Colic was first mentioned in recorded history by the ancient Greeks (Cirgin Ellett, 2003) yet in 2005 the cause remains unknown. Colic occurs in around one in five newborn babies, it is characterised by acute abdominal pain and the associated heart-wrenching crying that any parent of a child with colic will recognise. An otherwise healthy baby who cries excessively or inconsolably is often diagnosed as suffering from colic. While the exact cause is unknown several factors are thought to contribute including poor digestion, lactose intolerance and wind. Colic tends to start at around two to four weeks of age and has usually disappeared by around four months. In spite of all the distress colic can cause to the baby and the parents, babies with colic tend to feed and gain weight normally.
Since the 1970s, numerous studies have indicated that certain components of cow’s milk may lead to colic. In a clinical trial to test the effects of cow’s milk whey proteins, 24 out of 27 infants with colic showed no symptoms of colic after whey protein was removed from their diet. In fact crying hours per day dropped from 5.6 hours to 0.7 hours (Lothe and Lindberg, 1989). In transient lactose intolerance, the enzyme lactase is not produced while there is illness in the gut, but is manufactured again once the gut has recovered. In a review investigating transient lactose intolerance as a cause of colic, a range of studies showed that crying time was reduced when formula or breast milk was incubated with the enzyme lactase (Buckley, 2000). It has been suggested that infant colic has a multiple aetiology; in other words, colic may be caused by a number of different factors including whey proteins, lactose and others.
The fact that the incidence of colic is similar in formula fed and breast fed infants has led scientists to investigate the role of the maternal diet in this condition and many reports now link the maternal intake of cow’s milk to the occurrence of colic in exclusively breast fed infants. The breast milk of mothers who consume cow’s milk and milk products has been shown to contain intact proteins from these foods. To test the possible role of cow’s milk proteins in breast milk, researchers have investigated the effects of eliminating all dairy products from the mothers’ diet. An early report linking cow’s milk proteins in human breast milk to infantile colic date back to a letter published in the Lancet in the late 1970s (Jakobsson and Lindberg, 1978). The letter described how the symptoms of colic disappeared in 13 out of 19 infants whose mothers eliminated cow’s milk from their diet. In a subsequent clinical trial designed by the same researchers, 66 breast feeding mothers of infants with colic were put on a diet free from cow’s milk. The colic disappeared in 35 of the infants and subsequently reappeared in 23 of them when cow’s milk protein was reintroduced to the mothers’ diet (Jakobsson and Lindberg, 1983). The authors suggest that a diet free of cow’s milk may be useful as a first trial of treatment of infantile colic in breast fed infants.
Researchers at the Washington School of Medicine in Missouri US found that mothers of infants with colic had significantly higher levels of the cow’s milk antibody immunoglobulin G (IgG) in their breast milk than mothers of infants without colic (Clyne and Kulczycki, 1991). The authors of this study suggest that bovine IgG present in breast milk may be involved in the development of colic. This link was confirmed more recently and again it was suggested that the maternal avoidance of milk and dairy products may be an effective treatment for colic in some breast fed infants (Estep and Kulczycki, 2000).
In a substantial review of 27 controlled trials published in the British Medical Journal, the elimination of cow’s milk protein was deemed to be a highly effective treatment for infantile colic. The reviewers remained uncertain about the effectiveness of low lactose formula milks and the effectiveness of substitution with soya-based formula milks (although no adverse events were reported) while supporting the substitution of normal cow’s milk formula for whey or casein protein hydrolysate (hypoallergenic) formulas, in which the milk protein is partially broken down to ease digestion (Lucassen, 1998).
Interestingly, Dr Benjamin Spock, author of the hugely popular book Baby and Child (over 50 million copies sold worldwide) warns that the proteins in cow’s milk formulas can cause colic (Spock and Parker, 1998). Spock acknowledges that some infants that are allergic to cow’s milk formula may be allergic to soya-based infant formula as well and that these infants are often given expensive hydrolysate formulas. However, he states that soya formulas have an important advantage over cow’s milk formulas in that they contain none of the animal proteins linked with colic (and type I diabetes) and are free of lactose.
