The Causes of Breast Cancer
The risk of developing breast cancer is very small in young women and increases as women get older; more than half of breast cancers occur in women over the age of 65 (Cancerbackup, 2007). Some factors may slightly increase a woman's risk of developing the disease, these are listed below:
- Having had breast cancer
- Having benign (non-cancerous) breast disease
- Genetics - breast cancer in the family (see below)
- Early puberty/menstruation - before the age of 11
- Late menopause - after age 54
- Having a first child late in life
- Having no or few children
- Not breast-feeding long term
- Exposure to radiation
- High dietary fat intake
- Overweight and obesity - particularly for postmenopausal women
- Moderate to heavy consumption of alcohol
- Oral contraceptives (the pill) and hormone replacement therapy (HRT) may very slightly increase the risk of breast cancer
In addition to the above, studies have included a small number of chemicals identified as mammary carcinogens or hormone disruptors which may have implications for breast cancer. However, evidence is emerging for associations between breast cancer and polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs) and organic solvents (Brody et al., 2007). PCBs are persistent organic pollutants that do not degrade easily and so are widespread in the environment. They are generally present at low concentrations in most foods, especially fat-containing foods such as milk and meat (FSA, 2000). PAHs are ubiquitous in air pollutants produced from vehicle exhausts (Brody et al., 2007). Organic solvents are commonly used in detergents (citrus terpenes), dry cleaning (tetrachloroethylene), paint thinners (toluene and turpentine), nail polish removers and glue solvents (acetone, methyl acetate, ethyl acetate) and in perfumes (ethanol).
Just how much some of these factors contribute to the risk of breast cancer is difficult to say. However, the aim of this report is to investigate the somewhat overlooked role of dietary factors. That said, the role of genetics in breast cancer deserves further discussion.
The genetic link
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. A fault in either of these two genes can increase the chances of getting breast cancer. However, even among women with high-risk BRCA1 and BRCA2 gene mutations, evidence suggests that nongenetic (environmental) factors influence risk. A substantial review of the research, published in the journal Cancer, reported that more women born after 1940, carrying a fault in either, or both of these genes, were diagnosed with breast cancer by the age of 50 than those born before 1940 (Brody et al., 2007). In other words, the women born after 1940 were exposed to some environmental factor that increased their risk of developing breast cancer.
There are two other very rare genes which are thought to account for less than two per cent of all breast cancers: the P53 gene and the AT (ataxia telangiectasia) gene (Cancerbackup, 2006).
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. Interestingly, with a faulty gene, the probability of developing cancer has increased over the last 30 or more years from about 40 per cent to about 70 per cent, probably due to environmental and lifestyle factors (CANCERactive, 2007). In other words you can cut your risks, even if you have a faulty gene, by making changes to your diet and lifestyle.
The discovery of genes linked to breast cancer has given rise to a certain degree of 'genetic fatalism', encouraging some to think that their chances of getting breast cancer are entirely down to fate. However, scientists estimate that only around five to 10 per cent of breast cancers are due to inheriting abnormal genes (Cancerbackup, 2007). This means that the vast majority of cancers (90 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 more at risk of developing the condition than someone who does not have one of the abnormal genes.
An increasing body of scientific evidence links certain foods (such as meat and dairy products) to an increased risk of breast cancer. Conversely, other studies have identified foods that may lower the risk. As communications technology advances, scientists have become more able to compare disease rates and dietary patterns around the world. This has afforded them some useful incites into the causes of disease.
East versus West
Cross-cultural studies show that as the consumption of a typical Western diet (containing high levels of saturated fat, cholesterol and animal protein) spreads from country to country, so does the incidence of the so-called 'diseases of affluence' (such as obesity, heart disease, diabetes, osteoporosis and certain cancers, including breast cancer). It has been suggested that the incidence of these diseases varies because of genetic differences between different races. However, when people migrate from an area of low incidence of the so-called affluent diseases to an area of high incidence, they soon acquire the same high incidence shared by the population into which they have moved. This correlation must then be attributed, at least in part, to environmental factors such as diet and lifestyle.
