Generous of your time to explain this, what doctors rarely know. Yeah just ask for a fasting insulin test and see what happens, or any discussion on insulemia or possible genetic factors...Hi Clash, thanks for post.
1. That is true, pure glucose causes the biggest spike in insulin response among a randomised group of people. However, within that same of randomised group of people, the peaks will look vastly different depending on their metabolic health profiles, which comes back to the original point, what causes metabolic disease, which in turn is the primary causal factor for hypertension, CVD, dementia, obesity, and all the other leading causes of deaths that I mentioned earler? Sucrose has a moderate glycemic index, but a substantially higher glycemic load, thanks to its fructose molecule that dilutes the pure glucose effect it has in these indicies when used for calculation, despite fructose, as opposed to fiber in most other foods as a component of total carbs, is just as bad if you were to build a metabolic index. The body appears to be excellently designed to handle a sudden rush of food, or glucose, with relative ease. However, repeated occurrences will eventually degrade that functionality.
2. Yes, as I had mentioned earlier, glucose causes the biggest increases in insulin response, but glucose is not found in pure form in nature, except through sucrose in the form of fiber rich fruits. It is very clear that amylose and amylopectins isocalorically given both lower peaks in insulin and lower AUC. These are crticial but not the only points needed to develop insulin resistance. Therefore, it is natural to conclude that pure sucrose is the easiest way to induce insulin resistance, not just for its readily absorbed glucose molecule, but also for its insulin independent fructose molecule.
3. That is not what the data show. It does not take extreme conditions to make the liver impaired, which I am assuming here your definition of that is oversupplied by energy and accumulated hepatic fat deposits through diet. In fact, you would be surprised to know that 30% of Americans have NAFLD, and up to 50% of the population in Korea, one of the remaining few countries that still uses HCFS (again, indistinguishable from sucrose as mentioned previously). It has been shown that countries that use HCFS as a sweetner had 20% more prevalence of diabetes, and much more for pre-diabetes, and this was adjusted for sugar intake, suggesting a calorie is not just a calorie. I would even go far as to say these figures are understating the problem. A 5% fractionation ja the official diagnosis of steatosis, I would love to see their serum hepatic lipase enzyme concentrations, using pre-diabetes to diabetes as an analogy, where the former is 80% of the problem, diabetes in itself is a small step towards disease compared to the more prevalent, more problematic, and less attention receiving hyperinsulinemia. So how would you make sure that DNL is at its highest? Simple, you consume sucrose, as also mentioned in a previous post, it works on two pathways independent of each of each other using glucose and fructose to create the ultimate DNL and cholesterol synthesis factory.
4. Good catch, I've been typing on my phone all this time which isn't the easiest thing to do.
5. Data points to that it does. This is especially evident in longitudinal studies, one of the key missing ingredients in most of the prospective or RCTs done. Much like ASCVD, It is a disease of progression.
6. I'm not very clear on your point. The pathopathology of type 1 and 2 diabetes is somewhat well understood, and sucrose consumption, especially in excess caloric surplus, is the primary driver of the latter.
7. They are not directly triggered by glucose or fructose ingestion, that is correct. They are triggered by the response of insulin which is normal and healthy, it is when insulin levels are both high and chronic, that issues arise. High levels of insulin, even in the presence of normal blood glucose levels as in pre-diabetics, I would argue make up 50% of the global population at minimum, can directly activate immune cells, particularly macrophages. Insulin can stimulate these cells to produce pro-inflammatory cytokines like TNF-alpha, IL-6, and IL-1β. Hyperinsulinemia can activate key signaling pathways within immune cells that sway kt towards a pro-inflammatory state. For example, the NF-κB pathway, a central regulator of inflammation, can be activated by high levels of insulin. This activation leads to the transcription of various genes involved in the inflammatory response. Insulin acts on the endothelium (the inner lining of blood vessels) and can influence the interaction between endothelial cells and immune cells. In a state of hyperinsulinemia, this interaction can become dysregulated, contributing to endothelial dysfunction and promoting the adhesion and migration of immune cells into tissues, thereby exacerbating inflammation. In conditions associated with hyperinsulinemia, such as obesity and metabolic syndrome, adipose tissue becomes inflamed and is characterized by an infiltration of immune cells. High insulin levels can exacerbate this inflammation in adipose tissue, leading to the release of more pro-inflammatory cytokines and adipokines. Chronic hyperinsulinemia can contribute to insulin resistance in immune cells themselves. This low-grade chronic inflammation is a hallmark of various metabolic disorders.
8. Sounds contradictory. You might want to re-read that one again, in the context of what I had said.
9. This is not true, given the data I have provided in this post and past posts. Pure fructose is not needed, and possibly inferior to sucrose in inducing non-subcutaneous adipose deposits.
10. To make it simple. Sucrose consumption, high insulin, fat liver deposits, liver insulin resistant, liver exports more glucose and TG which creates ROS, triggers immune response, immune cells insulin resistant and can neither utilise glucose or tell that glucose is now under control being in a perpetual inflammatory state, this is also partially done by reducing glucocorticoids that are anti-inflammatory in nature, cortisol eventually rises in insulin resistance as it fails to respond, cells become insulin resistant and glucocorticoid resistant, insulins mitogenic properties are still functional leading to stiffening of artierial walls and endothelial dysfunction raising blood pressure, liver exporting much higher lipoprotein particles due to increased DNL and inhibited glucogenesis get pushed against the damaged endothelial wall more readily and get stuck, more immune response, plaque formation and CVD. It is a vicious self feeding cycle.