The heart and the circulatory system

Lichtenstein (2003) states that 15 million deaths in the late 1990s could be attributed to cardiovascular disease. The American Heart Association has pointed out that coronary heart disease and the related cardiovascular disease is the number-one killer in the US, accounting for almost one in two deaths among Americans and more deaths than are caused by all the forms of cancer combined. The impact on disability and the attendant economic loss are enormous.
Atherosclerosis ('hardening of the arteries') is the term used to describe a number of pathological events occurring in arteries and which are responsible for coronary heart disease, stroke and diseases of the peripheral circulatory system (Fisher 1991).
Atheroma (from the Greek ather = porridge) comprises deposits of fatty material on the walls of arteries - a material comprising cholesterol, triglycerides, brous tissue and red blood cells. As it builds it restricts blood ow and if this is in the coronary artery then heart attack and death may follow, as the heart muscle does not receive suf cient oxygen. Atheroma has also been associated with the development of cataracts, macular degeneration in the retina and the development of cancers (Emerit et al. 1991; Tunick et al. 1994). If the atheroma accumulation (plaque) is ruptured a blood clot may form which not only can accelerate the blockage of the artery concerned but also may break loose and plug another artery, increasing the risk of heart attack or, if the newly blocked artery is in the brain, a stroke.
Plainly, the intake of saturated fats and cholesterol increases the risk, although it must be realised that four- fths of the cholesterol is made in our bodies and does not come through the diet. The quantity of cholesterol produced is increased in propor­tion to the level of saturated fatty acids in the diet (polyunsaturated fatty acids reduce blood cholesterol), and also the trans saturated fatty acids, i.e. those that are produced industrially by catalytic hydrogenation (Krisetherton 1995). High sugar intake can lead to high formation of saturated fats in the body. Indeed, any imbalance in metabolism such that there is an excess of calories over those needed to sustain the body will lead to an accumulation of fat. Obesity, hypertension, diabetes, sedentary living and the use of cigarettes all increase the risk of atherosclerosis.
As cholesterol and other lipids such as the triglycerides are insoluble in aqueous systems, they are transported through the body by combination with proteins, as lipo-proteins. The principal carrier of cholesterol is low-density lipoprotein (LDL) and there is a strong positive correlation between its level and the risk of atherosclerosis. Hence LDL is frequently referred to as 'bad cholesterol'.
A lower percentage (20-30%) of the blood cholesterol is in the form of high-density lipoprotein (HDL), which is responsible for transporting cholesterol away from the arter­ies to the liver where it is metabolised. This role has caused HDL to be named 'good cholesterol', such that high levels of HDL appear to afford protection against heart attack. Thus there is an inverse correlation between levels of HDL and atherosclerosis.
There is now a plethora of papers arguing that moderate consumption of alcohol counters coronary heart disease [see, for example, Dyer et al. 1977; Hennekens et al. 1978; Ramsey 1979; Marmot et al. 1981; Gordon & Kannel 1983 (the Framingham study); Kozarevic et al. 1983; Yano et al. 1984; Moore & Pearson 1986; Klatsky et al. 1992; Maclure 1993; Verschuren 1993]. Alcohol causes a lowering of LDL cholesterol in the plasma and an increased level of HDL cholesterol (HDL2 and HDL3) and apo-lipoproteins A-I and A-II (Clevidence et al. 1995; Goldberg et al. 1995; Jansen et al. 1995; Parker et al. 1996).
Alcohol also appears to lower the risk of blood clotting by reducing the level of brinogen in blood plasma (Stefanick et al. 1995) and lessening the tendency of blood platelets to aggregate (Renaud et al. 1992). The bene ts apply to both men and women
(Nanchahal et al. 2000).
Doyens of the eld have included Arthur Klatsky in Oakland, California, Norman Kaplan of the University of Texas Southwestern Medical Center, and Sir Richard Doll in Oxford, England.
The phenomenon has taken the name the 'French paradox', on account of the unex­pectedly low risk of cardiovascular disease in a country noted for its intake of very fatty foods. We can look back nearly two centuries to the rst noting of this effect, when an Irish doctor, Samuel Black, remarked on the much greater incidence of angina in France as opposed to Ireland, which he believed was ascribable to 'the French habits and modes of living, coinciding with the benignity of their climate and the peculiar­ity of their moral affections' (Black 1819). The occurrence is now sometimes called the European Paradox because it re ects dietary characteristics beyond France alone
(Bellizzi et al. 1994).
Various laboratories have reported U-shaped curves (e.g. Doll et al. 1994) or J-shaped curves (e.g. Tsugane et al. 1999) (Fig. 6.1) to illustrate the impact of various intakes of alcohol on coronary heart disease and on all causes of mortality. For the most part it seems that the J shape relates to the relationship between alcohol intake and total mortality, with the U shape better describing that between alcohol consumption and coronary heart disease. The clear evidence is that the intake of some alcohol has a bene cial impact. In many instances consumption of between 1 and 3 units daily perhaps offers the best advantage, with higher intake progressively shifting the risk upwards again.
The low point (nadir) in these curves has been reported at various levels, for example, 69 g alcohol per week for men in the US (26 g per week for women), but 116 g per week for men in the UK (White 1999). It seems that bene ts for women are especially notable after the menopause (Fuchs et al. 1995; Nanchahal et al. 2000).
Even the American Cancer Society reported this type of effect (Boffetta & Gar nkel 1990). The study began in 1959 with 276,802 men between the ages of 40 and 59. Assigning 1.0 as a standard value for risk of death in non-drinkers, it was shown that the risk of death dropped to 0.84 (i.e. by 16%) for those taking one alcoholic drink per day. The risk of death for those claiming to consume six drinks per day was still lower than for abstainers, at 0.92.