One in four people in England will die of cancer. More than one in three people will develop cancer at some stage in their lives. Over 200,000 people are diagnosed each year with the disease; that is 600 new cases each day. Cancer is now the single most common cause of death in men and women in the UK (Department of Health, 2000). Whichever way the statistics are presented cancer remains the disease that people fear most.
Mortality from cancer over the last 50 years has remained fairly constant (Department of Health, 2000). This is very worrying when you consider the vast improvement in both cancer diagnosis techniques and cancer treatment methods. It means that even more people are getting cancer and the medical profession are running just to stand still.
Most people now recognise that smoking is the biggest single preventable risk factor for cancer. Indeed smoking causes one third of all cancers including cancers of the lung, mouth, nasal passages, larynx, bladder and pancreas. Smoking also plays a role in causing cancers of the oesophagus, stomach, kidney and in leukaemia. Smoking kills around 120,000 people in the UK per year (Department of Health, 2000). Stopping smoking, even when middle-aged, can dramatically reduce the risk of developing cancer.
However, it is less well known that a poor diet is the second largest preventable risk factor for cancer, coming close behind smoking. It is becoming clearer as research continues that nutrition plays a major role in cancer (Donaldson, 2004). A diet rich in saturated animal fats, cholesterol, animal protein, sugar, salt and processed foods has been shown to increase the risk of certain cancers. Indeed a poor diet may be responsible for up to a third of all cancer deaths (Department of Health, 2000). Cancers specifically linked to diet include cancers of the bowel, stomach, mouth, larynx and oesophagus. A poor diet can also greatly contribute to the risk of many other cancers including breast and prostate cancer (Cancer Research UK, 2005). There is an increasing amount of evidence linking the consumption of cow’s milk to certain cancers. One of the reasons for this is the increasing levels of hormones and other bioactive compounds present in the milk that result from intensive farming practices (taking milk from pregnant cows). In other words, in an effort to increase milk production, the dairy industry has intensified farming techniques to such a high level that between 75 per cent and 90 per cent of marketed milk and milk products are derived from pregnant cows (Danby, 2005). (See The undesirable components of milk and dairy products)
A plant-based diet containing less saturated animal fats, cholesterol, animal protein, sugar, salt and processed foods protects against cancer. Confirmation of the protective role of a vegetarian diet came in 1994 in a landmark study published in the British Medical Journal (Thorogood, 1994). Researchers found that vegetarians suffer 40 per cent less cancer mortality than the population average, even with controls for smoking, body weight and socio-economic status. The authors of this study stated that while their data do not provide justification for encouraging meat-eaters to change to a vegetarian diet, those who do might expect reductions in premature mortality due to cancer. In other words, you might choose not to give up eating meat but if you do, you will probably live longer.
In Professor T. Colin Campbell’s extensive China Study (one of the largest studies in the world on the effects of diet on health) a startling observation is made. Based on previous work and his own studies, Campbell saw a direct link between dietary protein intake and cancer; the more protein in the diet, the higher the risk of certain cancers, such as liver cancer. But this was not all protein, just animal protein. Campbell decided to look at the relationships between animal protein intake and the incidence of cancer in different cultures.
Colorectal cancer is the fourth most common cancer in the world; it is the second most common in the US. Campbell notes that while North America, Europe, Australia and wealthier Asian countries such as Japan and Singapore have relatively high rates of colorectal cancer, Africa, Asia and most of Central and South America have much lower rates. For example the Czech Republic has a death rate of 34.19 per 100,000 males, while in Bangladesh the figure is just 0.63 per 100,000 males (Campbell and Campbell, 2005). Campbell is not alone in revealing the enormous differences in the incidences of certain cancers between countries. The International Agency for Research on Cancer (IARC) provides startling figures comparing the incidence of breast cancer and prostate cancer in England and Wales to that in rural China. In 1997, in England and Wales, the IARC reported the incidence rate of breast cancer in women was 68.8 per 100,000 compared to just 11.2 per 100,000 in rural China. Similarly the incidence of prostate cancer in men in England and Wales was 28.0 per 100,000 compared to just 0.5 per 100,000 in rural China (IARC, 1997).
Figure 4.0 A comparison of animal protein intake in the US, the UK and rural China.
Source: Campbell and Campbell, 2005; FSA, 2003a.
It is widely acknowledged that the incidence of certain cancers is much greater in some countries than others, what intrigued Campbell was the relationship between these cancers and dietary animal protein. Figure 4.0 shows the differences in animal protein intake between the US, the UK and rural China. In the US, over 15 per cent of total energy intake comes from protein of which 70 per cent is animal protein (Campbell and Campbell, 2005). In the UK, over 16 per cent of food energy comes from protein, and of this, 62 per cent comes from animal foods (FSA, 2003a). While in rural China, the figures are quite different; nine to 10 per cent of total energy comes from protein and only 10 per cent of that is from animal protein (Campbell and Campbell, 2005).
