Does insulin make you fat?

Whether or not insulin is to blame for the obesity epidemic is one of the hot questions being debated on heath and diet blogs.  On the surface, this seems like an arcane question that would mainly interest physiologists and diet researchers.  After all, who really cares about the underlying mechanisms of fat storage and release?   Most of us just want to know some practical steps we can take to lose excess weight and keep it off and, beyond that, to stay healthy.

It seems like a simple yes-or-no question of fact that you could settle by studying populations and doing lab studies. But it’s not so much a question about facts as one about causation.  Questions of causation are often the thorniest ones. This particular question has taken on almost political or religious overtones, provoking emotion and acrimony in the diet blogosphere. On one side are defenders of the Carbohydrate/Insulin Hypothesis, like Gary Taubes and Michael Eades.  This is laid out in detail in Taubes’ book  Good Calories, Bad Calories (2007), and more compactly in “Why We Get Fat: And What To Do About It” (2010). On the other side are opponents such as James Krieger and CarbSane, who find the Carbohydrate/Insulin Hypothesis to be oversimplified and deeply flawed, citing recent scientific advances. People tend to chose up sides in this debate.  I’ve been participating in this debate myself (while still learning a lot) on the websites of Jimmy MooreJames Krieger, and CarbSane. I won’t rehash all the technical details here. Instead, I’d like to propose a “frameshift” that recognizes and integrates the strong points from each side, attempting to overcome their shortcomings.

First, here’s an overview of what each side has to say:

Proponents of the Carbohydrate/Insulin Hypothesis, as articulated by Taubes, posit four main points:

  1. Obesity is a disorder of excess fat accumulation, not voluntary overeating or inactivity, caused by an imbalance in hormonal regulation of adipose tissue and fat metabolism.
  2. Insulin is the primary regulator of fat storage.  When insulin levels are elevated–either chronically or after a meal–we accumulate fat in adopose tissue.  When insulin levels fall, we release fat and oxidize it for fuel.
  3. Elevated blood insulin levels increase hunger and the drive to eat, while decreasing energy expenditure and activity
  4. By stimulating insulin secretion, carbohydrates make us fat and ultimately cause obesity

In short: Carbohydrates drives insulin, which drives fat.

Opponents of the Carbohydrate Hypothesis challenge each of the above points.  I’ve paraphrased four main counterpoints here:

  1. Fat accumulation and obesity result from positive caloric balance (more calories consumed than expended), without regard to the macronutrient class of calorie (carbohydrate, protein, or fat).
  2. Your body can store fat even when insulin is low, via the action of the hormone ASP (acylation stimulating protein)
  3. Insulin doesn’t make you hungry; rather, it suppresses appetite. (The critics proffer that low carb diets may work because protein is more satiating than carbohydrates, but they merely report this observation and don’t attempt to explain it).
  4. Carbohydrate doesn’t uniquely stimulate insulin; many proteins are equally or more insulinogenic.

In short: Calories in minus calories out drives fat.

On the surface of it, these two models of fat metabolism appear to be diametrically opposed.  But are they really?  There is at least one large point on which both sides appear to agree:

Obesity, particularly of the abdominal type, is associated with insulin resistance.

What that means is that people with abdominal obesity (the characteristic “apple” or pot belly shape, rather than those with “pear” shaped backsides or extra subcutaneous fat)  tend to secrete more insulin after eating and have high basal insulin levels, ultimately leading to elevated blood glucose, triglycerides, elevated blood pressure, unfavorable cholesterol ratios, and a host of other issues associated with metabolic syndrome or “Syndrome X”.  Nobody seems to deny this. Sometimes leptin resistance is also cited as an independent or alternative marker of obesity.  But I’ll focus here primarily on insulin resistance, because it seems to be more closely involved with regulation of nutrient partitioning than is leptin.

Where the two sides disagree,  however, is on the causal chain behind the association between obesity and insulin resistance.  Advocates of the carbohydrate/insulin hypothesis tend to arrange the causal the order, from causes to effects, as:

carbohydrates > insulin spikes > hyperinsulinemia > insulin resistance > obesity

Whereas Krieger and CarbSane argue that the order of causality should be:

positive caloric balance > obesity > insulin resistance > hyerinsulinemia

When you look more deeply, however, there is acknoweldgement on both sides that insulin resistance is not a simple monocausal condition, but is likely multifactorial.  There is evidence of many contributing factors, including:

  • specific dietary components: fructose, sucrose, saturated fats, gluten, lectins, dairy, allergens
  • micronutrient deficiencies: vitamin D, magnesium, omega-3 fatty acids
  • metabolites:  triglycerides, free fatty acids (“FFA”, also called non-esterified fatty acids or “NEFA”)
  • inflammatory conditions
  • lack of physical activity and exercise (particularly strenuous exercise)
  • genetics

There is as yet no broad scientific consensus as to the relative importance of each of these factors in causing insulin resistance. But it is almost certain that there is no single cause.  Regardless of the cause, however, it is important to understand what insulin resistance is on a cellular level: a reduction in the number and sensitivity of insulin receptors, such as GLUT4 receptors.  Different tissues can experience different degrees of insulin resistance.  Typically, muscle tissues are the first to become insulin resistance and fat tissue is one of the last.  Insulin resistance in different organs like the brain or the skin can have different effects.  Some have argued that certain pathologies such as Alzheimer’s disease and acne are associated with organ-specific insulin resistance. I’ve proposed elsewhere on this blog (“Change your receptors, change your set point“) that receptor number and sensitivity can serve as a kind of dynamic “set point” for weight and other physiogical states governed by hormone-receptor and neurotransmitter-receptor balances.

So here is where I think that a frameshift in the debate about insulin can reconcile the two sides, at least in good measure:

Insulin resistant (IR) individuals respond in a qualititatively different way to carbohydrates and fats in their diet.

Let’s see what that means specifically:

First, consider insulin resistant (IR) individuals, regardless of how they got that way.  IR individuals have elevated basal insulin levels, usually defined as a fasting insulin of at least 15 μIU/mL, or perhaps higher.  If you have a protruding belly, high triglycerides and a high blood pressure, you are probably in this category.  Under these conditions, dietary carbohydrate, and to a lesser extent protein, add fuel to the fire by spiking an already elevated insulin level. And let us grant here the point of Krieger and CarbSane that ASP is a potent faciliator of fat storage.  It is known than insulin significantly enhances the action of ASP.  In addition, insulin upregulates lipoprotein lipase (LPL) a fat-storage  promoting enzyme and inhibits the action of hormone sensitive lipase (HSL) an enzyme that favors hydrolysis of stored lipids to free fatty acids.  Combine all three effects and we should expect that IR individuals store dietary fat easily, even with moderately low carbohydrate diets.

For these individuals, the elevated levels of basal insulin will tend to shift the balance of glucose and fatty acids from the blood stream into the tissues.  (Krieger and CarbSane are correct that insulin may not play a big direct role in driving fat sequestration, but its indirect stimulatory effects on ASP and LPL and inhibitory effect on HSL are quite significant, reducing the concentration of fatty acids in the blood stream by shifting the equilibrium towards the adipocytes).  This will also tend to stimulate appetite and eating, leading to more fat storage and a worsening IR condition. Sugarholics and those with carbohydrate cravings tend to be insulin resistant. Appetite has a large conditioned component, whereby preprandial levels of insulin, ghrelin, and other hormones are secreted based upon temporal cues and specific sensory cues.  It has been found that this pre-prandial secretion is much more pronounced in overweight, IR individuals.

One of the best ways to break this cycle is to go on a very low carbohydrate diet, something like the Atkins induction diet.  Since there is no insulin response to dietary fat, a high fat, very low carb, moderate protein diet will allow basal insulin level to gradually drift down.  This will shift the balance, reducing (but not eliminating) the actions of ASP and LPL, and disinhibiting the action of HSL. This will increase release of glucose and fatty acids, supplying energy and providing satiety, further lessening the drive to eat.  The vicious cycle is replaced by a virtuous one. Unfortunately, a reduced calorie, high carb diet will not work for IR individuals, because their appetite is so easily triggered by any increase in insulin, which leads to a faster than normal drop in blood glucose.  Note that blood glucose does not have to be “low” to induce hunger.  There is evidence that hunger is triggered merely by a rapid drop in glucose levels.   On the Deconditioning Diet page of this blog, I describe a method for extinguishing this conditioned pre-prandial insulin response.

Claims that insulin suppresses appetite is based on studies involving central administration of insulin while artificially infusing glucose. Krieger is correct about the “central” effect of insulin within the hypothalamus and upon the vagal afferent fibers. However, as with many hormones, insulin can have opposing effects at different locations and times. We need to consider the important appetite-inducing effect of insulin secreted into the “periphery”, without the simultaneous supplementation of glucose or other nutrients.  This is a particular issue for IR individuals who are vulnerable to insulin-induced cravings, and less of an issue for those with good blood sugar control.

Now let’s consider insulin sensitive (IS) individuals. These are people with less than 10 μIU/mL, ideally less than 5 μIU/mL insulin.   The situation is quite different for these folks.  As a result of much lower basal insulin levels, they have more stable blood glucose and fatty acid levels, because the lower insulin levels reduce inhibition of glucose and fatty acid release from glycogen and adipose tissue.  So IS individuals are less prone to hunger cravings, because they can access their own energy stores more easily. They are much better able to tolerate higher levels of carbohydrate in the diet, because their insulin response is well controlled and glucose readily gets to the cells and brain after eating.

This may also provide a plausible explanation for why certain populations such as the Okinawans, the Kitavans, and other cultures remain lean on a relatively high carbohydrate diet:  their low basal insulin levels and high insulin sensitivity permit them to handle carbohydrates easily.  According to Stephan Guyunet’s Whole Health Source blog:

Grains, refined sugar, vegetable oils and other processed foods are virtually nonexistent on Kitava. They get an estimated 69% of their calories from carbohydrate, 21% from fat, 17% from saturated fat and 10% from protein. Most of their fat intake is saturated because it comes from coconuts. They have an omega-6 : omega-3 ratio of approximately 1:2. Average caloric intake is 2,200 calories per day (9,200 kJ). By Western standards, their diet is high in carbohydrate, high in saturated fat, low in total fat, a bit low in protein and high in calories.

