Alcohol and cancer risk

Ethanol may cause cancer through the formation of acetaldehyde, its most toxic metabolite. Acetaldehyde has mutagenic and carcinogenic properties, and bonds with DNA to increase the risk of DNA mutations and impaired cell replication. Ethanol may also cause direct tissue damage by irritating the epithelium and increasing the absorption of carcinogens through its effects as a solvent. In addition, alcohol can increase the level of hormones such as oestrogen, thereby increasing breast cancer risk, and increase the risk of liver cancer by causing cirrhosis of the liver, increased oxidative stress, altered methylation and reduced levels of retinoic acid. Lifestyle factors such as smoking, poor oral hygiene, and certain nutrient deficiencies (folate, vitamin B6, methyl donors) or excesses (vitamin A/ß-carotene), owing to poor diet or self-medication, may also increase the risk for alcohol-associated tumours.

POSITION STATEMENT - Cancer Council Australia

Key messages and recommendations

• Alcohol use is a cause of cancer. Any level of alcohol consumption increases the risk of developing an alcohol-related cancer; the level of risk increases in line with the level of consumption.

• It is estimated that 5,070 cases of cancer (or 5% of all cancers) are attributable to long-term, chronicuse of alcohol each year in Australia.

• There is convincing evidence that alcohol use increases the risk of cancers of the mouth, pharynx, larynx, oesophagus, bowel (in men) and breast (in women), and probable evidence that it increases the risk of bowel cancer (in women) and liver cancer. (Convincing and probable are the highest levels of evidence as determined by the World Cancer Research Fund and American Institute for Cancer Research and denote that the relationship is causal or probably causal in nature).

• Together, smoking and alcohol have a synergistic effect on cancer risk, meaning the combined effects of use are significantly greater than the sum of individual risks.

• Alcohol use may contribute to weight (fat) gain, and greater body fatness is a convincing cause of cancers of the oesophagus, pancreas, bowel, endometrium, kidney and breast (in post-menopausal women).

• Cancer Council recommends that to reduce their risk of cancer, people limit their consumption of alcohol, or better still avoid alcohol altogether.

• For individuals who choose to drink alcohol, Cancer Council recommends that they drink only within the National Health and Medical Research Council (NHMRC) guidelines for alcohol consumption.

Introduction

Alcohol use is widespread in Australia and has had a dominant role in defining Australian culture for more than 200 years.1,2 However, it is also an important cause of illness, injury and death, whether resulting from short-term episodes of intoxication or from long-term, chronic use.3

Addressing the health and social damage resulting from risky drinking is one of the three key priority areas identified by the Australian National Preventative Health Taskforce.4 Levels of harm from alcohol use are increasing, and a range of policy measures have been proposed to address the current drinking ‘culture’ in Australia.4

In this position statement, Cancer Council Australia provides a brief overview of the evidence concerning alcohol use and cancer, and gives its current recommendations regarding alcohol consumption.

Evidence linking alcohol and cancer

It has been known for more than 20 years that long-term chronic use of alcohol can cause cancer. In 1988, the International Agency for Research on Cancer (IARC) stated that ‘the occurrence of malignant tumours of the oral cavity, pharynx, larynx, oesophagus and liver is causally related to the consumption of alcoholic beverages’ and classified alcoholic beverages as Group 1 carcinogens—known to cause cancer in humans.5 Ethanol, the chemical present in all alcoholic beverages and which induces the altered physical and mental responses experienced with alcohol use, has also been listed as a Group 1 carcinogen.6

The most recent comprehensive review of the scientific evidence by the World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR) concluded that there is convincing evidence that alcohol is a cause of cancer of the mouth, pharynx, larynx, oesophagus, bowel (in men) and breast (in women), and probable evidence that alcohol increases the risk of bowel cancer (in women) and liver cancer.7 Convincing and probable are the two highest levels of evidence set by the World Cancer Research Fund and American Institute for Cancer Research that identify a causal relationship between a particular aspect of food, nutrition, physical activity or body composition, and cancer.7 Scientific research is continuing to identify other cancers that could be associated with alcohol use. For example, there is some evidence that heavy alcohol consumption may be associated with a higher risk of prostate cancer.8,9

There is a dose-response relationship between alcohol and cancer risk for men and women, with studies showing that the risk of cancer increases with increasing consumption of alcohol on a regular basis.7,10-12

There are a number of biological mechanisms that may explain alcohol’s contribution to cancer development. Ethanol may cause cancer through the formation of acetaldehyde, its most toxic metabolite. Acetaldehyde has mutagenic and carcinogenic properties, and bonds with DNA to increase the risk of DNA mutations and impaired cell replication.13,14 Ethanol may also cause direct tissue damage by irritating the epithelium and increasing the absorption of carcinogens through its effects as a solvent.7 In addition, alcohol can increase the level of hormones such as oestrogen, thereby increasing breast cancer risk,7 and increase the risk of liver cancer by causing cirrhosis of the liver, increased oxidative stress, altered methylation and reduced levels of retinoic acid.14 Lifestyle factors such as smoking, poor oral hygiene, and certain nutrient deficiencies (folate, vitamin B6, methyl donors) or excesses (vitamin A/ß-carotene), owing to poor diet or self-medication, mayalso increase the risk for alcohol-associated tumours.14

Estimates of cancer incidence attributable to alcohol use in Australia

Several estimates of the numbers of cases of cancer attributable to alcohol use in Australia have been calculated using different methods.3,15-17 However, these calculations pre-date the confirmation of alcohol use as a convincing cause of bowel cancer in men. Because the incidence of bowel cancer in Australia is high,18 calculations which exclude bowel cancer are likely to lead to a substantial underestimate of the true burden of
alcohol-caused cancer in Australia.

In order to estimate the incidence of cancer in Australia attributed to alcohol use, Table 1 provides a complete set of attributable fractions for cancers associated with alcohol for the United Kingdom, collated by the World Cancer Research Fund19 and applied to Australian cancer incidence data for 2005.18 Attributable fractions for the UK have been used here, on the assumption that Australian patterns of drinking more closely mirror those
in the UK than those in the USA, Brazil or China, the other countries for which the World Cancer Research Fund presented data.

Using this method, it is estimated that 5,070 cases of cancer (or 5% of all cancers) are attributable to long term, chronic use of alcohol each year in Australia. This figure includes cancers for which there is convincing evidence that alcohol use increases the risk of disease. When cancers for which the risk is probably increased by alcohol use are included, the tally rises to 5,663 (or 5.6% of all cancers).

