NB: EatingAcademy is undergoing a major rebrand and redesign to bring you more high-quality longevity, self-optimization, and health-related content than ever before. Subscribe and tune in to peterattiamd.com on January 8th to learn more.

The personal blog of Peter Attia, M.D.

The great medical disconnect

The great medical disconnect

There is probably no greater disconnect in medicine than the root cause of obesity.  Even if you think you already know the answer to this “obvious” question, it’s still worth reading on.  The reason this question matters, of course, is clear to everyone.  Obesity (and more broadly the syndrome we define as metabolic syndrome) predisposes us to virtually every disease afflicting us in the modern age.  Above is a simple graphic from the journal Nature showing the linkage between obesity and all of its sequela.

When you are obese, your risk of disease goes up.  This is not disputed. Here is where the controversy starts…what actually makes us obese?

Obesity is a disorder of fat accumulation – fat cells accumulate too much fat, relative to how much fat the body breaks down.  Conventional wisdom, however, says obesity is a disorder of eating too much and/or exercising too little. These are not the same thing.

Let’s turn to a well-respected source of medical information, Lehninger’s Principles of Biochemistry (the so-called “bible” of biochemistry).

Go to the index and query, what makes fat cells fat? (the technical way of asking this question is, what causes adipose cells to accumulate triglycerides) and you’ll get the following response:

“High blood glucose elicits the release of insulin, which speeds the uptake of glucose by tissues and favors the storage of fuels as glycogen and triacyglycerols, while inhibiting fatty acid mobilization in adipose tissue.”

Let me translate this: Eating glucose (carbohydrates) increases insulin levels in our body.  Insulin drives glucose into liver and muscle cells as glycogen (in small, finite amounts) and into fat cells as triglycerides (in unlimited amounts). Insulin also inhibits the breakdown and utilization of fat.  Parenthetically, this means no one disputes this graph.

Next, query the exact same text book, what makes people fat (the technical way of asking this question is, what causes human obesity) and you’ll get the following response:

“To a first approximation, obesity is the result of taking in more calories in the diet than are expended by the body’s energy-consuming activities.”

Pretty straight forward, right?  People get fat because they eat too much relative to how much they exercise.

But how can both of these statements be correct?  Fat cells get fatter because of insulin’s influence on them, but people get fat because of overeating?  One of these statements is correct and the other is not.  I hope to help you understand why the first one is correct and the second one is not.

Let’s look at another example of this tragic medical disconnect.  I say “tragic” because the failure of most physicians (including me up until recently) to understand this is a large part of why the problem persists.  When people grow vertically (i.e., when people get taller) no one disputes that a hormone drives this action.  The hormone primarily responsible for this, of course, is growth hormone.  Sometimes, in rare cases, people develop a tumor in their pituitary gland (from where growth hormone is secreted) and they end up secreting too much of this hormone.  The result is that they grow vertically in an unregulated manner.  That is, they get too tall.  Again, no one in medicine disputes this.

Why is horizontal growth (i.e., obesity) different?  I, and many others, argue that unregulated horizontal growth is also regulated by a hormone – insulin.  In both cases – growing vertically or growing horizontally – the responsible hormone drives (literally induces) the person to eat more than they burn.  The fellow on the left in the figure below (nearly 9 feet tall) ate a lot to get that tall, but he did not get that tall because of eating too much.  He got that tall because he had too much of a certain hormone that drove him to over-eat relative to what he was able to burn.  The medical establishment tells us the girl on the right got to be that size because she ate too much.   Wrong.  She ate too much (relative to her energy expenditure) because she had too much of a different hormone – insulin – driving her to eat too much.


This subtle difference in actual causality, and the resulting misunderstanding that has led to current health and nutrition policies, is the root cause of the health problems afflicting us today.


About the Author:

Peter Attia, M.D., is a physician in private practice in NYC and CA. His practice focuses on longevity and healthspan. His clinical interests are nutrition, lipidology, endocrinology, and a few other cool things.


  1. Amir Drory  December 28, 2011

    Hi Peter,

    A short question: is it important to switch from regular diet to low sugar / high lipid diet in a gradual manner? Will it be possible for the body to change its metabolism to ketosis if the switch is a sudden one, not a gradual one?

    Happy Holidays, Amir

    • Peter Attia  December 28, 2011

      If you took the most radical shift possible – complete removal of carbohydrates (or even complete starvation) – your body would generate sufficient ketones to satisfy your brain within about 48 hours (by which point you will have little glycogen left in your body). Without this ability to produce ketones in the absence of any glucose you would actually die of hypoglycemia within a few days of starvation. I think the real question you’re asking, however, is what is the best way to transition from a state of high-carb eating to one of low-carb (or even ketotic) eating? There is no right answer. Metabolically, it only takes a short while to switch over, but the full period of adaptation can take anywhere from a week to several weeks. Furthermore, for some people (like me) it was easier – at least psychologically – to do it in stages. I’ll be writing about this in much more detail later on.