While this is a “high carbohydrate” diet, the carbohydrates are not typical western foods: The Kitavan diet consists mainly of foods like tubers, fruit, coconut, fish and vegetables. Even with the high carbohydrate levels, their insulin levels are much lower than that of typical Westerners.  One could argue that these foods have low levels of fructose and sugars, and are generally quite non-inflammatory, so they should promote insulin sensitivity.  According to Lindeberg, their fasting insulin levels averaged 3.12 and 3.29 IU/ml for males and females, respectively.  This is about half the basal insulin levels of Swedes: 6.98 and 6.65 IU/ml for males and females, respectively. Fasting blood glucose levels for the Kitavan’s were about 27% lower than that of the Swedes.

Furthermore, IS individuals should be able to lose fat quite easily by restricting carbohydrate, intermittent fasting and/or exercise. With resulting very low basal insulin levels, it should be even easier to release fat from adipose tissue and oxidize it for energy, or to go into ketosis. It is known that Type 1 diabetics, who have no insulin, shed fat readily and have trouble holding onto it without injections.  But someone with low basal insulin can achieve a naturally lean state easily, while also being able to handle insulinogenic meals without difficulty.  Based on my own experience over time, as my fasting insulin level has dropped, intermittent fasting and even fasted workouts become easy, and this does not preclude a reasonable level of carbohydrates in my diet.

Now let’s ask the question of whether insulin sensitive (IS)  individuals can accumulate body fat on a high-fat, low carb diet. According to Krieger and CarbSane, this should be no more difficult than on a high-carb diet.  You just have to eat a “caloric surplus” of fat, with no or little carbohydrate, and ASP will do the job, even without insulin.  But will this really have the predicted effect?  Without doing the study, it is hard to know for sure.  But my prediction would be that it is unlikely to play out as they suggest, for several reasons:

  1. Despite the claims that ASP works without any insulin, the primary sources don’t show this. For example in the paper by Saleh et al., which CarbSane cites in support, there is still some insulin and carbohydrate present to stimulate ASP, with or without the action of chylomicrons.
  2. Even assuming that the ASP could drive fat accumulation without insulin present, the lack of insulin would also favor downregulation of LPL and activation of HSL, which will tend to balance ASP’s action by liberating fatty acids from the adipocyte.
  3. Under low insulin conditions, even with excess fatty acids being fixed within the adipocytes, one would expect a reasonably high equilibrium level of free fatty acids in the blood stream.  This would favor satiety, so that eating the fat meal would be self-limiting.  This contrasts with the action of insulin which, when elevated, will tend to deplete the blood stream of glucose and fatty acids.

I will conclude with the following synthesis between the above opposing positions:

  1. Obesity is a disorder of excess fat accumulation resulting from insulin resistance (and leptin resistance), which stimulates appetite and naturally leads to caloric imbalance, including overconsumption of both carbohydrates and fats.
  2. Insulin and ASP together regulate  fat storage and release. While ASP acts directly to transport and fix fatty acids within fat cells, insulin acts to induce fat storage via ASP and LPL, and to inhibit fat release via HSL and epinephrine and norepinephrine. Reduced levels of both insulin and ASP favor lipolysis and fat loss. The synergy of insulin and ASP further explain why the combination of dietary carbohydrate and fat is particularly fattening.
  3. In insulin resistant individuals, elevated blood insulin levels stimulate hunger and the drive to eat; this effect is largely absent for insulin senstive individuals due to superior blood glucose control
  4. In insulin resistant individuals, the pancreas compensates for reduced receptor sensitivity by secreting more insulin, leading to hyperinsulinemia.

So the answer to the question is to shift the blame from the hormone insulin to the condition of the insulin receptors.  Insulin spikes at meal time are no problem, so long as basal insulin remains low. Restriction of dietary carbohydrate is one very effective strategy, which should be chosen not for the short term benefits in weight loss, so much as the longer term benefits in improving insulin sensitivity and reducing basal insulin.  With the focus on “regrowing” and “reconditioning” insulin receptors, we should look at the full arsenal of tools, including intermittent fasting, nutrients such as vitamin D, magnesium and fish oil, and high intensity interval training.

Let me emphasize here that my proposed explanation is meant as a tentative conceptual framework rather than a conclusive scientific analysis.  I’m still learning about the details and I fully expect that our understanding of the underlying mechanisms of fat metabolism will continue to be revised and evolve.  But I do think that there has been too much emphasis placed on hormones and neurotransmitters, which fluctuate every day,  and not enough on receptor health, which is something we can can influence over the long term by commitment to scientifically informed practices.

If you are interested in this general framework for diet and how it fits into my overall philosophy of Hormetism, check out my podcast interview with Jimmy Moore which just went live today.

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  1. Wow, haven’t read anything new from you in a while! What has it been, a month!?

    Anyway, even though it’s not my area of expertise I really think you’re up to something here.

    With your intermittent fasting you seem to have found a hack for a lot of modern day problems!

    • Todd,
      I always enjoy your insights! I hold myself PERSONALLY responsible for my “poor” eating habits. When I went to school, maybe 1 kid in 25 was “obese”. But for the fun of it, I “rate” myself as a “2″ or “3″ in your pictures going from left to right. It is not “fun” to admit “self-induced” problems, but that type of “honesty” can encourage you to “solve the problem” — yourself. This is your (and my) central thesis in engineering and science. Otis

  2. Brian

    While this particular entry isn’t that relevant to me (I weigh 130 pounds at 5 foot 8), I’d like to encourage you to keep writing. I actively incorporate the suggestions on this website, and would love to read more of your thoughts on the matter.

    Also, do you have any good research articles regarding fasting and bdnf?

    • Todd


      I’m glad to hear that you are finding some of the information here helpful. Regarding BDNF, this Wikipedia article is a good start for the basics. On my post about Calorie restriction and hormesis, I referenced two good articles, by Gomez-Panilla and Araya on the benefits of intermittent fasting to upregulate BDNF. Let me know it you were looking for something more detailed than that.

      I’d be interested in your feedback on which topics are of most interest to you. You might also consider joining in the discussions on the Forum linked to this blog.



  3. Awesome post! I tilt more towards the Taubes’ theory than the CarbSane one, but I’m not convinced that Taubes has the whole story right.

    I’ve lately been thinking his theory is analogous to looking at looking at a series of arson-related fires and saying “well, the houses wouldn’t burn if they weren’t made of wood, so let’s make houses out of brick” rather than focusing on the arsonist … i.e., what actually makes us insulin-resistant.

    My bet is on what Kurt Harris calls the neolithic agents — wheat, excess fructose, and excess linoleic acid — which damage the liver leading to IR. Peter@HyperLipid has a great post on this here:

  4. Steve

    I think the thing to understand about obesity as it relates to insulin as the primary driver of fat accumulation, relative to ASP and other mechanisms, is that Insulin sets off a feedback loop. ASP does not. You don’t get asp hyper secretion or asp resistance etc… That I’m aware of. There’s nothing to dis-regulate long term. So maybe its possible to constantly overeat fat in the absence of carbohydrate, but I suspect that would be very unusual. What exactly does that diet look like? Just sitting around eating sticks of butter?

    So while I believe ASP can store fat without insulin (although it seems true that the effect is stronger in the presence of insulin.. they feed each other and work better together) I don’t think it matters when we’re talking about obesity as a long term chronic condition where fat is accumulating more and more over time.

    I think part of the problem in all these obesity/calories/asp/insulin arguments is that there is not just a single scenario that these issues pertain to.

    A person who is deep on the path to full blown metabolic syndrome with hypertension and fatty liver and nearing type 2 diabetes is NOT the same as a person who has to lose 15 lbs to get to a low body fat percentage for some beach modeling gig. In the latter case overeating fat probably matters a lot and the whole calorie thing may indeed come into play, because the natural healthy fat level for that person’s body at their age may simply be more than they want or need for some reason. Often these people diet as a living, but it’s common for instance to see people like body builders drop to low body fat percentages pre contest and then return to normal fat levels day to day between contests. I think when Taubes and proponents of insulin as the main causal agent in obesity are talking, they are speaking directly to the most common cause of long term chronically disregulated fat.

    • LeonRover

      I can drink pints of double cream but only in the presence of

      a)a few ripe strawberries
      b)a little sucrose or sweet syrup
      c)a sprinkling of sucralose

      then whipping it all together.

      To eat a stick of butter, I add a nominal amount of hot mashed potato, salt and a scrap of onion, then puree ‘em together. Wow!

      What happens to insulin when a meal is consumed is really not relevant – else protein is also “implicated”.

      Chronic high basal insulin aka hyperinsulinemia blocks the continuing mobilisation of fat fuel from adipose tissue, when the liver glycogen depot has been exhausted and blood sugar is low.

      This is the story of Le Magnen’s rats as so eloquently related by GT.

      However, on page 435 of GCBC, GT states “..this hypothesis (implies) that that both weight gain and hunger will be promoted by factors that work to deposit fatty acids in the fat tissue and inhibit their mobilization”. The final addition to this sentence is fatally flawed “i.e. anything that elevates insulin”, as he does not distinguish between the levels of insulin necessary to store the glucose and/or amino acids resulting from digestion which are quite healthy, and chronic high basal insulin which prevents fat mobilisation which is quite unhealthy.

      “Methinks the lady doth protest too much”

      applies, and/or

      “Gilding the lily”

      Lustig in his review in Nature takes a cool scientific look at the hormonal regulation of feeding

      and also discusses how there can be a great hormonal disregulation in “satiety signalling” in the hedonic pathway.

      • Todd


        I’m with you on this. The problem is not “anything that elevates insulin” but chronic high basal insulin levels. The question is what causes these chronic high levels. In some way or another, insulin resistance and leptin resistance are at the center of the storm. So the “control points” for obesity are receptors, not the signalling compounds (hormones and neurotransmitters themselves) as argue in my post on “Change your receptors, change your set point“.