So if certain diets and lifestyles increase the risk of these diseases, it stands to reason that you can reduce the risk of disease by changing your diet and lifestyle.
As the typical Western diet pervades around the world, it takes with it typical Western diseases such as heart disease, diabetes, obesity and certain cancers. The World Health Organisation (WHO) states that dietary factors are estimated to account for around 30 per cent of all cancers in Western countries and 20 per cent of cancers in developing countries. They predict the number of cancers linked to diet in developing countries will grow as these countries become more urbanised (WHO, 2007). Other estimates are even higher. In 1997, the World Cancer Research Fund published a substantial review of the scientific literature linking foods, nutrition, food processing, dietary patterns and related factors, with the risk of human cancers worldwide (WCRF, 1997). The report concluded that policy-makers should now recognise that the incidence of cancer throughout the world can be reduced by 30 to 40 per cent by feasible changes in diets and related lifestyles.
Sadly there has never been a better time to observe the detrimental effects of the Western diet as countries in the East (such as China and Japan) move from a traditional plant-based diet rich in fruit, vegetables and grains towards a more Western diet characterised by meat, dairy and processed foods.
In a recent study, the effects of a Western diet on breast cancer risk was assessed among participants of the Shanghai Breast Cancer Study, a large population-based survey involving 1,446 Chinese women from Shanghai diagnosed with breast cancer and matched to 1,549 control subjects without the disease (Cui et al., 2007). The authors of the report identified two distinct dietary patterns which they describe as "vegetable-soy" including a high intake of vegetable, soya products and fish and the Western-style "meat-sweet" diet characterised by various meats, poultry, fish, confectionary, puddings, bread and milk. The "vegetable-soy" diet contained higher levels of fibre, vitamins C and E and soya protein while the "meat-sweet" diet was rich in total and saturated fat.
Results showed no overall association of breast cancer risk with the "vegetable-soy" pattern but demonstrated that a Western-style diet could double the rate of breast cancer among postmenopausal overweight women. Previous work has suggested that a "vegetable-soy" type diet can lower the risk of breast cancer. However, the authors of this study found that the "vegetable-soy" diet did not protect from breast cancer. This, they suggested, might due to the negative effects of the fish content of the "vegetable-soy" diet, or that cooking the vegetables may have diminished their protective effects (see below). The authors of this study concluded that for postmenopausal women in traditionally low-risk Asian populations poised to adopt foods characteristics of Western societies, the low consumption of a "meat-sweet" dietary pattern plus successful weight control may protect against breast cancer.
While previous work has shown that red meat increases the risk of bowel, stomach and pancreatic cancer, recent research now links red meat to breast cancer as well (Cho et al., 2006). Researchers from Harvard Medical School in Boston looked at the diets of over 90,000 premenopausal women (aged 26 to 46) over 12 years and found that women who ate more than one-and-a-half servings of red meat per day (the equivalent of a sausage and a burger) almost doubled their risk of oestrogen receptor-positive breast cancer. The authors of this study concluded that a high red meat intake may be a risk factor for breast cancer.
They suggest several biological mechanisms that may explain how this occurs. For example, cooked or processed red meat is a source of carcinogens (cancer-causing agents such as heterocyclic amines, N nitroso-compounds, and polycyclic aromatic hydrocarbons), that may increase breast cancer risk. Hormone treatment of beef cattle for growth promotion (banned in European countries but not in the United States) is also a concern. Red meat is a source of haem iron (a highly bioavailable form of iron and a major source of stored body iron), which has been shown to enhance oestrogen-induced tumour induction. Finally, they state that fat intake in general has been hypothesised to raise steroid hormone levels (see below). However, in a previous study, this research group found that intake of animal fat, but not vegetable fat, was related to elevated risk of breast cancer (Cho et al., 2003).