It could be argued that the difference in cancer incidence between cultures reflects genetic differences between ethnic groups rather than environmental (dietary) effects. However, migrant studies have shown that as people move from a low-cancer risk area to a high-cancer risk area, they assume an increased risk within two generations (WCRF/AICR, 1997). Therefore these vast differences in cancer rates must be largely attributable to environmental factors such as diet and lifestyle. Campbell concludes that animal-based foods are linked to an increased cancer risk whereas a whole grain plant-based diet including fibre and antioxidants is linked to lower rates of cancer (Campbell and Campbell, 2005). One possible mechanism for this may be the different composition of animal and plant proteins.
Plant proteins contain a different balance of amino acids than animal proteins. More specifically, plant proteins contain less of the essential amino acids methionine and lysine than animal protein and more of the non-essential amino acids arginine, glycine, alanine and serine. It has been suggested that consuming mostly a plant-based diet has a knock-on effect of limiting the biological activity of certain chemical substances involved in cancer development and that a sufficient consumption of plant proteins has a protective role against cancer (Krajcovicova-Kudlackova, 2005). So a vegetarian diet is a healthier option, not just because it excludes meat and other animal foods but because of the range of beneficial, protective factors present. Vegetarian diets contain less saturated fats and more of the good fats (omega-3 and omega-6 unsaturated fatty acids), more complex carbohydrates, more fibre and more vitamins, minerals and antioxidants. These factors help to explain the reduced risk of cancer in vegetarians.
Increasing your fruit and vegetable consumption is considered the second most effective strategy to reduce the risk of cancer (after stopping smoking). Indeed, one of the most important messages of modern nutrition research is that a diet rich in fruits and vegetables protects not only against cancer, but against many other diseases too including heart disease and diabetes (Donaldson, 2004). It has been estimated that eating at least five portions of fruit and vegetables a day could reduce the risk of death from chronic diseases such as heart disease, stroke and cancer by up to 20 per cent (Department of Health, 2000). In 1998, the Department of Health’s Committee on Medical Aspects of Food Policy and Nutrition reviewed the evidence and concluded that a higher vegetable consumption would reduce the risk of both colorectal and gastric cancer. There was also some evidence that higher fruit and vegetable consumption would reduce the risk of breast cancer (Department of Health, 1998). According to the WHO, low fruit and vegetable intake is estimated to cause about 31 per cent of ischaemic heart disease and 11 per cent of stroke worldwide. Furthermore, they estimate that up to 2.7 million lives could potentially be saved each year if fruit and vegetable consumption was sufficiently increased (FAO/WHO, 2004). This is particularly important for children who eat even more unhealthily than adults in the UK (Cancer Research UK, 2004). Children’s consumption of fruit and vegetables is generally low, with children from disadvantaged families consuming far less than those from high income families. One in five children does not eat any fruit in a week, and three in five eat no leafy green vegetables (Department of Health, 2000).
In a joint report the American Institute for Cancer Research and the World Cancer Research Fund estimate that recommended diets, together with maintenance of physical activity and appropriate body mass, can in time reduce cancer incidence by 30 to 40 per cent. At current rates, on a global basis, this represents between three to four million cases of cancer per year that could be prevented by altering diet and lifestyle (WCRF/AICR, 1997). Increasing our understanding and awareness of the importance of diet and influencing the choices people make about their own diets may significantly reduce the risk of cancer.
There are a number of other factors that can contribute to the development of cancer, including obesity (breast and endometrial cancer), alcohol (mouth, throat, liver and breast cancer), sunlight (skin cancer), radon (lung cancer) and physical activity can protect against some cancers (colorectal).
Cancers of the breast, lung, colorectum and prostate constitute around 50 per cent of all cases of and deaths from cancer in the UK (Department of Health, 2000). The role of cow’s milk and dairy products in breast, colorectal, ovarian and prostate cancer is discussed in more detail.
One in nine women in the UK will develop breast cancer at some point in their lives. In 2003 nearly 40,000 new cases were diagnosed, representing a third of all cancers in women, and in the same year around 10,500 women died from this disease. Between 1971 and 2003, the incidence rates of breast cancer have increased by 80 per cent (National Statistics, 2005). Figure 5.0 shows that while the incidence of breast cancer has risen sharply, mortality from breast cancer has remained fairly constant over the same period thanks largely to improved diagnostic methods and more efficient treatment.
Figure 5.0 Incidence of and mortality from breast cancer in England and Wales
between 1971 and 2001. Source: National Statistics, 2005.