        Thanks also for posting the excellent Lustig article. He nicely connects the insulin and leptin issues with these two sentences: “Insulin and leptin share a common central signalling pathway, and it seems that insulin functions as an endogenous leptin agonist. Suppressing insulin ameliorates leptin resistance, with ensuing reduction of caloric intake, increasing spontaneous activity, and improved quality of life.” This also makes clear that there is no inconsistency between hormonal control theories and “calories in, calories out”. They both move in concert, but the hormones are the horse and the calories are the cart, not the other way around.

        • In

          Nice article, but you seem a little biased towards low carb. Two gaping holes in your arguments:

          1. You don’t go into why some are IR in the first place. Since most modern fat people are descended from non-fat carb eaters – it seems to me that carbs perse aren’t the cause (certain types of carbs could be, but not carbs as a whole).

          2. So if some IR person goes low carb, long term is his ability to handle carbs increased or decreased? Obviously while you are low carb you can’t handle carbs as well. But if you were to try to adapt back to eating carbs, would you be more or less IR? Seems to me that is the crux of the matter. I’m skeptical that people do best on high fat in general so if you want optimal health, the goal would be to handle carbs better, be IS and eat carbs. Maybe some people can’t become IS eating carbs, but for the vast majority it doesn’t seem plausible to me that eating a high fat diet beyond a relatively short period of time would make one more IS eating carbs.

          • Todd

            Thanks for your comments, In. As to the causes of IR, I think my post states quite clearly that this is likely to be multifactorial, and I list some of the factors that research has associated with IR. I certainly do not take the position that carbohydrates per se cause insulin resistance, if you look closely at what I wrote. Low carb, intermittent fasting, and high intensity intermittent exercise may help IR individuals become more insulin sensitive. Weight loss in and of itself can help improve insulin sensitivity. Ultimately, however, I agree that strict adherence to a low carb diet is probablly counterproductive. Including periodic but limited carb “spikes” in the diet — perhaps even every day or two — seems to be a good way to develop “carbohydrate tolerance”, and a healthy insulin response. So while I’m moderately low carb and Paleo in my diet, by no means do I exclude carbohydrates. I eat small high carbohydrate meals every few days to “exercise” my insulin. But I think a low basal insulin level is associated with good insulin sensitivity.

            As to the value of high fat diets, the answer here may be complex. Certain fats (omega fatty acids, and short or medium chain saturated fatty acids like coconut oil) seem to be compatible with, or even to help improve, insulin sensitivity. Eating certain saturated fats in combination with high carb may worsen IR. So I don’t think there is a black and white answer to the question of whether high fat diets are wise.

  5. I’m happy to see that you’ve taken a stab at reconciling these two opposing theories. Like you, I suspect that the truth lies somewhere in between and I applaud your efforts here!

    I have two thoughts I want to bounce off you.

    First, it seems your theory might suggest a two-phased weight loss approach for IR individuals. Go VLC until it stops working and you plateau; then focus on caloric restriction, a more moderate carbohydrate intake, and weight training/IF to bump up insulin sensitivity further.

    I mention this for a couple reasons (a and b):

    a) I know a lot of low-carb folks who lose a ton of weight to a point but don’t ever get really lean. They keep low-carbbing. They don’t count calories. They stall completely on the plateau.

    b) I’m one of the individuals mentioned in a) and more or less stalled on body recomposition for two years while trying all sorts of IF and weight training but never counting calories and, randomly falling off the carb wagon for a day here and there, kept carbs pretty low all the time (say <50gm/day).

    Fast forward to the last few months where I've followed Martin Berkhan's LeanGains — high-carb on weight lifting days, IF all the time, caloric restriction on non-weight lifting days, generally low-fat/high-protein all the time. I've blasted through the plateau and am the leanest ever and a few pounds lighter (but significantly more lean) than the lowest weight I got while trying IF and low-carb (successful body recomposition).

    This brings me to the second thought I had. I think it's important to remember that insulin is kept low to allow fat to get out of the cells *to be burned by your body as energy when in a caloric deficit*. In other words, low carb folks who exclusively focus on low-carbing and don't count calories might find weight loss easy for awhile due to satiation and rehabilitating a busted metabolism thanks to keeping insulin in check, but once metabolism is more or less fixed and diet is still kept low-carb, I wonder if ASP isn't upregulated in order to allow the body to still be successful at maintaining caloric homestasis. Forgive my lack of technicality here, but I could see the body adjusting to a "new normal" with chronically low-carb dieters once metabolism/insulin is "fixed." It is here where caloric restriction really starts mattering for further weight loss/fat loss.

    I, for one, have found that maintaining low-carb seems to help me maintain my weight at a certain point while not worrying much about caloric intake. I'm hopeful (optimistic) that at a certain leanness,
    I will be able to focus less on total caloric intake and simply keep carbs in check enough to eat whatever fats I like and not worry about weight gain. That will be the real epilogue in my own forays into diet and nutrition over the last three years!

    • Justin, I’m seeing very similar results with my current experiment. Low carb / unlimited calories will make you healthier*, but you won’t get ripped lean eating as many calories as you want.

      I’m currently experimenting supplementing with pure glucose– which also happens to taste so much better than sucrose or HFCS-55, on workout days. I think the insulinogenicity of whey protein is enough to prompt muscle recovery, but when you’re combining a ketogenic diet, with intermittent fasting, and hard workouts you’ll run into a problem with you bodies bicarbonate buffering system and if you don’t eat enough protein (that can be synthesized to glucose) you won’t replenish your glycogen.

      A short summary of what I’m seeing as the chain is
      increase fat consumption / cut carbs -> body upregulates fat burning for energy (i.e ketosis) -> at plateau for fat loss increase protein intake while dropping fat intake and maintain low carb (~ 100 a day depending on activity levels) -> down regulated glucose metabolism, increased fat metabolism.

      If you think about it, your body would stop storing as much fat when you’re eating a bunch of fat. If you’re eating low-fat, your body goes oh crap I gotta store all the fat, because I’m not getting enough. Backing out of 20 years of eating like that can be difficult.

    • Todd


      I tend to agree with your two suggestions. On the first point, about doing low carb before caloric restriction/IF: that’s exactly what I suggest on the Diet page of the blog. Until your basal insulin levels are reasonably low, it may be hard to skip meals with the backlash of cravings, lightheadedness etc. I agree that weight training and interval training are a further boon. And my other suggested addition to this is deconditioning using cue exposure therapy, as discussed on the Diet page.

      Your second point is also plausible, that metabolism may adapt to a high fat diet to make it easier to store the fat. What I don’t know is whether this can be explained completely in terms of ASP upregulation. I think that Steve, in his comment above, makes a good point about feedback loops. In the case of insulin resistance, it is the damage, densitization or downregulation of the insulin (GLUT4) receptors that sets up a long term problem with hyperinsulinemia. Receptor levels don’t adjust as quickly as the hormone levels. Steve’s excellent question is whether there is any such feedback loop in the case of ASP. If not, then it would seem you would have to force yourself to continuously eat high fat to keep ASP high, and that taking even a short break, would allow it to plumment. By cutting calories and IF, yet still keeping percent fat high, you would seem to avoid this problem. Perhaps some of our experts on ASP, like CarbSane, can answer this.

      I’m impressed with the progress you made using Martin’s protocols. I’m a fan of his as you know, and I credit his advocacy of IF and fasted workouts with first encouraging me to try that. I’m still ambivalent about high carb on weight lifting days or running days. I see the advantages for gaining muscle mass, but I also want to train myself to preferentially “run on fat” as much of the time as possible. Since cutting out carbs on running days I find that my endurance has improved. Take a look at this article “Fuel on Fat for the Long Run” for details. For those reasons, I do eat some small carb treats and add moderate carbs to many meals, but I never have entire high carb days.

      • If you haven’t read Mark Twight’s thoughts on endurance training and fat oxidation (and training your body to burn fat), you might check out his post here:

        I understand the ambivalence about high carb days. My take on high carb days matched to weight lifting days is that the fasting + weight lifting prime muscle to absorb glycogen and promote an anabolic state. It might also go a ways to offset hormonal signals telling the body that it should conserve energy/go into starvation mode (signals that would be spawned by the overall caloric deficit, but also the more acute deficit on the day before a high-carb day and the day after). The next day, you cycle down calories and carbs; glycogen stores in muscle don’t go anywhere. If I had to guess I’d say liver glycogen is depleted and fat stores are released to make up any caloric deficit, and minimal lean tissue catabolism takes place. Repeat the roller coaster the next day with another day of training.

        The cyclicality of it/the diversification of macronutrients — both of these are appealing to me. I’m not sure we’re meant to be chronically low-carb just as I’m 99% sure we’re not meant to go chronically low-fat. An appeal of lean gains is that it suggests a diet that hits at a range of macro-combinations. That said, on the fat loss protocol for leangains, it’s pretty low-fat overall — very high protein. I’m most curious how, on being very lean, I will be able to maintain without paying as much attention to specific diet parameters (1) and increasing fat intake overall (2).

        Unfortunately, I had a minor diet setback this past weekend — 30th birthday and ate a LOT of cake and junk food. Hopefully won’t set me back more than a week or so. We’ll see. If I had to guess, I’d say I’ve got another 5-6 weeks before I’m about as lean as I’d want to be. We’ll see.

  6. I am beginning to believe that perhaps the crux of all this has to do with that fact that in the West most carbs are grain-carbs. Eating to caloric excess becomes easy with such nutrient poor foods and liquid calories and that toxins in these foods may eventually lead to a disruption of hormone signaling in leptin leading to leptin resistance leading to IR. Have you ever seen Stephan’s posts on leptin and lectins? He posits an interesting hypothesis that the lectins in grains may damage leptin by binding to it thus creating leptin resistance over time. This leads me to wonder what results would be found in an experiment where several groups of people were to be put on a Kitavan diet with the differences being that one would be the traditional Kitavan diet, one would replace the carbs with gluten-grains, one would replace the carbs with rice, one with corn, and one with pseudo-grains (amaranth, millet, quinoa). I wonder which groups would fatten and which wouldn’t.