Exactly how red meat may increase the risk of breast cancer remains unclear. This uncertainty inevitably casts some doubt on the role of red meat as a causative agent, particularly among enthusiastic meat-eaters. However, the mechanism by which red meat causes bowel cancer was only just proposed recently (Lewin et al., 2006) despite its causal role being suspected for many decades. In other words, we know that increasing consumption of red meat increases the risk of developing breast cancer, but scientists do not yet know exactly how.
Some studies link dietary fat to the risk of breast cancer. 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. It was concluded 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 help prevent breast cancer (Wu et 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 (Cho et al., 2003). 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 authors of this study suggest 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. They do state that the fatty acid composition in fat from animal and vegetable sources differs greatly and may therefore have different associations with breast cancer risk. So it could be that a high-fat plant-based diet has less effect than a high-fat diet containing lots of meat and dairy products. They also suggest that some other component such as the hormones in cow's milk might play a role in increasing the risk of breast cancer.
The conflicting effects of animal and vegetable fats on breast cancer risk have led many research groups to focus on the endogenous (naturally produced) hormonal content of animal-based foods, which has not been widely discussed. Oestrogens are contained in meat and eggs, but the major source of animal-derived oestrogens in the human diet are cow's milk and dairy products which account for 60 to 80 per cent of the animal-derived oestrogens consumed (Hartmann et al., 1998).
Furthermore, 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 animal-based foods that have been linked to the development of hormone-dependent cancers such as breast cancer.
Numerous studies show that women consuming a Western-style diet tend to have different hormone profiles compared to women eating traditional diets. This means the level of oestrogen in their blood varies according to the type of diet they have. For example, a review of studies carried out over a 10 year period in the Department of Clinical Chemistry at the University of Helsinki in Finland showed that women who consume a high-animal fat, high-animal protein diet with mostly refined carbohydrates and sugars have higher levels of oestrogen in their blood (Adlercreutz, 1990). This study also made the observation that the hormone pattern (high oestrogen), found in association with a Western-type diet tends to prevail among breast cancer patients. In other words, what you eat can affect the level of oestrogen in the blood, and high oestrogen levels are found in women with breast cancer.
A number of other studies confirm 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 (Thomas et al., 1997). Compared to 179 age-matched controls, oestradiol levels were 29 per cent higher in women who later developed breast cancer.
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 (Hankinson et al., 1998). 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.
In a review looking at 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 (Ganmaa and Sato, 2005). 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. The authors of this review concluded that the increased consumption of animal foods may increase the development of hormone-dependent cancers. Among dietary risk factors of particular concern to the authors were milk and dairy products, because so much of the milk we drink today is produced from pregnant cows, in which hormone levels are markedly elevated.
Milk contains many biologically active (bioactive) molecules including enzymes, hormones and growth factors. In 1992, Pennsylvania State University endocrinologist Clark Grosvenor published an extensive review of some of the known bioactive hormones and growth factors found in a typical glass of milk in the US. The list included seven pituitary (an endocrine gland in the brain) hormones, seven steroid hormones, seven hypothalamic (another brain endocrine gland) hormones, eight gastrointestinal peptides (chains of two or more amino acids), six thyroid and parathyroid hormones, 11 growth factors, and nine other biologically active compounds (Grosvenor et al., 1992).
A more recent survey of the published data on the occurrence of hormones and bioactive constituents in cow's milk and milk products also provides an extensive list of gonadal, adrenal, pituitary, hypothalamic and other hormones (Jouan et al., 2006). The authors of this survey state that there is a need to update the data concerning hormonal levels in milk and milk products, especially in the light of changes in the genetic background of dairy cattle in the last decades, as well as in animal feeding and husbandry and new processes that have emerged in the milk industry (Jouan et al., 2006).
The enormous detrimental health effects of consuming cow's milk and dairy products are more widely discussed in the VVF's fully-referenced scientific report White Lies. This report describes how the saturated animal fat, animal protein, cholesterol, hormones and growth factors in dairy products are linked to a wide range of illnesses and diseases including some of the UK's biggest killers such as heart disease, diabetes, prostate cancer as well as osteoporosis, eczema, asthma, Crohn's disease, colic, constipation and even teenage acne.