Much has been made of the link between genes and breast cancer. The genes BRCA1 and BRCA2 have received the most attention since they were first discovered in 1994 and 1995 respectively. There are two other very rare genes which probably only account for less than two per cent of all breast cancers: the P53 gene and the AT (ataxia telangiectasia) gene. These recent discoveries linking genetics to cancer has given rise to a certain degree of genetic fatalism. However, current estimates are that only about five per cent of breast cancers are due to abnormal genes (BACUP, 2005). This means that the vast majority of cancers (95 per cent) are not caused by abnormal genes. Secondly, it is important to remember that having an abnormal gene does not mean that a person will definitely develop breast cancer, but does mean they are considerably more at risk of developing the condition than someone who does not have one of the abnormal genes (BACUP, 2005).
The age-adjusted incidence rates per 100,000 for breast cancer differ markedly from one country to another. For example, Uruguay has a very high rate at 114.9, followed by 92.1 in the US and 87.1 in Israel. Much lower rates are seen in Korea at just 12.7, 20.0 in Mali and 16.1 in Thailand (Ganmaa and Sato, 2005). In response to this discrepancy, an increasing amount of attention is now focusing on the links between diet and breast cancer, particularly the relationship between the consumption of cow’s milk and dairy products and breast cancer.
Studying cancer incidence among particular groups of people can provide useful insights into the links between diet and disease. Researchers from the London School of Hygiene and Tropical Medicine recently reported breast cancer incidence is substantially lower, and survival rates higher, in South Asians living in the UK than other women (Farooq and Coleman, 2005). No data on diet was collected but the authors of this study suggested that differences in diet and lifestyle could explain the different rates observed. Earlier research published in the British Journal of Cancer also showed that South Asian women living in the UK are less likely to be diagnosed with breast cancer than other women, but found that the risk varied according to their specific ethnic subgroup. This research showed that Muslim women from India and Pakistan are almost twice as likely to develop breast cancer as Gujarati Hindu women. This study did examine the diet and found that the Gujarati Hindu women were more likely to be vegetarian and therefore had more fibre in their diet due to their higher intake of fruit and vegetables (McCormack et al., 2004). There are several mechanisms by which the diet might influence breast cancer risk. One possible mechanism is through an effect on hormones: increasing the amount of fibre in the diet may reduce breast cancer risk by altering the levels of female hormones (oestrogens) circulating in the blood (Gerber, 1998).
A number of studies show that women with breast cancer tend to have higher levels of circulating oestrogens. Prospective studies follow groups of people over time. Generally these people are alike in many but not all ways (for example, young women who smoke and young women who do not). The prospective cohort study will then look for a link between their behaviour and a particular outcome (such as lung cancer). A prospective study conducted on the island of Guernsey examined serum levels of the oestrogen hormone oestradiol in samples taken from 61 postmenopausal women who developed breast cancer an average of 7.8 years after blood collection. Compared to 179 age-matched controls, oestradiol levels were 29 per cent higher in women who later developed breast cancer (Thomas et al., 1997). Another prospective study (this time from the US), compared oestrogen levels in 156 postmenopausal women who developed breast cancer, after blood collection, with two age-matched controls for each cancer patient. Results showed increased levels of the hormones oestradiol, oestrone, oestrone sulphate and dehydroepiandrosterone sulphate in women who subsequently developed breast cancer thus providing strong evidence for a causal relationship between postmenopausal oestrogen levels and the risk of breast cancer (Hankinson et al., 1998). A review of studies carried out over a 10 year period in the Department of Clinical Chemistry at the University of Helsinki in Finland suggested that the Western diet (characterised by milk and meat products) increases levels of these types of hormones and concluded that the hormone pattern found in connection with a Western-type diet is prevailing in breast cancer patients (Adlercreutz, 1990).
While some research has identified dietary factors that reduce the risk of breast cancer, such as fibre, other studies have identified dietary factors that increase the risk, such as dietary fat. Case-control studies use a group of people with a particular characteristic (for example older women with lung cancer). This particular group is selected and information collected (for example, history of smoking), then a control group is selected from a similar population (older women without lung cancer) to see if they smoked or not, then a conclusion is drawn (smoking does or does not increase risk of lung cancer). A combined analysis of 12 case-control studies designed to examine diet and breast cancer risk found a positive association between fat intake and this disease. The reviewers estimated that the percentage of breast cancers that might be prevented by dietary modification in the North American population was 24 per cent for postmenopausal women and 16 per cent for premenopausal women (Howe et al., 1990).
In 1999 researchers at the Department of Preventive Medicine at the University of Southern California Medical School in Los Angeles published a review of 13 dietary fat intervention studies that were conducted to investigate the effect of fat intake on oestrogen levels. The results showed decreasing dietary fat intake (to between 10 and 25 per cent of the total energy intake) reduced serum oestradiol levels by between 2.7 and 10.3 per cent. It was concluded that dietary fat reduction can result in a lowering of serum oestradiol levels and that such a dietary modification may offer an approach to breast cancer prevention (Wu at al., 1999).
