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The straight dope on cholesterol – Part IX

The straight dope on cholesterol – Part IX
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Previously, across 8 parts of this series we’ve laid the groundwork to ask perhaps the most important question of all:

What should you eat to have the greatest chance of delaying the arrival of cardiovascular disease?

Before we get there, since this series has been longer and more detailed than any of us may have wanted, it is probably worth reviewing the summary points from the previous posts in this series (or you can just skip this and jump to the meat of this post).

What we’ve learned so far

  1. Cholesterol is “just” another fancy organic molecule in our body but with an interesting distinction: we eat it, we make it, we store it, and we excrete it – all in different amounts.
  2. The pool of cholesterol in our body is essential for life.  No cholesterol = no life.
  3. Cholesterol exists in 2 formsunesterified or “free” (UC) and esterified (CE) – and the form determines if we can absorb it or not, or store it or not (among other things).
  4. Much of the cholesterol we eat is in the form of CE. It is not absorbed and is excreted by our gut (i.e., leaves our body in stool). The reason this occurs is that CE not only has to be de-esterified, but it competes for absorption with the vastly larger amounts of UC supplied by the biliary route.
  5. Re-absorption of the cholesterol we synthesize in our body (i.e., endogenous produced cholesterol) is the dominant source of the cholesterol in our body. That is, most of the cholesterol in our body was made by our body.
  6. The process of regulating cholesterol is very complex and multifaceted with multiple layers of control.  I’ve only touched on the absorption side, but the synthesis side is also complex and highly regulated. You will discover that synthesis and absorption are very interrelated.
  7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion.  Anyone who tells you different is, at best, ignorant of this topic.  At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up.  To see an important reference on this topic, please look here.
  8. Cholesterol and triglycerides are not soluble in plasma (i.e., they can’t dissolve in water) and are therefore said to be hydrophobic.
  9. To be carried anywhere in our body, say from your liver to your coronary artery, they need to be carried by a special protein-wrapped transport vessel called a lipoprotein.
  10. As these “ships” called lipoproteins leave the liver they undergo a process of maturation where they shed much of their triglyceride “cargo” in the form of free fatty acid, and doing so makes them smaller and richer in cholesterol.
  11. Special proteins, apoproteins, play an important role in moving lipoproteins around the body and facilitating their interactions with other cells.  The most important of these are the apoB class, residing on VLDL, IDL, and LDL particles, and the apoA-I class, residing for the most part on the HDL particles.
  12. Cholesterol transport in plasma occurs in both directions, from the liver and small intestine towards the periphery and back to the liver and small intestine (the “gut”).
  13. The major function of the apoB-containing particles is to traffic energy (triglycerides) to muscles and phospholipids to all cells. Their cholesterol is trafficked back to the liver. The apoA-I containing particles traffic cholesterol to steroidogenic tissues, adipocytes (a storage organ for cholesterol ester) and ultimately back to the liver, gut, or steroidogenic tissue.
  14. All lipoproteins are part of the human lipid transportation system and work harmoniously together to efficiently traffic lipids. As you are probably starting to appreciate, the trafficking pattern is highly complex and the lipoproteins constantly exchange their core and surface lipids.
  15. The measurement of cholesterol has undergone a dramatic evolution over the past 70 years with technology at the heart of the advance.
  16. Currently, most people in the United States (and the world for that matter) undergo a “standard” lipid panel, which only directly measures TC, TG, and HDL-C.  LDL-C is measured or most often estimated.
  17. More advanced cholesterol measuring tests do exist to directly measure LDL-C (though none are standardized), along with the cholesterol content of other lipoproteins (e.g., VLDL, IDL) or lipoprotein subparticles.
  18. The most frequently used and guideline-recommended test that can count the number of LDL particles is either apolipoprotein B or LDL-P NMR, which is part of the NMR LipoProfile.  NMR can also measure the size of LDL and other lipoprotein particles, which is valuable for predicting insulin resistance in drug naïve patients, before changes are noted in glucose or insulin levels.
  19. The progression from a completely normal artery to a “clogged” or atherosclerotic one follows a very clear path: an apoB containing particle gets past the endothelial layer into the subendothelial space, the particle and its cholesterol content is retained, immune cells arrive, an inflammatory response ensues “fixing” the apoB containing particles in place AND making more space for more of them.
  20. While inflammation plays a key role in this process, it’s the penetration of the endothelium and retention within the endothelium that drive the process.
  21. The most common apoB containing lipoprotein in this process is certainly the LDL particle. However, Lp(a) and apoB containing lipoproteins play a role also, especially in the insulin resistant person.
  22. If you want to stop atherosclerosis, you must lower the LDL particle number. Period.
  23. At first glance it would seem that patients with smaller LDL particles are at greater risk for atherosclerosis than patients with large LDL particles, all things equal.
  24. “A particle is a particle is a particle.”  If you don’t know the number, you don’t know the risk.
  25. With respect to laboratory medicine, two markers that have a high correlation with a given outcome are concordant – they equally predict the same outcome. However, when the two tests do not correlate with each other they are said to be discordant.
  26. LDL-P (or apoB) is the best predictor of adverse cardiac events, which has been documented repeatedly in every major cardiovascular risk study.
  27. LDL-C is only a good predictor of adverse cardiac events when it is concordant with LDL-P; otherwise it is a poor predictor of risk.
  28. There is no way of determining which individual patient may have discordant LDL-C and LDL-P without measuring both markers.
  29. Discordance between LDL-C and LDL-P is even greater in populations with metabolic syndrome, including patients with diabetes.  Given the ubiquity of these conditions in the U.S. population, and the special risk such patients carry for cardiovascular disease, it is difficult to justify use of LDL-C, HDL-C, and TG alone for risk stratification in all but the most select patients.
  30. To address this question, however, one must look at changes in cardiovascular events or direct markers of atherosclerosis (e.g., IMT) while holding LDL-P constant and then again holding LDL size constant.  Only when you do this can you see that the relationship between size and event vanishes.  The only thing that matters is the number of LDL particles – large, small, or mixed.
  31. HDL-C and HDL-P are not measuring the same thing, just as LDL-C and LDL-P are not.
  32. Secondary to the total HDL-P, all things equal it seems smaller HDL particles are more protective than large ones.
  33. As HDL-C levels rise, most often it is driven by a disproportionate rise in HDL size, not HDL-P.
  34. In the trials which were designed to prove that a drug that raised HDL-C would provide a reduction in cardiovascular events, no benefit occurred:  estrogen studies (HERS, WHI), fibrate studies (FIELD, ACCORD), niacin studies, and CETP inhibition studies (dalcetrapib and torcetrapib).  But, this says nothing of what happens when you raise HDL-P.
  35. Don’t believe the hype: HDL is important, and more HDL particles are better than few. But, raising HDL-C with a drug isn’t going to fix the problem. Making this even more complex is that HDL functionality is likely as important, or even more important, than HDL-P, but no such tests exist to “measure” this.

Did you say “delay?”

That’s right. The question posed above did not ask how one could “prevent” or eliminate the risk cardiovascular disease, it asked how one could “delay” it.  There is a difference.  To appreciate this distinction, it’s worth reading this recent publication by Allan Sniderman and colleagues.  Allan sent me a copy of this paper ahead of publication a few months ago in response to a question I had posed to him over lunch one day.  I asked,

“Allan, who has a greater 5-year risk for cardiovascular disease, a 25 year-old with a LDL-P/apoB in the 99th percentile or a 75-year-old with a LDL-P/apoB in the 5th percentile?”

The paper Allan wrote is noteworthy for at least 2 reasons:

  1. It’s an excellent reminder that age is a paramount risk factor for cardiovascular disease.
  2. It provides a much better (causal) model for atherosclerosis than the typical age-driven models, and explains why age is an important risk factor.

What do I mean by this?  Most risk calculators (e.g., Framingham) take their inputs (e.g., age, gender, LDL-C, HDL-C, smoking, diabetes, blood pressure) and calculate a 10-year risk score.  If you’ve ever played with these models you’ll quickly see that age drives risk more than any other input.  But why?  Is there something inherently “risky” about being older?

Sniderman and many others would argue (and I agree) that the reason age is a strong predictor of risk has to do with exposure to apoB particles — LDL, Lp(a), and apoB-carrying remnants. Maybe it’s because I’m a math geek, but such models just seem intuitive to me because I think of most things in life in terms of calculus, especially integrals, the “area under a curve.”

[I once tried to explain to a girlfriend who thought I wasn’t spending enough time with her that my interest in her should be thought of in terms of the area under the curve, rather than any single point in time.  That is, think in terms of the integral function, not the point-in-time function.  Needless to say, she broke up with me on the spot (in the middle of a parking lot!), despite me drawing a very cool picture illustrating the difference, which I’ve re-created, below.]

Integral

The reason age is such a big driver of risk is that the longer your artery walls are exposed to the insult of apoB particles, the more likely they are to be damaged, for all the reasons we covered in Part IV of this series.  [This paper also reviews the clinical situation of PCSK9 mutations which builds a very compelling case for the causal model of apoB particles in the development of atherosclerosis].

What does eating have to do with cardiovascular risk?

So now that everyone is on the edge of their seat in anticipation of this punch-line, let me provide two important caveats.

First, there are no long-term studies – either in primary or secondary prevention – examining the exact question we all want to know the answer to with respect to the role of dietary intervention on cardiovascular disease.  There are short-term studies, some of which I will highlight, which look at proxies for cardiovascular disease, but all of the long-term studies (looking at secondary prevention), are either drug studies or multiple intervention studies (e.g., cholesterol-lowering drug(s) + blood pressure reducing drug(s) + dietary intervention + exercise + …).

In other words, the “dream” study has not been done and won’t be done for a long time.  The “dream” study would follow 2 randomized groups for many years and only make one change between the groups.  Group 1 would consume a standard American diet and group 2 would consume a very-low carbohydrate diet.  Furthermore, compliance within each group would be excellent (many ways to ensure this, but none of them are inexpensive – part of why this has not been done) and the study would be powered to detect “hard outcomes” (e.g., death), instead of just “soft outcomes” (e.g., changes in apoB, LDL-C, LDL-P, TG).

Second, everything we have learned to date on the risk relationship between cardiovascular disease and risk markers is predicated on the assumption that a risk maker of level X in a person on diet A is the same as it would be for a person on diet B.

Since virtually all of the thousands of subjects who have made up the dozens of studies that form the basis for our understanding on this topic were consuming some variant of the “standard American diet” (i.e., high-carb), it is quite possible that what we know about risk stratification is that this population is not entirely fit for extrapolation to a population on a radically different diet (e.g., a very-low carbohydrate diet or a ketogenic diet).  Many of you have asked about this, and my comments have always been the same.  It is entirely plausible that an elevated level of LDL-P or apoB in someone consuming a high-carb diet portends a greater risk than someone on a ketogenic or low-carb diet.  There are many reasons why this might be the case, and there are many folks who have made compelling arguments for this hypothesis.

But we can’t forget the words of Thomas Henry Huxley, who said, “The great tragedy of science is the slaying of a beautiful hypothesis by an ugly fact.”  Science is full of beautiful hypothesis slayed by ugly facts. Only time will tell if this hypothesis ends up in that same graveyard, or changes the way we think about lipoproteins and atherosclerosis.

The role of sugar in cardiovascular disease

Let’s start with what we know, then fill in the connections, with the goal of creating an eating strategy for those most interested in delaying the onset of cardiovascular disease.

There are several short-term studies that have carefully examined the impact of sugar, specifically, on cardiovascular risk markers.  Let’s examine one of them closely.  In 2011 Peter Havel and colleagues published a study titled Consumption of fructose and HFCS increases postprandial triglycerides, LDL-C, and apoB in young men and women. If you don’t have access to this journal, you can read the study here in pre-publication form.  This was a randomized trial with 3 parallel arms (no cross-over).  The 3 groups consumed an isocaloric diet (to individual baseline characteristics) consisting of 55% carbohydrate, 15% protein, and 30% fat.  The difference between the 3 groups was in the form of their carbohydrates.

Group 1: received 25% of their total energy in the form of glucose

Group 2: received 25% of their total energy in the form of fructose

Group 3: received 25% of their total energy in the form of high fructose corn syrup (55% fructose, 45% glucose)

The intervention was relatively short, consisting of both an inpatient and outpatient period, and is described in the methodology section.

Keep in mind, 25% of total energy in the form of sugar is not as extreme as you might think.  For a person consuming 2,400 kcal/day this amounts to about 120 pounds/year of sugar, which is slightly below the average consumption of annual sugar in the United States.  In that sense, the subjects in Group 3 can be viewed as the “control” for the U.S. population, and Group 1 can be viewed as an intervention group for what happens when you do nothing more in your diet than remove sugar, which was the first dietary intervention I made in 2009.

Despite the short duration of this study and the relatively small number of subjects (16 per group), the differences brought on by the interventions were significant.  The figure below shows the changes in serum triglycerides via 3 different ways of measuring them.  Figure A shows the difference in 24-hour total levels (i.e., the area under the curve for serial measurements – hey, there’s our integral function again!).  Figure B shows late evening (post-prandial) differences.  Figure C shows the overall change in fasting triglyceride level from baseline (where sugar intake was limited for 2 weeks and carbohydrate consumption consisted only of complex carbohydrates).

impact on TG

The differences were striking.  The group that had all fructose and HFCS removed from their diet, despite still ingesting 55% of their total intake in the form of non-sugar carbohydrates, experienced a decline in total TG (Figure A, which represents the daily integral of plasma TG levels, or AUC).  However, that same group experienced the greatest increase in fasting TG levels (Figure C).  Post-prandial TG levels were elevated in all groups, but significantly higher in the fructose and HFCS groups (Figure B).  The question this begs, of course, is which of these measurements is most predictive of risk?

Historically, fasting levels of TG are used as the basis of risk profiling (Figure C), and according to this metric glucose consumption appears even worse than fructose or HFCS.  However, recent evidence suggests that post-prandial levels of TG (Figure B) are a more accurate way to assess atherosclerotic risk, as seen here, here, and here.  One question I have is why did the AUC calculations in Figure A show a reduction in plasma TG level for the glucose group?

The figure below summarizes the differences in LDL-C, non-HDL-C, apoB, and apoB/apoA-I.

impact on lipoproteins

Again, the results were unmistakable with respect to the impact of fructose and HFCS on lipoproteins, and by extension, the relative lack of harm brought on by glucose in isolation.  [Of course, removal of glucose and fructose/HFCS would have been a very interesting control group.]

One of the simultaneous strengths and weaknesses of this study was the heterogeneity of its subjects, who ranged in BMI from 18 to 35, in age from18 to 40, and in gender.  While this provided at least one interesting example of age-related differences in carbohydrate metabolism (older subjects had a greater increase in triglycerides in response to glucose than younger subjects), it may have actually diluted the results.  There were also significant differences between genders in the glucose group.

What was most interesting about this study was the clear difference between the 3 groups that was not solely a function of fructose load.  In other words, the best outcome from a disease risk standpoint was in the glucose group, while the worst outcome was not in the all-fructose group, but in the 50/50 (technically 55/45) mixed group.  This is a very powerful indication that while glucose and fructose alone can be deleterious in excess, their combination seems synergistically bad.

The role of saturated fat in cardiovascular disease

In the next week or two I’ll be posting an hour-long comprehensive lecture I gave at UCSD a few weeks ago on this exact topic. Rather than repeat any of it here, I’ll highlight one study that I did not include in that lecture.  The study, Effect of a high saturated fat and no-starch diet on serum lipid subfractions in patients with documented atherosclerotic cardiovascular disease, published in 2003, treated 23 obese patients (average BMI 39) with known cardiovascular disease (status post coronary artery bypass surgery and/or stent placement) with a high-fat ketogenic diet.  Because the study was free-living and relied on self-reporting, not all subjects had documented levels of elevated serum B-OHB. However, the subjects were instructed to avoid starch and consume 50% of their caloric intake via saturated fat, primarily in the form of red meat and cheese. There were no restrictions on fruits and vegetables, which may have accounted for the observation that not all subjects were ketotic during the 6-week intervention.  In total, only 5 of the 23 patients achieved documented ketosis.

All of the subjects were on statins and entered the study at a goal LDL-C level target of 100 mg/dL, which may have been the only way the authors could get the IRB to approve such a study.

The table below shows the changes in lipoprotein fractions following the intervention (there was no control group):

Table 2

This study was conducted during the height of the “outcry” over the Atkins diet.  While most doctors reluctantly agreed that Dr. Atkins’ diet could reduce body fat, most believed it was still very dangerous.  In the words of Dean Ornish, “Sure you can lose weight on a low-carb diet, but you can also lose weight on heroin and no one would recommend that!”

Fair point.  In fact, the authors of this study acknowledged that they “strongly expected” this dietary intervention to increase risk for cardiovascular disease, which is why they only included subjects on statins with low LDL-C.  However, as you can see from the table above, the authors were startled by the results.  The subjects experienced a significant reduction in plasma triglycerides and VLDL triglycerides, without an increase in LDL-C or LDL-P.  In fact, LDL size and HDL size increased and VLDL size decreased – all signs of improved insulin resistance.  Furthermore, fasting glucose and insulin levels also decreased significantly.   The mean HOMA-IR was reduced from 5.6 to 3.6 (normal is 1.0) and TG/HDL-C from 3.3 to 2.0 (normal is considered below 3, but “ideal” is probably below 1.0) in just 6 weeks.  Taken together, these changes, combined with the dramatic change in VLDL size, suggest insulin resistance was dramatically improved while consuming a diet of 50% saturated fat!

As all of these patients were taking statins, we’re really robbed of seeing the impact of this diet on LDL-P, which did not change.  Also, CRP levels rose (though not clinically or statistically significantly).

Putting it all together

It is very difficult to make the case that when carbohydrates in general, and sugars in particular, are removed or greatly reduced in the diet, insulin resistance is not improved, even in the presence of high amounts of saturated fats.  When insulin resistance improves (i.e., as we become more insulin sensitive), we are less likely to have the signs and symptoms of metabolic syndrome.  As we meet fewer criteria of metabolic syndrome, our risk of not only heart disease, but also stroke, cancer, diabetes, and Alzheimer’s disease goes down.

Furthermore, as this study on the Framingham cohort showed us, the more criteria you have along the spectrum of metabolic syndrome, the more difficult it becomes to predict your risk, due to a widening gap in discordant risk markers, as shown in this figure.

LDL-C vs. LDL-P in MS

As I noted at the outset, the “dream” trial has not yet been done, though we (NuSI) plan to change that. Until then each of us has to make a decision several times every day about what we will and won’t put in our mouths.  Much of this blog is dedicated to underscoring the impact of carbohydrate reduction on insulin resistance and metabolic syndrome.

The results of the trials to date, combined with a nuanced understanding of the lipoprotein physiology and their role on the atherosclerotic disease process, bring us to the following conclusions:

  1. The consumption of sugar (sucrose, high fructose corn syrup) increases plasma levels of triglycerides, VLDL and apoB, and reduces plasma levels of HDL-C and apoA-I.
  2. The removal of sugar reverses each of these.
  3. The consumption of fructose alone, though likely in dose-dependent fashion, has a similar, though perhaps less harmful, impact as that of fructose and glucose combined (i.e., sugar).
  4. The addition of fat, in the absence of sugar and starch, does not raise serum triglycerides or other biomarkers of cardiovascular disease.
  5. The higher the level of serum triglycerides, the greater the likelihood of discordance between LDL-C and LDL-P (and apoB).
  6. The greater the number (from 0 to 5) of inclusion criteria for metabolic syndrome, the greater the likelihood of discordance between LDL-C and LDL-P (and apoB).

I would like to address one additional topic in this series before wrapping it up – the role of pharmacologic intervention in the treatment and prevention of atherosclerotic disease, so please hold off on questions pertaining to this topic for now.

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About the Author:

Peter Attia, M.D., is the co-founder and President of the Nutrition Science Initiative (NuSI), a non-profit based in San Diego, CA. He received his B.Sc. from Queen's University in Canada and his M.D. from Stanford Medical School in California. After his surgical residency in general surgery at Johns Hopkins he worked as a consultant at McKinsey & Company. He founded NuSI with scientific journalist Gary Taubes in 2012.

Discussion

  1. David Nelsen  July 12, 2012

    Peter, another excellent post. I don’t think anyone was on the edge of their seats with regard to the outcome, but it was good for the train to get to the station. I have been low carbing for about 6 months and although I know it is the best for my long term health, I really miss some of my favorite old foods. I read forums like yours to keep on the straight and narrow as they say.

    Maybe Ornish is on to something – a diet trial of Heroin users vs. Low Carb – winner take all!!! As to you old ex girlfriend that story reminded me of an Agatha Christie quote – “The best husband a woman can have is an Archaeologist – the older she gets the more interested he is in her”.

    (reply)
    • Peter Attia  July 12, 2012

      I love the idea of the diet trial: Heroin (and NO food at all) vs. ultra-low fat vs. ultra-low carb…

    • david  April 2, 2014

      All other things being equal (if such were possible), I understand that controlled and sanitary heroin increases life span. Who knows?

      What we do know is that legal drugs kill more Americans than illegal drugs. And that prescription drugs are the 4th leading cause of death in the US.

  2. Pierre Legrand  July 12, 2012

    Peter great post as usual. Is being keto adapted an either or situation or more along the lines of once you are keto adapted you can drift in and out of burning fat depending on your carb intake?

    (reply)
    • Peter Attia  July 12, 2012

      It really seems to be a pretty distinct metabolic state, primarily in terms of providing the brain with enough B-OHB to offset the reduction in circulating glucose levels.

  3. Ash Simmonds  July 12, 2012

    The bottle of gin in that bag looks weird.

    (reply)
  4. Raymund Edwards  July 12, 2012

    New to your blog Peter. Just marvelous work, thank you.

    I wonder if you have seen this fellows work and also where Vitamin D might fit in the picture ?

    Dr. Gerhard Spiteller ==>

    http://www.ncbi.nlm.nih.gov/pubmed/16843819

    http://www.ncbi.nlm.nih.gov/pubmed/20230283

    http://www.ncbi.nlm.nih.gov/pubmed/11976183

    http://www.ncbi.nlm.nih.gov/pubmed/16270286

    (reply)
    • Peter Attia  July 12, 2012

      Raymund, I’ll be doing a (mini) series or at least a post or two in Vitamin D in the future.

  5. Sean  July 12, 2012

    Peter, do you think a low-carbohydrate diet becomes more effective (i.e., exponential) at reducing risk-factors the longer someone adheres to the diet or is the reduction fairly linear over the entire duration? If it’s the former, then a long-term study might be even more revealing about the potency of a low-carb diet for reducing CVD risk-factors. As you mentioned in this article, there’s yet to be any long-term clinical studies on a low-carb diet, but based on your own practice and observations from your colleagues (such as Dr. Dayspring’s patients), what is your take on this?

    (reply)
    • Peter Attia  July 13, 2012

      My intuition says it probably depends on where one is starting form in terms of risk. Quicker plateaus for those starting with less risk, or those starting later in life. All speculation.

  6. Jeff Johnson  July 12, 2012

    I’m listening to Lana Del Rey sing “Blue Jeans” as I compose this – Jesus – she’s something else – in a good way -

    Anyway – back to reality – here’s my lipid results from last week -

    TC – 165
    LDL – 104
    HDL – 51
    TG – 54
    VLDL – 11
    NON – HDL – 114
    Apo – B – 76 (Particle Count about 850)
    Apo – A1 – 127

    I was a little bit dissapointed my Apo – B wasn’t lower And my Apo – A1 wasn’t a little higher -

    (reply)
    • Peter Attia  July 12, 2012

      I don’t think anyone could complain with those numbers.

    • D. M. Mitchell  September 1, 2012

      Aren’t there studies showing that higher cholesterol in older people is more protective than low cholesterol and that people, especially senior citizens, with very low cholesterol number tend to die at a higher rate for all causes, include suicide. (Too low cholesterol is bad for the brain. Certain violent criminals have been found to have very low cholesterol.)

    • Peter Attia  September 1, 2012

      It’s certainly true and well documented that people with very low cholesterol die sooner than those with “normal” cholesterol, though not of coronary heart disease. Combine this with the also-documented fact that folks with very high cholesterol (e.g., FH) actually have protection from other causes of death, such as infection. This body of literature suggests three things I subscribe to:
      1. Cholesterol is vital for life! Very low levels probably lead to reduced immune function, among other things.
      2. The lower the cholesterol (really, the lower the level of LDL particles) the less your cardiac risk.
      3. It’s a balancing act — too much or too little is associated with a shorter life.

    • Craig  April 18, 2013

      In men , the U shaped curve is true according to the Framingham study, but what about women where the curve is flat and if anything, the higher the cholesterol the better the survival rate?

  7. Nils  July 12, 2012

    Great post as always, thanks.

    However, I do think you might have overlooked one critical aspect of diet. The conversion of fructose to triglycerides is generally very low (<10%), however, when fructose (and this goes for carbohydrates in general) is provided as calories in excess, that is when triglyceride levels really start ramping up. So while I agree that fructose, and other carbohydrates can shift 'cholesterol' to VLDL and small LDL, I do think it is important to emphasize that in hypocaloric conditions the effects really are not so disastrous (take for example the Kitavas of Papua New Guinea who have undetectable incidence of heart disease, yet eat a considerable amount of carbohydrates 70% of total intake).

    I'm very interested in your take on this, and on your take on statins in the next post. Sincerely, Nils

    (reply)
    • Peter Attia  July 12, 2012

      The conversion has a lot to do with not just caloric load, but also glycogen storage capacity. At the end of a marathon, if someone has virtually no liver glycogen remaining, even a pretty large does of fructose will preferentially be converted to glycogen over TG/VLDL. However, modest doses of fructose in the presence of largely full glycogen reverse causes the reverse. So, yes the issues is load and glycogen capacity dependent. But remember — how many folks are running marathons AND limiting their fructose consumption to just the amount necessary to re-fill (hepatic, not muscle) glycogen stores?

    • Nils  July 12, 2012

      Thanks for the answer, I do however believe you are overestimating fructose to TG conversion in humans. While in many animals (rats, hamsters etc) the conversion is very great. In humans the picture is definitely somewhat different (again, assuming hypo or iso caloric conditions).

      http://physrev.physiology.org/content/90/1/23.long

      Showed that about 50% of fructose is converted to glucose, 25% to lactate, some to liver glycogen stores and then some is oxidized on the spot and the remainder is converted to TG. This might also explain why sucrose and HFCS work synergistically, as fructose intake in addition to glucose might push the conversion more to TG.

    • Salim Morgan  November 20, 2013

      Yeah, but the Kitavans:

      1) Eat very little fructose
      2) Their fat, while a small portion of calories are nearly all saturated and about zero Omega-6
      3) They eat ONCE A DAY

      Their “carbs” are almost entirely glucose-producing starches. It fits everything in this post.

  8. TheFatNurse  July 12, 2012

    Wow that 2003 study is very interesting Dr. Attia. With this post on carbohydrates, saturated fat and insulin resistance…I was wondering what your opinion was on the ADA diet which is low saturated fat (less than 7%) and high in whole grain carbohydrates with diabetics.

    Additionally, your last post on HDL motivated me to look up Dr. Dayspring’s lecture on it and make another comic if you’re interested! http://thefatnurse.wordpress.com/2012/07/05/hdl-for-all-ages/

    (reply)
    • Peter Attia  July 12, 2012

      Next week I’ll be posting a talk I gave on saturated fat. By the end of that 55 minute talk you’ll know exactly where I stand on the ADA recommendation of <7% SFA! Promise!

  9. jw  July 12, 2012

    I guess that Sniderman’s paper dovetails nicely with the Paleo theory. For the last 99,900 years, if your heart made it to 50 (assuming you made it to 15 or 20 first, that was the trick), it had done its job and the rest was gravy (I crack myself up sometimes…).

    In order to maintain a heart that was not designed to overcome the “advantages” of modernity, we need to either apply technology (statins) or revert to a pre-modern diet.

    (reply)
    • Peter Attia  July 12, 2012

      I think that is a logical extrapolation.

    • Henk Poley  July 13, 2012

      Reminds me of the research by Geoffrey B. West on invariances between organisms.

      http://www.darkcoding.net/research/gbwscl99.pdf

      At a heart rate of 75bpm and the invariant of 1.5e9 beats per lifetime that puts the expected human lifespan at 38 years. Apparently we are doing sometime right that we live about double that amount nowadays.

  10. fashion trends  July 12, 2012

    Peter Attia..You have written very good post.I just came a cross here and found so interesting discussion here.Love your blog and especially your for effort .You are doing excellent work.Have a great regards for your awesome and adorable work

    (reply)
  11. Vasco Névoa  July 12, 2012

    Beautiful write-up, Peter. Again a very pertinent choice of proof and fool-proof reasoning as far as I can see. :) Thank you for the effort.

    Your question: “One question I have is why did the AUC calculations in Figure A show a reduction in plasma TG level for the glucose group?”
    My answer: because the liver mainly needs to convert non-glucose to TG; I bet that the extra dietary glucose went straight into blood sugar, bypassing TG transport.

