A.R. Shipman; G.W.M. Millington


The British Journal of Dermatology. 2011;165(4):743-750. 

In This Article

Obesity and Skin Cancer

Obesity is associated with a number of noncutaneous cancers.[95,96] One Canadian study has found an association with nonmelanoma skin cancers (NMSCs),[97] whereas another Australian study found no association with basal cell carcinoma.[98] Various epidemiological studies have found a link between excess adiposity and malignant melanoma (MM).[9,99–103] However, others have found no significant association with MM.[104] It may be that obesity is a more relevant risk factor for skin cancer in areas of lower ultraviolet radiation (UVR) exposure,[97] but this needs further evaluation.

There is some clinical genetic evidence of a link between obesity and phototype I skin with red hair, which are features of the rare syndrome associated with a homozygous mutation in the proopiomelanocortin (POMC) gene.[105] Linkage between POMC and other traits suggests that it forms part of a common genetic obesity predisposition.[106,107] Also, experimental evidence shows that POMC neurones in the brain are the target of circulating leptin (thus inhibiting feeding), suggesting that the two are linked crucially in body weight homeostasis.[27] Heterozygous mutations in POMC are characterized by obesity in the absence of red hair.[108] Similarly, homozygous and heterozygous mutations in MC1R (the gene for the cutaneous receptor for the POMC gene products) are commonly associated with phototype I skin, red hair and an increased risk of both NMSC and MM.[105]MC1R heterozygous mutations in the absence of red hair are even commoner than in those expressing a red hair phenotype and they still give an increased risk of both NMSC and MM over MC1R wild-type genotypes.[105] What is not known is whether POMC heterozygosity (associated with obesity without red hair) is associated with increased skin cancer risk. A recent genetic epidemiology study identified a POMC single nucleotide polymorphism in caucasians which was not found to correlate with an increased risk of either NMSC or MM,[109] but this may not be a relevant mutation with respect to alteration of the function of the POMC protein with regard to skin cancer risk.

Other evidence from animal experiments suggests that alteration in the leptin pathway, leading to obesity, correlates with an aberrant cytokine response to UVR.[110] It is quite possible that an alteration in the expression of adipocytokines associated with obesity, compounded by the effects of UVR, could contribute to cutaneous carcinogenesis.[110] This model might fit more with the observation linking obesity with cancer in general.


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