For more information on British dairy farming methods see Viva!'s fully-referenced report The Dark Side of Dairy.
IGF-1 signalling trouble
In addition to the animal fat, various chemical contaminants and hormones found in animal-based foods, certain growth factors have been implicated in the proliferation of human breast cancer cells. In particular, a growth factor called insulin-like growth factor 1 (IGF-1) has attracted much attention.
IGF-1 is a signalling molecule produced in the liver and body tissues of mammals. It promotes cell growth and division, which is important for normal growth and development of mammals. However, IGF-1 levels decline with age, consistent with their role in growth.
Over the last decade IGF-1 has been linked to an increased risk of childhood cancers, breast cancer, lung cancer, melanoma and cancers of the pancreas and prostate (LeRoith et al., 1995; Chan et al., 1998) and gastrointestinal cancers (Epstein, 1996). Indeed IGF-1 may be used as a predictor of certain cancers, in much the same way that cholesterol is a predictor of heart disease (Campbell and Campbell, 2005).
IGF-1 from cows is identical to human IGF-1 in that the amino acid sequence of both molecules is the same (Honegger and Humbel, 1986). Amino acids are the building blocks of proteins and there are 20 different amino acids. All proteins consist of amino acids joined together like beads on a string and the nature of the protein (how it behaves) is determined by the order in which the amino acids occur along the string. In both human and bovine IGF-1 the same 70 amino acids occur in exactly the same order, which would suggest that bovine IGF-1 behaves the same way in humans as it does in cows.
As stated above, two-thirds of milk in the UK is taken from pregnant cows. It is not only the hormone content that is markedly elevated at this time; the amount of IGF-1 present is also higher in milk produced by pregnant cows. IGF-1 is relatively stable to both heat and acidic conditions and can therefore survive the harsh conditions of both commercial milk processing and gastric acid to maintain its biological activity (Playford et al., 2000). Some scientists are concerned that IGF-1 not destroyed during pasteurisation may cross the intestinal wall in the same way that another hormone, epidermal growth factor (EGF), has been shown to do. EGF is protected from being broken down when food proteins (such as the milk protein casein) block the active sites of the digestive enzymes (Playford et al., 1993). This allows the molecule to stay intact and cross the intestinal wall and enter the blood. Dr J.L. Outwater of the Physicians Committee For Responsible Medicine (PCRM) in Washington, DC, warns 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).
Furthermore, some research shows that various hormones and growth factors (including oestrogens, adrenocorticotropic hormone, thyrotropin, luteinizing hormone, follicle-stimulating hormone, platelet-derived growth factor, epidermal growth factor and fibroblast growth factor) can affect IGF-1 production within the body (Yu and Rohan, 2000). This indicates that certain foods, such as cow's milk, may increase endogenous IGF-1 production in humans. So diet can determine the amount of IGF-1 present in the blood.
The critical role IGFs play in regulating cell growth and death has led to much speculation about
their involvement in cancer development (Yu and Rohan, 2000). IGF-1 regulates cell growth, development and division and can stimulate growth in both normal and cancerous cells. Indeed, IGF-1 has been shown to stimulate the growth of human breast cancer cells in the laboratory and it has been suggested that it may be involved in the transformation of normal breast tissue to cancerous cells (Outwater et al., 1997). The concern here is that if IGF-1 can cause human cancer cells to grow in a Petri dish in the laboratory, it might have a cancer-inducing effect when consumed in the diet. This is very worrying as even small increases in serum levels of IGF-1 in humans are associated with increased risk for several common cancers including cancers of the breast, prostate, lung and colon (Wu et al., 2002).
In the first prospective study to investigate the relationship between the risk of breast cancer and circulating IGF-1 levels, researchers at Harvard Medical School analysed blood samples originally collected from 32,826 women aged between 43 and 69 years during 1989 and 1990 (Hankinson et al., 1998a). From this group, 397 women were later diagnosed with breast cancer. Analysis of IGF-1 levels in samples collected from these women compared to samples from 620 controls (without breast cancer) revealed a positive relationship between circulating IGF-1 levels and the risk of breast cancer among premenopausal (but not postmenopausal) women. It was concluded that plasma IGF-1 concentrations may be useful in the identification of women at high risk of breast cancer.