    The take-away points, for me, are:
    From the first study:
    - Fructose and glucose/fructose combination make our metabolic system spike intensely between post-prandial and fasting levels. This, in itself, may be a very important key in the development of the disease – aggressive serum peaks in TG, BG, Insulin, and LDL may very well cause more damage than an elevated continuous base / fasting level. High glicated hemoglobin along low fasting BG in certain subjects I know comes to mind. The damage may actually be coming primarily from the prandial spikes, and not from the area under the curve. Sorry, I don’t mean to contradict you, it just comes out naturally. ;)
    - Glucose is not that bad, in fact our metabolic system seems to regulate it very well along time, preventing extreme highs and lows. I like it that fasting TG is more levelled when feeding on glucose, it shows that the system behaves well in this situation. But you’ve made no comment about blood glucose, and I dare say that the subjects in group 1, although they have lower TG they will have higher BG (including post-prandial spikes) and this will cause higher oxidative stress and AGE production. So I’m not that sure they are so better off. Total reduction of sugars (glucose sources included) is probably better than just fructose reduction.

    Regarding the second study.
    - Partial confirmation of my personal anecdote that LDL does not increase visibly with saturated fat consumption (I’m not on any meds). However, my HDL went up and CRP and Homocistein went down, whereas theirs didn’t. Ignoring for a moment my personal difference, is it possible that their free consumption of sugary fruit interacted with the high fat and caused a little extra inflammation? Again, the best course of action seems to be radical elimination of all sugar sources.
    - Improved IR with sat fat. Vindication of the “a calorie is not a calorie” mantra. :)

    Keep’em coming, the party is just starting! :D

    (reply)
  12. geo  July 12, 2012

    To further Pierre’s great question. Assuming the standard state of ketosis is 80-65 mg/dl, if someone is fluctuating between 75 and 100 mg/dl on the ketone monitor within any given day, could it be problematic switching between ketones and glucose fuel? Let’s say someone tests 3 times a day to test what amounts of foods are causing them to spike glucose.

    (reply)
  13. Pierre Legrand  July 12, 2012

    Peter, thank you for the response.

    Do we know whether a person needs to stay within a range of .5 to 3.mmol in order to avoid going through induction again? My intepretation of induction is training the body to use ketones as an energy source. Or is it a period of time a person remains less .01 mmol that breaks his bodies ability to burn ketones and causes there to be a need to go back to induction?

    Thank you for any light you can shed.

    (reply)
    • Peter Attia  July 12, 2012

      Not sure what you mean by induction. Do you mean transition? I know the term “induction” is used in the Atkins diet to refer to a period of initial ketosis before transitioning to low-carb-non-ketosis.

      When you’re out due to “dietary violation” it can take between 1 and 5 days to get back in.

    • Pierre Legrand  July 12, 2012

      Sorry Peter, I wasn’t clear about induction. In Atkins there is a period of time called induction where you must eat less than 20g of carbs in order to train your body to use ketones. Thank you for interpreting what I said and still answering my question!

  14. JohnJ  July 12, 2012

    Good comment of cardiologist Dr. William Davis on diet and treatment Apo E4;

    http://www.wheatbellyblog.com/2011/07/who-is-dr-william-davis/comment-page-6/#comment-12342

    First, no need to panic. Apo E4, even in homozygotes (2 “doses” of the gene), is highly variable. It is not an all or none situation.

    My approach is a bit different than what is generally preached. I say prioritize all the metabolic parameters and clean them up, one by one. I advocate undergoing lipoprotein testing, e.g. NMR lipoprotein testing, as well as other metabolic markers, such as HbA1c, glucose, insulin, vitamin D.

    You are likely to find that you have a lot of small as well as large LDL particles. The small come from carbohydrates and excess weight. The large come from fat consumption. Prioritize: Tackle the small LDL particles first by cutting carbohydrates, then ratchet fat intake back to reduce the excess of large LDL particles.

    Also, my forum on the http://www.trackyourplaque.com website provides discussions of such more complicated issues, if you are interested in pursuing.

    (reply)
  15. John Pane  July 12, 2012

    By “all signs of improved insulin resistance”, do you mean, “all signs of reduced insulin resistance”?

    (reply)
    • Peter Attia  July 12, 2012

      Yes, by improving IR, I mean reducing it or become more IS.

  16. Mark Breckenridge  July 12, 2012

    are you/we/anyone at the point to say its not safe to eat even lots of complex carbs like fruit and potatoes every day? I’d really like to tell my Fruitarian friend that its NOT healthly to eat 5lbs of fruit every day.

    (reply)
    • Peter Attia  July 12, 2012

      Look at how much fructose they are eating. This makes a very powerful case for even a fraction of that amount being troublesome.

    • Vasco Névoa  July 12, 2012

      Mark,
      I’m at the point of saying that Steve Jobs committed premeditated suicide by ingesting nothing other than fruit and carrots for 32 years. It is pretty clear to me that such a behaviour would most probably result in metabolic organ failure sooner or later. His pancreas and his liver just gave out. I think that the thing that made him last 3 decades on this diet instead of just 2 is the fact that he insisted a lot in “purging” himself with meditation and fasting. While meditation is more or less proven to reduce stress factors, fasting is also proven to recycle cellular material through autophagy. I bet that if he didn’t do those things, he would have died about a decade earlier. Frutarianism just isn’t biologically sustainable for a human being in the long term, IMHO.

  17. steve  July 12, 2012

    I have to say that the whole series has been brilliant and moreover educational to all who have taken the time to read it. Regarding dietary recommendations, it seems to me that if your LDL-P and HDL-P(to lesser extent) is at goal for your age and risk factors( do you have CAD,family history,etc) then the amount of carbs in the diet may not matter. Do you agree? If not why not, since the issue of artery damage is related to penetration of the wall by the particles, so the lower the particle level the better.
    In my own case, I produce abnormally high particles whether i low carb or high carb. Only with meds(Crestor and Zetia) can I get LDL-P to goal(despite having a low TRG-75 on high carb and low LDL-C-73 without meds). What i do see if go zero starch and sugar on meds is that I virtually eliminate( <90) small LDL-P with some size increase, but no difference in total amount of LDL-P. So if size does not matter, it would appear to me that I can eat some level of carbs( berries, potatoes and rice only), based on this series, but Dr Krauss and Davis seem to think otherwise: they think small LDL is worse unlike Dr.Dayspring. Would be nice to have a debate among the titans. At nearly 62, I want to be as precise as possible. Thanks again for your great work!

    (reply)
    • Peter Attia  July 13, 2012

      Don’t forget, of course, mitigating disease risk is but one (albeit) important outcome of improving your nutrition. Don’t forget about body composition, athletic performance, energy levels, mental acuity.

  18. steve  July 12, 2012

    One other comment: The effect of sat fat no starch diet study you reference does not do one important thing: it does not address whether CAD progression slowed or stopped in these patients. That is more important than any bio-marker. To really know one would need to do calcium score on these people or better yet IVUS which would show the health of the arteries and any narrowing of the lumen.

    (reply)
    • Peter Attia  July 12, 2012

      It did not address that, but other studies have showed us that non-pharmacologic interventions can *reverse* atherosclerosis. Unfortunately, the interventions were too numerous to identify which ones. I wrote about this study in Lancet in my Weight Watchers post.

  19. Edward  July 12, 2012

    “In the words of Dean Ornish, ‘Sure you can lose weight on a low-carb diet, but you can also lose weight on heroin and no one would recommend that!’” “Fair point.”

    Not even remotely a fair point. This is just a logical fallacy called “Appeal to fear.” We are afraid of heroin, so we should be afraid of low-carb even though there is no relationship between heroin consumption and low-carb diets.

    (reply)
    • Peter Attia  July 12, 2012

      Point taken…I try to bend over sometimes to give my antagonists the benefit of the doubt. Thanks for keeping me honest.

    • David Nelsen  July 12, 2012

      Edward, I have eaten low carb on and off for a few years. In the early days I felt that it was a great tool to lose weight but that I might be doing long term harm to my health. After doing a lot of reading (this blog included) I no longer think that is the case. It’s 180 degrees from that, the only way to improve my health long term is to eat low carb. Which to me is a pretty amazing set of circumstances.

      In 1995 I had a liver biopsy and they told me I had Steotosis of the liver (fatty liver). The only thing they told me to do was to not drink alcohol. I didn’t know then I could cure my issue by eating low carb. Since then this Internet thing has mushroomed and it’s a lot easier to find information. Unfortunately, a lot of it is BS. For any position on health you want to hold (almost) you can find someone somewhere who will support that view. It then comes down to who and what you want to believe. If it is T. Colin Campbell then you go Vegan and see how that does for you. In my case, I could never go without meat so that’s a non starter.

      As far as the Heroin diet, I would say Keith Richards would be the poster boy for that one. He has a good BMI, but that’s probably about it. I have a secret suspicion that he’s been dead for some time but that nobody bothered to tell him.

    • Stephen Quirke  May 25, 2013

      This would be a good place to be able to hit “Like”. There is so much hype around this topic, as if my diet has an impact on the lives of everyone else. It has the flavour of religious war. One of the reasons I am ploughing through the detail in these posts and responses is the general ‘even keel’ around here.

  20. tess  July 12, 2012

    “There were also significant differences between genders in the glucose group.”

    aw, c’mon, Doc! :-) you can’t drop a bomb like that and then not explain what it was (unless it’s in those little graphs and i missed it…).

    (reply)
    • Peter Attia  July 13, 2012

      Although there were no significant sugar-gender interactions for any of the primary or secondary outcomes, men exhibited larger increases of fasting TG, non-HDL-C, apoB, and sdLDL-C concentrations and postprandial LDL, non-HDL-C, and sdLDL-C concentrations in response to sugar consumption than women.

    • greensleeves  July 13, 2012

      Hi Tess:

      “There were also significant differences between genders in the glucose group.”

      What that means is that estrogen protects a woman’s heart & arteries until menopause. Then the free ride’s over.

    • Vasco Névoa  July 13, 2012

      That’s a very interesting subject and, I think, underexplored in the “paleo / LC blogosphere”.
      Several friends of mine started following my “paleo / primal” dietary advice (I point them to Gnolls.org and Mark’s Daily Apple for everyday advice), and for the most part with resounding success.
      The only exceptions: 2 women, one in her late 30s, another in her early 40s. They say that eating fat makes them fat, and cutting carbs did not yield visible weight loss. They do, however, report increased energy levels on low carb.
      Since all the men I know who have tried this get immediate positive results, I’m inclined to think that female metabolism is fundamentally different from male at some level, and should be looked into more carefully.
      Do you know of any low-carb blogs maintained by women?

    • Jennifer  July 23, 2012

      Vasco,
      Here is a blog “Paleo for Women: Evolutionary Health, Revolutionary Womanhood”
      http://www.paleoforwomen.com/blog/

  21. AWD  July 12, 2012

    How long after first attaining a ketotic state and maintaining it (say 30g or so of carbs a day) should it take for blood numbers to noticeably improve? Is there a transition time where the blood numbers will temporarily get worse? Blood numbers being taken from a standard lipid test. For example, LDL up, HDL down, triglycerides above 200?

    (reply)
    • Peter Attia  July 12, 2012

      Different for different folks, and highly dependent on the ketotic state and lots of other variables. Some people experience changes in 3 months, other 3 years.

    • jake3_14  July 12, 2012

      Chris Masterjohn, a lipid research and advocate of ancestral eating, advises waiting 6 months *after* your weight stabilizes (if you are, in fact, losing weight) before you get a lipid panel done. There are just too many factors that make lipid readings go out of the normal range during weight loss for a lab test to be considered useful, except in extreme cases. For example, during weight loss, it’s normal for LDL readings to go up for a number of months as your body increases the transport of fatty acids liberated from adipocytes to be used as fuel. While this goes on, urine-based ketone detection strips will likely show a decrease in the concentration of ketones, because they don’t detect the form of ketones (hydroxybutarate) that are most likely circulating in the bloodstream (and are well used by the brain). If you’re being pressured to get a lab test, push back and insist on at least a 90-day wating period, and preferably 6 months.

    • Peter Attia  July 12, 2012

      Correct. Many folks have suggested this. Typically, an improvement in TG and HDL-C will be seen before weight stabilization, though. This is possibly more the case for LDL.

    • AWD  July 13, 2012

      Thanks! This info is exactly what I was looking for. I have been pretty much in a constant ketotic state for a month or so. I just had a free blood test (simple lipid panel) at work. My LDL was up noticeably, my HDL was down noticeably (low 20s, it has been consistently about 40 or just under for years), and my triglycerides weren’t near as low as I thought they would be. I think they were low to mid 200s. I was expecting under 100. I thought triglycerides were pretty fast to respond to low-carb. Total cholesterol was over 300 for the first time ever. I am NOT worried, just trying to make sense of it. I’ll try and get checked again at my doctor’s office in 2-3 month and hopefully at least see some improvement in each of those even if it isn’t as improved as it will be. I workout pretty hard lifting heavy weights 4-5 times a week and I am 44 yrs old and male.

  22. Wayne  July 12, 2012

    Hi Peter

    I love your blog. It makes very complex subjects so much more accessible to the layperson such as myself. I have read through this series on cholesterol with great interest as I have recently had a lipid panel test and I was trying to interoperate the results. Convention states that the results are disastrous and my doctor will freak when I see him again. However, I’m not conventional and am not ready to panic yet, until I read the summary quote in part IV: “If you want to stop atherosclerosis, you must lower the LDL particle number: ” –

    Looking at my lipid panel my LDL is very high. Naturally I was concerned, even though I have no faith in the lipid hypothesis. Question I need to answer is should I worry or not about the figures? I have had a very low carb diet for the last 8 months and followed it with religious zeal thinking that it the best path to good health. I follow advice from this site and Mark’s Daily Apple. However, I was stunned when I got the results:

    GLUCOSE: 5.4mmol/dl (not sure of the conversion)
    TRIGLYCERIDES: 1.2 mmol/l (46mg/dl)
    CHOLESTEROL: 7.1 mmol/l (274mg/dl)
    HLD: 1.5 mmol/l (58mg/dl)
    LDL: 5.1 mmol/l (196mg/dl)

    Having followed a low carb diet with regular intense exercise, I cannot account for such a large LDL number. Reading these articles though has made me wonder if the numbers are worthless, but still feel I need to look into this further.

    (reply)
    • David Nelsen  July 12, 2012

      I’m not Peter, but if you’ve been paying attention you would know that he recommends getting the NMR Lipid profile from Liposcience. It’s all about the particles, so get the test done so you’ll know where your LDL-P is at. Since you’re reporting all your values in mmol/dl you may not be in the US so that test could be problematic.

    • jake3_14  July 12, 2012

      Wayne,

      Refer to my post above about odd LDL readings during weight loss. Another possibility to explain your results is one discussed at length by Paul Jaminet, author of the Perfect Health Diet. You might be in the population that needs more starch than a very low-carb diet, where carbs come only from vegetables, provides. He’s written a multi-part series of blog posts titled “Dangers of low-carb diets x” where x is a roman numeral, that is worth reading. If your lipid panel is still showing these types of results 6 months *after* your weight stabilizes (if you are, in fact losing weight), consider adding starches like sweet potatoes and white rice, to your diet, and see what happens.

    • Doc´s Opinion  July 16, 2012

      Wayne. You´re right. Total cholesterol and LDL-cholesterol levels are relatively high. I suppose you know this may be genetically determined. In such cases it may be very hard to lower total and LDL-cholesterol through diet. However, there are other things you should look at. TG/HDL ratio is low which is a positive thing. You will also have to look at other risk factors such as smoking, high blood pressure etc. If the elevated total and LDL cholesterol are your only risk factors I would not worry to much about it.

  23. Catherine  July 12, 2012

    Just to be philosophical for a moment, regarding age: If the number one cause of death is CVD, do *I* really want to be the one proselytizing “the truth” to relatives or friends, since the probabilty is good they will eventually die of CVD either way? (The truth being Statins / NNT dubious reality for most and HFLC is probably positive)
    As a scientist, you are in a totally different situation as you have an audience comprised of appreciative open individuals that are seeking the truth (and responsible for changing their own course if/when warranted)
    People need to realize the dynamics of trying too hard to convince family members of health decisions unless you want to be blamed when Uncle Billy kicks the bucket.

    (reply)
    • Catherine  July 12, 2012

      Much gratitude for the Cliff Notes! ….sure helps me

  24. Lea  July 12, 2012

    Peter,

    I find myself on all these blogs (including MDA) reading medical papers, reading books, watching documentaries on what we should be feeding our bodies. I have personally been Paleo/Primal for 3 months (wasn’t over weight to start, but in amazing shape now) in a bid to show my parents (one pre-diabetic, another type-2 diabetic) that it all starts and ends with food. I send them articles…give them cook books….lead those horses to water, but their doctors and nutritionists tell them opposing information like: “don’t eat eggs, and no oils”. I’m going crazy cause my parents think I’m the wacko. Why do these doctors continue to perpetuate nonsense?

    (reply)
    • Peter Attia  July 12, 2012

      I share your frustration. This is why we’re putting NuSI together to tackle this problem structurally and scientifically.

    • Vasco Névoa  July 13, 2012

      Peter, the more I research on cholesterol and atherosclerosis, the more different theories and variables I collect.
      I think it would be very useful and pertinent to gear the NuSI trial with as many measurements as possible, to avoid those bias pitfalls so common in the studies we criticize. I know it all comes down to having enough money, and usually this is the stopping point, but a study that collects enough information from individuals to compare the various disease theories (and not just confirm/unconfirm one of them) would do a lot more for the science than the usual single-minded design…
      For example, it should probably take into account all the measurable factors related to cholesterol both in synthesis, transport, and assimilation at the cells, as well as the oxidation factors. For example, by measuring Vitamin E, oxidized LDL, and a few genetic markers for LDL receptors, the trial would be able to prove/disprove Chris Masterjohn’s theories of arterial disease. I wish there was a study that encompassed enough measurements to cover ALL the main disease theories so that we could actually find the true correlation.
      Along with “hard” outcomes, of course.

  25. lorraine  July 12, 2012

    Death, yes, definitely a hard outcome. As a 50-something reader who’s well aware that age accounts for more and more of the variance of risk as we…well, age, I find myself reading studies and discussions of risk reduction with the following thought background: I wonder how the risk works in people (like moi) who have decades of consistent, multi-factorial risk reduction behaviors on their side. Concurrent to reading this post, I also viewed last night, Dr. Davis’ presentation at Lecturepad on RBC fatty acid status and CVD. I went to sleep thinking, a little bit of this, a little bit of that. So, while you can have great biomarkers within a year of implementing risk reduction behaviors, and you can have those same great biomarkers 20 years after implementing and maintaining those behaviors, it’s hard to tell from the biomarkers how much that risk has actually been reduced in you by implementing risk reduction over a long period of time as you age. By consistent behaviors I mean 15+ years of carb restriction (I was all over Protein Power and The Zone when they first came out), fish oil for a decade, 30 years of sane and consistent training effect after a very active childhood and athletic teens and 20′s, a good history of refreshing sleep, active stress management, meditation, high pleasure, and a little BHRT thrown in more recently for good measure. Is there a synergy that over time confers something that we will never be able to determine from examining discreteness? And maybe that even impacts what amount of the variance is accounted for by age?

    Well, that would be cool, but I think many of us may be here (in the field, looking at our family histories, reading research and blogs) because of that very personal awareness of the hard outcome. I know I sure am. The two families that make up my genetic heritage have fascinated me as they’ve aged; partly because they’re each so huge that I got to see what killed people and what didn’t. I’ve mentioned here before that my father had a beautiful lipid panel and ECG three months before he dropped dead of the big one at the age of 64 on the living room floor after an early spring round of golf and a bagel. My dad was the oldest son of an impoverished Irish immigrant family of 8 siblings. My grandfather died of a massive MI at 55; following multiple “smaller” heart attacks which he dealt with by cracking open a cold one and sitting it out in his rocking chair. Believe me, my father’s young death following his father’s younger death got the attention of two generations of *everybody* as it related to all of our family history risk. But, they were also both bad smokers with high stress and type A -reactive personalities. In spite of how truly awful this family’s diet was (your basic highly refined carb poverty diet which none of them ever really changed after leaving the family home), in the almost 20 years since my father’s death, the only other sibling to die was another smoker. The surviving siblings (6) now range in age from 68 to 86, with only one case of heart disease, which required angioplasty, and he too was a past smoker. My mother’s family has great longevity; another immigrant family of small means and 9 children, my mother being the youngest, now at age 80. This family distinguished itself for me by all the females being very interested in health and nutrition, and my grandfather having a huge garden. This grandmother died in her late 90′s. My grandfather in his 70′s from lung cancer, he was a smoker. The only siblings who have died are the three males, all from emphysema, all smokers. All the female siblings are alive, and we had a reunion just this week. They range in age from my mother at 80 through her oldest sister at 95. So, two large families with very different diets and different risk factors, and the only people who died on either side were the smokers. It’s my personal experiment of n=21, and the take home for me is don’t smoke and eat my vegetables! As each of these 17 people in my parents’ generation had the Catholic requisite pile of kids, my generation includes around 60 cousins, and it’ll be interesting to see what happens to all of us. I don’t think there are any smokers. I am hoping that the synergy of my long term risk reduction behaviors confers some beneficial epigenetic mojo on my own aging.
    Peter, I don’t know how many times we can thank you for your work on this series before it loses its impact on you, but it is much appreciated. Btw, you would have had me at “integral function”.

    (reply)
    • Peter Attia  July 13, 2012

      Ha ha, Lorraine. You’re the only one!

    • jw  July 13, 2012

      Something tells me that Peter’s ex-girlfriend well understood out-of-sample extrapolations…

    • Peter Attia  July 13, 2012

      Ha ha!

  26. Nina  July 12, 2012

    Peter,
    Another amazing lecture. Thank you, once again, for all you do on this site. It is so inspiring and very appreciated.

    (reply)
  27. Jeff D  July 12, 2012

    Another great article, Peter. Do you know of any studies that have been done on fasting vs non-fasting lipid levels in high carb vs low carb dieters? I’ve often wondered if lipid numbers among low carb eaters aren’t naturally higher than those of high carb eaters, since their bodies are conditioned to releasing fat stores. Of course, their muscle cells would also be conditioned to consume that fat, so perhaps the net result is the same.

    (reply)
    • Peter Attia  July 13, 2012

      Not exactly. Lots of work on fasting vs non-fasting vs AUC, but I don’t know off the top of head of the side-by-side you describe. I’ve done some self-experiments on this with IF vs “regular” eating.

  28. Peter  July 12, 2012

    You are too charitable to esteemed folks like Ornish & Hirsch (labeled as ‘emeritus’ twice in one sentence in the latest NY Times diatribe against Ludwig’s findings.) Their dogma have trained medical providers to give such advice to a relative of mine( female in her mid 60′s):

    Blood Tests: Range 6/12/2012
    Hemoglobin A1C (Blood Sugar) 4.8 – 5.9% 7.0
    Cholesterol <200 181.0
    Triglyceride /=40 58.0
    LDL calculated <100 79.0
    Cholesterol/HDL (Formula) <4.3 3.1

    For decades now, she ate conventionally 'healthy': nil fat and sugar, lean protein and mostly complex carb and veg. Still slim and trim, she has crossed over to Type 2 Diabetes.
    Her doc's advice: maintain her current hi-carb diet composition. And start taking Simvastatin (Z0c0r) 20 mg. daily.
    Bad ideas, when implemented, have terrible consequences.
    Peter, thanks ever so much for your evidence-driven quest for facts and most importantly, the willingness to question one's beliefs when contradicted by new findings.

    (reply)
  29. jake3_14  July 12, 2012

    I’m confused by the introduction to the illustration with four graphs. The introduction says, “The figure below summarizes the differences in LDL-C, non-HDL-C, apoB, and apoB/apoA-I.” Isn’t non-HDL-C the same thing as LDL-C?

    (reply)
    • Peter Attia  July 12, 2012

      non-HDL-C is a proxy for LDL-C + VLDL-C

  30. Corinne  July 12, 2012

    Thanks for all this. My learning curve is slowly improving. Still a bit confused about how to assess specific lipid info. After much pestering I was able to get an order for ApoB and ApoA1, but the insurance company denied payment saying such tests are investigational and experimental. Their full defense of the paradigm can be found here:

    http://www.aetna.com/cpb/medical/data/300_399/0381.html

    Be that as it may, my latest lipid numbers are:
    TC – 275
    TG – 96
    HDL -106
    LDL -150
    non HDL-C – 169
    Chol/HDL – 2.6
    apo B – 144
    apo A1 – 200

    I am not sure if this means I have discordence with my ldl measurements. Also wondering about the high HDL & apo A1. I’ve been very low carb for 6 months. Without giving my med hx, I’d like some guidance on understanding the apoB and apoA1, particularly relative to my “basic lipids.” Can you point me to any info on how to correlate specific apoB numbers to ldl-p?

    Really looking forward to NuSci!!

    (reply)
    • Peter Attia  July 13, 2012

      There are formula to correlate them, but they are probably not worth fiddling with. Just have your doctor walk you through the risk assessment based on the apoB (assuming it was measured, not “estimated”).

  31. John Hanson  July 12, 2012

    Good doctor, of course all of this sounds like sugar is an evil, but these studies really don’t tell us if it leads to heart disease. In this world of science we cannot claim that if B causes C, and A causes B, then A must cause C. We are seing this faulty logic exposed in studies of in-development meds that increase HDL — they do not reduce heart disease. Dr. Krause has shown this with Saturated fat; which I’m sure you will cover. SF increases LDL-C, maybe, but SF is not associated with heart disease. Just because something affects a heart risk indicator doesn’t automatically make it bad. Further study is of course needed to link A to C or Sugar to heart disease. Studies such as the University of Warwick’s work with LDL MGmin need to be included in these discussions.

    (reply)
    • Peter Attia  July 13, 2012

      Yes, John. You are correct. The type of studies you’re talking about use “hard outcomes” (e.g., death, rates of cancer, number of heart attacks) rather than “soft markers.” Until such studies are done — and I personally have EVERY indication of ensuring the 100,000 person 5-year study to test these things is done — you, me, and everyone still has to make a choice about sugar. In the words of our good friend, Clint Eastwood, “Do you feel lucky?”

  32. george henderson  July 12, 2012

    On a VLC diet post-prandial TAG will be high, due to higher levels of chylomicrons.
    Do chylomicron TAGs matter?

    (reply)
    • Peter Attia  July 13, 2012

      Good question. It ultimately depends on their fate (biological). If said TAGs end up being oxidized by muscle cells, it’s great. If they end up in adiopose cells…not so good.

  33. Tony  July 13, 2012

    I have a thought about age being a major risk factor for atherosclerosis…
    I think it is more that just time exposed to ApoB. This would make sense if we were talking about water in a metal pipe, but we are dealing with living cells that are constantly dying and being regenerated. What’s the avg. life of an endothelial cell before it dies and is replaced? When we get older stuff eventually starts to go wrong, breakdown, and/or not have the same integrity that it once did (wrinkled skin, gray hair, failing eyesight, etc). It makes sense to me that this would also apply to the lining of our arteries. If the endothelium has lost some of its integrity due to the aging process, perhaps it creates an environment for ApoB to gain a foothold. The same basic theory could apply to cancer as it relates to old age too I suppose.

    (reply)
    • Peter Attia  July 13, 2012

      Very likely synergistic mechanism as you suggest. I would say it’s at least possible that age contributes to the maladaptive response of the immune system to the apoB particles.

    • jw  July 13, 2012

      Can’t wait for the IX part series on telomeres…

    • jw  July 13, 2012

      This will teach me to be sarcastic:

      Association of Marine Omega-3 Fatty Acid Levels With Telomeric Aging in Patients With Coronary Heart Disease

      http://jama.jamanetwork.com/article.aspx?articleid=185234

      Abstract:
      Context Increased dietary intake of marine omega-3 fatty acids is associated with prolonged survival in patients with coronary heart disease. However, the mechanisms underlying this protective effect are poorly understood.

      Objective To investigate the association of omega-3 fatty acid blood levels with temporal changes in telomere length, an emerging marker of biological age.

      Design, Setting, and Participants Prospective cohort study of 608 ambulatory outpatients in California with stable coronary artery disease recruited from the Heart and Soul Study between September 2000 and December 2002 and followed up to January 2009 (median, 6.0 years; range, 5.0-8.1 years).

      Main Outcome Measures We measured leukocyte telomere length at baseline and again after 5 years of follow-up. Multivariable linear and logistic regression models were used to investigate the association of baseline levels of omega-3 fatty acids (docosahexaenoic acid [DHA] and eicosapentaenoic acid [EPA]) with subsequent change in telomere length.

      Results Individuals in the lowest quartile of DHA+EPA experienced the fastest rate of telomere shortening (0.13 telomere-to-single-copy gene ratio [T/S] units over 5 years; 95% confidence interval [CI], 0.09-0.17), whereas those in the highest quartile experienced the slowest rate of telomere shortening (0.05 T/S units over 5 years; 95% CI, 0.02-0.08; P < .001 for linear trend across quartiles). Levels of DHA+EPA were associated with less telomere shortening before (unadjusted ? coefficient × 10?3 = 0.06; 95% CI, 0.02-0.10) and after (adjusted ? coefficient × 10?3 = 0.05; 95% CI, 0.01-0.08) sequential adjustment for established risk factors and potential confounders. Each 1-SD increase in DHA+EPA levels was associated with a 32% reduction in the odds of telomere shortening (adjusted odds ratio, 0.68; 95% CI, 0.47-0.98).

