Coronary heart disease
Diseases of the heart and circulatory system are collectively called cardiovascular disease (CVD) and are a leading cause of death in the UK. Coronary heart disease (CHD) is one of the two main forms of CVD along with stroke. Over 1.6 million men and over one million women are affected by CHD. It is responsible for more than 88,000 deaths in the UK each year, an average of 224 people each day or one death every six minutes. Around one in six men and one in nine women die from CHD (BHF, 2013). Most deaths from CHD are caused by heart attacks. In the UK, there are about 124,000 heart attacks each year. There are also around 152,000 strokes in the UK each year, resulting in over 43,000 deaths (NHS Choices, 2012k).
CHD occurs when there is a build-up of fatty deposits (plaques) along the walls of the arteries that supply the heart with oxygenated blood. These plaques build up and clog the arteries making them narrower and restricting the blood flow. Blood clots can form at the site of a plaque in the coronary artery and cut off the blood supply to the heart. This can result in heart attack and sudden death. Like the heart (and other organs), the brain needs the oxygen provided by blood to function properly. If the supply of blood is restricted or stopped, a stroke may occur and brain cells could begin to die, it can lead to brain damage and possibly death. The plaques that block the arteries are made up of a fatty substance that contains cholesterol. Cholesterol is essential for cells but too much can lead to CHD and stroke. Lipoproteins carry cholesterol to and from the cells in the blood. Low-density lipoprotein (LDL) takes cholesterol from the liver to the cells, and highdensity lipoprotein (HDL) carries excess cholesterol back to the liver for excretion. HDL is known as the ‘good fat’ while LDL (‘bad fat’) tends to build up on the walls of the arteries increasing the risk of CHD and stroke.
There are several well-documented risk factors for CVD including:
- Smoking – significantly increases the risk of CHD
- Obesity – more than a quarter of adults in England are obese and around 30 per cent of boys and girls aged two to 15 in England and Scotland are overweight or obese
- Alcohol – more than a third of men and over a quarter of women regularly exceed the government recommended level of alcohol intake
- Blood pressure – around one in three adults in England and Scotland have high blood pressure and nearly half of them are not receiving treatment for it
- Cholesterol – around six in 10 adults in England have cholesterol levels of 5mmol/l or above (you should aim to have a cholesterol level under 4mmol/l)
- Poor diet – less than one third of men and women currently eat the recommended five portions of fruit and vegetables per day in Britain, only around one in five boys and girls aged five to 15 consume the recommended amount
Source: BHF, 2013
Some risk factors put you at greater risk of CHD and stroke than others but the more risk factors you do have, the greater your chance of developing CVD. However, having a risk factor does not necessarily mean you will develop CVD, it just means it is more likely. So, limiting your risk factors reduces your risk.
Figure 7.0 shows how the number of deaths from CHD has fallen markedly since the late 1960s. This is because of a combination of factors including improvements in medical treatment and lifestyle changes. For example a vast improvement has been made in the speed at which so-called clot-busting drugs are applied, which has had a huge impact in preventing death. Furthermore, nearly two million people receive drugs called statins that lower cholesterol levels and reduce the risk of heart disease. Research suggests that statins may prevent cardiovascular events and reduce subsequent mortality by up to 60 per cent (Mills et al., 2008).
Many people have quit smoking, which has had a significant effect on lowering their risk of heart disease. Figures from the UK’s Office of National Statistics’ Opinions and Lifestyle Survey show that 45 per cent of adults smoked in 1974 compared with 20 per cent in 2012. This has contributed to the decline in smoking-related heart disease and subsequent mortality. The risk of CVD dramatically decreases when a person quits smoking and continues to fall rapidly for the first year and after five years the risk of CVD returns to the level of that of a non-smoker (Glantz and Gonzalez, 2012). UK Government initiatives encouraging people to reduce their salt intake (linked to high blood pressure) are also likely to have contributed to the decline in high blood pressure-related mortality (Office for National Statistics, 2013).
However, while fewer people are dying from CVD, the number of people living with it has remained relatively constant over the last decade. Figure 8.0 shows that from 2000 to 2010, the percentage of men and women (aged over 16 years) with CVD in Great Britain varied moderately, remaining between nine and 12 per cent (falling no lower than 9.4 and rising no higher than 11.9). The benefits we should be seeing, due to the advances in medical treatment and the reduction in smoking, are being negated by an increase in deaths attributable to rises in body mass index and diabetes.
