There’s some controversy about the so-called Hormonal-Obesity model. I’d like to dig into some of the details here and this may get technical so bear with me if you want to get to the heart of the differences.
For the Hormonal-Obesity side let’s look at Jason Fung’s IDM site (12-Part Hormonal Obesity series). Some of the points from Fung’s position are:
- Exercise doesn’t result in weight loss (Exercise-Part 1).
- Caloric restriction doesn’t result in weight loss (Calories-Part 1).
- If certain foods (what to eat) or dietary habits (when to eat) affect metabolic rate, then a calorie is not simply a calorie (Calories-Part 2).
- The body tries to maintain a set-point and involuntarily raises Calories-Out to match Calories-In (Calories-Part 3).
- Fat stores are regulated by hormones (Calories-Part 4).
- Total Energy Expenditure drops when Calories-In are decreased (Calories-Part 5).
- Control of Calories-In, ie, portion control, is doomed (Calories-Part 6).
- The body will reduce expenditures even after the weight loss is done in order to regain the lost weight (Calories-Part 7).
- Weight loss stimulates hormones which cause the weight to be regained (Calories-Part 8).
- Viscous cycles of dieting and re-eating are the result (Calories-Part 8b).
- Low Fat-Low Calories have been shown in studies to not result in long term weight loss (Calories-Part 9).
- Overfeeding (eating more calories) results in increases in Total Energy Expenditure (Calories-Part 10).
- Dietary composition (macro ratios) determines weight loss/gain (Calories-Part 11).
- Historically, excessive carb consumption (starches and refined carbs) were recognized as the cause of body fat until fat became the villain in the 1950’s. (Hormonal Obesity-Part 1).
- Dietary goals were set by the US Government in 1977 which led food producers to change their products to be higher in carbohydrates and lower in fat and the result was people got fatter (Hormonal Obesity-Part 2).
- Obesity was hypothesized to be a hormonal dysregulation of fat mass. That is, there is a hormonal signal from the body that controls fat mass. For example, thyroid stimulating hormone (TSH) controls the thyroid. Growth hormone (GH) controls growth of cells. Sex hormones (testosterone and estrogen) control sexual maturation. These are called endocrine glands and the substances that control them are hormones. This is the hormonal Obesity Theory (HOT). (Hormonal Obesity-Part 3).
- Insulin causes Weight gain not Calories-In/Calories-Out (Part 4).
- We get fat because our insulin levels are too high. If we increase insulin, we gain weight. If we decrease insulin, we lose weight (Hormonal Obesity-Part 5).
Throughout each of these pages, Dr Fung presented quite a few lines of evidence for each of his point. Many of them are formal studies and others are anecdotal but each has persuasive value. It is worth reading each article to see the lines of evidence that he uses for each point.
Putting Dr Fung’s Theory to the Test
Fung’s position is that efforts which lower fasting Insulin levels will inevitably result in weight loss, so his cure is two-fold. One part is a Low Carbohydrate, High Fat (LCHF) diet. The other aspect of the cure is restricted time eating, ie, Intermittent Fasting (IF).
Foods containing carbohydrates cause Insulin release so Fung limits them. Fat causes almost no Insulin to be produced by the body. Protein, while necessary, causes Insulin release so Fung limits protein to relatively low levels. This is all towards the goal of reducing Insulin release from the body to the least amount possible.
The only problem here is that reducing a diet to protein and fat almost always results in a caloric deficit. And when people up their caloric intake they often gain some weight even with Low Carb/High Fat diets (albeit not too much typically).
I know Fung’s approach matches my personal experience when I gained a lot of weight while I was on Insulin and lost an incredible amount of weight quickly as I got my Insulin levels down. I lost over 30 lbs in the first month of LCHF.
I did keep food logs in the beginning as well which show I was eating at a caloric deficit at the time and had plenty of body fat to offset the deficit from fat stores. I’ve also overfed many times and not had much weight gain.
The Diet that You Do is the One that Works
For me, compliance has been relatively easy with Low Carb/High Fat and Intermittent Fasting. I tend to slip into these eating patterns anyway.
The Other Side of the Issue
The other side of this issue contends that it’s not as much about hormones, rather it is all about calorie balance. In one sense, this can be seen as a cart/horse question. But which is the cart and which is the horse? Or is it a more tangled problem like a chicken/egg problem? Which came first?
Representative of the Other Side
For the other side, I picked Lyle McDonald because he has written on the subject in a thoughtful manner. From (Insulin Sensitivity and Fat Loss, September 5, 2008):
- Protein is a given with any diet (LM recommends 1-1.5 g per lb of Lean Body Mass for bodybuilders).
- Some people do well on LCHF and others do well on LFHC diets. There may be genetic differences between people which dictates which diet works better for which person.
- A link between diet effectiveness and both insulin sensitivity and insulin secretion after a meal has been proposed.
- Insulin is a storage hormone released in response to eating with carbohydrates having the largest impact on insulin secretion, protein having the second greatest and fat having little to no impact on insulin secretion.
- Insulin sensitivity refers to how well or poorly the body responds to the hormone insulin. Individuals who are insulin resistant tend to have higher baseline insulin levels because the body is releasing more in response to try and overcome the resistance.
- Some research suggests that a tendency to release too much insulin in response to feeding may predispose people towards weight/fat gain.
- High insulin secretion tends to make people eat more.
- Studies of diabetics find that decreasing insulin secretion with drugs tends to cause a spontaneously lower food intake.
All of those points are very helpful insights but honestly it is difficult to distinguish between Lyle’s position and Fung’s position from that article. Lyle’s position is that the right diet will result in calorie restriction and that caloric restriction will result in weight loss. Whether eating Low Carb lowers Insulin levels leads to weight loss (Fung) or eating Low Carb results in eating less resulting in weight loss (Lyle) is a difference that makes little difference in practice. And, it could be a combination of both.
From a later Lyle article (Insulin Resistance and Fat Loss, August 12, 2015):
- [The] analogy for how hormones work is the lock and key analogy…. insulin has an insulin receptor. When insulin binds to that receptor, stuff happens … And that insulin receptor is found all over the body, in the brain, in skeletal muscle, in the liver, and in fat cells.
- Think of insulin as a storage hormone. Released in response to eating carbohydrate and protein (but not in response to fat, which can impact on insulin resistance in other ways) insulin puts the body in an energy storage mode.
- In skeletal muscle, insulin stimulates the storage and/or burning of carbohydrate for fuel. In the liver, it shuts down glucose production. In fat cells, it both stimulates the storage of calories and inhibits the release of fat (it inhibits lipolysis).
- When a fat cell becomes insulin resistant, that means that insulin not only doesn’t store calories but that insulin can’t inhibit fatty acid release as well.
- Chronic elevation of a hormone tends to cause receptor resistance itself. So it becomes a bit of a vicious circle.
From (Endocr Pract. 2010 Jan-Feb;16(1). Identifying prediabetes using fasting insulin levels. Johnson JL, Duick DS, Chui MA, Aldasouqi SA.):
Further analysis using the area under the curve revealed that at a fasting insulin level > 9.0 microIU/mL, prediabetes would be correctly identified in 80% of affected patients.