Evidence shows that body fat is an endocrine organ – it produces hormones that help control body weight and energy metabolism, as well as inflammatory cytokines. It’s not inert insulation that just sits there. It does stuff and if you have too much of it, it does bad stuff. Like:
- Body fat secretes leptin, the “I’m full” hormone. Leptin indicates “plenty” to the body, and it scales up with body fat. The more body fat you have, the more leptin you secrete, the less you eat. It’s one way our body keeps itself in energy balance, and it works pretty well – up to a point. Unfortunately, excessive amounts of body fat secrete more leptin than the body can handle, the leptin receptors become resistant to the effect of leptin, the “I’m full” message cannot be received, and hunger grows unabated. Thus, obesity often perpetuates itself by blunting the appetite-suppressing effect of leptin.
- Body fat also secretes adiponectin, an anti-inflammatory hormone involved in glucose regulation, fatty acid oxidation, triglyceride clearance, and insulin sensitivity. More adiponectin means better fat burning, favorable blood lipids, improved glucose tolerance, and lower insulin levels. Unfortunately, the relationship between body fat and adiponectin secretion isn’t like the one between body fat and leptin. The more body fat you have, the less adiponectin you secrete. That’s why the obese and overweight tend to have lower levels of the beneficial hormone.
- Body fat secretes resistin, a hormone that increases insulin resistance. Both genetic and diet-related obesity increase resistin levels, suggesting that resistin is a function of obesity and excessive body fat rather than the lifestyle factors that lead to obesity. If a bad diet and poor exercise habits increase resistin, it’s only because they also increase body fat.
- Body fat secretes inflammatory cytokines, also known as adipokines. Adipokine-derived inflammation may be causing or exacerbating the insulin resistance and other conditions often associated with obesity. Thus, obesity is inherently inflammatory.
Watch Your Fructose Intake
In rats, fructose feeding inhibits leptin receptors. Rats were given a diet of 60% fructose for several weeks and then injected with leptin. In normal rats, leptin injections reduce energy intake and hunger. The leptin binds with leptin receptors in the hypothalamus and satiety is induced. In the fructose-fed rats, leptin had no effect. Energy intake continued unabated, while normal rats reduced their intake in response to the leptin. Rats on the fructose diet gained even more weight when switched to a high-fat diet.
Fructose appears to affect the leptin pathway in two ways. First, fructose directly renders the hypothalamus resistant to leptin. Normally responsive receptors in the brain have a muted, or even silent, response to leptin when fructose intake is high. Second, high blood triglycerides – brought on by a high fructose intake – block the passage of leptin to the brain. High tris actually physically prevent leptin from passing through the blood-brain barrier, and the leptin that does get through elicits a poor response from leptin receptors.
As we all know, a high-fat, low-carb, low-fructose diet generally decreases serum triglycerides and increases satiety; perhaps the lower triglycerides are allowing more leptin to pass through and inhibit hunger. The fructose found in reasonable amounts of fruit, like berries, shouldn’t affect leptin sensitivity.
Not Seeing Results?
As a personal trainer, I would venture to guess that around 1/4th of my clients over the past decade believed that they had some type of thyroid or other metabolic disorder that was preventing them from losing fat. I would now like to bring your attention to a classic paper published in The New England Journal of Medicine titled Discrepancy Between Self-Reported and Actual Caloric Intake and Exercise in Obese Subjects (click on the link to download the full paper).
In this study, the researchers decided to examine the discrepancy between the actual quantity of calories consumed and exercise performed and the reported quantity of calories consumed and exercise performed by obese subjects who were struggling in their weight loss endeavors. The results were shocking. The researchers found that all of the obese subjects who believed that they had “diet-resistance” in fact had normal metabolisms. What then was causing their alleged diet-resistance? Get this: They were underestimating/under-reporting their caloric intake by a whopping 47% and overestimating/over-reporting their physical activity by 51%!
1. Berardi, JM. Long haul training: An interview with Gary Homann.
Testosterone Magazine 23 Dec 2004. http://www.tnation.com/readTopic.do?id=536382.