The Link Between Obesity and Cancer in Women
Dr. Kate Dudek • December 30, 2020 • 5 min read
Global obesity rates are rising at an alarming rate. Across parts of the Middle East, obesity prevalence rates are as high as 40% and, with poor dietary habits and insufficient physical activity across the region, these rates are unlikely to decline any time soon. Obesity is associated with a myriad of health problems, including type 2 diabetes mellitus (T2DM), high blood pressure, cardiovascular disease, stroke, premature death and cancer.
Obesity has been linked to an increased incidence of various cancers, including:
- Meningioma
- Thyroid
- Oesophageal
- Breast
- Multiple Myeloma
- Liver
- Kidney
- Gall bladder
- Stomach
- Endometrium
- Ovary
- Pancreas
- Colorectal
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In fact, a large scale, population-based study revealed that in 2012, approximately 3.6% of all adulthood cancers could be attributed to obesity. This made obesity the second leading risk factor for cancer after smoking. Cancer mortality increases with a higher BMI and those who are obese are between 40% and 80% more likely to die from cancer.
This article aims to explore the link between obesity and female gynaecological cancers in more detail. However, as demonstrated by the list above, the problem is far more extensive than this; having a high BMI will increase your risk of developing many different types of cancer. Therefore, if you are overweight or obese, it is imperative that you make reducing your BMI a priority.
Gynaecological Cancers
- Endometrial, or womb cancer is a type of cancer that develops in the cells lining the uterus. A link between obesity and endometrial cancer was first identified in the 1960s and it is now thought that women who are obese or overweight are 2 – 4 times more likely to develop this type of cancer. In those who are extremely overweight, the risk can be as high as 7-fold higher.
- Ovarian cancer. A 5 unit increase in BMI is associated with a 10% increased risk of ovarian cancer.
- Breast cancer. A 5 unit increase in BMI is associated with a 12% increased risk of breast cancer in postmenopausal women. Those who are obese are considered to have a 20 – 40% increased risk of developing breast cancer. They will also have a worse prognosis at diagnosis and increased chance of metastatic disease.
Why does obesity increase your risk of developing cancer?
Two of the main factors that are thought to link obesity to gynaecological cancer are hormonal changes and inflammation.
Oestrogens are synthesised from androgens by the enzyme aromatase. In healthy, premenopausal women most of this conversion occurs in the ovaries and the oestrogen that is produced regulates the menstrual cycle. After the menopause, the ovaries no longer synthesise oestrogen; however, production of this hormone continues at distal sites, including within adipose (fat) tissue. In fact, one of the major sites of oestrogen synthesis in the postmenopausal female is the adipose tissue, which has high levels of aromatase. Obese females have more adipose tissue, resulting in an increase in unopposed circulating oestrogens. This can have beneficial effects with regards to maintaining bone strength (reducing the risk of osteoporosis), but it also increases the risk of endometrial hyperplasia (a precursor of endometrial cancer) and oestrogen-dependent breast cancer.
Obesity is considered to be a state of chronic, low-grade inflammation. This proinflammatory state is thought to trigger DNA damage and promote an oncogenic environment for the proliferation of cancer cells. Specifically, inflammation promotes tumour initiation and progression. Adipose tissue also produces adipokines, which can exert proliferative effects on tumour cells, as well as targeting other cell growth regulators. The net effect being an environment that, given the right conditions, can contribute to tumour development.
With regards to breast cancer, recent studies have attempted to probe the microenvironment of breast adipose tissue in more detail. It was found that obesity leads to mechanical niches in adipose tissue, which promotes carcinogenesis. Altered tissue structure can increase the malignant capabilities of mammary cells, providing one possible explanation for why obese breast cancer patients tend to have a significantly worse prognosis.
Type 2 diabetes, obesity and cancer
There is a strong association between obesity, T2DM and cancer and it is likely that multiple metabolic abnormalities contribute to the increased risk of cancer in those with T2DM.