    • Galina L.

      Some of answers for your questions you will find in the “Nutrition and Physical Degeneration” by Weston Price. Some of healthy eating societies he observed eat grains (I remember rye and milk products combination in isolated villages in Switzerland and oats and fish in some Gaelic islands ). The book is available on internet for free –

  7. David I

    Hi. Excellent discusssion of the problem.

    However, I think this amounts to “Taubes is 95% correct, though not always for the reasons he puts forth.”

    The Drs Eades also seem to fall into this category of 95% correct.

    I’d love to see a 100% correct theory of obesity, but 95% seems to have been good enough for me and many others. I lost 60 pounds of weight while gaining 10 pounds of muscle (all verified by preiodic hydrostatic weighing) by a combination of 1) resticting carbs, 2) upping protein intake, and 3) exercise. When last measured, I was ay 12% body fat.

    I did this without restricting calories, and at a higher caloric intake that I’d had previously.

    Is it because I controlled my insulin, and that cut my fat storage directly, or is it because I cut my insulin and that cut my fat storage directly and also inhibited ASP? As you point out, probably the latter. And it’s interesting to know. And I’m sure we don’t know everything yet.

    But CarbSane’s frothing rage at Taubes seems to me to be rather misplaced. It has overtones of disputes between various denominations of the same religion.

    Keep up the good work!

  8. Just wanted to thank you for an excellent analysis of the two competing hypothesis. I’ve been amazed at the emotion involved in the discussion from the CarbSane and Krieger camps (Taubes seems to be very good at keeping his rebuttals intellectual rather than personal). My impression is that your analysis is probably correct but would LOVE to see a study that proves it!

  9. Galina L.

    Thank you very much for your article. It was excellent! I hope it will contribute to the peaceful resolution of nutritional fights. I am grateful to Jimmy Moore for inviting you because it brought me to your blog.

    I am the person who practices a ketogenic diet for health reasons with very satisfactory results, recently I added IF to it. Before LC I tried Dr. Weal diet advice (very close to Mediterranean diet) and gained weight as a result. Your picture represents a man, I am a female and in a middle-body look more like the second person from the left. So, not exactly IR type, but I think I am very carb sensitive.

    What do you think about the Dr.Shai study His diet report demonstrate superiority of Mediterranean diet(MD) for Diabetes II(they suppose to be extremely IR)and equal effectiveness of MD and LC(low-carb) diets for a weight loss. The results completely contradicts to what Dr.Bernstein recommends for Diabetics, it contradicts my personal and other people experiences, but it is a well design research. CarbSane regularly mentions it as a proof of her theory. It is very confusing for me.

    I understand you may not have all answers for all questions. Model of body functioning is extremely complicated and still not completely understood.You made a great effort to go further. Right now the safest rout for me is to treat my body as a black box, comparing what is on entrance with a data on exit and not to worry much about things in-between.

    • Todd

      Thanks for your comments, Galina.

      I am quite familiar with Weston Price and read his book about 15 years ago. It was eye opening and inspired me to move beyond simple low carb towards more of a paleo focus on unprocessed foods. I don’t avoid grains, although I’m very moderate in how much I partake.

      I did read the Shai study, but I come to a different conclusion than CarbSane. If you read it carefully, you’ll see that the authors conclude that both the low carb and Mediterranean diets are roughly equal in their weight loss benefits and impact on biomarkers, and that both are superior to low fat diets. The weight loss chart shows that low carb and Mediterranean plateau with weight loss of of about 5 pounds, but the standard deviations were more than 5 pounds — so that tells me that there is a lot of variability in individual response to the diets, as your personal story indicates. The Mediterranean diet results did show some benefits in lowering fasting blood glucose, and the low carb group had the best reduction in triglycerides. Why not combine the best of both diets — low carb with healthy omega 3/ omega 6 fatty acid ratios, fish and nonstarchy vegetables?


      • Galina L.

        I know the theoretical benefits of eating fish, I eat fish myself, but I have some personal doubts about its benefit as a major sours of a protein (at least, for myself). First, the satiety issue. In general, I think it is better not to use any food as a staple if I can eat a big amount of that particular food it one setting (exercise my gluttony). It is my case with a fish, especially if I saute it with tomatoes and bay leaves, but not necessary. Second, the sea food is, unlike beef or lamb or pork, a very widespread cause of food allergies (I am allergic to some seafoods, but not to all). So, by treating my body as a black box, I see the evidence that the fish is the inferior food compare to meat (for me).

  10. Insulin doesn’t make you fat. Eating too much (for your activity level) makes you fat*.

    It just so happens that eating anything (except pure fat, which raises ASP) raises serum insulin.

    Eating protein raises serum insulin. Eating fat increases the insulin response produced by the other food groups.

    *Bodybuilders can gain significant muscle mass relative to fat mass by doing resistance training with weights.

    Cheers, Nige.

    • Galina L.

      Hi, Nigel,

      Protein causes the insulin secretion, but not so strong as carbohydrates.
      Do you think, that amount of secreted insulin matters?

      • Dietary fat (and many low-carbers get most of their calories from dietary fat), increases the insulin response of protein possibly by reducing the insulin sensitivity of target tissues (liver, muscle & fat cells).

        Therefore, its incorrect to say that people eating low-carb diets have low serum insulin levels.

        The amount of insulin secreted depends on how much food has been eaten and the insulin sensitivity of target tissues. I’m not sure what you mean by “matters”.

        • Galina L.

          Yes, the article in your post proves your point that protein may be sufficiently insulinogenic. There is something else going on, I think. As you possibly remember, I am interested more in staying in ketosis for health reasons then in loosing weight .Raise in insulin supposed to get me out of ketosis, but ,according to my testing strips, beef, lamb, eggs , fats keep me there, but not fruits and country cheese or grains. I cook my meats in a coconut oil and it may interfere one way or another. I should check more. Also, there is a lot of evidence that insulin injection treatments are fattening and increase appetite. Not typical body reaction on proteins consumption. Something doesn’t fit there.
          I like Todd’s attempt to bring together different sides, because the idea that the truth is more complex that the theory that insulin doesn’t affect a weight loss or the amount of eaten fat never causes a weight gain, is very appealing to me. High fat low carb diet works for me, but there are posts of numerous people who can’t loose weight on a LC.

        • Hi Galina. I can’t reply to your reply so I’ll reply here.

          Being in ketosis is mostly to do with restricting carbohydrate. Protein is somewhat (~50%) anti-ketotic (probably due to its glucagon response). Carbohydrate is 100% anti-ketotic and fat is 100% pro-ketotic. Coconut oil is pro-ketotic and a very stable cooking fat.

          Injecting insulin increases appetite by inducing low blood glucose. Eating protein doesn’t induce low blood glucose due to its glucagon response, which keeps blood glucose stable.

    • David I

      “It just so happens that eating anything (except pure fat, which raises ASP) raises serum insulin.”

      That’s a little like saying, “Any exercise, including sitting up in a chair, burns calories and increases strength.” True, but misleading. It makes it sound like all forms of exercise are similar in effect.

      Some foods cause far greater secretion of insulin than others. Protein does encourage an insulin response, but it also encourages the release of glucagon, which tends to mobilize fat rather than store it.

      Smelling food, or even thinking about food, causes an insulin response. But that doesn’t mean that smelling food is metabolically equivalent to eating five slices of white bread.

      • The glucagon response affects serum glucose, but I’m not talking about serum glucose. I’m talking about serum insulin. The insulin response to protein is bigger than you think, especially in people with impaired insulin sensitivity, people most likely to be on a low-carb diet. See

        Mobilising fat is pointless if it doesn’t get burned by muscular activity. It lingers in the blood, which is atherogenic.

        The cephalic insulin response is negligible (see ) so it’s nothing like eating five slices of white bread.

  11. David I

    I’m afraid I don’t quite see your point.

    Yes, activity matters, especially in terms of reducing insulin resistance.

    But I have never found a level of activity where I can eat more than 150 grams of carbohydrates a day without gaining weight–even if I keep food intake down below 1200 calories. About 15 years ago, I was gaining weight, and so I went on an ultra-low-fat, carb-oriented diet, with vigorous activity. My weight declined slightly and then rebounded and turned into steady and progressive weight gain.

    On the other hand, when I went on a low-carbohydrate diet, the pounds just peeled off, even though my caloric intake was about 2,000 cal per day or more. And this was without any physical activity (I had sprained my ankle severely).

    I’m not sure what your theory is, but I’d like to know how it can explain my particular results.

    (I’m a scientist, by the way, and have had two semeters of Thermodynamics and three semesters of Physical Chemistry–two and a half years of studying thermo. So please don’t tell me that I don’t understand the First Law.)

    One of the rules of science is that while there is no number of experiments that can prove a theory true, one experiment can prove a theory false. So dismissing my experience as “anecdotal” doesn’t cut it.

    The National Weight Control Registry–which by and large endorses a low-fat, high-carb approach to eating–has found that among the registry members (who have lost more than 30 pounds and kept it off), the low-carbers 1) ate an average of 300 calories more a day, 2) had lower levels of exercise, and 3) engagend in almost no portion control.

    I’d like an explanation of these results–and my own. Any explanation I’ve seen that comes close seems to include insulin.

    • Your personal experience suggests that you are getting some kind of magic from a low-carb diet vs a high-carb one. How were you measuring your calorie intake on each way of eating?

      Without being in a metabolic chamber or using doubly-labeled water, it’s impossible to know how many calories you’re burning on each way of eating. NEAT makes a big difference and tends to be high on a way of eating that makes you feel less sluggish. Other than that, I can’t explain your results.

      I’m not trying to discredit Gary Taubes or low-carb diets. The fact is that there are people out there who cannot lose weight no matter how low they cut their carb intake. For them, there is no magic. It’s calories that count.