      Conclusion Among this cohort of patients with coronary artery disease, there was an inverse relationship between baseline blood levels of marine omega-3 fatty acids and the rate of telomere shortening over 5 years.

  34. Gerry C  July 13, 2012

    Two Questions on the analysis of the saturated fat diet study. You mentioned that HDL and LDL size increases and VLDL size decreases were signs of improved insulin resistance. Didn’t you explain in past posts that particle size doesn’t matter, that is is all about count? Also, if size were to matter I get that a larger size HDL and LDL would be seen as improving but why with VLDL is smaller size seen as improving? My understanding was that all LDL starts its life as VLDL.

    Thanks so much for the blog. I enjoy all the info.
    Gerry

    (reply)
    • Peter Attia  July 14, 2012

      Great question, Gerry. Yes, size does not matter when it comes to getting sterols into the sub-endothelial space. A large apoB-carrying lipoprotein is no better or worse at this than a small one. BUT, size (in a drug naive person) is a marker for what is going on. Larger VLDL and smaller LDL particles often — but not always — suggest something bad is going on, almost always related to the over production of hepatic TG.

  35. Catherine  July 13, 2012

    …..I worry a bit about oxidation in capsules. You could take the things for years…
    I use the Carlson’s liquid now but am transitioning over to Paul Jaminet’s preference to just eat a pound of oily fish/ week. Gotta hedge your bets, baby (unless you are feeling lucky)
    My understanding is omega-3 stability is provided by the biolayer.
    Or, like a good portfolio, diversify your sources at least.

    (reply)
    • Peter Attia  July 14, 2012

      I only use capsules when I travel and am too lazy to bring small bottles of oil. I prefer the oil for many reasons, not the least of which is the cost. Your concern may be valid, also.

  36. LeonRover  July 13, 2012

    Peter,

    “In the words of our good friend, Clint Eastwood, “Do you feel lucky?””

    This is the logic used by the “diet heart” hypothesisers in 1970′s, ’80′s and ’90′s – arguing a position in advance of the data – in respect of saturated fat.

    That style of logic (WRT sat fat) is regarded as wrong.

    How may it be correct now? What happens if the data does not support your position?

    Slainte

    (reply)
    • Peter Attia  July 14, 2012

      Are you suggesting the evidence implicating saturated fat as the cause of CHD is even in the same metaphysical category as the evidence implicating apoB- trafficking lipoproteins in CHD?

      I still stand by my assertion. If you feel lucky, keep eating all the sugar in the world. The case against sugar and the case against saturated fat are very different. In fact, this week’s post will give you more detail about the SFA-CHD story than you’ll probably want to hear, but I’d urge you to contemplate that story with the current story.

      Don’t confuse one very important distinction: Acquiring hard outcomes to set policy to drive a mass behavioral change vs. using the best available data PLUS common sense PLUS sound mechanistic understand to make a *personal* choice. These are very different. The SFA debacle was an example of the former; my caution on sugar is an example of the latter.

      Ultimately, though, it is your choice. Hence my reference to Clint.

  37. gabby  July 13, 2012

    Awesome stuff, Doc. Helpful.

    (reply)
  38. Tony  July 13, 2012

    Regarding conclussion #4: 4.The addition of fat, in the absence of sugar and starch, does not raise serum triglycerides or other biomarkers of cardiovascular disease.

    What about eating high fat in the presence of moderate or high carbs? I could be wrong, but I seem to recall that in their book “Protein Power” the Drs. Eades say that fat with carbs are a very bad combo, while in the Q & A section of “Why We Get Fat”, Gary Taubes says that fat is not bad no matter if it is in the presence of carbs or not.

    Anyone know of good evidence one way or the other? I’ve been eating low carb for a couple years so it’s mainly just a curiosity thing for those rare moments when I decide to indulge in ice cream after a ribeye steak (I have a weakness for ice cream)!

    Hey Peter, are you following the Tour de France?

    (reply)
    • Peter Attia  July 14, 2012

      Correct. It’s quite possible that high fat in the presence of sugar (e.g., ice cream, waffles with maple syrup, virtually all fast food) is “extra” bad. If it’s ice cream you crave, make it sugar free. I have a recipe floating around the comments section somewhere.

    • Nicole  July 17, 2012

      Hey Tony,

      If it’s ice cream you crave there’s an excellent low carb/high fat option from So Delicious. Check out the “No Sugar Added” ones.

      http://www.sodeliciousdairyfree.com/products/coconut-milk-ice-creams

      A quick look at the (no sugar added) Butter Pecan flavor:
      Serving Size 1/2 Cup (85g)
      Calories 140
      Calories from Fat 110
      Total Fat 13g
      Saturated Fat 7g
      Total Carbohydrate 17g
      Dietary Fiber 10g
      Sugar 1g
      Protein 1g

  39. Lexi  July 13, 2012

    Dr. A, let me add to the many votes of support for what you are doing to educate us. I sincerely appreciate your work, your time, and your wife’s tolerance. I’ve become an avid reader, particularly of this series.
    I have the impression, I believe from reading lipid researcher Mary Enig, that as a result of long-term consumption of an unhealthy ratio of omega-6:omega-3, our cell membrane structure can be compromised. I think she used the term “flabby.” Aside from sheer number of LDL particles, could this be part of the explanation for apoB-containing particle penetration of the endothelial wall?

    (reply)
    • Peter Attia  July 14, 2012

      Possible, certainly. Though I don’t think it’s about the ratio of n-6 to n-3, and more related to the absolute amount of 2 very important n-3′s: EPA and DHA. I’ll be doing a series on this at some point (soon) I hope.

  40. Bill  July 14, 2012

    “I only use capsules when I travel and am too lazy to bring small bottles of oil. I prefer the oil for many reasons, not the least of which is the cost.”

    I have not supplemented omega-3 or fish oil for several years, but I do make sure to eat salmon or other fatty fish twice a week or so. I recently did a comprehensive Nutreval test and was happy to see that my RBC EPA and DHA were quite high (3.26% and 6.0% by weight respectively).

    So it may not be necessary, or even desirable, to supplement for omega-3 fatty acids, depending on diet.

    I’m no longer certain how much this matters, but my RBC % omega-3′s by weight was a high 12.5%, my AA/EPA was a low 5, and my omega 3 index was a high 9.2. I do avoid omega 6 oils as much as I can. Bill Lands would approve, I think. Not sure about Bill Harris.

    (reply)
    • Peter Attia  July 14, 2012

      Correct. Bill Lands and Bill Harris are on opposite sides of the n-6 argument. I’ve spent lots of time with both of them and will be assimilating the information for a series on this topic.

  41. Maryann  July 14, 2012

    Hi Peter! Thanks again for your excellent work! You mentioned that there is only one more installment left; however, previously you mentioned that you planned to do a post on the Apolipoprotein E Genotype. Would this not be a cholesterol-related topic? I didn’t see it listed on your coming-soon page, so I am not sure if you still plan to cover it. Thank you so much for all of your hard work! I don’t mean to add to it :)

    (reply)
    • Peter Attia  July 14, 2012

      I may need to take a small break from the series after a “wrap up.” I will write about apoE eventually, but not in part X.

  42. steve  July 14, 2012

    Would be interested in your take in this interview with Dr.Ron Kruass where he says sat fat raises LDL levels and small LDL-P is worse for CAD than large LDL-P:
    http://www.meandmydiabetes.com/2010/03/26/ldl-cholesterol-ron-krauss-md/

    My takeaway from your great series on cholesterol is that if LDL-P is at goal for a given person, the diet composition may not really matter since LDL-P causes CAD. Is this a correct conclusion? Thanks.

    (reply)
    • Peter Attia  July 15, 2012

      Size is a marker for risk, but at a given LDL-P or apoB it stops mattering. 2,000 large particles is just as bad as 2,000 small particles. In fact, 2,000 large particles is worse than 1,500 small particles. Check out the post where I review this concept with data. I think it was part III or IV, maybe V.

    • steve  July 15, 2012

      I read all your posts which are great. Just found it curious as to why Dr. Ron Krauss would seem to feel the small particles are worse. Since i do not know how to contact him I thought I would ask you.

      Now if total particles is all that counts regarding CAD, and one is at the right LDL-P for their risk factors, does diet then really matter?

    • Peter Attia  July 15, 2012

      I can’t speak for him. There is a great deal of confusion around the difference between a something (e.g., small LDL-p) being prognostic of other problems (e.g., IR) vs. an absolute risk in and of itself.

  43. Maryann  July 14, 2012

    I completely understand. An update: I found very thorough information on the HDL website.

    (reply)
  44. Ellen Urciola  July 15, 2012

    Thank you so much for your comments and all of your posts and responses. Your series on cholesterol and “What I Actually Eat” are informative, thought provoking and make sense (even to a lay person such as me). Thank-you for such quick responses to questions. I consider your blog and reader responses as important as reading the morning newspaper. You most certainly deserve to take a break. But give us plenty of notice please, so the withdrawal won’t be too bad.

    (reply)
  45. Steve  July 15, 2012

    I was eating a lot of Omega-3 foods until that Omega-3 study that had to be ended abruptly, because a large percentage of the participants developed prostate cancer. I haven’t heard that mentioned here.
    Any responses?

    (reply)
    • Peter Attia  July 15, 2012

      Please send over link to actual study. I’ve seen epidemiological data suggesting this, but not prospective data. Hard to draw conclusions for the former.

    • Raymund Edwards  July 16, 2012

      Dr. Gerhard Spiteller suggests it is because of these substances that a fish diet is beneficial while a fish oil supplement maybe is not so in comparison.

      http://www.ncbi.nlm.nih.gov/pubmed/16296395
      Furan fatty acids: occurrence, synthesis, and reactions. Are furan fatty acids responsible for the cardioprotective effects of a fish diet?

    • Peter Attia  July 16, 2012

      This doesn’t strike me as particularly compelling.

  46. Lex  July 15, 2012

    If a person is already on statins (not me; the brother-in-law), would the NMR LipoProfile still be useful? If he’s been on the statins a short time, a few weeks, is it still a good call to get the test? Maybe a good baseline to evaluate the effectiveness of the statins, if in his case it was the right call? I’m concerned he could be a one of those w/ confounding data, as his cholesterol is high, but TG are WNL and HDLs are quite good.

    (reply)
    • Peter Attia  July 16, 2012

      Absolutely, especially if combined with the sterol panel from HDL, Inc., as it gives more information about whether or not the statin is even indicated.

  47. steve  July 16, 2012

    Now if total particles is all that counts regarding CAD, and one is at the right LDL-P for their risk factors, does diet then really matter?

    (reply)
    • Peter Attia  July 17, 2012

      Of course. The role of diet on cardiac disease is important, but there are many other reasons to consume an optimal diet. Even if LDL-P is ideal on a sub-optimal, other things could likely be improved.

  48. Nicole  July 16, 2012

    Good afternoon Dr. Attia,

    First I’d like to thank you for your tireless knowledge sharing. I expect wild success from NuSi.

    Second, I would like to know when I can reasonably expect a post where you at least touch on the suitability and efficacy of a low-carb lifestyle for pregnant/nursing women, nursing infants and children. I’d be especially interested in whether a ketogenic diet would have any effect on women’s breast size, being that they are nearly all fatty tissue (as I understand them).

    Third, I’d like to share something. This is a mini-lecture from a class I am taking in college called ‘Basic Weight Training for Life.’ I am wondering if you can name a single study (or even basic science) off the top of your head that would effectively argue against this, something I could reference in my rebuttal . I already know this to be patently untrue per your generous knowledge sharing, that of Gary Taubes and my own personal experience in transitioning to a low-carb lifestyle. (I am aware you can not respond to EVERY comment so if I do not receive an answer I will not harbor any negative feelings.)

    “Carbs Are Good: No Carbs Mean Fatter Person – - We use food and stored food to make the energy we need to live, be active, and exercise. In aerobic metabolism, where copious amounts of energy can be converted to be used, the process begins with the breakdown of glucose. Glucose is our blood sugar or blood carb. Through a series of steps these glucose molecules produce some usable energy, but also leave a by-product substrate called pyruvate. The conversion of pyruvate in combination with oxygen, allows stored fat to be used as fuel substrate as well. To put it simply. Fat can only burn in the flame of carbohydrates. If you do not have carbs, you cannot burn fat. If you cut down on carb intake, you get fatter. Again, we are not talking about weight, but about fat. Muscle doesn’t weigh less than fat, it is more dense. At the same weight muscle takes up less room. That means you can tighten your belt a notch even though the needle on the scale does not move.”

    Thank you,
    Nicole

    (reply)
    • Peter Attia  July 17, 2012

      1. My pleasure. Looking forward to introducing NuSI to everyone.
      2. Not sure…too many things in the mix right now, and I’d hate to make a promise I can’t keep.
      3. Turn the tables on them. Ask them for proof of this statement.

  49. David Studhalter  July 16, 2012

    This series has been nothing short of fantastic. You should… seriously… write a book. Your enthusiasm and straight-talking style are just what are needed. How about calling it «Everything You Know About Diet and Health is Wrong (and What You Need to Know to Eat Right and Minimize Health Risks)»

    (reply)
    • Peter Attia  July 17, 2012

      Just what I need…another project!

  50. Tim  July 20, 2012

    Dr. Attia – Just started reading your website really enjoy it. Quick question about my blood panel.
    HDL- 58
    LDL-196
    VLDL -5
    TG -24
    I know my TG number is good and HDL is ok but I’m little worried that my LDL is so high
    Little more information – I’m 33 , blood pressure is 112/68, am 6′ tall 183 pounds, exercise in short intense sessions 2-4 times a week and try and walk several miles day on off days. Get good sleep and eat basically way you have described yourself. I don’t eat any grains or vegetable oils or sugars. Mostly grass fed meat I buy direct from farmer, eggs, wild caught fish, coconut oil and some veggies and few berries.
    Do you think the LDL number is a cause for concern? I realize you state numerous times its more about the LDL-C and LDL-P ratio just thought that number was pretty high and not sure why
    Thanks

    (reply)
    • Peter Attia  July 20, 2012

      Tim, I can provide medical advice, unfortunately. A TG/HDL ratio of less than 0.5 is excellent, though.

  51. Lex  July 21, 2012

    I have been reading your site chiefly because of what appears to be a bad news lipid panel on my husband (high LDL, low HDL, high TG, and TG:HDL over 8). This is 5 years after a seemingly “good” panel. Good news is I asked for and got our doctor to order the NMR LipoProfile. You have recommended, from other posts, to combine this with a sterol panel from HDL, Inc. What is this sterol panel, and is such a panel not available from a lab other than HDL? We are able to get the NMR at LabCorp.
    Also, just reading your explanation of discordance makes me think that even with a “good” standard lipid panel, such as I have, makes me concerned that even I should have the NMR. I mean, if a bad numbers aren’t necessarily bad, then good numbers can’t be relied upon to be good either?
    RE the husband, his age, size, genetics, and athleticism (though not as intense) are fairly similar to the before-you. One of my mental problems about this, however, is that we already had de-emphasized carbs for several months; and we eat very low n6, grains or sugar; eat all grassfed & pastured meat, raw milk from grassfed cows, good vegetables, coconut oil and grassfed butter. He is on board with all that I do on the eating, he just eats a bit more fruit than I, but nothing excessive. In fact he eats less than I do, even though he outweighs me by about 160%.
    It seems to me from all my reading on these issues, that he could be either (1) needing more carb-cutting – currently trying that out – or (2) he one of those who gets the “bad” numbers from the already low carb diet, as suggested by Westman and other readers here. When we get the NMR results, if by some chance the LDL-P is not so bad, then great. But if it’s high as I expect, then I would think more extreme carb-cutting is in order. Am I thinking straight here? And after how much time would you recommend trying that before re-testing?
    Sorry for the long/multiple questions. I’ve been reading as much as I can, of articles and comments, saving up my thoughts.
    Looking forward to your post about EPA and DHA!

    (reply)
    • Peter Attia  July 21, 2012

      Only Health Diagnostic Labs, Inc. (HDL, Inc.) does the sterol test. They send out to LipoScience for the NMR portion of the test and do all else in house.

  52. Matt  July 21, 2012

    I appreciate the depth of research in this post. Unfortunately I have not had success on a low-carb diet in terms of my lipid profile.
    My Apo B, LDL-C, are extremely high. Apo B is 167. LDL-C is 245.

    This was from a VAP test, which I sought out after the normal lipid panel scared me.

    Trigs are ok (101), HDL is fair (50). LDL pattern is A.

    Blood sugar and blood pressure are excellent, weight is good, I feel fine, and work-out 3 times per week. Why is my cholesterol so damn high?
    My Doctor wants to put me on statins of course.

    (reply)
    • Peter Attia  July 21, 2012

      Can’t really address this, Matt. The only thing I can say, though, is the apoB here is calculated. It may not accurately represent a measured apoB or a measured LDL-P.

  53. Ellen Urciola  July 21, 2012

    Hi Dr. Attia,

    Glad to see your blog is up and running again. Your presentation provided me with such a clearer understanding of the science behind weight. Also, thanks for the Francis bacon reference. I am staring my masters and want a true take on the scientific method.
    How about an update on NuSI? The lecture mentioned 3-4 weeks.
    Thanks

    (reply)
    • Peter Attia  July 21, 2012

      Thanks, Ellen. We’re running full speed ahead with NuSI, but we’ve postponed our public launch until early September.

  54. Amber  July 22, 2012

    Dr. Attia, thank you for this. I’m very excited about your work. At this moment though, I just wanted to say that I for one would have swooned at such an explanation of your interest and time, though I may have argued that what I really wanted was frequent high peaks, not just a large aggregate.

    (reply)
    • Peter Attia  July 22, 2012

      Amber, where were the girls like you when I was in college?

  55. george henderson  July 27, 2012

    I’ve linked to this post in my essay on calories vs carbs as drivers of Hepatic de novo lipogenesis:
    http://hopefulgeranium.blogspot.co.nz/2012/07/what-does-hypercaloric-actually-mean.html

    (reply)
  56. Richard David Feinman  July 28, 2012

    Correct me if I am wrong but I don’t think that you have shown points 1. and 2. What the data show is that fructose, in the context of a high carbohydrate diet raises TAG. Isn’t this just as well described as the effect of high glucose on other parameters.
    This is the point of my latest blog post at http://wp.me/16vK0 which examines a similar study from Havel’s group.

    (reply)
    • Peter Attia  July 28, 2012

      Richard, great to have you commenting on this blog. [For those who don't know Richard, he's a world-class scientist who has been studying this topic for many years.] You are correct, my conclusions are in the context of a “Standard American Diet.” In the context of a LCD, especially when hepatic stores of glycogen are depleted, fructose will be preferentially converted to glycogen (as you know, but many may not, at a rate that exceeds that of glucose conversion to hepatic glycogen). Thanks for making the distinction for the readers. If you’re going to be in Boston for AHS, I hope we can meet in person.

  57. Jennifer  July 29, 2012

    Dear Peter,
    Thank you so much for writing this marvelous series on cholesterol! I went to UCSF to become a nurse-midwife and I’ve learned as much from this series as from some entire classes in grad school. It is so well-explained and I’ve learned a tremendous amount that I didn’t know before. I have a couple of questions–

    1. It seems to me from reading the series and checking out many of the studies you mention that we should just replace the standard profile with this improved way of testing, since the LDL-C is not a great predictor and the LDL-P is a great predictor. But in reading the comments I see that you perhaps agree with some who say we should not do that, but should only use the NMR for certain people (or maybe you were bending over backwards to be reasonable but lean towards thinking we should switch over for everyone too). It seems to me that if this became the standard the cost would probably come down over time as it became more common. But more importantly, since some degree of insulin resistance probably characterizes most adults in the U.S., it seems to me that the standard profile would not be the best idea for at least a majority (if not all) of the patients. I suppose you could identify people who were concordant with the NMR and then plan to do their future screenings with the cheaper test, but that would assume they weren’t developing insulin resistance over the following years and that they would stay concordant.

    2. Do we know why there is a lot of discordance between the 2 measures in insulin-resistant people? At first I was thinking it was due to the calculation for the LDL-C being dependent on triglycerides but then I see in the example of an NMR report that the LDL-C and LDL-P are discordant and the triglycerides are not high.

    Thank you again for writing this incredible series!!!

    (reply)
    • Peter Attia  July 30, 2012

      Jennifer, it probably does not make sense to use NMR as the standard lipid test for everyone. For starters, there is only one company in the world that can do the test, and they wouldn’t be able to test even 5% of the US population. But even if the test was readily available, on average, it may not make sense for every single person to get the test. Of course, on a personal basis, it’s harder to make that claim. We all want perfect information for ourselves. To your second question, the biggest driver of discordance is probably the over-abundance of TG in lipoproteins at the expense of CE — driven most often (but not always) by IR.

  58. Lex  August 8, 2012

    I just got a call from my internist and we discussed my labs and lipids results. I’m about doing the happy dance because (1) TG of 48, with a TG:HDL 0.58; and (2) after telling her why I was not concerned about what she felt was high cholesterol and LDL-C, my doctor said, “You know more than I do.”
    Thank you Dr. Attia, for your generous education. You have helped me immeasurably, and I’d go so far as to say you are helping me save my husband’s life. He had blood drawn today for the NMR-LP and LP-IR, is losing weight, and complying with a VLCHF diet. As a bonus I’m hoping our internist will learn a bit and be able to help other patients. Further, I spread your blog to anyone who’ll listen!

    (reply)
    • Peter Attia  August 9, 2012

      If only more doctors had this level of humility and curiosity, the world would be a better place.

  59. Trisha Eldridge Gilkerson  August 15, 2012

    Not sure which cholesterol post this question fits most appropriately (hope you haven’t answered a million times). I know you recommend NMR when checking cholesterol, so that was one of the tests on my list that I requested the doctor run when I was in last week. He said that unfortunately the lab he works with does VAP tests and not NMR, but agreed the NMR was the best. I asked him if the VAP measured number of particles and he didn’t really answer the question he just said it was also a really good test and would tell me about particle size etc. Of course, from reading your post, I know that it’s the number of particles I need to be concerned about! I’ve searched in vain online and I can’t seem to find the answer. There are a number of people on my mom’s side of the family with pretty early heart disease (early 50′s) and though I have a couple of decades, I’d just like to be sure I’m on the right track even now! Hoping the VAP test isn’t completely worthless!

    (reply)
    • Peter Attia  August 15, 2012

      Hmmm, the VAP really isn’t an adequate test, as it doesn’t even measure apoB (it estimates it). At least see if you doctor can do a Berkeley labs apoB test, or go better yet, see if he/she can go through HDL, Inc for the NMR (rather than directly through Liposcience).

  60. Gerry C  August 15, 2012

    Peter:

    Was wondering if you had a chance to read the research just published by Western University Dr. David Spence claiming that eating egg yolks is almost as harmul as smoking as it relates to atherosclerosis, and what your thoughts were on it?

    (reply)
    • Peter Attia  August 15, 2012

      Addressed in 4 other comments. What are your thoughts on it, now what you’ve hopefully been educated on i) cholesterol and the pathogenesis of atherosclerosis, and ii) bad science?

    • Jack  August 17, 2012

      I would like a response to the study published by Western University Dr. David Spence claiming that eating egg yolks is almost as harmful as smoking as it relates to heart disease, and I didn’t see any on this website.

    • Peter Attia  August 17, 2012

      Yes sir! I’m so sorry I don’t have one up. Will you forgive me? Pardon the sarcasm, but the tone of your question — demanding and entitled — really rubs me the wrong way. I apologize if I’m misreading it.
      If you want a response to this, you should read the multiple posts on cholesterol. You should also read the posts that talk about poorly done research, of which this study is classic example. You may even want to read the summaries of others, which I’ve already referenced 7 or 8 times in the past 3 days. Jack – let me blunt – you’ve got to learn to think for yourself. I don’t write the blog because I’m board and have too much time on my hands. I write it to TEACH you how to think critically. This would be a good time for you to start putting those skills into practice. You should be the other readers on this site why this study is flawed.

  61. Gerry C  August 15, 2012

    It sounded absurd to me, and goes against everything I now understand. I seem to need constant reassurance for some reason.

    Thanks,
    Gerry

    (reply)
    • Peter Attia  August 15, 2012

      Don’t worry, Gerry, we’ll get you confident enough to resolve this on your own and explain it others.

  62. Lex  August 16, 2012

    The NMR LipoProfile is also available from LabCorp, according to theparticletest.com site. There are many locations, even though there’s only one LipoScience. This could be an alternative for many folks.

    (reply)
    • Peter Attia  August 16, 2012

      As long as they send to LipoScience to do the actual NMR.

    • Bob H  August 21, 2012

      Labcorp does send the blood work to LipoScience to do the NMR. I use privatemdlabs.com for my blood work and this is what their site says:
      “*Please note, the NMR LipoProfile® is processed through LipoScience, the cardiac c-reactive protein and Lp(a) is processed through Labcorp, results are provided on a Labcorp Report.”

  63. Ted  August 19, 2012

    I’ve just had head and neck MRAs and CTIs done as follow up to a MRA of the head showing extreme narrowing of the left Middle Cerebral Artery. The CTI showed reconstitution of the arterial bed distal to the narrowing of the MCA. However, the same CTI also showed extreme narrowing of one Vertebral Artery and moderate narrowing of the other. A neck MRA follow up confirmed that finding. My Neurologist was not familiar with NMR lipid panels and ordered your standard panel. LDLs were 151, Total C was 222, Trigs were 65, HDLs were 58, VLDLs were 13. I’m worried about further arterial narrowing, naturally. I’m taking Plavix and Lipitor (20mg) daily and have been following Dr. Furhman’s Eat to Live regimen, eliminating oils, dairy and saturated animal fats while eating complex carbs (beans and greens with fruit to boot). After reading your fine article I’m going to ask my PCP to order an NMR panel to get an LDL-P measure as a baseline in anticipation of an October consult with the Neurologist, at which time another NMR lipid panel will be ordered. Since Radiological studies have shown stenosis in the Vertebral Arteries, I feel I’ve left the realm of interpretation of lipid measures and have direct evidence of “the thing itself”. The question I have is, what should I eat to arrest and hopefully regress the stenosis? Evidence-based responses would be helpful in presenting my case for whatever diet I need to be on to my Neurologist. Thanks in advance.

    (reply)
    • Peter Attia  August 19, 2012

      Ted, I think you’ll find all of the evidence-based responses on this blog. It’s certainly possible that the plant-based diet you’re consuming is preventing greater acceleration of your disease, but it’s likely due the amount I suspect you’ve cut down on sugar and starch, rather the reduction in oil, meat, and saturated fat. Watch the video in this post: http://eatingacademy.com/nutrition/how-did-we-come-to-believe-saturated-fat-and-cholesterol-are-bad-for-us

    • Ted  August 28, 2012

      Just got my NMR Lipoprofile back. Background: Been eating Dr. Fuhrman’s plant-based diet for 5 weeks. Had been an omnivore of the Paleo/Primal ilk (Devaney, Sisson, Enig, Drs. William Davis, Kurt Harris, etc.) for years prior to getting a neck MRa in July that showed severe stenosis in both verterbral arteries. Hence the change in diet. Not picking a fight; just saying that I had to change something given the stenosis that was imaged. Since July 13th I’ve dropped 15-20 pounds. I’m 6 foot, 170lbs, with no abdominal fat at the moment. Take 20mg of Lipitor generic, 75mg of Plavix, 100mg of CoQ10 and a moderate amount of B12 daily. Here are the numbers: July 13th/August 21st – Total C 222/118, Trigs 65/76, LDL-C 151/64, HDL-C 58/39. CRP May 4th 2012/August 21st: 1.7/0.47. LDL-P and small LDL-P were not measured on July 13th. The last they were measured was March 2, 2011 via NMR. Here’s the comparison: March ’11/August ’12: LDL-P 2384/732. small LDL-P 558/442. Fantastic news!! But why is it that my neurologist, with whom I shared these numbers said, “Regarding the LDL-P, there have so far been no conclusive evidence based studies to evaluate the optimal value and the best management of this value for stroke prevention. Therefore, current stroke guidelines still recommend looking at LDL.” Are there any studies that you know of that I could show her that give peer-reviewed support to the use of LDL-P values in managing stroke prevention? I’m very happy with the latest NMR results, naturally, and am hoping that the Radiology studies at the end of this year will show plaque regression (or at least non-progression) associated with the very low LDL-P number (732) that you’ve indicated in the article above: (“If you want to stop atherosclerosis, you must lower the LDL particle number. Period.”) as well as the low Total C and LDL numbers that are crucial to stopping the development of atherosclerosis/plaque progression. I’ll keep you posted but am interested to hear from you what you make of my NMR results. Thanks for your great site and the way you keep up with the correspondence. Don’t know how you do it, but sure glad you do.