Hyperinsulinaemia is a symptom of T2DM, characterised by an excess of circulating insulin. It is not unique to patients with T2DM, but is strongly associated with the condition. With increasing BMI, there is a linear increase in the levels of circulating insulin. This means that the body’s tissues become resistant to insulin and the body compensates by producing more. High levels of insulin have been shown to promote the development of certain cancers, including endometrial cancers. There is also a strong positive relationship between insulin resistance and postmenopausal breast cancer, potentially due to insulin having a direct effect on the levels of sex hormones, including oestrogen. Insulin receptors are also highly expressed in tumours of the breast.
Postmenopausal women with T2DM have a 17% increased risk of developing breast cancer. Furthermore, it has been shown that Metformin treatment, used regularly in the management of T2DM, exerts a protective effect, reducing the risk of breast cancer in postmenopausal women with diabetes. Additional studies have shown that mortality rates for both breast cancer and endometrial cancer are higher in those women with concurrent T2DM.
It is important to note that women with type 1 diabetes do not demonstrate the same increased risk of developing cancer.
Final comments
The relationship between obesity and cancer is a complex one and the exact nature of the physiological events that link the two, remains to be fully elucidated. As has been alluded to in this article, it likely involves the interplay of various factors, including hormones, growth factors, inflammation and structural tissue changes. Insulin resistance seems to play a pivotal role in the etiology of obesity-associated cancer.
Whilst there is evidence that those who gained less weight during adulthood have a lower risk of developing breast, endometrial and ovarian cancer (as well as colon and kidney cancer); there is little evidence that intentional weight loss improves recurrence rates or prognosis for those who have already been diagnosed with cancer.
Another topic that requires further attention is whether being obese can affect the efficacy of the most widely used cancer treatments. It is known that obese patients have a less diverse gut microbiome, which may contribute to increased inflammation. However, preliminary studies in mice also suggest that changes in the microbiome might affect the immune response to treatment. This is a theory that requires validation using human subjects, but provides one explanation for why patients respond differently to treatment.
Nabta is reshaping women’s healthcare. We support women with their personal health journeys, from everyday wellbeing to the uniquely female experiences of fertility, pregnancy, and menopause.
Get in touch if you have any questions about this article or any aspect of women’s health. We’re here for you.
Sources:
- Arendt, Lisa M., and Charlotte Kuperwasser. “Working Stiff: How Obesity Boosts Cancer Risk.” Science Translational Medicine, vol. 7, no. 301, 19 Aug. 2015, doi:10.1126/scitranslmed.aac9446.
- Arnold, Melina, et al. “Global Burden of Cancer Attributable to High Body-Mass Index in 2012: a Population-Based Study.” The Lancet Oncology, vol. 16, no. 1, Jan. 2015, pp. 36–46., doi:10.1016/s1470-2045(14)71123-4.
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- Gallagher, Emily Jane, and Derek Leroith. “Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality.” Physiological Reviews, vol. 95, no. 3, July 2015, pp. 727–748., doi:10.1152/physrev.00030.2014.
- Ligibel, Jennifer A., and Howard D. Strickler. “Obesity and Its Impact on Breast Cancer: Tumor Incidence, Recurrence, Survival, and Possible Interventions.” American Society of Clinical Oncology Educational Book, vol. 33, 2013, pp. 52–59., doi:10.1200/edbook_am.2013.33.52.
- “Obesity and Cancer Fact Sheet.” National Cancer Institute, https://www.cancer.gov/about-cancer/causes-prevention/risk/obesity/obesity-fact-sheet#r48.
- Seo, Bo Ri, et al. “Obesity-Dependent Changes in Interstitial ECM Mechanics Promote Breast Tumorigenesis.” Science Translational Medicine, vol. 7, no. 301, 19 Aug. 2015, doi:10.1126/scitranslmed.3010467.
- Sivan, A., et al. “Commensal Bifidobacterium Promotes Antitumor Immunity and Facilitates Anti-PD-L1 Efficacy.” Science, vol. 350, no. 6264, 27 Nov. 2015, pp. 1084–1089., doi:10.1126/science.aac4255.
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International Journal of Environmental Research and Public Health ([MDPI](https://www.mdpi.com/journal/ijerph)), 20(5), 3021.