Researchers from the Department of Applied Health Research, at the University College London used a well-known, tried and tested epidemiological model (IMPACT) to analyse the total population of England aged 25 and older in 2000 and 2007 (Bajekal et al., 2012). They included all the major risk factors for CHD plus 45 current medical and surgical treatments in their model. They found that half (52 per cent) of the recent CHD mortality fall in England was attributable to improved treatment uptake. However, opposing trends in major lifestyle risk factors meant that the net contribution of these interventions amounted to only just over a third of the CHD deaths averted. In other words, despite the medical advances of the last ten years, plus the large drop in the number of smokers in the UK, we are not reaping the benefits as much as we could because of poor lifestyle and dietary choices. You could say it is a case of ‘two steps forward and one step back’. Furthermore, concerns are that the decline in deaths from heart disease may be short lived due to the increasing levels of inactivity, the rise in obesity, the increase in cholesterol levels and the rise of type 2 diabetes.
The quest to identify dietary and lifestyle risk factors for CHD dates back over five decades. In 1946 Los Angeles physician Dr Lester Morrison began a study to determine the relationship of dietary fat intake to the incidence of CHD (Morrison, 1960). He reduced the dietary fat intake of 50 heart attack survivors and compared their health to 50 other heart attack survivors whose fat intake was left unchanged. After eight years, 38 of the control group had died compared to 22 of the low-fat group. After 12 years, the entire control group had died but 19 ofthe low-fat diet group were still alive. Around the same time, the residents of Framingham, just outside Boston Massachusetts in the US, took part in a study to investigate the role of diet and lifestyle in CHD. The study began in 1948, and by observing who suffered from CHD and who did not, the Framingham Study established the concept of risk factors such as cholesterol, high blood pressure (hypertension), lack of physical exercise, smoking and obesity (Kannal et al., 1961).
It is important to note that dietary risk factors for CVD do not just apply to adults. Various studies warn of the increased risk of CVD (later in life) associated with the consumption of cow’s milk and cow’s milk infant formula in young children. A review on infant feeding practices published in the US journal Pediatrics suggests that the consumption of whole milk should be discouraged in infants because of its potential role in atherosclerotic heart disease (Oski, 1985).
In 2002, a substantial report of a joint WHO/FAO expert consultation review of the evidence on the effects of diet and nutrition on chronic diseases stated that:
“Data from most, but not all, observational studies of term infants have generally suggested adverse effects of formula consumption on the other risk factors for cardiovascular disease (as well as blood pressure), but little information to support this finding is available from controlled clinical trials. Nevertheless, the weight of current evidence indicates adverse effects of formula milk on cardiovascular disease risk factors; this is consistent with the observations of increased mortality among older adults who were fed formula as infants. The risk for several chronic diseases of childhood and adolescence (e.g. type 1 diabetes, coeliac disease, some childhood cancers, inflammatory bowel disease) have also been associated with infant feeding on breast-milk substitutes and short-term breastfeeding” (WHO/FAO, 2002).
A more recent review of the current literature concurred that being breastfed as an infant (as opposed to cow’s milk formula-feeding) is associated with a reduction in blood pressure, cholesterol and a lower risk of obesity and diabetes in adult life. The authors stated that although the effects on CVD risk factors are modest, breastfeeding rates are suboptimal in many countries and strategies to promote breastfeeding could therefore confer important benefits for cardiovascular health at a population level (Robinson and Hall, 2012). The authors concluded that there is a growing recognition of the need for a life course approach to understanding how adult diseases, such as CVD, develop and there is now significant evidence that links patterns of infant feeding to different health outcomes both in the short and longer term.
As stated, a number of risk factors are now firmly associated with CHD including high cholesterol levels, high blood pressure, family history of heart disease, diabetes, obesity and smoking. Additionally, there is much evidence linking CHD to poor dietary practices, including the high consumption of saturated fats, salt and refined carbohydrates, and the low consumption of fruits and vegetables (WHO/FAO, 2002).
A certain amount of cholesterol is essential for good health, but high cholesterol levels in the blood are associated with an increased risk of CHD and stroke. This is because cholesterol contributes towards the build-up of fatty plaques on the artery walls which results in the narrowing of the arteries and can lead to a blockage and subsequent failure or death of the organ that the artery provides blood to. The organs affected often include the heart (heart attack) and brain (stroke), but may affect other organs such as the kidneys (kidney failure). But what determines blood cholesterol levels? Contrary to popular belief, most of our cholesterol does not come from the diet but is produced within the body by the liver. Only a small amount of our cholesterol (estimates vary from 15 to 20 per cent) comes from the diet. Cholesterol is found only in animal foods and is particularly concentrated in eggs and organ meats. Even high-fat plant foods, such as avocados, nuts and seeds, contain no cholesterol whatsoever, so a plant-based vegan diet is cholesterol-free. We have no actual dietary requirement for cholesterol, in other words we do not need to eat foods that contain cholesterol as the liver can manufacture as much as is required. However, there is no mechanism limiting the amount of cholesterol produced by the liver and cholesterol production can rise to unhealthy levels.
