Prostate Cancer

Prostate cancer

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.