Table 1: Estimated incidence of cancers caused by alcohol use in Australia, applying population attributable fractions for the UK to Australian cancer incidence data for 2005

Sources: World Cancer Research Fund and the American Institute for Cancer Research;7,19 Australian Institute of Health and Welfare18

Burden of disease and injury

Australian data show that alcohol is an important contributor to the overall burden of disease and injury in Australia.3 Burden of disease and injury is measured in disability-adjusted life years (DALYs), which calculate the amount of time lost due to both fatal and non-fatal events; that is, years of life lost due to premature death coupled with years of “healthy'” life lost due to disability.3 In 2003, alcohol was ranked sixth after tobacco,high blood pressure, high body mass, physical inactivity and high blood cholesterol as a cause of burden of disease and injury in Australia.3 Alcohol was responsible for 3.1% of the burden of disease and injury due to cancer.3*

Because alcohol is frequently consumed in excess by young people, it is responsible for many lost years of life.20 The financial cost of disease, injury and crime caused by alcohol in Australia has been estimated to be about $15.3 billion.15 The proportion of these costs which can be attributed to alcohol-related cancer is not specified.15

Combined effects of drinking and smoking

For some cancers the combined effects of drinking alcohol and smoking tobacco greatly exceed the risk from either factor alone. Smoking and alcohol together have a synergistic effect on upper gastrointestinal and aero-digestive cancer risk.21 Compared with non-smoking non-drinkers, the approximate relative risks for developing mouth and throat cancers are up to seven times greater for people who smoke tobacco, up to six times greater for those who drink alcohol, but more than 35 times greater for those who are regular, heavy users of both substances (consuming more than four alcoholic drinks and smoking forty or more cigarettes daily).22 The synergistic effect of alcohol and smoking has been estimated to be responsible for more than 75% of cancers of the upper aero-digestive tract in developed countries.22

* These data pre-date confirmation that bowel cancers are caused by alcohol use and are therefore likely to be an underestimate.

Alcohol and weight gain

The relationship between alcohol consumption and body weight and fat is complex and appears to vary with sex and drinking pattern.23 From a nutritional viewpoint, alcoholic drinks represent ‘empty kilojoules’—that is, alcoholic drinks are high in kilojoules but low in nutritional value, especially when added to sugary mixer drinks. Alcohol itself has a comparatively high energy content (29 kilojoules per gram) compared with other
macronutrients.24

If people drink alcohol in addition to their normal dietary intake – that is, without a compensatory reduction in energy intake – they are liable to gain weight. Alcohol provides extra kilojoules and slows fat and carbohydrate oxidation. On the other hand, if drinking replaces healthy eating patterns, it can lead to nutritional deficiencies and serious illness.23,25

Therefore as well as being a direct cause of several cancers, alcohol might also contribute indirectly to those cancers associated with excess body fatness. There is convincing evidence that body fatness increases the risk of cancers of the oesophagus, pancreas, bowel, breast (in post menopausal women), endometrium and kidney, and probable evidence that body fatness increases the risk of gallbladder cancer.7

Alcohol and heart disease

Earlier research which reported that low to moderate levels of alcohol consumption might reduce the incidence of coronary heart disease may be flawed.26 For example, misclassification error may be a factor in some studies, in which the category of non-drinkers includes former drinkers who might have stopped drinking for reasons such as ill-health or becoming older.27 It might reasonably be assumed that this population would be more likely to have coronary heart disease.27 Other reviews have suggested that unmeasured confounding in epidemiological studies of alcohol and heart disease is likely to be widespread and that it is almost impossible to account for this confounding without randomised controlled trials.28-30

The putative benefits of moderate alcohol consumption on heart disease appear to be confined to middleaged and older people.31 However, the ongoing debate over the potential impact of uncontrolled confounders on estimates of the size of the cardio-protective effect, and whether or not moderate alcohol consumption should be recommended for protection against heart disease is difficult to resolve in the absence of randomised controlled trials. Acknowledging these issues, the World Health Organisation (WHO) stated in 2007 that ‘…from both the public health and clinical viewpoints, there is no merit in promoting alcohol consumption as a preventive strategy.’26 In Australia, the National Heart Foundation explicitly advises against the consumption of red wine and other types of alcoholic drinks for the prevention or treatment of heart disease.32

Alcohol consumption in Australia

Adults

In 2007, 83% of Australians aged 14 or older had consumed at least one drink in the previous year (“recent drinkers”).1 Of recent drinkers, about half drank on a weekly basis, and one in ten drank daily. Seventeen percent of adults were either ex-drinkers or never-drinkers. Males were more likely to consume alcohol than females.1

Although most drinkers (61%) aged 14 years or older consumed alcohol at levels regarded as low risk to health in the short or long term, nearly one in 10 drinkers (8.6%) consumed alcohol at risky or high risk quantities to their health in both the short and long term.1# These drinking patterns have persisted since 2001.1 The majority of people classified as recent drinkers reported that they had made an effort to reduce their alcohol consumption. The most common reason given for doing so was because of health considerations.1

It is worth noting that the data on levels of personal alcohol consumption contained in these national surveys are based on self report by participants. When compared with the volume of alcohol known to be cleared for consumption (on the basis of statistics on sales figures, taxation and customs data) there is a significant shortfall. It is therefore probable that individuals under-report their personal levels of consumption.34,35

Quantities of alcohol consumed by Australian adults aged 15 years or over appear to have remained relatively stable over the past fifteen years at just fewer than 10 litres per capita.36 Compared with other countries within the Organisation for Economic Cooperation and Development (OECD), Australia is middle ranking on the basis of per capita alcohol consumption.36 In 2008, apparent per capita consumption of alcohol in the population aged 15 years or more was 9.95 litres, about half of which was consumed in the form of beer.37 Consumption of ready-to-drink, pre-mixed spirits increased between 2006 and 2007 but has since stabilised.37 Consumption of undiluted spirits dropped between 2006 and 2007 and increased between 2007 and 2008.37 It is likely that these trends reflect alcohol taxation policy in place at the time.

