Problems with low-fat diets
In recent years there has been much said about how the dietary villain is not cholesterol and egg yolk but sugar, and some have mistakenly blamed the Mediterranean diet for the low-fat diet that has resulted in a marked increase in carbohydrate intake, with increases in diabetes and obesity.16 However, the low-fat diet did not result from the discovery of the Mediterranean diet. With its high fat content (40% of calories from fat, mainly olive oil)10 and emphasis on whole grains, the Mediterranean diet is actually a low glycaemic diet.
The result of this discussion has been a widespread and popular, but entirely mistaken, move to increased use of low-carbohydrate (low-carb) diets, with a high intake of cholesterol and animal fat. This is disastrous, and to a great extent due to propaganda of the food industry.17 Like the sugar industry18 the meat and egg industries spend hundreds of millions of dollars on propaganda, unfortunately with great success.19–21 Box 1 provides links to information about this issue.
Box 1Links to videos about egg industry propaganda
An Israeli diet study22 provided perhaps the best evidence that the Cretan Mediterranean diet is actually better than a low-carb diet for diabetes and insulin resistance. Overweight residents in an institution, who obtained their meals from the cafeteria, were randomised to a low-fat diet, a low-carb diet or the Mediterranean diet. Adherence was 95% at 1 year and 86% at 2 years, unusually good for dietary studies. Weight loss was identical on the low-carb and Mediterranean diet, and both were significantly better than the low-fat diet. Among participants with diabetes, fasting glucose, fasting insulin levels and insulin resistance were clearly the best on the Mediterranean diet.22
Propaganda of the egg industry and the red meat industry
Following an exposé of the propaganda of the sugar industry in which the ‘smoking gun’ was unearthed in archives,18 Nestle17 commented on the attempts of the food industry in general to influence public beliefs. I commented on the egg industry and the meat industry.19
The two pillars of the egg industry propaganda are a red herring and a half-truth. The red herring is a misplaced focus on the effects of diet on fasting lipids. Diet is not about the fasting state; it is about the postprandial state.23 24 For ~4 hours after a high-fat/high-cholesterol meal, there is marked oxidative stress, endothelial dysfunction and arterial inflammation.25
The half-truth is the slogan ‘eggs can be part of a healthy diet for healthy people’. This is based on two US studies that did not find harm from egg consumption except among participants who became diabetic, in whom an egg a day ‘only’ doubled coronary risk.26 27 However, as discussed above, the US diet is so bad that it is difficult to show harm from any component (figure 3). In Greece, however, where the Mediterranean diet is the norm, an egg a day increased coronary risk fivefold among persons with diabetes, and even 10 g per day of egg (a sixth of a large egg) increased coronary risk by 54%.28 Egg consumption also increases the risk of diabetes.29
Figure 3Diet is the worst of the risk issues in the USA. Prevalence (unadjusted) estimates for poor, intermediate and ideal cardiovascular health for each of the seven metrics of cardiovascular health in the American Heart Association 2020 goals, US children aged 12–19 years, National Health and Nutrition Examination Survey (NHANES) 2011–2012. *Healthy diet score data reflect 2009–2010 NHANES data. (Reproduced with permission from Wolters Kluwer, Mozaffarian et al.
5)
The 2016 US guideline
In 2016, when the new US dietary guideline was released, there were headlines trumpeting ‘It’s OK to eat cholesterol again; the new guideline says so’. But it was not true. In the first paragraph, the press release said that there were insufficient data to recommend a specific limit to cholesterol intake, as in the past (300 mg/day for healthy people or 200 mg/day for those at risk of vascular disease).30 However, the second paragraph said: ‘However, cholesterol intake should be as low as possible within the recommended eating pattern’ (which resembles a Mediterranean diet). The paragraphs should have been reversed. There are still good reasons to recommend a cholesterol intake below 200 mg/day (less than one large egg yolk), and other guidelines do so.31
It is little understood that ‘people at risk of vascular disease’ essentially means everyone who aspires to achieve a healthy old age.32 A 20-year-old man might think he can eat eggs and smoke with impunity, because his stroke or myocardial infarction are 45 years in the future. But why would he want to bring it on sooner?33
Effects of the intestinal microbiome
Although dietary cholesterol does not increase fasting lipid levels by much, it clearly does increase coronary mortality.34 35 However, there is increasing recognition of the importance of the intestinal microbiome.36 While cholesterol content is essentially the same for any kind of animal flesh, red meat has more saturated fat, and has ~4 times as much carnitine as chicken or fish. Carnitine from red meat37 and phosphatidylcholine from egg yolk37 are converted by the intestinal bacteria to trimethylamine, in turn oxidised in the liver to trimethylamine n-oxide (TMAO) (figure 4). TMAO causes atherosclerosis in animal models,37 and in patients undergoing coronary angiograms plasma levels in the top quartile of TMAO levels after a test dose of two hard-boiled eggs predicted a 2.5-fold increase in the 3-year risk of stroke, myocardial infarction or vascular death.38 A 12-ounce Hardee’s Monster Thickburger39 contains 265 mg of cholesterol and 320 mg of carnitine. The yolk of a 65 g egg contains 237 mg of cholesterol and 250 mg of carnitine, so two egg yolks are worse than the 12-ounce burger. Patients at risk of stroke should avoid red meat and egg yolk.
Figure 4Trimethylamine n-oxide (TMAO) is produced by the intestinal bacteria from phosphatidylcholine. Carnitine (largely from red meat) and phosphatidylcholine (largely from egg yolk) are converted by the intestinal bacteria to trimethylamine, which in turn is oxidised by the liver to TMAO. TMAO causes atherosclerosis in animal models and markedly increases the risk of stroke, myocardial infarction and cardiovascular mortality, particularly in persons with renal impairment. It also accelerates decline of renal function. (Permission requested to reproduce from Wang et al.
58) FMO, flavin-containing monooxygenase.
Besides TMAO, there are other toxic metabolites produced by the intestinal bacteria from amino acids, including P-cresyl sulfate, hippuric acid, indoxyl sulfate, P-cresyl glucuronide, phenyl acetyl glutamine and phenyl sulfate. These toxic metabolites of the intestinal microbiome are renally excreted, so they may be termed ‘Gut-derived Uremic Toxins’ (GDUT). Their blood levels are very high in patients with renal failure. Other uraemic toxins that have high plasma levels in renal failure are thiocyanate, asymmetric dimethylarginine and homocysteine. Homocysteine accounts for only ~20% of the effect of renal impairment on carotid plaque burden40; we hypothesised40 that GDUT may account for much of the very high risk associated with renal failure.41 Renal function declines linearly with age, and by age 80 the average estimated glomerular filtration rate in patients attending a stroke prevention clinic is below 60 mL/min/1.73 m2.40 We have evidence that even moderate renal impairment significantly increases plasma levels of the GDUT (submitted for publication). This means that persons with renal impairment, including most elderly patients, should avoid red meat and egg yolk.