Will Taking the Pill Increase my Risk of Developing Cancer?
Will taking contraceptive pill increase developing cancer risk, It is estimated that as many as 140 million women worldwide take the [oral contraceptive pill](https://nabtahealth.com/the-oral-contraceptive-pill/). It is a simple, effective way for a female to control her own fertility and has also been utilised as a treatment for heavy periods, [acne](https://nabtahealth.com/why-do-i-get-acne-breakouts-before-my-period/) and [](https://nabtahealth.com/what-medications-are-recommended-for-endometriosis/)[endometriosis](https://nabtahealth.com/glossary/endometriosis/). However, safety concerns over its usage persist, and one of the major issues is a suspected link between the pill and cancer. So, what does the science say? Does taking the pill increase your risk of developing cancer, or can it actually serve a protective role? **The pill as an anti-cancer agent** ------------------------------------ **The pill reduces the risk of ovarian, endometrial and colorectal cancer.** * **Ovarian cancer**. Ever-users of the pill are significantly less likely to develop [ovarian cancer](https://nabtahealth.com/the-diversity-of-ovarian-cancer/) than never-users. In fact, studies have suggested that for every 5 years of pill use there is a 20% reduction in ovarian cancer risk. Furthermore, these protective effects are maintained for at least 30 years after discontinuation of pill use. * **Endometrial cancer**. The pill exerts a substantial protective effect against the development of [endometrial cancer](https://nabtahealth.com/a-guide-to-endometrial-cancer/). The risk is thought to be reduced by between 30 and 50%, depending on the duration of use. Protection lasts for at least 20 years after cessation of treatment. * **Colorectal cancer**. Ever-users of the pill are approximately 15% less likely to develop colorectal cancer than those that have never taken it. Whether increased duration of use has a beneficial effect is difficult to know as the quality of data from these studies is poor. **The pill’s carcinogenic effects** ----------------------------------- Oral contraceptive use is a risk factor for breast and cervical cancer. * **Breast cancer**. The association between breast cancer and the oral contraceptive pill is small, but significant. Studies suggest that those women who are currently on the pill are 20% to 24% more likely to receive a breast cancer diagnosis. The increased risk is lost once the pill is discontinued and, after ten years, prior pill users are at no greater risk than never users of getting breast cancer. The risk also falls significantly once a woman goes through the [menopause](https://nabtahealth.com/glossary/menopause/). Pill use is associated with clinically challenging types of breast cancer, including the [triple negative form](https://nabtahealth.com/breast-cancer-staging/), which usually has a worse prognosis and higher mortality rate. The exact mechanisms linking the two are unclear, although many breast cancers have a hormonal component. It is thought that increased lifetime exposure to oestrogens increases the risk of breast cancer, primarily because the hormone promotes or initiates tumour growth. Studies have failed to find an elevated risk of breast cancer in pill users with a family history of the disease. However, the data may be skewed by the fact that these women are less likely to use the pill due to their already increased susceptibility. The established link between [oestrogen](https://nabtahealth.com/glossary/oestrogen/) and breast cancer may [lead](https://nabtahealth.com/glossary/lead/) you to wonder whether using the progestin-only ‘mini pill’ would be a safer option. There have been very few studies on this form of contraception, probably because it is not as widely used as the combined pill (which