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Lifestyle factors

Lifestyle factors are behaviours that are part of everyday life that are associated with increased or decreased risk of breast cancer

Lifestyle factors associated with an increased risk of breast cancer include bodyweight and weight gain, and alcohol consumption, and may include processed meat consumption and smoking.

 

Overweight and obesity

Convincing

There is compelling and consistent evidence that the factor increases or decreases the risk of breast cancer.

After menopause

Being overweight or obese is associated with an increased risk of breast cancer for women who have experienced menopause (postmenopausal women).

Body fatness can be measured in several ways including:

  1. body mass index (BMI);

  2. waist circumference.

Both measures are associated with increased risk of breast cancer among women after menopause.

For each 5-unit increase in BMI after menopause, the risk of breast cancer increases by about 12%.

For each 10 cm increase in waist circumference, the risk of postmenopausal breast cancer increases by about 6%.

It is estimated that 8% of postmenopausal breast cancers each year in Australia are attributable to overweight or obesity.

The way in which body fat increases or decreases the risk of breast cancer is not fully understood. The most likely explanation is that higher body fatness after menopause influences the levels of circulating hormones in the body, including oestrogen, which can affect the risk of breast cancer.

Before menopause

In contrast to the effect of higher BMI in women after menopause, having a higher BMI before menopause is associated with a decreased risk of premenopausal breast cancer.

For each 5-unit increase in BMI the risk of premenopausal breast cancer is decreased by about 7%.

The link between body fatness and premenopausal breast cancer is complex and not well understood.

* Body mass index (BMI) is a measure of body fat based on your weight in relation to your height, and applies to most adult men and women aged 20 and over. 

Commonly accepted BMI ranges are underweight: under 18.5 kg/m2, normal weight: 18.5 to 25 kg/m2, overweight: 25 to 30 kg/m2, obese: over 30 kg/m2.

Evidence classifications:
  • Convincing (adult body fatness - marked by BMI, waist circumference and waist‒hip ratio - and increased risk of postmenopausal breast cancer)1

  • Probable (body fatness before the menopause and decreased risk of premenopausal breast cancer)1

There is convincing evidence that being overweight or obese is associated with an increased risk of breast cancer in postmenopausal women. Being overweight or obese before the menopause is probably associated with a decreased risk of premenopausal breast cancer.

Body fatness can be measured in several ways including:

  1. Body mass index (BMI);

The increased risk of postmenopausal breast cancer associated with BMI in adulthood is estimated as RR 1.12 (95% CI 1.09–1.15) (per 5 kg/m2).

The decreased risk of premenopausal breast cancer is estimated as RR 0.93 (95% CI 0.90–0.97) per 5 kg/m2 during the premenopausal period. 1

  1. Waist circumference.

Waist circumference was associated with an increased risk for postmenopausal breast cancer (RR per 10 cm increase = 1.06, 95% CI 1.01–1.12; based on studies adjusted for BMI).1

Despite BMI being associated with a decreased risk of premenopausal breast cancer, waist circumference was associated with an increased risk of premenopausal breast cancer (RR per 10 cm increase = 1.14, 95% CI 1.04–1.26; based on studies adjusted for BMI).1

Mechanisms

The mechanisms by which differences in body fat and fat distribution affect breast cancer are complex, particularly during early life and young adulthood, but are likely to involve the effects of adipose tissue on circulating sex hormone levels.2 Obesity in premenopausal women probably reduces ovarian progesterone production.1 Obesity in postmenopausal women increases the production of oestradiol.1 Both hormones are associated with breast cancer.  In addition, studies are increasingly implicating obesity as associated with a low-grade chronic inflammatory state and the activation of inflammatory cascades is one process that may predispose to carcinogenesis.1

Evidence 

WCRF/AICR (2018) summarised a vast literature in relation to measures of body fatness across the life-course and risk of premenopausal and postmenopausal breast cancer (see above).1  The International Agency for Research on Cancer (IARC) concluded in 2016 that ‘the absence of excess body fatness decreases the risk of cancer of the breast in postmenopausal women’, citing an approximately increased risk of 1.1 per 5 kg/m2  BMI.2,3

