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Sugar 101 – How harmful is sugar?

Sugar 101 – How harmful is sugar?
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Any discussion on the culpability of poor nutrition as the cause of our health woes begins with a discussion on sugar. One of the world’s experts on this topic is Dr. Robert Lustig, a pediatric endocrinologist at UCSF.  Dr. Lustig has great experience treating children with obesity and is really on the front lines of what is becoming an epidemic of childhood obesity.  About two-and-a-half years ago, he gave a lecture on the perils of fructose (fruit sugar, which also makes up half of table sugar and high fructose corn syrup). It’s about 90 minutes in length, but the time goes by pretty quickly as Dr. Lustig is an engaging speaker. In addition, Gary Taubes wrote a great piece on sugar toxicity in the NY Times Magazine last year, which references the work of Dr. Lustig.  You can find it here.  Gary’s article on this topic was the fourth most read feature of 2011 on NYTimes.com (and the most read of all health-related topics).   Here’s the video of Dr. Lustig’s lecture:

I’ve highlighted the key points (with corresponding time in video), for those who may not want to watch the video in its entirety:

  • 0:09:40 – Helpful summary showing the reduction in fat consumption in the U.S. from 1960 to 2000 (about 45% to 30%) and the concomitant rise in obesity (about 12% to 31%) [Which, of course, doesn't "prove" anything, it's just another correlation.]
  • 0:23:00 – Change in fructose consumption over time: Prior to WWII (16-24 gm/day); 1977-78 USDA survey (37 gm/day); 1994 NHANES III (54.7 gm/day); Adolescents today (73 gm/day).
  • 0:24:00– Perfect political storm of 3 events:
    • Nixon and USDA secretary (1973) – insistence to stabilize/reduce food prices.
    • Invention of High Fructose Corn Syrup (HFCS), which was half the price of cane sugar and enabled cheap substitution.
    • USDA, ADA, AHA, AMA – all call for reduction in fat intake.  Why? (For a quick primer on “cholesterol,” you may want to check my previous post on, What is cholesterol?)
      • Early 1970’s – LDL-C (The so-called “bad” cholesterol) is discovered (more specifically, a test to measure LDL-C is discovered)
      • Mid 1970’s – Observation that dietary fat is correlated with rising LDL-C (“A implies B”) in a subset of people.
      • Late 1970’s – Observation that elevated LDL-C is correlated with heart disease and cerebrovascular disease (“B implies C”) [Note: It's not actually clear this correlation has causation attached to it, in fact most evidence today would tell us that elevated LDL-C does not lead to heart disease and stroke.]
      • Early 1980’s – The following connection is (erroneously) made: A implies B, and B implies C, hence A implies C, so no-A means no-C.  [I guess it’s easy to see how an untrained person could make this mistake, but anyone who has taken even an intro course in logic knows that if A implies C, it is not the case no-A implies no-C, it is only the case that no-C implies no-A. It’s hard to believe such poor logic was, and is, used to drive health policy. Last editorial point on this – any card-carrying lipidologist today will tell you that the so-called “bad” LDL-C is as relevant to your getting heart disease as your eye color.  Heart disease is caused by lipoprotein particles carrying oxysterols into your artery walls.  This is not measured or reasonably predicted by LDL-C.]
  • 0:33:00 – Overview of Ancel Keys’ flawed “Seven countries study:” Showed the correlation of fat intake and coronary mortality, but failed to explain the cross correlation of sucrose with the fat (that is, sugar consumption rose too, but this was ignored in the analysis).
  • 0:58:00 – Fructose metabolism overview (technical, but interesting – feel free to skip if you don’t like biochemistry): Fructose requires more ATP for the first step in its metabolism (fructose to fructose-1-P) than glucose.  This requires an AMP scavenger to recycle the ADP and AMP.  AMP goes to IMP, which goes to uric acid.  This creates the link between fructose consumption and gout and hypertension (uric acid blocks nitric oxide synthase).  In addition, the byproducts of fructose-1-P to pyruvate, such as xylose-5-P, upregulate the enzymes that favor the reaction of citrate being turned into acetyl CoA being turned into fatty acids (staying in liver, causing fatty liver) and VLDL (exported out of liver) [i.e., de novo lipogenesis].  In other words, on a per unit basis, much more fructose is hepatically converted into fat than glucose.
  • 1:09:00 – Comparison of chronic ethanol exposure and fructose exposure; very high overlap (not surprising, given that ethanol is fermented fructose).  As Lustig correctly puts it, fructose is ethanol, but without the buzz…

You could leave Lustig’s lecture thinking that fructose alone is the cause of obesity.  There is little doubt that a massive reduction in fructose (e.g., elimination of dietary sucrose and HFCS, and only modest consumption of fruit) does a lot to reduce obesity.  But does this mean the rest of carbs get off the hook?

The problem with the “fructose-alone-is-the-root-of-all-evil” argument

Much of what Dr. Lustig says may be correct, but I believe he overstates the importance of exercise in controlling weight (though he acknowledges that most “experts” fail to realize the calorie burning component of exercise is meaningless), the role/importance of fiber, and the lack of harm associated with glucose.  I am going to write extensively about these topics at a later date.  The “fiber story” is another sad example of observational epidemiology causing more harm than good.

Back to fructose…the main flaw in Dr. Lustig’s argument, in my humble opinion, is that he claims glucose is benign and that fructose (alone) is the culprit of obesity and metabolic syndrome.  In this sense, he is partially correct.  Fructose, in excess, may be “evil,” to be sure.  However, Lustig claims that glucose is “good” in any amount.  He does this based on the assumption that the metabolic priority for glucose metabolism is, first, direct oxidation (i.e., real-time use by organs that need it), and second, glycogen formation and storage by the liver and skeletal muscles.   He overlooks a few problems, though.