    • Jane  March 29, 2013

      Peter,

      Ted’s n of 1 study is very interesting. I am quite sympathetic to his plight, and am impressed by how disciplined his dietary interventions seem to have been.

      Despite great efforts, I have failed to find any publication of the results of any randomized controlled trial comparing a very low carbohydrate diet with a very low fat (Ornish) diet that includes the lipoprotein analyses that you have explained,, or even VLCD with a vegan Atkins type diet.

      Have you found such a study? Would NUSI be supporting such a study? The one of greatest utility in the short run would be one comparable to Gardner’s 2007 study that was set up to compare results based on little more than sending each study group out with the instructions of the Atkins, Ornish, LEARN, and Zone books. Perhaps analyzing the data by stratifying the groups into the four concordant vs disconcordant patterns of lipoproteins would yield useful results to physicians and the millions of IR individuals who stumble on the results. Perhaps a relatively inexpensive study could be done on the blood samples already collected for Gardner’s study? Have you spoken with him about this?

      Thank you very much for all your work.
      Jane

    • Peter Attia  March 30, 2013

      You’re correct. This is, indeed, in the works.

  64. Ted  August 20, 2012

    Thanks for the thoughtful response, Peter. I’m a 57 year old guy who one year ago had an NMR lipid panel which showed an LDL particle number slightly over 2000. At the time I was eating red meat, lean meat, fish, butter, half and half, etc. I continued thusly until this May when, quite by accident, I learned of the stenosis in my vertebral arteries. I’ve only recently (July 12th to be exact) eliminated dairy, saturated fats and most oils from my diet, grudgingly. I had already minimized if not eliminated processed grains and cheap carbs from my diet these past several years. I’ve chosen the Eat to Live plan with some modifications because, frankly, I’ve done the low-carb, high protein and fat diet without the grains and my LDL particle number was astronomical. I appreciate that you say that it’s possible that the new (since July of this year) plant-based diet may be slowing the acceleration of the stenosis. I hope to arrest and regress it! Thanks for your time and I’ll let you know how things are going in a couple of months.

    (reply)
  65. Jim Bowron  August 28, 2012

    A short article in the recent Scientific American titled “Cholesterol Confusion” referred to a paper in the April “Journal of the American Heart Association” that concluded that HDL particles with apolipoprotein C-III ‘may nearly double the risk of heart disease in healthy men and women” while HDL particles without apoC-III may be especially heart protective. As one commentator on the study said, “…there’s a lot more to be learned about HDL and how it acts”
    I only hope that NuSi will not be overloaded with questions ‘where there is a lot more to be learned’.

    (reply)
  66. Eric  August 29, 2012

    After reading your guest post on Marks Daily Apple, the question arose in my mind about cumulative effects of arterial plaques and long term repairability. I got the impression from your desription of an arterial plaque that it’s likely there to stay once in place. Is there any data on how repairable the damage might be?

    (reply)
    • Peter Attia  August 29, 2012

      Turns out the plaques can regress, through either pharmacological intervention and/or lifestyle modification (e.g., smoking cessation, dietary change).

  67. Steve  August 30, 2012

    Hi there Peter,

    I was wondering when Part X will be released? Or has it been already?

    Thanks!

    (reply)
    • Peter Attia  August 30, 2012

      It’s still in my head…not sure when it will be released, but probably not for another few weeks, and certainly not before NuSI’s launch.

  68. Alexandra M  August 30, 2012

    I’m sure you’ve been bombarded with the news about the failed* calorie restriction study:

    http://www.nytimes.com/2012/08/30/science/low-calorie-diet-doesnt-prolong-life-study-of-monkeys-finds.html

    “Rafael de Cabo, lead author of the diet study, published online on Wednesday in the journal Nature, said he was surprised and disappointed that the underfed monkeys did not live longer. ”

    Disappointed? I understand that they were expecting a different result, but I’m anything but disappointed! Who wants to have to choose between a somewhat longer lifespan of semi-starvation and a normal lifespan of not starving? I’ll be thrilled to death if this idea ends up on the rubbish heap of disproved hypotheses. As someone said in another story about CR:

    “They say you can live longer doing this, but after a few days of it, you won’t want to.”

    *Failed, adj Not validating the wishful thinking of the researchers.

    (reply)
    • Peter Attia  August 30, 2012

      Yes, I was also a bit surprised by that sentence when I read this article. Thanks for sharing with everyone.

  69. Nathan  September 5, 2012

    I’m new to your blog and just finished reading the cholesterol series. This is an excellent resource, thanks for putting this together. This is of particular interest to me given I’m 36 and presumably have familial hypercholesterolemia (heterozygote). I have had a long, drawn out internal debate/rationing process regarding statin use given this is my only risk factor for heart disease. I’m particularly interested in the upcoming “role of pharmacologic intervention in the treatment and prevention of atherosclerotic disease” referenced above. Any time-table for releasing this blot post?

    (reply)
    • Peter Attia  September 6, 2012

      Nathan, glad you’re enjoying it. That installment is probably at least a month away. With NuSI’s launch just a week away, and 12 other things up the air, I won’t be able to address this properly for a while.

  70. Steve  September 6, 2012

    Peter,

    Direct Labs has their NMR Lipo Profile lab test on sale this month if anyone is interested. I don’t work for them!

    (reply)
  71. Jonathan Carey  September 11, 2012

    As an individual with heterozygous familial hypercholesterolemia who has switched from a Dean Ornish diet to a Paleo approach and tripled my HDL-C, I still find the LDL-P datasets enigmatic. While I may have LDL-P of 2800 (top 0.1%), I in no way resemble my cohort-mates in any other blood measures since I have very low TGs, low CRP, low VLDL, very high HDL-C, and 90% large LDL. I am an outlier. Must my cardiovascular future be correlated with my “peers?”

    (reply)
    • Peter Attia  September 11, 2012

      It’s a great question, Jonathan. We just don’t know the answer, even in the absence of your FH. We need more clinical trials to understand what high LDL-P in the absence of other markers means for someone eating like you.

    • Raymund Edwards  September 12, 2012

      On Inflammation !

      This paper is on Vitamin D and erectile dysfunction .

      However it has a wider aspect than that. Covering some of the Vitamin D and cardiovascular disease mechanisms. Esp Inflammation .

      http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427191/?tool=pubmed

      “Vitamin D may promote vascular health by inhibiting inflammation. Vitamin D supplements and injections may lower CRP levels as much as 40% and improve cytokine profiles; it inhibits the production of proinflammatory cytokines while stimulating the production of anti-inflammatory cytokines. One pro-inflammatory cytokine, TNF?, is inversely related to regular exposure to sunlight and artificial sources of UVB among women, and the same is probably true for men. Two CAMs induced by TNF? are also significantly decreased after incubation with activated vitamin D.1 In addition, Oh and colleagues have shown that in patients with type 2 diabetes, active vitamin D inhibits foam cell formation and suppresses macrophage cholesterol uptake, inhibiting the inflammatory atherosclerotic process described earlier.

      We hypothesize that vitamin D optimization through sunlight exposure or vitamin D3 supplementation would decrease vascular damage caused by inflammation and reduce the risk of ED. We searched pubmed.gov for evidence contradicting our hypothesis regarding VDD and ED but found none.”

      Would seem to be important not to be Vitamin D deficient.
      ==>
      “Understanding the Entire Lipid profile
      Thomas Dayspring MD, FACP
      There is only one absolute in atherosclerosis: sterols (predominantly cholesterol) entering the
      artery wall and being internalized by macrophages, creating foam cells (the histologic diagnostic
      marker of atherosclerosis) and the associated inflammatory process. ”

      There are also papers that connect Vitamin D to Increase in HDL…

      In my circle this has been the case.

    • Raymund Edwards  September 18, 2012

      Peter – Beta – Amyloid deposits and heart disease ? I had not heard of that before.

      I found this interesting . It also made me think about the reports linking insulin to faulty Amyloid clearance in the brain–

      Eg “Elevated insulin levels are implicated in the brain cells’ failure to clear beta-amyloid. ” Maybe not just the brain ? Maybe all the Blood Vessels too.

      In any case more on Vitamin D and inflammation ..

      http://www.bbsrc.ac.uk/news/health/2012/120116-pr-vit-d-combat-ageing-in-eyes.aspx

      “The researchers identified two changes taking place in the eyes of the mice that they think accounted for this improvement. Firstly, the number of potentially damaging cells, called macrophages, were reduced considerably in the eyes of the mice given vitamin D. Macrophages are an important component of our immune systems where they work to fight off infections. However in combating threats to the aged body they can sometimes bring about damage and inflammation. Giving mice vitamin D not only led to reduced numbers of macrophages in the eye, but also triggered the remaining macrophages to change to a different configuration. Rather than damaging the eye the researchers think that in their new configuration macrophages actively worked to reduce inflammation and clear up debris.

      The second change the researchers saw in the eyes of mice given vitamin D was a reduction in deposits of a toxic molecule called amyloid beta that accumulates with age. Inflammation and the accumulation of amyloid beta are known to contribute, in humans, to an increased risk of age-related macular degeneration (AMD), the largest cause of blindness in people over 50 in the developed world. The researchers think that, based on their findings in mice, giving vitamin D supplements to people who are at risk of AMD might be a simple way of helping to prevent the disease.

      Professor Jeffery said “When we gave older mice the vitamin D we found that deposits of amyloid beta were reduced in their eyes and the mice showed an associated improvement of vision. People might have heard of amyloid beta as being linked to Alzheimer’s disease and new evidence suggests that vitamin D could have a role in reducing its build up in the brain. So, when we saw this effect in the eyes as well, we immediately wondered where else these deposits might be being reduced.”

      Professor Jeffery and his team then went on to study some of the blood vessels of their mice. They found that the mice that had been given the vitamin D supplement also had significantly less amyloid beta built up in their blood vessels, including in the aorta.

      Professor Jeffery continues “Finding that amyloid deposits were reduced in the blood vessels of mice that had been given vitamin D supplements suggests that vitamin D could be useful in helping to prevent a range of age-related health problems, from deteriorating vision to heart disease.”

    • Adam Long  October 16, 2012

      Jonathan, I read this on the site Paleo Premise (link: http://thepaleopremise.blogspot.com.au/)

      “The number of LDL particles (LDL-P) can be estimated by apolipoprotein B (ApoB) and lipoprotein A (Lp(a)). The size of the LDL particle is no longer a significant risk factor when adjusted for ApoB, ApoB is no longer a significant risk factor after adjusting for HDL-C and triglycerides and LDL-C is no longer a significant risk factor after adjusting for systolic blood pressure and smoking” from his analysis of the EPIC study. So if what he calculated jibes with what Dr. Attia is saying (the part about size of LDL not being important) and the following statement is correct, it would show that those with high ApoB levels (which correlate with LDL-P, right, or at least help estimate it) can be healthy if your HDL-C is high and your trigs are low. Is this correct?

  72. James  September 15, 2012

    I haven’t seen any advice on lowering LDL (C or P). Perhaps the next post?

    I was on a statin for years but went off – I don’t know if statins long term are healthy, either. I don’t know LDL-P but as of last week had LDL-C of 150, HDL-C of 64 and TG <50.

    No clue about Apo B.

    If Apo B is low, would I expect LDL-P to be low or must they both be assessed? If Apo B is low and LDL-P is moderate / high would I still need to focus on lowering LDL-P. In thinking about what you've written, I would think it very odd to have discordance between ApoB and LDL-P.

    Thoughts?

    (reply)
    • Patrick  September 16, 2012

      I would agree with conclusion that it would be very odd to have discordance between ApoB and your LDL-P. Seeing as your TG/HDL ratio is .78, which is phenomenal, I would venture to guess that you would likely find that you also have a low LDL-P. The TG/HDL ratio is a quick check as to whether you may want to proceed with further analysis via an ApoB and LDL-P test. I would then further venture to guess that there is likely not much discordance between a sub 1.00 TG/HDL ratio and low ApoB/LDL-P. Also, as has been pointed out here and other places, I would not focus on lowering your LDL-C. Further, you should not be surprised to see it in fact rise on a HFLC diet….as Dr. Attia and others have pointed out. As we know, however, you do see alot of discordance between a high LDL-C and ApoB/LDL-P.

  73. David Ma  September 18, 2012

    Hi Peter,

    I’ve come across the concept of post-prandial dysmetabolism where after a fatty meal is ingested, there are large amounts of chyloromicrons in the blood. This can then be deposited or cause an MI. But also read that such a thing may only occur in the presence of high glucose.
    Will you be blogging on this, and is this phenomenon a serious consequence?

    (reply)
    • Peter Attia  September 19, 2012

      Probably not in the near term.

    • David Ma  September 21, 2012

      So the phenomenon doesn’t really apply to the ketogenic diet?

  74. Ian  September 24, 2012

    “One question I have is why did the AUC calculations in Figure A show a reduction in plasma TG level for the glucose group?”
    Easy answer I think, glucose stimulates insulin release hence incresaed activity of lipoprotein lipase therefore decreased TAGs. Fructose doesn’t stimulate insulin release.

    (reply)
  75. Diana Attuso  September 29, 2012

    Hi Peter et al,

    I love it when doctors experiment on themselves! I just read this article:
    http://azsunfm.blogspot.com/2012/09/font-definitions-font-face-font-family.html (Does LDL-P Matter?)
    And my take away was this: Dr. Rakesh Patel switched from a SAD diet to a Low-Carb diet, his Lipid Numbers got worse but his actual artery thickness number (CIMT) got smaller and his CT score is 0… besides the fact that this is super cool, I didn’t know one’s coronary artery disease could “improve”. Here, in Peter’s post it says CAD can only be delayed, which, for me, translated to “whatever you have now can’t get better, you can only slow down the progression”.

    Do you see my confusion? Can you ‘heal” CDA with a low-carb diet and how does that translate to “you’re going to get it anyway eventually”?

    Thanks for any response!
    Diana

    (reply)
    • Peter Attia  September 29, 2012

      Yes, Dr. Patel was kind enough to share this post with me a few weeks ago. I was very happy to see this. Here’s what it tells me: we need new trials to evaluate the predictive power of biomarkers in the absence of (most) carbohydrates in the diet.

  76. Dave  October 2, 2012

    Hey Peter so are you familiar much with Anthony Colpo’s stance on cholesterol? I haven’t read his book “The Great Cholesterol Con”, but from some of his articles on his website, I get the impression he believes LDL has nothing to do with CVD and that its complete nonsense. Since it seems there is a strong correlation between LDL particle count and CVD, would you say he’s completely wrong on this or is it possible he’s right and that even LDL-P isn’t a causal factor?

    (reply)
    • Peter Attia  October 3, 2012

      I have no idea what he thinks/believes.

  77. Ted  October 4, 2012

    I’ve just completed a compare-contrast (A-B) study on myself involving manipulation of diet and statins to determine the effect either might have on my LDL-P. My diet was essentially Vegan. My statin was 20mg of atorvastatin. My LDL-P on the statin + vegan diet as determined by NMR was 732 on August 21st. I went off atorvastatin for 5 weeks and then had another NMR done on September 28th. My LDL-P had skyrocketed to 1659! In fact, LDL-C rose from 64 to 147 (so I’m concordant, I gather…), TC went from 118 to 210 and Trigs went from 79 to 90! My weight dropped from 187 to 163. I’m very lean now, which is one good thing that’s come of a Vegan diet. Before proceeding, though, I should note that it’s possible I have hyperlipidemia and/or hypercholesterolemia. Why do I think so? I have about 4 xanthomas, subcutaneous fatty nodes, on my arms and legs and these are considered suggestive of being hyperlipidemic. Also, about a year and 3/4s ago I had an LDL-P reading of 2384 without being on statins and eating a moderately low-carb diet. The biggest issue facing me these days is that I have stenosis in both vertebral arteries. I’m back on statins as of yesterday! I can’t be having elevated LDL-P with stenosis in both of those arteries!! I’m thinking of going low-carb, high fat while continuing with atorvastatin. Any comments from Peter or other readers would be appreciated.

    (reply)
    • Jane  March 29, 2013

      Ted,
      Clarifying question:
      Weren’t you on Paleo without statin before switching to Vegan plus statin? big improvement
      So now you’ve done an ABC study, with C being the Vegan diet without the statin? back to high LDL-P

      And now you are proposing a Paleo plus statin trial? (or an Attia/Taubes plus statin trial?)

      Please do let us know the results of your self study,; at least it will be another case study supporting a diet treatment.

      Without good randomized studies on these interventions that have external validity, it seems all we can do to minimize our risk or attempt to reverse the disease process is to experiment on ourselves.

      Thank you for sharing your results.
      Jane

  78. Mike A.  October 8, 2012

    Dr. Attia,

    I’m curious if you have any advice on questions that patients should ask when interviewing prospective doctors for the purpose of primary prevention of cardiovascular disease. Also, do you feel that cardiologists are best suited for this role, typically, or other specialists such as endocrinologists?

    It’s difficult to choose a doctor for many of us, so your input on this matter would be greatly appreciated.

    Thanks.

    (reply)
    • Peter Attia  October 8, 2012

      This is a great question. I’d start with an open discussion of their philosophy of the role of nutrition in human health. Are they wed to the food pyramid and conventional wisdom (fat is bad, grains are good)? As to what kind of doctor, it depends on the problem you’re trying to address. A good family doctor or internist should be the “quarterback” of your healthcare, with specialists being brought in for specific issues (e.g., lipid-related, hormone-related).

  79. ruben marcos  October 8, 2012

    Great blog. Where is part X???

    (reply)
    • Peter Attia  October 8, 2012

      In my head at the moment, but I’m hoping to get it out in the next 4-6 weeks.

  80. Dave  October 8, 2012

    You may find his peer-reviewed paper here interesting if you have some spare time.

    http://www.jpands.org/vol10no3/colpo.pdf

    (reply)
    • Peter Attia  October 8, 2012

      What is “spare” time? Sounds like an interesting, albeit theoretical, concept.

  81. Raymund Edwards  October 9, 2012

    Peter there are many interesting papers on the “ancient pathway called autophagy”

    Its activation is linked to starvation , Ketones , and vitamin D ( also papers looking at hibernation in animals )

    My Question ( linked to the niacin question )

    Is this .. –> It seems a lot known about the cholesterol question is only known as averages in a population suffering carbohydrate excess and vitamin D deficiency .

    Probably such people have this “ancient pathway called autophagy” down regulated . ( “we don’t eat ourselves enough” ( papers suggest this is so and a cause of age related diseases ) .

    How many other pathways might be effected .? ( previous question on Niacin )
    Maybe many concerns on the cholesterol question become altered .
    Maybe a Ketogenic diet and Vitamin D could reverse and prevent arteriosclerosis and that other things like autophagy become important than cholesterol numbers ?

    I am reading the work of Thomas Seyfried on Cancer and I have a family member with Epilepsy doing much better on a ketogenic diet. I have adopted a Ketogenic diet myself.

    The diet seems to change multiple systems in the body and has seen in epilepsy works through many pathways.

    http://www.sciencedaily.com/releases/2011/09/110908124140.htm

    Process That Clears Cholesterol Could Reverse Major Cause of Heart Attack

    ScienceDaily (Sep. 9, 2011) — Researchers at the University of Ottawa Heart Institute (UOHI) have discovered that an ancient pathway called autophagy also mobilizes and exports cholesterol from cells.

    http://www.sciencedaily.com/releases/2011/09/110908124140.htm

    Coronary atherosclerosis: Significance of autophagic armour

    “Autophagy is a lysosomal degradation pathway of cellular components such as organelles and long-lived proteins. Though a protective role for autophagy has been established in various patho-physiologic conditions such as cancer, neurodegeneration, aging and heart failure, a growing body of evidence now reveals a protective role for autophagy in atherosclerosis, mainly by removing oxidatively damaged organelles and proteins and also by promoting cholesterol egress from the lipid-laden cells. Recent studies by Razani et al and Liao et al unravel novel pathways that might be involved in autophagic protection and in this commentary we highlight the importance of autophagy in atherosclerosis in the light of these two recent papers.”

    http://www.wjgnet.com/1949-8462/full/v4/i9/271.htm

    (reply)
    • Peter Attia  October 9, 2012

      Raymund, your point does speak to an issue I and others have raised. I don’t know the answer and can only speculate, which I’ve done. Curious as the thoughts of others, also. Thanks for compiling.

  82. Kyle Knapp  October 11, 2012

    Just read the series after coming across the synopsis on Mark’s Daily Apple a few weeks back. Thanks for the effort and information. As someone trying to learn as much as possible for myself, my family, friends and clients, series like this are invaluable. Your analogies are very helpful in discussing these things and are a must have when interacting with people who have conventional wisdom filled brains and a little less biology in their backgrounds. I look forward to exploring your site in more detail. Thanks again!

    (reply)
  83. Brian  October 16, 2012

    Peter,

    First off, I know you can’t give medical advice over the internet. I respect that. I am however at a bit of a loss. I did 3 months on a strict ketogenic diet (not one cheat day and all “clean” whole foods). I got my standard lipid profile and an NMR.

    TC: 229
    LDL-C: 169
    HDL-C: 55
    TG: 22
    LDL-P: 2192

    I was obviously happy with my TG and HDL (previous “healthy” diet HDL was 36). But my LDL-P number is concerning me.

    Without asking for medical advice, is there something that could have effected the test to make that number so high? Was I not on the diet long enough? I’m definitely disappointed in that number. I’m hoping that maybe something went wrong somewhere and that’s not an accurate number. Anything you can tell me would be much appreciated but I understand and respect your limitations.

    Brian

    (reply)
    • Peter Attia  October 16, 2012

      Brian, I am definitely going to be doing a post on this exact topic, so I hope you can hold tight till I get there. The short answer is this: I actually don’t know what to make of a high LDL-P in the presence of remarkable TG and HDL-C…but I’m working very hard with some of the country’s experts to sort this out. In the mean time, I could suggest folks in your situation consider non-invasive testing to further stratify risk, such as hs-CRP, Lp-PLA2, CIMT, MPO. I won’t leave you hanging, but I need a bit more time to aggregate information. There is a great post you might want to read that addresses this: http://azsunfm.blogspot.com/2012/09/font-definitions-font-face-font-family.html

    • Randy  August 17, 2013

      Brian,

      Hey, I just posted my numbers at the bottom. They are similar to yours, but LDL-P is actually worse than yours. I feel your pain. I don’t know what to make of it either.

    • Pam  August 18, 2013

      I fall in the discordant group, too, that is mentioned here. Super wonderful “standard” tests including TG/HDL (<.5), eating strategy ketogenic (tested by meter), feel great, last NMR 2400+. Cartoid arteries clear of plaque. I was the one that told my doctor about NMR and they didn't resist to having it done. That was in May. Next one December. I continue to do what I have been doing and choosing not to worry. Looking happily toward the day when your post on this, Peter, appears. Thanks for all you do.

  84. Cara Zaller  October 26, 2012

    I listened to you on a few podcasts and wanted to get your opinion on my lab results.
    I’m a 5’2″ 44 year old female who is pretty lean. I eat a low carb diet (probably not under 50, but under 75 – never calculated it). Here are my #’s
    Total Chol 299
    HLD-C 85
    Trigs 50
    LDL-P 1,981
    LDL-C 204
    HDL-P 41.6
    Small LDL-P 173
    LDL Size 21.4
    My Insulin resistance score was 6
    My doctor is insisting I go on a statin. Is my lipid profile dangerous that I would need a statin? I’m pretty sure they don’t show to help females at all, but he says I have familiar Hypercholestrolimia so that would need medication. Should I cut down on my saturated fat consumption? I consume coconut oil, MCT oil, coconut milk and coconut flakes and red meat daily. I have never been overweight and I strength train and am athletic. Do hormones affect your LDL? I just got lab work from an endocrinologist since I don’t seem to make any hormones and thought maybe the 2 were related since cholesterol makes hormones, maybe it’s a pituitary issue that’s driving my numbers up. Any insight to my concerns and confusion would be great. Thank you.

    (reply)
    • Peter Attia  October 27, 2012

      I’m sorry Cara, I can’t provide medical advice.

  85. Bernard P.  December 12, 2012

    I have been holding my breath for part x, the one that probably interests a lot of people: the role of pharmacologic intervention.

    It must not be easy to write about this. It’s one thing to describe and explain relatively objective facts, but not so simple to wade in the more controversial waters of medication use.

    I am looking forward to your post on this.

    (reply)
    • Peter Attia  December 12, 2012

      Bernard, I sure do hope I can get to this, but there a few pressing issues ahead of it.

  86. Todd  December 20, 2012

    Peter,
    You posted somewhere (and I can`t find) a multi-day recording of your NMR numbers and their variability which I believe was significant.
    Where was this ?
    Was your diet constant throughout ?
    Thank You

    (reply)
    • Peter Attia  December 20, 2012

      I have not posted it yet, but I did allude to it in a post. Variability on LDL-P was over 10%, while apoB and LDL-C were less than 5%. Yes, diet constant through the 3 days.

  87. Ty  December 28, 2012

    Hi Peter,

    I’ve only skimmed through most of this, but so far I’m impressed. Excellent work.

    Disclaimer: I am not requesting medical advice, but rather a dietary compromise.

    Here is my situation. After reading Gary Taubes “Why We Get Fat”, I switched to a high fat low carb diet, which I’ve faithfully adhered to for the past 4 months. When I started this diet I was about 185 lbs (I’m 5’8). After two months on the diet I dropped down to 168 lbs, which has been pretty much been maintained for the past two months.

    Now I started this diet knowing I would have a physical coming up, and my wife has said “If your cholesterol goes up, this diet stops”.

    Well, I had my physical last week and here were the results:

    LDL = 170 mg/dl
    HDL = 74 mg/dl
    TG = 64 mg/dl

    My PCP said my LDL jumped 80 points since my last physical (a year ago). For the sake of full disclosure, I’m on ramipril 5mg for hypertension, and I exercise infrequently (averaging 3 or 4 days every other week).

    Anyway, once my wife finds out about my LDL, there’s going to be a “debate” about the future of my diet, and I’m wondering what sort of compromises I can offer that will keep me in ketogenic mode (honestly i feel great), but are friendly to the anti-saturated fat/anti-cholesterol group.

    Here’s my typical diet:
    Breakfast: 3 eggs, 3 or 4 slices of bacon, 3 sausage links, pretty much everyday
    Lunch: chicken (thighs, legs), burgers (no bun), 4 or 5 servings of spring mix, sometimes fish.
    Dinner: same as above (lunch is usually left overs)
    snacks (salami, roast beef deli meat, deli cheese, polio string cheese, almonds, cashews)

    Thanks in advance

    (reply)
    • Ty  December 28, 2012

      Correction:

      LDL = 179 mg/dl
      TG = 54 mg/dl
      TG/HDL ratio = 0.73

      Thanks again.

    • Ty  December 28, 2012

      This is a science question.

      Cholesterol is used for steroid hormones synthesis. One such hormone is aldosterone, which is responsible for fluid and sodium retention. Now going backwards until I get to my point, aldosterone secretion is triggered by angiotensin II, which is converted from angiotensin I by angiotensin converting enzyme (ACE), correct? Well, ramipril is an ACE inhibitor, so that entire process is interrupted. Less angiotensin I is converted to angiotensin II, meaning there is less available to trigger aldosterone secretion.

      If less aldosterone is secreted, could that mean that less is synthesize? And if so, is it possible that the raw materials to produce the aldosterone are continuing to be supplied in spite of demand by the adrenal glands? And if so, could that account for the elevated LDL-C count?

      Thanks.

    • Peter Attia  December 28, 2012

      I don’t think the production of aldosterone is significant enough to account for the difference you describe.

  88. Ari  January 2, 2013

    Peter,

    Have read through this entire series, it was very well done, thank you. I have also tried to read through as many comments as I can to find an answer to my question but there are a lot throughout the series. My question is how you would suggest going about finding a primary care physician that is staying on top of the most current research and theories as you do. In my experience, most of the doctors I have had contact with seem to be a decade behind, and given this subject, that is too far. My family has always had issues with cholesterol and heart disease. My father has gone the route of avoiding cholesterol in food and using statins as suggested by his doctor (a very well known doctor in the media). He has been maintaining a decent total/LDL level for a while but I get the feeling his risks are not reduced, especially after your series. I myself have had good numbers but my ApoB level is elevated (not sure if it is an estimated or directly measured value) and want to get NMR testing as you have pointed out. In the end a doctor who can help me manage these numbers and figure out a way to reduce my risks using the most up to date (and credible) research out there instead of what they have learned 20 years ago. Any suggestions on how to find the right physician would be greatly appreciated.

    Thanl

    (reply)
    • Peter Attia  January 3, 2013

      Ari, beyond the stuff you’ve already probably tried, I’m not sure I can offer much, other than to suggest you not rest until you find a doctor that meets your standards.

    • Ivan  January 3, 2013

      Hi Ari, have you looked into Jimmy Moore’s (livinglavidalowcarb) list of low-carb doctors?

    • Maryann  January 5, 2013

      Hi Ari and Peter,

      There are a couple of websites that can be of potential help to you and others. Lipidboard.org and lipid.org have databases of members by area of the country. Some of these lipidologists are also cardiologists and primary care physicians. Best wishes, maryann

  89. William T  January 13, 2013

    I’m still working through the material, so forgive me if this has already been answered.