However, other studies of fat intake and the incidence of breast cancer have yielded conflicting results. The discrepancy in results may reflect the difficulties of accurately recording fat intake. Dr Sheila Bingham of the Dunn Human Nutrition Unit in Cambridge has developed a data-collection method which may overcome these problems. Bingham used food frequency questionnaire methods with a detailed seven-day food diary in over 13,000 women between 1993 and 1997. The study concluded that those who ate the most animal saturated fat (found mainly in whole milk, butter, meat, cakes and biscuits) were almost twice as likely to develop breast cancer as those who ate the least. It was also concluded that previous studies may have failed to establish this link because of imprecise methods (Bingham et al., 2003).
In a subsequent prospective cohort study involving over 90,000 premenopausal women, researchers from Harvard Medical School confirmed that animal fat intake was associated with an elevated risk of breast cancer. Red meat and high-fat dairy foods such as whole milk, cream, ice-cream, butter, cream cheese and cheese were the major contributors of animal fat in this cohort of relatively young women. Interestingly, this research did not find any clear association between vegetable fat and breast cancer risk; the increased risk was only associated with animal fat intake. It has been suggested that a high-fat diet increases the risk of breast cancer by elevating concentrations of oestrogen. However, the author of this study, Dr Eunyoung Cho, suggests that if this were true a diet high in animal fat and a diet high in vegetable fat should both lead to higher rates of cancer, and that was not the case in this study. Cho suspects that some other component such as the hormones in cow’s milk might play a role in increasing the risk of breast cancer (Cho et al., 2003).
Such conclusions have led many research groups to focus on the endogenous hormonal content of milk (hormones produced by the cow and excreted in the milk), which has not been widely discussed. The milk produced now is very different from that produced 100 years ago; modern dairy cows are frequently impregnated while still producing milk (Webster, 2005). Two-thirds of milk in the UK is taken from pregnant cows with the remainder coming from cows that have recently given birth. This means that the hormone (oestrogen, progesterone and androgen precursor) content of milk varies widely. It is the high levels of hormones in milk that have been linked to the development of hormone-dependent cancers such as ovarian and breast cancer.
In a review of the relationship between breast cancer incidence and food intake among the populations of 40 different countries, a positive correlation was seen between the consumption of meat, milk and cheese and the incidence of breast (and ovarian) cancer. Meat was most closely correlated with breast cancer incidence, followed by cow’s milk and cheese. By contrast, cereals and pulses were negatively correlated with the incidence of breast cancer. This review concluded that the increased consumption of animal foods may have adverse effects on the development of hormone-dependent cancers. Among dietary risk factors of particular concern were milk and dairy products, because so much of the milk we drink today is produced from pregnant cows, in which oestrogen and progesterone levels are markedly elevated (Ganmaa and Sato, 2005).
In addition to animal fat and various chemical contaminants, cow’s milk and dairy products contain hormones and growth factors, which have been implicated in the proliferation of human breast cancer cells. In a review of the evidence linking dairy consumption with breast cancer risk, researchers from Princeton University in New Jersey concluded that milk may promote breast cancer by the action of the growth factor IGF-1, which has been shown to stimulate the growth of human breast cancer cells in the laboratory (Outwater et al., 1997). In another review, examining the role of IGF-1 in cancer development, Yu and Rohan state that IGFs play a critical role in regulating cell growth and death. This function has led to speculation about their involvement in cancer development. Laboratory experiments demonstrate the ability of IGFs to stimulate growth of a wide range of cancer cells and to suppress cell death or apoptosis (Yu and Rohan, 2000). The concern here is that if IGF-1 can cause human cancer cells to grow in a Petri dish in the laboratory, they might have a cancer-inducing effect when consumed in the diet. IGF-1 is present in all milk and is not destroyed during pasteurisation. Dr J.L. Outwater of the Physicians Committee For Responsible Medicine (PCRM) in Washington, DC, warns that IGF-1 may be absorbed across the gut and cautions that regular milk ingestion after weaning may produce enough IGF-1 in mammary tissue to encourage cell division thus increasing the risk of cancer (Outwater et al., 1997).
In her book Your Life in Your Hands, Professor Jane Plant CBE, the chief scientist of the British Geological Survey, describes a very personal and moving story of how she overcame breast cancer by excluding all dairy products from her diet (Plant, 2000). Plant was diagnosed with breast cancer in 1987. She had five recurrences of the disease and by 1993 the cancer had spread to her lymphatic system. She could feel the lump on her neck, and was told that she had just three months to live, six if she was lucky. However, Plant was determined to use her scientific training to find a solution to this ‘problem’. She began researching breast cancer in other cultures and found a much lower incidence in China. The data showed that in rural China breast cancer affects just one in 10,000 women compared to one in 10 British women (now one in nine). However, Plant observed that among wealthy Chinese women with a more Western lifestyle (for example in Malaysia and Singapore), the rate of breast cancer is similar to that in the West. Furthermore, epidemiological evidence shows that when Chinese women move to the West, within one or two generations their rates of breast cancer incidence and mortality increase to match those of their host country. This suggested that diet and lifestyle (rather than genetics) must be a major determinant of cancer risk.