  • Direct oxidation of glucose at rest (the state we are in >90% of the time) is quite low.  At rest, most adults oxidize less than 20-25 grams of glucose (about 60-90 kcal/hour of glucose).  In fact, even during exercise, it is difficult for the mitochondria to oxidize more than 1 gram of glucose per minute.  In other words, while this “sink” for glucose is a high priority, it is very limited in size and rate.  Most of the time we consume carbohydrates (i.e., glucose precursor) we are supplying much more than we can oxidize at that moment in time.
  • Conversion of glucose into glycogen is limited to how much “room” is left in the glycogen tank.  Even the most highly trained athlete can only store a finite amount of glucose in the form of liver and muscle glycogen: approximately 400 kcal (120 gm of glucose) in the liver and approximately 1200 kcal (~400 gm of glucose) in the sum of all skeletal muscles, assuming one is starting from a completely depleted reservoir (a profoundly rare physiologic state).  The body does not have the potential to store excess glucose, beyond this amount, in a form that is recoverable as glucose.  Any excess glucose that is not immediately metabolized, or converted to glycogen, is turned (irreversibly) into fatty acid for storage.  At about 47:00 min into the video, Dr. Lustig talks about the fact that glycogen is non-toxic (true) and that regardless of how much the liver stores, it doesn’t cause hepatocellular damage, unlike fructose (true).  The problem is, he fails to mention the storage capacity issue.  When the liver stops storing glycogen, which it does at about 120 grams, it does convert the excess to fat.
  • While the most highly-trained, insulin sensitive individual might be able to replace glycogen (assuming liver and/or muscle have capacity) when they ingest carbohydrate, rather than store fat, an insulin resistant individual is less able to import glucose into muscle to form glycogen.  Furthermore, when insulin levels are elevated, fat lipolysis is inhibited, and obviously this problem is confounded in the insulin resistant individual.

Even in the absence of fructose, a diet high in glucose, beyond everything I’ve stated above, still stimulates insulin release from the pancreas.  Elevated levels of insulin “turn off” our ability to burn fat and increase our capacity to store fat (see figure below – you’re probably getting used to seeing this figure by now).

Insulin levels versus fat breakdown

Clearly fructose is a significant culprit in obesity and metabolic syndrome.  I’ve personally seen many patients with fatty liver (usually a tell-tale sign of alcoholic liver disease), who rarely consumed alcohol, but consumed high amounts of sugar.  At the time (i.e., when I was operating on them), I couldn’t make sense of this observation.  Now I can.

The impact of chronic sugar exposure is probably more significant than that of tobacco.  I’m actually not being hyperbolic. However, eliminating fructose alone will not cure metabolic syndrome and its associated pathology.  It will go a long way, but not all the way, at least not in all people.  We simply eat too much glucose in our current carbivore lifestyle.

Scientists have done studies showing that if one removes all fructose (e.g., all sucrose, high-fructose corn syrup, and fruit) from subjects’ diets, they tolerate glucose better, PROVIDED glucose intake is limited, in keeping with the constraints I outlined above.  If, however, in the presence of fructose restriction, we consume massive amounts of glucose, we will still convert glucose into fat and, as importantly, through elevated insulin levels, switch off our ability to oxidize our fat stores.

To quote Dr. Lustig from this talk, “it’s a numbers game.”  We consume far too much glucose to simply fill our glycogen tanks.  Invariably, we keep them topped off, and continue to pour the extra glucose into fat, all the while we force our bodies to survive in a high insulin environment.

 

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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. Priya Rawat  January 14, 2012

    What would most of us do without the marvellous ideas you share on this site? Who has the patience to deal with crucial topics for the health of common subscribers like me? I actually and my buddies are very delighted to have your blog among the ones we often visit. It is hoped you know how a great deal we value your effort! Best wishes coming from us all.

    (reply)
  2. Dave  January 15, 2012

    Are you saying that the maximum storage capacity of the liver is 120 grams of glucose and 120 grams glycogen independent of each other?

    What is the conversion factor for glucose to glycogen in the liver and in the muscles?
    Are these factors relatively constant in the population?

    Thanks much!

    (reply)
    • Peter Attia  January 15, 2012

      I’m sorry, this is my mistake in being a bit too liberal with the terminology. I (and most folks) use “glycogen” and “glucose” interchangeably, though this is technically not correct. The body’s cells use glucose, which is a 6-carbon ring, but the body stores glucose in the form of a structure called glycogen, which is simply a bunch of glucose molecules linked together in a large polymer. So, to be rigorous, the liver and muscle store about 120 gm and 400 gm of glycogen (pretty much equivalent to that mass of glucose), respectively. These numbers, especially muscle glycogen, are quite variable in the population and have to do with muscle size and metabolic efficiency. The more insulin resistant an individual is, the less efficiently they convert excess glucose to glycogen. This is a bit of an over-simplification, but is decent rule of thumb.
      But keep in mind the main point: There is a relatively small amount of storage space in the body for glycogen, especially relative to the typical Western diet.

  3. Tom  January 18, 2012

    So here is my question. If I do consume too much glycogen, say a fruit salad for lunch at the office or some other form of sugar, am I better off working out afterward (or prior) with some high intensity in order to try and deplete the glycogen stores to inhibit the fat retention in my cells? what would the timing be prio or after eating? It is probably more a question of science/interest than it would have a significant impact or am I wrong?

    BTW, love the sight and the emails. Though I don’t work out 3-4 hours a day I do compete (and I use that term loosely) in endurance events but have never had the lean body. Always been fit but fat even running marathons. I have been following your advice and dropping weight like crazy and feeling much better. no loss in stamina and much of the time it is improved. Thank you for time, passion, and effort!

    (reply)
    • Peter Attia  January 18, 2012

      Tom, I think you’re asking, “when is the best time to consume fructose?” Or glucose? Technically, you don’t consume glycogen – glycogen is the storage form of glucose. With that caveat, the best time to consume fructose would actually be right after a long enough workout that depleted your liver’s reserves of glycogen. In this setting, fructose would be preferentially diverted into replacing liver glycogen, rather than being stored as fat and/or exported as VLDL. Keep in mind the quantities, though. Let’s say you depleted half of your liver’s glycogen. This means you can put another 200 kcal or so in place, or about 55 to 60 gm of fructose. A large Fuji apple has about 30 grams. So a long workout doesn’t make it “ok” to drink 3 bottles of gatorade.

    • Tom  January 20, 2012

      You actually answer both my suspicions and question. First was the timing and second is the real fact that significant fructose consumption has little remedy in terms of exercise. Makes complete sense. Thanks again!

  4. Eliott  January 22, 2012

    I am currently reading the Art and Science of Low Carbohydrate Living by Drs. Volek and Phinney. It was a book that Dr. Eades said he wished he had written. It is extremely interesting but also terribly complicated for a laymen like me but covers several of the points you make. I was wondering if you were familiar with it and if so your thoughts. My partner and I are endurance athletes and while we ate a low carb diet were always concerned about running out of fuel. This has put our fears to rest. We are so excited to have found your blog and look forward to the information and experiences you have been and will be generous enough to share. Thanks,E.