This said, it should be emphasised to parents who breast feed, it is a good idea to continue breast feeding as weaning on to formula milk may make the colic worse. If eliminating cow’s milk and milk products from the maternal diet does not help, cutting out other foods may help. Researchers at the University of Minnesota tested a range of foods including cruciferous vegetables (cabbage, cauliflower, sprouts and broccoli) in an elimination diet in mothers of babies with colic. While the results showed that cow’s milk had the strongest association with colic, other foods more weakly associated included onions, chocolate, cabbage, broccoli and cauliflower (Lust et al., 1996).
Constipation is a condition in which bowel movements are infrequent or incomplete. While it is normal for some people to go to the toilet several times a day, others go less frequently. A change in the normal frequency of trips to the toilet can be an indicator of constipation. Similarly if you are going as frequently but having trouble passing stools, having to strain, this too may indicate constipation. Common symptoms include stomach ache and cramps, feeling bloated, nausea, a sense of fullness, headache, loss of appetite, fatigue and depression (NHS Direct, 2005).
Constipation may be caused by a range of factors including insufficient fluid in the diet, lack of fibre (fruit, vegetables and cereals) in the diet, lack of physical exercise, certain drugs (diuretics or painkillers, antidepressants and antacids that contain iron, calcium or aluminium), too much calcium or iron in the diet, pregnancy, an excessive intake of tea or coffee (this increases urine production and so decreases the amount of fluid in the bowel). Other factors include surgery, haemorrhoids (piles) and psychological problems such as anxiety. Constipation may be a symptom of another medical condition such as irritable bowel syndrome (IBS).
The link between constipation and milk intolerance was first made in medical literature in 1954 (Clein, 1954). More recently there have been several studies published confirming that this link exits. Researchers at the University of Palermo in Italy studied 65 children (aged from 11 to 72 months) suffering from chronic constipation (Iacono et al., 1998). All of these children had been treated with laxatives without success. After 15 days of observations (in a double-blind crossover study) each child received either cow’s milk or soya milk for two weeks, and then had a week off when they could eat and drink anything they wanted. Then the feeding order was reversed, so that the group that had previously drunk cow’s milk switched to soya and vice versa. The researchers (and children) were unaware of the order of treatment. Careful recordings of the bowel habits were made and a response to the treatment was defined as eight or more bowel movements during the two week treatment period. Results showed that 44 of the 65 children (68 per cent) had a response while receiving soya milk compared to none of the children receiving cow’s milk. The results were most dramatic in children who had frequent runny noses, eczema or wheezing, which may have been a symptom of milk allergy in these children. Sometimes however, constipation can be the only symptom of cow’s milk intolerance or allergy. More recently further research has confirmed the link between the consumption of cow’s milk and constipation (Daher et al., 2001; Andiran et al., 2003; Turunen, 2004).
Cow’s milk may lead to constipation by two distinct modes of action: cow’s milk intolerance or cow’s milk allergy. In either case, studies suggest that cow’s milk intolerance or allergy should be considered as a cause of constipation although the underlying mechanism still requires further investigation. In general it should be noted that dairy products supply children with unnecessary saturated fat while providing no dietary fibre whatsoever. Fibre is essential in the diet to maintain good bowel health through regular movements.
Diseases of the heart and circulatory system are collectively called cardiovascular disease (CVD) and are the main cause of death in the UK, killing one in every three people. Coronary heart disease (CHD) is one of the two main forms of CVD along with stroke. CHD is the most common cause of death in the UK; around one in five men and one in six women die from this disease (Petersen et al., 2005).
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. 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. Lipoproteins carry cholesterol to and from the cells in the blood. Low-density lipoprotein (LDL) takes cholesterol from the liver to the cells, and high-density 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.
Figure 7.0 Death rates from CHD for people aged under 65 from 1970 to 2002.
Source: BHF, 2005.
Figure 7.0 shows how the number of deaths from CHD has fallen markedly since the 1970s. This may be because of improvements in treatment and lifestyle. 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. Many people have given up smoking, which has a significant effect on lowering the risk of heart disease.
