Excess weight is a well-supported cause of increased cancer risk at at least 13 sites in the body, with the strongest associations for uterine, colon, liver, and post-menopausal breast cancer. The evidence rests on large meta-analyses and is indirectly confirmed by the finding that weight loss substantially reduces risk. People who lose weight thereby likely also reduce their cancer risk, although it is not yet clear whether all methods of weight loss are equivalent.
Overweight and obesity increase the risk of cancer in at least 13 different sites in the body. Worldwide, an estimated nearly 12% of all cancers in men and just over 13% in women are attributable to excess body weight. This is not a suspicion but a conclusion supported by a large and consistent body of research.
The strongest associations have been demonstrated for cancers of the uterus, colon, breast (post-menopause), liver, and pancreas. The extent to which risk increases can be gauged indirectly from research on bariatric surgery: women who underwent such surgery and lost substantial weight had a 62% lower risk of uterine cancer, 44% lower risk of post-menopausal breast cancer, 65% lower risk of liver cancer, 48% lower risk of pancreatic cancer, and 37% lower risk of colon cancer compared with people with obesity who did not have the surgery. That marked reduction in risk following weight loss is one of the reasons researchers consider excess weight itself to be the cause, rather than some other factor.
Overweight has also been linked to cancers of the ovary, gallbladder, oesophagus (a specific type, adenocarcinoma), stomach, kidney, and thyroid, as well as to meningioma and multiple myeloma. The evidence here is somewhat less strong, and for thyroid cancer, kidney cancer, and multiple myeloma, weight loss through surgery did not show a clear protective effect in the studies examined. That does not mean the association is absent, but rather that it is less well understood.
How can excess weight promote cancer? Two biological mechanisms are well supported. First, adipose tissue produces hormones, particularly oestrogens, and promotes a smouldering, low-grade inflammation in the body. That inflammation has been linked to a worse prognosis in breast and tongue cancers. Notably, this adipose tissue inflammation can also occur in people with a normal BMI, which means that body weight alone does not fully explain the risk. Second, obesity impairs the functioning of T-cells, the immune cells that detect and eliminate cancer cells. This allows the immune system to keep tumours in check less effectively. This mechanism, however, has so far been demonstrated mainly in animal models and still needs to be confirmed in humans.
A separate finding from animal research deserves attention, but with appropriate caution: losing weight through dietary restriction restored T-cell function in mice, whereas losing weight through the weight-loss drug semaglutide did not, even though the animals lost an equivalent amount of weight. This suggests that the method of weight loss may matter for the immune system. How this plays out in humans is still unknown and needs to be investigated in clinical studies.
Based on multiple systematic reviews and meta-analyses (PMID 30445141, 37047163, 39279764, 31722374), a mechanistic-pathological review (PMID 27903155), an immunological animal study (PMID 38565540), and an observational cohort study (PMID 39287872). The evidence for uterine, colon, breast, liver, and pancreatic cancers is the strongest. The surgical data are observational, not derived from randomised trials.