    (reply)
    • Peter Attia  January 23, 2012

      I’ve read the Art and Science by Jeff and Steve twice. It’s a nice complement to Gary’s incredible work. I look forward to writing more and more about athlete-specific issues of low-carb nutrition. In fact, Steve and Jeff really helped me personally as I was transitioning to ketosis while trying to maintain 21 hours a week of heavy training. By their admission I was the most different person they had ever seen through that transition. We all learned a lot from my trial and error.

  5. Deb  January 23, 2012

    What would you do if you had a fat child? I haven’t discovered a successful model for kids though I have read GCBC, WWGF and watched Lustig and Taubes lectures. As kids enter school it becomes more difficult to control their diet. (I’d love to know how Taubes feeds his kids, though they sound very young.) I have 3 kids, all under 10, two of whom are fat. One of my children was born 6.5lbs, was exclusively breastfed, and nonetheless was very fat by 4 months. I thought I had a nicely chubby baby but now that the child is older I realize that the tendancy to gain fat was in the child from birth. While both my husband and I have obese relatives, neither of us is obese and my pregnancy weight gain was normal. I do and did have a huge sweet tooth. No gestational diabetes. In summmary, would love information, ideas and links to resources for fat kids. Thanks.

    (reply)
    • Peter Attia  January 24, 2012

      Deb, great question. The same principles apply to children, though we have less data. For this reason, I would not necessarily advocate for a child to be fully ketoic (although nutritional ketosis is a known and proven treatment for intractable epileptic seizures in children and has been shown to be safe). For overweight children, I would look to the work of Dr. Lustig – strict restriction on ALL sugar, plus I would greatly reduce highly refined carbs and grains. You point out an obvious problem, of course, with respect to “food infrastructure” – i.e., what they are bombarded with outside of the house. Perhaps being very strict in the house (e.g., no cereal with any sugar, no soda, no juice) might be a start?

    • Joe  February 16, 2012

      Dr. Attia,
      I was trying to find an appropriate spot on your site to ask your thoughts on this question. I am a pediatric dentist and ran across an article just published, “Association between Childhood Obesity and Dental Caries”. It appears to be a retrospective observational study. They found that a smaller proportion of obese and overweight children initially presented with tooth decay than underweight/healthy weight children. I expected the opposite. I would think that a child with a high refined carbohydrate diet would be more likely to be obese and have more dental decay. As an anecdote, when I think about, I observe a similar trend in my practice. Any thoughts on why an obese child would have lower dental caries incidence?

    • Peter Attia  February 17, 2012

      Hmmm. Very interesting question. As you point out, the retrospective and observational nature make it practically impossible to conclude anything. I would suspect some confounding variable, like socioeconomic status, though I don’t have a great idea exactly what?

  6. Anon  January 25, 2012

    I no longer drink soda or juice, but still drink diet soda. Does diet soda cause a spike in insulin, even though it contains no carbs? Will it slow down weight loss? How about coffee (without sugar or sweetener)?

    (reply)
    • Peter Attia  January 25, 2012

      I’ve written an entire post on this exact topic, but it’s still “in line” to be put up. Please sign up for the blog and you’ll get an email as soon as I post it. Promise.

  7. Helga  January 29, 2012

    I eagerly await the alcohol and type 1 diabetes posts. My best friend is type 1 and has always struggled with her weight. I personally don’t mind giving up most carbs, but I do love to have some wine.

    (reply)
    • Peter Attia  January 29, 2012

      Don’t worry, you don’t need to give up wine.

    • Jeff Currin  February 5, 2012

      Will you be writing about wine & spirits? I’ve cut sugar and most all carbs and have lost a few pounds but not as much as I’d hoped. I realize now that I’m consuming too much protein and not enough fat — but should I be cutting alcohol?

    • Peter Attia  February 5, 2012

      I will. Please stay tuned.

  8. David  January 31, 2012

    Peter, have you investigated diets like the Anabolic Diet from Dr. Pasquale or guys like Charles Poliquin. For people who are insulin sensitive, they recommend periodic carb refeeds, although its still a low carb diet. For example, Dr. Pasquale would have clients eat low carb (<30grams per day) high fat for 5-6 days and then have a day or two of carb refeed (length of carb refeed was based on keeping you in ketosis). Seemed to combine benefits of low carb while providing benefits of carbs and insulin. Poliquin (if my memory serves me) does not recommend these refeeds unless you have a fairly low bodyfat.

    (reply)
    • David  January 31, 2012

      Sorry, Dr. Mauro DiPasquale

    • Peter Attia  January 31, 2012

      I have not read their work, but at the surface I see much downside to constantly going into and out of ketosis – from personally experience, this makes it very difficult for your body to completely adapt metabolically.

  9. Shiv Kumar  January 31, 2012

    Hi Peter,

    In answer to Eliott’s question above you say, “By their admission I was the most different person they had ever seen through that transition”.
    Can you explain that some more please? Also, what (in their experience) is “normal”?

    (reply)
    • Peter Attia  January 31, 2012

      Sorry, typo, supposed to say most “difficult” person. Probably because of my caloric requirement and my refusal to reduce training volume during the transition period.

  10. Shiv Kumar  January 31, 2012

    Hi Peter,

    Have you seen Dr. Richard Johnson’s (Kidney Disease researcher) videos on YouTube? He discovered a connection between Fructose and elevated triglycerides, hypertension, kidney disease, and Obesity. He also uncovered links to a biochemical condition which link an addiction process that may be induced in some people from the Fructose. His thought is that it may have originated as an evolutionary process among the people who evolved in Eastern Europe as a mechanism to survive the cold winters in which the people had very little access to food.

    Part 2 starts at the point where he starts to talk about fructose and Metabolic syndrome.

    Part 1
    Part 2
    Part 3

    (reply)
  11. Joe  February 2, 2012

    Peter – as a young “ish” person, I just want to thank you for picking up the torch with Gary. Poor Taubes has been at it alone for over a decade now, and its high time someone (with a medical degree) helped him out! My wife and I follow your blog closely and enjoy reading about low carb from the perspective of an elite athlete.

    Just wanted to point you to this lecture by Dr. David Diamond at USF. It involves his own personal journey in discovering what was making him fat and at risk for heart disease. I found it very informative, and, like your own story, compelling because it was from a medical professional’s own experience.

    http://www.youtube.com/watch?v=3vr-c8GeT34

    Keep fighting the good fight (against insulin)!

    (reply)
    • Peter Attia  February 2, 2012

      Thank you, Joe. I’ll try to watch this video when I get some time. I seem to be a bit lacking in that department right now, though.

  12. Warren Dew  February 6, 2012

    Thanks for this post. I’ve been worried about how much mind share “safe starches” have gained in the low carb community based on Lustig’s video.

