Another cup of coffee?
Different studies have associated coffee with both cardiovascular risks and benefits. Coffee contains more than 1000 different biologically active substances; some (like caffeine) are detrimental to the heart, while others (like antioxidants) are protective.
Study design seems to influence results, explains Ahmed El-Sohemy, Canada Research Chair in Nutrigenomics (University of Toronto, Canada). Case-control studies have shown that increased coffee consumption was associated with an increased risk of coronary heart disease (CHD), while prospective cohort studies have shown either no effect or a protective effect for moderate intakes. “Such discrepancies suggest that coffee may have acute effects on the risk of CHD, which are revealed in case-control studies, but obscured in cohort studies by the time lag between exposure assessment and outcome,” says El-Sohemy.
The method of coffee preparation appears to be important. Boiled (unfiltered) coffee raises serum cholesterol levels to a greater extent than filtered coffee. The cholesterolraising factors have been identified as the diterpenes, substances that are extracted by hot water but retained by filter paper, neatly explaining why filter coffee does not affect cholesterol. Coffee may protect against type 2 diabetes, a risk factor for CHD. Coffee contains the antioxidant chlorogenic oxide, which can inhibit the glucose-6-phosphatase system and decrease intestinal absorption of glucose.
The way the body metabolises caffeine may affect CHD risk. In a recent study El-Sohemy and colleagues showed that coffee was associated with an increased risk of nonfatal MI among individuals with slow caffeine metabolism, but not among fast metabolisers. Caffeine is metabolised by the polymorphic cytochrome P450 1A2 (CYP1A2) enzyme, and people who are homozygous for the CYP1A2*1A allele are "rapid" caffeine metabolisers, whereas carriers of the variant CYP1A2*1F are "slow" metabolisers.
Eggs unscrambled
The popular belief is that cholesterol in the diet is automatically translated into cholesterol in the blood, which is then laid down in the coronary arteries. Since eggs represent the richest source of dietary cholesterol, with a yolk containing between 50 and 250 mg cholesterol, they have taken much of the rap for the adverse effects of dietary cholesterol. New evidence suggests this reputation is unjustified.
Studies by Henry Ginsberg in the 1990s showed that men who ate up to four eggs a day increased their total serum cholesterol by 0.038 mmol/L per 100 mg of added dietary cholesterol, and that women increased their total serum cholesterol by 0.073 mmol/L per 100 mg of added dietary cholesterol.
In 1999 researchers from the Harvard School of Public Health found no relationship between egg consumption and cardiovascular disease when they followed 80,000 women for more than 14 years in the Nurses’ Health Study and almost 38,000 men for eight years in the Health Professionals Follow-up Study. One egg per day, the authors concluded, had no impact on heart disease risk.
In addition, since eggs are low in calories, yet have a high satiety index, they may offer an effective approach to weight loss.
Many earlier studies showing links between dietary cholesterol and blood cholesterol were confounded by the fact that dietary cholesterol and saturated fat frequently occur together in the diet, making it difficult to distinguish between their individual effects.
Red wine or white?
Regular consumption of red wine has been suggested as the explanation for the "French paradox", whereby French people have a relatively low incidence of coronary atherosclerosis compared to other Western populations with identical smoking habits and lifestyles.
A Lancet report by Renaud and De Lorgeril noted that the annual mortality rate per 100,000 population from CHD was 78 in Toulouse, France, compared to 348 in
Belfast, UK, and 380 in Glasgow, UK, despite similar intakes of saturated fat. Analysing 17 countries, Renaud and De Lorgeril found that wine was the only foodstuff to show a negative correlation with mortality, indicating a protective effect. When this news appeared on 60 Minutes in the US in 1991, red wine drinking increased by 44% and some wineries began lobbying for the right to label their products “health food”.
