Not understanding the logic?
Carbohydrate-induced hypertriglyceridemia. It's counterintuitive on the surface, I know, but the link between dietary fat intake and blood lipid levels is actually the
opposite of what you'd guess. It's a paradox. The data from the last 20 years flies directly in the face of the "low-fat, eat more fruit" tactic we were bombarded with in the 80s and 90s.
The short-term TG-raising effect of a very low-fat diet is dependent upon the nature of the carbohydrate, with a greater effect of a sugar-rich than a complex-carbohydrate-rich diet.
pubmed.ncbi.nlm.nih.gov
After a high-carbohydrate, low-fat meal, overweight men had a lower fat oxidation and a higher fractional hepatic fat synthesis than did lean men.
pubmed.ncbi.nlm.nih.gov
These results support the concept that both hyperinsulinemia and a low-fat diet increase DNL, and that DNL contributes to hypertriglyceridemia.
pubmed.ncbi.nlm.nih.gov
The elevation of blood lipid concentrations in response to the consumption of low-fat high-carbohydrate diets is known as carbohydrate-induced hypertriacylglycerolaemia (HPTG). An understanding of the mechanisms involved in the interaction between carbohydrates and plasma lipids may help...
pubmed.ncbi.nlm.nih.gov
It has been known for decades that low-fat, high-carbohydrate diets can increase plasma triglyceride levels, but the mechanism for this effect has been uncertain. Recently, new isotopic and nonisotopic methods have been used to determine in vivo whether low-fat, high-carbohydrate diets increase...
pubmed.ncbi.nlm.nih.gov
When the content of dietary carbohydrate is elevated above the level typically consumed (>55% of energy), blood concentrations of triglycerides rise. This phenomenon, known as carbohydrate-induced hypertriglyceridemia, is paradoxical because the increase in dietary carbohydrate usually comes at t …
pubmed.ncbi.nlm.nih.gov
You can improve your LDL with a higher fat intake if you focus on the right ones, even with higher dietary cholesterol.
Low-carbohydrate high-fat (LCHF) diets are a highly contentious current topic in nutrition. This narrative review aims to provide clinicians with a broad overview of the effects of LCHF diets on body weight, glycaemic control and cardiovascular risk factors while addressing some common concerns...
pubmed.ncbi.nlm.nih.gov
Overweight and obesity are both a risk factor for developing and exacerbating type 2 diabetes (T2D). While the most common diet used to treat overweight and obesity focus on high-carbohydrate, low-fat, energy deficit diets, recently, low-carbohydrate, high-fat diets (LCHFD) have become popular...
pubmed.ncbi.nlm.nih.gov
Several dietary approaches have reduced cardiovascular events in randomized clinical trials. Replacing saturated fat with polyunsaturated fat prevented coronary events in men, and a Mediterranean diet and fatty fish improved survival. None of these trials had much impact on total fat intake but...
pubmed.ncbi.nlm.nih.gov
Background Previous results provide supportive but not conclusive evidence for the use of omega-3 fatty acids to reduce blood lipids and prevent events of atherosclerotic cardiovascular disease, but the strength and shape of dose-response relationships remain elusive. Methods and Results This...
pubmed.ncbi.nlm.nih.gov
LDL may not be a useful marker anyway, and the hype/panic around it unnecessary. (Or worse, exploited for marketing purposes)
For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is...
pubmed.ncbi.nlm.nih.gov
(Full article
https://www.tandfonline.com/doi/full/10.1080/17512433.2018.1519391)
<p>In this study of people with Type 1 diabetes in clinical practice, LDL-C was not a good predictor of CVD. We found no support for an LDL-C cut-off point < 2.6 mmol/l. TC/HDL-C seems more reliable as a marker for CVD risk when considering primary prevention.</p>
pubmed.ncbi.nlm.nih.gov
I also know that some research suggests that lipophilic statins may be more likely to cause brain related side effects over hydrophilic
I'm already way over tl;dr so I'll save you from 20 more links (unless you want them), but it seems like you've already researched a bit. You probably noticed that after the FDA issued its alert and forced a warning labeling change for statins, publications like JAMA were flooded with quick studies with conclusions that can be paraphrased as "It's worth the risks" and "If you're worried about cognitive effects, just stop taking it". If you didn't, go back and look at some, and pay attention to who funded those. I would also go to the
FDA's FAERS site and look up the specific one you're taking.
For me, if I can control my numbers by paying attention to what I eat, taking a pill to fix it the easier way is not worth the risk of going crazy in 15 years.
