Obesity induced by high-fat diets increases the risk of several cancers, including breast cancer in several animal species [ 3 ].
On the contrary, soybean products act as cancer preventive agents in rodents and other animals [ 4 ]. Epidemiological studies provide clear evidence of association between breast cancer incidence, mortality, and dietary patterns or dietary constituents in humans, but frequently there is a discrepancy between the studies on human populations and investigations performed in more controlled conditions, such as cellular or animal studies.
Many other variables, such as race, age, menopausal status, onset of puberty and the number of pregnancies, are in fact associated with diet and lifestyle in humans, acting as confounding factors [ 5 ]. Among the prospective epidemiological studies on diet and breast cancer incidence, to date, there is no association, that is strong, reproducible, and statistically significant, with the exception of alcohol intake, overweight, and weight gain [ 6 ].
Over the past decade, there have been fundamental advances in breast cancer genomics. As nutrition deeply impacts on genome, it is critical to investigate this interaction. Nutrigenomics can clarify how genetic and epigenetic variations, which control gene expression, are influenced by nutrients and how development, progression, and recurrence of cancer are modified by foods [ 7 ]. In this review, we will summarise the current scientific evidence regarding the association between food, lifestyle, and breast cancer risk in women. Increased body mass index BMI is associated with a significant increase in the risk of breast cancer, although with some differences in age and menopausal status.
The association between being overweight defined as a BMI of 25 to Most studies and meta-analysis showed an increased risk of breast cancer for postmenopausal women and an inverse association between obesity and survival after breast cancer [ 8 ]. Controversial data exist in premenopausal subjects.
Can I Lower My Risk of Breast Cancer Progressing or Coming Back?
On the contrary, obesity increases breast cancer incidence in premenopausal women in the Asian population [ 10 ]. Furthermore, abdominal fatness is closely associated with premenopausal cancer risk [ 11 ]. Obesity, abdominal obesity in particular, has been associated with the production of adipokines in fat tissues [ 12 ], which, in turn, causes insulin insensitivity in peripheral tissues [ 13 ].
Body fat increases oestrogen production through the aromatisation of steroidal precursors of both ovarian and adrenal origin. Tumorigenic properties of oestrogen are regulated through the oestrogen receptor ER , making the understanding of the mechanisms that activate this receptor highly relevant. Recently, a possible interaction between leptin and insulin, and obesity-related markers of inflammation has been linked to breast cancer outcomes.
Numerous studies have examined the relationship between obesity and prognosis in breast cancer: the majority of them demonstrate an inverse association between obesity and survival after breast cancer [ 15 , 16 ]. However, it is still unknown whether intentional weight loss improves outcomes for women with breast cancer [ 17 ] and the number of trials of weight loss interventions in these patients, while increasing, is still small [ 18 ].
Recently, the International Agency for Research on Cancer IARC and the World Cancer Research Fund WCRF have remarked that diet strongly influences cancer prevention, disease development, treatment tolerance, and cancer recurrence and also provide advice and recommendations for body weight management in breast cancer primary and secondary prevention [ 19 , 20 ]. A number of epidemiological studies have provided convincing evidence that alcohol consumption is an important risk factor for the incidence and mortality of breast cancer [ 21 , 22 ].
A pooled analysis of six prospective cohort studies showed that alcohol consumption is associated with a linear increase in breast cancer incidence. Furthermore, the Million Women Study showed that the relative risk of developing breast cancer increases by 7. The relationship between breast cancer and alcohol was confirmed by the reanalysis of 53 epidemiological studies performed by Hamajima et al [ 22 ].
Ferrari et al collected data on of men and women among whom 20, fatal events occurred for which information on lifetime alcohol use was available, allowing separate consideration of former drinkers from lifetime abstainers. The mechanisms of carcinogenesis induced by alcohol on breast cancer are still unknown, but there is accumulating evidence that regular intakes of moderate amounts of alcohol affect sex hormone levels in premenopausal and postmenopausal women [ 25 ].
Several lines of evidence indicate that acetaldehyde, a product of alcohol metabolism, might play a role in alcohol-related carcinogenic effects in different target tissues [ 7 , 22 ]. As alcohol is a lipid solvent, the substance could modify cell membranes enhancing cellular permeability to carcinogens. Furthermore, alcohol can modulate their metabolism, enhance the production of reactive oxygen species ROS , and inhibit deoxy ribonucleic acid DNA repair [ 26 ].
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The role of alcohol intake on breast cancer survival was investigated in The Life After Cancer Epidemiology LACE Study, a cohort of 2, early-stage breast cancer survivors designed to examine modifiable lifestyle predictors of recurrence, survival, and quality of life. Alcohol consumption also impairs folate metabolism and may alter gene methylation since folate plays a pivotal role in DNA methylation [ 7 ]. The analysis of methylation of a cluster of cancer-related genes has revealed that alcohol consumption is associated with a specific pattern of DNA methylation, thus suggesting that alcohol produces specific epigenetic changes.
