Is Insulin REALLY To Blame For Making People Fat?
Almost two years ago now, I read “Good Calories, Bad Calories” by Gary Taubes, and my world was officially rocked. It all made sense….Carbs make us fat, plain and simple. Carbohydrates and insulin combined are the devil, and together are responsible for obesity, diabetes, heart disease, cancer, and every chronic disease the average person can think of, given five solid minutes. But is that really true? Is this simplistic, yet entirely plausible hypothesis the truth, or just another off-the-mark explanation for a problem that we cannot possibly understand?
Stephan Guyenet of the “Whole Health Source” blog posted an article on January 21st of 2012 entitled “Insulin and Obesity: Another Nail in the Coffin”, that attacks the insulin hypothesis, and hopes to put the controversy to rest. Whether the article is convincing enough to actually be counted as a “nail in the coffin” is really up to you, but if you read the article comments, you’ll see some people who agree and others who obviously do not.
Is insulin REALLY to blame for making people fat?
“There are several versions of the insulin hypothesis of obesity, but the versions that are most visible to the public generally state that elevated circulating insulin (whether acute or chronic) increases body fatness. Some versions invoke insulin’s effects on fat tissue, others its effects in the brain. This idea has been used to explain why low-carbohydrate and low-glycemic-index diets can lead to weight loss (although frankly, glycemic index per se doesn’t seem to have much if any impact on body weight in controlled trials).”
True. In my experience, although the glycemic index helps to give us a valuable insight into the speed at which food items absorb to affect our blood-glucose levels, it’s not really usable for weight-loss.
“I have explained in various posts why this idea does not appear to be correct (1, 2, 3), and why, after extensive research, the insulin hypothesis of obesity lost steam by the late 1980s. However, I recently came across two experiments that tested the hypothesis as directly as it can be tested- by chronically increasing circulating insulin in animals and measuring food intake and body weight and/or body fatness. If the hypothesis is correct, these animals should gain fat, and perhaps eat more as well.”
“They found that all doses of insulin reduced body weight gain, but only the 2 unit dose was statistically significant. They speculated that the 6 unit dose was less effective at reducing weight gain because it was sufficiently high to cause hypoglycemia (low blood sugar), which is a potent trigger for food intake. Total food intake was suppressed at all doses by insulin as well, but this was apparently not due to illness.”
“Contrary to what the insulin hypothesis of obesity predicts, chronically elevated insulin if anything seems to oppose weight and fat accumulation in animal models. This likely involves insulin’s action in the brain to constrain body fat accumulation.
The evidence suggests that:
- Experimentally preventing the increase in circulating insulin that occurs on fattening diets does not alter the course of fat gain in rodents or dogs (7).
- Experimentally elevating circulating insulin by creating liver insulin resistance does not lead to fat gain in rodents (8).
- Experimentally increasing circulating insulin by infusing it directly into the blood does not cause fat gain in rodents, but instead makes them leaner (above).
- Roughly a quarter of obese humans have normal circulating insulin and normal insulin sensitivity (“metabolically healthy” obese) (9).
- In Pima (Akimel O’odham) native Americans, one of the most obesity-prone populations in the world, and certain other populations, insulin resistance and higher insulin secretion consistently predict less body fat gain over time (10, 11, 12, 12a, 12b). This has not been observed in all populations, but the fact that it occurs in some casts further doubt on the idea that elevated insulin is a central contributor to fat gain.
Researchers have been studying insulin’s impact on food intake and body fatness for a long time, and among those who are the most intimately involved in the field, the idea that elevated insulin leads to body fat accumulation seemed rather unlikely by the late 1980s (13). Although biology is complex, and you can never be totally certain where scientific progress will lead, we have enough evidence at this point to say that this hypothesis is probably not correct. We now know that food intake is regulated by a complex ‘symphony’ of signals originating from the brain, fat tissue, the gastrointestinal tract and the pancreas, and insulin seems to play little or no role in this process on a meal-to-meal basis (14). In the long term, it may constrain food intake and body fat mass due to its actions in the brain, in a manner similar to leptin (although less potently).