    On the first part you wrote “…Everything I have learned and continue to learn on this topic has been patiently taught to me by the words and writings of my mentors on this subject: Dr. Tom Dayspring, Dr. Tara Dall, Dr. Bill Cromwell, and Dr. James Otvos.”

    What role did they actually play? Did you have a personal dialogue with them, or was this a condensation of their research and knowledge passed via other sources? Have any of these individuals reviewed this series of articles or commented on it?

    Thank you for this excellent series, Peter. I hope to see lots more in the future.

    (reply)
  90. Spar  January 14, 2013

    Hi Peter, I am just trying to understand how much do Coconut/MCT oil “extend” Ketosis? Do they help you produce Ketones even if you go a bit more that 50g of carbs?

    Also hypothetical question, if I am eating lets say 80g of carbs, I am probably not producing Ketones and therefore probably not getting enough glucose for the brain? So is it not healthy to be just above Ketosis?

    (reply)
  91. James Fox  January 14, 2013

    Dr. Attia thank you for this excellent and educational series on cholesterol, and also to all those who have provided a valuable contribution with their questions and comments. I have one question which I would like to ask, it’s a point I’ve seen discussed on other forums but no one has been able to provide a proper answer:
    It relates to a person who is following a low to very low carbohydrate paleo diet, has no obvious health problems, non smoker who looks after his/her health but with a family history of CVD. Following an NMR test the person finds out he/she has a LDL-P count of 3000 nmol/L, Trig/HDL-C = 0.75 (HDL-C77, LDL-C 220, Trig 57), Lp (a) 70, IR score of 25, hs-CRP 0.20, Lp-PLA 250, Apo E 3/4 . With such a high particle count what options does this person have? What should he/she be doing if a low carb / high fat diet has been followed for some time?

    (reply)
    • Peter Attia  January 15, 2013

      One should wait for part X of the cholesterol series.

  92. Joe B  January 16, 2013

    Dr. Attia,
    IMO you have written the most informative series on cholesterol I have seen. I am waiting for X hoping that the contents will answer a question that is very important to me. I recently had a drug-alluding stent placed through my 88% occluded circumflex artery. In addtion, my right coronary artery is 100% occluded but has found a collateral blood supply so that area of the heart is healthy according to cardiology. This stent requires drug therapy for about a year after placementt, so I must take Plavix for that period of time. As Plavix is used to prevent blood clotting, does it conflict with taking Vitamin K-2? Also, I have been on a high dose statin from 1988 until about 2 years ago when I stopped it after developing neuropathy in my feet and severe muscle pain in my legs and shoulders. I have acheived about the same cholesterol levels after about a year on low carb as I did with the statin,
    while losing close to 40 pounds. I also participate in a very high level of excercise now that I’m angina free. I am very interested in seeing your view on drug therapy for lowering cholesterol. Lipitor will lower LDL but there may be a painful price to pay in the process. I fear that the truth is yet to be told about these drugs.

    (reply)
  93. Richard Cannon  January 23, 2013

    Dr. Attia

    I greatly appreciate your efforts to educate us about nutrition and health. It is difficult for most folks to objectively evaluate often seemingly contradictory information on healthy eating. The following link to an article published in the Journal Circulation (2010) argues that dietary cholesterol from foods like egg yolks present a serious risk associated with increased vascular inflammation. Can you comment?
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989358/

    (reply)
    • Peter Attia  January 23, 2013

      You realize Spence is the same guy who thinks eating eggs is as harmful as smoking in terms of vascular disease, right? Oh, and that’s all based on observational epidemiology.

    • Richard Cannon  January 23, 2013

      Dr. Attica,

      Thank you for your comments on the article. This is my back story and why I asked about egg yolks. I am a lean 65 year old who exercises daily and avoids sucrose and high glycemic foods – following a low glycemic diet (protein and veggies) for over twenty years. My doc uses the NMR Lipoprofile. My traditional markers are always well within range but particle number and size values are not optimal. For example, LDL-P is approximately 1200. I have been working with a naturopathic doc to try to improve these values. I added eggs to my diet (1-2/day) as a protein source last year. My lab valves all significantly improved with one major exception. My LP Plac2 values increased < 50 to 255. My docs were shocked but offered no explanation. So now I'm stuck in the quandary of wanting to maintain the optimal lipid profiles while addressing the inflammatory marker. I was thinking about avoiding or drastically reducing egg yolks (reducing extra dietary cholesterol and arachidonic acid) and supplementing with choline but realizing that this may be flawed reasoning. Any thoughts or insight on how to approach this dilemma?

  94. Richard Cannon  January 26, 2013

    Dr. Attia,

    I’ve also been attempting to locate information regarding non vascular causes of elevated Plac 2, but have not finding anything on google scholar or pub med. Do you have any suggestions?

    LDL-associated PLA2 (PLAC) (Info from Cleveland Clinic website)

    This blood test measures the level of lipoprotein associated-phospholipase A2 (Lp-PLA2), an enzyme associated with inflammation, stroke and heart attack risk. However, elevated levels also may be due to non-arterial causes.

    http://my.clevelandclinic.org/heart/services/tests/labtests/testscad.aspx

    (reply)
    • Peter Attia  January 28, 2013

      Yes, there are no doubt some false positives. I suspect there are false negatives, too. Speaks to the need for a triangulating approach. This is why, at least in my clients, I use many markers and modalities (e.g., lipids, inflammatory markers, CIMT, family history, genetic markers).

    • Richard Cannon  January 28, 2013

      Dr. Attia,

      Hmm, I think a retest might be informative. Thank you for giving your time and knowledge to help others.

  95. James  March 4, 2013

    Hi Peter,
    Just spotted this article linked in Sisson’s website:

    http://www.sciencedaily.com/releases/2013/02/130227151254.htm

    Not sure you mentioned some of the things studied by Mr. Fred Kummerow in this otherwise amazing series of articles!

    J.

    (reply)
    • Peter Attia  March 4, 2013

      I’m actually not familiar with this gentleman, but he observations seems reasonable.

  96. Richard Earnshaw  March 4, 2013

    Hi there,

    Wow, great information. I am a Critical Care Paramedic, and participate in daily workouts, weights, cardio ( burn some 350 calories) and stretching. i have been unable, at age 56, to reduce my abdominal fat. It is clear now that the muffin and pie that I consume is killing me, too much sugar. While I look to remove that from my diet, I am intrigued by the Vegan diet, and its seemingly profound benefits, documented by Dr.C.Campbell and Dr. Esselstyn, I am considering making a bold move in a dietary sense. I have not been successful just with exercise and their comments certainly seem pragmatic. I do have a family history of cardiac risk with elevated cholesterol and a CT scan which demonstrated scaring at my LAD.

    What do you think?

    Cheers,
    Richard

    (reply)
  97. Mike  March 7, 2013

    Hi Peter,

    Have very much enjoyed the series. I know you cannot provide medical advice but am curious as to what you think is a better measurement, if you had to choose, LDL-P or Apolipoprotein B. After about 8 months of basically removing most sugar, exercising 4 times a week and dropping 20 lbs, I got my LDL-P down to 1461- from over 2100. My ApoB is 89. I’m curious as if both measurements are available, what is the best measurement to look at? Looking forward to part X

    Best regards

    Mike

    (reply)
    • Peter Attia  March 7, 2013

      If the LDL-P is measured with NMR, it is probably more important than apoB.

  98. Andreas  March 8, 2013

    Hello Peter!

    I want to sincerely thank you for all this free information on heart health. I’m a Danish paramedic and I read a lot of science and health blogs as a little hobby probably spawned by my work. It’s very interesting to learn what really goes on “behind” the endless ECG’s. You are definitely one of my “regulars” along with Chris Masterjohn, Chris Kresser, Mark Sisson and Gary Taubes. Keep up the great work!

    I run kind of an n=1 experiment featuring myself from time to time. This time it’s rice MicroRNA and the impact on LDL receptors. I have a doctor who willingly has blood tests done on me when I ask him nicely. (He’s very interested in nutrition and sees the point in experimenting, although he does tend to think that 3 eggs a day and the lauric acid in coconut is gonna kill me!) Normally it’s a standard lipid panel, but this time I had an ApoB/Apoa1 test done and sent to the States Serum Institute for analysis. I’m waiting for the results right now. However, I honestly don’t know what numbers to expect or what to hope for. What would be some heart-healthy numbers for this test (ApoB and ApoA1 values) apart from a low ratio? I have searched a lot for this information but somehow it has escaped my attention. Would you be able to help me out?

    (reply)
  99. Jeff  March 11, 2013

    I discovered this blog last night and have spent most of the last 24 hours getting up to speed and I am giddy with excitement. I’ve been attempting to follow the growing scholarship over sugar and its effects on blood chemistry and cholesterol, and I have been absolutely appalled at the state of nutritional observational research, as well as the state of medical advice I have received. (I can’t count the number of times I have screamed “correlation is not causation” at mainstream media…I assumed I was missing something.) I am so incredibly happy to have Dr. Attia (and some of the scholars to which he links) to synthesize current research for me. At age 30, I had my first cholesterol test (about 11 years ago). My TC was 375 (I don’t even know my specific numbers now, other than my HDL/LDL ratio was “normal”). Because I exhibit no other signs of metabolic syndrome (I look young, I’m thin and athletic), nobody seems to know quite what to do with me. I once had a cardiologist tell me that with high doses of statin, he could probably fix me and if not, not to worry, he could filter my blood of cholesterol (!!). So…that made me worry (and not visit him again). Since then, I have been prescribed a variety of statins by confused doctors that have various levels of success at bringing down LDL (and giving me very achey hips and legs), while my HDL has remained high. I’ve been consistently underwhelmed by the general profession’s knowledge of the intricacies of high cholesterol and decided to take matters into my own hands, which is how I landed here. A couple questions…when is the next volume regarding the use of pharmaceuticals coming out? I feel like I need to make a decision about statins on my own, but finding useful information is well nigh impossible. Two…how does one go about getting LDL-P and apoB tested? I know you have listed companies that do so, but…how do you actually do it? I don’t have a lot of faith that my doctor is going to have any idea. Can I direct a sample to them? Send it myself? I know this seems like a silly question. Thank you very, very much for what you are doing.

    (reply)
    • Peter Attia  March 13, 2013

      I think currently you need a doctor to order the test.

    • Maryann  March 14, 2013

      Hello Jeff, I heard Jimmy Moore recommend privatemdlabs.com as the lab he uses for his testing. No doctor is needed. Best wishes, maryann

  100. Dawn  March 14, 2013

    Hi, firstly can I say I think what your doing is amazing and I love your blog. Sorry if I am posting this in the wrong area. I am from the U.K and I came across your blog from Zoe Harcombe’s forum, I started following her eating plan about 6 weeks ago and because of the way I am, I cant just take her word for it, I have to find real evidence that what I am doing is the right thing, hence why I like your blog! I have a question that I hope you may be able to advise me on.
    I had my gallbladder removed last October and I have read on zoe’s forum that because I don’t have a gallbladder I may not be able to absorb the nutrient’s from the fat I am eating and that I may even store some of the fats, which obviously I don’t want to do. I have read a lot about people gaining weight after gallbladder surgery, which would be explained if your storing fat and not digesting it properly. I have read that taking bile salts can help with this but have also read that bitters (herbs) would be a better option because they would stimulate my liver to produce more bile, today I read else where that in fact bitters are not recommended after gallbladder removal. So as you can imagine I am quite confused as to what is the best thing to do. I know you cant advise me medically but I am wondering if you could point me in the right direction regarding this topic, maybe a trusted website or book? I cant ask my doctor because his advise would be eat a low fat diet, that is what all the doctors say about gallbladders in the u.k.
    I am an active member of ” Unofficial The Harcombe Diet” facebook page and there are a few of us on there with gallbladder problems and ones like me who don’t have gallbladders anymore, we would all be extremely grateful for any advise you may be able to offer on this subject, thanks! :-)

    (reply)
    • Peter Attia  March 18, 2013

      This is a bit misleading, Dawn. The gallbladder is just a reservoir for bile (which the liver produces to help with fat and cholesterol absorption, among other things). Absent a GB, your livers still makes normal amounts of bile, but it’s true for that for some people status post cholecystectomy (GB removal), the absolute amount of bile delivered in one instant can be reduce. If you notice malabsorption after a fatty meal, it would suggested slowing down or spreading it out over more time is the prudent thing to do.

  101. Rob  March 18, 2013

    Peter, thanks so much for your blog. My wife and I have been on a Keto Adaptive diet for about three months now and we both have been very happy. Lots of energy, improved alertness and a significant change in body composition. Neither of us are overweight but we have been able to maintain our weight while reducing body fat. All good. I have had one bump in the road related to my Lipid Panel. One year ago my numbers where: Total Cholesterol – 237, HDL C – 84, TG – 46, LDL C – 144. Last week I had my annual physical (age 53) and the numbers have changed: Total Cholesterol – 327, HDL C – 97, TG – 36, LDL C – 223. Going in for a re-test as my doc is quite concerned. Should I pursue a NMR LipoProfile? Not sure why my LDL would react to the keto diet in this way. Thanks for your opinion.

    (reply)
    • Peter Attia  March 18, 2013

      I’ll try to address this (common) theme in part X of the cholesterol series.

    • Bill  March 19, 2013

      My panel went from this (doctor no like):

      Total: 382
      HDL: 157
      LDL: 217
      Triglycerides: 39

      to this (doctor like):

      Total: 284
      HDL: 162
      LDL: 117
      Triglycerides: 23

      I suspect this drastic LDL reduction resulted from a modest reduction of dietary sat fat (not sat fat avoidance, just using olive oil instead of butter to cook sometimes, allowing more pork instead of beef, adding a bit of nuts, allowing a modest amount of starch once or twice a day, etc.).

      A recent Neutreval test showed, in accordance with this dietary change, a small reduction of RBC sat fat and small increases in RBC mono and polyunsaturated fats compared to an earlier test.

      My doctor and I were both extremely surprised that such a modest dietary change could cause such a tremendous LDL reduction, apparently. I have no idea what the health consequences of this reduction may be, positive or negative, but my relationship with my doc certainly improved :-)

      I was also impressed by even further reductions in fasting triglycerides, and increase in my already ridiculously high HDL, even as I added back starch. I speculate that my period of VLC maybe fixed my metabolism so I can tolerate modest amounts of carbohydrate better. Intermittent fasting (no breakfast) and very brief, intense, once-a-week, Body by Science style weightlifting, may be contributing as well.

    • Ari  March 20, 2013

      Peter,

      Maybe this is part of what you are going to comer in part X, but I was going to post a question and reference to a study that discussed the implication of high LDL-P to future CVD events, but when adjusted for HDL-C and TG levels, the association disappears and is statistically insignificant (at 95%). I was interested in finding this since, similarly to the numbers I am seeing in these recent comments, my TC, LDL-C, ApoB are high, but so is my HDL-C and my TG/vLDL-C/LPa are low, which causes a disconnect for me:

      TC 241
      LDL-C 160
      HDL-C 71
      TG 52
      vLDL-C 10
      LPa 1
      ApoB 138

      Overall I am in pretty good health and recently measured at 10.85% body fat hydrostatically. I train a lot and eat a mod protein, high fat, lowish carb paleo style diet (30%/20%/50% P/C/F by calories).

      Here is the study
      http://content.onlinejacc.org/mobile/article.aspx?articleid=1188679

      The population is on average, in their words, elderly at mid-60′s where as I am in my late thirties so not sure it is comparable or even if this study is relevant in your opinion. Do you know this this study? Is it meaningful? Would the fact that my HDL and TG levels (and the ratio between them) perhaps indicate that my elevated LDL-C may in fact not be an issue?

      On a similar note, these numbers are from this past December, previously I was tested in July ’12 and between the two tests my TC/LDL-C/HDL/ApoB increased and TG dropped (ApoB & LDL-C raised at about the same rate so maybe particle size stayed constant), the main things that changed in my diet in between was that I was supplementing Dextrose or Maltodextrin post workout with whey and also increased my saturated fat a lot through coconut oil/butter and grass-fed butter. After reading your series I quickly dropped the sugar post workout and also the whey and am sticking to whole foods, but I still wonder if the increased saturated fat is partly or the whole reason my levels went up in the various lipid measures. Right now my saturated fat is around ~35% of total fat, but I consume 150-200 grams of fat a day.

      Thanks for entertaining my question and also for all the great information you provide and the hard work you put into it

      -Ari

    • Peter Attia  March 24, 2013

      This conclusion applies under 2 conditions: to this population (not sure how discordant they were) and at the population level. It’s up to you if you want to infer from those 2 conditions to yourself, personally.

  102. Indy M  March 27, 2013

    Dr. Attia -

    after trying for over an Year to lower my LDL-P from ~1500 to <= 1000, with diet and lifestyle, I did not succeed(South Asian genes) and decided to give medications a try.
    With Ezetimbe10mg+Simvastatin10mg together my LDL-P is now '582' , LDL-C '55' , HDL-C '66' and HDL-P '31.6'(Dr. Daysprings's case paper 132 talks about a Woman where with these same medications, the patient had a big drop like mine; my Statin dosage is smaller) .

    My question, if you have 10 secs, is that can one have too low LDL-C and or LDL-P?? The lowest LDL-P I see on the chart is ~720.

    Thanks in advance!
    Indy M.
    Sunnyvale.

    (reply)
    • Peter Attia  March 28, 2013

      Yes, at some point, you can be too low. Not clear where, but probably below 30-35 mg/dL of LDL-C (not sure you can have too little LDL-P, but as you know 582 is probably in the 3rd to 5th percentile.

  103. Guido Vogel  April 5, 2013

    Hi Peter,

    I was exicted to get my blood test results after 7 months of low carb dieting (really low, like Atkins induction phase). Unfortunately, I didn’t do a test when I started out.

    These are the results:

    Cholesterol 6,3 mmol/l
    HDL 1,4 mmol/l
    Triglycerides 1,2 mmol/l
    Cholesterol ratio 4,5
    LDL 4,36 mmol/l
    ApoB 1,29 g/l

    I found them to be a little dissappointing for a 42 year old male with no family history of CVD (most numbers pretty high).

    But my question is how to assess the ApoB results:
    1. It says 1,29 g/l on the result form. That is 129 mg/dl right?
    2. The result form gives 0,49 g/l – 1,73 g/l as range for normal values. So I should be ok
    3. However I found numerous sources stating that <90 mg/dl or even <80 mg/dl are the safe ranges. So now I am confused. is 1,29 g/l a safe result or not?

    Thanks for your help (and I donated 100 dollars to NuSi. Any news on when the first experiments will start)?

    (reply)
    • Peter Attia  April 7, 2013

      Guido, thanks so much for your generous donation. The first experiments will begin this year. Look for the announcements in time…

    • Guido Vogel  April 8, 2013

      You’re welcome. I am also bringing a lot of your stuff into the Dutch discussion fora to show that a calorie is not a calorie. Trying to convince (among others) the author of leading new diet over here (Dr. Frank diet).

      But any thoughts to share on how to assess the ApoB values? Are these normalized accross labs or might it be somewhat different per lab? Again 129 mg/dl is much higher than safe ranges of <90 or even <80 that I see.
      Or should I tell my family that I will quit drinking coffie with heavy cream and fatty meats :-) ?

    • Peter Attia  April 8, 2013

      I will hopefully address this concern in Part X.

  104. Guido Vogel  April 8, 2013

    Oops, “Or should I tell my family that I will quit drinking coffie with heavy cream and fatty meats?” should be: “Or should I tell my family that I will quit drinking coffee with heavy cream and stop eating fatty meats?

    We might not have the best culinary culture in the Netherlands, but we don’t put (fatty) meat in our coffee :-)

    (reply)
  105. IS  April 9, 2013

    Hi Peter!

    Your articles are avesome. I have been on a ketogenic diet for two months.
    Average values:
    Carbs under 30 grams
    Protein 15% of total daily intake
    Fat 85%, saturated fat 33%, monounsaturated 27%, omega3 : omega6 ratio = 1 : 1,4.

    My blood test before:
    Cholesterol 5,11 mmol/l
    Triglicerides 0,5 mmol/l
    HDL 2,17 mmol/l
    LDL 2,71 mmol/l

    My Blood test after:
    Cholesterol 7,2 mmol/l
    Triglicerides 0,6 mmol/l
    HDL 3,0 mmol/l
    LDL 3,7 mmol/l

    As you can see the ratios stayed the same, all the values just increased exactly by 40%.
    Now for the next two months i am going to increase the monounsaturated fats and reduce the saturated fat because i would like to lower my LDL. What dou you think abaout the blood values and do you think this strategy might work??

    Keep up the good work and thank you for the answer!!

    (reply)
    • IS  April 9, 2013

      Oh yess and i would like my total cholesterol level to get lower, do you think it could decrease by reducing the consumption of saturated fat???

    • Peter Attia  April 9, 2013

      Will try to address these issues in Part X.

  106. Eric  April 12, 2013

    Dr. Attia,

    You’ve discussed the importance of omega-3 to omega-6 fatty acid ratio in dietary intake. Some recent anecdotal evidence I’ve come across suggests that VERY high doses of omega-3 fatty acid in the form of fish oil has a strong correlation with improving cholesterol profile. By very high dose I mean 30-40 grams per day. What are your thoughts on this?

    (reply)
    • Peter Attia  April 14, 2013

      If true or not, I’m not sure. It’s probably somewhat dependent on apoE status. However, EPA and DHA (the “active” ingredients in fish oil) are by no means benign. You can definitely get too much. Side effects range from anti-anabolism to spontaneous bleeding and easy bruising. I titrate my levels very closely.

  107. Joan Borysenko  April 18, 2013

    First of all, Peter, you’re an ace. Thank you so much for writing these brilliant and thoughtful blogs. I’m a former cancer cell biologist (I’ve got a doctorate from Harvard Medical School) and have been greatly affected by the work of Dr. John Ioannidas, demonstrating how poorly designed most biomedical research really is. The fact that “evidence-based” interventions are so often based on poor logic is really an eye opener. Your posts really point out where we need to go and what’s missing in nutritional science, which makes me extra delighted that NuSi has recently received some serious funding. Congratulations.

    Now, for a question about lipids. My husband and I have been eating a low carb diet (probably around 100 gms of carbs a day) for about 9 months. We started it because my husband Gordie has a scary calcium reading of 600 in his coronary arteries. We tried an Ornish-type diet first for about 18 months. The result was poor. His LDL particle which were previously large and fluffy reverted to small. My blood pressure went through the roof. So, I began to distrust the low fat literature. On the low carb diet my LDL-C is 86. My HDLs are 76. My triglycerides are 54. BUT…LDL-P is 1355 even though fasting insulin is very low. My husband has similar values in lipids other than somewhat higher LDL-C. BUT…His LDL-P is even worse than mine- up around 1500. His cardiologist wants him on statins to reduce LDL-P (and LDL-C). My reading of the research suggests that statins are unlikely to reduce LDL-P (and I’m not particularly concerned about the LDL-C). Furthermore, I’m not a fan of potential statin side effects, especially since my husband doesn’t need any help reducing inflammation. His CRP is actually zero. Since neither of us has metabolic syndrome, and we’re both slim, is the discordance between our LDL-P and LDL-C values still likely to correlate with an increased risk of CVD? If so, should we be reducing fat to decrease LDL-P? I can’t find anything else that might reduce it but niacin and I wonder about that, too.

    (reply)
    • Peter Attia  April 20, 2013

      Joan, discordance does not imply risk, per se, but it does suggest advanced testing (i.e., apoB/NMR) is warranted to properly stratify. I’m not able to comment on numbers. Sorry.

  108. Justin  April 24, 2013

    Peter,
    Thank you for compiling this information. I am trying to think about how to apply what I have learned here and I think I’ve come to this: cholesterol is vital to our survivial and the body has very efficient feedback loops to regulate its production. If we are not consuming enough, we will produce it and vice versa. So, aside from omega 6s, etc, it does not matter how much cholesterol we eat. However, as it relates to our cardiovascular system, inflammation is the real culprit of our problems and testing for these markers (CRP, etc) seems to take a greater importance than the standard lipid profile that we are used to. Do you agree and can you elaborate on this?
    Thanks again for all this info.

    (reply)
    • Peter Attia  April 24, 2013

      Justin, I’m actually giving a talk this weekend at ASBP which will address this. But don’t confuse non-causal markers (e.g., CRP) with causal markers (e.g., LDL-P) or even targets of treatment. I’ll try to address in part X.

  109. Jeff  April 26, 2013

    First began reading you a few months ago. I am a physically fit 41 year old male (approximately 11% body fat) with a history of exceptionally high cholesterol (unmedicated, 250 – 375 TC), along with a decent ratio of LDL/HDL and typically elevated but not abnormally high triglycerides. I had tried low fat diets in the past and saw zero change in LDL, so have been on statins for most of the last 10 years. I began reading your and Taubes’ material and decided that, although I don’t have typical signs of insulin resistance, I would try a very low carb diet. I have spent the last 8 weeks cutting out almost all sugars and carbs (not ketogenic as I ate legumes and drank primarily milk), but no grains or sugars. Just got my NMR lipid profile. Yikes. TC is above where it was last year (309). LDL-P numbers are through the roof (3247) and LDL-C higher than before. HDL-C lower than before, and HDL-P numbers not so hot (30). My triglycerides are higher than they have ever been as well. I am happy to have run a self experiment on this, but it looks like, at least for me, low carb is not helpful and, in fact, worsens my blood chemistry. My test claims I’m high risk for insulin resistance, which seems odd considering the low carb/sugar diet is the first time I have shown up as possibly insulin resistant. I only have with-statin standard blood tests to work with, so now I plan to do 8 weeks of my normal diet on 20 mg daily statins and see where I stand. I can’t really justify not taking statins now that I have failed to improve things on either a low fat or a low carb diet. Running out of diet options. Sigh.

    Still, I’m a huge fan of what you and Gary Taubes are doing. Thank you so much.

    (reply)
    • Peter Attia  April 28, 2013

      It may be less about your carb restriction and more about the types of fat you’re using. Obviously, I can’t suggest anything particularly insightful from a distance, but maybe switching from high saturated fat to less (and replacing it with monounsaturated) and more leafy veggies? I have seen this work in the past, for what that is worth.

    • Richard S  April 28, 2013

      Jeff,

      I’ve been lucky, in that my experience has been much like Peter’s. I’m older (57) and don’t exercise as much (who does?) but my weight has dropped from 207 to 173, and I no longer need statins or BP meds. I’m confident that eating fewer than 50 carbs/day (and closer to 20/day) is a BIG part of my success.

      One thing I think I’ve learned from my low carb dieting is that the effects of eating fewer carbs are not linear for many (if not most) people. In other words, one cannot simply eat more fat and reduce carbs, and expect great results, or even good or better results.

      You might want to check out “The Art & Science of Low Carbohydrate Living” by Phinney and Volek. In the book, the authors note that increasing one’s dietary fat from 30% to 60% (of daily energy intake) can actually make one’s insulin sensitivity worse. However, when energy from fat climbs over 60%, then one’s insulin sensitivity starts to improve. (By increasing dietary fat, they also mean reducing carbs.)

      In other words, getting incrementally fewer carbs and more fat might not help, and it can actually hurt, if you’re still eating enough carbs to cause an unwanted insulin response. (I’d been avoiding carbs, generally, for years, with no clear benefit. But when I REALLY stopped eating carbs, my weight started dropping and my lipid numbers improved.

      If you’re still drinking milk and eating legumes, you’re probably not on a real low-carb diet (or I should say, not low enough for you, since everything depends on how we each react). To find out whether the diet works for you or not, you might need to reduce carbs significantly, to somewhere between 20g-50g per day.

      At least, that is what worked for me. Good luck!

  110. Jeff  April 29, 2013

    Thanks to both of you for responding, although I do note that the suggestions are polar opposites (one is higher saturated fat and the other lower saturated fat). I intend to continue experimenting, but my numbers are so off the chart that it feels irresponsible to not include a statin at this point (which is what my very patient primary care doctor is begging me to do). One of the problems with self experimenting is with so many possible variables, by the time I figure out what might work for me, it might be too late.

    How outside of the norm is a LDL-P number of 3247? It seems to be literally off the charts.

    I have no physical markers of insulin resistance. I.e., I am thin, I do not gain weight or lose weight easily (or really, at all, no matter what I do). What is the best way to determine insulin resistance? It seems more likely that I have hypercholesterolemia, which doesn’t seem “treatable” by diet change. I haven’t reviewed this paper, but it sounds like my case may be one in which statins are actually required.

    http://eurheartj.oxfordjournals.org/content/29/21/2625.full

    (reply)
    • Richard S  April 29, 2013

      Jeff,

      In no way did I mean to contradict Peter. (He knows much more about all this than I do.) I also don’t think I did contradict him.

      Peter suggested that you change the type of fat you are eating (less saturated fat, more monounsaturated fat) and eat more leafy vegs. I’m not disagreeing with that, and have no insight on those points. You mentioned IR in your first post, and I just wanted to share the observation that eating fewer carbs might not help IR, unless one gets the carb intake down significantly. (A no carb diet might not help you, but you might need to try fewer than 50g of carbs a day to really know.)

