Truthing Out

Hiding unhealthy heart outcomes in a low-fat diet trial: the Women's Health Initiative Randomized Controlled Dietary Modification Trial finds that postmenopausal women with established coronary heart disease were at increased risk of an adverse outcome if they consumed a low-fat 'heart-healthy' diet

Abstract

The Women's Health Initiative Randomized Controlled Dietary Modification Trial (WHIRCDMT) was designed to test whether the US Department of Agriculture's 1977 Dietary Guidelines for Americans protects against coronary heart disease (CHD) and other chronic diseases. The only significant finding in the original 2006 WHIRCDMT publication was that postmenopausal women with CHD randomised to a low-fat 'heart-healthy' diet in 1993 were at 26% greater risk of developing additional CHD events compared with women with CHD eating the control diet. A 2017 WHIRCDMT publication includes data for an additional 5 years of follow-up. It finds that CHD risk in this subgroup of postmenopausal women had increased further to 47%-61%. The authors present three post-hoc rationalisations to explain why this finding is 'inadmissible': (1) only women in this subgroup were less likely to adhere to the prescribed dietary intervention; (2) their failure to follow the intervention diet increased their CHD risk; and (3) only these women were more likely to not have received cholesterol-lowering drugs. These rationalisations appear spurious. Rather these findings are better explained as a direct consequence of postmenopausal women with features of insulin resistance (IR) eating a low-fat high-carbohydrate diet for 13 years. All the worst clinical features of IR, including type 2 diabetes mellitus (T2DM) in some, can be 'reversed' by the prescription of a high-fat low-carbohydrate diet. The Women's Health Study has recently reported that T2DM (10.71-fold increased risk) and other markers of IR including metabolic syndrome (6.09-fold increased risk) were the most powerful predictors of future CHD development in women; blood low-density lipoprotein-cholesterol concentration was a poor predictor (1.38-fold increased risk). These studies challenge the prescription of the low-fat high-carbohydrate heart-healthy diet, at least in postmenopausal women with IR, especially T2DM. According to the medical principle of 'first do no harm', this practice is now shown to be not evidence-based, making it scientifically unjustifiable, perhaps unethical.

pubmed.ncbi.nlm.nih.gov/34290045/

This study examined the effect of dietary fat on mental ability in older adults. It found that increasing fat in the diet resulted in better mental function.

"Our findings support that PUFAs in dietary sources were associated with lower risks for cognitive impairment partially via lowering oxidative stress. Dietary PUFA supplementation may potentially reduce risk of cognitive impairment via antioxidative mechanism."

Oxidative Stress Mediates the Association Between Dietary Fat Intake and Cognition in US Older Adults

https://www.sciencedirect.com/science/article/abs/pii/S106474812200001X

"Since the Framingham study it has long been considered common knowledge that total serum cholesterol is a strong independent risk factor for cardiovascular disease."

"Sixty years ago the impressive Framingham study, a longitudinal epidemiological study that included about five thousand people, gave out the basis to find the risk factors of ischemic heart disease: smoking, high blood pressure, high cholesterol, diabetes mellitus, obesity and family history. The extrapolation of data found in a small village near Boston to the rest of the world gave birth to decades of theories and investigation efforts ending in current clinical practice. The majority of those risk factors have been proven in clinical practice. All those factors increase inflammation and oxidative stress all over the body. But as mentioned above, cholesterol is there, maybe not creating the problem, but trying to solve it as an important anti-inflammatory tool used by the body´s defence systems."

"The HUNT 2 study, a very elegant prospective study in Scandinavia (the same region where the 4S took place) included 52087 Norwegians, aged 20-74, that were followed-up on cause-specific mortality for 10 years. This is 510.297 person-years in total. The statistical power and the lack of conflict of interest make this a heavy evidence source, even stronger than Framingham. Based on their results, they clearly contradict the popularized idea of a positive, linear relationship between cholesterol and fatal disease, and conclude that the underlying assumptions regarding cholesterol in clinical guidelines for prevention might be flawed."

"Sugar, processed food, stress, heavy metals and radiation are surrounding us on a daily basis. They are the main source of free radicals, oxidative stress and inflammation nowadays. Many physicians are just prescribing cholesterol lowering drugs because we have been blaming the wrong culprit and we still are. Population studies reveal that, although we live longer, the quality of life in terms of a “doctor free life” is dropping down dramatically. The 3rd cause of mortality in the US is iatrogenic caused diseases. In an optimal healthcare system, solutions for many disorders would begin with nutrition, then natural interventions, then pharmaceuticals. But it is important to blame the correct culprits."

"The lack of exposure-response in the trials between changes in LDL-cholesterol and clinical and angiographic outcome, the inverse association between change of cholesterol and angiographic changes seen in the observational studies, the significant increase in complicated atherosclerotic lesions in the treatment group after cholesterol lowering by diet, and most of all, the fact that high cholesterol predicts longevity rather than mortality in old people, suggests that the role, if any, of high cholesterol must be trivial. The most likely explanation for these findings is that rather than promoting atherosclerosis, high cholesterol may be protective, possibly through its beneficial influence on the immune system."

academic.oup.com/qjmed/article/96/12/927/1533176