    • Dan Simonelli  December 29, 2011

      “If people let the government decide what foods they eat and what medicines they take, their bodies will soon be in as a sorry state as the souls who live under tyranny.”
      -Thomas Jefferson

  2. Jack  December 30, 2011


    I think you should read a lot more studies on the actual distribution of nutrients rather than fixating on all of the known physiological effects of insulin. In particular, you should read the metabolic tracer studies of Dr. Hellerstein at Berkeley. While it is true that insulin is an anabolic hormone, the most negative effect of a high carbohydrate diet is that it strongly promotes the oxidation of carbohydrates. You see, the body actually cares about and monitors carbohydrates, while being oblivious to fat intake and storage. On a diet high in carbohydrates, ingested fat will be sent directly to adipose tissue while almost all the carbohydrate will be oxidized. It may not be a large issue in practical terms (you will still be adding fat) it will not be due to insulin directing glucose into the fat cells to be converted to fat. In fact, that would be the best possible outcome, since the process is inefficient enough that you would only gain around 65% of the weight you would gain by directly storing fat. You see, very little conversion from carbohydrates to fat happens in humans. It has been calculated (see Hellerstein) that less than 10% of the fat in your body was synthesized by lipogenesis rather than ingested as fat. For folks on a standard diet, a full 50% of their ingested fat will go directly into a fat cell rather than be oxidized. For folks on a high carbohydrate diet, they will have to consume more calories than they can burn or store as glycogen to even begin to show appreciable conversion of carbohydrate into fat. So, can insulin stimulate this process? Yes, but it is a minor metabolic pathway in humans, and most glucose will be disposed into muscle and liver.

    • Peter Attia  January 8, 2012

      Jack, thanks for your question. Please email the study you’re referring to and I’ll be happy to take a look when I get a moment. I am familiar with some of the work of Hellerstein, and contrary to your comment, I do actually read a lot – as much as I can (but I do wish I could read more)! In fact, I do have a paper by Hellerstein and Schwartz that looks at what you’re describing. The thing you need to keep in mind – and I’m sure you already know this, but some folks do get confused – is that many of these studies actually under-feed glucose, relative to what “real” people eat. In other words, if I took a group of subjects and removed all (and I mean *all*) fructose from their diet (e.g., no fruit, no sucrose, no HFCS), and fed them small amounts of glucose, you’re right, I could prevent a great deal of de novo lipogensis. But, and this is a very big BUT, I would need to ensure that I was only feeding them a small amount of glucose, probably less than 60 gm/hour. This way, I could force a metabolic prioritization from direct glycolysis (first) to glycogen formation (second). But keep in mind what happens when these two sources are “full” – you will make fat out of glucose. Even the most highly trained and muscular athlete can store roughly 400 kcal of glycogen in their liver and 1200 kcal in their skeletal muscle. And that’s assuming both “tanks” are completely empty – a nearly impossible physiologic condition. Unfortunately, most people consume so much glucose (and fructose), that the tight experimental conditions of Hellerstein do not apply.

      As we’ve learned from Rob Lustig (and I’m actually going to post on this very topic this week), gram for gram, fructose is converted to fat more readily than glucose, but this does not mean glucose is not converted to fat (i.e., when glycogen stores are full and you are not immediately oxidizing it). Finally, and perhaps most importantly, keep in mind that there is another “sinister” effect of glucose (that is not true of fructose, by the way): glucose raises insulin levels. When insulin levels are high, we stop beta-oxidation of fat. So even in the “best” case (i.e., a case when we are not making new fat as we eat glucose) we’re not burning fat when we eat glucose. This is profoundly important and should not be overlooked.

    • Shiv Kumar  February 1, 2012


      At the end of your reply to Jack you say, “Finally, and perhaps most importantly, keep in mind that there is another “sinister” effect of glucose (that is not true of fructose, by the way): glucose raises insulin levels.”

      From my research and understanding (I believe from Dr. Richard Johnson and/or Dr. Robert Lustig), Fructose does not spike blood glucose, but *does* raise insulin levels. Glucose raises blood glucose levels and thus causes insulin to be secreted. I believe Dr. Robert Lustig, says that Fructose keeps insulin levels elevated thus causing more fat storage.

      Dr. Richard Johnson finds that Fructose, by raising uric acid and inhibiting nitric oxide, completely blocks the effect of glucose to stimulate the secretion of insulin to increase the uptake of glucose in cells, thus causing insulin resistance.

      I should add that there is a lot more in all of the biochemistry involved that I truly grasp 🙂 and so I may have misunderstood some of this stuff.

    • Peter Attia  February 1, 2012

      That’s correct. Fructose does not actually raise insulin levels. The beta-cell of the pancreas does not “recognize” it, and it is transported into the liver via the GLUT 2 transporter (rather than the insulin-activated GLUT 4 transporter that puts glucose into cells). I think what you may be thinking about is that fructose DOES indirectly contribute to insulin resistance, but at the moment you are ingesting it, it’s not raising insulin levels, per se.

  3. Sam  February 21, 2012

    Petter thanks for your great blog. I have been very low carbing for a few years and had achieved normal weight and good health but since reading your blog I reduced the proteins and increased the fat. Wow I now feel fabulous it have given me so much more energy, have more endurance, less hunger, clearer mind. I could not believe I could be improving so much more doing a ketonic diet.

    I wanted to ask you about lipids since I have no way of doing a NMR or VAP. There is some discussion now (Jimmy Moore)that the best indicator for CAD is TC/HDL but I had read that the most accurate predictors is TG/HDL even equal to LDL-P like it said here what do you think? What is your opinion on what best if no NMR or VAP is available?


    Dr Karim El Harchaoui (Academic Medical Center, Amsterdam, the Netherlands) and colleagues report their findings online January 22, 2007 in the Journal of the American College of Cardiology.
    Coauthor Dr Matthijs Boekholdt (Academic Medical Center) told heartwire that, in patients with only moderately elevated LDL-C, clinicians would do better to pay attention to HDL levels and triglycerides as markers for future CAD risk rather than worrying about testing LDL-P.

