Tweet by Prof David Diamond:
David Diamond
@LDLSkeptic
In the past several years, editors have been sending manuscripts on diet and heart disease to me as a part of the peer-review process. I've been honored to be seen as an expert worthy of providing input to editors as to whether a manuscript deserves to be published. The below text in bold/italics is a subset of a review I wrote recently in which I evaluated a manuscript written by authors who promoted the DASH diet and were critical of low carb diets and red meat consumption, and they promoted the perspective that high LDL causes CVD. I've removed any mention of the authors' names, as well as the journal identifier. The essence of my review (below) may be of value for those who wonder about misinformation on LDL, heart disease and diet.
My review: "The idea that the first stage of atherosclerosis is the accumulation of LDL-C is not supported by a broader assessment of the literature. If high LDL-C simply gains access to the artery wall, thereby choking off the artery and causing premature CVD death, then all people with high LDL-C should die prematurely of CVD. Whether one reads the older [1] or recent [2] literature, one finds that people with familial hypercholesterolemia (FH) have a normal lifespan. Indeed, after 70 years of age, people with FH have a lower rate of CVD events and mortality than the general population [2].
Smokers and hypertensives have a far higher rate of events than healthy FH people, so a vulnerability factor must precede LDL accumulation in the artery wall to increase CVD events and mortality. Population studies also demonstrate that people with the highest LDL live as long, or even longer, than people with lower LDL [3]. The fact that diabetics with uncontrolled elevated blood glucose have an extremely high rate of CVD, independent of LDL, points to blood sugar-induced damage to the endothelium as a prime candidate for CVD vulnerability. Finally, careful analysis of the FH literature demonstrates that the subset of FH individuals that develop premature CVD are those with evidence of hypercoagulation (which can be triggered by high blood sugar), independent of their LDL [4,5].
The flawed epidemiological literature and recent promotion of plant-based diets has ignored the extensive literature demonstrating that a meat and high carb diet is unhealthy, but red meat, alone, has not been shown to be associated with CVD risk. Research critical of the view that red meat is harmful has been summarized here [6,7].
An important component of the DASH diet is the restriction of sugar, which thereby makes an important component of the DASH diet overlap with the LCD. The obvious flaw with the DASH diet is the control group. Has the DASH diet ever been studied with a comparison diet that solely restricts carb consumption. If not, how can the other components of the DASH diet be considered important when it may be solely the sugar restriction that provides the benefits of the DASH diet?
The authors may not be familiar with the LCD literature which may explain why they have misrepresented it. The idea that up to 45% of calories from carbs can be considered a low carb diet is incorrect and has been promoted by authors who are critical of the diet. A low carb diet that has been studied in numerous RCTs is one in which carbs are typically less than 10% of the calories [8,9].
Benefits of LCDs were described in the 19th century as a treatment for type 2 diabetes and obesity. This literature was reviewed in the mid-20th century by Pennington [10], and in JAMA [11] and then popularized by Atkins in 1972. Since then, there have been dozens of LCD RCTs [e.g., 8,9] In 2015, a large group of scholars reviewed the LCD literature and concluded the LCD was the ideal first approach to the treatment of type 2 diabetes [12], which of course, is a condition that is associated with a high risk of CVD.
The warning against consuming red meat is an anachronism based solely on biased epidemiological work that has not been supported by rigorous analyses [6,7].
References 1. Harlan WR, Graham JB, Estes EH. Familial Hypercholesterolemia - a Genetic and Metabolic Study. Medicine, 45(2), 77-& (1966).
2. Mundal L, Sarancic M, Ose L et al. Mortality Among Patients With Familial Hypercholesterolemia: A Registry-Based Study in Norway, 1992-2010. J Am Heart Assoc, 3(6) (2014).
3. Ravnskov U, Diamond DM, Hama R et al. Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review. Bmj Open, 6(6) (2016).
4. Ravnskov U, de Lorgeril M, Kendrick M, Diamond DM. Importance of Coagulation Factors as Critical Components of Premature Cardiovascular Disease in Familial Hypercholesterolemia. International Journal of Molecular Sciences, 23(16) (2022).
5. Ravnskov U, de Lorgeril M, Kendrick M, Diamond DM. Inborn coagulation factors are more important cardiovascular risk factors than high LDL-cholesterol in familial hypercholesterolemia. Medical Hypotheses, 121, 60-63 (2018).
6. Leroy F, Smith NW, Adesogan AT et al. The role of meat in the human diet: evolutionary aspects and nutritional value. Anim Front, 13(2), 11-18 (2023). 7. Leroy F, Cofnas N. Should dietary guidelines recommend low red meat intake? Crit Rev Food Sci, 60(16), 2763-2772 (2020).
8. Westman EC, Tondt J, Maguire E, Yancy WS. Implementing a low-carbohydrate, ketogenic diet to manage type 2 diabetes mellitus. Expert Rev Endocrino, 13(5), 263-272 (2018).
9. Volek JS, Phinney SD, Krauss RM et al. Alternative Dietary Patterns for Americans: Low-Carbohydrate Diets. Nutrients, 13(10) (2021).
10. Pennington AW. Treatment of obesity: developments of the past 150 years. Am J Dig Dis, 21(3), 65-69 (1954).
11. Thorpe GL. Treating overweight patients. J Am Med Assoc, 165(11), 1361-1365 (1957).
12. Feinman RD, Pogozelski WK, Astrup A et al. Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base. Nutrition, 31(1), 1-13 (2015)."
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7:21 PM · Nov 7, 2023
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! Good day and good luck 
to everyone!