contains [oestrogen](https://nabtahealth.com/glossary/oestrogen/) and progestin). The work that has been performed has suggested that women who take the mini pill still have a higher risk of breast cancer than those who have never used oral contraceptives, perhaps by as much as 21%. The link between progestins and breast cancer is poorly understood and likely to be complex. However, it is validated by studies on postmenopausal women who take hormone replacement therapy. Those on combined [oestrogen](https://nabtahealth.com/glossary/oestrogen/) plus progestin therapy have a higher breast cancer risk than those who take just [oestrogen](https://nabtahealth.com/glossary/oestrogen/). Thus, the mini pill should no longer be considered a safer contraceptive option for those with an elevated risk of developing breast cancer. * **Cervical cancer**. Taking the pill for five or more years is associated with a significantly increased risk of developing cervical cancer. The duration of use increases the risk, so that women who take the pill for 5 years have a 10% increased risk, but those who take it for longer, are more than 60% more likely to be diagnosed. Ten years after stopping the pill there is no increased risk of developing cervical cancer. One important thing to note is that as a risk, oral contraceptives will always be cofactors that interact with high risk [human papillomavirus](https://nabtahealth.com/when-should-i-get-a-pap-smear/) ([HPV](https://nabtahealth.com/glossary/hpv/)) strains to induce cervical carcinogenesis. This means that oral contraceptives in isolation are not a risk factor in women who are [HPV](https://nabtahealth.com/glossary/hpv/) negative; however, for those who are [HPV](https://nabtahealth.com/glossary/hpv/) positive, the pill can exacerbate the risk. Steroid hormone receptors (mainly [progesterone](https://nabtahealth.com/glossary/progesterone/)) are found in cervical tissue and are thought to enhance the expression of high risk [HPV](https://nabtahealth.com/glossary/hpv/), contributing to cancerous changes in the [cervix](https://nabtahealth.com/glossary/cervix/). **Conclusion: the pill and cancer** ----------------------------------- It is very difficult to state conclusively whether the pill should be used or avoided based on its associations with cancer. The net effect is likely to be positive, with one long-term, UK-based study finding that taking the pill resulted in a 12% reduction in overall cancer risk. It is also challenging to assess the absolute risk posed by oral contraceptive use. Cancer can have a long latency period, meaning the time between exposure to a particular risk factor and cancer diagnosis can span many years. Most women who develop cancer will have been exposed to multiple risk factors during their lifetimes, including [parity](https://nabtahealth.com/is-pregnancy-linked-to-developing-cervical-cancer/) (the number of times she has been pregnant and carried the baby to term), [obesity](https://nabtahealth.com/the-link-between-obesity-and-cancer-in-women/) and whether or not she has breastfed (breastfeeding can exert [protective effects](https://nabtahealth.com/benefits-of-breastfeeding-for-the-mother/)). Ascertaining how much of a role each of these factors plays in a later cancer diagnosis is likely to be extremely difficult. One final thing to consider is that the pill has changed in formulation over the decades since it was first utilised as a type of contraception. The specific synthetic hormones in use have changed, as has their concentration. Today, a triphasic pill is commonly used, whereby the hormone concentration changes across the month. This is designed to more closely mimic the normal ovulatory cycle. These different formulations will have differing risks and benefits. The consequence of this is that women who were prescribed the