    “Although it’s good to be aware of LDL-P, it’s expensive to test. We show that HDL-C and triglycerides provide similar predictive information. Most doctors do not look at HDL-C or triglycerides because, unlike LDL-C, treatment for these parameters is not mainstream clinical practice. It would be more useful to be aware of these results, particularly in those with the metabolic syndrome, abdominal obesity, or diabetes,” he said.

    • Peter Attia  February 21, 2012

      Sam, it’s certainly a good place to start by looking at TG to HDL-C ratio, and that it probably more helpful than LDL-C, but at least 30-40% of people with low or normal LDL-C have elevated LDL-P. So the questions is how predictive is TG/HDL-C of LDL-P? To be clear, the damage is CAUSED by LDL-P, so by *definition* nothing is more accurate for predicting artherosclerosis than LDL-P. It’s like saying hair color is a good predictor of eye color. Sure it can help…but it’s no where near as good as eye color is for predicting eye color! There is great resistance in the medical community to move away from LDL-C and HDL-C, just like there’s great resistance to move away from the idea that fat is harmful, despite much evidence. If you’re at even modest risk, and/or your TG/HDL-C is above 2.0, I’d strongly recommend you pay for the NMR, even out of your own pocket.

    • Sam  February 21, 2012

      Thanks Peter. My TG/HDL thankfully is below 1. My total TC is below 200 so I don’t have a doctor bothering me about fat in my diet. But I have always advice friend and family that TG/HDL was a better predictor than TC/HDL because that what I had read. So just wanted to be sure that I was giving the correct advice since they all only had the standard lipid panel that the doctor orders.

    • Peter Attia  February 21, 2012

      Sam, make sure your units for both TG and HDL are mg/dl. If in mmol/L you must convert.

  4. Deirdre  May 15, 2012

    Hi Peter,

    Thank you for sharing your perspective. You started this blog with 2 explanations for “what makes fat cells fat” – and then followed up by stating, “One of these statements is true, the other is not”. I respectfully disagree that the second statement was false, and I will explain why.

    I think the biggest mistake that many make when studying the etiology of obesity, which is a multi-faceted and multi-dynamic phenomenon, is to simplify it. While I agree with your explanation on insulin’s anabolic effects, the story doesn’t start and end with Insulin. There are other huge “players” involved as well, such as leptin, ghrelin, melanocortins, neuropeptide Y, dopamine, opioids, & amylin – and I’m sure many more that I’m forgetting. And what about the role that the lateral hypothalamus in our brain plays with regards to motivation, drive and reward?

    We can’t pluck one hormone as the culprit because really, insulin is just part of the end game. When we look at the whole picture, or the whole “system” if you will, it is a brilliant concert of cascading hormones, neurotransmitters and psychoactive chemicals which respond in unison to a primal and evolutionary drive – and that is to store energy [survival].

    When we look at the changes in our current food environment, and compare it to the natural food environment for which this brilliant system was designed to survive in, it’s obvious we don’t stand a chance. Our hedonic drive to over consume is purposeful and unchanged, and far more powerful than our homeostatic cues. For our children, obesity is the default, and without early intervention, education and big changes in policies, future generations will follow along the same collision course. The bottom line is, we have to change the food environment, our attitudes and our beliefs about food before we can save them.

    • Peter Attia  May 16, 2012

      I see your point, and I agree, but with one distinction. The second statement, “To a first approximation, obesity is the *result* of taking in more calories in the diet than are expended by the body’s energy-consuming activities,” implies that over-eating is the cause of obesity. I agree – while obesity always implies over-eating took place – the cause and effect are backwards. The hormonal drive to obesity is what creates an energy imbalance through a combination (it varies in everyone) of over-eating and under-expending. Insulin is the major hormone driving this process, though it does not act alone.

  5. Scott B  May 16, 2012

    Deirdre – for me, it’s a bigger mistake to over-complicate obesity than simplify it. If I simplify it, I know what to do – quit eating carbs (and get my kids to as well). If I complicate it, and start hand-wringing over the food environment and the hedonic drive, I lose my way and start to think “I don’t stand a chance”. Nonsense. I read this brilliant blog from the perspective of an individual and a father. The bottom line is – save yourself first, save your kids next, save the world next. This is how we make progress . . .

  6. Charlotte  September 6, 2012

    Hi Peter
    Great blog.
    I still am confused because I believe in the concept of low carb for insulin resistance and fat and ketosis but research seems to show a clear link between high protein diets and inflammation in the body that leads to disease. Is it that Ketosis gets rid of this link whereas low fat protein diets like Dukan don’t?

    • Peter Attia  September 7, 2012

      Actually, ketosis is (contrary to popular misconception) a normal protein diet. In fact, high protein intake outright prevents ketosis.

  7. Charlotte  September 7, 2012

    So therefore adding the fat keeps the protein lower and keeps inflammation lower in the body?

    • Peter Attia  September 8, 2012

      If you believe protein is inflammatory.

  8. larry  December 7, 2012

    Peter,here they go again. I just finished reading today Dec 6,2012 about a new “study” reported on MSNBC ( which reportedly will influence World Health Organization guidelines) touting low fat for weight loss. I don’t know if this thread on your blog is still active, but if it is, I’d appreciate it if you could comment on this study which is getting a lot of press notwithstanding that the conclusions seem suspect.
    I’m a certified fitness nutrition trainer and I’m sure I’ll be getting questions.

