The Negative Domino Effect: Why We Must Address the Role of Obesity in Cancer Development


Over the past few decades, researchers have discovered a strong association between obesity and the development of 13 types of cancers, namely breast, bowel, womb, oesophageal, pancreatic, renal, hepatic, gastric, gallbladder, ovarian, thyroid, myeloma, and brain cancer. [1] Alarmingly, these include some of the most common and aggressive cancers. Consequently, it should not come as a surprise that excessive weight is thought to account for around 18,000 cancer cases within the United Kingdom annually and is second only to tabacco as being the most preventable cause of cancer worldwide. [2]

Fat (adipose tissue) is crucial for survival. This tissue stores calories from food and beverages as lipids, which are degraded to release energy when carbohydrate levels are low. Moreover, fat sends chemical signals involved in the regulation of growth, metabolism, appetite, immunity, and menstruation. [3] However, excessive fat stores are associated with detrimental impacts on health, including the promotion of tumour development. [4] Specially, high fat levels are linked to chronic inflammation, high estrogen levels, and increased insulin production – three mechanisms that potentially induce cancer growth, survival, and migration:

1. Fat is the main source of oestrogen production following menopause in women; consequently, overweight postmenstrual women generally have higher levels of the circulating hormone than their healthy counterparts, which has been shown to increase breast and womb cancer risk. [5]

2. Insulin is involved in the regulation of metabolism, controlling cellular glucose uptake from blood. Overweight individuals contain high levels of circulating fatty acids, which reduces sensitivity to insulin. Insulin production increases to compensate, altering insulin-related growth factors available to cells. The rise in insulin and changes to growth factors can promote cellular growth and resistance to apoptosis, thereby encouraging cancer development. [6]

3. Macrophage (a type of white blood cell that engulfs harmful substances) numbers within an individual’s adipose tissue significantly rise as one becomes increasingly overweight, potentially to clear dead fat cells. However, these macrophages release chemical signals that attract various inflammatory cells, ultimately inducing a state of chronic inflammation that can aid uncontrolled cellular division and migration that are distinct characteristics of cancer. [7]

Although researchers are beginning to unravel the mystery of how excessive weight may increase cancer risk and are investigating potential treatments targeting these pathways, the picture is still extremely complex. Obesity influences a myriad of physiological processes and affects everyone differently. Our lack of mechanistic understanding highlights the importance of tackling the underlying cause – excessive weight gain – as a preventative cancer strategy. This is increasingly important since more than two thirds of adults in England were classified as overweight or obese in 2015. This prevalence is expected to reach three quarters of adults and cause 670,000 associated cancer cases by 2035 if current trends in weight gain continue. [8]

The public must be made aware of the association between excessive weight and cancer, in order to reduce the number of obesity-related cancer cases. Cancer Research UK recently investigated the level of public awareness regarding this topic, with an unprompted question revealing that only 25% of individuals were informed. Moreover, the lowest socioeconomic grade and men in general were less likely to be aware of this association than the highest socioeconomic grade and women. This is alarming since excessive weight is more prominent in these least informed groups. Finally, very few people who were aware of the association between obesity and cancer were also informed that the association included cancers not pertaining to the digestive tract. [9] Clearly there is a desperate need to improve the current lack of public awareness. Fortunately, there is strong incentive to do so; reducing the prevalence of overweight/obese individuals by 1% below forecast rates is predicted to prevent 64,200 novel cancer cases and save £42 million from NHS cancer care (saving £300 million in NHS and social health care costs) over the next two decades. [8]

The government must be responsible for producing comprehensive and feasible policies that aim to raise public recognition of obesity-related cancers and reduce the prevalence of overweight/obese individuals. It is time to consider increasing taxes on foods containing foods with a high fat/sugar content, subsidising healthier foods, restricting junk food options within public domains such as schools, continue prioritising accessibility to transport that promotes physical activity (pedestrian and bike lanes), and importantly pressuring food and beverage producers to make healthier commodities. Fortunately, the government are beginning to implement changes that should impact the current increase in obesity. For example, the soft drink sugar tax due to commence in early 2018 will see drinks containing over 5g or 8g of sugar per 100ml being taxed 18p and 24p per litre, respectively. [10] Although there is a long way to go, such actions show the government has recognised the negative impact overweight and obesity-related problems are predicted to have on the physical and economic health of the nation.

About the Author:

Jennifer Wood is undertaking an MPhil in Clinical Sciences (Experimental Medicine) at the University of Cambridge, currently investigating a potential novel treatment for Pulmonary Arterial Hypertension within the Department of Clinical Medicine.

References:

[1] Kyrgiou, M., Kalliala, I., Markozannes, G., Gunter, M., Paraskevaidis, E., Gabra, H., Martin-Hirsch, P. and Tsilidis, K. (2017). Adiposity and cancer at major anatomical sites: umbrella review of the literature. BMJ, p.j477.

[2] Parkin, D. & Boyd, L. (2011) 8. Cancers attributable to overweight and obesity in the UK in 2010. British Journal of Cancer. [Online] 105S34-S37. Available from: doi:10.1038/bjc.2011.481.

[3] Coelho, M., Oliveira, T. & Fernandes, R. (2013) State of the art paper Biochemistry of adipose tissue: an endocrine organ. Archives of Medical Science. [Online] 2191-200. Available from: doi:10.5114/aoms.2013.33181.

[4] Nieman, K., Romero, I., Van Houten, B. & Lengyel, E. (2013) Adipose tissue and adipocytes support tumorigenesis and metastasis. Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids. [Online] 1831 (10), 1533-1541. Available from: doi:10.1016/j.bbalip.2013.02.010 [Accessed: 30 March 2017].

[5] Travis, R. & Key, T. (2003) Oestrogen exposure and breast cancer risk. Breast Cancer Research. [Online] 5 (5). Available from: doi:10.1186/bcr628 [Accessed: 30 March 2017].

[6] Djiogue, S., Nwabo Kamdje, A., Vecchio, L. & Kipanyula, M. et al. (2012) Insulin resistance and cancer: the role of insulin and IGFs. Endocrine Related Cancer. [Online] 20 (1), R1-R17. Available from: doi:10.1530/erc-12-0324.

[7] Wagner, M., Samdal Steinskog, E. & Wiig, H. (2014) Adipose tissue macrophages: the inflammatory link between obesity and cancer?. Expert Opinion on Therapeutic Targets. [Online] 19 (4), 527-538. Available from: doi:10.1517/14728222.2014.991311.

[8] Bhimjiyani, A., Knuchel-Takano, A. & Hunt, D. (2017) Tipping the Scales: Why Preventing Obesity Makes Economic Sense. 1st edition. London, Cancer Research UK Policy Research Centre for Cancer Prevention.

[9] Hooper L, Anderson A, Forster A, Rosenberg G & Vohra J (2016) Public knowledge of the link between obesity and cancer. Cancer Research UK.

[10] Soft Drinks Industry Levy - GOV.UK. [Online]. 2017. Gov.uk. Available from: https://www.gov.uk/government/publications/soft-drinks-industry-levy/soft-drinks-industry-levy

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