Children

Experience with alcohol is common among teenagers, and likelihood of use increases with age.38 The Australian Secondary Students’ Alcohol and Drug (ASSAD) survey (2005) shows that by age 15 about 90% of students had tried alcohol, and by age 17, 70% of students consumed alcohol in the month prior to the survey.38 The proportion of students drinking in the week prior to the survey increased with age, from 10% of those aged 12 to about half of 17-year-olds.38 About 5% of 12- to 15-year-olds and 20% of 16- and 17-yearolds had consumed alcohol at levels which could lead to short term harm during the week prior to survey.~ Teenagers were most likely to drink alcohol in the form of pre-mixed drinks or spirits.38

Indigenous Australians

Although Aboriginal and Torres Strait Islander Australians are more likely to abstain from alcohol use than the non-Indigenous population, of those who do drink, a higher proportion drink at risky or high-risk levels.39 In 2004-05, 29% of Indigenous Australians had not had a drink in the previous 12 months, about twice the prevalence of non-Indigenous Australians (15%).39 Among the populations who had consumed alcohol, however, 34% of Indigenous Australians had consumed at long-term risky or high-risk levels, compared with 22% of non-Indigenous Australians.39

The effects of alcohol use are felt especially heavily in this population. In 2003, drinking caused 8% of all Indigenous deaths and was responsible for 6% of the total burden of disease and injury for Indigenous Australians,40 approximately double that for the total Australian population.3 Liver cancer, and cancers of the lip, mouth and pharynx occur at more than twice the rate^ in Indigenous Australians compared with non-Indigenous Australians.41 The higher rates of liver cancer are likely to be attributable to elevated rates of infection with the hepatitis B virus and excessive alcohol consumption in some Indigenous males.41 The likelihood of developing cancers of the lip, mouth and pharynx is elevated in people who use tobacco and who drink alcohol; and the risk is much higher in people who use both substances.41 As well as risky drinking, smoking is more prevalent among Indigenous people than in the non-Indigenous population.39

# These measures are based on the NHMRC Australian Alcohol Guidelines (2001).33
~ For the purposes of ASSAD, risk of short term harm is defined as follows: Those males who consumed seven or more alcoholic drinks on at least one day of the preceding seven days and those females who consumed five or more alcoholic drinks on at least one day of the preceding seven days.38 These measures are based on the NHMRC Australian Alcohol Guidelines (2001) current at the time.33


Cancer Council Australia’s recommendations on alcohol use

Alcoholic drinks and ethanol are carcinogenic to humans.6,7 There is no evidence that there is a safe threshold of alcohol consumption for avoiding cancer, or that cancer risk varies between the type of alcoholic beverage consumed.7

Cancer Council recommends that to reduce their risk of cancer, people limit their consumption of alcohol, or better still avoid alcohol altogether. For individuals who choose to drink alcohol, consumption should occur within in the Australian National Health and Medical Research Council (NHMRC) guidelines.42 Cancer Council Australia’s key recommendations are summarised at the beginning of this statement and outlined in Box 1.

Cancer Council Australia is a strong advocate for evidence-based action to reshape social attitudes concerning drinking, and to reduce the burden of morbidity and mortality caused by alcohol use.

^ Age-standardised rate. These estimates are based on combined data from Cancer Registries in Western Australia, the Northern Territory and South Australia, and together provide the most detailed picture of Indigenous age-specific cancer incidence rates currently available.

Box 1. Key evidence-based points and recommendations

Alcohol use is a cause of cancer in humans (Group 1 carcinogen, highest level of evidence, classified by the International Agency for Research on Cancer (IARC)).5,6

Ethanol, the chemical present in all alcohol beverages, is also a cause of cancer in humans (Group 1 carcinogen, classified by the IARC).6

There is convincing evidence that alcohol use increases the risk of cancers of the mouth, pharynx, larynx, oesophagus, bowel (in men) and breast.7 (Convincing evidence, as classified by the World Cancer Research Fund (WCRF) and the American Institute for Cancer Research (AICR), is the strongest level of evidence and denotes a causal relationship*).

Alcohol use probably increases the risk of bowel cancer (in women) and liver cancer. (A probable relationship, as classified by the WCRF and the AICR, is the second highest level of evidence and denotes that the relationship is probably causal in nature*).

Alcohol use may contribute to weight (fat) gain, and therefore contribute in an indirect way to those cancers which are associated with overweight and obesity.

Greater body fatness is a convincing cause of cancers of the oesophagus, pancreas, bowel, endometrium, kidney and breast (in postmenopausal women)7 (the WCRF and the AICR’s strongest level of evidence, denoting a causal relationship*).

Cancer Council recommends that to reduce their risk of cancer, people limit their consumption of alcohol, or better still avoid alcohol altogether.

For individuals who choose to drink alcohol, Cancer Council Australia supports drinking only within the NHMRC Australian guidelines to reduce health risks from drinking alcohol *.

The NHMRC guidelines are listed in abridged form in Box 2. Full text of the guidelines is available from: http://www.nhmrc.gov.au/publications/synopses/ds10syn.htm

Cancer Council bases its recommendations about alcohol use on the weight of scientific evidence which has accumulated about the relationship between alcohol consumption and cancer.

*See reference 7, Section 3.5.2, p. 59

Box 2. NHMRC alcohol guidelines, abridged

The Australian standard drink contains 10g of alcohol (equivalent to 12.5 mL of pure alcohol). In Australia a standard drink is 100 mL wine (13.5% alcohol), a 285 mL glass of beer (~5% alcohol) or a 30 mL nip of spirits.

Guideline 1: Reducing the risk of alcohol-related harm over a lifetime

The lifetime risk of harm from drinking alcohol increases with the amount consumed. For healthy men and women, drinking no more than two standard drinks on any day reduces the lifetime risk of harm from alcohol related disease or injury.

Guideline 2: Reducing the risk of injury on a single occasion of drinking

On a single occasion of drinking, the risk of alcohol-related injury increases with the amount consumed. For healthy men and women, drinking no more than four standard drinks on a single occasion reduces the risk of alcohol-related injury arising from that occasion.

Guideline 3: Children and young people under 18 years of age

For children and young people under 18 years of age, not drinking alcohol is the safest option.

Guideline 4: Pregnancy and breastfeeding

Maternal alcohol consumption can harm the developing foetus or breast feeding baby.

A -For women who are pregnant or planning a pregnancy, not drinking is the safest option.
B -For women who are breast feeding, not drinking is the safest option.

The National Health and Medical Research Council states that, “the advice in the guidelines cannot be ascribed levels of evidence ratings as occurs with other NHMRC guidelines, due to the analytic approach taken in their development”. Guidelines one and four however are underpinned by evidence equivalent to NHMRC level III-1.

