https://www.youtube.com/watch?v=oystPZFrEDM
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https://my.clevelandclinic.org/health/diseases/22206-insulin-resistance
When glucose enters your cells and the levels in your bloodstream decrease, it signals your pancreas to stop producing insulin. For several reasons, your muscle, fat and liver cells can respond inappropriately to insulin, which means they can't efficiently take up glucose from your blood or store it. This is insulin resistance.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7792751/
In contrast, no change in total cholesterol or LDL cholesterol was observed in insulin-sensitive and insulin-resistant postmenopausal women, after 4 wk, when dietary cholesterol was increased from 113 mg/d to 319, 523, or 941 mg/d as part of a Step I diet . However, in this study only 8-11 women were included in each treatment subgroup, and

https://www.webmd.com/diabetes/insulin-resistance-syndrome%23:~:text=Insulin%2520resistance%2520is%2520when%2520cells,blood%2520sugar%2520levels%2520go%2520up.
Insulin resistance doesn't guarantee that you'll get diabetes. But it's important to make changes to your eating habits and activity level, since healthy daily habits can protect your health.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6428207/
The mechanisms by which IR influences lipid metabolism are complex and may depend on the disease state associated with the IR, i.e. obesity, metabolic syndrome, T2DM and T1DM. The relationship between IR and dyslipidemia is likely reciprocal and the direction of the causality remains incompletely defined.

https://diabetesjournals.org/care/article/27/6/1496/22705/Lipids-and-Lipoproteins-in-Patients-With-Type-2
Insulin resistance may play a pivotal role in the development of diabetic dyslipidemia by influencing several factors. In insulin resistance and type 2 diabetes, increased efflux of free fatty acids from adipose tissue and impaired insulin-mediated skeletal muscle uptake of free fatty acids increase fatty acid flux to the liver (26,27).

https://diabetesjournals.org/care/article/30/8/2164/28570/Insulin-Resistance-Dyslipidemia-and-Cardiovascular
At the same time, migration of macrophages into the subendothelial layer leads to foam cell formation with the CD-36 receptor, which internalizes oxidized LDL, increased in the proinflammatory state of insulin resistance. Insulin resistance is associated with increased factor XII, both directly as an effect of insulin and indirectly via

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10351747/
Statins should therefore prevent rather than exacerbate insulin resistance because they lower dyslipidemia (LDL cholesterol and triglycerides). In this study, we intended to shed more light on the diabetogenic effects of statins through a thorough examination and synthesis of the literature published during the last 10 years.

https://www.ahajournals.org/doi/10.1161/ATVBAHA.121.316159
The mechanisms for statin-related T2D are unclear. There is evidence that statins may adversely impact both insulin resistance and secretion. In that context, studies have shown that treatment with statins is associated with increase in fasting insulin 13-15 as well as increase in insulin resistance as assessed by measures obtained during the oral glucose tolerance test (OGTT). 9,16 For

https://drhyman.com/blog/2024/02/16/podcast-ep856/
Now, small dense LDL cholesterol particles are the worst actors. They have a greater tendency to damage the lining of your arteries to become oxidized and to trigger the development of plaque and they're highly correlated with A OB. So you can use your A OB if your doctor doesn't want to check your lipoprotein fractionation, although they

https://www.ajconline.org/article/S0002-9149(99)00355-0/fulltext
The 3 major components of the dyslipidemia of insulin resistance are increased triglyceride levels, decreased high-density lipoprotein (HDL) cholesterol, and changes in the composition of low-density lipoprotein (LDL) cholesterol. Hyperinsulinemia and the central obesity that typically accompanies insulin resistance are thought to lead to overproduction of very low-density lipoprotein (VLDL

https://zoe.com/learn/what-are-normal-insulin-levels-for-women
We measure insulin blood levels in milli-international units per liter (mIU/L) or picomoles per liter (pmol/L). It's important to remember that everyone is different, and there's no agreement among experts about what's a normal, low, or high fasting insulin level. One source lists normal ranges as either 5-15 or 5-12 mIU/L (30-90 or

https://www.endocrinepractice.org/article/S1530-891X(20)40965-6/fulltext
The insulin resistance syndrome has been shown to be a key initiator of cardiovascular disease. In this communiqué, the role of dyslipidemia in the insulin resistance syndrome and in subsequent cardiovascular disease will be assessed with use of a statistical tool called factor analysis. Factor analysis is a technique that uses statistical

https://link.springer.com/chapter/10.1007/978-3-030-56514-5_16
The incidence and prevalence of overweight and obesity have increased dramatically in the United States during the last generation [4,5,6,7].Figure 16.1 shows the prevalence of obesity among US adult men and women, based on representative samples of the population, from 1960 to 2014. The prevalence of obesity nearly tripled during this time; the increases have been mainly attributable to the