pill in its infancy, in the 1950s and 1960s should certainly not be compared to those taking it today in the 21st Century. Perhaps the advent of the mini pill came with initial optimism that the risks associated with the combined pill would be alleviated by removing the [oestrogen](https://nabtahealth.com/glossary/oestrogen/) component. Unfortunately, it appears that women taking this form of contraceptive have a comparable cancer risk to those taking the more commonly prescribed combined oral contraceptive pill. Nabta is reshaping women’s healthcare. We support women with their personal health journeys, from everyday wellbeing to the uniquely female experiences of fertility, pregnancy, and [menopause](https://nabtahealth.com/glossary/menopause/). Get in [touch](/cdn-cgi/l/email-protection#5f263e33333e1f313e3d2b3e373a3e332b37713c3032) if you have any questions about this article or any aspect of women’s health. We’re here for you. **Sources:** * Brynhildsen, Jan. “Combined Hormonal Contraceptives: Prescribing Patterns, Compliance, and Benefits versus Risks.” Therapeutic Advances in Drug Safety, vol. 5, no. 5, Oct. 2014, pp. 201–213., doi:10.1177/2042098614548857. * “Does the Contraceptive Pill Increase Cancer Risk?” Cancer Research UK, 4 Mar. 2019, [https://www.cancerresearchuk.org/about-cancer/causes-of-cancer/hormones-and-cancer/does-the-contraceptive-pill-increase-cancer-risk](https://www.cancerresearchuk.org/about-cancer/causes-of-cancer/hormones-and-cancer/does-the-contraceptive-pill-increase-cancer-risk). * Gierisch, J. M., et al. “Oral Contraceptive Use and Risk of Breast, Cervical, Colorectal, and Endometrial Cancers: A Systematic Review.” Cancer Epidemiology Biomarkers & Prevention, vol. 22, no. 11, Nov. 2013, pp. 1931–1943., doi:10.1158/1055-9965.epi-13-0298. * Knowlden, Hilary A. “The Pill and Cancer: a Review of the Literature. A Case of Swings and Roundabouts?” Journal of Advanced Nursing, vol. 15, no. 9, Sept. 1990, pp. 1016–1020., doi:10.1111/j.1365-2648.1990.tb01981.x. * Li, Li, et al. “Association between Oral Contraceptive Use as a Risk Factor and Triple-Negative Breast Cancer: A Systematic Review and Meta-Analysis.” Molecular and Clinical Oncology, vol. 7, no. 1, 12 May 2017, pp. 76–80., doi:10.3892/mco.2017.1259. * Murphy, Neil, et al. “Reproductive and Menstrual Factors and Colorectal Cancer Incidence in the Women’s Health Initiative Observational Study.” British Journal of Cancer, vol. 116, no. 1, 29 Nov. 2016, pp. 117–125., doi:10.1038/bjc.2016.345. * Mørch, L S, et al. “Contemporary Hormonal Contraception and the Risk of Breast Cancer.” New England Journal of Medicine, vol. 377, no. 23, 7 Dec. 2017, pp. 2228–2239., doi:10.1056/NEJMoa1700732. * “Oral Contraceptives (Birth Control Pills) and Cancer Risk.” National Cancer Institute, [https://www.cancer.gov/about-cancer/causes-prevention/risk/hormones/oral-contraceptives-fact-sheet](https://www.cancer.gov/about-cancer/causes-prevention/risk/hormones/oral-contraceptives-fact-sheet). * Roura, Esther, et al. “The Influence of Hormonal Factors on the Risk of Developing Cervical Cancer and Pre-Cancer: Results from the EPIC Cohort.” Plos One, vol. 11, no. 1, 25 Jan. 2016, doi:10.1371/journal.pone.0147029. * Schairer, Catherine. “Menopausal Estrogen and Estrogen-Progestin Replacement Therapy and Breast Cancer Risk.” Jama, vol. 283, no. 4, 26 Jan. 2000, pp. 485–491., doi:10.1001/jama.283.4.485. * Smith, Jennifer S, et al. “Cervical Cancer and Use of Hormonal Contraceptives: a Systematic Review.” The Lancet, vol. 361, no. 9364, 5 Apr. 2003, pp. 1159–1167., doi:10.1016/s0140-6736(03)12949-2. * Soroush, Ali, et al. “The Role of Oral Contraceptive Pills on Increased Risk of Breast Cancer in Iranian Populations: A Meta-Analysis.” Journal of Cancer Prevention, vol. 21, no. 4, 30 Dec. 2016, pp. 294–301., doi:10.15430/jcp.2016.21.4.294.