    • Peter Attia  December 7, 2012

      Too much to comment on right now. May pen a letter to BMJ editorial board to point out the (obvious) flaws with this study.

  9. Sherwood  February 18, 2013

    I don’t see why you see a conflict between the two statements:

    “High blood glucose elicits the release of insulin, which speeds the uptake of glucose by tissues and favors the storage of fuels as glycogen and triacyglycerols, while inhibiting fatty acid mobilization in adipose tissue.”

    “To a first approximation, obesity is the result of taking in more calories in the diet than are expended by the body’s energy-consuming activities.”

    The second statement is a verbal statement of the conservation of mass/energy. Store = Input – Output
    The first statement is a statement about the mechanics of the storage operation. They are both true.

    The mechanism is in place for good reason: For most of our history grocery stores weren’t a 5 minute drive away, and carrying fuel is a well distributed layer over our body was an easy form of transport.

    Now we don’t have a nice yearly hungry moon or two or three, and our plenty is doing us in.

    Question: Is the insulin receptor on a fat cell any different than the ones on a muscle cell? What would happen if you were able to either block or eliminate the insulin receptor on fat cells. At first blush it would make it far more difficult to make fat. That would be good. But the reverse side of that would be far more drastic spiking of blood sugar levels wouldn’t it? Would people adapt their eating habits to compensate?

    Blog entry on how cells regulate the number of receptors?

    Blog: What drives hunger?

    • Peter Attia  February 19, 2013

      The first describes a cause. The second is the (necessary) result. The second statement is meaningless in that it only states the obvious (except that attempts to assign cause). I would say the correct statement is: “When obesity results, more calories have been taken in the diet than are expended by the body’s energy-consuming activities.”

      The question is why did this happen? And why does it happen more today than 40 years ago?

    • gary luzio  May 12, 2014

      “To a first approximation, obesity is the result of taking in more calories in the diet than are expended by the body’s energy-consuming activities.” So the only way to monitor this is to do a daily calorie count, and obesity is totally caused by eating too many calories and has nothing to do with hormones and food composition. This is a totally short sighted and obviously invalid because it assumes that

      1. A gram of protein, fat or carbohydrate are burned in a bomb calorimeter identically to how humans burn these substances. Each biochemical pathway is different, with different enzyme efficiencies etc. The differences between how cells metabolize each substance differently would take an entire book to discuss. Thus a calorimeter is an inaccurate measure of how humans “burn” food. There a major differences within even inside one food group, such as comparing cellulose to starch, or glucose to fructose metabolism. The variations make the assumption as direct comparison of humans to calorimeters invalid.

      2. Second the assumption does not take into account, gut absorption efficiency of various foods.

      3. Third the assumption does not take into account how composition of food effects hormones which have feedback mechanisms to alter how fats, carbs or proteins are metabolized by individual cells and their relative efficiencies. Does a muscle have an identical metabolic efficiency to a brain cells in absorption and metabolism of glucose based on hormonal feedback signals and pathways. Maybe it does, but the law, as stated, indicates that it must be and this may not be true.

      There are more assumptions that invalidate this argument but I want to wrap this up. I wished people stopped looking at a calorie is a calorie and started looking at actual data of how people, on low carb diets, actually loose weight and keep it off. I argue, that a fat calorie is not identical to a carb calorie and food composition plays a larger role in weight control than most people want to admit. At the end of the day people are loathe to giving up their sugar and high refined carbohydrate diets. They would rather eat 100 grams of sugar each day than 100 grams of meat and assume that they are identical in how much fat they might gain.

      The first statement in this comment is only applicable if one can accurately measure, for each individual human being, how they actually convert various food substances to energy or to store it as fat, or muscle etc. and I submit that this is not feasible to do correctly. Values obtained from bomb calorimeter measurements are of little value in this regards. It is far better to look at how compositions affect weight gain or loss and there are numerous studies to suggest that high sugar and starch ingestion is not the way to proceed. At the end of the day eating100 grams of lean meat does not equal 100 grams of sucrose in weight control even though they both represent 400 calories.

  10. Maria  February 20, 2013

    Although I am not diabetic I have many hypoglycemia crisis, reason why I decided to become fat adapted. First attempt was tough, because I would pass out just from fat, if I didn’t ate carbs. Now I am fat adapting and day by day I’m feeling better. Experiencing with nutritional ketosis and I don’t need carbs at every hour and I can snack on nuts and fat without feeling hypoglycemia symptoms after. I’m just on the 2 week.. and I’m not fully fat adapted yet but getting there. This is totally giving my life back, the only problem is I’m experiencing a pain in the right side. On my liver. And I’m drinking 2l of water per day… But it still hurts. Does this suggest something? Should I stop or this eventually go away after becoming fat adapted?

    • Peter Attia  February 21, 2013

      Maria, I would not attempt to made a diagnosis this way. Best for you to connect with your doctor. I do agree, though, that paradoxically, the best way to overcome symptomatic hypoglycemia is actually to lower RQ (through diet), as you have.

  11. Guido Vogel  February 26, 2013

    Hi Peter,

    I wonder if there is a direct relationship (causation) between the high intake of carbohydrates and the diseases in the diagram. If I understand correctly, the logic is:you get fat because you eat too many carbohydrates. Because you are to fat you get ill.