Process, acknowledgements

This statement was developed by Cancer Council Australia’s Alcohol Working Group with input from its Nutrition and Physical Activity Committee and reviewed by the organisation’s principal Public Health Committee. It has also been approved for publication by Cancer Council Australia’s Board.

The statement has been peer reviewed by the Medical Journal of Australia and, following amendments to the content as part of that process, published by the MJA on May 2011. It can be accessed on the MJA website at:

http://www.mja.com.au/public/issues/194_09_020511/contents_020511.html.

Cancer Council Australia wishes to acknowledge Associate Professor Tanya Chikritzhs, who assisted in drafting the section on alcohol and heart disease, and Professor Jeanette Ward and Professor Dallas English, who kindly reviewed an earlier draft of the position statement.

Cancer Council Australia, GPO Box 4708, Sydney NSW 2001
Ph: (02) 8063 4100 Fax: (02) 8063 4101 Website: http://www.cancer.org.au/

References

1. Australian Institute of Health and Welfare. 2007 National Drug Strategy Household Survey: detailed findings. Drug statistics series no. 22. Cat. no. PHE 107. Canberra, Australia: Australian Institute of Health and Welfare; 2008.
2. Lewis M. (1992); A rum state: alcohol and state policy in Australia, 1788-1988. Canberra: Australian Government Printing Service.
3. Begg S, Vos T, et al. The burden of disease and injury in Australia 2003. Canberra: AIHW; 2007.
4. National Preventative Health Taskforce. Australia: The Healthiest Country by 2020 National Preventative Health Strategy the roadmap for action. Canberra, Australia: National Preventative Health Taskforce; 2009.
5. World Health Organization and International Agency for Research on Cancer. (1988); IARC monographs on the evaluation of carcinogenic risks to humans. Volume 44. Alcohol drinking. Summary of data reported and evaluation. Lyon France: IARC.
6. International Agency for Research on Cancer. Monographs on the evaluation of carcinogenic risks to humans: alcoholic beverage consumption and ethyl carbamate (urethane). Lyon: IARC; 2007.
7. World Cancer Research Fund and American Institute for Cancer Research. Food, nutrition, physical
activity and the prevention of cancer: a global perspective. Washington DC: AICR; 2007.
8. Fillmore KM, Chikritzhs T, et al. Alcohol use and prostate cancer: A meta-analysis. Molecular Nutrition &
Food Research 2009;53:240-55
9. Gong Z, Kristal AR, et al. Alcohol consumption, finasteride, and prostate cancer risk: results from the Prostate Cancer Prevention Trial. Cancer 2009;115:3661-9
10. Allen NE, Beral V, et al. Moderate Alcohol Intake and Cancer Incidence in Women. J Natl Cancer Inst 2009;101:296-305
11. Collaborative Group on Hormonal Factors in Breast Cancer. Alcohol, tobacco and breast cancer-- collaborative reanalysis of individual data from 53 epidemiological studies, including 58,515 women with breast cancer and 95,067 women without the disease. Br J Cancer 2002;87:1234-45
12. Corrao G, Bagnardi V, et al. A meta-analysis of alcohol consumption and the risk of 15 diseases. Prev Med 2004;38:613-9
13. Druesne-Pecollo N, Tehard B, et al. Alcohol and genetic polymorphisms: effect on risk of alcoholrelated cancer. Lancet Oncol 2009;10:173-80
14. Seitz HK, Stickel F. Molecular mechanisms of alcohol-mediated carcinogenesis. Nat Rev Cancer2007;7:599-61210
15. Collins D and Lapsley H. The costs of tobacco, alcohol and illicit drug abuse to Australian society in 2004/05. Canberra, Australia: Department of Health and Ageing; 2008.
16. English D, Holman CDJ, et al. The quantification of drug caused morbidity and mortality in Australia. AGPS; 1995.
17. Ridolfo B and Stevenson C. The quantification of drug-caused mortality and morbidity in Australia, 1998. Canberra: AIHW; 2001.
18. Australian Institute of Health and Welfare. Cancer in Australia: an overview, 2008. Canberra: AIHW; 2008.
19. World Cancer Research Fund and American Institute for Cancer Research. Policy and action for cancer prevention. Food, nutrition, and physical activity: a global perspective. Washington DC: AICR; 2009.
20. Collins D and Lapsley H. The avoidable costs of alcohol abuse in Australia and the potential benefits of effective policies to reduce the social costs of alcohol. National Drug Strategy Monograph No. 70. Canberra, Australia: Department of Health and Ageing; 2008.
21. US Department of Health and Human Services. The health consequences of smoking. Cancer. A report of the US Surgeon General. USA: Department of Health and Human Services, Public Health Service, Office on Smoking and Health; 1982.
22. Blot WJ, McLaughlin JK, et al. Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res 1988;48:3282-7
23. Wannamethee SG, Shaper AG, et al. Alcohol and adiposity: effects of quantity and type of drink and time relation with meals. Int J Obes (Lond ) 2005;29:1436-44
24. Food and Agriculture Organisation of the United Nations. Food energy - methods of analysis and conversion factors. FAO Food and Nutrition Paper 77. Report of a technical workshop Rome 3-6 December 2002. Rome, Italy: FAO; 2003.
25. Tolstrup JS, Halkjaer J, et al. Alcohol drinking frequency in relation to subsequent changes in waist circumference. Am J Clin Nutr 2008;87:957-63
26. World Health Organization. Prevention of cardiovascular disease. Guidelines for assessment and management of cardiovascular risk. Geneva: World Health Organization; 2007.
27. Fillmore KM, Stockwell T, et al. Moderate alcohol use and reduced mortality risk: systematic error in prospective studies and new hypotheses. Ann Epidemiol 2007;17:S16-S23
28. Fuchs FD, Chambless LE. Is the cardioprotective effect of alcohol real? Alcohol 2007;41:399-402
29. Jackson R, Broad J, et al. Alcohol and ischaemic heart disease: probably no free lunch. Lancet 2005;366:1911-2
30. Naimi TS, Brown DW, et al. Cardiovascular risk factors and confounders among nondrinking and moderate-drinking U.S. adults. Am J Prev Med 2005;28:369-7311
31. Hvidtfeldt UA, Tolstrup JS, et al. Alcohol intake and risk of coronary heart disease in younger, middleaged,and older adults. Circulation 2010;121:1589-97
32. National Heart Foundation of Australia. Position statement Antioxidants in food, drinks and supplements for cardiovascular health. National Heart Foundation of Australia; 2010.
33. National Health and Medical Research Council. Australian Alcohol Guidelines: health risks and benefits. Canberra: AGPS; 2001.
34. Stockwell T, Donath S, et al. Under-reporting of alcohol consumption in household surveys: a comparison of quantity-frequency, graduated-frequency and recent recall. Addiction 2004;99:1024-33
35. Stockwell T, Zhao J, et al. What did you drink yesterday? Public health relevance of a recent recall method used in the 2004 Australian National Drug Strategy Household Survey. Addiction 2008;103:919-28
36. Organisation for Economic Co-operation and Development Health Division. OECD Health Data 2008 - Frequently Requested Data. Alcohol consumption. Paris, France: OECD; 2008.
37. Australian Bureau of Statistics. Apparent Consumption of Alcohol, Australia, 2008-09. Canberra: Australian Bureau of Statistics; 2010.
38. White V. and Hayman J. Australian secondary school students' use of alcohol in 2005. Monograph Series No. 58. Report prepared for Drug Strategy Branch, Australian Government Department of Health and Ageing, by the Centre for Behavioural Research in Cancer, Cancer Control Research Institute, The Cancer Council Victoria. Canberra, Australia: Department of Health and Ageing; 2006.
39. Australian Institute of Health and Welfare. Australia's health 2008. Cat.no.AUS 99. Canberra, Australia: AIHW; 2008.
40. Vos T, Barker B, et al. The burden of disease and injury in Aboriginal and Torres Strait Islander peoples, 2003. Brisbane, Australia: School of Population Health, University of Queensland; 2007.
41. Threlfall T and Thompson J. Cancer incidence and mortality in Western Australia, 2007. Perth, Australia: Department of Health; 2009.
42. National Health and Medical Research Council. Australian guidelines to reduce health risks from drinking alcohol. Canberra: NHMRC; 2009.

