Regarding the lowcarb RCTs and what they prove:

What I mean to say is that those RCTs strictly speaking only prove that they have been designed, namely that a low carb diet is an effective method to lose weight. The LCHF method you refer to is more a diet than a diet. If it works to lose weight, it is expected that that pattern also works to prevent obesity.

Is that proof that highcarb, so to speak, is the cause of obesity? No. An example. Amphetamine has been in vogue as a slimming agent for a while, was very effective, and has some plausible mechanisms: it suppresses hunger and increases basal metabolic rate. Is that proof that overweight is caused by too low a basic metabolism or too much appetite? No of course not.



How you judge the value of my other arguments, you must know for yourself. For the sake of completeness, the logic behind it:

If too much consumption were the cause of obesity, I would expect a next route.

1. There is often a lot of KH eaten.
2. The body wants to keep the blood sugar level within narrow margins and reacts with insulin.
3. This results in an average higher insulin level.
4. The dynamics of fat storage in fat cells gets disturbed, because of the higher insulin level (higher peaks, longer duration of release) more fat is stored than released.
5. In response to that average higher insulin level, the number of receptors for insulin is regulated again, insulin resistance is created. This is a natural reaction that also exists for many other receptor modulated systems (think of habituation to opiates).


Once with this route?
What do the studies on insulin resistance mean? In my eyes, studies that show resistance and consequence of being overweight make the route too much plausible due to too much KH. Well it is possible that this high insulin level is there, but that this leads to obesity more quickly than it leads to resistance. I do not know if that is the case, but it seems less plausible to me. First, insulin resistance is also measured by measuring insulin secretion, so you would expect to find a higher level in that measurement. In the first instance, this is not the case with obese people. Secondly, the reduction of the number of receptors physiologically is much faster than the growth of fat cells. But it may work differently than I sketch here.

Why is this question relevant? Because I think that prevention is better than cure. Yes, it seems that LCHF is one way to prevent obesity. But other dietary patterns with many unprocessed, natural foods may also be. And perhaps it is fine if such a pattern contains KH-en, such as fruit and vegetables.


Why is that relevant? Because, if it is the case that KH are wrongly appointed as the major culprit and this philosophy becomes a widely public 'fact' (just like decades ago with fat happened), this will lead to all sorts of strange, highly processed products that are 'healthy'. because they do not contain KH. Whether that fruit or similar foods will be seen as less healthy due to too many KH-and. I know that this does not correspond with the idea behind LCHF, as if you interpret it, but it can indeed be a consequence of certainly suggesting that KH and the main cause of obesity. I am in favor of being nuanced about this.

Another hypothesis? An idea:
Too many processed foods lead to obesity due to dysregulation of the metabolism (among other things due to inadequate bioactive substances such as vitamins and minerals).

Substantiation? Well, for example, the LCHF interventions. Or interventions with fruit that I already mentioned. Again a plausible biochemical mechanism, to be found in the textbooks.

First order? This is possible, given that only 2% eat according to the recommendations (which must guarantee sufficient intake of various bioactive substances). And because these substances are essential in metabolism.

Reliability? If this hypothesis is correct, people can more easily compose their daily expenses (because there are just more options) than with LCHF alone.