      Since you don’t have a weight issue, your case is certainly different from mine, so I’m probably not much help. Sorry. I will add that I stayed on statins until I got my fitness level up and weight down. Then I dropped the statins for a few weeks, to take the tests and confirm that I don’t need them.

      Please let keep us posted on what you learn, if you don’t mind.

  111. Jeff  May 1, 2013

    I will keep posting my test results and my experiments. I love this community, and Dr. Attia’s work, and appreciate any and all insights. Certainly didn’t mean to insinuate otherwise. I was highlighting the difficulties inherent in self-experimentation (and, more globally, the attempts to provide meaningful nutrition guidance). So many variables, but limited time and resources. It is well-nigh impossible to alter just one variable at a time and would take several lifetimes (many ending in adverse cardiac events!!) to try to do so and collect meaningful personal data.

    For the next 8 weeks, I intend to be on 20 mg of statin and continue to abstain from as much sugar and carbs as I can. I don’t have the lifestyle and/or self-control to conduct more nuanced moves. I will repost when I get my next lipid profile.

    (reply)
  112. Jeremy S.  May 3, 2013

    Dr Attia,

    I just got the results from an NMR profile I requested after my Dr. freaked over my 270 TC…I can see generally that I’m in pretty good shape, but welcome you pointing out any outliers that jump out at you…

    NMR Lipoprofile
    CVD Risk:
    HDL-P = 34.7
    Small LDL-P = 157
    LDL Size = 21.5

    Insulin Resistance/Diabetes Risk
    Large VLDL-P = <0.7
    Small LDL-P = 157
    Large HDL-P = 11.6
    VLDL Size = Too small to measure
    LDL Size = 21.5
    HDL Size = 9.9
    Insulin Resistance Score = 4, (0-100)

    NMR Lipoprotein Test
    LDL-P = 1589

    Lipids
    LDL-C (Calculated) = 160
    HDL-C = 81
    Triglyceride = 25
    Total Cholesterol = 246

    Thanks, Jeremy

    (reply)
  113. Stephen Quirke  May 27, 2013

    Hi Peter

    I have been searching for information after receiving my last lipid profile from our local lab. As an aside, they were reluctant to draw and submit the blood without the referral from a GP. I referred them to the 7 megatrends of Paul Keckley, specifically that with ‘unconstrained connectivity’ users will be managing their own healthcare information. Eventually they let me do it.

    My LDL number is slightly down on the test I did two months ago but still very high and perhaps the drop was within normal weekly variance.
    I also asked for an apo-A1 and apo-B count which they did. My apo-B is very high. The apo-B/apo-A1 is just over 1 (1.66/1.56) which I believe is in a high risk zone. I know you have asked us not to send our numbers but that is just for illustration.

    I am concerned about what you have said about the link between high LDLs and atherosclerosis. So I would like to bring the LDL numbers down. However I want to take ownership of this journey of health and research. After some searching I came across a posting by Chris Kresser in which he talks about way goiterogens in cruciferous veggies impede the uptake of LDLs. As it happens, for the last few months I have been using Himalayan salt which has zero iodine. And I have been eating brussels sprouts and brocolli which apparently are high in goiterogens.

    I am not keen to start taking statins. My general cholesterol level went from just over 5 when I started LCHF in October last year to 8.7 in the last profile. And I have a sense that by research and some discipline I can get my numbers into an acceptable range, based on what you present.

    Therefore my strategy is to start with an iodine supplement (and a selenium which supports the uptake of iodine) both of which I get from a multivitamin. I will also eat more seafood. A lot of the advice on bringing down cholesterol comes from the old thinking that you and others are challenging so is not so useful. But I have decided to take on more soluble fibre and have started eating a couple of spoons of psillium a day. Oh yes I have also started eating kefir which, according to the best material I could find, has been shown to have no effect on LDL count but it seems healthy and is tasty. I have decided to continue with the high fat diet as before, which includes butter, cream, coconut oil and olive oil as well as leafy veg and some protein (mostly chicken).

    I am also reasonably active and surf or run most days of the week.

    I guess I am posting this just to hear any comment from you or anyone else and to give feedback when I do my next test. This is hardly a controlled observation but may provide some anecdotal input. I am really enjoying coming to grips with the science you offer in your postings. The terminology is slowly sinking in and I can now read most of the way through your ‘straight dope’ series before starting to feel lost. And your video postings are high value to this understanding for me – so thanks again.

    (reply)
  114. Amanda  June 7, 2013

    Thank you so much for this very informative series. I’ve read through twice (what can I say-the material is dense and my background is non- existent). Reading your personal journey helped me understand how to apply the material to myself.

    I had my standard lipid profile this week through the nurse’s station where I work, and my numbers seemed…off. My TG and HDL-C are perfect, but my LDL-C was in the very high range. A year ago, I would have been alarmed. Now, I know to calmly ask my primary care doctor to run the NMR panel. This saved me a whole lotta’ stress.

    (reply)
    • Peter Attia  June 8, 2013

      Or apoB…that will be less expensive, if they don’t want to do NMR.

  115. Joan Mercantini  June 13, 2013

    Should I continue a low carb, moderate protein diet after cardiac bypass surgery?
    As I type 1 diabetic, I realize I must keep the carbs low in order to minimize insulin requirements.
    I eat moderate protein, ie. grass feed beef ,.free ramge chicken, eggs and small servings of cheese on occasion.
    The hospital has now tells me to minimize the saturated fat. In the past I have cooked with coconut oil and butter.
    Your help is appreciated.

    (reply)
    • Peter Attia  June 13, 2013

      Joan, it may depend on what you replace the saturated fat (SFA) with. If you replace it with carbs, there is little doubt in the literature that your risk for heart disease goes up, not down; with MUFA, maybe down slightly; PUFA unclear. As far as cooking, you really need to be using SFA (butter or coconut oil) for stability reasons, though your diet sounds pretty good already! Ask the hospital what evidence they have for their recommendation?

    • Jane  June 13, 2013

      “As far as cooking, you really need to be using SFA (butter or coconut oil) for stability reasons”

      I confess, I am quite confused now. You mentioned before that one struggling with high LDL might try switching from saturated fats.

      Is it a fair summary to say that you recommend cooking with coconut oil and using olive oil for salads? (EVOO?)

      What about avocado oil for cooking? It has a high smoke point, and tastes better than the coconut oil I have tried.
      (In fact no one in our household will tolerate the Trader Joe’s coconut oil. Maybe there is a coconut oil out there with a more neutral taste?)

      Thanks again.

    • T.S.  June 14, 2013

      Hey,

      I hope you don’t mind if I pitch in here quickly. There’s two things you need to look at when considering an oil for cooking.

      1) The fatty acid composition
      2) The smoke point

      Fatty acids naturally start to oxidize (that is, become rancid) when exposed to oxygen, and this process is accelerated by light or heat. By definition what makes certain fats “unsaturated” is what makes them more prone to oxidation. Therefore the most stable are SFA, then MUFA, then PUFA. For this reason you should use SFA for cooking.

      The smoke point depends on how “pure” or refined the oil is. It’s not the fats that start to burn and cause smoke at high temperature, rather it’s the impurities in the oil. For example, sunflower oil is very high in heat sensitive PUFA, but because it’s very refined it can be heated very high without giving off smoke. While butter is full of SFA which are more heat stable, but due to the milk solids that are prone to burning it has a low smoke point. So, if you are going to cook at a higher temperature look for a coconut oil that suits your taste or perhaps try clarified butter, also known as “ghee”, which is pure butterfat that has had the milk solids removed from it.

      Personally, just to be on the safe side of things, I tend to prefer to cook on low heat (i.e. slow cook meat in the oven, steam vegetables) and then add fat towards the end just for taste (and nutritionally seen as a source of energy).

      EVOO is very high in MUFA, which Peter pointed could possibly to some extent lower your risk of heart disease. I don’t see any reason at all to avoid it and quite frankly there isn’t any other oil that tastes as good in salads.

      Also, if you do plan to follow a diet that is high in fat, and are considering to cut down on SFA it seems inevitable that you’ll consume more PUFA which will increase your intake of omega-6. My understanding is this can be problematic because omega-6 competes with omega-3 in some of the metabolic pathways that are used to convert certain forms of omega-3 into one’s that are more highly regarded by your body. Therefore it might be wise to supplement daily with fish oil or an algae based omega-3 supplement. I believe it’s specifically important to get an adequate amount of DHA (docosahexaenoic acid) as it’s the most desirable and versatile.

      Perhaps Peter could chime in here if I’m not off-base with my recommendation.

    • Peter Attia  June 14, 2013

      I think both of these are important, though I focus more on #1 (which makes #2 less essential). Hence, cooking with SFA, safer than MUFA, safer than PUFA, as a general rule. Agree that lower heat is probably better for cooking for many reasons.

    • Jane  June 15, 2013

      Thanks, T.S. and Peter.

  116. Maryann  June 23, 2013

    Hi Peter,

    Does Crestor cause weight gain? Eager to see part 10 when you have the time :) Thanks!

    (reply)
    • Peter Attia  June 23, 2013

      If it does, it’s not a common side-effect.

  117. Jane  June 26, 2013

    Hello again, Peter et al,

    I have done a bit more research into published RCTs on the efficacy of very low carbohydrate diets. The data are usually presented as means for the groups of dieters, so it is difficult to find as much information as needed to really find out the distribution of effects on LDL-C or LDL particle numbers.
    However, at least one study, by Westman’s group at Duke, reported (in vol 140 issue 10 in 2004 of the Annals of Internal Medicine) reported a significant increase in LDL-C in 30% of those on the very low carb diet.

    Afterr a few months of very low carb dieting, My LDL-C calc increased by 20%. Now that I have looked at what Dr. Dayspring has to say about this effect in some, and of course, consulted my physician, I am doubling my statin dose to bring down my LDL -C. I am also cutting way back on all saturated fats, switching to olive oil almost exclusively.
    That said, I remain delighted by my significant weight loss and improved glycemic control. And, i should say, my apparent troubles with LDL may have preceded my weight gain and insulin resistance by decades, as far as I can tell. Doctors have always told me to eat a low fat diet, which, of course, until recently, I thought I was doing!

    Frankly, I am troubled by the fact that this effect on LDL seems to be downplayed in the discussions online about very low carb diets, and that folks are being encouraged, by some advocates, to regard butter, cream, and cheese as completely healthy for everyone. Unfortunately, many of us seem to be as vulnerable to the saturated fats as we are to the excess carbs. (I am still unclear about the coconut oil , but I will avoid it for now.)

    Of course, the fact that the adverse effect on serum lipids is often obscured in the reports of RCTs is also troubling.

    Peter, thank you for your work on the NuSI initiative. I hope that the data will be available to all, and reported in ways that are useful for the broad spectrum of individuals.

    I value your analyses and commentary, and look forward to more blog posts on ketosis and cholesterol.

    (reply)
    • Peter Attia  June 26, 2013

      Jane, I can’t wait to dive into the content for Part X.

    • Jane  June 26, 2013

      Thanks Peter. by the way, i also found your TED talk to be very moving and persuasive. we all need to hold open our minds to different and probably more complex answers from the future studies,

      I want to mention one more idea about my own weight loss effects. This is kind of obvious, but I omitted before.

      maybe it wasn’t the eating of fat, but the burning of my own fat, or something else about the process, that increased my own generation of increased LDL-C. I am not clear about the biochemistry. Looks to me like the body pretty much breaks down everything we eat and reassembles and generates a new balance based on our own individual situation.
      Who knows, maybe my brain and nervous system need more endogenous cholesterol? That, of course, raises the Quality of Life question, yet another complex web of interactions.

      Regardless, Even if I can shed the last 10 pounds (back to where I was before perimenopause), and I certainly plan to, I will not be able to learn whether the olive oil substitution would have been effective, because of the statin.

      So far, I have not figured out how to get the VAP or NMR testing done here to find out about the particle size effect.
      But even if only my concentration of LDL is increased by the eating pattern or fat loss, the advice from Dayspring or my doctor would probably still be to increase the statin dose. The consensus about LDL and about statins is so powerful, I dare not defy it now.

    • Peter Attia  June 26, 2013

      Sorry to hear you’re having trouble getting advanced testing done. It’s not that statins are “bad,” it’s just important to be sure they are being used on the right patients, and for the right indication.

    • Maryann  June 26, 2013

      Hi Jane, did you have your sterol absorption and synthesis markers tested? You could be a hyper-absorber. Also, some people suggest that apo-E folks might need to watch saturated fat. Best wishes!

    • Maryann  June 26, 2013

      Apo-E 4, to clarify.

    • Jane  June 26, 2013

      Thanks Maryann,
      The absorption ans synthesis markers are also outside the range of my HMO system. I have yet to even pursue the more detailed lipid testing.
      And I do not know about my Apo E status, or anything about its heritability. That is the “Alzheimer’s” set of genes, isn’t it? Dominant or recessive?
      In any event, we can only control our own choices anyway, and just the idea of dementia is enough to motivate me!

    • Jane  June 26, 2013

      Peter,
      Thanks for emphasizing that point. I should make some more calls, perhaps drive farther, to get that testing. But wouldn’t I need an order from an MD?

    • Peter Attia  June 26, 2013

      Yes, your doctor will need to coordinate. Sometimes they are unaware of the tests (and not sure how to interpret).

    • Maryann  June 27, 2013

      Hi Jane, ApoE-4 is primarily a cardio risk marker (although there are associations with alzheimer’s risk, as you mentioned). Jimmy Moore has a lab he uses for independent testing, perhaps you might like to look into that. Best wishes, maryann

  118. Phil Sergent  June 26, 2013

    Your Ted Talk was So Very Intense! I’ve lost 60 lbs in the past year, I’m 6’2″ and most people didn’t notice but the more I loss, the higher my glucose count (GC) got. I take 2000mg of Metformin a day to stay at or under a GC of 150.
    A friend linked me to your talk and to be honest, then and now, I’m fighting back such an emotional wave that my eyes won’t stop watering.
    The bottoms of my feet, especially my toes, feel like my socks are bunched up in my shoes, even in my sandals.
    Is there anyway possible that I can be a part of your studies?

    (reply)
    • Peter Attia  June 27, 2013

      Phil, thank you for your kind words. NuSI doesn’t run the studies, but the investigators will be enrolling patients over the coming months and years. Look for it.

    • Maryann  June 27, 2013

      Hi Peter,
      I signed up for emails from NuSi when you first launched and have never received any…have there been none?
      Thank you, maryann

    • Peter Attia  June 27, 2013

      We’ll get there.

    • Paula  July 8, 2013

      Hi Phil,

      I’m a Type II diabetic, and I’ve done my own research and self-experiementation because I can’t tolerate Metformin. It gives me severe brain fog. One thing I learned is that it is possible to get your glucose intake so low that your liver will actually put out more glucose to compensate. Eating some carbs before bed prior to your fasting glucose test might improve your numbers.

  119. Jane  July 1, 2013

    Dear Peter,

    I must not have been reading carefully enough, but I must have missed the point that the same enzyme, hmg coa , in critical in both the synthesis of cholesterol in the liver AND the synthesis of ketones. And, it is active in both the mitochondria and the cytoplasm. And, via the cholesterol path, it is key to steroidal synthesis, which may be upregulated when stress is high. It would thus seem to be key to both normal steroid regulation, such as sex hormone balances, and to emotional and cognitive health via cortisol and brain-based synthesis of various proteins in the brain.

    Please correct me if I am wrong here. Am I confused or off track here? ( No doubt, I lack the basic knowledge of biochemistry and physiology necessary to sort through this.)

    If not, Can you direct us to a source that discusses both the ketone and the cholesterol pathways and how they are balanced in humans?

    This is the enzyme targeted by statin drugs, such as atorvastatin, simvastatin, pravastatin, etc. which are so widely prescribed to prevent heart disease (and other consequences such as strokes, multi-infarct dementia, . . . ).?

    Can you direct us to a good source discussing the several roles of this hmg coa enzyme in humans?

    What about the statins? Where can we educate ourselves about their effects, both theoretical and demonstrated?

    I have run across commentary online positing their possible role in depression and diabetes, but have not found a good review article about these issues. The internists seem to be so focused on vascular health, that they cannot even think about all the other cascades of effects in their patients.

    Thanks again so much for your work.

    (reply)
    • Peter Attia  July 1, 2013

      Jane, pretty elaborate discussion. The data linking statins to other diseases are interesting — and my have some merit — but they are observational, so we can’t parse out cause and effect. For a great set of reading on this, check out the work of Tom Dayspring, which can be found at LecturePad and fhit.org

    • Jane  July 2, 2013

      It was Dayspring’s discussion of number 291 on LecturePad (which, of course, I learned about from you) that explained to me the metabolic pathway for potential (well, actual for me and case 291 and many others ) connection between a ketogenic diet and an observed increase in LDL-C.
      Then I began to riff, mentally, about other sites for cholesterol synthesis and other theoretical effects of ketosis, statins,. . . .

      When Dayspring discussed saturated fats, he mentioned coconut oil. But, it was not entirely clear to me what he meant about it: the long- vs medium- vs short-chain fatty acids and whether some of us make more apoB or LDL-P from coconut oil. . . . Doesn’t coconut oil include some long-chain FA? I will have to look that up.

      The more I learn, the more questions I have! To me, this is really fun. But oh my, it is sedentary.

      As to the observational studies, the ones I have run across are at least longitudinal, not cross-sectional, and do control for other potential confounding effects. Not gold standard RCTs, but worth considering. Certainly hypothesis-

      But my memory is far from perfect. . . . I am on a statin after all!

    • Mayda  July 13, 2013

      Jane and Dr. Attia — belated thanks for your replies and information. I’ve been studying the protocol supplied by Benjamin Lynch (if anyone here has searched on “MTHFR,” his website will come up). Again, I’ve had the MTHFR677 TT genotype identified. I will look into Deplin once I retest in a few months. Perhaps the subject of methylation does not belong in the Cholesterol discussion, but surely it is all related: CHO, hormones, neurotransmitters – our health, happiness and productivity! Thanks again.

  120. Mayda  July 2, 2013

    Dr Attia,

    Many thanks in advance for your response and the incredible resources of your site and intellectual generosity. 58 yr old female, athletic, normal weight. I have recently been diagnosed as homozygous for the MTHFR 677 mutation (elevated risk of CAD and thrombosis, low SAM-e) w high homocysteine, high TC, excellent ratio. Low-carb, “high” fat for 25 years (except when I fall, FALL, off the wagon) after diagnosis of hyperinsulemia. Supplementing w 3 mg Naltrexone for app. 9 months which has helped with what I absolutely feel is a sugar addiction since adolescence – years of trying to self-medicate for what I now know is low dopamine, serotonin, and resultant high excitotoxins. The more I read, the more I believe that all of my imbalances stem from the MTHFR mutation. Just started on 1 mg daily each methylcobalamin and l-methylfoate. Beginning to work w Alan Magaziner in NJ — any direction to specialists in this area highly appreciated.

    (reply)
    • Peter Attia  July 2, 2013

      Mayda, MTHFR mutations can be pretty common, but of course it depends on C/C, C/T mutation, etc. Perhaps the most important implications are 1) do you require additional folic acid supplementation? and 2) are you at greater risk for thrombosis? Given the mutation, your elevated homocysteine may be due to folic acid utilization, rather than inflammation.

    • Jane  July 2, 2013

      This is a fascinating subject, Mayda. Thank you for bringing it up. I am deeply sympathetic to your plight as a sweets addict.

      I think that the brain chemistry involved in the overeating problem, now a pandemic, needs a lot more attention. Robert Lustig clued me into it in his talks on YouTube.

      Peter, I hope that NuSI addresses the various hormones involved in appetite, beyond the perhaps more indirect roles of blood glucose and insulin in eating regulation and body comp homeostasis. Now that we know about how common the MTFHR genetic variation is in some populations, and are generating good questions about its consequences in our current food environment, it seems clear that more research is needed there too.

      Mayda, I have a little comment about your folate treatment, related to one of your supplements and Peter’s point (1).
      This is sort of a “for what it’s worth” comment.
      I know very little about it, but have heard and read that the FDA has actually approved as a medical food an l-methylfolate brand-named Deplin. It is very expensive, and not covered by insurance as far as I can tell. It comes in dosages of 7.5 mg and 15 mg. I believe that I read that it was the 15 mg dose that was shown to be effective in treating depression, at least in the one or more trials that the FDA considered.
      I know someone who takes it and testifies to its effectiveness. That’s why I looked it up.
      I just thought you might want to know about the fact that Deplin is supplied at doses much higher than the 1 mg that you report taking. (I know nothing about the other supplement you mentioned.)
      It certainly seems plausible to me that smaller doses might be helpful, and it makes sense to me to try the more minimal intervention first. After all, folic acid supplementation typically is at 0.4 to 0.8 mg levels.

      Mayda, I do hope that you will continue to contribute here, and let us know how you are doing and whether the supplements seem to be effective for you. I believe that there are millions of folks who share your plight, and if we can prevent the decades of suffering . . . .

  121. Mike  July 9, 2013

    In your summary, you state:

    “The addition of fat, in the absence of sugar and starch, does not raise serum triglycerides or other biomarkers of cardiovascular disease.”

    Listening to an interview with Jimmy Moore and Dr. Dayspring (see http://www.askthelowcarbexperts.com/2012/10/29-dr-thomas-dayspring-cholesterol-testing-what-matters-most/ ) there is some discussion about individuals who see their LDL shoot up when going on a low-carb diet (and also the possibility of elevated LDL due to weight loss).

    It seems like these two ideas are in conflict — it seems like there may be some people for whom a ketogenic or low carb diet could cause LDL-P to skyrocket (I suspect I may be one of these people, but obviously haven’t permuted through the possible variables).

    If this is true, it seems like the benefits of a low-carb diet on heart disease markers may need an asterisk for some portion of the population…very confused here! Any light you could shed on this?

    (reply)
    • Peter Attia  July 9, 2013

      That’s correct. This will be discussed in part X of the cholesterol series if I can get to it.

    • Jane  July 19, 2013

      Peter,

      Do you have a best guess about when you will be likely to get to Part X ?

      Your explanations are so clear! It looks to me like there are several (many? hundreds? thousands?) of us out here who are very eager for your next cholesterol tutorial.

      Thank you again.

    • Peter Attia  July 19, 2013

      My goal is to get to Part X before I stop blogging (the date for which I have not yet decided, of course).

  122. Mark  July 10, 2013

    http://www.nytimes.com/2013/07/10/health/rare-mutation-prompts-race-for-cholesterol-drug.html?nl=todaysheadlines&emc=edit_th_20130710&_r=0&_r=0

    Not a cut and dried issue IMO because the drug will lower not only sdLDL-C, but large. Also, typical it doesn’t address the possible side effects either. Thoughts?

    (reply)
  123. KCJerry  July 18, 2013

    I sent this information to my cardiologist
    01-13-2012 12-18-12 02-23-13 07-02-13
    LDL-P 1137 1099 1103 1209
    Small LDL P 761 731 711 677
    He replies “Just keep in mind that no one knows if these are markers of risk or mediators of risk. If they are just markers, then changing them won’t matter. It takes clinical trials to learn whether changing the readings meaningfully changes your health. The healthcare highway is littered with the burned out wrecks of therapies that treated markers, not mediators.”
    What do you do to stay healthy when you are trying to do what is best?

    (reply)
    • Peter Attia  July 18, 2013

      True, but in this case the data are pretty good that LDL-P or apoB track closely, at least in SAD-consuming populations.

  124. Maryann  July 20, 2013

    Hi Dr. Attia, I don’t remember which part of the Cholesterol Series discussed calcium, but I remember it was not advisable to take calcium supplements because calcium can be involved in plaque formation. On a low carb or ketotic nutrition plan, should a female (because of the concern for the prevention of bone loss) who is lactose intolerant supplement calcium at all, or to some specific dose, since no dairy or cheese is in the diet? Thank you very much, maryann

    (reply)
  125. CraigL  July 29, 2013

    Dr. Attia, I appreciate the work you are doing. I have a few risk factors that probably place me with metabolic syndrome. I’m trying to do the research and determine what diet I should adopt, as a lifestyle – not a quick fix. This has proven to be a much more difficult task than I imagined. I’ve tried to limit my reading to sites that seem to operate with academic integrity. I’ve gleaned a lot of information from your site but was surprised and frustrated when I read in point #7 above where you wrote:

    “Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up. To see an important reference on this topic (the link you provided takes you to a site where only 2 pages of the research document are available)

    Here is where I was surprised – You took such a dogmatic approach, stating that anyone who thinks differently is either ignorant or a charlatan. Really? I don’t necessarily think differently because I don’t know what to think yet. I’m looking for the truth – which has become very hard to find. I read the 2 pages that were available on the link. The article that you are pointing to as proof states, “the relation between dietary cholesterol and the risk of CHD is not clearly understood”. That doesn’t sound like very compelling proof. Am I missing something? The last paragraph in the available 2 pages states that both LDL and HDL appear to be influenced by dietary cholesterol. There is more to the paper that I didn’t have access to. But, the abstract clearly states that the relationship between dietary cholesterol and CHD is not clearly understood. So, if the relationship isn’t clearly understood, how could you label people that disagree with your opinion, which you are calling a fact, as ignorant or a charlatan?

    Again, I don’t have any agenda other than trying to find the truth to help me determine what diet changes I need to make. A big question for me while gathering information is, can I trust the author? The way you stated your cased on this issue called that into question for me. It’s surprising, because up until I read this it appeared that writing with integrity was very important to you. I’m sure I must have misunderstood something because you seem to be a person of high character, ethics, and integrity. Please let me know what I’ve misunderstood.
    Thank you,
    Craig

    (reply)
    • Peter Attia  July 30, 2013

      Craig, many things are still unknown. This, however, is not one of them. So while I’m not dogmatic with respect to many things in nutrition, I am with respect to this. And the laws of gravity. BTW – the statement that dietary dietary cholesterol and the risk of CHD is not the same as the (much simpler) statement I made — dietary cholesterol levels have little impact on (serum) cholesterol levels in the body. Does this nuance make sense? Consider the following, also, look at the largest association study of dietary cholesterol and serum cholesterol (Framingham Heart Study). Here is what they found, though this was unpublished in 1968 at the time of the first publication. They compared cholesterol intake of those with serum levels above 300 mg/dL to those below 170 mg/dL. No difference. They concluded, “There is considerable range of serum cholesterol within the Framingham Study Group. Something explains this inter-individual variation, but it is not diet (as measured here).” So while SFA consumption impacts HDL-C and LDL-C, it’s not the dietary cholesterol per se. Another way to think about this is by considering the chemistry of cholesterol (i.e., esterified vs. free) and the path for CE to enter the body via the NPC1L1 transporter on enterocytes. Can’t happen unless cholesterol is UNesterified. Back to laws like gravity.

  126. Randy  August 13, 2013

    Peter,

    I’m glad to say that today I finally went and got my blood work(NMR Lipo Test) done after following a pretty restrictive Ketogeic diet for about 5 1/2 months now. My only regret is that I didn’t know about the in’s and out’s of this diet and your teachings until about a quarter of the way through. I’ve lost 38 pounds to date and feeling great. I’ve post on your blog before and there is a lot of information to digest on here, so even using your search tool its hard to find specific things sometimes. Like yourself, I think I’m very carb sensitive and have to keep em pretty low to stay in Ketogenic state. I’ve looked on the blog for a simple breakdown of what you think the ideal numbers should be for the NMR Lipo Test (The particle test). Is there a quick guide that you know of that explains the numbers line by line or an NMR for dummies. Are your numbers of your most recent test listed anywhere on the blog? I get my results back in a couple days and I want to know what I’m looking at. What should my LDL-P be (in a perfect world) considering i’ve been doing this for 5 to 6 months now.

    Side Note:
    You weren’t lying when you said most doctors wouldn’t be familiar with this test. This MD had never even heard of LDL-P, much less NMR LipoProtein test. I told him that if he knew what I knew, he would never prescribe another standard Lipid test again. This guy was about 50 I think. I told him not to feel bad about it because he was probably never taught these things in med school and its probably not required reading once you got your credentials behind your name. He actually admitted that he wasn’t up to snuff on all the things he should know on cholesterol. I was highly surprised he said that, but I wasn’t a prick about it. He was curious how I knew so much about the subject and I told him a MD by the name of Peter Attia told me on youtube and his blog. So it’s funny, I had to go to a doctor to get a prescription for a test that the doctor had never heard of. I had to pay him for his lack of knowledge on the subject because I couldn’t go straight to the source and get what I needed. He should have waived the fee for the office visit in my personal opinion, that’s definitely what i would have done if it were my practice . Then, I go to the lab and they’ve never heard of the test and they were curious how I knew so much. Crazy right? So, they drew the blood and sent it to Labcorp. Quest didn’t offer the test. It was about 166 bucks in case your readers as interested. Its amazing how curious people get when you tell them you lost 38 pounds in 5 months with no exercise. Women seem to get way more curious than guys for some reason. I’m always happy to tell them that all you have to do is break your addiction to sugar, which is harder than to stop drinking alcohol and regulate a low insulin level all day every day.