Source : Cancer Council Australia

http://bit.ly/x59zT7

Soy, phyto-estrogens, and cancer prevention

Safe and efficacious levels of phyto-oestrogens have yet to be established for cancer prevention. As the results of some experimental studies suggest adverse effects from phyto-oestrogens, high dose phyto-oestrogen supplementation is not recommended or justified at this stage, especially for women with existing breast cancer.

Approved Public Health Committee – September 2006, update August 2009

POSITION STATEMENT - Cancer Council nsw
Soy, phyto-oestrogens and cancer prevention

Key messages

• Phyto-oestrogens are bioactive substances found in plant foods, with naturally occurring oestrogenic activity. Soy beans and other foods containing soy, such as tofu, tempeh and soy milk, are rich sources of phyto-oestrogens.

• There is limited suggestive evidence that soy foods may lower the risk of prostate and stomach cancer. The evidence for soy foods and cancer of the pharynx, oesophagus, pancreas, breast and endometrium is limited with no conclusion possible. There is no association between soy foods and the risk of other cancers, including bowel cancer.

• While they may have a protective effect, there is also some evidence that phyto-oestrogens might stimulate the growth of existing hormone dependent cancers.

• Cancer Council supports the consumption of soy foods in the diet. This is consistent with Cancer Council recommendations and national dietary guidelines to eat a diet high in plant based foods.

• Cancer Council does not recommend or support the use of supplements such as soy protein isolates or isoflavone capsules for healthy men and women to prevent cancer.

• Cancer Council does not recommend or support the use of supplements for breast cancer survivors. There is evidence to suggest that women with existing breast cancer or past breast cancer should be cautious in consuming large quantities of soy foods or phyto-oestrogen supplements.

Rationale

The purpose of this position statement is to evaluate and summarise the evidence linking soy foods and phyto-oestrogens with cancer. There is increasing interest in soy foods and phyto-oestrogens regarding their possible health benefits for a number of conditions, including cardiovascular disease, menopausal symptoms, osteoporosis and cancer. It is important that Cancer Council evaluate the associations between soy and cancer risk in order to develop its messages and recommendations, especially for women who already have breast cancer.

Background

Phyto-oestrogens are phytochemicals (bioactive substances that occur in plant foods) with naturally occurring oestrogenic activity. Particularly high concentrations of phyto-oestrogens are found in soy beans and other foods containing soy.

Phyto-oestrogens achieved notoriety in the 1940s in Western Australia when sheep fed large quantities of clover fodder developed a reproductive abnormality known as clover disease, which resulted in fertility problems and loss of productivity. The phyto-oestrogens in the clover were subsequently identified as the bioactive substance responsible for the reproductive abnormality.1

The lower breast and prostate cancer mortality rates in Asian countries and the potential anti-oestrogenic effects of phyto-oestrogens have led to speculation that soy foods reduce cancer risk.

Types of phyto-oestrogens

There are three important classes of phyto-oestrogens:

• Isoflavonoids/isoflavones - found in legumes, with soy beans being the richest source.
• Lignans - a constituent of dietary fibre and found mainly in nuts, seeds, legumes, cereals, vegetables and fruits.
• Coumestans - found in sprouted beans, alfalfa and clover.

Soy beans and soy products provide the main sources of phyto-oestrogens in the human diet. Soy phyto-oestrogens (isoflavones) comprise mainly genistein (60%) and daidzein (30%), with smaller quantities of glycitein (10%).2 Isoflavonoids are stable to heating and some processing techniques.2 Genistein and daidzein have a similar structure to oestradiol, and are able to bind to oestrogen receptors, albeit with a lower affinity than oestradiol.2

Food sources

Foods containing soy include tofu, tempeh and soy milk, which are rich sources of phyto-oestrogens. A list of different soy foods and their relevant phyto-oestrogen content is shown in table 1. Although fermentation of soy can reduce the amount of isoflavones present, the bioavailability of isoflavones is higher in fermented products.3 Generally, it is thought that 30-50mg of isoflavones is enough to offer health benefits.


Table 1. The phyto-oestrogen content of different soy foods3,4

Food Total Isoflavone (mg/100g)

Soy beans ------------2 - 221
Tofu ----------------- 4 - 67
Tempeh --------------103
Soy milk -------------- 1 - 21


Dietary intake of phyto-oestrogens

In communities consuming traditional soy foods, estimates of average isoflavone intakes range between 11 and 54mg/day.5,6 This is equivalent to one or two serves of soy foods on a daily basis.

