Dietary factors are suggested to account for about 30% of cancers in Western societies (Key et al., 2002), which makes diet – along with physical activity and smoking – one of the most important modifiable determinants of cancer risk (Riboli & Norat, 2003). The contribution of diet to risk of cancer in developing and Asian countries is lower, estimated at around 20% (Willett, 2001; Messina, 1999). Breast cancer rates indeed vary widely throughout the world, with women in Westernized countries usually exhibiting five times as high a frequency of the disease as women in most Asian and developing countries (Willett, 2001).
Populations migrating from low-incidence to high-incidence areas generally show an increase in breast cancer rates within two to three generations, which shows that the specifics of the new environment rather then genetic differences are the most responsible for this discrepancy in rates. Mainly for this reason, major hypotheses regarding the connection between diet and breast cancer risks have been derived from investigation of the existence of such correlation in various populations. As early as the 1970s, studies showed that diets high in animal products, fat, and sugar – characteristics of industrialized Western societies – generally led to higher rates of various types of cancers, including of the breast, than those of the developing countries, where the dietary emphasis was on a limited number of starchy staple foods, with low intake of animal products, fat, and sugar (Key et al., 2002).
One of the most striking confirmations of the correlation between the specifics of individual diets and the risk of cancer is the example of Japan in the second half of the twentieth century. Japan was one of many countries where people’s diet changed substantially during this period, generally with increases in the consumption of meat, dairy products, vegetable oils, fruit juice, and alcohol, while the consumption of starchy staple foods like bread, potatoes, rice, and maize flour decreased. In fact, the consumption of meat and dairy products in Japan between 1950s and 1990s has increased ten-fold, while the consumption of staple grains like rice decreased by 35% in the same period. Additional contributing factors were the more sedentary lifestyle and higher prevalence of obesity associated with it. The result was a seven-fold increase in cancer rates in Japan over these four decades (Key et al., 2002).
Still, the breast cancer mortality rate in Japan at the end of the twentieth century remained about one-quarter of that in the U.S. (Messina, 1999). This fact, along with other indicators of lower incidence and mortality rates from breast cancer among Asian women compared to Caucasian women, prompted an increase in the number of studies exploring the protective qualities of non-meat, non-dairy protein-substitute foods consumed among Asians in high quantities, such as soy. These studies concentrated along the two main lines: the potential antiestrogenic effects of the soybean isoflavones, and the reduced number of 7,12-dimethylbenzanthracene-induced mammary tumors observed in animal trials (Messina, 1999). Some of the studies – including one in the U.S. – produced the results confirming the inverse relationship between soy foods intake and breast cancer rates, while others showed no such effect. While this ambiguity of results does not necessarily nullify the legitimacy of the studies that found such correlation, the relatively small overall number of studies conducted in this area shows that much more research of this type must be conducted before unambiguous, evidence-based conclusions can be drawn.
Adjustments in an individual’s diet have been shown to influence the level of breast cancer risk in various populations. Trichopoulou et al. (1995) explored the influence of the consumption of olive oil, margarine, and a range of other food groups on the risk of breast cancer. Their findings indicated that an independent association between vegetable and fruit consumption and statistically significant reductions in breast cancer risks existed. Regular consumption of olive oil produced an even more significant reduction in the risks of this type of cancer, while increased consumption of margarine actually increased these risks. La Vecchia et al. (1995) independently confirmed these conclusions through their own study of the correlation between dietary fats and the risk of breast cancer. According to their results, all types of vegetable oil used in the study (olive, safflower, corn, peanut, and soy) produced an inverse relationship to breast cancer risks, while animal-derived dietary fats (butter and margarine) produced a direct relationship between the levels of their consumptions and the risks of breast cancer.
Riboli and Norat (2003) conducted a comprehensive meta-analysis of case-control and prospective studies on fruit and vegetable intake and cancer risk. Their results showed a significant protective effect of vegetables against breast cancer, but no such effect on the part of fruit; in fact, one of the studies they analyzed showed an increased risk of breast cancer in women older than 50 years whose consumption of fruit was increased significantly.
