[bad_user]

The cause of insulin resistance is energy poisoning (i.e. people eating too much). The only cure for insulin resistance is weight loss. That's it.

There's no study, not one, showing reversal of IR with keto/fasting independent of weight loss.

Macros are absolutely irrelevant for either weight gain or weight loss in controlled studies. Only protein seems to have an effect on satiety, but the effect is not very significant in the context of whole foods.

Even more serious is that drops in HbA1C, a surrogate marker for blood glucose, cannot be shown to drop independent of weight loss. Ketoers might avoid sugar spikes after meals better, they might get off some meds sooner, but this is only disease management and for the HbA1C, which represents a 3 months average, it doesn't seem to matter.

The whole notion that insulin resistance is cause by sugar or carbohydrates, or that the cure is cutting carbs, is bullshit similar with anti-vaxxing and homeopathy. Not evidence based.

[partyboat1586]

How do you explain skinny people getting type 2 diabetes? They can't be in caloric surplus or they would be gaining weight.

[bad_user]

Skinny people getting T2D have a less flexible adipocytes tissue (aka fat tissue). They cannot store excess energy as subcutaneous fat, because they don't have a subcutaneous fat layer that can store that energy. But once you look at their organs, they are covered in visceral fat.

Adipocytes, the fat cells, have a limited capacity and new adipocytes can be created, but only in certain conditions and slowly. This isn't an infinite supply and genetics play a role. In other words people have a "personal fat threshold":

https://portlandpress.com/clinsci/article/128/7/405/71158/No...

https://diabetes.diabetesjournals.org/content/63/12/4369

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774584/

Once the adipocytes start rejecting the energy excess, with that energy excess building up in the bloodstream as glucose and triglycerides, being then pissed away, this is effectively insulin resistance, which is actually a defensive reaction to "energy poisoning":

https://pubmed.ncbi.nlm.nih.gov/11872656/

However it's important to understand that this energy poisoning can happen as a result of overeating fat or protein as well, even if the pathways are different from that of glucose:

https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2362....

https://pubmed.ncbi.nlm.nih.gov/11872656/

https://pubmed.ncbi.nlm.nih.gov/3421919/

More importantly is that "weight loss" is the only measure shown in tests on humans to revert insulin resistance significantly. Another factor would be exercise, which was shown to work independently of weight loss, but the effect wasn't significant AFAIK.

Everything else is confounded by weight loss. And this goes in the other direction — most (not all) risk factors for the diseases associated with the metabolic syndrome, including high blood pressure and heart disease, are confounded by weight gain. There are independent risk factors of course, like smoking or a high LDL, which most often has genetic causes, but most negative effects of foods you've heard about are in the context of a caloric surplus.

This includes fat driving cholesterol and triglycerides up. Including sugar causing fatty liver. Sugar (fructose) was never shown to cause fatty liver unless it's in the context of a caloric surplus, sugar was never shown to cause T2D unless it's in the context of a caloric surplus, but that didn't stop some people writing books claiming otherwise.

[partyboat1586]

With naturally skinny people having less flexible adipocytes does that not put them at higher risk of diabetes? Since they have less area to store the fat they will more quickly reach their threshold and start developing insulin resistance. Why then is there a classical association between obesity and diabetes? Or perhaps the definition of obesity is flexible depending on genetics?

On the topic of refined sugar my understanding was that because it is processed by the body more quickly it spikes blood sugar levels short and sharp rather than more spread out in the case of protein and fat which take longer to digest. Because of the limited rate of creating adipocytes this means that the same concentration of blood sugar delivered over a shorter time period would stimulate insulin resistance where if it were delivered over a longer period of time blood sugar levels would not cross that threshold. I'm sure that if you eat a caloric surplus that you will trip the threshold but could it not also be tripped by eating lots of high sugar foods to the same amount of calories of fat and protein which would not cross the threshold?