Many behavioural choices during life are likely to enhance the risk of developing breast cancer.
There is strong scientific evidence that not having children or having them after 30 years, avoiding breast feeding, prolonged use of the contraceptive pill, and having hormone replacement therapy after menopause all increase the incidence of mammary tumours. Other aspects of lifestyle have also been investigated. Among these, physical activity is associated with lower risk of invasive breast cancer [ 28 ]. However, breast cancers are heterogeneous for histopathology, hormone receptor status, and gene expression profile, and whether increased physical activity offers a true protection in all cases, is controversial.
A considerable number of studies have been conducted worldwide on physical activity and breast cancer risk. These results were confirmed in the recent European Prospective Investigation into Cancer and Nutrition EPIC study which demonstrated that moderate and high physical activity are associated with modest reduction in breast cancer risk [ 30 ].
A number of studies deal with the relationships between dietary habits and breast cancer incidence and mortality. In evaluating the impact of diet and physical activity on cancer progression and survival, evidence from prospective observational studies suggests that physical activity and diet may be associated with improved cancer progression and recurrence [ 32 ].
This protective effect was more evident in women with hormone-receptor-negative breast cancer [ 2 ]. Pierce et al have also shown that patients that consume a healthy diet and are physically active may increase their years of survival after diagnosis of breast cancer and those who reported eating a minimum of 5 vegetable and fruit servings daily and performing weekly physical activity equivalent to 30 minutes of walking at a moderate pace for 6 days a week had a higher year survival rate than those who did not adhere to these lifestyle practices [ 34 ].
Spark et al evaluated postintervention maintenance of physical activity and dietary behaviour change outcomes; their findings suggest successful maintenance was more common in trials using a theoretical model for intervention development that included behavioural change strategies [ 35 ]. Due to these positive results, many public health agencies tend to promote a healthy lifestyle focused on reducing adiposity through a low-fat, high-fibre diet and regular physical activity.
Substances contained in vegetable foods are studied as possible ways to prevent cancer, since a number of studies have suggested that people who eat more fruit and vegetables are less likely develop cancer. Although there is evidence to show that a diet rich in plant foods may be protective against cancer risk and provide many health benefits, published data are not univocal [ 36 ]; in particular, the analysis of the correlation between diet and breast cancer is still a controversial issue.
By the s, most reports dealing with the prevention of chronic diseases recommended relatively high intakes of vegetables and fruit, either because these foods were seen as nourishing substitutes for energy-dense fatty or sugary foods, or else because they were identified as positively protective agents against cardiovascular diseases.
Evidence that vegetables and fruit might be protective against some cancers emerged in the s [ 37 ].
Can I Lower My Risk of Breast Cancer Progressing or Coming Back?
Since the s, a number of studies tried to understand what the role of plant foods was in the prevention of various types of cancer, including breast cancer, but despite this, evidence in support of this statement are inconclusive. The risk decreased for cancers of the mouth and pharynx, oesophagus, stomach, colorectum, and lung. Breast cancer risk was not affected [ 38 ]. Other large prospective studies have investigated whether high intakes of fruit and vegetables might be associated with a reduced risk of breast cancer, but the results are close to null.
However, a more recent meta-analysis, which reviewed fifteen prospective studies, revealed a lower risk of breast cancer for the highest versus the lowest intake of fruit and vegetables combined, but when fruit and vegetable were separated, data were significant only for fruit consumption [ 40 ]. Interestingly, this study highlights that dietary changes during follow-up can obscure associations between dietary intake and disease risk if dietary intake is only assessed at baseline; in support of this statement, one of the studies analysed in this systematic review reported a RR of 0.
This finding supports the hypothesis of epigenetic modulation through nutrition in early life and their role in the prevention of chronic diseases. In addition, the results seem to be clearer when they are analysed in combination with the different type of tumours, in particular the expression of the ER. It should be stressed that one of the main difficulties in these kinds of studies is the assessment of food intake, highly variable because of the different methods and nutrient database utilised [ 36 ].
To improve knowledge in this issue, exposure assessment can be measured using biomarkers of fruit and vegetable intake, such as circulating carotenoids. A pooled analysis of eight cohort studies published in analysed the associations between circulating carotenoids and breast cancer risk. Results showed statistically significant inverse associations between circulating levels of total carotenoids and breast cancer risk. Associations were generally stronger among women of a healthy weight and for ER-negative tumours [ 42 ]. Several potential mechanisms may explain the inverse association between fruit and vegetables and breast cancer risk.
