In the past you could see Dr Lustig turning the traditional perception of the obesity development upside down. He said that it was not due to the behavior, when people reach for energy dense food and prefer to stay physically inactive because they can. It rather was the sole role of biochemistry that drove the behavior of people to overeat, remain sedentary and gain weight. He even strengthened this premise by pointing at obese 6 months old, probably expecting that all cases of obesity should be explained by exactly the same mechanism.
Another cases he used to support this biology driven reason for obesity were his patients after suffering a hypothalamic trauma. The hypothalamus of these people could not read the leptin which would otherwise stop them eating when full and preventing them to store extra adipose tissue. But because this mechanism was not working in these people, as a result of overeating they developed insulin resistance, which further drove the metabolic diseases, associated with obesity. As a proof that the obesity can only be fixed from the inside, Dr Lustig demonstrated how he managed to fix it by artificially reducing the release of insulin first by using a drug and then watching how the patients started to lose weight and even enjoy the physical exercise. And, as a proof that this has the effect on people without the hypothalamic trauma, he demonstrated this on another patient who was just being obese, proving himself right in his point. He also illustrated this mechanism on an example of two children receiving a cookie: a slim child became hyperactive but an obese child did not, because it was leptin resistant, most likely due to the hyperinsulinemia as a result of insulin resistance. But how they become hyperinsulinemic in the first place?
We should look back when it all started. I mean the individuals without the hypothalamic trauma or leptin receptors deficiency, which are the majority of obesity and metabolic disease cases worldwide. Before they developed insulin and leptin resistance they were perfectly metabolically healthy, but the wrong dietary and lifestyle choices made them gradually overweight, obese and metabolically sick. They did not express the gluttony and sloth before but they have developed them after wrong dietary choices and a prolonged time of positive energy balance. Dr Lustig never discussed this order of events properly. Even when elaborating on how the food industry and the lack of effective policies promote these unhealthy choices, it was not about the unhealthy choices themselves in his argumentation other than our likeness for sweet taste, which fructose provides in foods. The blame was always put on somebody else, never on the individuals that actually made those choices and put the food items into their mouths. What is more, Dr Lustig constantly focuses on already diseased people how powerless they are under their condition and applies their conditions and ill metabolism on the healthy people as if the origins of the consequences were identical among these people.
As you have noticed by now, Dr Lustig illustrated that it was not the behavior that drove obesity levels in his patients suffering a hypothalamic trauma. When thinking about the differences, I have realised that these patients were firstly resistant to the leptin present in their bodies and then they started to eat like crazy, storing excess fat and slowly developing insulin resistance. In other cases, without this trauma, it is either the regular spikes of insulin that makes the hypothalamus less responsive to leptin, or gradually developing the insulin resistance (most likely due to the constant positive energy balance), that makes them leptin blind. These are two different premises. However, Dr Lustig constantly pictures the later stages of obesity development or gradually developed insulin resistance as a cause of obesity or metabolic diseases. He uses a mechanism of consequence as a mechanism of cause in these people without the hypothalamic traumua. WHY? I suspect he is biased by his medical profession where he mainly treats symptoms rather than looking at the cause of the problem in its nature and since his fructose agenda become a worldwide thing he tries to adjust other physiological mechanisms to fit this proposed frame.
I have a different opinion.
In the video from which is the following slide, Dr Lustig uses the same tactic again. In order to dismiss the generally perceived and accepted adipocentric model of the metabolic syndrome development (and insulin resistance within), he used an extreme case such as familial partial lipodystrophy. This is a result of a serious genetic mutation and you can see on the patient that he is not quite like the rest of us:
The patient was genetically predisposed where he stored and did not store the extra fat, or rather from which body regions the affected people start losing the subcutaneous fat as they mature and age. Although we all have this differentiated fat storage places - we store extra fat on our hips, stomach, arms, but not too much on palms of hands, on our ear lobes or hair area - people like this patient are too different from the most of us due to having other metabolic problems including 'inability to properly breakdown a simple sugar known as glucose (glucose intolerance), elevated levels of triglycerides (fat) in the blood (hypertriglyceridemia), and diabetes'.
What that means? The patients with this genetic condition do not develop metabolic diseases despite of not storing fat under their skin but because of their genetic susceptibility for them, in addition to the gradual loss of subcutaneous fat. In fact, the inability to store potentially excess energy intake in the subcutaneous fat depot can actually contribute to their metabolic disturbances.
So this was another inappropriately used supporting example by Dr Lustig proving NOTHING about the allegedly non-existent causal link between the excess subcutaneous adipose tissue and metabolic health of the average population. And, as one researcher (M. Constantine Samaan from McMaster University) pointed out when I discussed the origin of insulin resistance:
"One other organ to be considered is the brain. Evidence from animal models suggests that high fat diet causes animals to become insulin resistant prior to weight gain, and that this is the result of hypothalamic inflammation. Whether this applies to human MetS is unknown."
So here you have two different views on the origin of insulin resistance in relation to hypothalamus. Can the high fat diet be a culprit of hypothalamic insulin resistance in normal people, making them leptin resistant and subsequently develop obesity? Remember that insulin is also a hormone regulating food intake: hypothalamus reads increased glucose and a subsequent insulin release as a sign of food intake and Dr Lustig agreed with this as well.
But the insulin resistance in hypothalamus is not the same as overall body hyperinsulinemia. Read more about why we might be hyperinsulinemic today here.
Now, how fructose comes into this? Almost 100% fructose is metabolized by the liver, only micromole concentrations appear in blood whereas glucose appears in millimole concentrations, a thousand times higher amount. Can liver cause all these problems? Read more about this issue here.
No comments:
Post a Comment