    (reply)
    • Peter Attia  February 6, 2012

      Glad you liked it, Warren. I think the work of Lustig is fantastic, but I did want to call this point to attention. Zero fructose + small amounts of glucose at the right time might be ok, but that’s not what folks actually eat.

  13. Josh Turknett, MD  February 7, 2012

    Great to see another physician challenging the nutritional dogma in a public forum.

    Another major issue with fructose is its tendency to form advanced glycation end products(AGEs). As you know, protein glycation is the primary mechanism by which diabetes leads to tissue destruction. Fructose, however, is about 10 times more likely to form AGEs than glucose. Since AGEs are a common feature in the pathology of many chronic/degenerative disorders that affect non-diabetics, fructose may well play a crucial role in their pathogenesis. This includes several neurodegenerative disorders – I discussed the link between AGEs and Alzheimers’ in a
    recent post.

    Anyhow, food for thought (no pun intended). Keep up the good work!

    (reply)
    • Peter Attia  February 7, 2012

      Josh, thanks so much for the comment. Absolutely, this is a great point. It’s hard for me to “endorse” fructose consumption in any amount beyond the most modest amount. Thanks for bringing this up. By the way, I’ll be writing a post or two (or a series) on the role of this in Alzheimer’s disease.

    • TwitchyFirefly  January 20, 2013

      Steve Jobs, reportedly, was practically a fruitarian. I have long wondered if that contributed to his pancreatic cancer.

    • Peter Attia  January 21, 2013

      Be careful of extrapolating from this. He may have had the same illness regardless of what he ate.

  14. Mike  February 8, 2012

    I was a vegan and twice tried the 80/10/10 diet (90% fruit), more recently with bad consequences. Although, it possibly appears there are people who thrive on it, I could not. Granted, I could not eat fruit at every meal everyday, which left some oil and other fats in my blood, which is a large no-no. My first experiment led to hard training doing “Power 90″ for 70 days with get this, no body fat loss, no weight loss and no muscle gains! When I recently tried the diet again, I swear I was having memory issues, my typing was horrible, almost as if I had a disconnect between my mind and fingers and I was dipping into deep depression.

    I finally made a connection to possible insulin resistance myself. I just could not get that 70 days of working out with no results out of my mind. This led me to the Primal Diet and I figured I could try it and see what happened. It’s about a week in, my depression has lifted, I am never hungry, My typing issues went away and I dropped some water weight.

    I am still learning to avoid carbs and it’s not easy at first. I firmly believe low fat is NOT where it’s at. I also believe insulin resistance and overuse of carbs is the #1 issue in the country. I am going to continue on this path. Next week I am going to begin training weights only using the Body By Science methodology with a professional trainer familiar with it. I am only going to do cardio for fun. I have also found a supplier for grass fed beef and free range chicken. I had my first grass fed burger no bun tonight. I have also been eating avocados with no guilt and feasting on flax fed chickens omega three eggs.

    I still have issues ethically with animals being used to feed me, but right now nothing is more important than dropping this 30-40 pounds of fat off my 204 pound frame and my health.

    (reply)
    • Peter Attia  February 8, 2012

      Wow, Mike. When I get comments like this, it makes me think I need a “testimonial” section on this blog. You’re right, there are some people out there with good enough genes (probably 10-20% of the population, including my wife) who can do ok (and even “well”) on this type of diet. Unfortunately, most of us cannot. I really understand your concern over eating animals from and ethical perspective and completely respect that choice. I do think your logic is water tight, though, with respect to the trade-offs. I think you really minimize meat intake and make huge strides, especially if you’re ok with fish and dairy. PLEASE keep me posted on your progress.

  15. Harold  February 12, 2012

    Several people commented that they were having trouble loosing weight despite a seemingly good low carb program. No one mentioned thyroid problems as the possible cause. If weight loss fails on a low carb lifestyle the thyroid should be carefully checked out. The TSH is not a reliable test and is often the only test done. A free T3 needs to be done and possibly a free T4. You won’t loose weight if you are hypothyroid and it is easily corrected.

    (reply)
  16. Youval  February 16, 2012

    Hi,

    After reading Gary Taubes’s books and some online material (including this very impressive and enjoyable blog), here are a few lingering questions:
    * Has there been any serious response by “the establishment” to the low-carb, high fat claims? It’s easy to be convinced by hearing one side of the argument (especially when it’s presented so thoroughly an eloquently), but to really judge its merit it’s useful to hear the other side (if there is one).
    * Is it really the case that our bodies can’t store fat when we’re on a low-carb diet? Does energy use by our cells just go up indefinitely? Do we somehow secrete the un-needed nutrients?
    * Are there any estimates regarding “safe” levels of (unrefined) glucose and fructose consumption? I would assume that in many of the places where diseases of civilization were absent prior to the introduction of western foods, people were consuming significant quantities of fruit, starchy vegetables and maybe even grains.

    (reply)
    • Peter Attia  February 16, 2012

      These are really good questions and worth much more time than I can give them right here. I’ll try to very briefly address them.
      1. The medical establishment has 2 main disputes with what folks like me, Gary, and Lustig say: 1) they do not believe what we call the “alternative hypothesis” (see glossary), and they believe that saturated fat is harmful.
      2. This is a bit of an oversimplification. It’s probably more accurate to say, when we’re not consuming carbohydrates, the hormonal milieu in our bodies make fat storage less likely.
      3. Highly dependent on your genes, activity level, and timing of ingestion.

  17. Lisa  February 18, 2012

    I’m enjoying your website. I find it supportive when I’m literally betting my life on this approach to lower my insulin.

    I’m a 4+ year breast cancer survivor and extremely interested in the role of nutrition in disease. Since completing conventional treatment, I’ve spent the better part of the past four years educating myself by reading studies trying to learn the best way to eat to increase my odds of long term survival. By genetic profile of my tumor, I’m at high risk of distant recurrence so this is obviously very important to me. I’ve finally settled on a low carb, high fat approach largely based on the work and opinions of Thomas Seyfried at Boston College and a few others. The carbs I allow myself are all ones that have a good chance of improving my odds of survival – cruciferous vegetables and leafy greens being the mainstay. I’m also very careful about my Omega 3 to Omega 6 ratio and exercise moderately to further reduce insulin levels.