These foods are important sources of fibre which may prevent breast cancer by binding oestrogens and reducing reabsorption of oestrogens in the colon. Moreover, fruit and vegetables are good sources of various phytochemicals, such as carotenoids, glucosinolates, indoles, and isothiocyanates, which may prevent breast cancer by inducing the activity of detoxifying enzymes, reducing oxidative stress, inflammation and changing the epigenome [ 43 ].
Soybeans and its products have been a staple part of the Asian diet for centuries; they are the predominant source of isoflavones, which belong to the family of phytoestrogens. Genistein and daidzein are the most known and studied phytoestrogens. Laboratory data show that isoflavones have a wide range of biological actions, including the growth inhibition of breast cancer cell lines [ 44 ]. From this, much has been said about their role in carcinogenesis but what we know about the role of soy consumption in breast cancer risk in human is unclear.
Since , after the publication on Lancet by Lee HP and colleagues [ 45 ], many observational studies reported that soy intake may lower breast cancer risk, but these findings are highly variable. On the contrary, due to the apparent oestrogenicity of genistein, women diagnosed with breast cancer have frequently been advised to avoid it. So, it would be useful to make sense of this issue. In , Wu et al conducted two separate meta-analyses of studies carried out in Asian and Western populations.
A meta-analysis of eight studies showed that Asian women consuming the highest amount of dietary isoflavones had a reduction in breast cancer risk, as compared with those with low consumption of isoflavones. In contrast, a meta-analysis of 11 studies of women eating Western diets found no association between isoflavone intake and breast cancer risk [ 46 ].
A more recent meta-analysis tried to discriminate soy isoflavone intake and breast cancer risk for menopausal status with similar results [ 47 ]. Studies that investigate the relationship between soy food intake after the diagnosis of breast cancer and health status reported a slightly protective effect especially among the Asian population [ 48 , 49 ] confirming the results collected so far.
There are different mechanisms that try to explain these various outcomes: first, the role of diet in the epigenetic modulation especially during early life; indeed, the protective role of soy is more evident in Asian countries, where soy products are the basis of the typical diet since childhood. In support of this statement, several case—control studies found that soy intake during childhood or adolescence affects breast cancer risk in adulthood [ 50 ]. Similar studies also show that lifetime soy consumption at a moderate level may prevent breast cancer recurrence through mechanisms that change the biology of tumours; in particular, women who consumed soy during childhood are more likely to develop breast cancers that express significantly reduced Human epidermal growth factor receptor-2 levels hEGFR2.
Another mechanism that may explain the differences between populations could be related to the intestinal microbial transformation of phytoestrogen, since the metabolism of isoflavone can vary greatly between individuals. Equol EQ , a metabolite of daidzein produced in the intestine, is absorbed more efficiently and has higher oestrogenic activity then daidzein, but it was found that more than half of the adult population did not have a gut microbiota able to convert daidzein into EQ.
The prevalence of EQ producers appears to be higher in Japanese than in Caucasian women, which might explain the additional benefits conferred on Japanese women in terms of reduced breast cancer risk [ 52 ]. It is possible that the consumption of soy since early life can promote a suitable gut microbiota; however, there is a lack of data to support this hypothesis.
Appetite Changes (Over-Eating, or More Hungry than Usual)
In summary, there is no evidence to advise against soy food consumption for the female population or women diagnosed with breast cancer. It is important to have a different approach with isoflavones supplements, as they provide a greater concentration of phytoestrogen, which indicates that interactions with biological mechanisms can be hazardous to health. Milk and dairy consumption has, over time, been suspected of playing a role in the development of breast cancer. The hypotheses that have been put forth to suggest an increased cancer risk associated with milk consumption include overall high dietary fat content, contaminants in milk and hormones contained in milk such as oestrogens and IGF-1 [ 53 ].
IGFs are also self-produced by the human body and have both immediate and long-term effects on various cellular activities, for example impact on cell proliferation, differentiation, migration, and survival.
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The mitogenic and survival function of IGFs is not only observed in normal mammary cells, but also in breast cancer cells. Additionally, in some cases the IGF-1 receptor is overexpressed and highly activated in breast cancer tissue compared with normal or benign tissue. What is important to emphasise is that the actions of IGFs can be modulated by interaction with a family of six insulin-like growth factor-binding proteins IGFBPs and their functions at the cellular level are not fully understood [ 54 ]. In a consistent systematic literature review that summarised and quantified the current findings on milk and dairy products consumption and its effect on the serum concentration of IGF-1, 10 cross-sectional studies showed statistically positive correlation between milk consumption and the circulating IGF-1 level and randomised controlled trials indicated that the circulating IGF-1 level was significantly higher in the milk intervention group.
However, only three out of 12 studies reported a statistically positive correlation between dairy products consumption and IGF-1 serum concentration [ 55 ].