The conclusions of IARC (2016) and WCRF/AIRC (2018) are supported by more recently published analyses.  For example, a recent meta-analysis of data from seven prospective cohort studies also found a significantly increased risk of postmenopausal breast cancer associated with higher BMI (hazard ratio [HR] per 1 standard deviation (SD) increase = 1.15, 95% confidence intreval [CI] 1.03–1.27).A pooled analysis of Australian cohort studies reported an increased risk of postmenopausal breast cancer associated with increasing waist circumference (relative risk [RR] per 1 SD increase = 1.06, 95% CI 1.01–1.12).5 

Several cohort studies have shown that the association between body fatness and postmenopausal breast cancer risk may only occur, or may be greater, in women who do not use menopausal hormone therapy (MHT).1,4,6,7However, another cohort study did not find an effect of MHT use on the relationship between BMI and postmenopausal breast cancer risk.8

In a large, multicentre pooled analysis of premenopausal women aged 18–54 years, BMI at all ages during the premenopausal period was negatively associated with risk of breast cancer, with a dose–response relationship (RR per 5 kg/m2 0.77, 95% CI 0.73–0.80).9 The effect was greater for younger age groups.

It is estimated that 8% of postmenopausal breast cancers each year in Australia are attributable to overweight or obesity.10

Read the full Review of the Evidence

References
  1. World Cancer Research Fund/American Institute for Cancer Research (2018). Continuous Update Project Expert Report 2018. Diet, nutrition, physical activity and breast cancer. London, UK.
  2. Lauby-Secretan B, Scoccianti C, Loomis D, et al. (2016). Body Fatness and Cancer – Viewpoint of the IARC Working Group. New England Journal of Medicine 375(8);794–8
  3. International Agency for Research on Cancer (2016). IARC handbooks volume 16: questions and answers, IARC, Lyon, www.iarc.fr/en/media-centre/iarcnews/pdf/Q&AHandbook16.pdf.
  4. Freisling HM, Arnold M, Soerjomataram I, et al. (2017). Comparison of general obesity and measures of body fat distribution in older adults in relation to cancer risk: meta-analysis of individual participant data of seven prospective cohorts in Europe. British Journal of Cancer 116(11):1486–1497.
  5. Harding JL, Shaw JE, Anstey KJ, et al. (2015) Comparison of anthropometric measures as predictors of cancer incidence: A pooled collaborative analysis of 11 Australian cohorts. International Journal of Cancer 137 (7):1699–708
  6. Horn-Ross PL, Canchola AJ, Bernstein L, et al.  (2016). Lifetime body size and estrogen-receptor-positive breast cancer risk in the California Teachers Study cohort. Breast Cancer Research 18(1):132.
  7. Collaborative Group on Hormonal Factors in breast cancer (1996). Breast cancer and hormonal contraceptives: collaborative reanalysis of individual data on 53 297 women with breast cancer and 100 239 women without breast cancer from 54 epidemiological studies. Lancet 347(9017):1713–1727
  8. Neuhouser ML, Aragaki AK, Prentice RL, et al. (2015). Overweight, obesity, and postmenopausal invasive breast cancer risk: a secondary analysis of the Women’s Health Initiative randomized clinical trials. JAMA Oncology 1(5):611–621.
  9. Premenopausal Breast Cancer Collaborative Group (2018). Association of body mass index and age with subsequent breast cancer risk in premenopausal women. JAMA Oncology e181771.
  10. Kendall BJ, Wilson LF, Olsen CM, et al. (2015) Cancers in Australia in 2010 attributable to overweight and obesity. Australian and New Zealand Journal of Public Health 39 (5):452–457.
Weight gain

Convincing

There is compelling and consistent evidence that the factor increases or decreases the risk of breast cancer.

Postmenopausal women
Gaining weight as an adult is associated with an increased risk of postmenopausal breast cancer.

The risk of postmenopausal breast cancer increases by about 6% for each 5 kg increase in a woman’s weight. This corresponds to approximately a 12% and 26% increased risk for 10 kg and 20 kg weight gain, respectively.

The way that weight gain affects breast cancer risk is likely to involve hormones. Weight gain means that the body is storing more fat, which can affect levels of circulating hormones.

In postmenopausal women, weight gain increases the levels of circulating oestrogen. This can affect the risk of some types of breast cancer.