    Low carb, high fat is a really hard approach to follow because I have no support from my doctors and all conventional advice is to lower fat and add more complex carbs. There’s conflicting studies about high fat vs. low fat diet and the risk of breast cancer. The one study that causes me to doubt my approach is the Women’s Health Initiative study which showed a modest reduction in risk of BC with a low fat diet. This was not always statistically significant except for my particular tumor type, (ER+/PR-) in which case there did appear to be a benefit from low fat. Of course, that is risk, and not survivability or odds of recurrence, but it does make me wonder about this approach and is my one concern.

    Here’s hoping I’ve guessed right! If you’re familiar with the WHI study and have any thoughts, I would love to hear them in a future post.

    (reply)
    • Peter Attia  February 18, 2012

      Lisa, I won’t pretend to understand what you’re going through, but I think your approach makes all the sense in the world as far as doing everything in your power. I will be writing a post (or two) on the role of insulin in cancer, so please stay tuned.

    • Edward  May 19, 2012

      One approach to maximizing the possibly cancer-fighting micro-nutrients you want to get from your cruciferous vegetables and leafy greens is to juice the vegetables. You don’t have to chew up a big volume of fiber that way. A Breville juicer seems to be the best at juicing greens.

    • Peter Attia  May 19, 2012

      Perhaps? But what is the actual body of evidence that says the juice of vegetables prevents or halts cancer?

    • Edward  May 19, 2012

      I don’t know of any. I was just responding to her idea that the veggies were her mainstay in her fight against cancer. I’m not really sure the “micro-nutrients” in veggies even exist for carnivores. I actually meant to ask you specifically about juicing, especially after I watched “Fat, Sick and Nearly Dead” a couple of times.

      I, like you, prefer to let animals eat plants and then eat the animals. That is what used to be taught in nutrition classes when I was in nursing school in 1977. Even undernourished animals we were told were still nutritious and therefore created a buffer between us and a less than nutritious environment. Of course, this was prior to the feedlot cattle and chicken factories.

    • Peter Attia  May 19, 2012

      I love vegetables. Don’t get me wrong. I just don’t buy any evidence that they are uniquely healthy or “special.” It’s important to differentiate between something as “essential” versus “not harmful.” These are not the same thing. I put most vegetables in the latter category.

  18. Maryann  February 18, 2012

    Hi Peter! Thank you for all of the great work you do, and for so generously sharing it with us. You are changing lives! I found you from a link on Gary’s site. Is wine considered ethanol? (You have it pictured in your last email alongside beer.) For example, are the following equally bad for our health: wine, cognac, scotch on the rocks, champagne, gin with diet tonic, or a skinny margarita? Some of these have no carbs at all. Are all alcoholic drinks to be avoided regardless of the carb content? If so, is that because they are all ethanol or because they are all considered sugar? Thank you :)

    (reply)
    • Peter Attia  February 19, 2012

      Maryann, yes wine is a form of ethanol, as is all “alcohol” we drink. I would not say all beverages are equal, but you need to look at each one individually: how much ethanol is it (this will mostly get turned into fat by your liver, but does not stimulate insulin)? How much sugar is in it? How much other stuff is in it? The sugar and carb content of the drinks you list is actually quite different.

    • Maryann  February 20, 2012

      Thank you for your kind reply, Peter. I don’t understand the distinction between carb and sugar content. I’m sorry!

    • Peter Attia  February 20, 2012

      We’ll get to it.

  19. Birgit  February 21, 2012

    I read “Wheatbelly” and gave up wheat, then read Gary Taubes and started low-carb, then found your blog and learned more about storing glycogen. I have no doubts that this is working as I have lost 3 pounds from 139 to 136 on over 2000 calories with moderate exercise and borderline hypothyroidism in only 2 weeks. I also have much more energy in the afternoons and evenings and finally make progress in my running. I’ve been low-carb (about 50-60 grams)for a week and realized I don’t know what to do before my long run of 2 1/2 hours now, should I eat any extra carbs, and how much? Same for half marathon coming up on March 3.
    Your blog is outstanding and I love the clear and systematic thinking. Makes it so much easier. Keep up the great work!
    Birgit

    (reply)
    • Peter Attia  February 21, 2012

      Birgit, if you’re eating right, you don’t need additional carbs for long exercise. I rode for 5 (very tough) hours on Sunday with nothing but water. Had a high fat breakfast 2 hours before. It takes your body some time to adjust, but if you get enough fat, enough salt, and keep carbs low, you can access infinite fat stores. Take it easy and keep experimenting.

    • Birgit  February 22, 2012

      Peter, thanks so much for your reply. Fortunately I read your blog “My Pet Peeve” this morning because when I went for a run earlier my heart rate was up at a much lower speed than normal (using Maffetone method with heartrate cap at 134) and I decided to stop after only 3 miles. I’m still a beginning runner (18 months) but I also realize that after only six days my body still needs to get used to burning fat and seems a little stressed by the new challenge. Frankly without the heart rate monitor I wouldn’t have been able to tell, though. :)
      I’m very much looking forward to more of your blogs and am trying to spread the work on facebook and sparkpeople.
      Birgit

    • Peter Attia  February 22, 2012

      Keep in mind, it took me about 12 weeks to really really adjust my exercise habits around being in nutritional ketosis, so go easy on yourself.

    • Birgit  February 22, 2012

      That really helps to know. I’ll be careful. I’m not very competitive nor do I like to push myself too hard, LOL, I know patience will pay off. :)
      Birgit

  20. Edward  May 19, 2012

    In your discussion of Dr. Lustig’s lecture, you mention that, “Any excess glucose that is not immediately metabolized, or converted to glycogen, is turned (irreversibly) into fatty acid for storage.” Surely you didn’t mean irreversibly. We would never be able to lose weight that way, I would think. Maybe I missed something. I often do…

    (reply)
    • Peter Attia  May 19, 2012

      Correct. What I mean is once it’s converted to fat, it’s always fat. It can’t go back to glucose/glycogen. So the only way to “do” anything with it is to oxidize it.

  21. Aviv  June 10, 2012

    Weston A price. Long, long time before Lustig, very cool short video…

    http://vimeo.com/33089450

    Or

    http://www.youtube.com/watch?v=UHNDmsYOY8c

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  22. Joe  June 12, 2012

    Dr Attia,
    I really appreciate your work and find your site an invaluable resource! I think Dr. Lustig’s video is fantastic. Do you have any suggestion or know of a more basic presentation? In my pediatric dentistry practice, I am looking for an effective way to present this information to teenagers who consume high amounts of the high sugar beverages. Any thoughts would be much appreciated. Thank you.

    (reply)
    • Peter Attia  June 13, 2012

      Hmmm, good question. I can see the value in that, but can’t think of anything off the top of my head, beyond your thoughtful explanation to patients and parents. Anyone else?