    Does that mean that people with the “lucky genes” who don’t get fat also don’t get ill and can eat any amount of carbs? All things equal of course?

    If this is not true then lean people might get the diseases mentioned (e.g. via intakes of lots of sugar), but it is not noticable via their weight. I don’t what other symptoms are but they might be even at greater risk then.

    • Peter Attia  February 27, 2013

      Very good question. The short answer is no. Between 7 and 9% of lean to normal weight individuals have MetSyn. In fact, a lean person with type 2 diabetes may do worse than an overweight person with diabetes. Stay tuned for more on this. This topic will discussed in my upcoming TED talk in April.

  12. Vanessa  April 1, 2013

    Hi Peter,

    First, I really like the way you put the science back into this discussion and that is what actually prompted me to reach out to you. What does the science on nutritional ketosis and pregnancy say? Clearly our ancestors survived and thrived which would imply that babies were being born but I am having a hard time finding more than the “traditional” discussion about pregnancy and diet. Thank god women are not asked to lay about in our bedrooms for 9 months as they did in the Victorian age but as an active person, I don’t feel like this aspect of medicine has come very far. I love my steady energy levels, I like the way my body looks and more importantly, the way it functions. I don’t really believe that I can be this healthy and feel this alive and not be able to support a healthy pregnancy with an end result of a healthy baby. Do you have any thoughts on this subject or any sources that I could look at to continue my search?

    • Peter Attia  April 7, 2013

      Vanessa, I’ve commented on this a few times across the comment forum. Please take a look.

  13. Holly  April 25, 2013

    Hi Peter,
    I have been investigating “The fasting diet” advocated by Dr Michael Mosley- with claims to help reverse/reduce the effects of met syn, by eating normally for 5 days of the week and reducing calorie intake the other 2 (below 500 for women and 600 for men). I would be interested to know if you could achieve similar results by changing the fasting days to lipid only days. Or would the effect be lost due to ingestion of carbs on non fasting days?

  14. Emil  August 13, 2013


    There is a study which has shown that “administration of 3-hydroxy-butyrate increases tumor growth by ?2.5-fold.” Here is a link to it http://www.ncbi.nlm.nih.gov/pubmed/20818174.
    Unfortunately I do not have the proper education to really understand what they are talking about but it sounds like they have shown that B-OHB fuels cancer growth. I have previously thought that cancer cells are exclusively fueled by glucose and never ketones. On my low carb diet I have expected to be safe from developing cancer, but this piece of information suggests that all the ketones in my blood could potentially be feeding cancer cells. What are your thoughts?

    • Peter Attia  August 13, 2013

      Funny…sort of…I just responded to this exact question from another reader yesterday. Not such which post it was under, but should be easy to find since yesterday. Short answer: I choose to disregard this study outright for several reasons.

  15. Hazel  November 13, 2013

    “But how can both of these statements be correct? Fat cells get fatter because of insulin’s influence on them, but people get fat because of overeating?”

    The statement above exemplifies the insanity of the US “health care” system, which in reality is the US “conventional medicine and pharmaceutical industry care” system.

    If “they” don’t want to look at what’s right in front of their eyes, “they” won’t see the solution to the problem. “They” being doctors and big pharma, who don’t benefit when people are well.

  16. Bernice  November 28, 2013

    Hi Peter,

    I have been on a “balanced” Low GI diet for a while, where I am eating quite similarly to that of someone that has diabetes.

    This has been said to keep blood glucose and insulin levels constant, which should, in turn, promote insulin sensitivity.

    Anyway, my question is: I do eat a lot of fruit and vegetables. Specifically fruit as a snack, between breakfast /lunch or Lunch/Dinner… I have started combining it with a protein, whether yogurt or an egg or whatever to prevent that spike.

    Yet you mention that fruit (Which contains Fructose) contributes to insulin resistance?
    Can this be true, even when fructose is ingested from a natural source and combined with a form of protein?

    • Bernice  November 28, 2013

      I am very interested in this due to my current studies on PCOS and its relation to insulin.

    • Peter Attia  November 28, 2013

      Dose is the issue. See the post on sugar toxicity.

    • Boundless  November 29, 2013

      >> Can this be true, even when fructose is ingested
      >> from a natural source and combined with a form of protein?

      Have you actually measured blood sugar response to sugars combined with protein (or fats, as I often see people conjecture that such mixing slows down the uptake)? I don’t know the answer, but I suspect that there’s not much difference.

      > Dose is the issue.

      I’m going to argue that we need to distinguish between glucose and fructose. Glucose merely becomes blood sugar directly. Fructose has other considerations.

      I see people who, for example, religiously eschew HFCS (which is 55-60% free fructose) but use apple syrup (which is likely 65% free fructose). They are fooling themselves about fruit sugars, fructose specifically, and fruit consumption generally. An apple a day keeps no doctor away.

      An interesting work on this topic is “The Fat Switch”* by sugar researcher Richard J. Johnson. It lays out the issues with fructose metabolism. My take: modern humans are adapted to pack on the fat when fructose is available (historically, seasonal fruit), and then burn it off in unwanted unplanned ketosis in deep winter (or other challenging circumstances, such as any of several conjectured prehistoric population bottlenecks).