      The National Weight Control Registry uses self-reported intake data which is horrendously inaccurate, so 300 calories is down in the noise. See

      • David I

        Calories matter, but the way bodies work is quite complex and poorly understood. My problem with the Calories In/Calories Out crowd is that in general they vastly oversimplify. Yes, nothing comes from nowhere, and nothing magically vanishes, but that in fact tells us very little about what our body is doing with our intake.

        To take simple example, consider soluble fiber. It combusts at about 4 cal/g, but we aren’t direct-combustion furnaces. So do we count it?

        Most people say fiber should not be counted as it isn’t digested. But bacteria in our gut digest it, and we absorb the short-chain fatty acids SCFAs they produce. In effect, when we eat soluble fiber, we are eating fat.

        But how much fat? Well, it varies. Some estimates peg the amount of SCFAs produced and absorbed at 1.8-2.0 cal/g of soluble fiber. But if you eat large amounts of insoluble fiber with it, it decreases the availability of the soluble fiber to the bacteria, so it can be lower. Or your gut flora may be unhealthy. So, how many calories do we absorb from soluble fiber? Some place between 0 and 50% of the heat of combustion.

        Do we absorb all the fat we eat? Apparently not, as sometimes feces are so fat-laden they float.

        And, back to fiber, the reason fiber lowers cholesterol is because it tends to lock up bile (which is largely cholesterol) and carry it out of the body. Of course, bile is secreted mainly in response to fat, so how much cholesterol is carried out of the body depends on both fat and fiber intake (and probably other factors we haven’t considered). There are some calories flowing right back out of the body–and not in response to our exercise levels, either.

        In my case, I suspect NEAT makes a big difference. My body temperature also drifts up after meals that include a lot of fat, so I suspect there is a lot of “futile cycling” happening. Similarly, when many people go on low-calorie diets, their metabolism slows and their hands and feet get cold.

        I don’t object to the idea that weight maintenance is a matter of

        Calories In = Calories Out

        What I object to is that both sides of the equation are vastly more complex than most people allow–and both sides of the equation interact with one other. What you eat, rather than its strict caloric measure, affects how you process those calories, how efficiently you absorb them, how efficiently you transform them (gluconeogenesis is energetically costly), whether you lose caloric material through your digestive system (see bile, above) and what your body is inclined to do (fidgeting, sleeping, sweating). Not all calories are created equal in terms of what they do in the body.

        High-protein, low-carb diets increase energy expenditure even without exercise; in one metabolic chamber experiment, the increase amounted to an average of 81 Calories per day. This is about the same magnitude as the legendary extra slice of bread that makes people gain 8-10 pounds per year. And that’s resting energy expenditure. If the subjects were free to exercise, the spontaneous increase in activity might have resulted in much larger differences.

        42 percent of that 81 Calories is gluconeogenesis, so has nothing to do with activity. The rest is is unexplained, but might also be metabolic rather than a matter of activity.

        “Calories” explains a lot, but it doesn’t explain everything.

        You might want to look at the photo of the woman in Taubes’s new book–although it’s a bit horrific. She has two melon-sized lumps of fat on the front of her thighs. They are there because those are the sites where she injected insulin over many years. I suspect that if you starved her and made her run 20 miles on a treadmill every day, she’d still have huge lumps of fat on her thighs. The regular bath of insulin around those cells makes the stored fat very hard to access.

        Insulin doesn’t explain everything, but neither do “calories.” The problem certainly wasn’t that the woman in that picture needed to Eat Less and Move More.

        • Soluble & insoluble fibre affect the “kcals in” side of the Energy Balance equation (even though they appear to be on the “out” side). It means that we don’t really know how many calories we’re eating.

          Have you read Lyle McDonald’s The Energy Balance Equation?

          “Do we absorb all the fat we eat?” Over 98%, unless we are ill (e.g. coeliac disease) or taking a lipase inhibitor (e.g. Xenical). This has already been discussed on GT’s blog. See If you Find “Kinbrum”, you can see all my comments there, spread over GT’s 2 blog posts.

          “You might want to look at the photo of the woman in Taubes’s new book–although it’s a bit horrific. She has two melon-sized lumps of fat on the front of her thighs. They are there because those are the sites where she injected insulin over many years.” Insulin certainly affects fat-mass distribution. However, it can’t create fat-mass out of nothing.

          In people not injecting insulin (the vast majority of the population), insulin levels around the body are constant. Therefore, in the vast majority of the population, fat-mass distribution around the body due to insulin is constant. Other hormones affect fat-mass distribution, hence android & gynoid body shapes.

  12. David I

    Exactly my point. We don’t know how many calories we are consuming, and we don’t know how many we are expending, and we don’t know how many we are failing to absorb, and we don’t know how many we are spilling.

    That is why I find “Energy In = Energy Out + Energy Stored” to be singularly uninstructive. It is nothing but a truism.

    Practical applications of it are usually oversimplistic, since it is often a priori assumed that we can affect one part of the equation without affecting the others. But changing Energy In can have an effect on Energy Out. And changing the type of Energy In can affect Energy Out–and also Energy Stored.

    No one suggested that fat is being created out of nowhere.

    As to whether continuously high levels of circulating insulin predispose to accumulating fat, I didn’t realize there was a debate on the topic. It certainly isn’t a concept that Taubes invented. And Taubes may be overfocused on insulin responses to carbohydrates. I think his biggest failing, however, is that he hasn’t been more concerned with insulin resistance as a factor.

    There is also considerable evidence that how you burn calories has an effect on weight/fat loss and gain. As good as walking is for you, it doesn’t deplete muscle glycogen in most of the body, or go far toward restoring insulin sensitivity. Intense exercise, and some degree of anaerobic activity, predispose not only to increased insulin sensitivity, but also to an increase in the number of mitochondria. Yet many people continue to insist that the only relevant factor is the number of calories burned in an exercise session.

    • I think that we’re on the same wavelength. I also think that the basic problem is Insulin Resistance (IR). Instead of drastically reducing their carb intake to suit their IR, people should be tackling their IR. A change of diet is still a good idea, as the SAD & SED are pretty dire.

      On Wednesday, 2 February 2011, I blogged about how to tackle IR. I’m not posting a link, as I don’t want to end up in the spam folder again!

  13. David I

    By the way, CarbSane’s own diet approach for weight loss was Very Low Carb.

    If it’s all about calories, why does she say on the sidebar to her blog that, “I’ve struggled with my weight my entire adult life but consider myself to have finally conquered that demon. I shed 80+ eating VLC (<20g) most days with planned cheats."

    • Because VLC allows her to keep “calories in” under control. LC allows me to keep “calories in” under control.

      Just because counting calories doesn’t work doesn’t mean that calories don’t count.

      We are not saying that it’s all about calories. What we are saying is that you cannot be as gluttonous as you like on protein & fat and not gain weight. GT says that you can. What say you?

      • David I

        I am as “gluttonous as I like” and don’t gain weight. I never, ever deliberately restrict my caloric intake. I eat until I don’t want to eat another bite.

        The key there, of course, is partly “as I like.” I find fat and protein highly satiating, and find that the satiating effects last for a long time. That last bite of a cheese omelette cooked in butter often isn’t appealing. In fact, sometimes thinking about one more bite makes me queasy.

        Of course, those who want to be outraged over Taubes invariably define gluttony as deliberately eating more than you want to eat. This reminds me a great deal of how conservative commentators dela with statements by Obama–they deliberately spin the words to mean something outrageous, and then get outraged about their own deliberate misintepretation. I’ve asked around, and most people think that gluttons are just people who eat all they want.

        In any case, if I deliberately stuffed myself with as much protein and fat as I could bear that I still wouldn’t gain weight? Probably not.

        On the other hand, overfeeding studies show quite clearly that deliberate intake of massive numbers of calories does not result in weight gain that is directly proportional to the caloric intake. Various mechanisms (including many we probably haven’t yet discovered) kick in to prevent infinite fat storage, and people in overfeeding studies invariably find that their weight plateaus at some point.

        I think that one of the reasons I was unable to lose weight easily even with calorie restiction on a high-carb diet was that it tended to slow my metabolism.

        But I also believe that when the body adapts to use of fatty acids it does so by upping the enzymes and other mechanisms needed for burning fat as the primary fuel, and this makes it easier to draw on fat reserves for energy. I think that when the body is geared to running on glucose these mechanisms are not maximized and therefore the rate of fat loss is inherently limited. In such a case, in the absence of enough readily processed fuel, I think the body’s choice is to go into energy-conservation mode, tending to lower BMR, NEAT, and spontaneous physical activity.

        Insulin is a player in all of this, but it isn’t the only player.

        We know from short-term experiments that low-carb diets sufficient to result in gluconeogenesis result in an extra burn-off of about 80 Calories a day–although the gluconeogenesis itself accounts for only 34 Calories of that total. I suspect that when the body optimizes itself for running on fats (which wouldn’t be seen in these short-term lab expriments), that the total average burnoff is probably higher–but there may be a great deal of individual variability in this regard.

        The National Weight Control Registry isn’t perfect, since everything is based on self-reporting. But the average 300 calories per day greater intake reported by low-carb eaters in the NWCR is in a range that seems reasonable to me. We know that low-carb burns at least some extra calories through gluconeogenesis and some other metabolic effect. Add in perhaps a slightly higher RMR on top of that, and maybe higher NEAT and spontaneous physical activity–and maybe factors we don’t yet understand–and I don’t find 300 additional Calories a day at all unlikely.

        Do calories matter? Sure, but in the same way that interest rates matter to the economy.

        My problem with the standard Calories In – Calories Out dogma is twofold.

        First, it doesn’t tell someone what effect they will get by cutting a set amount of Calories from their diet, even if deliberate exercise is held constant. Knock out 100 Calories a day, and you might lose the predicted 0.194 pounds. Or you might lose more. Or your metabolism or NEAT might slow, and you might even gain weight.