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It is generally safe to undergo anaesthesia whilst pregnant, but in order to limit the time you are under general anaesthetic, your doctor will probably recommend postponing reconstructive surgery until after delivery. [Radiotherapy](https://nabtahealth.com/glossary/radiotherapy/) is not recommended during pregnancy and wherever possible your doctor will attempt to delay this type of treatment until after delivery. This is because it increases the risk of [foetal malformations](https://nabtahealth.com/glossary/foetal-malformations/) and can delay [neurocognitive](https://nabtahealth.com/glossary/neurocognitive/) development. If breast preservation is desired, the disease is not advanced and diagnosis has occurred towards the end of pregnancy, it may be possible to treat with immediate lumpectomy and [radiotherapy](https://nabtahealth.com/glossary/radiotherapy/) after delivery. It has been shown that a six week window between lumpectomy and commencement of [radiotherapy](https://nabtahealth.com/glossary/radiotherapy/) does not have a detrimental effect on outcome. [Chemotherapy](https://nabtahealth.com/glossary/chemotherapy/) should not be given during the first [14 weeks of pregnancy](https://nabtahealth.com/articles/week-by-week-pregnancy-weeks-14-26/). It can cause severe [teratogenicity](https://nabtahealth.com/glossary/teratogenicity/) during organ development, which primarily occurs in the first trimester. In the second and third trimester, [chemotherapy](https://nabtahealth.com/glossary/chemotherapy/) can be administered. There have been no reports of later ill effects in children born to mothers who had [chemotherapy](https://nabtahealth.com/glossary/chemotherapy/) at this stage of their pregnancy. Most doctors will recommend stopping [chemotherapy](https://nabtahealth.com/glossary/chemotherapy/) at about week 36 to reduce the risk of infection or bleeding during delivery. Hormone therapy is not recommended for women who are pregnant or breastfeeding. Whilst, there are treatment options for women with PABC, additional work is required to establish a more effective treatment approach for these women. Certainly, as women postpone having children, the rates of PABC are likely to increase over the next few years. **Prognosis** ------------- The prognosis for women with PABC is generally lower than for women with breast cancer who are not pregnant. This is likely due to: * Less aggressive therapy being used due to concerns over the effect of harsher regimens on the developing baby. * Later stage of diagnosis because of difficulty in distinguishing physiologically-relevant changes from normal pregnancy-related changes. * The pregnancy having a direct effect on outcome, although knowledge regarding the exact mechanisms relating to this is currently lacking. * An increased percentage of [oestrogen](https://nabtahealth.com/glossary/oestrogen/) receptor negative cases. This is known to be associated with an increased risk of metastatic disease, which has a poorer prognosis. In terms of the developing foetus, women with PABC should be reassured that there are no reports of breast cancer spreading from the mother to the baby during pregnancy. In rare cases cancer cells will be found in the [placenta](https://nabtahealth.com/glossary/placenta/), so the doctor will always check this immediately after delivery. During pregnancy, a woman should remain under observation by a multidisciplinary team of healthcare professionals, including gynaecologists and oncologists to ensure that the support she receives is optimal for both her and her baby. Growth scans will be performed regularly to ensure that the baby is developing as he or she should be. If possible, the medical team will try to ensure that the woman delivers her baby as close to her due delivery date as possible. After delivery, treatment options will be reassessed. Get yourself the [post-surgery pack](https://nabtahealth.com/product/post-surgery-selfcare-pack-copy/) Nabta is reshaping women’s healthcare. We support women with their personal health journeys, from everyday wellbeing to the uniquely female experiences of fertility, pregnancy, and [menopause](https://nabtahealth.com/glossary/menopause/). Get in [touch](/cdn-cgi/l/email-protection#99e0f8f5f5f8d9f7f8fbedf8f1fcf8f5edf1b7faf6f4) if you have any questions about this article or any aspect of women’s health. We’re here for you. **Sources:** * “Breast Cancer.” Breast Cancer during Pregnancy | Cancer Research UK, 21 Nov. 2017, [https://www.cancerresearchuk.org/about-cancer/breast-cancer/living-with/breast-cancer-during-pregnancy](https://www.cancerresearchuk.org/about-cancer/breast-cancer/living-with/breast-cancer-during-pregnancy). * “Breast Cancer, Pregnancy and (Green-Top Guideline No. 12).” Royal College of Obstetricians & Gynaecologists, [https://www.rcog.org.uk/en/guidelines-research-services/guidelines/gtg12/](https://www.rcog.org.uk/en/guidelines-research-services/guidelines/gtg12/). * Johansson, A L V, et al. “Diagnostic Pathways and Management in Women with Pregnancy-Associated Breast Cancer (PABC): No Evidence of Treatment Delays Following a First Healthcare Contact.” Breast Cancer Research and Treatment, vol. 174, no. 2, Apr. 2019, pp. 489–503., doi:10.1007/s10549-018-05083-x. * Keyser, E A, et al. “Pregnancy-Associated Breast Cancer.” Reviews in Obstetrics & Gynecology, vol. 5, no. 2, 2012, pp. 94–99.