  23. Michele  June 13, 2012

    http://www.box.com/s/100d8671b8160e03867e

    Hi Joe, Peter,

    There’s the link again to the presentation I put together for my dad who is diabetic. It’s a different audience but might have some use in helping Joe frame his “elavator speech” for his patients. I think teenagers might get this.

    Best of luck and hope I can help.

    (reply)
    • Joe  June 16, 2012

      Thank you. I really found the http://www.sugarstacks.com helpful. I had forgotten that I have used that successfully in the past. A picture is worth a thousand words!

  24. Mike A.  June 25, 2012

    Dr. Attia,
    I’m hoping you can clear up a point of confusion for me. I thought that glucose typically is the culprit in causing the insulin response that we are trying to minimize in order to free up our stored fat. However, in the Lustig video, he indicates that the fructose is metabolized in the liver, and that the free fatty acids that result elicit an insulin response. I assume that this insulin response would be no worse than what would result from consuming dietary fat. Is that indeed the case?
    Secondly, how is it that many fruits, which I believe only contain fructose (and not glucose) can have high glycemic index values, which I thought measured the rise in blood sugar? In this case, are we measuring fructose (as opposed to glucose or glycogen) in the blood stream before the liver can metabolize it?

    Thanks for any insight that you can provide.

    Mike

    (reply)
    • Mike A.  June 25, 2012

      Additional note which I meant to include from http://www.ajcn.org/content/86/4/895.full … “Glucose stimulates insulin release from the isolated pancreas, but fructose does not.”

    • Peter Attia  June 25, 2012

      Yes, Lustig is correct. While fructose elicits no DIRECT insulin response, it ironically contributes indirectly to insulin resistance. I believe I outlined the mechanism in one of the blog posts (sorry I don’t recall exactly which one).

    • Mike A.  June 25, 2012

      Thanks Dr. Attia. I will try to track that down.

    • Bob West  June 25, 2012

      Mike, just a note on the question of whether fruits only contain fructose, the Wikipedia article on fructose http://en.wikipedia.org/wiki/Fructose gives an enlightening table of frucose, glucose and sucrose content of some common fruits. It seems that most fruits have significant glucose, and some have significant sucrose (glucose/fructose combo) as well.

      For example, apples show 5.9 g/100g of fructose, 2.4 of glucose and 2.1 of sucrose; bananas have 4.9 fructose, 5.0 glucose and 2.4 sucrose.

      I know some Type 2 diabetics, who monitor their blood glucose and use insulin to control it, who have to inject additional insulin to allow for orange juice or fruit when they have it.

      Changes the whole idea of fructose being the only fruit sugar….

    • Mike A.  June 25, 2012

      Bob- Thank you for pointing that out to me. Much appreciated.

  25. Josh O  July 16, 2012

    Thanks for the great blog.
    As it is likely to be used only in low volumes and with other foods, I’m not sure how important it is, but I am curious…
    What’s your take on the use of balsamic vinegar? Besides increasing satiety, it’s supposed to reduce the insulin response when added to a meal. Of course, in addition to having some sugars, it is fermented ethanol, which, as you and Lustig point out, is fermented fructose, which does its damage without as significant an insulin spike as glucose.
    So, would you say balsamic vinegar is good for you? Or just “less bad” (perhaps) than, say, ethanol, fructose, etc.?
    Thanks.

    (reply)
    • Peter Attia  July 17, 2012

      Fortunately (for most of us), balsamic vinegar is something we consume in minor amounts. I think a few spoons of it is fine, but I’d hold off on drinking the stuff by the cup.

  26. David Nelsen  August 6, 2012

    Peter, did you attend this conference in San DIego?
    http://evolvinghealthscience.blogspot.com/2012/04/sugar-showdown-science-responds-to.html?spref=tw

    Seems like sugar is ok after all!! Great news for all the diabetics and pre-diabetics out there. It would appear they were trying to rough up Dr. Lustig a bit based on that article.

    Cheers,
    Dave

    (reply)
  27. David Nelsen  August 6, 2012

    Reminds me of those Tobacco industry researchers who never could quite find the link between smoking and lung cancer – the jury was always out. Granted the signal to noise ratio on smoking is much larger than on metabolic affects of sugar, but they seem to be voting along the lines of who is signing their paychecks. The congnitive dissonance has to be overwhelming…….

    (reply)
  28. Evan  August 14, 2012

    There is an Australian study (The Australian Paradox
    Professor Jennie Brand-Miller and Dr Alan Barclay, they even have a website hitting back at critics, theaustralianparadox dot com dot au) claiming that consumption of nutritive sweeteners in Australia has declined over the same period in which we have seen an increase in obesity. I have not read it in full but the impression I am getting is they are saying that sugar is no worse than other carbs.
    Could you comment on this article?

    (reply)
    • Peter Attia  August 14, 2012

      Evan, observational studies do *nothing* to establish causality.

  29. Mario  September 13, 2012

    I’ve found raypeat’s articles on sugar to be very helpful in explaining some of the confusion surrounding the “sugar is bad for you” camps. His argument is that sugar is being blamed for the damage being caused by all the polyunsaturated fats in our diet, context is everything! It seems to also explain why the people I see do better with control of their blood sugar when they remove PUFA’s from their diet including the supposedly beneficial omega 3 fish oils. I’m glad I can finally enjoy my coffee with sugar again.

    (reply)
  30. Joseph  January 26, 2013

    How do vegans and fruitarians stay lean if they’re constantly maxing out they hepatic glycogen stores? Is it, perhaps, a matter of calorie balance–that even though the excess fructose doesn’t get stored in the liver as glycogen, and is effectively converted to fat and VLDL through DNL, the excess fat is oxidized due to insufficient calories? Tangentially, are there cases that fructose is converted to glycogen in skeletal muscle?For some reason, I was under the impression that DNL occurs only when fat intake is under around 10%, and that excess carbs lead to fat gain indirectly, by inhibiting the oxidation of fat, but clearly you make the case that excess fructose (as well as glucose) is directly converted to fat. In that case, my prior belief that excess carbs are oxidized (thereby inhibiting fat oxidation) would be null:(

    (reply)
    • Peter Attia  January 27, 2013

      First off, not all vegans and fruitarians are lean, just as not all fill-in-the-blank-other-way-of-eating population is lean. As I just commented to another reader, my wife could eat Oreo’s, M&M’s, and ice cream all day, and not gain one ounce. The only thing that tells me is that she is very insulin sensitive, probably has little LPL on her adipose tissue, lots of HSL and LPL on her myocytes, perhaps something going on in her hypothalamus, etc.