Premenopausal women

There is no conclusive evidence that weight gain in premenopausal women is associated with increased risk of breast cancer. Only a small number of studies have been done and the evidence was inconclusive.

Evidence classifications:
  • Convincing (postmenopausal breast cancer)

  • Inconclusive (premenopausal breast cancer)

There is convincing evidence that adult weight gain is associated with an increased risk of postmenopausal breast cancer. The increase in risk is estimated as 6% for each 5 kg increase in weight (RR 1.06, 95% CI 1.05–1.08).1

The evidence for an association between adult weight gain and risk of premenopausal breast cancer is inconclusive. There are only a small number of studies examining this association.

Mechanisms

Long-term weight gain in adults is associated with increased storage of body fat. This may increase the risk of breast cancer in postmenopausal women by reducing levels of serum hormone binding protein, which results in higher levels of circulating oestrogen.2 

Evidence 

The International Agency for Research on Cancer (IARC) concluded that there was sufficient evidence for a cancer-preventive effect of avoidance of weight gain for postmenopausal breast cancer;3 and the World Cancer Research Fund International/American Institute for Cancer Research (WCRF/AICR) concluded that there was convincing evidence that greater weight gain in adulthood is a cause of postmenopausal breast cancer.1 A dose-response analysis provided a relative risk per 5 kg increase in weight of 1.06 (95% confidence interval [CI] 1.05–1.08).1

WCRF/AICR reported that the increased risk associated with weight gain was significant only for oestrogen receptor positive, progesterone-receptor positive (ER+PR+) breast cancer, and not ER+PR- or ER-PR- disease. Contrary to the IARC review, risk was not affected by use of menopausal hormone therapy (MHT).1

For premenopausal breast cancer, IARC concluded that the available evidence suggested a lack of a cancer-preventive effect of avoidance of weight gain.3 WCRF/AICR considered the evidence for an association between adult weight gain and premenopausal breast cancer to be limited, and no conclusion was made.1

Findings from two more recent cohort studies are consistent with the findings of the WCRF/AICR.4,5

Read the full Review of the Evidence

References
  1. World Cancer Research Fund/American Institute for Cancer Research (2018). Continuous Update Project Expert Report 2018. Diet, nutrition, physical activity and breast cancer. London, UK.
  2. Endogenous Hormones Breast Cancer Collaborative Group (2003). Body mass index, serum sex hormones, and breast cancer risk in postmenopausal women. Journal of the National Cancer Institute 95(6):1218–1226.
  3. International Agency for Research on Cancer (2002). Weight control and physical activity, IARC Handbooks of Cancer Prevention, vol 6, IARC, Lyon.
  4. Neuhouser ML, Aragaki AK, Prentice RL, et al. (2015). Overweight, obesity, and postmenopausal invasive breast cancer risk: a secondary analysis of the Women’s Health Initiative randomized clinical trials. JAMA Oncology 1(5):611–621.
  5. Nitta J, Nojima M, Ohnishi H, et al. (2016). Weight gain and alcohol drinking associations with breast cancer risk in Japanese postmenopausal women: results from the Japan Collaborative Cohort (JACC) Study. Asian Pacific Journal of Cancer Prevention 17(3):1437–1443.
Alcohol

Convincing

There is compelling and consistent evidence that the factor increases or decreases the risk of breast cancer.

Drinking alcohol on a daily basis is associated with an increased risk of breast cancer in postmenopausal women. Drinking alcohol is probably associated with an increased risk of breast cancer in premenopausal women also.

Women who drink one standard glass of alcohol each day have a 7% higher risk of breast cancer than women who never drink alcohol. The risk of breast cancer increases as the number of drinks regularly consumed increases.

It is estimated that nearly 6% of breast cancer cases each year in Australia are due to alcohol consumption.

There does not appear to be a ‘safe’ level of regular alcohol consumption for risk of breast cancer, according to the evidence.

Alcohol may increase risk for breast cancer in a number of ways, including helping cancer-causing molecules to enter cells or damaging cell DNA. Alcohol is also thought to increase levels of the hormone oestrogen, which can influence breast cancer risk.