Figure 8.0 Prevalence of CHD in England in 1994 and 2003.
Source: BHF, 2005a.
However, while fewer people are dying from CHD, the number of people living with this disease is rising. Figure 8.0 shows that over ten years, between 1994 and 2003, the number of women with CHD increased from 4.1 per cent to 4.5 per cent, and the number of men with CHD increased from 6.0 per cent to 7.4 per cent. There are now an estimated 2.6 million people in the UK facing life with CHD (BHF, 2005a). Furthermore, concerns remain 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 the 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 of the 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).
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 including egg yolks, red meat, butter, whole milk, cheese, cakes and chips to reduce the intake of saturated fat (NHS Direct, 2006).
Dietary risk factors for CVD do not just apply to adults. A review on infant feeding practices published in the US journal Pediatrics suggested that the consumption of whole milk should be discouraged in infants because of its potential role in atherosclerotic heart disease (Oski, 1985). More recently the WHO stated that the current evidence indicates undesirable effects of formula milk on CVD risk factors; this is consistent with the observations of increased mortality among older adults who were fed formula as infants (WHO/FAO, 2002).
A number of risk factors are now firmly associated with CHD including high blood 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. 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 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 and increased binding of LDL to receptors (Sirtori et al., 1977).
The cholesterol-raising effects of saturated fat have received far more attention than animal protein. In a review of the current 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. 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 (FSA, 2006). Like saturated fats, trans fats can also raise cholesterol levels. Trans fats are found in foods that contain hydrogenated fats, including processed foods such as biscuits, cakes, fast food, pastry, margarines and spreads (FSA, 2006).
The good news is that there are foods that can reduce blood cholesterol. Eating a diet that contains plenty of soluble fibre could also help to reduce the amount of cholesterol in the blood. Good sources of soluble fibre include oats, beans, peas, lentils, chickpeas, fruit and vegetables (FSA, 2006). 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, about 56 per cent of global heart disease is attributable to total cholesterol levels above 3.2mmol/l (WHO, 2006). 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.
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. Some studies suggest it may have an even more important role in determining the health of individuals than cholesterol (Walsh, 2003). Homocysteine is converted into the amino acid methionine in the presence of 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 B12, B6 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 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 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 plant-based 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 (NHS Direct, 2006). 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 whole grain, 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.
Crohn’s disease is a chronic inflammatory bowel disease (IBD). Its symptoms are similar to other bowel conditions such as irritable bowel syndrome (IBS) and another IBD ulcerative colitis. Crohn’s disease commonly occurs in the ileum (the lower part of the small intestine), but it can affect any part of the bowel. In fact it can occur anywhere along the entire alimentary tract from the mouth to the anus. In most cases though, Crohn’s disease occurs in sections of the bowel which become inflamed, ulcerated and thickened. Symptoms include diarrhoea, abdominal pain, weight loss and tiredness. According to the National Association for Colitis and Crohn’s Disease, the disease affects about one in every 1,600 people in the UK. Other studies have reported higher figures; up to one in 690 in one regional study. A reasonable ballpark figure may be around one in every 1,000 people (FSA, 2002a). Crohn’s disease affects men and women equally but occurs more commonly in white than black people. It usually occurs in the age group between 15 and 40 although it can affect people of any age.
Although the cause of Crohn’s disease remains unclear, it may be due to a combination of factors including a genetic predisposition, an abnormal immune response and environmental factors, probably relating to a response to microorganisms in the bowel but also possibly related to other dietary factors (FSA, 2002a).
It has been proposed that an environmental factor leading to Crohn’s disease is a pathogenic bacterium. The most popular candidate is the infectious bacterium Mycobacterium avium subspecies paratuberculosis(MAP). MAP infection is widespread in domestic livestock and is present in commercial pasteurised cow’s milk in the UK. There are concerns that water supplies may also be contaminated. MAP is a robust and versatile pathogen which has been shown to cause chronic inflammation in the intestines of many species of animal, including primates. MAP causes a chronic gastrointestinal infection called Johne’s disease in cattle and other ruminants. However, the link between MAP and Crohn’s has remained somewhat controversial.