So what causes high cholesterol production in the liver? The answer lies in the types of foods we eat: diets high in animal protein and saturated animal fats have been shown to increase cholesterol. The cholesterol-raising effects of saturated fat are well-documented. In a review of the literature, researchers from the Department of Nutrition at the Harvard School of Public Health in Boston, Massachusetts, found compelling evidence that the types of fat are more important than total amount of fat in determining the risk of CHD (Hu et al., 2001). Here the culprit is saturated fat, and controlled clinical trials have shown that replacing this type of fat with polyunsaturated fat is more effective in lowering cholesterol and reducing the risk of CHD than reducing total fat consumption. In 1985, research published in the Journal of the American Medical Association suggested that dairy products are a major source of dietary saturated fat and cholesterol and that ingestion of high-fat dairy products raises both total and LDL ‘bad’ cholesterol levels (Sacks et al., 1985). It is now widely accepted that diets high in animal fats are unhealthy and that reducing the saturated fat intake is very important for reducing the risk of CHD. The UK Government recommends avoiding or cutting down on fatty foods. Foods high in saturated fat include: meat pies, sausages and fatty cuts of meat, butter, ghee, lard, cream, hard cheese, cakes and biscuits and foods containing coconut or palm oil (NHS Choices, 2013c). Like saturated fats, trans fats can also raise cholesterol levels. Trans fats are found naturally at low levels in meat and dairy products and foods containing hydrogenated vegetable oil, including processed foods such as biscuits, cakes, fast food, pastry, margarines and spreads. However, most people in the UK don’t eat a lot of trans fats as many supermarkets in the UK have removed hydrogenated vegetable oil from their products.
As stated, replacing saturated fat with polyunsaturated fat is more effective in lowering cholesterol and reducing the risk of CHD than reducing total fat consumption. Studies on the protective effect of seafood polyunsaturated omega-3 fatty acids (EPA and DHA) have produced mixed results because of the relatively high levels of pollutants found in oily fish. A 2012 meta-analysis published in the Journal of the American Medical Association of 20 studies and 68,680 patients found that fish oil supplementation did not reduce the chance of death, cardiac death, heart attack or stroke (Rizos et al., 2012). Furthermore, some positive results have been wildly exaggerated (NHS Choices, 2012l). In a meta-analysis of studies looking at the plant-based omega-3 fatty acid ALA (found in soya beans, walnuts and canola/rapeseed oil) it was found that each gram per day increment of ALA intake was associated with a 10 per cent lower risk of CHD death (Pan et al., 2012). The authors state that compared with seafood omega-3 fatty acids, ALA from plant sources is more affordable and widely available globally. Thus, whether ALA can reduce the risk of CVD is of considerable public health importance. It should be noted that algal sources of EPA and DHA are now available in supplement form for people concerned about their omega-3 intake.
In The China Study, Campbell observes that animal protein intake correlates directly with heart disease incidence, which he attributes to the cholesterol-raising effect of animal protein. Conversely, Campbell notes that eating plant protein lowers cholesterol (Campbell and Campbell, 2005). Studies have shown that replacing animal milk protein (casein) with soya protein reduces blood cholesterol,even when the fat intake remains unchanged (Lovati et al., 1987; Sirtori et al., 1999). Exactly how soya protein lowers cholesterol is uncertain, although a range of theories have been proposed. One hypothesis suggests that the amino acid composition of soya protein causes changes in cholesterol metabolism (possibly via the endocrine system). Others propose that non-protein components (such as saponins, fibre, phytic acid, minerals and isoflavones) associated with soya protein affect cholesterol metabolism either directly or indirectly (Potter, 1995). The most popular theory currently accepted is that soya protein reduces cholesterol metabolism in the liver by increasing the removal of LDL ‘bad’ cholesterol. The precise mechanism is thought to involve enhanced LDL-degradation by increased binding of LDL to receptors (Sirtori et al., 1977; Lovati et al., 2000).