Evidence classification: Convincing (postmenopausal breast cancer)1

Evidence classification: Probable (premenopausal breast cancer)1

There is convincing evidence that alcohol consumption is associated with an increased risk of breast cancer, particularly in postmenopausal women. The risk of breast cancer among women who regularly drink alcohol compared to women who never drink alcohol is estimated by the World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR 2018) to increase by 7% for every 10 grams increase in daily alcohol consumption (RR 1.07, 95% CI 1.05–1.09).1 This corresponds to an increase in risk of breast cancer by 15% for 2 drinks per day and 31% for 4 drinks per day. (One ‘standard’ drink contains approximately 10 grams of alcohol).

Mechanisms

Several mechanisms have been proposed for how alcohol may increase breast cancer risk. Alcohol is a lipid solvent and can help carcinogens to enter cells. Alcohol can also increase the level of free-radical oxygen species, which can lead to DNA damage in cells. Genetic differences in ethanol metabolism can affect breast cancer risk. Alcohol consumption has also been associated with higher circulating oestrogen concentrations which can influence risk of breast cancer.1

Evidence 

The International Agency for Research on Cancer (2012) concluded that there is ‘sufficient evidence’ that ‘alcohol consumption causes cancer of the breast’.2 

The findings of World Cancer Research Fund International/American Institute for Cancer Research (2018)1 were based on evidence from 62 studies, 23 of which were included in dose–response meta-analyses. A relative risk (RR) for every 10 g/day increase in alcohol consumption of 1.05 (95% confidence interval [CI] 1.02–1.08) was reported for premenopausal breast cancer and of 1.09 (95% CI 1.07–1.12) for postmenopausal breast cancer.1 There is no threshold for consumption with an increased risk of breast cancer observed even at low levels of daily alcohol consumption.1,3,4  A pooled analysis of prospective cohort studies has indicated a positive association between oestrogen receptor-positive (ER+) and alcohol consumption, but not oestrogen receptor-negative (ER-) breast cancers,5 as observed in analyses by WCRF/AICR (2018).

It is estimated that about 5.8% of breast cancer cases each year in Australia are due to alcohol consumption.6

Read the full Review of the Evidence

References
  1. World Cancer Research Fund/American Institute for Cancer Research (2018). Continuous Update Project Expert Report 2018. Diet, nutrition, physical activity and breast cancer. London, UK.
  2. International Agency for Research on Cancer (2012). Personal habits and indoor combustions, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, volume 100E, IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, Lyon, http://monographs.iarc.fr/ENG/Monographs/vol100E/mono100E.pdf.
  3. Bagnardi V, Rota M, Botteri E, et al (2013). Light alcohol drinking and cancer: a meta-analysis. Annals Oncology 24: 301–308.
  4. Seitz HK, Pelucchi C, Bagnardi V, et al. (2012). Epidemiology and pathophysiology of alcohol and breast cancer: Update 2012. Alcohol and Alcoholism  47(3): 204–212
  5. Jayasekara H, MacInnis RJ, Room R, et al. (2016). Long-term alcohol consumption and breast, upper aero-digestive tract and colorectal cancer risk: a systematic review and meta-analysis. Alcohol and Alcoholism  51(3): 315–330.
  6. Pandeva N. Wilson LF. Webb PM et al (2015) Cancers in Australia in 2010 attributable to the consumption of alcohol. Australian and New Zealand Journal of Public Health 39 (5): 408–13
Smoking

Suggestive

The evidence is indicative of an association between the factor and increased or decreased risk of breast cancer, but there is not sufficiently strong evidence to be more certain.

There are many studies showing that tobacco smoking may be associated with a increased risk of breast cancer. While there are some limitations to the evidence, studies have been generally consistent in supporting a link between tobacco smoking and increased risk of breast cancer.

Tobacco smoking may be associated with an increased risk of breast cancer particularly in women who start smoking when they are younger or who start smoking many years before having their first child.

Tobacco smoke contains more than 5,300 chemicals, including more than 70 chemicals that are known to cause cancer.

Tobacco smoking is the major known and preventable cause of cancer worldwide. Smoking causes lung cancer and cancers of many other organs including the nasal cavity, throat, stomach, liver, kidney, bowel, and bladder.