Tofu contributes the largest amount of soy to most Asian diets.7 In Western diets, the majority of the isoflavone/phyto-oestrogen intake comes from non-soy foods, such as soy additives in baked goods, tuna or coffee.8 A high dietary intake of phyto-oestrogens in most studies in Western populations corresponds to a low intake in most studies of Asian populations.9

Epidemiological evidence

The results from experimental studies have been conflicting, with soy foods and phyto-oestrogens showing both risk enhancing and risk reducing effects. Caution is required in interpreting the results of epidemiologic studies relating to phyto-oestrogens due to potential exposure misclassification, confounding and lack of a dose response.

Breast cancer

A meta-analysis found that soy intake is associated with a modest reduction in breast cancer risk (odds ratio (OR)=0.86, 95% confidence interval (CI)=0.75-0.99).9 This meta-analysis included results from 12 case-control and six cohort studies. However, the heterogeneity across studies limited the ability to interpret the findings and the authors advised against making any recommendations for using soy as a cancer prevention agent.

The inverse association between soy exposure and breast cancer risk was slightly stronger in premenopausal women (OR=0.70, 95% CI=0.58-0.85) than in post menopausal women (OR=0.77, 95% CI=0.60-0.98).9

An earlier meta-analysis found that consumption of soy foods was associated with a lower risk of breast cancer (OR=0.78, 95% CI=0.68-0.91).10 This study was funded by the soy food industry. This meta-analysis included results from 11 case-control and three cohort studies.

Prostate cancer

A meta-analysis showed that soy consumption was related to a lower risk of prostate cancer in men (OR=0.70, 95% CI=0.59-0.83).11 It should be noted that this study was funded by the soy food industry. This meta-analysis included results from six case-control and two cohort studies.

Another review,12 although not a systematic review, identified different case-control and cohort studies to the meta-analysis11 described above. It concluded that there was inconsistency with few studies showing a statistically significant protective effect.12

Some trials (although not randomised) suggest that phyto-oestrogen supplements may benefit some patients with prostate cancer, by decreasing or stabilising PSA values but the evidence is too limited to recommend supplementation.13,14

Colorectal cancer

There does not appear to be an association between soy consumption and colorectal cancer.15 Although most case-control and cohort studies show weak inverse associations between higher soy consumption and colorectal cancer, the results have not been statistically significant, with most of the confidence intervals crossing one.15

Other cancers

There is no association between soy foods and the risk of other cancers. There is some limited evidence to suggest that phyto-oestrogens have enough oestrogenic activity to stimulate cell growth in the endometrium of post menopausal women, although the evidence overall is inadequate to draw conclusions on whether phyto-oestrogens taken by perimenopausal or post menopausal women eventually would cause endometrial cancer.16

Views on soy and phyto-oestrogens in cancer prevention reports

The World Cancer Research Fund found in 2007 that there was limited suggestive evidence that pulses (legumes), including soy and soy products, lowered the risk of prostate and stomach cancer. WCRF also found that the evidence for soy and soy products was limited with no conclusion possible for cancer of the pharynx, oesophagus, pancreas, breast and endometrium.17
The World Health Organization concluded in 2003 that there was insufficient evidence that soy foods or phyto-oestrogens reduce the risk of breast cancer.18

Potential mechanisms of action

Breast cancer

As phyto-oestrogens are strikingly similar in chemical structure to oestradiol, a potential mechanism of action for phyto-oestrogens is their ability to bind to oestrogen receptors. However phyto-oestrogens also have effects that are unrelated to oestrogen activity. They act as antioxidants to inhibit free radical damage, and have anti-proliferative properties to inhibit tumour growth.

Most of these actions of phyto-oestrogens occur only at pharmacologic concentrations (30-185μM) in experimental studies, rather than at the lower concentrations achievable from a dietary intake. However, at concentrations within the range achievable from dietary soy exposures (<4μM in the blood), genistein (a type of phyto-oestrogen) exhibits oestrogenic properties, some of which could theoretically enhance breast cancer risk.19

In contrast, daidezin, the other key phyto-oestrogen in soy, enhances tamoxifen efficacy at physiologic levels in a rat model.20

Timing of exposure

Early life may be a critical period for soy exposure. Animal studies have shown that pre-pubertal exposure to phyto-oestrogens reduces carcinogen-induced breast cancer in rats.21-24 Some human epidemiologic studies have also shown that there is an inverse association between childhood soy exposure and reduced breast cancer risk.25,26 As Asian women are likely to have been exposed to soy during early life, this may explain the stronger protective association seen in studies of Asian populations.

Prostate cancer

The exact mechanism of action by which soy consumption is associated with a lower risk of prostate cancer remains to be elucidated. Short intervention studies show that serum sex hormone-binding globulin concentrations increase in men consuming tofu.27,28 Intake of phyto-oestrogens may lead to a reduction in cell proliferation and angiogenesis and an increase in apoptosis.29-32

Issues for women with existing breast cancer

It is not clear whether it is safe for women with existing breast cancer to consume soy supplements or even large quantities of soy foods. The results of scientific studies are contradictory, with cell culture studies reporting both the oestrogenic stimulation of oestrogen receptor positive breast cancer cell lines and the antagonism of tamoxifen activity at physiological phyto-oestrogen concentrations.33,34

Thus phyto-oestrogens (genistein and daidzein) may stimulate existing tumour growth and antagonize the effects of tamoxifen.33,35 Women with current or past breast cancer should be aware of the risks of potential tumour growth when taking soy products.

There are no clinical trials available to definitively answer this question.

Menopause

Soy phyto-oestrogens are seen by some as an alternative to oestrogen therapy to treat post-menopausal symptoms. However the oestrogenic effect of soy in potentially promoting tumour recurrence raises concern for its use by breast cancer survivors.36

A systematic review found that phyto-oestrogens available as soy foods, soy extracts and red clover extracts do not significantly improve hot flushes or other menopausal symptoms.37 Most of the trials lasted only three to four months, so the long term effects remain unclear.37

Recommendations

Although the evidence is not conclusive for soy foods to protect against cancer, soy foods can be encouraged as part of a varied and nutritious diet. This is consistent with Cancer Council recommendations and national dietary guidelines to eat a diet rich in plant foods.

Safe and efficacious levels of phyto-oestrogens have yet to be established for cancer prevention. As the results of some experimental studies suggest adverse effects from phyto-oestrogens, high dose phyto-oestrogen supplementation is not recommended or justified at this stage, especially for women with existing breast cancer.