    (reply)
    • Peter Attia  August 13, 2013

      Randy, I have not done a how to read your NMR test per se. Most of the info is embedded within the cholesterol series, though. Sorry it’s such a hassle to get the test done, but glad you did.

  127. Andrew Logan  August 13, 2013

    In response to Randy’s difficulties in getting his NMR profile done, there is a way, in the USA at least of ordering this yourself without going through your doctor. There is a company called health testing centres healthtestingcentres.com who will arrange any blood test you might want e.g. nMr profile currently costs $129 I think. You pay for the test online and then arrange to have blood drawn at a convenient location, results get emailed to you in a few days. NMR is not available in New Zealand where I live so I organised this when I was in San Francisco earlier this year at a conference. It worked flawlessly. The only problem is that you then have to interpret the data. Even though I am a physician (not a lipidologist though) it took me several goes to understand the data. They give quite a good risk profile assessment as part of the report which helps. I would think that, if you are not fully conversant with the ins and outs of NMR, doing your apoA and apoB would be be easier to understand, and maybe give a simpler assessment of the effect of any intervention you are undertaking, and give almost as much information as the NMRprofile at a lower cost.

    (reply)
  128. Andrew Logan  August 13, 2013

    I guess I wondered, in the absence of expert interpretation of an NMR, it would be easier for an individual to make sense of apoA and apoB. The test is also going to be cheaper and does not need fasting to do. One of the problems I could foresee in ordering a test without your doctor’s OK or against his advice, is that said doctor may feel quite threatened by this , particularly if you appear to be more knowledgeable or adopt an assertive position, and become ” non cooperative” with one’s future health care. Sadly, not all doctors have as much openness and humility as you Peter!

    (reply)
    • Peter Attia  August 14, 2013

      Very similar information. The “expertise” is necessary to put numbers in context, based on other risk factors.

  129. Randy  August 14, 2013

    Thanks for the input guys.

    (reply)
  130. Randy  August 17, 2013

    Peter,

    Got my results back today and they were pretty discouraging. Really couldn’t believe them. I’ve lost weight down to my goal of 172, I feel great, I sleep great, energy level is up all day, and I’m making plenty of ketones. Maybe you can give me some advice. I’m eating pretty much all or alot of the same things as yourself. Here are my NMR RESULTS:

    LDL -P 1579 nmol/L
    LDL -C 150 mg/dl
    HDL -C 55 mg/dl
    Triglycerides 100 mg/dl
    Total Cholesterol 225 mg/dl

    LDL and HDL PARTICLES
    HDL -P (Total) 27.5 umol/L
    Small LDL -P 586 nmol/L
    LDL Size 21.1 nm

    My LP – IR test assessment for insulin resistance was 24

    Any suggestions would be great.

    Thanks in advance.

    (reply)
    • Boundless  August 17, 2013

      I also had an NMR lipoprofile done lately. Had to escalate from GP to internist to get it, and the internist also supplied no interpretive guidance (but of course suggested going on statins, even though the two numbers that really matter, my small LDL and trig, are extremely low, and there are zero other indications; so much for his credibility). My total LDL-P, like yours, is highish (near the 1600 nmol/l level).

      I had the numbers looked at by an independent cardiac MD, who just happens to be working on (but hasn’t completed) a “how to read your numbers” article – which isn’t trivially simple, due to the variety of labs available.

      His assessment in my case was mild hypothyroid, possibly to be resolved merely by going back on the iodine (kelp) I had discontinued a month before the lab. I’ll be on it for the follow-up, and I will also be insistent on getting the complete thyroid panel I asked for last time (FT3, FT4, RT3) and didn’t get (TSH and TT4 are about as useful as TC and LDL-C). It is likely to be the case that once major other side effects of a full-time glycemic diet are cleared away, underlying thyroid problems will often be exposed, if they are correctly measured, assessed and treated (which, as with CVD, they usually are not). I also have family history of thyroid issues.

      The above, of course, might have no bearing on your case – where the first question that came to mind actually was: are you still losing weight? My understanding is that this does skew lipid reading whilst in progress.

  131. Randy  August 19, 2013

    Boundless,

    Thanks for you comments first off. My weight loss has stalled at 172 morning weight. I think because that’s actually how much I should weight normally. My belly button circumference is 32 inches now from 43 inches. It was my goal weight from the beginning and I just got there about 2 weeks ago. It’s very interesting that you bring up potential thyroid imbalance. Unlike you, I don’t really know of my family having thyroid issues, but I wouldn’t rule it out because my Mom and Dad really never cared about knowing there potential health problems. I will say that I have had an uncomfortable feeling in my throat for the last 3 months. It seems to come and go and feels kind of like a tugging or a constant pulling sensation. Doesn’t hurt though.

    A little background on my diet and exercise might shed some light. I have done essentially no exercise to lose the weight and like Peter I inhale saturated fat. A lot of the fat I’ve been taking in has been through the yogurt and heavy whip cream in my scrambled eggs and coffee. I’m beginning to think this is my problem. I should have done moderate exercise along the way, but didn’t. I just love telling people I lost all the weight and didn’t do any exercise. The look on their faces are priceless. I will be exercising for the next 3 months and building muscle. I will be eating more of the same things. I think I will go and get a thyroid work up. Its been in the back of my mind, but haven’t done it because I haven’t seen any of the commonly know symptoms. I have done some reading on the subject though and have found that most people that get diagnosed never even knew they had it.

    (reply)
  132. Beth  August 20, 2013

    I’ve been looking for part x on the role of pharmacologic intervention in the treatment and prevention of atherosclerotic disease and can’t find it. Am I missing it?

    (reply)
    • Peter Attia  August 20, 2013

      Still in my head, unfortunately.

    • Beth  August 21, 2013

      Is there any way I can convince you to write it? I’ve got a great almond ball recipe I’ll swap for it.

    • Peter Attia  August 21, 2013

      I will at some point. My day job is pretty demanding, though.

    • Beth  August 21, 2013

      Btw, thank you for an amazing series and blog! :)

  133. Randy  August 21, 2013

    This video may speak to my issue as it relates to active weight loss. The next 3 months shall be a good test. Steve Phinney
    http://www.youtube.com/watch?v=MNfjkTyBUdQ

    (reply)
  134. Christina  August 22, 2013

    I lost 26 pounds 154 to 128 lbs and my cholesterol went from 190 to 274 and my ldl went up as well. It occurred during menopause. I am not a fan of statins. Both my father and grandmother developed diabetes about a year after taking statins. Can you give me any advise?

    (reply)
    • Richard S.  September 12, 2013

      Christina,

      Happened to me, too. I’ve lost 30 pounds, my BP is fine now, and I stopped taking a statin and niacin. My total cholesterol and LDL-C are both high after my LC diet. But my TG/HDL-C ratio is now under 2, which makes me think I’m probably OK.

      This seems to be common (or not uncommon) occurrence after LCHF diets. They discuss it at length in “Cholesterol Clarity,” by Jimmy Moore and Eric Westman. Dr. Westman also said that after a patient has lost a lot of weight, he waits until the patient’s weight has been stable for a while before checking lipids and lipoproteins.

      The main thing I think most of the experts would say is for us to check our ApoB or LDL-P levels. If they are OK, then the old measurements of TC and LDL-C don’t matter. I plan to have mine checked before long.

  135. Randy  August 24, 2013

    I cannot give advice,but i will repeat what Peter has said. Cholesterol levels have little to do with what you feed your face and is probably an under lying issue causing higher than normal levels. By reading this blog, the problem seems pretty common. In my case, only a little bit of time will tell. i may have to re evaluate after that and until then i will keep doing more of the same. Correct me if im wrong Peter.

    (reply)
  136. Thomas Beresford  September 5, 2013

    Hi Peter,
    Brilliant resource on cholesterol, I think I stuck with it and follow ‘most’ of it. It’s quite a rabbit hole and I’ve read so much that I can’t see the wood for the trees. I have 2 very quick questions though. I have just had my blood tested (national health service here in the UK) lipids, liver, thyroid, electrolytes, b21 & folate, GFR. I understand that at best these are nothing more than an indication and their usefulness is limited. so 1) should I ignore them or only focus on certain ratio’s / numbers 2) if I should only focus on certain things, can you point me in a direction of a useful resource / website where I can make some sense or meaning from my results?

    (reply)
  137. Justin W.  September 10, 2013

    Dear Peter,
    Could you speak to the reported hyperlipidemia of children on KD for epilepsy? It has become common wisdom that their KD-induced hyperlipidemia can be corrected by lowering saturated fat and cholesterol in the diet. This seems to go against what you and many others have found to be true for adults on the KD. Here some examples of this common wisdom:
    http://jama.jamanetwork.com/article.aspx?articleid=197131
    http://can.sagepub.com/content/1/6/338
    http://www.sciencedirect.com/science/article/pii/S092012111100204X

    (reply)
    • Peter Attia  September 11, 2013

      Yes, there may be other things going on kids on KD, and to be honest, I’m not an expert on the formulations of the diets in kids, though I can only imagine how much more difficult it is. I had read the JAMA paper before and reached out to the lead author to learn more, but he did not respond, unfortunately. I would be curious what Elizabeth Thiel’s experiences have been. She’s at Boston Children’s Hospital and probably has one of the largest practices in the world using KD for epilepsy. I’d also like to know the apoCII status of the kids the respond well to switching out the SFA for MUFA and PUFA.

  138. Richard S.  September 12, 2013

    Peter,

    Reading this series was like reading a serial novel — I couldn’t wait to get to the next chapter.

    At one point, I think you said that those who were favorably discordant (high LDL-C, low LDL-P) had even lower risk that those who were low and concordant. Any theories why that would be so?

    I understand that insulin resistance is implicated in those with unfavorable discordance. Is there anything common about those who are favorably discordant? (Other than the fact that their LDL particles must be relatively large.) Just curious.

    Thanks for all you do.

    (reply)
    • Peter Attia  September 12, 2013

      Just based on the longitudinal survival data I presented. Not sure why, though. The differences is minor.

  139. Jerry White  September 16, 2013

    Dr Attia really takes on the lipid world. Well worth your time to look at his site if your health issues relate to heart, inflammation, sugar, diabetes or weight. Bravo for taking on the myths and fallacies with facts and concrete recommendations.

    (reply)
  140. Joan  September 17, 2013

    I will not send my numbers, but having read all nine parts – more than once – along with The Truth About Statins and much more, I still need to know…straight up…what should I do?

    I know you can’t and won’t give advice, so this is a hypothetical question. What do I do now? I’m 58, can’t handle any more mental fog than I already have! so really, really do not want to take statins. My doctor – who actually is very careful about reading the primary literature and who is well-versed in these questions – is still recommending statins.

    I don’t eat animal protein except for fish and an occasional egg (for reasons other than health; it is personal preference); I eat only slow carbs (low glycemic index), non-starchy vegetables, fruit. I exercise an hour a day and 3-4 hours on Saturday and Sunday. All since November 2012. Take 81 mg aspirin per day.

    The LDL-P is still in the very high range though its concordant with the LDL-C (all measured via NMR). HDL-P is low, triglycerides are low.

    Weight is appropriate, blood pressure is fine, blood sugar is fine.

    Family history unknown except for immediate family (father, two uncles, mother – no heart disease).

    What else can I do besides taking statins?

    (reply)
    • Joan  September 17, 2013

      Oh. forgot to say – I’m female.

  141. Randy  September 21, 2013

    Hey Peter,

    I was wondering if you’ve ever given any though to coming up with any nutribullet recipes. I just recently bought one to blend my bulletproof coffee. I just don’t know enough about food and nutrition to come up with my own. Making a quick list of 6 or 7 low carb vegetables and maybe 2 or 3 lowest sugar fruits. There’s gotta be some great tasting things that could benefit people to make the HFLC experience a little better. I’ve got about 6 people following the HFLC and people are always asking what I do. I’m trying to think of something to add to the FAGE yogurt to blend for a snake too. Give me your thoughts and move this thread to the appropriate sub section of your blog. I didn’t know where the best place was to pose this question.

    Thanks

    (reply)
  142. Randy  September 22, 2013

    An update to my previous post about elevated LDL – P and LDL numbers. This is very interesting and could be the cause of my not so good results. I think this could have very well affected my results because I did drink coffee with heavy cream and splenda everyday leading up to my test. Here’s the link:
    http://www.infobarrel.com/Can_You_Drink_Coffee_Before_a_Cholesterol_Test

    Hope this helps.

    (reply)
  143. Greg  October 22, 2013

    This is an awesome site and article. It’s so cool to find people that are just genuinely interested in things and enjoy thinking. I’ve developed a huge interest in nutrition recently (age 26) because I was raised on really bad food and am just now really doing everything in my power to change my habits. But to find research like this is just wonderful.

    I’m doing an experiment right now… cutting all wheat out and all sugar except for some high cocoa dark chocolate occasionally. I haven’t been worrying about fat in it’s most natural forms such as meats, eggs and dairy… and have upped my vegetable intake from occasionally to multiple times a day.

    I am no scientist, I didn’t even go to college. (I make music videos and want to direct feature films), but I think that what I am eating now is a big improvement, and I can feel it both mentally and physically (whether it be placebo or not). At least a step in the right direction by eating REAL foods.

    Thanks for this site, and keep doing what you’re doing.

    (reply)
  144. Garth  November 1, 2013

    Is Part X published yet?

    (reply)
  145. Garth  November 1, 2013

    Fascinating and insightful set of articles. Like you, I am a surgeon, and I applaud your effort at educating the public about this complex issue. I, for one, an just learning, via your site, about the nuances of lipid mgmt, so a big thanks to you.

    (reply)
  146. Craig Roberts  November 2, 2013

    Throughout this execelent series there is no mention of the form cholesterol sulfate. It is produced at the skin layer with the production of vitamin D sulfate. Are the two of them water soluable? and if so, can they transport in blood without a protein vessel?

    (reply)
  147. Norm  November 17, 2013

    Hi Peter,

    I’m sure lots of us are anxiously waiting for your take on increase in LDL-C and LDL-P on a low carb diet.

    Regards

    (reply)
  148. Sui  November 26, 2013

    Excellent series, Peter. Thank you for all the efforts in research, writing and generously sharing with us on your blog. I also enjoyed your TED talk.

    I am a physician (neurologist) based in London (England). As per previous poster, I was alarmed by my personal lipid profile: high LDL (calculated, not NMR – though I’m planning to travel to USA if needed to get the test done), though good levels of HDL (high) and TG (low). This is against a background of good lifestyle, lean, active, etc, and in fact a move towards ‘Paleo’ type diet in the past 2 years. In your reply to the previous poster, you mentioned writing an article on this pattern of lipid profile. Have you written it yet?

    Keep up the good work! Will make a donation now to NuSI (just need to find the link now…). Best regards, Sui

    (reply)
    • Sui  November 26, 2013

      Donation done! Easy to find on google search
      http://nusi.org/donate/#.UpRQMGSgZhN

      Towards rigorous research in questions that matter!

    • Peter Attia  November 26, 2013

      Sui, thanks very much. Greatly appreciated.

    • Peter Attia  November 26, 2013

      I have not yet, Sui. It will be part X of this series. I will get to it…

    • Sui  January 2, 2014

      Hi again Peter. Many good wishes for 2014! I am looking forward to Part X…. ;)

      Meanwhile, following on from my earlier post, my n=1 numbers raises some questions about LDL-P perhaps? I was surprised when my basic cholesterol panel suggested a worryingly high LDL (a new finding since switching to a Paleo-style eating about 2 years ago) – Surprising because I am lean and have a ‘clean’ lifestyle with eating/ training (almost daily training with either strength/ intervals/ yoga etc). I thought it might be spurious because of LDL done by estimation/calculation rather than direct measurement, so I got a more extensive test including NMR done. The results, just back, show:

      LDL-C 158 mg/dL (ref 39)
      TG 32 mg/dL (ref <150)
      total Cholesterol 252 (ref <200)

      Particle concentration & size by NMR:
      LDL-P 1402 nmol/L (ref 34.9)
      LDL-size 21.8 (large pattern A)
      Lp(a) 17 mg/dL (ref <30)

      Insulin Resistance Score by lipid fractionation is 7.3)
      LDL S 116 nmol/L (ref <117)
      VLDL L <0.8 nmol/L (ref 9.6)
      LDL size 21.8 nm (ref >21.2)

      LpPLA2 (PLAC) 218 ng/dL(ref <200)

      I'm not sure what to make of the high LDL-P but an good LDL size. Hence Looking forward to Part X…. Will pledging another donation to NuSI be a good incentive?!? :)

    • Sui  January 2, 2014

      Reposting numbers because for some strange reason, I type it correctly on my screen but what I see after hitting ‘add comment’ button seem altered… Some clarifications:

      LDL-C 158
      HDL-C 88
      TG 32
      total Cholesterol 252

      Particle concentration & size by NMR:
      LDL-P 1402
      HDL-P 32.6
      LDL-size 21.8 (large pattern A)
      Lp(a) 17

      Insulin Resistance Score by lipid fractionation is <25 (Optimal)
      HDL L 14.1
      LDL S 116
      VLDL L <0.8
      HDL size 10.1
      LDL size 21.8

      LpPLA2 (PLAC) 218

  149. Andrea  December 4, 2013

    My 18 year old daughter has high triglycerides and is insulin resistant and I came across some interesting info and I was wondering if there is any truth in the following:
    Basic Diet Adjustments for Insulin Improvement

    The absolute worst possible dietary pattern of eating for a type 2 diabetic IS THE STANDARD DIET ADVICE GIVEN BY DIETICIANS AND DOCTORS ACROSS THIS COUNTRY FOR ALMOST ALL TYPE 2 DIABETIC PATIENTS, which helps lock in a national epidemic of type 2 diabetes. They routinely tell individuals to snack in order to maintain their blood sugar levels and to “stoke” their metabolism with fuel.

    In normal health, when you haven’t eaten for three hours, insulin levels return to a baseline. Now your pancreas makes a different hormone called glucagon. This hormone tells your liver to release the sugar (glycogen) it has stored to sustain your blood sugar levels, and as it does this it turns on your liver’s fat burning system. Thus, under the influence of glucagon your liver simultaneously uses sugar and fat to sustain your blood sugar – a true fat burning time that helps clear up stagnating levels of triglycerides in your blood.

    If you snack on anything surpassing 30 calories you will raise insulin, which automatically turns off glucagon, causes fat burning to stop, and blunts the use of sugar that has been stored in your liver. However, since you haven’t used the stored sugar in your liver, then insulin can’t put more sugar back in your liver as it normally would, meaning it will readily turn blood sugar into fat (even if you snacked on something with no fat).

    Don’t know who to trust anymore. Even her nutritionist said to eat every 3 hours.

    (reply)
    • Peter Attia  December 4, 2013

      Andrea, I think you will find the book by Dr. Richard Bernstein on this topic particularly helpful.

  150. Ron Blackburn  December 7, 2013

    Randy,

    I wanted you to know that i started the Keto Diet, on Aug 1st and checked my cholesterol 3 months later and i worked out with weight training 6 days a week and HIIT 3 days a week. My HDL stayed the same. Triglycerides dropped from 85 to 72 but my Ldl went from 130 to 207. Total Cholesterol went from 205 to 284. so i too went and had the NMR test…hoping that the calculations were wrong. They weren’t sad to say. In fact the LDL-P number was off the chart. very high is over 2000, mine was 2843. all other numbers were good. The test was very detailed.

    So i just wanted you to know that exercise may not be the culprit in your situation. I am now doing a new test for the next 3 months in which i eat the same diet however i will eat “healthy fats” and also add 1/3 cup of oat bran to my diet. I believe that is only 24 grams of carbs , so i should stay in Ketosis.

    I have never felt better in my life. I tell people that i no longer am held hostage by the cravings of that of carb eaters. I eat vegetables with every meal for the little carbs i do eat. I also feel euphoric often, seems to be mostly after large amounts of greens. I don’t drink coffee but i do drink Pu-er tea…a lot actually, about 100 oz per day

    I too have leveled out on my weight. although i didn’t lose as much as you did. i went from 197-177. i am 6’3″ and vary from 177 – 181 throughout the week. for over 2 months now. This weight feels good but i think it would be fun to experiment with lower body fat percentages.

    My biggest hope is that being on a ketogenic diet, i will not need to worry about ldl-p as much as those on a high carb diet. however i don’t think i should roll the dice until we learn more.

    Looking forward to X

    Thanks for everything Peter!!

    (reply)
  151. Jeff Johnson  December 7, 2013

    It Would Seem………..
    …………………………………
    ……………………….

    Measuring Oxidation and Inflamation within all cell’s and lipids of the body would be a good idea – particullary the Liver – Bloodstream and Under/outer/layer itself of the endothelium and

    discover whatever processes are cuasing such – wether external or internal -

    this should be a part of a standard blood test

    The patient should be able to ask – how many oxidized LDL – LDL-P and what’s up with the Inflamation ? and get a simple anwser – or and how fast are my LDL-P being cleared by the liver or some other way ?

    A salient question I might ask is – do these parameters differ in people who never have soft-plaque build-up/heart-attacks and people who do ?

    One confounding idea being floated around is that half the people who suffer heart attacks have normal cholesterol -

    the confounding thing about this is – there are far more people with normal cholesterol numbers and fewer people with abnormal numbers – if you think about this a bit you will see the confounding involved – in other words – you need to know the percentage of all people with normal ‘numbers’ who sufffer heart trouble and the pertcentage of those with ‘abnormal’ numbers who suffer heart trouble and I do not think it’s any where near 50/50

    (reply)
  152. Jack  December 9, 2013

    Hi Peter
    Thanks for the great info. I’ve searched around here and a few other places but can’t find much on my two simple questions – ok simple to ask, but not simple to answer!

    1) Why did my cholesterol go up so much after starting a Paleo type diet?
    - I eat a pretty clean “paleo-type” diet – (daily coffee and gin n tonic though). However my cholesterol went up from 188 to 260 (tested 1 yr. after changing diet, and 2x since) HDL went from 58 to 93, but LDL (calculated) went from 114 to 61. Trigs went from 80 to 36.
    - I lift heavy weights 3 x week, run 2x week, some high intensity interval training
    – My doctor disregards the positive movement on HDL and trigs (see below). I’m going to have the detailed lipo panel done by WellnessFX next.

    Is there something I’m missing? I would have thought the LDL would improve or at least stay in range

    2) Is there an authoritative cholesterol resource that my GP doctor would trust that might set him on the road to asking more questions and challenging the “statins first” mantra. I just saw him this morning. here’s my experience if anyone’s interested
    - He advised going on statins within 30 seconds of walking in – without asking me about my exercise or diet
    - If I had side effects on statins, he would keep changing them until he found one until the side effects ceased
    - The doctor, his mother and father all are on statins
    - Statins result in 30-40% reduction in risk for patients without priorheart disease
    - Eat less saturated fat than I am eating – no coconut oil or butter. Substitute canola oil. Olive oil is good though
    - My high HDL is good, but he’s more concerned with high LDL.
    - Framingham heart study repeated as source of his advice
    - Some processed foods are OK to eat – no elaboration on what kinds though
    - He said the LDL particle size tests are useless since you wouldn’t do anything different. He compared it the ‘useless” CRP tests

    Besides getting a new doctor, I feel compelled to at least provide him a little information to see if he will become more skeptical about common wisdom. I might try Cholesterol Clarity (which I suspect he would dismiss) but was wondering if you had a good starting point for a doctor. These are the people we need to be learning this!
    Thanks again to everybody for the learning.

    (reply)
  153. Jack  December 9, 2013

    Oh, and my stats
    53 year old male, my weight stayed pretty much the same (165 lbs ) – I did lose an inch off my waist, but weight reduction is not my goal

    (reply)
  154. Bryan  December 13, 2013

    It was not until I dumped all dairy and meat from my diet that I was able to reach a healthy BMI, BP, total cholestoral dropped from 214 to 152 (LDL dropped from 131 to 76) and I am no longer medicated for gout. This begs the question that sources of dietary cholesterol had an impact on the cholestoral levels in my body. Is this inconsistant with the 7th point you make in the first part of this blog entry? The link to the reference is not working and I would like to learn more about “Eating cholesterol has very little impact on the cholesterol levels in your body.”

    (reply)
  155. Paul Johnson  December 16, 2013

    Just thought I’d add my voice to the clamour of readers asking for Part X!

    I was diagnosed with CVD and had a stent fitted to a severely narrowed LAD age 41 despite being otherwise fit and with none of the traditional risk factors (eventually, I discovered very high Lp(a) as the most likely culprit after asking a private cardiologist to get this tested). Inevitably, a statin was given top billing in the cocktail of drugs I was prescribed on discharge and I took it for about 18 months. However, I have become more and more of a statin-sceptic, and moved to low-carb eating, after reading Gary Taubes, Ben Goldacre, the UK’s Malcolm Kendrick as well as your blog. However, my GP, cardiologist and two professors of endocrinology all tell me I’m mad not to take the statin. As a result, I’m very interested in your view on the role of statins – even if it’s not yet definitive.

    (reply)
    • Peter Attia  December 16, 2013

      I hear you, Paul. I’ll get there.

  156. Norm  December 20, 2013

    Hi Peter,
    Is it safe to say that particle number of lipoprotein is a bigger problem in heart disease than inflammation as these particles cause inflammation in the artery wall which makes things worse?

    What makes “sub-endothelial space” vulnerable to the landing of lipoproteins in there? Can this be prevented other than having less particle?

    Thanks

    (reply)
    • Peter Attia  December 20, 2013

      Technically, we don’t know, as the analysis of LDL-P vs. oxLDL has not been done. We know for sure that LDL-P parallels risk and many (including me) believe it drives risk. The role of inflammation is clear, but to measure and quantify it at the artery and particle level and see if that independently predicts risk is another story which has not been resolved.

  157. Andreas  December 22, 2013

    Hi Peter.

    Just now I saw your “Straight dope on cholesterol” talk from AHS once again, and there’s one thing I really think is missing from the chart showing increased discordance of LDL-C to LDL-P with an increased number of criterea of metabolic syndrome. (The one with 6 x blue and red pillars as seen above).
    You mentioned when showing this chart that with no criterea for MetSyn there is concordance between the two. I would like to see another set of pillars from that study: What if a person has no criterea for MetSyn but has a high LDL-C? Would that necessarily mean a high LDL-P? According to you (at the time of that talk ofcourse) a reading of let’s say 180 mg/dl LDL-C would equal a reading of around 1800 mmol/L of LDL-P. Don’t you think it could just as well be that a high LDL-C in a person with no criterea for MetSyn could equal a low LDL-P reading? This could be an effect of very low triglyceride count and some elite cholesterol packing LDL’s =)
    I can easily imagine that LDL-P pillar just staying in place while its LDL-C buddy shoots up a bit. Maybe this is even slightly favorable when looking at some of the other charts of your cholesterol series suggesting that lowest risk of coronary events is a high LDL-C tin conjunction with a low LDL-P.
    Thank you for taking your time to provide all the information on this site!

    Andreas.

    (reply)
    • Peter Attia  December 22, 2013

      Andreas, what that graph says is that, on average, if one has no signs of MetSyn, LDL-C and LDL-P will be concordant.

    • Boundless  December 24, 2013

      Andreas, you may be giving lipid panel result LDL-C more credibility than it merits.
      Lipoprotein panel result LDL-P is what we need instead, and almost never get.

      For for a concise critique of LDL-C, see the remarks starting at
      “LDL cholesterol is calculated, not measured ” in article
      http://www.wheatbellyblog.com/2013/11/a-grain-eaters-cholesterol-panel/
      on Dr. Davis’ blog. Dr.D. is a cardiac specialist.

    • Andreas  December 25, 2013

      Boundless: That’s perfectly clear. I too am convinced the LDL-P test is superior when trying to predict developement of atherosclerosis. My question was in regards to the specifics of this one chart above.

  158. Andreas  December 23, 2013

    I know, Peter, but if that was actually true, then in people with no signs of MetSyn high LDL-C by itself would be a strong predictor of future atherosclerosis right? Assuming high LDL-C = High LDL-P.

    And that would mean that most people with high LDL-C (even MetSyn-free people) are at high risk for developing atherosclerosis. Conventional wisdom was right?

    That’s why I ask: Don’t you think it is very possible to have high LDL-C but with low LDL-P?

    (reply)
    • Peter Attia  December 23, 2013

      I think you may be misunderstand concordance vs. discordance. LDL-P and LDL-C are *concordant* when they both predict equal risk. This is likely to happen when one does not have IR (i.e., 0 signs of MetSyn), but this fact does not change the point. It’s like saying blue eyes predicts CHD risk. Well, it does when someone has blue eyes and high LDL-P, but that doesn’t mean blue eyes predict CHD risk. That fact the *sometimes* LDL-C is concordant with LDL-P says nothing about the CW being right.

    • Andreas  December 25, 2013

      Alright, that makes sense. And it puts me somewhat at rest – having no IR, but high LDL-C after 2 years with around 70% of energy intake from a blend of mono and saturated fat. Doc’s very concerned though! ;-)
      Thank you for clarifying and merry christmas!