Evidence classification: Suggestive

The evidence is suggestive of an association between tobacco smoking and risk of breast cancer. The evidence from a large number of cohort studies is generally consistent in showing a positive association between current or former tobacco smoking versus never smoking and risk of breast cancer. The associations are stronger among women who started smoking at a young age or many years before their first birth. However the evidence for a dose-response effect is inconsistent.

Mechanisms

Tobacco smoke contains more than 5300 chemical compounds, including more than 70 that are known to be carcinogenic.1 Tobacco smoking has been classified by the International Agency for Research on Cancer (IARC) as a Class 1 carcinogen and has been identified to cause cancer of the lung and many other organs, including the nasal cavity, oral cavity and organs of the digestive and urinary tract.1 Some of the compounds in tobacco smoke, including polycyclic aromatic hydrocarbons and aromatic amines, can induce mammary tumours in rodents,1 and some have been found in human breast milk.2

Evidence 

IARC3 concluded that there was limited evidence to show a causal link between tobacco smoking and risk of breast cancer, although a positive association was acknowledged.

More recently published data, including a large pooled analysis of data from 14 international prospective cohort studies,4 and a large meta-analysis of 31 cohort studies and 44 case–control studies,5 show a small increase in risk of breast cancer with current or former tobacco smoking. Risk estimates from prospective studies are in the range of 1.07 (95% confidence interval [CI] 1.04–1.10)4 and 1.13 (95% CI 1.09–1.17)5 among current smokers compared to never smokers. No dose-response relationship was observed in the pooled analysis.

Higher risks of breast cancer compared with never smokers have been reported among women who start smoking 10 years before their first birth in the pooled analysis4 and more generally when starting smoking before first birth in a previous meta-analysis of cohort studies.7 A more recent large cohort study has also reported an increased risk of breast cancer for ever smoking versus never smoking, particularly for starting smoking at a young age.6  In this study there was also a dose-response relationship for number of pack-years and number of cigarettes per day after 10 or more years of smoking, although there was no association with duration of smoking.

Read the full Review of the Evidence

References
  1. Phillips DH, Martin FL, Grover PL et al. (2001). Toxicological basis for a possible association of breast cancer with smoking and other sources of environmental carcinogens. Journal of Women's Cancer 3:9–16.
  2. Thompson PA, DeMarini DM, Kadlubar FF, et al. (2002). Evidence for the presence of mutagenic arylamines in human breast milk and DNA adducts in exfoliated breast ductal epithelial cells. Environmental and Molecular Mutagenesis 39:134–142.
  3. International Agency for Research on Cancer (2012). Personal habits and indoor combustions, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, volume 100E, IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, Lyon, http://monographs.iarc.fr/ENG/Monographs/vol100E/mono100E.pdf.
  4. Gaudet MM, Carter BD, Brinton LA, et al. (2017). Pooled analysis of active cigarette smoking and invasive breast cancer risk in 14 cohort studies. International Journal of Epidemiology 46(3):881–893.
  5. Macacu A, Autier P, Boniol M et al. (2015). Active and passive smoking and risk of breast cancer: a meta-analysis. Breast Cancer Research and Treatment 154(2):213–224.
  6. Jones ME, Schoemaler MJ, Wright LB, et al. (2017). Smoking and risk of breast cancer in the Generations Study cohort. Breast Cancer Research 19:118.
  7. Gaudet MM, Gapstur SM, Sun J, et al. (2013). Active smoking and breast cancer risk: original cohort data and meta-analysis. Journal of the National Cancer Institute 105(8):515–525.
Processed meats

Suggestive

The evidence is indicative of an association between the factor and increased or decreased risk of breast cancer, but there is not sufficiently strong evidence to be more certain.

Eating processed meat may be associated with an increased risk of breast cancer. Studies have given inconsistent results, with recent studies suggesting that processed meat in the diet does increase the risk of postmenopausal breast cancer, but possibly not premenopausal breast cancer.

Processed meat is meat that has been salted, cured, fermented or smoked to improve its flavour or to preserve it. Most processed meat is pork or beef – for example, ham, sausages and corned beef.

The way in which processed meat might increase the risk of breast cancer is not known. Processing can produce some cancer-causing chemicals. Cooking of processed meat can also produce cancer-causing chemicals.

Evidence classification: Suggestive

There is suggestive evidence that consumption of processed meat may be associated with an increased risk of breast cancer, but there are some limitations to the evidence.