Health claims about soy

In 2004, the American Soybean Association petitioned the Food and Drug Authority in the USA for permission to use a health claim for the association between soy protein intake and lower risk of certain cancers, including breast cancer. The industry has since withdrawn their petition. The inconsistency of the evidence appears to have been the driving force in the withdrawal of this petition for a health claim.

In the USA, health claims on soy protein and lowered risk of heart disease are permissible.

Cancer Council does not support the use of health claims on food labels that suggest soy foods or phyto-oestrogens protect against the development of cancer.

Future research

It would be useful for future studies to report associations for both soy foods and specific phyto-oestrogens. Studies vary as to whether they report on the following exposures:

§ Fermented vs non-fermented soy.

§ Total soy vs soy protein.

§ Dietary soy consumption vs urinary isoflavones.

As with many other nutritional factors, there is a need for better quality, well-reported, larger and longer duration studies. Studies need to be performed in populations with sufficient variation in intake of soy and phyto-oestrogens. A better understanding of the factors that affect the bioavailability of ingested phyto-oestrogens, such as absorption rate, incorporation rate into the bloodstream, and metabolism of the intestinal bacterial environment, are required.

The issue of when soy foods are eaten during the lifetime needs to be resolved, with early life exposure to soy foods appearing to be of most benefit.

Clinical trials to assess the efficacy and safety of soy foods and supplements for women with existing breast cancer are also needed.

Further Information
Cancer Council New South Wales
PO Box 572 Kings Cross NSW 1340
www.cancercouncil.com.au
ABN 51 116 463 846

Contact
Kathy Chapman, Nutrition Program Manager: kathyc@nswcc.org.au

References

1. Shutt, Weston, Hogan. Quantitative aspects of phytoestrogen metabolism in sheep fed on Subterranean Clover (trifolium subterraneum cultivar Clare) or Red Clover (Trifolium pratense). Australian Journal of Agricultural Research. 1970; 21: 713-722.
2. Eldridge AC, Kwolek WF. Soybean isoflavones: effect of environment and variety on composition. J Agric Food Chem. 1983; 31(2): 394-396.
3. Cornwell T, Cohick W, Raskin I. Dietary phytoestrogens and health. Phytochemistry. 2004; 65(8): 995-1016.
4. Nakajima N, Nozaki N, Ishihara K, Ishikawa A, Tsuji H. Analysis of isoflavone content in tempeh, a fermented soybean, and preparation of a new isoflavone-enriched tempeh. Journal of Bioscience & Bioengineering. 2005; 100(6): 685-687.
5. Ho SC, Woo JL, Leung SS, Sham AL, Lam TH, Janus ED. Intake of soy products is associated with better plasma lipid profiles in the Hong Kong Chinese population. J Nutr. 2000; 130(10): 2590-2593.
6. Somekawa Y, Chiguchi M, Ishibashi T, Aso T. Soy intake related to menopausal symptoms, serum lipids, and bone mineral density in postmenopausal Japanese women. Obstet Gynecol. 2001; 97(1): 109-115.
7. Wu AH, Ziegler RG, Nomura AM, West DW, Kolonel LN, Horn-Ross PL et al. Soy intake and risk of breast cancer in Asians and Asian Americans. Am J Clin Nutr. 1998; 68(6 Suppl): 1437S-1443S.
8. Horn-Ross PL, Lee M, John EM, Koo J. Sources of phytoestrogen exposure among non-Asian women in California, USA. Cancer Causes Control. 2000; 11(4): 299-302.
9. Trock BJ, Hilakivi-Clarke L, Clarke R. Meta-analysis of soy intake and breast cancer risk. J Natl Cancer Inst. 2006; 98(7): 459-471.
10. Yan, Spitznagel. A meta-analysis of soyfoods and risk of breast cancer in women. International Journal of Cancer Prevention. 2004; 1(4): 281-293.
11. Yan L, Spitznagel EL. Meta-analysis of soy food and risk of prostate cancer in men. Int J Cancer. 2005; 117(4): 667-669.
12. Ganry O. Phytoestrogens and prostate cancer risk. Prev Med. 2005; 41(1): 1-6.
13. Hussain M, Banerjee M, Sarkar FH, Djuric Z, Pollak MN, Doerge D et al. Soy isoflavones in the treatment of prostate cancer. Nutr Cancer. 2003; 47(2): 111-117.
14. Kumar NB, Cantor A, Allen K, Riccardi D, Besterman-Dahan K, Seigne J et al. The specific role of isoflavones in reducing prostate cancer risk. Prostate. 2004; 59(2): 141-147.
15. Spector D, Anthony M, Alexander D, Arab L. Soy consumption and colorectal cancer. Nutr Cancer. 2003; 47(1): 1-12.
16. Sacks FM, Lichtenstein A, Van Horn L, Harris W, Kris-Etherton P, Winston M. Soy protein, isoflavones, and cardiovascular health: an American Heart Association Science Advisory for professionals from the Nutrition Committee. Circulation. 2006; 113(7): 1034-1044.
17. World Cancer Research Fund and American Institute for Cancer Research. Food, nutrition, physical activity and the prevention of cancer: a global perspective. Washington DC, AICR. 2007. 18. World Health Organisation. Diet, nutrition and the prevention of chronic diseases. Geneva, World Health Organisation. 2003.
19. Messina MJ, Loprinzi CL. Soy for breast cancer survivors: a critical review of the literature. J Nutr. 2001; 131(11 Suppl): 3095S-3108S.
20. Constantinou AI, White BE, Tonetti D, Yang Y, Liang W, Li W et al. The soy isoflavone daidzein improves the capacity of tamoxifen to prevent mammary tumours. Eur J Cancer. 2005; 41(4): 647-654.
21. Lamartiniere CA. Timing of exposure and mammary cancer risk. J Mammary Gland Biol Neoplasia. 2002; 7(1): 67-76.
22. Cabanes A, Wang M, Olivo S, DeAssis S, Gustafsson JA, Khan G et al. Prepubertal estradiol and genistein exposures up-regulate BRCA1 mRNA and reduce mammary tumorigenesis. Carcinogenesis. 2004; 25(5): 741-748.
23. Fritz WA, Coward L, Wang J, Lamartiniere CA. Dietary genistein: perinatal mammary cancer prevention, bioavailability and toxicity testing in the rat. Carcinogenesis. 1998; 19(12): 2151-2158.
24. Hilakivi-Clarke L, Onojafe I, Raygada M, Cho E, Skaar T, Russo I et al. Prepubertal exposure to zearalenone or genistein reduces mammary tumorigenesis. Br J Cancer. 1999; 80(11): 1682-1688.
25. Shu XO, Jin F, Dai Q, Wen W, Potter JD, Kushi LH et al. Soyfood intake during adolescence and subsequent risk of breast cancer among Chinese women. Cancer Epidemiol Biomarkers Prev. 2001; 10(5): 483-488.
26. Wu AH, Wan P, Hankin J, Tseng CC, Yu MC, Pike MC. Adolescent and adult soy intake and risk of breast cancer in Asian-Americans. Carcinogenesis. 2002; 23(9): 1491-1496.
27. Habito RC, Montalto J, Leslie E, Ball MJ. Effects of replacing meat with soyabean in the diet on sex hormone concentrations in healthy adult males. Br J Nutr. 2000; 84(4): 557-563.
28. Habito RC, Ball MJ. Postprandial changes in sex hormones after meals of different composition. Metabolism. 2001; 50(5): 505-511.
29. Bylund A, Zhang JX, Bergh A, Damber JE, Widmark A, Johansson A et al. Rye bran and soy protein delay growth and increase apoptosis of human LNCaP prostate adenocarcinoma in nude mice. Prostate. 2000; 42(4): 304-314.
30. Castle EP, Thrasher JB. The role of soy phytoestrogens in prostate cancer. Urol Clin North Am. 2002; 29(1): 71-ix.
31. Zhou JR, Gugger ET, Tanaka T, Guo Y, Blackburn GL, Clinton SK. Soybean phytochemicals inhibit the growth of transplantable human prostate carcinoma and tumor angiogenesis in mice. J Nutr. 1999; 129(9): 1628-1635.
32. Zhou JR, Yu L, Zhong Y, Nassr RL, Franke AA, Gaston SM et al. Inhibition of orthotopic growth and metastasis of androgen-sensitive human prostate tumors in mice by bioactive soybean components. Prostate. 2002; 53(2): 143-153.
33. de Lemos ML. Effects of soy phytoestrogens genistein and daidzein on breast cancer growth. Ann Pharmacother. 2001; 35(9): 1118-1121.
34. Limer JL, Speirs V. Phyto-oestrogens and breast cancer chemoprevention. Breast Cancer Res. 2004; 6(3): 119-127.
35. Duffy C, Cyr M. Phytoestrogens: potential benefits and implications for breast cancer survivors. J Womens Health (Larchmt ). 2003; 12(7): 617-631.
36. Balk E, Chung M, Chew P, Ip S, Raman G, Kupelnick B et al. Effects of soy on health outcomes. Evidence Report/Technology Assessment No. 126. Rockville, USA, Agency for Healthcare Research and Quality. 2005.
37. Krebs EE, Ensrud KE, MacDonald R, Wilt TJ. Phytoestrogens for treatment of menopausal symptoms: a systematic review. Obstet Gynecol. 2004; 104(4): 824-836.
Cancer Council Australia, GPO Box 4708, Sydney NSW 2001
Ph: (02) 8063 4100 Fax: (02) 8063 4101 Website: www.cancer.org.au