        Of course, if you don’t get the expected result, your doctor will tell you that it’s your measurements that are wrong, because, after all, we’re talking about the Laws of Physics here. (I have yet to meet a doctor or nutritionist whose understanding of the Laws of Physics is anywhere near as good as mine. In general, they only had enough physics and chemistry to get them into med school.)

        Taubes’s stuff–which is not, I hasten to add once more, original, but based on the work of many researchers–is oversimplistic, but it points the way to important research areas.

        So, I think Calories In matter. But I think the type of Calories matters as well, and that simply cutting Calories per se can lead to somewhat unpredictable effects–including obese people with startlingly low metabolic rates.

        I also think that Calories Out matter–and that the specific way the energy is burned (resistance exercise vs cardio vs HIIT vs cold-water immersion) also matter.

        So, yes, I think we’re in general on the same wavelength.

  14. “I am as “gluttonous as I like” and don’t gain weight. I never, ever deliberately restrict my caloric intake. I eat until I don’t want to eat another bite.” You are still getting magic. What about those who don’t?

    “On the other hand, overfeeding studies show quite clearly that deliberate intake of massive numbers of calories does not result in weight gain that is directly proportional to the caloric intake. Various mechanisms (including many we probably haven’t yet discovered) kick in to prevent infinite fat storage, and people in overfeeding studies invariably find that their weight plateaus at some point.” The body can’t increase metabolic rate ad-infinitum. Look-up 2,4,dinitrophenol. As weight increases, NEAT decreases. Look-up Manuel Uribe. He had almost infinite fat storage.

    “Insulin is a player in all of this, but it isn’t the only player.” I Agree.

    As you pointed out “change in weight = calories in – calories out” is a truism, but worthless. Our appetites & health are determined by what we eat and how active we are. I’m off for 2 rashers of bacon, 2 meaty sausages, 2 eggs & a small pile of veggies, followed by a long walk!

    • David I

      “You are still getting magic. What about those who don’t?”

      I’m not sure I’d describe it as “magic.” But, yes, I find consuming fat without carbohydrates to be self-limiting. I used to be able to take on a baked potato slatered with butter and sour cream, of a large bag of tortilla chips, but I find that my appetite for butter or sour cream or oil on their own to be quite limited. Even my appetite for heavily buttered broccoli is pretty limited.

      I have a friend who had a hard time losing weight and controlling appetite, even low-carb. But I found that friend was deliberately limiting fat, too, through careful portion control. Eating more fat turned out to solve that problem, my friend’s stall broke, and the excess appetite disappeared.

      I’m not saying that will work for everyone. For example, I also seem to be able to drink wine without drinking to excess–not because of my superb self-control, but because beyond some point, it doesn’t seem appealing. Again, doesn’t strike me as magic. I’d be more inclined to describe those who can’t stop drinking as having a disorder.

      Perhaps I’m lucky to have these self-limiting mechanisms. Or perhaps I’m just normal. (I’ve certainly met dozens of other people who have lost large amounts of fat and then maintained that loss on low-carb diets, without ever deliberately limiting calories.)

      Or perhaps there are several flavors of normal.

  15. Michael

    Using low carb for weight loss works well that’s for sure. I’ve lost the weight I put on eating lots of cakes by cutting all carbohydrates and overeating fat for a couple of days. I lost 2 pounds per day until I got close to my usually stable and decently lean pre-binge weight and the last two pounds clinged on a little longer. A few weeks before I tried to gain weight by overeating fat & protein for almost two weeks and the most weight I gained was 3 pounds and that extra weight went away overnight when I stopped overeating.

    I don’t know if overeating fat as opposed to eating the quantity that satisfies my appetite made some difference in the results but I experienced a weight loss and reached a weight gain plateau both times on a continuous high surplus of fat and protein and a very low level of carbohydrates.

    There’s probably like you suggest some hormonal interaction that sets this body fat set point, the one the body aims for. How it works I don’t know for sure but the simple caloric balance model which is the basis of the Eat-less & Move-more prescription, that needs to be updated.

    and it’s a good thing that the energy model for weight loss doesn’t work as advertised because counting the calories you eat gets annoying pretty fast.

  16. Kate

    Adding fats, in two phases, completely changed my system, and I still eat plenty of carbs, but mostly healthy ones as in multi-grain, etc.

    1) I used Seth Roberts’ olive oil (1-2 T each am, an hour before food), which seemed to decrease insulin levels (my hunger began to lessen, and I was satiated more quickly all day). I lost a good amount of weight, and was less hungry.

    2) I then dropped the oil, and began fasting all day until afternoon on weekdays(, during which my hunger has almost disappeared, except after several days in a row of eating all day, and I lost a good amount of weight, but still had an outsized belly (huge, with no bulge anywhere else!).

    3) I added saturated fats in huge volumes, as desired (as much as a 1/2 c. of coconut milk in coffees/teas, large glasses of raw whole Guernsey milk, and tons of pastured butter and raw milk cheeses) compared to my lowfat intake of years past, when I cooked with olive oil, rarely ate any butter, and ended up bingeing on ice cream pretty regularly. I no longer crave ice cream, am almost the same weight (5-7 pounds heavier, but still am about the same size), but have shifted from an apple shape to a pear shape.

    The positive profile shift to an insulin sensitive person from a borderline resistant person was a long process, but the carbs weren’t the problem, really, it was the lack of natural saturated fats, most likely. I still eat whatever I really want.

    Also, the gut research on obese people which shows issues in the flora was probably corrected by the raw milk “pathogens” which have helped in many unmentionable ways. ;)

    • Todd


      It’s great to hear this update from you. What your journey illustrates is that changes in body composition and insulin sensitivity don’t happen overnight, but are the result of concerted, sustained changes in diet and lifestyle. Last I heard from you I was aware that you had embarked on raw dairy as a source of natural saturated fats. I’d be interested to learn more about why you think raw milk is superior. Is it the composition of fatty acids, the microbial content, or something else? Are there any references we should read up on?


      • Kate


        I’ve been slacking in lots of ways, but have kept up with the healthy versions of saturated fats (coconut oil/milk, raw milk, pastured hens eggs, butter from pastured cows) and really don’t feel the need to eat much at all, especially compared to past years! The shape-shift is continuing…

        As for raw milk, it fits with my “avoid the industrial food complex because it’s all disgusting due to slack processing standards” rule. For safety’s sake, raw milk is better (pasteurizing means that filthy milk can be heated then sold to us – raw milk meets much higher standards, and is regulated in SC as grade A dairy where I buy it). I don’t like the idea of homogenizing the milk – the fat globule size/composition is altered and some studies suggest potential changes in our bodies as we process these unnatural globules. The heating changes the proteins, which may cause allergy issues for some – my daughter has seen improvements overall in her health, probably due to needing saturated fats (she’s a vegetarian). Bacteria which are beneficial are a main reason, including the “bad guys” which help us build up immunity slowly and consistently (so the odd ecoli burger has a lesser chance of hurting us). The “good guys” allow me to let milk sit out a few days, making curds and whey – the whey is used for lacto-fermenting veggies (remember Seth’s posts on fermented foods) more safely than heated pickling (according to the NC State Extension!), and it increases vitamin contact due to metabolism by the “bugs”. Whey is useful for soaking beans and grains, to “neutralize anti-nutrients” according to the literature – irritants to our systems, apparently. Spoiled raw milk never smells disgusting like the other stuff does, just “cheesy” in a much less gross way. Still haven’t interested my family in eating the curds, which are technically cream cheese. There’s a great book, (written by an N.D.) called The Untold Story of Milk, and is a catch-all for many traditional foods, but has a bit of a “joiner” feel to it. To read about raw milk specifically, look at which is a subtopic of weston a price foundation’s work.

        Once you drink raw whole milk for a little while, you won’t be able to drink the processed stuff, it’s just so filthy – not really milk, after all of the processing and “industry standard practices” additives blended in. Ditto eggs/meat from pastured chickens who live outside, graze on grass/bugs, and are slaughtered by the farmer. Clean = worth eating, in my book.

        You Californians can get Organic Pastures raw milk from your grocery stores, but I’d find a small farmer with organic pastures if you pursue good clean eggs. They have ridiculously rich yolks – darker than the color of cheddar cheese, and you can eat the yolks raw with no fear of salmonella.

        You’ve posted a bunch of new stuff – thanks for all of the excellent reading. I’m still trying to vary my fasting, and will focus on that and read your updated IF stuff – I tend to get stuck in a rut of just not eating til late in the day, and I know that’s not so good.

        Hey – My friend Ashish Mukharji (in SF) is publishing a barefoot running book to be released this year. I teased him about it (as if we need another book) but it turned out to be really good and helpful for beginners, and an interesting read for seasoned runners in general, lots of interviews, and a great foreword – check it out if you’re still interested in the topic – I’m not just saying this because I got a credit for reading it. ;)

        • Todd


          Thanks for the information on raw milk. I’ll look around to see if I can find the Organic Pastures brand you mention.

          Please do let me know how to get a copy of Ashish’s book on barefoot running. I just completed three 6-mile segments of a 200-mile relay from Calistoga to Santa Cruz. Last year I did the race in regular running shoes. This year, I ran it in my Vibram Five Fingers, and cut one minute off my pace! Plus, it was a lot of fun. The only real challenge I had was on a very steep downhill 3-mile section towards the end. Running downhill in Vibrams tends to jam your toes and requires a lot of control to avoid hitting your heels too hard. So I’m looking for advice on downhill barefoot/minimalist running technique.


  17. Todd

    Here is a very interesting new take on the causes of obesity. Beth Mazur summarizes a new study by diabetes researchers Unger and Scherer, suggesting that obesity is the body’s attempt to defend itself from the liver damage associated with hyperinsulinemia:

    According to Mazur, this new metabolic model may help bridge the chasm between the opposing sides I described above in my post:

    First, it fills in some of the gaps from theories like Taubes’ or Lustig’s that focus on one specific factor. If you’re like me and wonder why some (like Asians) do well on a traditional high-carb diet when Taubes makes such a good case against carbs, then a possible explanation is that their diets (at least until recently) included far less of the excess sugar and industrial oils found in our diet (they also don’t eat as much wheat).