A cross-sectional study of 1,033 pre- and postmenopausal women selected from the Oxford arm of the EPIC study (including 361 non-vegetarians, 570 vegetarians and 102 vegans) found that soya protein intake was inversely associated with total and LDL cholesterol levels. LDL (‘bad’)cholesterol in women with a soya protein intake of at least six grams per day was 12.4 per cent lower than that in women who consumed less than 0.5 grams per day (Rosell et al., 2004).
More recently, a meta-analysis of studies examining the extent to which soya foods could reduce LDL cholesterol found that replacing meat or dairy protein with 13 grams of soya protein resulted in a LDL cholesterol reduction of 0.15mmol/l, 50 grams of soya protein reduced the level by 0.25mmol/l (Jenkins et al., 2010). This represents a reduction of around 4.3 per cent in LDL cholesterol with a potential additional reduction of 3.6-6.0 per cent due to displacement of saturated fat and cholesterol depending on the diet and the foods displaced. Based on these assumptions, the authors concluded that soya foods have the potential to lower LDL cholesterol by as much as 10.3 per cent. The authors state that the displacement value may be unique to soya, because other cholesterol-lowering foods are added to the diet rather than exchanged for suboptimal (meat and dairy) foods. They say that this makes soya a particularly valuable tool in the dietary armamentarium to reduce serum cholesterol. In addition, many soya products could be beneficial to cardiovascular and overall health because of their high content of polyunsaturated fats, fibre, vitamins and minerals and low content of saturated fat. Replacing cheese, meat and other animal foods with soya can mean using tofu, soya beans (edamame) or soya milk (in a white sauce). Soya-based faux meats (such as soya mince) can be used although the amount of processed food in the diet should be limited as they can contain relatively high levels of saturated fat and salt, but still remain a healthier option than meat and dairy.
Many other plant foods (and components of them) are known to possess cholesterol-lowering properties including nuts, plant sterols and viscous (soluble) fibres. Individually, these plant food components can be expected to lower LDL cholesterol in the range of 3-10 per cent, far less than the 40-60 per cent reductions achievable with statins. However, collectively they could reduce LDL cholesterol by up to 30 per cent, which would have a considerable impact on preventing CHD (Jenkins et al., 2010).
Eating a diet that contains plenty of soluble fibre can help to reduce the amount of cholesterol in the blood and so reduce the risk of CHD. Good sources of soluble fibre include oats, beans, peas, lentils, chick peas, fruit and vegetables (NHS Choices, 2013c). Increased consumption of fruit and vegetables is associated with a reduced risk of CHD. A meta-analysis of twelve cohort studies including 278,459 individuals (9,143 CHD events) with an average follow-up of 11 years found that, increasing consumption of fruit and vegetables from less than three to more than five servings per day reduced CHD risk by 17 per cent. The authors state that these results provide strong support for the recommendations to consume more than five servings of fruit and vegetables a day (He et al., 2007). The government recommend that we eat at least five portions of fruit and vegetables each day. Dr Dean Ornish, best known for his Lifestyle Heart Trial, investigated the role of a low-fat, high-fibre diet coupled to lifestyle changes in heart disease patients. Ornish treated 28 heart disease patients with diet and lifestyle changes alone. They followed a low-fat plant-based diet including unrestricted amounts of fruits, vegetables and grains. They also practised stress management techniques and exercised regularly. After one year 82 per cent of the test group experienced regression of their heart disease, including a 91 per cent reduction in the frequency of heart pain compared to 165 per cent increase in the control group (Ornish et al., 1990). No conventional drug or surgery related therapies compare with these results (Campbell and Campbell, 2005).
A study published in the Journal of the American College of Nutrition investigating the risk factors associated with CHD found that African-American vegans exhibit a more favourable serum lipid profile (a healthier balance of fats in the blood) compared to vegetarians who ate milk, milk products and eggs (Toohey et al., 1998). This means that the vegans had healthier levels of total cholesterol, LDL and HDL in their blood compared to the vegetarians. The major factors contributing to this result were thought to be the lower saturated fat intake and higher fibre intake of vegans.
Examining the incidence of CHD in other cultures allows us to draw conclusions about the role of diet in disease. Several studies have shown that certified death rates from CHD are linked country-by-country with milk consumption (Moss and Freed, 2003). In The China Study, Campbell was astonished at the low rates of CHD in the southwest Chinese provinces of Sichuan and Guizhou; between 1973 and 1975 not one single person died of CHD before the age of 64 among 246,000 men and 181,000 women (Campbell and Campbell, 2005). Campbell suggests these figures reflect the important protective role of low blood cholesterol levels observed in rural China.