We need a better hypothesis to explain why low-carbohydrate diets cause fat loss in many obese people, and we definitely need a better hypothesis to explain why obesity arises in the first place. An alternative hypothesis, that insulin opposes fat gain through its action in the brain, is plausible and has received support from a variety of lines of evidence. Insulin resistance in the brain, leading to reduced insulin signaling in neurons, has been documented in animal models of obesity, and likely contributes to fat accumulation. Therefore, the ‘insulin hypothesis of obesity’ that makes sense is that a reduced insulin (and particularly leptin) signal in the brain contributes to fat gain.”
So, as usual, Stephan makes a pretty convincing argument. Head on over to the blog and read the rest of the article, to get the rest of the details. Stephan cites two insulin related studies, and shows how the outcomes help to support his standpoint.
Two years ago, I wouldn’t have even began to question that insulin is the devil, but now I’m basically on the fence. This is mostly due to the fact that I have spent a long time on a ketogenic-Paleo type of diet, where I was in ketosis for an extended period of time, and yet I reached a point where I actually began to gain weight again. I started to regain some stubborn fat around my middle, and no matter how low I dropped my carbohydrate intake, and no matter how hard I worked at the gym, I just couldn’t get rid of it. Research leads me to believe that the prolonged low-carb state was actually doing my body more harm than good, by causing the production of cortisol, and possibly causing my thyroid to bonk, which possibly all led to my stress-related fat gain. If Gary Taubes is correct however, considering the distinct lack of carbohydrates from my diet, I should never have been able to gain weight in the form of fat. But I did.
If the insulin-obesity hypothesis actually was the be-all and end-all, surely my low-carb practices should have quickly whittled my body-fat down to almost nothing with great ease…..but it didn’t happen. Obviously, there are MANY other factors at play in body-fat regulation. Like Stephan says, insulin grants triglycerides access into fat-cells, but does not play a regulatory role:
“Insulin is required for fat storage in fat cells but it doesn’t regulate fat storage. Permissive vs. regulatory.” – Stephan Guyenet
I’ve actually begun to experiment upon myself, by significantly raising my daily carbohydrate intake, to see what happens to my body composition. I’ve been eating lots of fruits, and also lots of starches (white rice and sweet potatoes etc), usually targeted around my workout times, and I’ve already noticed a significant amount of added muscle, even after only one week of experimentation. Granted, I’ve put on a little body-fat too, but I’m waiting to see if it will normalize after my body adjusts from being very low carbohydrate for so long.
So what do you think? Is insulin really to blame for making people fat? Is Stephen correct in his views? Let us know, by leaving a comment below, or on Facebook.
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Barry Cripps is a Paleo-based Nutrition and Wellness Consultant, who operates out of Bowling Green, Kentucky.
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I am confused! I know that a symptom of type 1 diabetes (pancreas fails to make insulin) is weightloss. People will often get very thin prior to diagnosis. I also know that in type 2 diabetics that use insulin, if excessive weight gain occurs, doctors will reduce the insulin and leave blood sugar higher to lower weight.
Hi Lyndsey,
I suspect the entire issue is far more complex than we know. Honestly, I didn’t even know of this until Barry posted the article. It requires more research, that is certain.
Thanks for commenting!
I have never been a Taubes-ite. It was too simplistic and there were too many non-conforming examples for me to take it as a complete explanation of obesity and fat storage. But it did teach me a good deal about hitherto unknown associations and pathways. When all the washing has been done and our brains have grown sufficiently large enough to be able to understand the entirely complex mess that is diet and weight gain I am sure that the only single factor that will be found to completely predict and control weight gain and loss will be the single factor of Total-lifestyle-and-total-diet