Taken together, the scientific literature strongly suggests a link between high circulating IGF-1 levels and cancer, but what has this to do with diet? The answer is a lot: circulating IGF-1 levels are higher in people who consume milk and dairy products. US researchers from Harvard Medical School investigating the link between IGF-1 levels and diet examined IGF-1 levels in 1,037 healthy women (Holmes et al., 2002). The most consistent finding of this study was a positive association between circulating IGF-1 levels and animal protein intake which, in this study, was largely attributed to cow's milk intake.
Researchers at the Fred Hutchinson Cancer Research Centre in Washington investigated the link between plasma levels of IGF-1 and lifestyle factors in 333 people (Morimoto et al., 2005). They too found that milk consumption was linked to IGF-1 levels. This concurs with an earlier study, from Creighton University in Omaha, NE, which observed a 10 per cent increase in blood levels of IGF-1 in subjects who increased their intake of non-fat milk from fewer than 1.5 servings of dairy foods to three servings per day (Heaney, 1999). Furthermore, a study from the Cancer Epidemiology Unit at the Radcliffe Infirmary in Oxford noted that vegan men had a nine per cent lower serum IGF-1 level than meat-eaters and vegetarians (Allen et al., 2000). This strongly suggests a link between the consumption of cow's milk and dairy products and higher IGF-1 levels circulating in the blood.
One study actually quantified the effect of cow's milk on circulating IGF-1 levels in 54 Danish boys aged two-and-a-half years old (Hoppe et al., 2004). In this study an increase in cow's milk intake from 200 to 600ml per day corresponded to a massive 30 per cent increase in circulating IGF-1.
Researchers at Bristol University investigating the association of diet with IGF-1 in 344 disease-free men found that raised levels of IGF-1 were associated with higher intakes of milk, dairy products and calcium while lower levels of IGF-1 were associated with high vegetable consumption, particularly tomatoes (Gunnell et al., 2003). In their study, published in the British Journal of Cancer, it was concluded that IGF-1 may mediate some diet-cancer associations.
In conclusion, the research shows that nutrition has an important role in determining serum IGF-1 levels (Yaker et al., 2005). Whether the increase in IGF-1 caused by cow's milk occurs directly (by IGF-1 crossing the gut wall), or indirectly (as a result of the action of other factors), the evidence suggests that some component of cow's milk causes an increase in blood serum levels of IGF-1, which in turn is linked to various cancers.
Bovine somatotrophin (BST)
Mammalian milk production is regulated by a complex interaction of hormones. Bovine somatotrophin (BST) is a natural growth hormone that occurs in cattle and controls the amount of milk that they produce. In 1994 Monsanto began marketing a synthetic version of BST, known as recombinant BST (rBST), which was sold as Posilac. Injecting dairy cows with rBST alters their metabolism to increase milk production by up to 15 per cent. Since its introduction in 1994, Posilac has become the largest selling dairy animal pharmaceutical product in the US. Sold in all 50 states, rBST is used in around one-third of the nine million dairy cows in the US (Monsanto, 2007).
While the US Food and Drug Administration (FDA) permit the use of rBST, its use is associated with severe animal welfare problems, for example increasing the incidence of lameness and mastitis. For these reasons, the use of rBST in the EU was prohibited in 2000. Indeed Canada, Japan and many other countries have banned the use of rBST because of its effects on animal health and welfare. However, there are no restrictions on the import of rBST dairy products, or any requirement to label them.