Plant decided to investigate the role of diet in breast cancer risk. She examined the results of the China-Cornell-Oxford project on nutrition, environment and health (Campbell and Junshi, 1994). This project was based on national surveys conducted between 1983 and 1984 in China. The project was a collaboration between T. Colin Campbell at Cornell University in the US, Chen Junshi from the Chinese Academy of Preventative Medicine, in Beijing, China, Li Junyao at the Chinese Academy of Medical Sciences, Beijing, and Richard Peto from Oxford University in the UK. The project revealed some surprising insights into diet and health. For example, it showed that people in China tend to consume more calories per day that people in the US, but only 14 per cent of these calories come from fat compared to a massive 36 per cent in the West. This coupled to the fact that Chinese people tend to be more physically active than people in the West, is why obesity affects far more people in the West than in China. However, Plant’s diet had not been particularly high in fat; indeed she describes it as very low in fat and high in fibre. Then Plant had a revelation: the Chinese don’t eat dairy produce. Plant had been eating yogurt and skimmed organic milk up until this time, but within days of ceasing all dairy, the lump on her neck began to shrink. The tumour decreased and eventually disappeared, leading her to the conviction that there is a causal link between the consumption of dairy products and breast cancer. Although Plant received chemotherapy during this time, it did not appear to be working and so convinced was her cancer specialist that it was the change in diet that saved her life, he now refers to cancer mortality maps in his lectures and recommends a dairy-free diet to his breast cancer patients.
Plant eventually defeated cancer by eliminating dairy products from her diet, replacing them with healthy alternatives and making some lifestyle changes. Plant advises that if you do only one thing to cut your risk of breast cancer, make the change from dairy to soya (Plant, 2000). Providing breast cancer patients with sound dietary advice could greatly increase survival rates. Taken together, these observations show that a plant-based diet can reduce many of the risk factors associated with breast cancer.
Cancers of the colon and rectum account for around one in every eight newly diagnosed cancers in the UK and one in every nine deaths from cancer (National Statistics, 2005a). In the UK it is the third most common cancer in men, and the second most common cancer in women (Cancer Research UK, 2005). Colorectal cancer occurs when the process of cell renewal in the bowel goes wrong. Abnormal cells can form polyps (small growths) which may develop into cancer. Risk factors for colorectal cancer include poor diet, obesity, alcohol and smoking.
Although the causes of colorectal cancer are not known, it is thought that there may be a link with a diet high in animal fats and protein and low in fibre (NHS, 2006). To reduce the risk of developing colorectal cancer, the Government recommends a healthy, balanced diet including plenty of fresh fruit and vegetables (NHS, 2006). It is also important to take regular physical exercise, maintain a healthy weight and avoid alcohol and smoking.
The protective role of a whole grain plant-based diet containing plenty of fruit and vegetables (and therefore fibre) is well-documented. Two large-scale studies (both published in the Lancet) have examined the relationship between diet and colorectal cancer; both confirmed that as dietary fibre intake increases, the risk of colorectal cancer decreases. In the first of these two studies, a research team from the National Cancer Institute in the US compared fibre intake of 3,591 people with at least one bowel adenoma or polyp (a benign growth that may or may not transform to cancer), with that of 33,971 people without polyps. They found that the participants in the top 20 per cent for dietary fibre intake had 27 per cent lower risk of adenoma than people in the lowest 20 per cent (representing a difference in fibre intake of 24 grams per day). It was concluded that dietary fibre, particularly from grains, cereals and fruits, was associated with a decreased risk of colorectal adenoma (Peters et al., 2003). In the second even larger study, researchers from the European Prospective Investigation into Cancer and Nutrition (EPIC) prospectively examined the association between dietary fibre intake and incidence of colorectal cancer in 519,978 individuals aged between 25 and 70 years-old, recruited from 10 different European countries. Participants completed a dietary questionnaire between 1992 and 1998 and were followed up for cancer incidence on average 4.5 years later. Again, people with the highest fibre intake (35 grams per day) had a 40 per cent lower risk of colorectal cancer compared to those with the lowest intake (15 grams per day). In populations with low average intake of dietary fibre, an approximate doubling of total fibre intake from foods could reduce the risk of colorectal cancer by 40 per cent (Bingham et al., 2003a). These studies provide convincing evidence that increasing the amount of whole grains and fruit and vegetables in the diet reduces the risk of colorectal cancer.