      Insulin resistance is not a disease process. It’s a “thrifty gene” adaptation that is now adverse due to the modern food chain and defective dietary dogma. As I’ve said elsewhere …

      For most modern humans:
      Metabolic Summer never ends.
      Metabolic Winter never comes.
      Metabolic Syndrome comes instead.
      * No, fructose isn’t the fat switch. Uric acid is, but fructose is the big chubby finger on that switch.

    • Bob West  November 30, 2013

      Boundless, I don’t know whether the narrative you propose about early adaptation to seasonal plenty and scarcity is right or not — it sounds good, but it’s hard to tell about the effects of any factors that long ago on our current genetics — but I do like it as a perspective on things.

      I am particularly struck by the “Metabolic Summer never ends/Metabolic Winter never comes” statement.

      In Alaska, in the winter (where I spent a little time a few years ago), you can get bananas or pineapple, or any other tropical fruit, any time you want. Or just about anything else that is eaten anywhere.


  17. Tim Claason  March 7, 2014

    I feel like I’m missing a piece here (sorry about the very late comment).

    I’m a layman, so please excuse my fumbling of terms…

    A person consumes carbohydrates, which triggers an insulin response, which limits the mobilization of fatty acids in adipose tissue. Simultaneously, glucose metabolism is prioritized over fat metabolism. Given the level of insulin in the body (along with excess glucose), lipogenesis occurs, and leads to fat accumulation.

    I’m trying to wrap my head around what happens in the event of very low carb intake, low protein intake, and very high fat intake.

    Is it true that fat consumption that exceeds the energy required by BMR will eventually get stored in adipose tissue?

  18. Luis  March 9, 2014

    Hi Pete,
    I have been on low carb diet for over 8 months, eating sat fats (bacon and eggs in the morning), good quality coconut oil, avocados, hardly no fruits and 0 sugar, you know the drill. I feel fabulous.
    I test my ketones level daily with urine strips and I am for the most part in the medium range. I am active physically (play tennis everyday). In other words, I really thought I was doing very well, cause I feel well.
    Here is my question to you . I got a blood test done the other day (fasting) and a few results caught me by surprise:
    My glucose level was measured at 111 (normal supposed to be under 100).
    LDL was 146 (although HDL was good at 79 and triglycerides very good at 63).
    I am thin, never been overweight. My blood pressure is low. I am puzzled by the high glucose being that I don’t touch an ounce of sugar of any kind and I watch very careful all the ingredients in everything I eat.

    Should I be concerned? thanks for your comments!

    • Naren  March 10, 2014

      Looking forward to Peter’s reply to this one. But it could be physiological insulin resistance (Look it up, you’ll find a detailed explanation). Happens to me quite frequently (I have a home blood glucose / ketone monitor) where my fasting blood glucose is higher than I would expect on a low-carb diet, but my post prandial taken the very same day (2 hrs after lunch) is lower than the fasting BG taken in the morning.

      My understanding is that the high fasting BG (on a keto diet) is nothing to worry about as long as your Post Prandial BG and HbA1c are normal.

    • Vicente  March 11, 2014

      “Almost” the same here: my fasting glucose is 98 and I didn’t like to see that number. Although I have been eating low-carb for 7 months, I started drinking kefir on a daily basis a few weeks before the blood test was done. Kefir has an insulinotropic effect that may have an impact on glucose management. Apart from that I eat lchf.

      I have read elsewhere about a physiological insulin resistance being different from the pathological insulin resistance, but I didn’t understand the difference neither the explanation for the elevated FG when eating low-carb. I guess checking the postprandial glucose levels with a glucometer is the best way of getting answers.

    • Vicente  March 21, 2014

      I found this link regarding fasting glucose levels and I think it can give some insight:
      “Impaired glucose tolerance in low-carbohydrate diet: maybe only a physiological state”

      “It should be common in clinical practice that patients submitted to oral glucose tolerance tests not be under severe carbohydrate restriction, since this could alter the response to the glucose overload. Thus, we suggest that the results from Bielohuby et al. (1) can be interpreted as a unique and not necessarily harmful metabolic condition, which is characteristic of this state, besides being transitory. As demonstrated by Kinzig et al. (4), the glucose intolerance and the peripheral insulin resistance are rapidly reversible with the reintroduction of carbohydrates in the diet.

      Additionally, the condition of induced insulin resistance is different from that induced by mitochondrial dysfunction, caused by oxidative stress generated by the glucose overload (3).”

  19. Norm  March 11, 2014

    HbA1c can also be off on a low carb diet apparently due to longer life span of red blood cells which means some folks can be discordant: low/normal blood glucose but higher HbA1c. Here is one example:


  20. Ron  March 12, 2014

    Yep, same here. I’ve been low carb for almost 2 years now, with an added protocol of IF most of the time. I was curious about the last few posts here so I checked my BG this AM and sure enough, it was 111. A few years ago (before my new lifestyle), I had my “labs” done and my fasting BG was 112 and the Doc warned me that I may be pre-diabetic! That was actually a rare occurrence prior to that (usually between 80-100), so it did cause a bit of anxiety at the time to say the least.

    I’m not too worried about it as all of my other health indicators have improved dramatically since starting IF/LC and I feel great as well. But it does baffle me why this occurs. The common denominator here seems to be lack of carbs. It would be nice to hear from a few more folks that practice similar lifestyles if this is just a common phenomenon (for now). Or, better yet, if someone knows why this happens.

    • Patti  March 12, 2014

      Yes this is happening to me as well. My blood sugar in the morning is higher than through out the day. Sometimes it is up over 105.