Other studies explored less specific but more comprehensive and long-lasting effects of dietary changes on the risks of breast cancer. Boyd et al. (1997) performed a two-year study of the effects of a low-fat, high-carbohydrate diet on the changes in density of the breast tissue. The hypothesis behind the study – and supported by existing research – was that women with higher breast tissue density were up to 75% more likely to contract breast cancer than women with low breast tissue density. The results of this study showed significant reduction in the area of mammographic density among the control group of women who were on a low-fat, high-carbohydrate diet for the two years of the study. On their part, Wu, Pike and Stram (1999) conducted a meta-analysis of the case-control studies exploring the correlation between the levels of dietary fat intake and breast cancer rates, specifically the levels of serum estrogen, which have been shown statistically to influence the development of breast cancer. This analysis produced inconsistent results, with one-quarter of the studies showing an increase in serum estrogen levels despite the significant reduction in dietary fat intakes. The researchers hypothesized that the reason for such a discrepancy was in the lack of control of this analysis over the consistency of the subjects’ other dietary intakes, such as fruit, vegetables, and dietary fibers. In other words, while the reductions in dietary fat intake have been consistent through all the analyzed studies, the levels of estrogen in the subjects’ blood may have been influenced by factors unrelated to dietary fat intake. This conclusion is supported by Stoll (1996), who found that not only high fat intake, but also low intake of fiber and carbohydrates were associated with low insulin sensitivity, which itself is a contributing factor for breast cancer risk. Similarly ambiguous results regarding the correlation between dietary fat intake and breast cancer rates were found in Key et al. (2002) and Willett (2001).
This ambiguity of empirical data leads to a conclusion that dietary fat alone cannot be looked at as the main factor contributing to an increase in breast cancer risk. It makes considerably more sense to explore such intake as part of the overall picture of nutrition in its contribution to a person’s lifestyle, which includes alcohol consumption and daily physical activities. In other words, the person’s propensity to excessive weight and obesity should be looked at in terms of correlation with breast cancer rates.
Obesity increases the risk of breast cancer in postmenopausal women by around 50%, most likely by increasing estrogen concentration in the blood (Key et al., 2002). It does not have the same effect for premenopausal women – in fact, it is associated with a moderate reduction in breast cancer risk in premenopausal women in developed countries, possibly due to breast tissue density reduction mentioned in Boyd et al. (1997), or to a reduction in hormone exposure because obesity frequently leads to anovular menstrual cycles (Key et al., 2002). However, if a woman is obese at a younger age, there is a high chance that she would remain so into menopause, which means that obesity is an important risk factor for breast cancer.
Lahmann et al. (2004) conducted a study to determine if one particular form of obesity was more likely to increase breast cancer risk than others, but their results showed such direct correlation only for the overall obesity, not such separate types of it like abdominal obesity. Additionally, this study produced a direct correlation between height of the subjects and the levels of breast cancer risk, producing an unrelated to research – and thus unexpected – but nevertheless significant result when considering the population groups with a higher risk of breast cancer than others.
Even in regards to obesity, however, ambiguity of results still exists. Stoll (1996) reported on a study in which low-fat, high-carbohydrate, high-fiber diet was applied to subjects, in combination with daily exercise, resulting in normalization of insulin sensitivity – and thus, theoretically, the reduction in the levels of breast cancer risks – despite the fact that the participants remained significantly obese or overweight at the end of it. The logical conclusion of this study is that the breast cancer risks can be reduced without inducing significant body mass reduction in a subject.