      DNL is a pretty complex topic, and I was actually thinking about putting a post together on the broader topic of fat flux to address part of this. There is no “rule” for DNL, and it varies greatly by hormonal regulation and certainly genetic variation.

  31. Berkhead Sheerin  March 8, 2013

    Hi, I’m just starting the low-carb lifestyle, and have already lost 12 pounds. I’m 46, stay home mom of three children, 5’7, started at 194 and am down to 182 after about three weeks. My question is, I’m confused about the discussions I’ve read about too much protein and not enough fat. How much protein should I limit myself to, and how much fat. I read the thread with an example of your daily intake, but your exercise routine is much different from mine as I walk on my treadmill for 90 minutes a day. Any suggestion would be greatly appreciated :)

    (reply)
    • Nicky Hansard  May 10, 2013

      Personally I think you wouldn’t want to go over 100g of protein a day and basically eat enough fat so you’re not hungry. Also personally I would shorten the amount of time you’re on the treadmill to under an hour but up the intensity, also I strongly suggest weight training a few days a week – the big three, squat, dead lift and bench press. If you consume to much protein it has a similar result in regard to ketosis as eating to many carbs (just to a lesser degree I believe). Personally I can eat an obscene amount of fat and lose weight, as long as I keep protein low on a ketogenic diet (I was eating roughly 2kg of bacon a day, for a period there and losing weight like crazy). Anyway just my thoughts but Peter might have different recommendations to me.

    • Pam  December 30, 2013

      Grab a copy of The Art & Science of Low Carbohydrate Living. It’s a good read and has a formula for figuring out target protein intake.

      http://www.amazon.com/Art-Science-Low-Carbohydrate-Living-ebook/dp/B005CVV2AE/ref=sr_1_1?ie=UTF8&qid=1388376051&sr=8-1&keywords=art+and+science+of+low+carbohydrate+living

  32. Andrew  July 6, 2013

    Peter, Do artificial sweeteners induce insulin release similarly to fructose/glucose?
    If so, does this imply that one must avoid all sweeteners?
    Thanks.

    (reply)
  33. Michael Hirasuna  July 11, 2013

    Dr. Lustig said that excessive fructose causes fatty liver which is correlated to insulin resistance, but he does not explain how fat makes skeletal muscles insulin resistant. Actually, the creation of fat from fructose is better than the alternative, fructose in the blood. More harm would come from fructose that did not get converted to fat and escaped into the blood. Here is a study which shows that fructose blood levels in diabetics are elevated.

    http://care.diabetesjournals.org/content/25/2/353.full

    It seems that fructose in the blood can do much damage to all protein, but the cell’s glucose transport protein may be particularly vulnerable. When these transport proteins are open in the presence of insulin, fructose can enter because they are similar to glucose, but get stuck because they are still different from glucose. Glycation can permanently damage the glucose transport protein and cause insulin resistance.

    The liver fat may still be dangerous, but insulin resistance in skeletal muscles is more easily explained by a direct reaction to fructose.

    (reply)
  34. Alec  September 7, 2013

    If it’s still any help to anyone, here’s Sean Croxton’s ten minute version of Lustig’s :https://www.youtube.com/watch?v=tdMjKEncojQ&feature=youtube_gdata_player

    (reply)
  35. Brent Rice  October 14, 2013

    Peter, I discovered your blog a little over a week ago and have been pouring over it ever since. It is fascinating and I’d like to say thank you for dedicating the time and resources you do.

    I have had small runs at “low-carb” in the past but never stuck with it. For the past week, I have been strictly following a diet high in fat quite similar to what you consume. My caloric intake is between 1,700 – 2,000 but not because of any control I have imposed. This is simply about how much I’m eating based on hunger levels.

    I was recently diagnosed with gout after three of the most painful days of my life. I drank a lot and ate many of what have been referred to as trigger foods, however I think it is safe to say the beer and alcohol in general as well as my obesity (6’2″ and 220lbs) played part in this. Much of what I have read (on other sites and forms) have indicated that a diet such as this could trigger gout. I have yet to feel a twinge. I currently take allopurionol and colchicine. What are your thoughts and/or experiences with the effect of this type of eating on gout symptoms? My thoughts are that people that continued to have problems were probably over-consuming protein but I’m curious on your take.

    Thank you,

    Brent

    (reply)
    • Peter Attia  October 14, 2013

      Over-consumption of protein can probably exacerbate gout due to purine breakdown. I believe alcohol and excess fructose play a greater role in most case, though.

  36. jim kennedy  December 28, 2013

    Peter,
    Thank you. This information is gold. Thank you. I am a type 2 and I eventually wound up at 360 lbs and 26 units of Lantis, Actos, Metformin, thyroid, lipotor meds. and still had terrible blood sugar control. I had tried exercise sometimes 2 one hour bouts a day. (aerobic) I would lose a little and then gain it back. So your information is invaluable. I had tried to follow Primary care physician’s advice (eat less exercise more) and it did not help. Now I understand why.

    At my peak I met a trainer. I took a chance and worked with them. (I had been contemplating lap band surgery). I figured if I could lose the weight without the surgery that would be the way to go. The trainer worked with me 3 sessions a week and made food recommendations. It took 2 years but I slowly peeled off 100 lbs. When I started I could not run 100 meters.

    As of now I am off all diabetic meds except metformin. (and thyroid) I run relay races (eg Ragnar) in both 12 people and 6 people teams. (double mileage, so 3 half marathons in 27 hours.) Training for my first 50K and 50 mile trail races. This information will be invaluable.(a trainer at Animal Athletics recommended your site)

    Again thank you. I hope more people benefit from your information.

    Jim Kennedy

    (reply)
    • Peter Attia  December 29, 2013

      Jim, this is a great and very inspiring story. I’m really glad you’ve shared it. I think more people will be benefit from the hope your experience gives them than from anything I write!

  37. Valerie  January 12, 2014

    Wow, I just found your site and all I can say is you’ve really put in some long hours into your posts. Thank you for that, it is greatly appreciated.

    Today is my first day on a ketosis diet, so I’m just in the learning process. My question is about honey – it’s supposed to be a great anti-fungal/bacterial and many indiginous people (I hear) ate honey at least occassionally. Is it beneficial for a ketotic diet? If so, how much? Will a teaspoon throw me out of ketosis? Any thoughts on molasses?

    Thank you for any ideas you can pass along on this.

