Thursday, 20 November 2014

Thinking inside the box again

I remember Dr Lustig elaborating in 2009 about how fructose leads to obesity because brain does not read it as a source of energy. The mechanism was explained and supported by some studies, that fructose is not a glucose and it does not rise insulin levels to the same level as glucose. According to this scenario the hypothalamus does not see the calories and therefore it does not stop the person eating more. We now know that is not true, but Dr Lustig had put a lot of effort in his presentation to convince you that he was right. I have not heard him saying that anymore. Instead of obesity he now focuses on fructose effect on metabolic diseases and again exacerbates things quite often. 

You could hear him elaborating with a similar passion in the video at 13:23 where he was explaining the mechanism of insulin and leptin resistance in obese people like if there were only these two hormones regulating appetite or hunger and the energy metabolism. He talked about how every attempt to cut down the energy intake for losing weight leads to decreased leptin concentration down to only 25% within 12 hours so now the poor obese folks not only are leptin resistant, but they no longer have enough leptin to stimulate those few responsive receptors in their brains and this is supposed to drive the hyperphagia (excessive eating) or yo-yo dieting further. The body supposedly thinks it is starving. 

Except one thing: the levels of released hormones in the body are not always constant and the leptin is rather a hormone of a long-term energy regulation than acting in a short-term manner. Our endocrine system is very complex and inter-dependent. Leptin levels can decrease even when the fat cells have not been significantly affected in the acute settings. Of course they could not, who loses fat within 12 hours? There are other functions for leptin in the body, not all are fully known and its levels are affected by other factors, too. 

I remember my professor of endocrinology saying that we have more anorexigenic hormones (make us to stop eating) but those orexigenic (the opposite) are more powerful.Take ghrelin which acts in a short-term manner in response to the actual food consumption, or rather not-consumption. Do not eat for several hours and you will get hungry, regardless of the leptin and insulin concentrations in blood. This study provides more information about other hormones which participate in appetite regulation and how the palatability of food affects the satiety signals. 

Switch your brain on and put it together in your head. And learn more about leptin before you will be fooled again. 

This is just a very unfortunate practice by many who are seeking sensations: taking things out of context and elaborating on them so much that it will become a topic of the week. People then do not understand or see the whole context and are disappointed that the media publish one thing one day and the complete opposite the next day. Does that sound familiar to you? 

I am not saying that Dr Lustig is completely wrong. I am saying that he again focused too much on one mechanism, which is not as important in isolation because our endocrine system is too complicated for that. After all, he is the endocrinologist, not me. 

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