Vitamin Supplements

The discovery of leptin, a hormone produced by the most unlikely of endocrine organs, fat, prompted researchers to look again at our blubbery stuff, and in 2001 it was announced that another hormone had been found. Adiponectin has a role in regulating energy balance, seemingly raising metabolic rate. Its production is not distributed evenly across our fat, but concentrated in our love handles and other unsavoury bulgy bits that migrate to our middles. Unlike leptin, where high levels are linked with being overweight, there’s a negative association between adiponectin and obesity. Low circulating levels of adiponectin have now been discovered to be a very accurate predictor of Type z diabetes risk. The lower the adiponectin, the worse the blood fats profile, the greater the risk of heart disease being associated with the diabetes.

The threads of this story are now beginning to come together. At the beginning, we talked about insulin, the hormone which controls sugar levels in the body by telling cells all over the body, in the liver and muscle, to absorb glucose from the blood. When people get Type z diabetes, first their muscles and liver, but not their fat, become insulin-resistant, meaning that despite production of increasing amounts of insulin, their cells are deaf to its exhortation to take up glucose. Too much fat, as we know, is likely to cause Type 2 diabetes — but curiously having too little causes exactly the same disease.

People who have a disease called lipodystrophy have almost no fat. You can have such a condition from birth, or acquire it because of _something like HIV. It sounds vaguely attractive, but actually is very disfiguring, making people look permanently sick and skeletal. Because the bodies of those with lipodystrophy can’t store fat, their bodies try to move it into muscle tissue or the liver instead. In people who are obese, there is also nowhere to store fat, but in their case it’s not because there is no fat, but because all the fat depots are already full to brimming. Just as in those with no fat, there is an attempt to shift it to muscle and liver. In both the obese and the thin, the consequence, especially in muscle, is that fatty acids spill into the cells, somehow altering the normal response to insulin. It is possible that adiponectin is the missing link between insulin resistance and obesity. If it is, it means that diabetes is not the sugar problem we’ve thought it was for the best part of eighty- five years, but a fat problem. As I write, no adiponectin is yet available for use in humans. When it can be made in sufficient quantity for human use, as it surely will, we may discover that this hormone can be used for treating both obesity and diabetes. But so far this is just surmise.

When I tell people that hormones can make them fat and about the fat thermostat, there are two reactions. One is relief and the other is suspicion, usually followed by ‘But it’s still about putting too much in and not enough out’, which for the majority of people is right. For years, management of obesity has been about the management of behaviour. Behaviour is only part of the obesity problem. The other part is hormones. And that’s the truth.

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