    (reply)
    • Boundless  January 12, 2014

      > My question is about honey –

      I’m not Dr. Attia, but I have an opinion on this. See: “Honey” at:
      http://wheatfreeforum.com/index.php/topic,895.0.html

      > Is it beneficial for a ketotic diet?

      I would bet on “no”.

      > Will a teaspoon throw me out of ketosis?

      I would bet on “yes”, as would a tsp of HFCS, which is what that “honey” may well be.

  38. Ken  January 16, 2014

    Peter,
    i have been following your “what i do eat from 2011″ and cutting out all sugar, grains etc for like 4 months.
    got blood work recently and all of my metabolic panel was in the normal range except the ALT which was 65
    what is a good way of lowering my ATL? your thoughts?

    here is my testing for my metabolic panel and choleterol.
    Glucose 60 – 99 mg/dL 83
    Creatinine. 0.7 – 1.3 mg/dL 0.9
    BUN 7 – 25 mg/dL 17
    Total Bilirubin 0.3 – 1.2 mg/dL 0.7
    Total Protein 6.0 – 8.3 g/dL 7.9
    AST 14 – 50 U/L 35
    ALT 10 – 35 U/L 65
    Albumin 3.4 – 5.0 g/dl 4.9
    Alkaline Phosphatase 35 – 104 U/L 60
    Calcium 8.6 – 10.3 mg/dL 10.0
    Sodium 135 – 145 mEq/L 137
    Potassium 3.6 – 5.0 mEq/L 4.5
    Chloride 98 – 107 mEQ/L 101
    Carbon Dioxide 21 – 31 mEQ/L 27
    Glom Filt Rate, Est >59.5 mL/min/1.72 m^2 88.2

    cholesteral
    Cholesterol, Total 125 – 200 mg/dL 203
    Pediatric ranges
    Desirable = 200mg/dl
    TRIGLYCERIDE 30 – 150 mg/dL 138
    Desirable <150 mg/dLadult or = 130 child
    Very high >499 mg/dL no child range
    HDL 40 – 75 mg/dL 38
    LDL Calculated = 130 mg/dL
    Non HDL Chol. (LDL+VLDL) 165

    (reply)
  39. Thomas  January 31, 2014

    Hello Peter,

    I have been enjoying your blog for the past few days now, I probably spend more time in the comments sections and am very impressed to see how often you respond. On the sugar topic I am wondering what you think about drinks like Kombucha, Jun, or Kefir? On a similar note how about cultured foods like kimchi, miso, natto and so on? Also Im looking to gain weight more then loose it, do you think this is achievable staying within nutritional ketosis? Thank you for all the information and have a nice day.

    (reply)
  40. david  March 24, 2014

    Peter,

    I have read pretty much every word Gary has ever written and much of your web site. I’m a big fan of the overall endeavor. I fear that you and Gary are both biased by your own experience. It’s likely that somehow you’re both prone to metabolic syndrome, and for you, cutting out sugar makes sense. And that may be true for many people. However, there is another group, as you have alluded to, that can eat sugar without restriction and generally not gain weight. I’m 54. I’ve been vegan for 30 years. For 30 years, I’ve eaten a low-protein, high-carb diet that includes plenty of sugar, and I eat more than most people my age. Yet I still weigh 155 pounds – the same I did in college. In my entire life, I’ve been as high as 160 pounds. And I exercise a lot less than I did 10 years ago.

    I feel there is probably a spectrum of insulin resistance, from extremely resistant (prone to diabetes) to extremely unresistant (prone to hypoglycemia), and that your research, if done properly, could uncover it. Might even be able to tell parents at birth where their kids are on it. We still need to know why so many more people are insulin resistant now than there were 30 years ago, but there are many many factors that could explain it, not just the rise of sugar. Much of your explanation doesn’t apply to me (and probably your wife). We need to be part of the picture. Please keep your eyes, ears, and minds open until you can really find the signal, because if you’re looking for a particular culprit, you’re bound to find it. Think about hypoglycemia as much as you think about metabolic syndrome and we may find some interesting answers.

    Sincerely,

    David

    (reply)
    • Peter Attia  March 25, 2014

      David, I appreciate the thoughtfulness with which you approach this. I agree that folks like my wife, and likely you, are largely “immune” to the deleterious effects of sugars and other dietary triggers of insulin resistance and metabolic dysregulation, which often leads to obesity and its related diseases.
      Perhaps an analogy, though admittedly overly simplistic, is smoking. While it’s certainly true that smoking dramatically (by over a factor of 10) increases ones chances of lung cancer, only about 1 in 6 smokers actually dies of lung cancer. Furthermore, a non-zero fraction of lifetime smokers seem to live essentially a normal lifespan free of disease. Now, it might be tempting to look at someone in that category and dismiss smoking as the most culpable environmental trigger of lung cancer. But we know this is a classic case of “survivor bias.” The fact that not everyone who smokes a pack a day for 50 years dies of lung cancer or heart disease or other lung disease doesn’t mean anything other than they have some immunity to the trigger.
      So pending new evidence, which I am very open to, it seems the most important studies to do are those can identify the dietary triggers of insulin resistance, obesity, and its related diseases, as experienced by the majority of folks.

    • Vicente  March 25, 2014

      Hi David,
      how do you know low-carb is not good for you? Weight is only one aspect of this way of eating. It can also improve your health and even your athletic performance. This has been my case (NAFLD disappeared, GERD medication no longer needed and cholesterol numbers better than ever). My iron levels are still a little bit elevated to be honest, but no more than before. And I can’t believe how my athletic performance has improved. So, do you really think the benefits of low-carbing don’t apply to you? May be you should open your mind just a little to give it a try. Check your health before and after a few weeks of low-carbing and see for yourself if sugar/carbs is doing you any good. I don’t think so.

  41. Cate  May 8, 2014

    Is there anyway to make a printer friendly version & button? This ends up being 30 pages with all of the side text and images :)
    thanks (student)

    (reply)
    • Peter Attia  May 8, 2014

      Copy and paste into Word and format to print as you see fit.

  42. Woody Payne  July 11, 2014

    Hey, Peter. I was doing some digging lately, and I discovered an article stating that when ketosis leads to increased production of acetone, some of this acetone is converted into methylglyoxal by the CYP2E1 enzyme. I’ve read scattered reports that methylglyoxal is only increased about 1.5 times by ketosis. I have also read it is upwards 40,000 times more potent an than sugar in produce AGE’s. I’m still intending to experiment with ketosis, but what are your thoughts on this matter?

    (reply)

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