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8708656/
Abstract. Type 2 diabetes mellitus and insulin resistance feature substantial modifications of the lipoprotein profile, including a higher proportion of smaller and denser low-density lipoprotein (LDL) particles. In addition, qualitative changes occur in the composition and structure of LDL, including changes in electrophoretic mobility

https://diabetesjournals.org/diabetes/article/62/2/401/15352/Ceramides-Contained-in-LDL-Are-Elevated-in-Type-2
Data are presented as means ± SEM. Plasma was collected from obese, insulin-resistant female subjects before (Pre-WL) and after (Post-WL) losing 12% body mass by diet or diet and exercise. F: Plasma ceramide in lipoprotein fractions. Data are presented as means ± SEM. *P < 0.05 vs. Pre-WL by paired Student t test. n = 14.

https://www.sciencedirect.com/science/article/pii/S0002916522001198
In contrast, the informative negative outcomes involving LDL cholesterol and LDL-P are clearly nonsignificant, although we lack power to rule out a small diet effect. In conclusion, we found that carbohydrate restriction had benefits for insulin-resistant dyslipoproteinemia and Lp(a), without adverse effects on LDL cholesterol or inflammation.

https://pubmed.ncbi.nlm.nih.gov/10418856/
The 3 major components of the dyslipidemia of insulin resistance are increased triglyceride levels, decreased high-density lipoprotein (HDL) cholesterol, and changes in the composition of low-density lipoprotein (LDL) cholesterol. Hyperinsulinemia and the central obesity that typically accompanies insulin resistance are thought to lead to

https://diabetesjournals.org/care/article/32/suppl_2/S373/26631/Triglycerides-and-HDL-CholesterolStars-or-second
The combination of low LDL cholesterol (<70 mg/dl), low C-reactive protein (<2 mg/l), and low TG (<150 mg/dl) was associated with the lowest event rates. However, although statins can reduce LDL cholesterol levels by as much as 50% or more, their effect on HDL cholesterol levels is modest, at best.

https://www.ncbi.nlm.nih.gov/books/NBK305900/
Atherosclerotic cardiovascular disease (ASCVD) is a major cause of morbidity and mortality in both men and women with T1DM and T2DM. In patients with T1DM in good glycemic control, the lipid profile is very similar to the general population. In contrast, in patients with T2DM, even with good glycemic control, there are frequently lipid abnormalities (elevated TG and non-HDL-C, decreased HDL-C

https://pubmed.ncbi.nlm.nih.gov/31672136/
Background: Dyslipidemia and inflammation are closely interrelated contributors in the pathogenesis of atherosclerosis. Disorders of lipid metabolism initiate an inflammatory and immune-mediated response in atherosclerosis, while low-density lipoprotein cholesterol (LDL-C) lowering has possible pleiotropic anti-inflammatory effects that extend beyond lipid lowering.

https://pubmed.ncbi.nlm.nih.gov/25815343/
To investigate this, we assessed if hepatic inflammation explains the predisposition towards insulin resistance in low-density lipoprotein receptor knock-out (Ldlr (-/-)) mice. For this, wild type (WT) and Ldlr (-/-) mice were fed a chow diet, a high fat (HF) diet, or a high fat, high cholesterol (HFC) diet for 2 weeks.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8118579/
The observed inverse correlation of LDL cholesterol concentrations and insulin-based estimates for insulin secretion is a result of enhanced insulin clearance in case of higher LDL levels. CEACAM1 as a key component of hepatic insulin clearance could possibly link hepatic insulin clearance and LDL metabolism in the liver, for which molecular