  159. Mike  December 24, 2013

    Just another, waiting anxiously to see if theirs any light to unraveling the high LDL-P issue in some of us.
    In summary, on HFLC, Im concordant, but with an LDL-C of 210 LDL-P 2000, small LDL-P is low at 180, IR 15. Ate lower fat, more carbs and LDL-C drops to 140 but LDL-P now is discordant and stays at 1800. small LDL-P jumps to 600. IR score is still less than 25. Does genetics simply have the final say in some of us no matter what we eat and high LDL-P is something we just cant do anything about?

    (reply)
    • Peter Attia  December 25, 2013

      Mike, genetics always plays a significant role in CHD risk, and this can often be driven through high LDL-P for many reasons.

  160. Norm  December 26, 2013

    Andreas,
    If I’m reading correctly what Peter said was that both LDL-C and LDL-P are LIKELY to be concordant (predicting equal risk) with NO signs of IR. All the best.

    (reply)
    • Peter Attia  December 26, 2013

      Correct…it’s all about probability.

  161. Nico  December 27, 2013

    Have any of the cholesterol posts discussed the role of oxysterols in atherosclerosis/disease processes in general? I started keto with a normal BMI and a fairly exemplary basic lipid profile (HDL 106, LDL 54, TG 45), so am not overly concerned about CAD in particular. However, I am somewhat concerned that eliminating fruits/legumes/starchy veg while increasing my consumption of oxysterols (via dairy, cooked fatty meats, heated oils) could increase my net oxidative load, if you will.

    I work in clinical research (specifically, oxidative stress and neuromuscular disease) and realize the data are quite murky regarding the risks/utility of antioxidant supplementation (especially vs. intake from food sources). However, I wonder if it may be warranted for those who have greatly reduced their intake of AOX-rich fruits with a concomitant increase in oxysterol intake.

    My thinking is that AOX’s documented ability to inhibit PUFA oxidation might curtail the production of ROS/free radicals that could trigger cholesterol oxidation downstream. For those of us in a low risk category for CAD, carotenoids, tocopherols, mineral ascorbates, even flavanoids are at best theoretically beneficial, and at worst, benign.

    I’d like to hear your thoughts on the matter!

    An article on the biological role of oxidized LDL, for anyone interested: http://www.jbc.org/content/272/34/20963.full

    (reply)
    • Peter Attia  December 29, 2013

      Nico, I’ve discussed it in various comment threads, but not yet in posts. Part of the problem is we don’t have a really good way to measure oxLDL. LpPLA2 is probably the best, and I’m still not sure how good it is. Clearly oxidation plays a role in atherosclerosis, but it’s not entirely clear (to me, at least), how to quantify it.

  162. Nonna  December 31, 2013

    Peter, If I had been that girlfriend in the parking lot I would have asked you to explain the significance of the area under the curve so that I could grasp exactly what you’re talking about and we probably would have been there for several hours hashing through it all! Thank goodness for people like you to share your enthusiasm and quest for understanding in so many areas important to us all. That energy, enthusiasm and thirst for knowledge comes through your on-line writings and talks. It is a real gift to all of us out here in the world trying to learn, understand and do the right thing by ourselves and our communities.

    Thank you!

    (reply)
    • Peter Attia  December 31, 2013

      Funny. I’m sure she has long forgotten that day…though probably has an awful memory of some loser she once dated.

  163. Norm  January 2, 2014

    I wonder how smoking and then quitting smoking affects cholesterol, if any?

    (reply)
  164. Karen  January 13, 2014

    The link “To see an important reference on this topic, please look here.” is not working…for item #7.
    7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan. Years ago the Canadian Guidelines removed the limitation of dietary cholesterol. The rest of the world, especially the United States, needs to catch up. To see an important reference on this topic, please look here.

    (reply)
  165. oori  January 18, 2014

    Thanks Peter, obviously you share priceless information.

    My question is, can you over ingest butter and other fats, ala bulletproof coffee for example, way above what your body needs and can handle and therefore have your cholesterol go thru the roof and liver enzymes elevated, whereas, if you eat 2 to 3 meals a day and use fat as a flavor like ingredients (cook in butter for example) cholesterol and liver enzymes would be normal, in other words is there a point in the curve that a ketosis diet can go from producing positive health results to negative ones. I assume every dirt would have such a point but is it easier to reach that point if you add fat to drinks, coffee etc..

    Thanks in advance

    (reply)
    • Peter Attia  January 19, 2014

      Absolutely, and it varies by person.

  166. Norm  January 20, 2014

    That means dietary fat DOES affect cholesterol levels, may be indirectly? With the aim of losing weight when one is fat adapted and they also are on a high fat diet, could there be too much fat available for their body in this situation? Could this explain why some people experience very high ldl on a low carb diet?

    (reply)
    • Peter Attia  January 21, 2014

      In some cases, yes. Tom Dayspring addressing this in a LecturePad post. I’ll revisit at some point.

  167. Norm  January 22, 2014

    Thanks Peter. Would really appreciate title/link of Dr Tom Dayspring’s post if it is out.

    (reply)
    • Peter Attia  January 22, 2014

      Lipidaholics case #291

  168. Norm  January 22, 2014

    Thanks Peter, helpful as ever. It is a great post and I would recommend reading of it to all who have experienced high LDL-C and LDL-P on a low carb diet. I truly hope that we do not go from one extreme to the other: from demonisation of fat to over consuming it believing that cholesterol/LDL-P is not relevant and it is all about inflammation as that’s what is being proposed by many in low carb community.

    (reply)
  169. Vincent Lin  February 8, 2014

    I enjoy very much of your posts, and please help me to understand the mechanism of atherosclerosis.

    The key of atherosclerosis is to understand how LDL particles go through single-layer vascular endothelial cells of arteries into the sub-endothelium. I have the following three related questions:
    (1) Can the LDL particles enter the single layer endothelial cells by transcytosis: endocytosis first, and then exocytosis? If yes, please cite the literatures;
    (2) If the number of LDL particles is major contribution factor to atherosclerosis, then (a) will the diameter of artery affect the atherosclerosis process; (b) why it occurs mainly at coronary artery or carotid artery, and rarely at the other arteries?;
    (3) Does calcium play any roles in the atherosclerosis process? If yes, could you comment its role?

    (reply)
    • Peter Attia  February 9, 2014

      (1) not to my knowledge
      (2) great question, and the issue is probably multifactorial — a combination of artery diameter (i.e., more susceptible to narrowing) and local factors that may damage the intima. Many arteries in the body experience athero, including large ones (aorta, femoral, renal). Lastly, collarerization plays a role in mitigation outside of the CV system
      (3) yes, addressed in previous posts

    • Vincent Lin  February 9, 2014

      Thank you for your prompt response to my questions.
      (1) Without understanding the mechanism of LDL being transported from the lumen side to the other side of sub-endothelium, all of the theories are only hypotheses to me. We need to understand the true mechanism to determine the real root cause of atherosclerosis.
      The endocytosis is proven by Brown-Goldstein when the cells themselves decide that they need more cholesterol by synthesizing more LDL receptors. If they don’t need more cholesterol, then they reduce or stop synthesizing the receptor. Thus, the cells are not forced to synthesize more receptors to take cholesterol disregarding that there too many LDL particles in the lumen. In my opinion, it is very unlikely that endothelial cells would import LDL particles by endocytosis and export by exocytosis to the other side of sub-endothelium simply because there are too may LDL particles in the lumen.
      Is it possible that there exist gaps or cracks in the endothelium cells; or the cells are forced to endocytosize not normal cholesterol but the oxidized cholesterol thru different receptors as suggested by some literatures; or from damaged endothelial cells; or too much calcium; or etc.?
      (2) If the number of LDL particles, LDL-P rather than LDL-C, has stronger impact in atherosclerosis, then it indicates that the number of times that a cell contacting with LDL particle in a unit of time is a more important determinable factor than the number or the size of particle. If this is case, then we should consider the velocity in addition to the number of the particle. The atherosclerosis should occur more frequently at the location where the number of contact time is higher.

  170. Fiona Shepherd Davis  February 11, 2014

    Can you comment on the role of diet in patients with Apo E 3/4 or 4 genotype? The conventional wisdom is that these patients should go on a low fat diet to improve cholesterol levels. Is there a decreased cardiovascular risk in these patients if their LDL cholesterol decreases on a low fat diet? What diet advice would you give to a ApoE 3/4 patient? Thank you!

    (reply)
    • Peter Attia  February 11, 2014

      Complex. 3/4 and 4/4 patients require special care and lots of tweaking to get right. Usually tolerate SFA less well and need less fat in diet. Also, rarely respond to monotherapy for lipid lowering.

  171. Norm  February 17, 2014

    Is it a good idea to have Apo E genotype tested for people who have experienced rapid increase in their LDL-C/LDL-P on a LCHF diet?

    (reply)
    • Peter Attia  February 17, 2014

      I think so, but that may not account for the response. ApoE is one of the few genes I think it’s worth knowing early in life.

    • Boundless  May 15, 2014

      > ApoE is one of the few genes I think it’s worth knowing early in life.

      When you get a chance, it might be useful to list the diet-related genes worth knowing about. If possible, please also identify some labs that report them. What actual adjustments to make for each might be beyond the scope of such an article.

      The only genes I’ve stumbled upon so far are AMY1, ApoE and MTHFR – and the low-cost DIY lab 23andme apparently does not report AMY1.

      I suspect that although the keto-paleosphere is distracted at the moment by resistant starches (and possibly “safe starches”) and is about to confront gut biome, the next big thing will be genotype-specific diets, and that’s going to require knowing.

  172. Norm  February 17, 2014

    Thanks Peter, can E3/4, 4/4 still get away with a high fat non ketotic diet by tweaking with SFAs and PUFAs or is it omega 6 that they need to be careful about? Would you please recommend any good readings (not too technical) on Apo E4 in the context of how such genotypes respond to dietary fat. Many thanks

    (reply)
    • Maryann  February 18, 2014

      Hi Peter, have you heard of Stephanie Seneff of MIT and this article: APOE-4: The Clue to Why Low Fat Diet and Statins may Cause Alzheimer’s. She discusses the defect as a cholesterol transport problem: “To summarize, I hypothesize that, for the apoE-4 Alzheimer’s patients, defective apoE has led to an impaired ability to transport fats and cholesterol from the blood stream, via the astrocytes, into the cerebrospinal fluid. The associated high blood serum cholesterol is an attempt to partially correct for this defect.”
      Dr. Perlmutter speaks of the need for low carb with increased healthy saturated fats to protect the brain even in cases of ApoE 4. As far as I know, there isn’t anything definitive suggesting to lower fat for 3/4, 4/4. Wouldn’t it put brain health at risk to do so? Thank you, Maryann

    • Peter Attia  February 18, 2014

      It’s not clear that optimizing around brain health and heart health have the same path in apoE 4/4 and 3/4.

  173. Maryann  February 19, 2014

    Thank you Dr. Attia, that’s interesting. A person would have to choose which he prefered to treat? Heart health or brain health and possibly to the detriment of the other?

    (reply)
    • Peter Attia  February 19, 2014

      It’s a bit more nuanced than that.

  174. Norm  February 22, 2014

    I would roughly guess that non ketotic low carb and low SATURATED fat might be the way to go for E3/4, 4/4 people?

    (reply)
  175. Elaine  March 3, 2014

    I am 68 and my cholesterol is 304. HDL 66, Trig. 98, LDL 218. The cholesterol went up from 250 to 304 after gallbladder removal. I have lone afib also but controlled with mag, etc. My cardiologist wants me to go on statins. I have no other heart issues, CT scan showed zero plaque and no risk of heart disease. The doctor was stunned as he thought I would have plaque. I think my cholesterol is familial. I did have the VAP test once which showed about 50/50 fractionated Ldl. A few of the numbers were off on the bad side. My Lpa is within range. My Ldl’s are always high. So, I’m wondering if I should do anything based on my results or? I do exercise and eat fairly low carb. Strictly no processed foods, grass fed beef, etc. Thanks for your info even though I don’t understand all of the in depth cholesterol info. It’s good to read as most docs just go by simple numbers and prescribe pills. I always said that it’s way more complicated than that and most docs are not treating people individually.

    (reply)
  176. Uzi Geiger  March 20, 2014

    Hi Dr. Attia

    I know this has only a vague connection to this post, but I am looking to know what are the timescales for enzymatic changes to the liver. For example, if I start eating lots of cholesterol (by the spoon fulls…), how much time will it take to my liver to downplay the cholesterol synthesis pathways? And if after that time I stop all cholesterol consumption – how much time until the liver starts cholesterol production again?

    Thanks.

    (reply)
    • Peter Attia  March 20, 2014

      I don’t know exactly, but I’ve seen the changes in as little as 4 weeks.

  177. sally  March 25, 2014

    Dr. Attria,

    I am looking forward to your article on APOE 3/4, 4/4. In the meantime I have a quick logical question, if one could get their gut in working order, reduce inflammation, eat a healthy diet, wouldn’t the whole APOE questions be reduced or eliminated? Since APOE 4 is the ancestral gene and our ancestors ate organ meats preferentially which is loaded with saturated fat, couldn’t one draw the conclusion that it is not the saturated fat per se but what is also in the diet that effects saturated fat metabolism?

    (reply)
    • Peter Attia  March 25, 2014

      I don’t really know. It’s unlikely the apoE 4 variant would have survived so long if it did not confer some benefit early in life (i.e., pre-reproduction), but that says nothing about the risks it poses later in life.

  178. SPP  March 30, 2014

    What could cause discordance between LDL-P and LDL-C in an individual with low triglycerides? Does LDL carry stuff other than cholesterol and triglycerides (vitamins and antioxidants?) I have been taking 4000 IU of Vitamin D as well as a number of anti-oxidants, and have seen a jump in D levels from 12 to 36. I had discordance in my first NMR and have been on a LCHF diet for maybe 6 months. Additionally, is there some sort of a half life for LDL? Typically does reduction in particle number happen steadily over a long period of time?
    Thanks so much for your work at NUSI and on this blog.

    (reply)
    • Peter Attia  March 31, 2014

      Particle size, phospholipids, a few other factors. Half life for LDL particle depends on size: for larger particles (pattern A), about 36 to 48 hours; for smaller particles (pattern B), more than 72 hours.

  179. Jane  April 5, 2014

    hello Peter,

    I am pursuing the question whether I can safely change my medication now that I have changed my diet to vey low carbs.
    I do still have two signs of metabollic syndrome: treated for blood pressure and persistent, but not worsening, HbA1c at 5.9
    TG is 60 and HDL is 60. waist is small enough. Doctor detected low visceral fat on physical exam.

    I have succeeded in getting an order for advance lipoprotein testing, so I now need to know:

    1. how long to go off of atorvastIn 40mg before I can get a valid baseline LDL-P.
    2. How safe is it to go off the statin?

    If the results are favorable, than I would also need to know

    3. which other lab measures (inflammatory markers?) would be needed, if any, for a statin decision,and

    4. which RCTs on post- menopausal women, or good meta analyses of them, would support changing the stain recommendation?

    Can you help me find answers to these questions?

    I am not asking for advice about treatment, just information from your data bank to help me navigate the system and communicate with my doctors.

    Thank you so much for your hard work for NUSI, for your advocacy and TED Talk, and for this educational blog.

    (reply)
  180. Vicente  April 8, 2014

    Hi Peter,
    I was reading the abstract of a study that said that when compared with a VLCHF diet, “an HCLF diet had more favorable effects on the blood lipid profile. This suggests that the potential long-term effects of the VLCHF diet for CVD risk remain a concern”. (http://www.ncbi.nlm.nih.gov/pubmed/18174038)

    But reading the full article, the conclusions say that “The HCLF diet had more favorable effects on LDL-C, whereas the VLCHF diet had more favorable effects on TG and HDL-C, suggesting that the latter approach may have relevance for the management of the metabolic syndrome.” (http://www.sciencedirect.com/science/article/pii/S0735109707032597)

    Am I the only one that sees a Jakyll/Hyde transformation here? I thought pubmed was a reliable source.

    PD: in Table 3 a change in LDL-C from 3.24 to 3.19 is NOT an increase of 0.06.

    (reply)
    • Vicente  April 8, 2014

      I have a correction to make: the transformation in the conclusions is not pubmed’s fault: the “hyde-conclusions” can be found at the beginning of the full article.

      Sorry pubmed. My wrong.

  181. Vito  May 2, 2014

    Hi Peter-
    Read this post awhile back, it has never quite sat right. Your 25 year old vs.75 year old risk example seems to imply that the area under the curve is unchangeable. That is, the damage done to arterial walls via particles is purely cumulative, and cannot be reversed or healed? What about a 65 year old with great numbers? 55 year old? 45? Perhaps I am reading too much into a high level population model on this one example? It is a thought provoking question-…

    (reply)
    • Peter Attia  May 4, 2014

      It’s probably not true in absolute, but on average. Of course, drugs and (the right) lifestyle changes will improve endothelial injury.

  182. Eva  May 18, 2014

    Dear Dr. Attia,
    thanks a lot for letting laypeople like me participate of both your personal journey and a lot of medical facts/news completed with explanations, so that also not-medically-trained people are able to follow.
    I really do appreciate your enthusiasm and your wisdom as well as your generousity in sharing your insights with the world.

    I´m an Austrian teacher and I´ve read nearly all your posts within the last weeks.
    I started LCHF just a while ago and I´ve got a question, which hasn´t be posted yet (as far as I can see).

    I wondered, if it is thinkable that a nutrition being high in fat leading to plaques in the artery-walls WITHOUT
    uppening the blood-lipids (aop-b-particle- number/LDL-C/total cholesterol)?

    What I´m wondering exactly is: Is it possible, that all blood-lipids- expecially the number of apo-b- particles, but also the LDL-C or even the triglycerides – are perfectly fine : No signs of the usually risk-factors for a cardio-vascular-desease. And that despite this- at the same time plaques are buildung within the artery-walls, even though the blood-lipids are perfect?

    Might it be possible, that the plaque-building goes on unwarned by blood-lipids?
    Or that there might be different risk-markers with high-fat nutrition than with a low-fat-nutrition?

    Yours Eva

    (reply)
    • Peter Attia  May 19, 2014

      I guess anything is possible, but it would be less likely, especially if specific inflammatory markers were also normal (e.g., LpPLA2, MPO).

  183. Dave  June 12, 2014

    “7. Eating cholesterol has very little impact on the cholesterol levels in your body. This is a fact, not my opinion. Anyone who tells you different is, at best, ignorant of this topic. At worst, they are a deliberate charlatan.”

    This is rubbish! I went on Dr. Esselstyn’s diet almost three years ago and it cut my LDL-C in half. My Cardiologist had me on a statin, but after awhile I stopped taking it completely for two months and then rechecked–still was half what it was before. I think you folks are the charlatans! I restarted on a different statin with less side effects and at a very low self-imposed dose (5 mg pravastatin/day)–just to hedge my bets. Checked it again last week and it’s 67. When I had my stent it was 134. Folks, go to http://www.heartattackproof.com and turn your lives around!

    (reply)
    • Peter Attia  June 12, 2014

      Your statement is no way a refutation of mine. Read my statement carefully. I did not say what you eat does not impact the cholesterol levels in your body. I said eating cholesterol… big difference, my friend.

    • Vicente  June 12, 2014

      Hi Dave,
      In my case a low-carb diet is enough to have perfect blood lipids. You seem to be eating high-carb and taking statins to try to fix the problems carbs create. I am sorry for you and I hope some day you can get rid of those drugs.

      I would recommend reading “Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors ” if you want to know what science has to say about improving your health without drugs.

      Have a nice day

    • Dave  June 13, 2014

      C’mon, doc. You know people equate eating cholesterol with eating animal products. You’re playing word games here.

      And Vicente, that study does nothing to move me. I agree that sugar and processed grains like white flour are no good, so if you cut that out of an animal product diet you’ll naturally fare better. No need to feel sorry for me, my endothelium’s in a lot better shape than the SAD diet I ate most of my life left it in. That’s what’s important, not eating to achieve good “numbers” (of which mine are substantially better just the same). If you don’t eat stuff that injures your arterial lining, your numbers mean little. What good is a high HDL if it really just means your liver is working overtime to mop up the residue from your bad eating habits?

      I’m outta here…

    • Vicente  June 13, 2014

      Hi Dave,
      with a low-carb diet I have better blood lipids (raised HDL, same LDL, lower triglycerides) and normal transaminases. My TG/HDL is 0.7

      My numbers are amazing, but you say this is in fact bad for me… You mean that now that my transaminases are ok, my liver and kidneys are indeed suffering? My high HDL “really just means my liver is working overtime”? While my health parameters improve my health deteriorates? Are you serious?

      I trust the numbers and the facts: 23 clinial trials using low-carb diets say my diet is healthy. But you “know” my diet is “bad eating”…

      Have a nice day

    • Kelley  June 15, 2014

      Dave: After a year and a half or so of following Peter Attia’s blog, I can say with pretty good confidence that one thing he does NOT do is play word games. That’s why I count on him as a trustworthy source of information. Which is not to say that you or I or anyone should accept what he presents uncritically (in fact, Attia would caution against doing so), but it’s possible to disagree without making ad hominem attacks on his integrity.

  184. Ellen  June 15, 2014

    I agree Kelley, I have been foolowing Peter’s blog for three years and it has been an incredible journey.

    Peter, I have finally gotten to the consciously unconscious stage and would like to start a light weight lifting routine for women over 50. I don’t know where to turn though. Any suggestions. I currently use the “Lower Back Basics” and ” Flexibility Training” by Brian Doftman. Thanks in adavance for any suggestions. Have a Great Father’s Day!

    (reply)
    • Peter Attia  June 16, 2014

      Thank you, Ellen. I’d recommend the book by Doug McGuff (Body By Science) and then a well-certified super slow coach to guide you.

  185. Lorenzo  June 19, 2014

    Hi Peter, I love what your are doing and the pasion you do this with is unique.

    (reply)
    • Lorenzo  June 19, 2014

      I meant passion not “pasion”. sorry.

  186. julianne  July 2, 2014

    I would like to get your comment on my lipid profile. You mentioned in your talks that you do not know whether a low carb diet that increases LDL is a worry when all other metabolic risks are low. I am one of those, normal blood pressure (115/75), low triglycerides (0.9) High HDL 2.2, and very high LDL: 6 That is 230 for you in the USA), almost all is large ‘non-atherogenic’ (I’m in New Zealand) However the shock is a very high oxidised LDL 2500.0 + ng/ml (reference range: 90 – 133.2)- a test not normally done in USA, I got mine done through a lab in Germany.
    I emailed Dr Dayspring, who said that it is likely the saturated fat in my diet “Your case is representative of many who pursue the high fat, low carb dietary methods. Due to individual genetic, some use the saturated fat as a substrate to significantly increase cholesterol synthesis – measuring the penultimate sterols in the cholesterol synthesis pathway ( desmosterol or lathosterol) in serum would confirm this.”
    As you said we just dont know if this is a problem or not. My husband also had his tested, and depite a similar diet, his LDL is also high (5), but virtually no oxLDL. Results from the lab (imupro) are in PDF format. I’d be happy to forward them to you if you are interested.
    As you can imagine – I’ve changed my diet – taken out coconut cream and oil which has caused problems for others LDL, and increased root veg and berry carbs. and added some supplements. I’m keeping track of everything so I can see what effect diet has.
    Regards
    Julianne

    (reply)
  187. Mike  July 18, 2014

    Hi Peter,

    Enjoy your posts, great stuff! Wanted to get your thoughts on the recent news about adverse effects of Niacin on hearth health. From your understanding does it really decrease LDL-P and increase HDL?

    http://www.foxnews.com/health/2014/07/17/dont-take-niacin-for-heart-health-docs-warn/

    Thanks

    Mike

    (reply)
    • Peter Attia  July 18, 2014

      Here’s the email I sent Tom Dayspring a week ago when I read the NEJM study:

      “Tom, So I read the NEJM piece (but have not seen your commentary yet, so forgive me if I’m repeating what you have written there)…
      This struck me as a study that asked the wrong question!
      They take a group of patients with already very low LDL-C (and presumably, though not a given, low LDL-P) and add one more agent to try to eke out a bit more LDL-C (and presumably LDL-P) reduction.
      But the agent they chose—-niacin-—is known to worsen IR.
      They do this in a patient population that is either all T2D or pre-diabetic. At best, they are “just” IR.
      So the trade-off is lousy. The upside-—LDL-P reduction—-is almost non-existent, yet the downside-—worsening IR-—is huge.
      Maybe I’m being too critical of the study. If this use of Niaspan is “common,” then it’s a good thing to have studied it the way they did, but it seems odd.”

  188. Jeff Johnson  July 19, 2014

    LDL-P

    !. If 100 hundred people enter the hospital or die having a heart attack (soft plauqe eroption) – how many of these people will have high LDL-P – ?

    a. A cofounder to this might be intermittent high LDL-P or high levels at some prior period – but aside from this possibility -

    they all should have high LDL-P -

    The number better be at least 50 – less than this and your LDL-P theory becomes not only useless and outright misleading – unless these is the best predictive available -

    I suppose or a least hope – the number is between 50 and a 100 hundred -

    Show me some numbers

    I have a feeling this may not be pretty -

    (reply)
    • Peter Attia  July 19, 2014

      How can this be done, Jeff, when about 50% of the time some presents with CAD, the first sign is sudden death? Furthermore, with so few people receiving advanced testing, the LDL-P info would be inconsistent.
      Look at the LDL-C data in one of these post (can’t recall which one) to see that distribution–LDL-C is not predictive in the hospital admitted patient population.
      If you look at studies that do use LDL-P testing, including this one (Atherosclerosis 235 (2014)) that came out a few weeks ago, mortality always tracks higher with LDL-P than any other metric.

    • Vicente  July 19, 2014

      Hi Jeff,
      1) let’s assume 5% of the population has a high LDL-P.
      2) let’s assume 25% of the people that die having a heart attack has a high LDL-P.

      Wouldn’t you say a high LDL-P is a risk factor?

  189. Andy  July 23, 2014

    Hi Peter,
    Thanks for the incredible posts and video lectures. Few questions, please:

    How does one lower ApoB? I’ve read that Tangeretin and Nobiletin inhibits ApoB production, but not sure that is addressing the cause. I’ve been Paleo for 2 years and my measured ApoB is 126 and apparently under 109 is acceptable range. ApoAI is 129, so the ratio is 0.98 where acceptable is <0.92. My Lp(a) is 4. So I'm struggling to understand why the ApoB is out of range.

    Also, how would one reverse endothelialc damage. If ApoB is lowered, can atherosclerosis be reversed? I supplement with theracumin to support this.

    Lastly, please could you let us have your viewpoint on Lp-pla2 – does this test have any merit? My score is 194 under the reference range of 200 which is a relief after my ApoB level.
    Sincere thanks,
    Andy

    (reply)
    • Andy  July 28, 2014

      HI Peter – sorry for the bump, but your viewpoint would really be appreciated. Cheers!

  190. Rob  July 25, 2014

    Hi Peter,
    Let me first say…..I’m a huge fan!
    My question for you is:
    If a person has metabolic syndrome, has had elevated triglycerides for some time (thus increased lipoproteins, boats), when this person adopts a nutritional ketotic diet and trigs fall through the floor does the measurement of HDL, LDL and overall cholesterol become elevated?…number of boats still the same but now carrying cholesterol (the intended cargo). If so, how long before the extra boats are decommissioned?
    Cheers,
    Rob

    (reply)
    • Peter Attia  July 26, 2014

      There may be a transient effect, but typically, a reduction in TG is matched by a rise in HDL-C within about a month or two. LDL-C is more variable, can go up or down depending on fat content of diet. VLDL-C also goes down typically.

  191. Rinat-ya  July 27, 2014

    Hi Peter,
    I am very confused do to the changes in my lipid profil in the last couple of months. I am 30 years old, I train on a daily basis ( I’m a kettlebell trainer, and I do crossfit and run 5k 2 a week). Everyday I try to be active. I weight 54 kg and my height is 1.60 cm and fat percentage is about 20%.
    Now, I’ve started Paleo diet on January this year and did my blood check at the same time and it turned out great (hdl 113, LDL 80). My paleo was less then 100 gr carbs per day. i decided to try ketogenic diet do to a lot of reading and quriuos on the way it will effect my training and body. On April I went into ketosis (under 20 gr carbs per day). I checked every day with blood strips my ketone and glucose. After 2 month I did blood checks again and I was very confused – my hdl rose to 154, but my LDL rose to 270. Glucose was 69, no CRP, thyroid ok, and triglycerid went just a little up. After a month I did blood checks again and my LDL rose again to 300. I checked my apo b and it was high (188), vldl was normal.
    I’ve decided to get out of ketosis and back to paleo ( I eat 80-100 gr fat, 70-100 gr carbs only from non starch vegetables and 1.2-1.5 per kg protein per day).
    I can’t understand the dramatic changes in my blood profil. I will state that before paleo I ate low fat low carb – a lot of vegetables, low fat dairy, no red meat, legumes, eggs , fish and chicken.
    I wonder if ketosis act different on active people. I’m quiet stressed at the moment, I’m used to be very healthy (as the modern age see it), and my doctor went nuts from my latest blood check. I really appreciate hearing your view on this.
    Much appreciate
    Rinat-ya

    (reply)

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