Source: Cancer Council NSW


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Soy foods, phyto-oestrogens and cancer

Australia Cancer Council recommends that women with breast cancer avoid soy and phyto-oestrogen supplements

What are phyto-oestrogens and where are they found?

Phyto-oestrogens are compounds found in plants that may act like the hormone oestrogen when consumed. Foods high in phyto-oestrogens include soy products (soy milk or yoghurt, tofu and tempeh), flaxseed, legumes and whole grains. The phyto-oestrogens in soy foods are also known as isoflavones.

Phyto-oestrogens have a very similar structure to the body's own oestrogen. The effects of phyto-oestrogens on the body are not fully understood, it is believed that they may act like weak oestrogen in some situations, but also block the actions of oestrogen in others.

Do phyto-oestrogens and soy foods protect against breast and prostate cancer?

Lower rates of breast and prostate cancer in some Asian countries, where soy is very common in the diet, led scientists to investigate the link between eating soy foods and protection against breast and prostate cancer. Due to their different dietary intakes, and also different genetics, it is difficult to determine whether it is the soy in the diet or some other factor. Overall in large studies on people it seems like a high consumption of soy foods may lower the risk of breast and prostate cancers, but only a little. Animal and test tube studies do support an anti-cancer effect.

More studies are needed to examine if phyto-oestrogens have a protective effect against breast and prostate cancer. From the current evidence, it is believed that a moderate consumption of soy foods (e.g. 1-2 serves of soy foods/day) along with an overall healthy eating plan is unlikely to have adverse effects. This is consistent with Cancer Council’s recommendations and dietary guidelines to eat a diet rich in plant foods.

There is no evidence supplements that contain high doses of soy or soy isoflavones are effective in preventing cancer, and are therefore not recommended.

Should women with breast cancer eat soy foods?

It is not clear if eating a diet high in phyto-oestrogens is safe for women who have breast cancer. Tamoxifen is a common treatment for women with oestrogen receptor positive breast cancer. Tamoxifen works by blocking the actions of oestrogen, and therefore stopping or reducing tumour growth.

For women with oestrogen receptor positive breast cancer who are taking Tamoxifen, it is still unclear whether eating soy foods or taking soy supplements will block or enhance the actions of Tamoxifen. Results of scientific studies are contradictory. A moderate consumption of soy foods, as part of an overall healthy eating plan, is unlikely to have any harmful effects.

Should women with breast cancer take soy supplements?

High dose soy or soy isoflavone supplements have not been tested for safety in women who have breast cancer or are taking Tamoxifen. The best advice is to eat soy foods in moderation as part of an overall healthy eating pattern, and not to suddenly increase the amount of soy phyto-oestrogens in the diet. Cancer Council recommends that women with breast cancer avoid soy and phyto-oestrogen supplements.

What can women with breast cancer do to improve their health?

Research is underway looking at the types of eating patterns that are protective for women who have had breast cancer. Evidence is starting to emerge that maintaining a healthy weight by eating a low-fat diet with plenty of fruit and vegetables and being physically active can improve survival and the overall health of breast cancer survivors.

Source: Cancer Council NSW

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