This conclusion, of course, takes the matter back to the subject of nutrition, both as a factor contributing to obesity and to the levels of breast cancer risk. As the above analysis shows, the role of specific dietary factors in breast cancer causation has not been unambiguously resolved as of yet. Enthusiasm for the hypothesis that dietary fat intake was responsible for the high rates of breast cancer, particularly in industrialized countries of the West, was based largely on the weakest form of epidemiologic evidence, represented by comparisons of such correlations among different countries. Existing research does not appear to support the concept that the increased levels of fat intake at an adult age have a major effect on breast cancer incidence later in life. On the other hand, excessive food intake and lack of physical activity at a young age leads to increased growth and earlier onset of menstruation, together with increased chances of obesity, all of which represent contributing factors for a significant increase in breast cancer risks later in life. The differences in early-life energy intake – both culturally and economically based – between the Western and Eastern countries can be considered an important contributing factor to the widely observed discrepancies in breast cancer occurrence and mortality rates among Caucasian and Asian women. The existing research also delivers some evidence that increased vegetable intake reduces the risks of breast cancer, although the detailed explanation of how this occurs is still missing. The best suggestion to date is that certain carotenoids in this type of food exhibit strong protective qualities (Willett, 2001). The only clearly established dietary risk factor for breast cancer is alcohol, with consistent correlation between alcohol consumption and increase of endogenous oestrogen levels, but more recent research showed that these adverse effects can be mitigated to a certain degree by an adequate intake of folic acid (Willett, 2001).
It is practically challenging to test the hypotheses relating childhood and adolescent diet to breast cancer risk in middle adult or older adult life because of inadequate methods of collecting and measuring diet in the distant past. Nevertheless, existing evidence points at the possibility to reduce breast cancer risk by avoiding unnecessary weight gain and limiting alcohol consumption. Studies presented here also offer empirical evidence that the risk of obesity – and subsequent co-morbid conditions like breast cancer and coronary heart disease – can be reduced by replacing animal-derived, saturated fat in one’s diet with plant-derived unsaturated fats.
Boyd, N. F., Greenberg, C., Lockwood, G., Little, L., Martin, L., Byng, J., Yaffe, M., & Tritchler, D. (1997). Effects at two years of low-fat, high-carbohydrate diet on radiological features of the breast: Results from a randomized trial. Journal of the National Cancer Institute, 89, 488-496.
Key, T. J., Allen, N. E., Spencer, E. A., & Travis, R. C. (2002). The effect of diet on risk of cancer. Lancet, 360, 861-868.
La Vecchia, I. C., Negri, E., Franceschi, S., Decarli, A., Giacosa, A., & Lipworth, L. (1995). Olive oil, other dietary fats, and the risk of breast cancer (Italy). Cancer Causes Control, 6, 545-550.
Lahmann, P. H., Hoffmann, K., Allen, N., Van Gils, C. H., Khaw, K-T., Tehard, B., Berrino, F., Tjonneland, A., Bigaard, J., et al. (2004). Body size and breast cancer risk: Findings from the European prospective investigation into cancer and nutrition (EPIC). International Journal of Cancer, 111, 762-771.
Messina, M. J. (1999). Legumes and soybeans: Overview of their nutritional profiles and health effects. American Journal of Clinical Nutrition, 70, 439S-450S.
Riboli, E., & Norat, T. (2003). Epidemiologic evidence of the prospective effect of fruit and vegetables on cancer risk. American Journal of Clinical Nutrition, 78, 559S-569S.
Stoll, B. A. (1996). Nutrition and breast cancer risk: Can an effect via insulin resistance be demonstrated? Breast Cancer Research and Treatment, 38, 239-246.
Trichopoulou, A., Katsouyanni, K., Stuver, S., Tzala, L., Gnardellis, C., Rimm, E., & Trichopoulos, D. (1995). Consumption of olive oil and specific food groups in relation to breast cancer risk in Greece. Journal of the National Cancer Institute, 87, 110-116.
Willett, W. C. (2001). Diet and breast cancer. Journal of Internal Medicine, 249, 395-411.
Wu, A. H., Pike, M. C., & Stram, D. O. (1999). Meta-analysis: Dietary fat intake, serum estrogen levels, and the risk of breast cancer. Journal of the National Cancer Institute, 91, 529-534.