    Second, it is FAR more satisfying an explanation than “calories in vs calories out” and a whacked-out interpretation of the laws of thermodynamics.

    Finally, it seems to me that this hypothesis might explain why diets that are very different seem to have good results when studied. For example, an Atkins or Eades low-carb diet versus an Ornish low-fat diet. Neither removes all three of the big three from above explicitly, but in practice, they certainly remove one or more: Atkins’ low-carb diet removes sugar and grains; Ornish’s low-fat diet removes most fat and also a lot of refined sugar and starch.

    The other nice thing about this “hepatic” theory of obesity is that it should be very testable.

    • First forgive my english, frenchman here. ;-)

      Todd wrote: “it seems to me that this hypothesis might explain why diets that are very different seem to have good results when studied”

      I keep reading stuff like this here and there, but never get to read the actual “studies” showing that very different diets could yeld good results.

      Actually, I’ve read a lot of studies which shows that most diets don’t get good results, if any results at all. I don’t mean after 3 weeks or so(even a badly designed low-cal diet can seem to be effective if studied this way) but after, say, a year, two years….

      But I’ve read a couple studies showing that low-carbs diets do far better than any other in the long run. Oh, and bring much better lipid profiles, BTW. Get it from a vegetarian, formerly convinced that low-carb diets were a fad, until he actually studied them…

      Personally, I think that all this talk about “different diets can be good, they’re just for different people” is just a reflection of modern cultural relativism. It doesn’t stand some objective, unbiased scrutiny.

      I’m willing to change my opinion, though. Where are the studies showing the good results of those diets **even when scrutinized for intepretation bias**..?



      • Todd


        I’m certainly not a cultural relativist; I believe in objective reality. But that doesn’t mean there are not different routes to objectively good health. I personally eat a low carb/Paleo diet and practice intermittent fasting to lower my basal insulin. I believe that low basal insulin results in numerous heath benefits, including low body fat, reduced inflammation and infection, reduced risk of CVD and cancer, etc. But there are other routes to reducing basal insulin besides eating low carb / high fat / moderate protein diets. As I mentioned above in the article, Stephan Guyenet has cited Lindeborg’s studies of the Kitavans, who eat a diet of 69% carbohydrate, 21% fat, and 10% protein, and they have average fasting insulin levels of 3-4 IU/ml, vs.. 6-7 IU/ml for Swedes. Similarly, the Okinawans eat a diet relatively high in low glycemic carbohydrates and low in fat, and yet have low insulin levels, and exceptional longevity.

        The common element in low carb Paleo, high carb Kitavan and low fat Okinawan may be the consumption of low levels of fructose (whether as a monomeric sugar or incorporated into sucrose), resulting in reduced insulin resistance, lower basal insulin, and a resulting reduced appetite that naturally leads to reduced intake of calories. (See O’Donnell and Lustig). These diets also all appear to be non-inflammatory.

        So we don’t have to be relativists to appreciate that there may be more than one route to health and longevity, and that behind these seemingly different diets there may be a common metabolic pattern.

  18. Kate


    I found a comment somewhere about metabolism increasing during fasting (of up to four days) due to higher levels of norepinephrine. As a result, I’ll be jumping off of the fast-5 wagon for a while and trying intermittent fasting. It’s possible that some benign atrial flutter and benign PACs (?) I had this past year have resolved during a month and a half of not doing fast-5 this spring (and gaining back ten pounds, a combination of not fasting and not being sure I could safely run, while heart testing took place). I had the heart weirdness before fasting, and it got better with weight loss, too. I also dropped all caffeine during these two months, so fasting/epinephrine might’ve had nothing to do with it. I’ve noted eatstopeat’s routine, and will do a 24 hour fast twice a week, and see how that works (I’ve never attempted the 36 hour fast you have done). I’m likely to be a light eater on “nonfasting” days, because I now really prefer not eating until late in the afternoon. On fasting days, especially, I’ll be running sprints. Thanks for being such a good resource – you save me lots of time surfing the tubes….

    • Todd


      Actually, I consider fast-5 to be a type of intermittent fasting, so you are already getting a lot of the benefits — including extended periods of low insulin and upgregulated adrenaline. Extending the fast will enhance those effects, but it is more a difference of degree than a difference of kind. If you have any concerns about your health, I’d advise extending the fasting period very gradually. Try a few 24-hour fasts over a few weeks before going any longer. My longest fast so far has been 75 hours, but I built up to this very slowly over many months, adding no more than 6 hours to my previous longest fast. And after a long fast, I’ll go back and mix up my pattern with some fast-5 days and 24-hour fasts. I think that Art DeVany’s New Evolution Diet is very smart about the virtues of randomizing eating patterns. He and Martin Berkhan also advocate the type of fasted workouts that you mention, and I find these invigorating.


  19. danimal

    Thanks Todd for your synthesis of the information and interesting conclusion.

    I haven’t read Taubes’s book but does he mention the Kitavans and other high carb eating groups? Based on Stephen’s info, that right there shatters taubes hypothesis that carbs drive insulin resistance drives fat. There must be something wrong that has accumulated (poor food choices is my guess) to drive the metabolism to the point of Taubes conclusions since the theory doesn”t hold water with normal people

    “Now let’s ask the question of whether insulin sensitive (IS) individuals can accumulate body fat on a high-fat, low carb diet. According to Krieger and CarbSane, this should be no more difficult than on a high-carb diet”

    Personally I think both types of diet would be hard to gain weight on. When I was low carb about 1.5 yrs ago and I stopped a little over a year ago I was my leanest ever. But I encountered Matt Stone’s blog and made me think again about potatoes. After that point, I reincorporated tons of white rice and potatoes, stuffing my self as much as possible with carbs, meat, eggs, and high fat greek yogurt, and I gained fat but very slowly even when I’d stopped exercising

    • Todd


      Actually, Taubes has been confronted with this criticism many times, and I think he answers it in his new book, “Why We Get Fat” and on his podcast interview with Jimmy Moore. The objection is raised for many populations, not just the Kitavans, but also the Okinawans, who eat a lot of rice, which is of course high in carbohydrate. The answer is threefold: (1) It is not the percentage of carbohydrate that drives insulin, but the absolute amount, the glycemic availability, and the frequency of carbohydrate. Because the Kitavans and Okinawans eat a fairly low calorie diet, the amount of carbs they eat each day is a fair bit lower than that of the average American. So while their percentage of carbs is higher, the actual “dose” of carbs is lower; (2) Taubes is clear to point out that carbohydrates are a necessary but not sufficient condition for getting fat. That is to say that many people can tolerate high carbs without becoming insulin resistant, either through individual or group genetics. But those who are not blessed with such genetics will get fat on carbs. He makes an analogy with smoking: Far less than 100% of the population will in fact get lung cancer from smoking; many people are apparently genetically protected. But for those who are vulnerable, smoking is a powerful inducer of lung cancer; (3) finally, under the influence of Robert Lustig, Taubes has recently highlighted fructose-containing carbs (which includes sugar) as the primary culprit in causing insulin resistance, and so he has somewhat modified his stance: carbs are fattening primarily if you include sugar and fructose in your diet. He points out that the Japanese and Kitavans eat very little sugar relative to other populations, so they are far less prone to the effects of carbs.

      I actually think he and Lustig may be right about fructose and sugar, at least at high levels. The picture that emerges from all of this is that obesity has two prerequisites: insulin resistance plus high carbs. They often go together, but it is possible to largely avoid getting fat if you have only one of the two. So the Kitavans eat carbs (but are not insulin resitance due to genetics and/or avoiding sugar); whereas those on high fat low carb diets may have some degree of physiolgical insulin resistance, but they can stay lean by limiting their carbs.

      Everyone is always looking to “disprove” the other guy. I prefer to believe that there is often enough truth in alternative hypotheses to learn from them and find out that they are merely parts of the same elephant, each being looked at under a restricted set of conditions. The way to accommodate the dueling hypotheses is often to identify the conditions under which each partial hypothesis is true, thereby finding a larger overarching hypothesis. Just as Newton’s physics represent an important subset of the more broadly valid Einsteinian physics, I think that Taubes’ theory remains useful and true for a wide range of conditions that we live in in the West. But certainly studying the apparent anomalies helps us find a more broadly correct perspective. And it may even have practical benefits. Specifically, if you can avoid becoming insulin resistant by limiting intake of sugar and certain fatty acids (like palmitic acid) , adding magnesium, Vitamin D and essential fatty acids to your diet, exercising, and perhaps doing intermittent fasting, then you may be able to tolerate a much higher carbohydrate intake than the average insulin-resistant American.

      I note that your recent diet of white rice, potatoes, meat, eggs, and high fat greek yogurt doesn’t have very much sucrose or fructose in it — does it? I’d be interested to know how often you consume sweets like ice cream, candies or pastries, or sugary fruits like bananas, peaches pineapples, watermelon (as opposed to low sugar fruit like berries and apples) at the same time you are on this diet with rice and potatoes.

  20. Mike Ellwood


    Thank you very much for the article, a much-needed contribution. I come to this as a “Taubsian”, since it was GC, BC (and Gary’s various online articles) that forced me to confront my use of carbohydrates, and set me off on a path to reducing my weight and improving my health.

    However, I try to be open-minded, and for example, I think Carbsane has made some salient points (when one gets past the emotion) that need addressing, although I’ve only read a fraction of her stuff.

    One of her points that I’m not sure you addressed above is fairly fundamental: She is convinced that Taubes (and others) are wrong when he says that adipocytes are the last thing to become insulin resistant. Her argument is probably more complex, but from memory, I think she says they are the first, and this is borne out by the fact that the obese usually have excessive amounts of FFAs/NEFAs circulating in their bloodstream. Fat therefore gets stored in the liver, in intra-muscular tissue, and maybe other places, and causes all sorts of problems. Since it’s such a fundamental difference to Taubes, it seems like it’s a mystery that’s worth solving, and one would think it were easily testable, but I only speak as an amateur.