Subsequent observational studies have shown consistent reductions in all-cause mortality among red wine drinkers. A number of mechanisms have been suggested - that alcohol increases HDL cholesterol, that alcohol inhibits platelet aggregation, and most recently that polyphenols in red wine activate a receptor on the surface of platelets, called PECAM-1, which inhibits platelet aggregation and thus prevents further thrombus growth.
“While observational studies have shown an association, this does not prove cause and
effect,” says Dylan de Lange from the Thrombosis and Haemostasis Laboratory, Utrecht, the Netherlands. The current debate centres on whether the “French Paradox” is because of components of the wine, or the result of confounding factors, such as the lifestyle of wine drinkers. Factors other than alcohol or red wine may have an influence on mortality - red wine consumers may buy healthier food products, while the “sick quitter phenomenon”, where abstainers have a higher all-cause mortality, may include people who stopped drinking because of health problems. One study showed that 27 out of 30 cardiovascular risk factors were more prominent in abstainers than in consumers of alcohol.
“What’s needed to resolve the issue is a double-blind placebo controlled trial with solid end-points, such as MI and death,” says de Lange. “But how do you blind a trial in which people have to drink alcohol? It’s easy to distinguish between a glass of red wine and a glass of grape juice.” He sees the only way forward as conducting a trial using polyphenols, “but, before we can do this trial, issues need to be resolved around bioavailability, and the best combinations of polyphenols.”
Omega-3 fatty acids
Interest in omega-3 fatty acids was first sparked in the 1970s when studies by Bang and Dyerberg showed that the Greenland Inuit, who consumed a diet rich in oily fish, had an exceptionally low incidence of cardiovascular disease compared to other populations. These basic observations about omega-3 fatty acids – a specific type of polyunsaturated fat found in fatty fish (such as wild salmon, sardines and mackerel)and plant food sources (such as flax, walnuts and canola oil) – spawned hundreds of other studies.
The strongest evidence for a beneficial effect comes from the Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico (GISSI)-Prevezione study, in which 5654 patients with coronary artery disease were randomised to either omega-3 fatty acids (850 mg/d) or usual care. After 3.5 years, those taking the omega-3 fatty acids had experienced a 20% reduction in overall mortality and a 45% decrease in risk for sudden cardiac death. Subsequent metaanalyses have shown a favourable effect of fish fatty acids on stroke and fatal coronary heart disease.
Further evidence suggests omega-3 fats have anti-arrhythmic effects (including reventing atrial fibrillation), anti-thrombotic actions, anti-atherogenic effects, antiinflammatory effects and the ability to lower blood pressure and improve endothelial function.
However, last year doubts were cast after the publication of a systematic review by Lee Hooper and colleagues from the University of East Anglia (Norwich, UK). The study – which included 48 randomised control trials and 41 cohort studies – found no strong evidence for a reduction in combined cardiovascular events in patients taking omega-3.
The authors, however, acknowledged that the inclusion of an observational study by Burr and co-workers advising 3000 men with stable angina to eat oily fish or take fish oil supplements was largely responsible for the net neutral effect.
A number of explanations have been offered as to why the angina study produced conflicting results. “It could be because the very long follow-up brought out the harmful effects of methylmercury, a fat soluble toxicant found in oily fish that is known to increase risks of MI,” suggests Marika Massaro, a nutrition researcher from
Institute of Clinical Physiology of the National Council of Research (Italy).
Marianne Geleijnse, a nutritionist and epidemiologist from Wageningen University Netherlands), believes that there may also be a biological explanation since the study was undertaken in angina patients who may be different from other patients. She said it was significant that the study suffered from several logistical problems and did not differentiate between fish and fish oil supplements.
To resolve the issue, Geleijnse and colleagues are undertaking a double-blind andomised placebo-controlled trial, where coronary patients are being randomised to margarine with or without fish oil. In the meantime, people are recommended to eat at least two servings of oily fish per week.
In Italy, says Massaro, the results of GISSI are thought so convincing that omega-3 is
now prescribed as secondary prevention treatment for patients who have suffered an MI.