    • Naren  March 12, 2014

      Here is probably why,

      Short answer – While your brain can get ~75% of it’s energy need from ketones/fat, ~25% needs to come from glucose, whereas other organs/muscle tissue can survive on fat/ketones alone. So when you are ultra low-carbing, sometimes in a fasted state you might have such little glucose in your body that your muscle tissue and other organs shut their doors (for lack of a better description) on this scarce supply of glucose by turning on (physiological) insulin resistance so that the limited glucose available is now saved for the brain and not used by muscles/other organs. And when the muscles are not consuming this glucose, you would, as expected, see a higher blood glucose reading.

      I noticed this first when my fasting blood glucose would be in the 80s some days (normally it is in the 60s or 70s when I am on a keto diet. I am an otherwise insulin sensitive 32 year old doing a keto diet not because I need to but because I enjoy it and seems to work best for my body-composition goals). My post-prandial on those days would be in the 70s. This seems to be in line with physiological insulin resistance.

      All based on n=1 experience and my not-so-strong/technical translation of what I have read in various places, of course.

  21. Bill  June 22, 2014

    Dr Attia,

    I am wondering if you could comment in your blog on the recent claim coming out of UCSD, that insulin resistance & Type 2 diabetes are triggered by a lack of oxygen in adipose cells which in turn can be caused by high-fat diets. http://health.ucsd.edu/news/releases/Pages/2014-06-05-connection-between-oxygen-and-diabetes.aspx.

    I have diabetes (T2D), have never been overweight, but by following LCHF have seen my A1c improve accordingly. Maybe Experience should trump (scientific) Theory. Nevertheless to those of us following a LCHF diet to combat diabetes, this UCSD result is a bit confusing and troubling. This result goes a little beyond a hypothesis it seems and proposes and actual mechanism. Talk about “Discordance”!

    • Peter Attia  June 22, 2014

      Mouse study…studying diabetes in mice is less than helpful. Also, “high fat” diets in mice contain about 20-25% sugar.

  22. claus wall  July 12, 2014

    Hi Peter,

    glad you are spreading the word.
    But you must feel like a voice crying in the wilderness.

    I live in Toronto and studied at UofT.
    My wake-up call came with Taubes’ books. Then the inside information of Michael Moss’s book. What has not been widely studied is the role that bad nutrition plays in brain function. “Grain Brain” by David Perlmutter opened my eyes.
    Finally the incredible pressure of lobby groups and the food giants is criminal.
    When Philip Morris bought Kraft Foods in 1988 that should have rung alarm bells. They use the same playbook book for foods as they did for cigarettes.
    The top 5 food companies are Pepsi (revenue of $44.3 billon), Dole (6.8 billon in 2009), General Mills (14.7 billion last year), Nestlé ($110 billion) and Krafts foods (40.4 billion).

    You have no idea how intricate their nets are since all of these companies buy up well-known brands and then continue to use that label. Junk food provides them with huge incomes.

    Bottom line:
    There will be a wave of coronary disease, diabetes-II, Alzheimers, and various forms of cancer in10 or 15 years. None of the food giants will pay a penny for these health costs because “we did not force anyone to eat our foods”.

    Keep up the good work. I use the ketogenic approach of Mike Sheridan (not an M.D.) but like others, a well informed trainer: His book is: Live it, NOT diet.

    Best wishes with your efforts
    Claus Wall

    • Peter Attia  July 12, 2014

      Thanks, Claus. Unfortunately, I do have a very good idea of the intricacies you refer to.

  23. Joe  July 14, 2014

    Now that you are just “flirting” with ketosis … do you still find it necessary to supplement sodium?

    • Peter Attia  July 14, 2014

      Only on days (like the other day) when I go all day without eating, despite a long ride or something. So I may only “require” bouillon a few times a month.

  24. Samantha Beowulf  September 22, 2014

    It seems to me that the issue folks have with the second statement (from the Biochemistry textbook) might be an issue of interpretation rather than a literal reading of the statement.

    Specifically, some folks are interpreting the statement

    “To a first approximation, obesity is the result of taking in more calories in the diet than are expended by the body’s energy-consuming activities.”

    to mean that obese folks must not have moved (exercised) enough to burn all the calories they consumed.

    But that is not what the statement (taken alone) actually says.

    The phrase “the body’s energy-consuming activities” is actually quite broad. It includes far more than exercise. It includes digesting, breathing, keeping your heart pumping, healing wounds, using your brain, and other energy-intensive functions. (Isn’t willful movement/exercise generally thought to be a relatively small percentage of “the body’s energy-consuming activities”, at least in a non-athlete?)

    The statement (standing alone) does not refute the possibility that the body’s actual use of energy might be negatively impacted by disease, metabolic derangement, sub-optimal diet, environmental factors, and/or other nuanced factors we might consider.

    I guess my point is that perhaps we don’t need to refute Biochemistry textbooks to advance society’s understanding of human metabolism. Perhaps we just need to argue against oversimplification (such as assuming the above statement implies that laziness and gluttony are the cause of obesity).

    Perhaps the textbook makes it clear that laziness and gluttony are its intended villains. If not, finding common ground with conventional teachings rather than railing against them might do more to help the obese by advancing the discussion more effectively and broadening acceptance of more recent scientific theories and findings.

