cholesterol.md

cholesterol.md

• «Zinöcker thought, “When we eat more polyunsaturated fat, the cells collect cholesterol from the blood, and build it into the cell membranes to ensure that they become rigid enough. This is where the cholesterol has gone when we measure less cholesterol in the blood!”

  And the opposite holds true as well – when we eat more saturated fat, the cell membranes become stiffer. The cells have less need to bring in stabilizing cholesterol and instead send it into the bloodstream. The cells also stop absorbing cholesterol, thus raising the blood cholesterol level.

  In the second instance, Zinöcker arrived at another understanding:

  The increase in blood cholesterol level as a result of more saturated fat in the diet may not be a sign of disease at all. On the contrary.

  "The increased blood cholesterol level is probably a sign that the regulatory mechanisms in the body are working the way they should," says Zinöcker.

  Perhaps the cholesterol in the blood of healthy people is simply a kind of emergency stockpile, which the body has at its disposal when the fluidity of the cell membranes needs to be adjusted.

  “Cell stiffness is probably so important that the body doesn’t take a chance on covering the need exclusively through food,” says Zinöcker.»

  «Most people with an increased risk of heart disease have a lot more than just their cholesterol levels out of balance. Their blood pressure and blood sugar are too high, the liver is too fatty and their insulin isn’t functioning properly.

  And critically, measurements show signs of chronic inflammation in people with heart disease risk.

  Several studies suggest that chronic inflammation in the body can disrupt many regulatory mechanisms in our cells.

  Zinöcker believes chronic inflammation may be the root of the problems.

  Could inflammation be leading to disturbances in regulating cholesterol and many other processes, which together increase the risk of heart disease?

  In this scenario, it is conceivable that high cholesterol in people with chronic inflammation is only a signal of the regulatory disturbances and not a cause of heart disease per se.

  Or maybe it plays a negative role, which it wouldn’t in a healthy body.

  Zinöcker believes cholesterol levels in a healthy body mean something different from cholesterol levels in a sick body. When we mix the results of healthy and sick people, the measurements don’t make sense.» - "New model could explain old cholesterol mystery" (2021)

• «The HADL model proposes a plausible mechanism, founded on human adaptive physiology, that explains the shifting dynamics of cholesterol in lipoproteins with changes in ratios of dietary PUFA/SFA. We argue that dietary fats differentially affect cholesterol concentrations in circulating lipoproteins to ensure that cellular function is maintained when the types of fatty acid consumed change. From this perspective, the LDL cholesterol–raising effect of dietary SFAs does not imply a pathogenic response, but rather a properly functioning cholesterol homeostasis. Additionally, the different interactions between SFAs and n-3 compared to n-6 fatty acids in the regulation of cell membrane fluidity could explain why combined n-3 and n-6 fatty acid intake may protect against ASCVD, while increased intake of n-6 fatty acids alone does not. If verified, our model speaks for a different approach to dietary recommendations for the prevention of ASCVD, and for the discontinuation of simplified expressions such as “good HDL cholesterol” and “bad LDL cholesterol.”» - "The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk" (2021)

• "Following their Nobel Prize-winning discovery of the defective gene causing familial hypercholesterolaemia, Brown and Goldstein misunderstood the mechanism involved in the pathogenesis of the associated arterial disease. They ascribed this to an effect of the high levels of cholesterol circulating in the blood. In reality, the accelerated arterial damage is likely to be a consequence of more brittle arterial cell walls, as biochemists know cholesterol to be a component of them which modulates their fluidity, conferring flexibility and hence resistance to damage from the ordinary hydrodynamic blood forces. In the absence of efficient receptors for LDL cholesterol, cells will be unable to use this component adequately for the manufacture of normally resilient arterial cell walls, resulting in accelerated arteriosclerosis. Eating cholesterol is harmless, shown by its failure to produce vascular accidents in laboratory animals, but its avoidance causes human malnutrition from lack of fat-soluble vitamins, especially vitamin D." - "The great cholesterol myth; unfortunate consequences of Brown and Goldstein’s mistake" (2011)

• "Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats." - "Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis" (2014)

• "The absolute risk reduction of CVD mortality in secondary-preventive cholesterol-lowering trials is quite small, rarely exceeding two percentage points, and no primary-preventive trial has ever succeeded in prolonging the life of the participants.

  The rate of serious adverse effects of statin treatment is highly underestimated.

  Adverse effects of statins are extensive, including diabetes, cognitive impairments, cancer, cataracts and musculoskeletal disorders.

  The small benefit seen in the cholesterol-lowering trials is independent of the degree of cholesterol lowering." - "How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease" (2015)

• "The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. Most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke. Although SFAs increase low-density lipoprotein (LDL) cholesterol, in most individuals, this is not due to increasing levels of small, dense LDL particles, but rather larger LDL particles, which are much less strongly related to CVD risk. It is also apparent that the health effects of foods cannot be predicted by their content in any nutrient group without considering the overall macronutrient distribution. Whole-fat dairy, unprocessed meat, and dark chocolate are SFA-rich foods with a complex matrix that are not associated with increased risk of CVD. The totality of available evidence does not support further limiting the intake of such foods." - "Saturated Fats and Health: A Reassessment and Proposal for Food-Based Recommendations: JACC State-of-the-Art Review" (2020)

• "Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in the New England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review’s objective, contributed articles for inclusion, and received drafts. The SRF’s funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry–funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development." - "Sugar Industry and Coronary Heart Disease Research - A Historical Analysis of Internal Industry Documents" (2016)