While it has been demonstrated that dietary fibre can protect again colorectal cancer, evidence suggests that animal foods (animal fat and animal protein) may be associated with increased colorectal cancer risk. In another EPIC study, researchers prospectively followed 478,040 men and women from 10 European countries that were free of cancer between 1992 and 1998. Information on diet and lifestyle was collected and after a mean follow-up of 4.8 years, 1,329 cases of colorectal cancer were documented. An investigation of the relationship between intakes of red and processed meat, poultry and fish revealed that colorectal cancer risk was positively associated with intake of red and processed meat (Norat et al., 2005).
In a recent study, the association between the consumption of dairy foods and calcium and colorectal cancer risk was assessed in a pooled analysis of 10 cohort studies from North America and Europe (Cho et al., 2004). In this study the authors concluded that the consumption of milk and calcium were related to a lower risk of colorectal cancer. However, the inverse association between calcium (and by inference, dairy) intake and colorectal cancer was only statistically significant among those with the highest vitamin D intake. This may be either because vitamin D enhances calcium absorption, or because vitamin D itself may decrease colorectal cancer incidence (Garland, 1999). In contrast to these findings, most prospective studies show only a moderate and not statistically significant decrease in the risk of colorectal cancer with increased dietary calcium intake (Ma et al., 2001).
Furthermore, as with breast cancer, there are growing concerns that the consumption of cow’s milk raises levels of IGF-1 in the blood (either directly or indirectly). For example, in a study of 204 healthy men and women aged 55 to 85 years, three servings of non-fat milk per day over 12 weeks increased blood serum levels of IGF-1 by 10 per cent (Heaney, 1999). Because elevated levels of IGF-1 are associated with increased risk of colorectal cancer (Ma et al., 1999; Giovannucci et al., 2000; Kaaks et al., 2000), an increase in IGF-1 attributable to the consumption of milk could potentially counter any protective effect conferred by dietary calcium (and vitamin D in US fortified milk). It may be that plant-based sources of calcium, including non-oxalate dark green leafy vegetables, dried fruits, nuts, seeds and pulses as well as fortified foods such as calcium-set tofu (soya bean curd) and calcium-enriched soya milk, provide a safer source of calcium. Vitamin D can be either obtained from the diet or synthesised in the skin following exposure to sunlight.
Ovarian cancer is the fourth most common cancer among women in the UK. Around 6,900 new cases are diagnosed each year (Cancer Research UK, 2006). The ovaries are two almond shaped organs located on either side of the uterus. They produce eggs and the reproductive hormones (oestrogen and progesterone). The cause of ovarian cancer is unknown however some risk factors have been identified. There may be an increased risk for this disease among women: over the age of 65; who have never been pregnant; who started having periods at an early age; who had their first child after the age of 30 or who go through the menopause after the age of 50. Furthermore, the prolonged use of fertility drugs might increase the risk of ovarian cancer (Cancer Research UK, 2006). Taking the combined contraceptive pill reduces the risk of ovarian cancer: the longer you take the pill, the more the risk is reduced (NHS Direct, 2006). Taken together, these risk factors suggest that hormonal factors are involved in the development of ovarian cancer although the precise mechanisms remain unclear. Additional risk factors include a genetic component; a small number of ovarian cancers (five to 10 per cent) are caused by an inherited faulty gene (NHS Direct, 2006). The use of talcum powder in feminine hygiene (direct application to the genital area) has also been implicated (Cramer et al., 1999).
It has been suggested that the milk sugar lactose is a risk factor for ovarian cancer. A positive relationship between ovarian cancer and dairy products was first reported in the Lancet in 1989 when it was suggested that lactose consumption may be a dietary risk factor for ovarian cancer (Cramer et al., 1989). More recently, data collected from the Harvard Nurses Health Study was used to assess the lactose, milk and milk product consumption in relation to ovarian cancer risk in over 80,000 women. Over 16 years of follow-up, 301 cases of one particular type of ovarian cancer were confirmed in this study group. Results showed that women who consumed the most lactose had twice the risk of this type of ovarian cancer than women who drank the least lactose. It was suggested that galactose (a component of lactose) may damage ovarian cells making them more susceptible to cancer (Fairfield et al., 2004).
In the same year, Susanna Larsson and colleagues of the Karolinska Institute in Stockholm, Sweden, published a study in the American Journal of Clinical Nutrition that examined the association between intakes of dairy products and lactose and the risk of ovarian cancer. In this study of 61,084 women aged 38 to 76 years, the diet was assessed over three years and after 13.5 years 266 participants had been diagnosed with ovarian cancer. Results showed that women consuming four or more servings of dairy a day had double the risk of ovarian cancer compared to low or non-dairy consumers. Milk was the dairy product with the strongest positive association with ovarian cancer. The authors of this study observed a positive association between lactose intake and ovarian cancer risk and concluded that high intakes of lactose and dairy products, particularly milk, are associated with an increased risk of ovarian cancer (Larsson et al., 2004).
