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Guilherme Marquezine (G.) @marqquezine
, 17 tweets, 6 min read Read on Twitter
There's an interesting concept in insulin action that I think add to the notion that a calorie is NOT just any calorie. That would be specially important in the metabolically sick people, aka people with metabolic syndrome, hyperinsulinemic, trying to lose weight.
Have you read about SELECTIVE insulin resistance?

That means that after insulin binds to its receptor, there are more than one pathway to follow and they stimulate very different actions. Unfortunately for us in abundant food times, some of them are lost as we get resistant.
Because we lose most anabolic functions of this wonderful hormone, we get hyperglycemia and impaired glucogenesis, for example. Lipid synthesis, however, may remain active and we are able to see that clinically - T2 diabetic with high VLDL, for example.
As we lose this actions and get high glucose, the pancreas senses this and starts trying to compensate with higher levels of insulin. If we were totally resistant to this new levels of insulin, no big deal. Glucose would rise, but sadly there is more.
Because resistance is selective, hyperinsulinemia becomes VERY deleterious. Signalling down MAP kinase pathway, which is responsible for the proliferative actions of insulin, gets a buff. All sorts of cardiovascular cells types have been shown to be activated by this
There have been described synergic effects with FGF, PDGF, vasopressin, the RAAS system and so on
When you read about it you get the impression the authors are covering the atherosclerosis pathophysiology...

Insulin resistance leads to loss of very important metabolic and CV actions (NO action, supression of NFkB, etc) AND accelerates proliferative actions....
Accelerates proliferative actions that could explain the extremely accelerated atherosclerosis observed in T2D patients (but not T1, for instance).
Coming back to my first tweet on this thread, what has all this to do with calories?

A high carb diet, no matter how "whole" or fresh or unprocessed they are, is bound to lead to higher than normal levels of insulin, specially in the post-prandial state.
This is what I observe that the fitness crowd doesn't really get: their clients tend to be younger and more physically capable to generate work and reverse metabolic damage.

It's hard to get an older, heavier and sicker diabetic to do all the work required to heal insulin.
On the other hand, diets low in carbs and high in fat act on two ends of the problem: they are able to feed and satiate the person without the glucose challenge that they usually have problems dealing with AND they very rapidly get to lower insulin.
We haven't yet been able to fully grasp how important insulin lowering is (not forgeting of the direct consequence: fat catabolism in key organs, which is the ketogenic part) in dealing with metabolic diseases.
I personally find it very unlikely that people are able to reverse this whole process with a WFPB diet WITH ONE EXCEPTION: that is is pretty low in calories and induces lipolysis by a much harder way.
It's doable, of course.

Usually requires a lot more meds ($$) also. It's an option.
Metformin, for instance, activates AKT.
Pioglitazone tries to increase insulin sensitity in muscle and adipose tissue, protecting visceral territory.
RAS system activation leads to water and sodium retention, hypertension.

All this can be done by addressing insulin with diet.
To finish up: ketogenic diets are not about foods and carbs. It's mainly about what type of hormonal response you get.

Depending on your metabolic picture, yes, you can be harmed by one small banana. You're not going to die from it, but it can surely get in the way of healing
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