They overfed lean and modestly overweight volunteers 50% more calories than they naturally consume … After 6 weeks of massive overfeeding, both lean and overweight subjects gained an average of 10 lb (4.6 kg) of fat mass and 6.6 lb (3 kg) of lean mass... Following overfeeding, subjects were allowed to eat however much they wanted for 6 weeks. Both lean and overweight volunteers promptly lost 6.2 of the 10 lb they had gained in fat mass (61% of fat gained), and 1.5 of the 6.6 lb they had gained in lean mass (23%).
To me, the most interesting aspect regarding human overfeeding studies like this is that, once the overfeeding period has ended, the participants return to their original weight without dieting. As Stephan indicates, this means that our bodies have the inherent ability to maintain our “normal weight.” Refer to the post I wrote on tribal fattening practices and the fact that the fattened women who refuse to overeat their real foods diet return to a healthy weight in short order. Normal weight, however, appears to be different for every individual. For example, when a person has a normal weight – a setpoint – that, by all standards, can be seen as obese, we are left with the question of just why in the heck this is happening. Why does the body insist on remaining in such a biologically abnormal state?
Many scientists and researchers claim that leptin – a hormone which regulates appetite – plays a key role in obesity, as many people who are overweight exhibit low levels of the hormone. Much research has been conducted on the validity of this theory and it is now recognized that leptin resistance – in which the body can no longer can recognize when it has had enough food – is what enables a person to eat more than they need, thus leading to obesity and keeping that person obese. And, surprise, surprise: artificial fructose is a prime culprit in leptin resistance because fructose doesn't stimulate leptin (or insulin for that matter). No stimulation, no appetite regulation.
Skinny Jeans & Skinny Genes
Okay, so leptin appears to play a role in weight maintenance. That's all fine and good, but why can some people eat and drink whatever they want -- including artificial fructose -- without affecting their body composition while some people become obese? This is where I believe heredity comes into play. Depending on what stage of degeneration a person is in – first, second, or third generation of processed food consumption, let's say, and/or what a person's mother ate while pregnant with him/her – obesity can be more or less of a potential complication.
In my case, for example, my mother wasn't overweight when I was in the woom and neither of my parents are overweight now. This is despite consuming a lot of high-fructose corn syrup and omega-6 vegetable oils for much of their lives. I was raised on this typical industrial diet and never experienced issues of overweight as a child, and I have no issues now. At age 18, I altered my diet and cut out processed foods, which is how I eat now, eight years later. But my older brother, now age 29, has continued to eat our childhood foods without gaining significant weight. Other health problems aside, my family has no weight issues. Is there something about us genetically that is behind all of this? I think it's a strong possibility. And maybe this is because, like Don Gorske, we may have a closer-to-pure hereditity. We are not yet degenerated to the point where the disease of obesity has set in.
In contrast, I know of a few childhood friends (two brothers) who now appear to be on the receiving end of metabolic discord through familial degeneration. In their twenties now, they are both experiencing weight problems. They also drink a lot of beer and don't seem to have the best diet in the world. Observing their parents, the mother has been overweight for at least half of her life (including several years before becoming pregnant) and the father has always been slim, despite drinking a lot of beer and not having the best diet in the world just like his sons. Why is dad slim while having very similar dietary habits to his overweight sons? Are his genetics more pure and less degenerated – less overall processed food consumption – than the mother's genes, which appear to have a hereditary predisposition to being overweight? This may be the case, and it would explain the weight issues of the two sons, as they would inherit half of their mother's genes.
Several studies have been done evaluating the role heredity may play in obesity. The most compelling subset of these studies are those that include data from adopted children, their adoptive parents, and their biological parents. Here's an abstract from one of these of these studies, called “Genetic contributions to human fatness: an adoption study:”
A strong relationship was found between the degree of fatness of biologic mothers and that of their adult offspring who had been separated from their mothers at birth and adopted during the first year of life. This relationship persisted even after age, height, and possible confounding environmental factors were controlled. There was little evidence for either selective placement on the basis of parental fatness or gene-environment interaction. There was no relationship between the degree of fatness of adoptive parents and that of the adoptees.
It's interesting that the weight of the child was directly affected by the weight of the biological mother and is not affected by the environment of the adoptive home. This supports my theory on the two sons who I described above. There is, however, one glaring confounding factor in all of this talk about obesity and heredity, and that is the increasing consumption of high-fructose corn syrup in the last 30 years. This amazingly effective human fattener was not significant in the industrialized diet until 1980, when Coca-Cola officially began adding this biochemically engineered sweetener to its popular soft drink. This also happens to be the time when obesity levels really began to take off. Check out the graph below from the paper, “High-fructose corn syrup in beverages may play a role in the epidemic of obesity:”
So does that mean that heredity may not be as important as diet in the development of obesity? Not necessarily. I believe the two go hand-in-hand and, as I said earlier, it's possible that it is heredity and the diet of the mother which determines susceptibility to the effects of HFCS or other processed foods.
So what lesson have we learned here? Well, there's still a lot of questions, but I think we can safely say that some people have more difficulty with weight than others, and that reason may not necessarily be connected to dietary choices in all cases. Rather, there are several lifetimes of degeneration that may be influencing each individuals propensity to gain – and keep on – the fat.
For solutions to inherited susceptibility to obesity, I refer you back to Stephan, who I think provides some good advice. As far as my recommendations, the best change anyone can make in their diet to make a difference in health, and perhaps body composition, is to simply eliminate the four nasties: artificial fructose, gluten, trans fats, and vegetable oils. Eat real food. And please, please, please raise your children on real foods so they don't have the same health difficulties that many of us adults have!