Larsson subsequently compared two groups of studies: three prospective cohort studies and 18 case-control studies. The results of the three prospective cohort studies showed a strong link between the intake of total dairy foods, low-fat milk and lactose and the risk of ovarian cancer. In contrast, the data from the 18 case-control studies failed to show such a link. It was a stalemate with no clear conclusion (Larsson et al., 2005). The differences between the findings of the cohort and case-control studies might be explained by a number of factors including selection bias (choosing individuals that are not representative of the norm) or changes in the diet following cancer diagnosis. Alternatively, the differences between the findings may be due to the time interval between diet assessment and cancer diagnosis. Cohort studies frequently record dietary practices many years before illness occurs, which may make the data more likely to be accurate compared to data collected in case-control studies which tends to be collected at the time of diagnosis.
In a study examining the link between diet and ovarian cancer, ovarian cancer incidence between 1993 and 1997 in different geographical locations was coupled to food consumption data from FAOSTAT Database Collections. The food items used for this study were animal fats, meat (beef, pork, poultry, mutton and goat meat), eggs, butter, milk, cereals, pulses, beans, soya beans, peas, fruits, vegetables, coffee, tea and alcoholic beverages. Results showed that Iceland had the highest rates of ovarian cancer affecting 16.2 women per 100,000, followed by 15.2 in Sweden and 13.7 in the UK. The lowest rate per 100,000 was 1.6 for Korea, followed by 2.1 in Mali and 4.0 in both China and Brazil. Again, results showed a strong link between dairy foods and cancer: milk was most closely correlated with the incidence of ovarian cancer, followed by animal fats and cheese. Conversely, pulses were negatively correlated with the incidence of this cancer (Ganmaa and Sato, 2005). This provides yet more evidence that animal-based foods tend to increase the risk of disease while whole grain plant-based diets reduce the risk.
In conclusion, the consumption of animal-based foods is associated with an increased risk of certain hormone-dependent cancers. Milk and dairy products are of particular concern: as already stated, most milk drunk today is produced from pregnant cows, in which oestrogen and progesterone levels are markedly elevated (Ganmaa and Sato, 2005). While there are several candidate components of milk that may increase the risk of ovarian and other hormone-dependent cancers, the precise mechanisms underlying their action remain unclear. However, as milk and dairy products have been identified as a risk factor for ovarian cancer, it stands to reason that this particular risk can be reduced by switching to a plant-based diet.
Prostate cancer is the most common cancer in men and the second most common cause of male cancer deaths after lung cancer. Although it rarely occurs in younger men, one in 14 men in the UK will be diagnosed with prostate cancer at some point in their lives (Cancer Research UK, 2005). Prostate cancer develops from cells within the prostate gland which is the size of a walnut and lies directly under the bladder. The prostate produces a protein called prostate-specific antigen (PSA) which turns semen into liquid form (NHS Direct, 2006). The majority of prostate cancers are slow growing and it may be some time before any symptoms are noticed, which can make this disease less treatable. Prostate cancer risk is associated with increasing age and is higher in people whose father or brother suffered the disease at an early age. Exposure to radioactive substances may increase the risk of prostate cancer. As for other hormone-dependent cancers, the highest incidence rates of prostate cancer occur in the developed world and the lowest rates in Africa and Asia (however, African-American men are more affected than white American men). This suggests that prostate cancer risk is mainly determined by dietary and lifestyle factors. This notion is supported by the observation that vegetarians are half as likely to get prostate cancer as meat-eaters (NHS Direct, 2006). This protection may be partly due to the protective role conferred by selenium and lycopenes (found in vegetables, particularly tomatoes).
Figure 6.0 Incidence of and mortality from prostate cancer in selected countries in 2002. Source: Cancer Research UK, 2005a.
Figure 6.0 shows how the incidence of prostate cancer varies widely around the world with the highest incidence rates seen in the developed world and the lowest rates occurring in Africa and Asia. The lowest European rates are seen in southern Europe while the highest occur in Finland and Sweden (Cancer Research UK, 2005a). Research shows that prostate cancer rates are lower in countries with low consumption rates of typical Western foods such as meat and dairy.
One of the earliest reports linking dairy consumption to prostate cancer was published in the 1980s when a study of over 27,000 Californian Seventh-Day Adventists who had completed dietary questionnaires 20 years earlier concluded that milk consumption was positively associated with prostate cancer mortality (Snowdon, 1988). Since then many more reports have confirmed an increased risk from the consumption of dairy foods, although the mechanism underlying this action remains unclear.