  25. Rob Coberly  December 23, 2014

    Lucan SC, DiNicolantonio JJ. How calorie-focused thinking about obesity and
    related diseases may mislead and harm public health. An alternative. Public
    Health Nutr. 2014 Nov 24:1-11. [Epub ahead of print] PubMed PMID: 25416919.
    (same two researchers have an op-ed in the NYT today – “Addictive Sugar Is Everywhere”)
    Nice article – some language in it made me recall this blog post of yours, and the exemplary contrasting photographs at the end of the blog text above. Thought a quote would go well with your theme – of course these are things you’ve already said…
    Article quote:” The problem for public health is that continuing to focus on quantifying calories may misdirect thinking on obesity and related diseases and promote destructive messages. For instance, in a 2013 editorial, the president of the Institute of Medicine listed gluttony and sloth as ‘obvious’ ‘deadly sins’ for public health to address. His argument… suggested obesity and related diseases are matters only of personal resolve and self-control; if people just had more motivation and will-power, they could consciously control their calorie balance sheets, eat less, move more and lose weight. It stands to reason that those subscribing to the Institute of Medicine logic might blame an overconsuming, inactive adolescent for growing fat. But would they blame the same overconsuming, inactive adolescent for growing tall? Just as children do not enter puberty and grow tall because they overeat and sleep more, neither do individuals start to fatten and become obese because they eat too much and move too little. In both cases overconsumption and inactivity are intermediate effects; neurohormonal changes are the cause. The case of pubertal growth represents normal development, but the case of fattening represents decided pathology; pathology that may be modifiable through dietary change. Perhaps if we shifted food production and people’s consumption away from added sugars and refined starches, we could avoid the resultant metabolic dysfunction and corpulence that have come to plague our populations.”

  26. T  February 3, 2015

    Hi Peter — Thanks so much for your incredibly insightful blog and all the work you are doing to better educate people about nutrition.

    Just wondering if you could address the issue raised by Luis’ comment on March 9, where he indicates high fasting blood glucose levels on a low carb diet. I’m experiencing the same issue — I now have an excellent TG to HDL-C ratio, but my fasting blood glucose level is higher than the norm. This surprised me, since I thought it would plummet on a low carb diet.

    Could this be “physiological insulin resistance” as suggested by others in the comment section – and not something to be concerned about?

    • Peter Attia  February 4, 2015

      Fasting glucose, unless really high, is only slight more insightful than eye color. Yes, it could imply PIR. Only way to confirm is short (3 days or so) CHO re-feed. Then do OGTT with glucose and insulin.

  27. Roland  April 13, 2015

    Thank you for all your valuable knowledge. I have high Uric Acid indicator and my doctor advised me to stop eating red meat among other things. Some online resources like this one (http://www.upmc.com/patients-visitors/education/nutrition/pages/low-purine-diet.aspx) advise to eat more carbs because uric acid gets trapped in the kidneys and the carbs help to get rid of it.
    My question is two folds: What is the relation between following a low carbs diet and having a high uric acid? How can I construct my diet on low carbs without worrying about potential side effects?
    Thank you,

    • abhishek  February 6, 2016

      Hello Roland

      I am probably in a similar boat as you.
      I have been following guidelines here and from reddit.com/r/keto for the past 2 months, and have lost 28 pounds. But, I have seen my already high Uric Acid level from 9.x to 10.9 mg/dL taken today.

      I am concerned since I had a Gout attack, my 1st (prior to starting on low carb diet), some 6months back.
      Please do share i f you were able to find more information.


  28. eva  October 17, 2015

    I am so happy to have found this blog,
    i have been trying to learn as much as i can about how ketogenic diet works through books and videos of you and Dr j,Volek,i really admire your work and effort to spread the knowledge.
    i read both good and bad as you can find almost in every type of diet,
    what i have experienced though is that i feel fuller,i like my food a lot more than i did before(being what i thought off as healthy dieter most of my life,now 28 years old female) and i don’t feel bloated anymore. i sleep better,i also remember most of my dreams,and i have lost a few pounds(not that i was ever obese,but i keep storing some fat in my thighs no matter what diet or work out,that just does not fit my overal appearence,thus i was triggered to find out more about the metabolic syndrome and it got me here),
    i found a few articles about physiological insulin resistance that got me a bit worried,and though you have been asked a lot about this,i would like to ask this : is PIR something normal that will go away after time when someone addapts on the ketogenic? or is it a problem that occurs when you have a metabolic syndrome thus you need to fix it and then try ketosis?

    thank you so much in advance!

  29. Tom Kuhne  November 6, 2016

    Hi Peter,

    This may be a naive question I’ve read on other sites that when adapting to NK you still need to have a carb day to restore lost glycogen and other aspects that your body needs from carbs. Based on your caloric intake do you not need to do this based on the fact that you are still consuming enough carbs but your percentages are in line due to your caloric intake? Which allows you to stay in NK. I’m experimenting on what works for me as I continue to adapt to NK. I’m concerned about nutrition deficiencies as I lower my carb intake and so far have eliminated fruits. I love the increased energy and weight loss so far.

    Thanks for your time. Great info that you are providing.

    Regards. Tom


Add a Comment

Disclaimer: This blog is for general informational purposes only and does not constitute the practice of medicine, nursing or other professional health care services, including the giving of medical advice, and no doctor/patient relationship is formed. The use of information on this blog or materials linked from this blog is at the users own risk. The content of this blog is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Users should not disregard, or delay in obtaining, medical advice for any medical condition they may have, and should seek the assistance of their health care professionals for any such conditions.