A joint report between the Medical Research Council and the British Heart Foundation states that the average blood total cholesterol level for people aged 16 and above in the UK is about 5.5mmol/l. In China (where there is much less heart disease), mean total cholesterol levels in the cities are about 4.5mmol/l for men and women aged 35-64, and levels in the countryside are even lower (MRC/BHF, 2006). According to the WHO, almost a fifth (18 per cent) of global stroke events and about 56 per cent of global heart disease is attributable to total cholesterol levels above 3.2mmol/l (WHO, 2003). It could be argued that genetic differences between races may affect the risk factors for CHD and other diseases. However, Campbell’s observations that Japanese men in Hawaii and California have much higher levels of blood cholesterol and incidence of CHD than Japanese men in Japan confirms that some risk factors are environmental rather than genetic. In other words, the choices we make about the food we eat and how we live can have a significant impact on heart health.
Since the early 1990s the amino acid homocysteine has become the subject of much interest among the scientific community. Evidence suggests that homocysteine damages the lining of blood vessels and enhances blood clotting. Elevated concentrations of homocysteine in the blood have been linked to an increased risk for both heart disease and stroke. Homocysteine is converted into the amino acid methionine in the presence of vitamin B12. In the same reaction, methyltetrahydrofolate is converted to folate which is used in the synthesis of DNA. This entire reaction relies on sufficient supplies of vitamins B6, B12 and folate. In B12 deficiency, the amount of homocysteine in the body can escalate to potentially dangerous levels and has been linked to a range of disorders including depression, dementia, damage to the inner lining of the artery walls and may be a trigger for CHD. While increased homocysteine levels have been observed in some vegetarians and vegans they do not occur in those ensuring an adequate B12 intake of three micrograms per day, whereas elevated homocysteine levels are not uncommon among meat-eaters due to a low folate intake (Walsh, 2003). Additionally, elevated serum homocysteine levels tend to increase in the elderly as incidence of B12 deficiency occurs more frequently. Interestingly, a recent study showed how a daily serving of breakfast cereal fortified with folic acid, B6 and B12 not only contributed to the plasma status of these vitamins but significantly reduced homocysteine concentrations in a randomly selected group of relatively healthy 50-85 year olds (Tucker et al., 2004).
The role of a vegetarian and vegan diet in nutrition and health was examined among a large group of vegetarians in the Oxford Vegetarian Study (Appleby et al., 1999). This was a prospective study of 6,000 vegetarians and 5,000 non-vegetarian controlled subjects recruited in the UK between 1980 and 1984. In this study vegans had lower cholesterol levels than meat-eaters (vegetarians and fish-eaters had intermediate or similar values). Meat and cheese consumption were positively associated, and dietary fibre intake was inversely associated, with cholesterol levels. After 12 years of follow-up, mortality from heart disease was positively associated with estimated intakes of total animal fat, saturated animal fat and dietary cholesterol. A subsequent review of the literature comparing the health of Western vegetarians to non-vegetarians found that vegetarians had lower cholesterol levels (by about 0.5mmol/l) and a lower mortality from heart disease (by about 25 per cent). It was suggested that the widespread adoption of a vegetarian diet could prevent approximately 40,000 deaths from heart disease in Britain each year (Key et al., 1999).
Taken together, the evidence shows that a plantbased diet reduces the risk of CHD. This may be for a range of reasons including the cholesterol-lowering effect of fibre. It has been suggested that the antioxidants (beta-carotene and vitamins C and E) contained in fruit and vegetables and cereals prevent saturated fats from being converted into cholesterol in your body. Whatever the precise mechanism, the evidence is clear: a plant-based diet containing plenty of fruits and vegetables and whole grains reduces the risk of CHD. There is much speculation about how the consumption of animal foods increases the risk of CHD. Again, the precise mechanisms involved may be unresolved, but it is clear that the more animal foods a person eats, the higher their risk. In summary, animal protein and saturated animals fats increase blood cholesterol and the risk of CHD while plant protein and fibre lowers cholesterol and reduces the risk. Therefore, to reduce the risk of CHD we should reduce the amount of animal foods in the diet and eat more wholegrain, plant-based foods.
There are of course other factors that can contribute to the risk of CHD. Exercise is extremely important as it increases HDL cholesterol levels, which in turn helps keep LDL cholesterol levels down. Exercise also helps control weight. As stated, smoking is a major risk factor of CHD as it hardens the arteries, causing them to narrow. Alcohol consumption can increase the risk so it should be limited and binge drinking avoided.