I've been trawling through low carb resources for the last 2 months, trying to understand the guts of their belief. They've got some excellent presentations that are aiding my understanding of pathophysiology of insulin resistance and DT2 dev't, weight gain, NAFLD
Some interesting snippets:
- on newer more sensitive dx tests, 35-40% of Westerners have elevated insulin, meaning they are insulin resistant.
- insulin resistance leads to non alcoholic fatty liver disease (NAFLD), metabolic syndrome, T2D, CVD.
- anyone with insulin resistance will convert more carbs to fat via denovo lipogenesis, even on a eucaloric diet, because fat cells cannot adequately uptake fat and glucose from the blood. This is a depth of understanding I've never heard from the PBWF team, some of whom deny DNL exists.
- a significant driver of IR is as adipocytes become more full of fat (triglycerides), the intra- and inter- adipocyte pressure compromises blood flow (hypoxia and reduced insulin delivery), macrophage attraction/inflammation/cytokine production, reduced angiogenesis (capillary sprouting) compromises capacity to create new adipocytes in a timely manner, leaky and reduced fat storage leading to spillover into circulation of triglycerides and FFAs, decreased insulin sensitivity and ability to take in glucose, elevated blood glucose. The higher circulating TAGs (triglycerides) and glucose go back to the liver and increase DNL, storage (NAFLD) and production of VLDL. Fat also gets stored ectopically in inappropriate tissue. On this basis, the most powerful strategy to reverse the process is weight loss, via a fast or significant Calorie deficit, and cardio exercise to increase blood flow through fat tissue. There is some substance to easing the work of a NAFLD liver by decreasing carbs, especially refined and fructose, of the weight loss diet. But on 1000 Cal deficit for most of us, low carb (<100g) should happen automatically.
So what starts insulin resistance?
Excess Calorie intake. doesn't matter what the macros are in my view, but they believe all carbs compound the problem. Once it starts, there's a lot of positive feedback making it difficult to reverse.
So the solution is : lose weight, move more. and secondarily get good sleep, manage stress.
Even though this guy recommends a very low carb ketogenic diet, I still think his presentation of the pathophysiology is excellent:
Dr. Worm is a highly respected nutrition researcher and author in the German speaking world.
___________________________________________________________
Another topic I've been fleshing out is how fiber contributes to appetite control. Here's a brilliant chart summary:
https://www.nature.com/ijo/journal/v39/ ... 1584a.html
International Journal of Obesity (2015) 39, 1331–1338; doi:10.1038/ijo.2015.84; published online 9 June 2015
The role of short chain fatty acids in appetite regulation and energy homeostasis
C S Byrne1, E S Chambers1, D J Morrison2 and G Frost1
An overarching model for the beneficial effects of colonic SCFA production on appetite regulation and energy homeostasis. FCs, fermentable carbohydrates; FFA, free fatty acids; FFA2, free fatty acid receptor 2; FFA3, free fatty acid receptor 3; GLP-1, glucagon like peptide-1; IGN, intestinal gluconeogenesis; PYY, peptide YY; SCFAs, short chain fatty acids; TG, triglyceride.