Although earlier evidence of a possible association between processed meat in the diet and breast cancer risk was inconsistent, recent meta-analyses have reported a positive association between high levels of processed meat consumption and risk of breast cancer. This association is observed for breast cancer overall, and postmenopausal breast cancer, but possibly not premenopausal breast cancer.

Mechanisms

Processed meat is meat that has been salted, cured, fermented, smoked or treated in some other way to improve its flavour or to preserve it. Processed meats are mainly pork or beef – for example, ham, sausages and corned beef – but can include other red meats, poultry, offal or meat by-products.

The International Agency for Research on Cancer (IARC) concluded that processed meat is carcinogenic to humans (Group 1 carcinogen), noting sufficient evidence that consumption of processed meat causes colorectal cancer.1,2

The mechanism by which consumption of processed meat might increase the risk of breast cancer is not known. Processing of meat can produce some carcinogenic chemicals, including N-nitroso-compounds and polycyclic aromatic hydrocarbons.1 Cooking processed meat, especially at high temperatures, can also produce known or suspected carcinogens.1

Evidence 

IARC reviewed 10 cohort and nested case–control studies and 16 case-control studies reporting on an association between consumption of processed meat and breast cancer risk.2 Four of the 10 cohort studies reported a statistically significant positive association with breast cancer risk for the consumption of red and processed meat combined. However, the case–control studies provided inconsistent evidence. IARC concluded that there was insufficient data to evaluate the association separately for premenopausal and postmenopausal breast cancer, or by hormone receptor status.2

The World Cancer Research Fund/American Institute for Cancer Research concluded that there was limited evidence for an association between consumption of processed meat and breast cancer risk, and did not make a formal conclusion.3

A recent meta-analysis of prospective cohort, nested case-control and clinical trial studies showed that high, compared with low, intake of processed meat was associated with overall breast cancer risk (relative risk [RR] 1.05, 95% confidence interval [CI] 1.03‒1.16) and postmenopausal breast cancer risk (RR 1.10, 95% CI 1.03‒1.17), but not with premenopausal breast cancer risk (RR 1.09, 95% CI 0.95‒1.25).4 Another recent meta-analysis of data from the United Kingdom Biobank cohort study, combined with data from 10 previous cohort studies, had similar findings.5

An earlier meta-analysis reported an increased breast cancer risk for the highest category compared with the lowest category of processed meat consumption, and a statistically significant dose-response relationship (RR per 50 g/day increment 1.09, 95% CI 1.02‒1.17).6

A French cohort study reported no association between processed meat consumption and risk of breast cancer.7 However, the level of consumption of processed meat was low in this study, which reduced the ability to detect any association.

Read the full Review of the Evidence

References
  1. Bouvard V, Loomis D, Guyton KZ, et al. (2015). Carcinogenicity of consumption of red and processed meat. Lancet Oncology 16(16):1599–1600.
  2. International Agency for Research on Cancer (2018). Red meat and processed meat, IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, volume 114, IARC Working Group on the Evaluation of Carcinogenic Risk to Humans, Lyon, https://monographs.iarc.fr/wp-content/uploads/2018/06/mono114.pdf.
  3. World Cancer Research Fund/American Institute for Cancer Research (2018). Continuous Update Project Expert Report 2018. Diet, nutrition, physical activity and breast cancer. London, UK.
  4. Farvid MS, Stern MC, Norat T, et al. (2018). Consumption of red and processed meat and breast cancer incidence: a systematic review and meta-analysis of prospective studies. International Journal of Cancer 2018 Sep 5 (Epub ahead of print).
  5. Anderson JJ, Darwis NDM, Mackay DF, et al. (2018) Red and processed meat consumption and breast cancer: UK Biobank cohort study and meta-analysis.  European Journal of Cancer 90:73–82.
  6. Wu J, Zeng R, Huang J, et al. (2016). Dietary protein sources and incidence of breast cancer: a dose–response meta-analysis of prospective studies. Nutrients 8(11):E730.
  7. Diallo A, Deschasaux M, Latino-Martel P, et al.  (2018). Red and processed meat intake and cancer risk: results from the prospective NutriNet-Santé cohort study. International Journal of Cancer 142(2):230–237.

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