    On a slightly different tack: I’ve been reading the fascinating comments by a contributor known as “Its the wooo2″ on Stephan Guyenet’s blong, on the subject of leptin resistance. She is also somewhat emotional, but seems to know her science. Her experience was that she reduced from obesity to extremely low body fat by low-carbing and she is in the Taubes camp on insulin resistance being the key, not leptin resistance. However, she then had problems (so she said) keeping the weight off because her adipocytes had grown in number during her weight-gain days (e.g. lots of “yo-yo” in childhood), and shrunk in mass during her weight loss, with the net effect that they were producing a oo-low level of leptin. They “needed” her to get fat again in order to stop sending the hunger signals.

    She noted that it was more importance in women than men, because in men, testosterone can to some extent do what leptin might otherwise do. It’s more involved than my brief paraphrase, but I found it a fascinating story. She had also taken part in a leptin trial, and had found that small doses of subcutaneous leptin enabled her to keep the weight off, and she said this proved she was not leptin resistant.

    Taubes and fructose: I think to be fair to Taubes, in GC, BC, he comes down pretty hard on fructose, and I seem to remember he fingers it as a good candidate for causing insulin resistance. It’s possible he’s been further influenced by Dr Lustig since then, but I don’t think it came exactly as a Damascus Road conversion. There was after all, an incredible amount of stuff in GC, BC, and an even larger amount of stuff had to be left out to keep it down to a “reasonable” 601 pages all-in.

    @David: One of my few criticisms of Taubes would be that he didn’t explain insulin resistance very well in GC, BC; I was left confused by it. I think it’s done better in WWGF, assuming his analysis is correct of course.

    @Matthew: I wonder if liver would be a good, and sufficient, and relatively natural source of glucose? There are other good reasons for consuming it, c.f. Masterjohn.


  21. Wayne Johnson

    Your synthesis seems reasonable to me until “3.In insulin resistant individuals, elevated blood insulin levels stimulate hunger and the drive to eat; this effect is largely absent for insulin senstive individuals due to superior blood glucose control”. I seem to remember a lot of clinical studies/reviews where insulin is called the “satiety hormone”. I probably am misrembering, or I’m guessing that this depiction is controversial, but…

    Your thoughts?


    • Todd

      Wayne, Your question is a good one, about a point which has confused many people. It turns out that insulin can act as both an appetite stimulant and an appetite suppressant depending on the site of action. In the periphery (the physiologist’s term for circulation to the organs and tissues other than the brain) elevated insulin acts to inhibit the availability of glucose and fatty acids. This effect is initially also experienced in the brain, since glucose and fatty acids freely diffuse across the blood brain barrier, leading to an increase in appetite vs. what would be experienced at lower insulin levels. Once insulin crosses the blood-brain barrier — which takes time — it acts in an OPPOSITE manner centrally (in the hypothalamus of the brain), leading to satiety. So elevated insulin initially increases appetite and later suppresses it. This counter-regulatory effect is nicely described in this reference:

      In those with pronounced insulin resistance, the diffusion of insulin across the blood brain barrier is impaired. In these individuals, it takes more time, and higher levels of insulin, for insulin to get into the brain and dampen appetite:


  22. Eric

    The HIIT training is almost irrelevant for someone’s goal of losing fat while retaining as much muscle as possible. It increases your metabolic need which increases your appetite, which makes you eat more to fill the extra energy used. Why not just eat a low-carb, high-fat, moderate protein eucaloric diet and skip the cardio?

    Your insulin will be low, you’ll be burning fat for energy and using ketones for a good portion of the blood sugar stabilization, and sparing your muscle.

    Better yet would be to skip the catabolic HIIT cardio and anabolically weight train instead. Then you are building up muscle (which increases your basal metabolism, i.e. you burn fat faster just by standing still). The added carbs you’ll require for weight training will be burned during the weight training session so you can get right back into ketosis after the session is over.

    Best of both worlds!

    Add intermittent fasting and now you are rockin’!

    Just my opinion however :)

    • Todd


      I’m with you on the benefits of low carb or ketogenic diets, intermittent fasting and weight training. But don’t discount the benefits of strenuous interval training — for example, sprints. This is a great way to build insulin sensitivity and conditioning. It doesn’t inevitably increase appetite, particularly if you combine it with IF or low carb. When I go running, I don’t “jog”, but push myself hard periodically. My appetite is usually suppressed for several hours after an intense run, although I always rehydrate and quench my thirst with water.


  23. Hector Wilberforce

    Don’t really agree with the conclusion.

    “Obesity is a disorder of excess fat accumulation resulting from insulin resistance (and leptin resistance), which stimulates appetite and naturally leads to caloric imbalance, including overconsumption of both carbohydrates and fats.”

    How is it then that people like myself can (I did this for experimental purposes) gain weight deliberately on a high calorie diet easily then? Most of the diet consisted of high fat rather than high carb. My appetite was next to nothing the whole time because I was “over eating” and my body didn’t want or crave food but I forced myself to eat 4000kcal every day. Sure enough weight gain happened but after I stopped it dropped off again in about 3 weeks. None of this gain of 16lbs in 6 weeks which occurred had anything to do with insulin resistance.

    • Todd


      Your experiment is an interesting one, and I have no doubt that people can force themselves to gain weight by deliberately overeating. But the term “obesity”, as most people use it, refers to a serious metabolic condition — now becoming an societal epidemic — in which people find themselves gaining extreme amounts of body fat, despite their wishes and their best efforts. It is a condition in which people are constantly hungry, craving food, even though there is no shortage of calories stored in their body. In your experiment, you did not become obese or suffer cravings, and your transient weight gain was easily reversed.

      Obesity is an abnormal, chronic condition that calls out for explanation. Obviously the obese overeat, but the critical question is what drives them to do so. And I think we can locate the problem in a metabolic disorder that involves a disturbance in appetite signalling, via resistance of hormone receptors to the hormones that control appetite — principally leptin and insulin, but there are others. I believe the key control point for appetite regulation lies in hyopthalamic circuits, as I discussed in Obesity starts in the brain. There are many possible upstream contributors to this regulation (type of food, stress, inflammation, genetics, etc.), but they all ultimately go through the hypothalamus.


  24. Hi Todd. Enjoyed reading your article. Many thanks for spending months working on a project so that I and others can spend minutes digesting it.

    You wrote: “It is known that Type 1 diabetics, who have no insulin, shed fat readily and have trouble holding onto it without injections.”

    As a member of the club, so to speak, I just wanted to make sure you understood the reality here.

    Without any insulin, and with initial blood sugar conditions in “normal range,” roughly 70-110 mg/dl, there is no hunger, everything’s operating pretty good, i.e., blood levels of nearly everything are normal. Yet, as a consequence of having no insulin, a type 1er’s BG will begin to rise.

    Above 120, but less than 240 mg/dl, a type 1er will start getting hungry, and will likely begin burning fat as fuel due to the process you outlined in your article.

    Above 240 mg/dl, a type 1er will burn only fat for fuel, and the ketones in the blood will quickly move the individual from ketosis to full blown ketoacidosis. They will certainly shed fat fast, then muscle tissue, then bone tissue, then brain tissue, then, after a month or so, die.

    The will also have polydypsia, polyphagia and polyuria, increased thirst, increased eating and increased urine production. That last item, polyuria, will help to lower the blood sugar, perhaps under 240, but only if they stop eating. Nevertheless, it doesn’t work that way, because the increased hunger will only drive the diabetic to eat more, and it will be almost impossible to get the BG under 240 without insulin.

    Why am I writing this? Well, because your one sentence was simply, pardon me, well, a little too simplistic. Because nearly every type one diabetic takes insulin, thus, they don’t shed fat readily at all!

    That exogenous insulin sets up us members of the club to burn glucose as a fuel almost as a rule, even if aiming for ketosis. the footnote here is that I advocate a near-zero carbohydrate diet, and theoretically, could be in ketosis, however, in order to mitigate the so-called dawn phenomenon, take only long-acting insulin–Lantus–once or twice a day. Nonetheless, it’s still insulin, but it does keep my BG fairly steady but only if I don’t eat carbohydrates. Any carbohydrates necessitates taking that fast-acting stuff.

    In short, we do not shed fat easily unless we don’t take exogenous insulin. We could shed it quite fast–the newer members typically do that–but that’s not a particularly sustainable process.

    Best wishes… – lc (nice initials, eh?)

    • Todd


      Good explanation. I did understand your point, which is why the last two words in my sentence were “without injections”. Clearly, with their normal injections of insulin, diabetics will not shed fat.

      While I agree with you that going without insulin injections is typically not sustainable, it is possible to cut back significantly and even eliminate insulin injections. Richard Bernstein outlines a comprehensive diet and exercise program for doing just that in his magnificent book, Dr. Bernstein’s Diabetes Solution.


  25. Vinod

    just a comment about eating a “caloric surplus” of fat compared to eating a caloric Surplus of carbs: after about 3-4 days of low carb high fat moderate protein diet, nutritional ketosis is reached, and when this is the case, the surplus calories from fat are actually excreted in the form of ketones (lungs, kidneys). Thus, it would be hard if not impossible to gain weight on a caloric suplus of fat (this is also my personal experience), since the amount of fat ingested would have to be so high as to compensate for the calories lost in urine and breath. This would not be the case for a caloric surplus of carbs, since after the storage capacity of the Body for glycogen is reached at around 300 g, the Surplus carbs are converted and easily stored as fat. The storage of fat in the liver then leads to a steadily increasing Insulin resistance.


  26. Vinod

    infact, in a carb surplus diet, apart from inreasing hepatic intracellar fat storage, the increasing level of glycogen storage in muscle and liver itself leads to increasing insulin resistance, increasing insulin levels and increased fat storage. All this does not happen with a fat surplus diet with moderate protein intake (1-1.5 g/Kg)

    In the case of non caloric-surplus fat and carb diets, the fat oriented diets have the advantage of not inducing non enymatic glycation of all proteins and increased oxidative and inflammatory stress leading to corresponding accelerated aging processes.


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