One possible mechanism for the action of milk in increasing prostate cancer risk may involve the calcium in milk. Researchers from Harvard Medical School have shown that high consumption of calcium is linked to advanced prostate cancer (Giovannucci et al., 1998). However, research on the roles of calcium and vitamin D in prostate cancer are inconsistent. It has been suggested that calcium increases prostate cancer risk by suppressing circulating vitamin D. In a study of 3,612 men observed between 1982 and 1992, 131 prostate cancer cases were identified and dietary intake analysed (Tseng et al., 2005). Results confirmed that dietary calcium was associated with an increased risk whereas vitamin D was not associated.
Another study considered the oestrogen content of milk as a causal factor, having noted that the typical Western diet (characterised by milk and meat products) contains higher levels of oestrogen than the foods eaten by Asian men who suffer much less from prostate cancer. This study measured the hormone contents of two kinds of commercial milks (from Holstein and Jersey cows) and found that levels were markedly higher than they were 20 years ago. This was attributed to modern dairy farming methods whereby around 75 per cent of commercial milk comes from pregnant cows (Qin et al., 2004).
The growth factor IGF-1 has been associated with increased prostate cancer risk in some epidemiologic studies, and as stated previously the diet can influence IGF-1 concentrations in the blood. In a Swedish study, levels of IGF-1 were measured in blood samples from over 800 men, 281 of whom were later diagnosed as having prostate cancer (Stattin et al, 2004). A strong correlation between IGF-1 and prostate cancer was observed and it was concluded that circulating IGF-1 levels are associated with an increased risk for this disease. Campbell suggests that IGF-1 is turning out to be a predictor of certain cancers, including prostate, in much the same way that cholesterol is a predictor of heart disease (Campbell and Campbell, 2005).
Interestingly, a study published in the British Journal of Cancer noted that vegan men had a nine per cent lower serum IGF-1 level than meat-eaters and vegetarians (Allen et al., 2000). In terms of follow-up on cancer incidence it is still relatively early days, but the EPIC-Oxford researchers intend to follow the long-term health of participants of this and other studies based in the UK and Europe over the next 10 years to identify any associations with dietary factors, with particular emphasis on cancer incidence and mortality rates (Davey et al., 2003).
While the precise molecular mechanism underlying the development of prostate cancer remains unclear, the effects of changing diet have produced positive results. Researchers at the Preventative Medicine Research Institute in California evaluated the effects of dietary changes in 93 volunteers who had chosen not to undergo conventional treatment for early prostate cancer. This was a unique opportunity to observe the effects of diet and lifestyle changes without the confounding effects of radiation or surgery. Participants in the lifestyle-change group were placed on a vegan diet consisting primarily of fruits, vegetables, whole grains and legumes supplemented with soya, vitamins and minerals. Two standard tests were used to assess disease status. The first was a routine blood test measuring PSA levels; this protein produced by the prostate gland can be used to assess disease progression. The second test relied on differences in the growth rates of a human prostate cancer cells (LNCaP) treated with patient serum. This is a standard laboratory test used for evaluating the effects of conventional treatments of prostate cancer.
While none of the experimental (vegan) patients underwent conventional treatment during the study, six control patients underwent treatment due to an increase in PSA and/or progression of the disease on magnetic resonance imaging. PSA decreased four per cent in the experimental group but increased six per cent in the control group. Although the magnitude of these changes was relatively modest, the direction of change may be clinically significant since an increase in PSA predicts clinical progression in the majority of men with prostate cancer. In the second test, the growth of LNCaP prostate cancer cells was inhibited almost eight times more by serum from the experimental than from the control group. Changes in serum PSA and also in LNCaP cell growth were significantly associated with the degree of change in diet and lifestyle. It was concluded that intensive lifestyle changes may affect the progression of early, low grade prostate cancer (Ornish et al., 2005).
Well over a decade ago, increasing the consumption of beans, lentils, peas, tomatoes, raisins, dates and other dried fruit was associated with a significantly decreased risk of prostate cancer (Mills et al., 1989). A more recent study of over 47,000 men confirmed an inverse link between fructose and prostate cancer indicating that eating fruit offers some protection against prostate cancer (Giovannucci et al., 1998). More recently, in a review of diet, lifestyle and prostate cancer it was observed that while meat and dairy are associated with an increased risk, the consumption of tomato products (which contain the antioxidant lycopene), vitamin E and selenium supplements have all been shown to decrease risk. A high level of physical activity was also identified as a factor decreasing the risk of prostate cancer (Wolk, 2005).
In summary, the data linking the consumption of cow’s milk and milk products to cancer provides a convincing argument for eliminating animal foods from the diet while increasing the intake of whole grains, pulses, fruit and vegetables.