The government's Veterinary Medicines Directorate does not carry out any testing of imported milk (Defra, 2006). Furthermore, Defra confirmed in correspondence with the VVF that, since the EU is a single market, once a product has entered, if it is transported on to another country within the EU, then the origin of the product will be the EU country rather than the originating country (Defra, 2006). In 2005, the UK imported over 1,000 tons of dairy products (mainly ice-cream) from the US (Defra, 2006a); these figures have declined from over 5,000 tons in both 2001 and 2002 but still remain a concern, especially as the consumer has a limited chance of discriminating against imports from the US. The sensible option is to avoid all dairy products.
Milk production increases in cows treated with rBST because it promotes the production of IGF-1 which then stimulates the glands in the cow's udders to produce more milk. Research shows that rBST use on dairy cows can substantially increase the levels of IGF-1 in their milk (Prosser et al., 1989). This raises concerns about the potential biological action of IGF-1 from cow's milk in humans especially because IGF-1 from cows is identical to human IGF-1. Professor Samuel Epstein,
an international leading authority on the causes and prevention of cancer, warns that converging lines of evidence incriminate IGF-1 in rBST milk as a potential risk factor for both breast and gastrointestinal cancers (Epstein, 1996).
So why should this concern us if we do not allow the use of rBST in the UK? Well in terms of human health, the concern is that milk and milk products imported from countries that permit the use of rBST may lead to the consumption of foods that promote increased levels of IGF-1 in humans. In 1999, the minister of state, Baroness Hayman, referred to a report from the Veterinary Products Committee (VPC) which stated that while the use of rBST does not increase the level of BST found naturally in cow's milk, there is a two-to-five fold increase in the level of IGF-1 in the milk, which she acknowledged may be implicated in the occurrence of colonic cancer. However, Hayman reiterated the VPC's view that the risk to human health was likely to be extremely small. Hayman also suggested that just 0.3 per cent of total milk and milk products imported into the UK come from the US where rBST is authorised for use (UK Parliament, 1999).
The damaging effects of dairy
In recent years an increasing body of evidence has accumulated linking the consumption of cow's milk and dairy products to breast cancer. In her book Your Life in Your Hands, Professor Jane Plant CBE, Anglo American Professor of Applied Geochemistry at Imperial College, London, describes a very personal and moving story of how she overcame breast cancer by excluding all dairy products from her diet (Plant, 2007). 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 comparing breast cancer incidence in the UK to that in other cultures.
As stated above, the age-standardised breast cancer incidence rate allows the comparison of cancer rates between populations that may have a different age structure. Plant looked at breast cancer incidence rates in rural China where, in 1997, the disease affected 11 out of every 100,000 women (compared to 70 in the UK). This rate was trebled in Chinese cities, probably Plant suggests, because of the pollution and an increased exposure to a more Western style diet. Interestingly, she observes, Hiroshima and Nagasaki have similar rates to those found in Chinese cities. Both places were attacked with nuclear weapons so you might expect to see some radiation-related cancers. However, by moving to Hiroshima and adopting a Japanese lifestyle, Plant reveals, a UK woman would slash her risk of developing breast cancer by half!
Furthermore 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 than 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 low-fat 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. Her book recounts not only her own story but that of others and it contains much research using the peer-reviewed scientific literature. Plant advises that if you do only one thing to cut your risk of breast cancer, make the change from dairy to soya (Plant, 2007). 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.
It's not just the food itself that can affect the risk of breast cancer; how you cook the food can influence its role in this disease. Recent evidence linking the consumption of barbequed and smoked meats to breast cancer was provided by a large study published in the journal Epidemiology (Steck et al., 2007). This study shows that postmenopausal (but not premenopausal) women with a high lifetime intake of grilled, barbequed and smoked meats have a 47 per cent increased risk of breast cancer. This study also reported that big meat-eaters who also skimp on fruit and vegetables were found to have a massive 74 per cent increase in risk. The authors concluded that these results support the accumulating evidence that the consumption of meats cooked by methods that promote carcinogen formation may increase risk of postmenopausal breast cancer. Why this effect was not seen in premenopausal women is unclear. That said, it would seem prudent for women of all ages to avoid barbequed and smoked meats in order to reduce the risk of breast cancer.