An increasing amount of evidence now supports the causal link between MAP and Crohn’s disease. Researchers at the University of Wisconsin used a range of modern molecular techniques to search for and confirm the presence of MAP in patients with IBDs including Crohn’s (Collins et al., 2000). The results showed MAP was present in around 20 per cent of Crohn’s patients compared to less than seven per cent of controls (without Crohn’s). Although these results may not have provided the substantive evidence initially anticipated the researchers concluded that MAP (or some similar species) infects a subset of IBD patients.
More recently, Professor John Hermon-Taylor and colleagues at St George’s Hospital Medical School in London tested a group of patients with and without Crohn’s disease for MAP (Bull et al., 2003). Using improved molecular methods that increased the sensitivity of the tests, this time 92 per cent of patients with Crohn’s disease tested positive compared to 26 per cent of the controls. These patients were from the UK, Ireland, US, Germany and United Arab Emirates, suggesting exposure to this pathogen occurs on an international basis. The discovery that MAP is present in the majority of Crohn’s patients would suggest a causal link between this bacterium and the condition. Since then, additional reports have confirmed MAP as a predominant feature of Crohn’s disease (Autschbach et al., 2005; Sechi et al., 2005).
But how does MAP infection occur? The answer may lie under our very noses, depending on what we are drinking. MAP can survive the pasteurisation process, indeed an FSA-commissioned survey in 2002 found MAP in two per cent of pasteurised milk on sale in the UK (FSA, 2002a). However, researchers from the Department of Surgery at St George’s Hospital Medical School in London detected MAP in 22 of 312 (seven per cent) of samples of whole pasteurised cow’s milk obtained from retail outlets throughout central and southern England from September 1991 to March 1993. Alarmingly this study revealed the presence of peak periods in January to March and in September to November, when up to 25 per cent of samples tested positive for MAP (Millar et al., 1996). Taken together with data on the prevalence of MAP infection in herds in the UK, the known secretion of MAP in milk from infected animals, and the inability of laboratory conditions simulating pasteurisation to ensure the killing of all these slow-growing organisms, the authors of this study concluded that there is a high risk, particularly at peak times, that residual MAP will be present in retail pasteurised cow’s milk in England. In response to concerns about the presence of MAP in retail milk, the FSA devised a strategy to control MAP in milk at all stages of the food chain (FSA, 2003). This strategy aims to ensure hygienic milking practices and effective pasteurisation of milk and reduce the level of MAP in dairy herds. Of course the overall aim is to reduce the likelihood of consumers being exposed to MAP. However, this strategy does not consider alternative routes of exposure.
MAP is a robust organism which can survive for months or even years in the environment which is a cause of much concern as infected animals excrete huge numbers of MAP in their faeces. In South Wales, researchers sampled river water from the Taff which runs off the hills and through the city of Cardiff and detected MAP in 32.3 per cent of the samples (Pickup et al., 2005). The hills are grazed by livestock in which MAP is endemic. Previous research in Cardiff has shown a steep increase in the incidence of Crohn’s disease. Given that inhalation is a probable route of MAP infection in cattle, it was suggested that the pattern of clustering of Crohn’s disease in Cardiff may be due to people inhaling aerosols carrying MAP from the river. Avoiding dairy products alone may not be enough to ensure avoiding exposure to MAP (although if everyone reduced their intake of animal products there would be fewer cattle and therefore less MAP present in the environment).
For patients that have developed Crohn’s disease avoiding foods that precipitate the symptoms has proved to be a successful way of avoiding drug (corticosteroid) therapy. In the Lancet in 1993, researchers from a Cambridge hospital reported that altering the diet was as effective in producing remission of Crohn’s disease as corticosteroid treatment thus providing an alternative therapeutic strategy to treating Crohn’s. The research showed that the food intolerances were predominantly to cereals, dairy products and yeast (Riordan et al., 1993). Manipulating the diet rather than relying on drug therapy may be particularly important as corticosteroid treatment in patients with Crohn’s disease has been linked to osteoporosis (Dearet al., 2001).