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Are Low-Carb & Keto Diets ‘Bad’ for Ovarian Cancer?

There has recently been significant discussion in clinical circles about the appropriateness of the ketogenic diet for the treatment of ovarian cancer. In this article, I summarise the available research on ketogenic diets and ovarian cancer to shed some light on whether it is or isn’t appropriate…

Key Findings:

  • Ovarian cancer cells are known to migrate to the omentum
  • These cells ‘co-opt’ fatty acids for use as fuel from adipocytes
  • Ketogenic diets do not worsen blood lipids in ovarian cancer patients
  • Ketogenic diets reduce total and visceral fat more than standard-care cancer diets
  • When compared to standard-care diet, a keto-diet might reduce cravings for fast food, sugar, and starch
  • Greater intakes of fat do not necessarily result in greater availability of fatty-acid fuels to cancers favouring this fuel-type
  • Dietary interventions should focus on reducing total fuel availability to cancer cells and also on reducing known drivers of cancer growth and proliferation
  • Low-carbohydrate and ketogenic diets that do not result in increased free fatty-acids or excessive serum ketone levels are likely to help reduce total fuel availability to ovarian cancer cells

There has recently been significant discussion in clinical circles about the appropriateness of the ketogenic diet for the treatment of ovarian cancer. There is, as with most cancer forms and their most appropriate dietary treatment, vociferous debate between advocates of low-carbohydrate and ketogenic diets, and those more inclined towards higher-carbohydrate approaches. There is also a lot of complexity due to the very diverse nature of cancers and cancer cells, even within an individual. In this article, I summarise the available research on ketogenic diets and ovarian cancer to shed some light on whether it is or isn’t appropriate…

Tumours of the abdomen, including ovarian cancer, are characterised by widespread and rapid metastases in the peritoneal cavity.1 In particular, they have a clear predilection to metastasis to the omentum (a large ‘apron-like’ fold of peritoneum that hangs down from the stomach). It has been demonstrated that adipocytes (fat cells) of the omentum promote migration and invasion by ovarian cancer cells and that these processes are mediated by inflammatory adipokines including interleukin-8 (IL-8). In addition, in vitro and in vivo analysis has shown that ovarian cancer cells induce lipolysis in adipose tissue and increased β-oxidation in the cancer cells, suggesting that adipocytes are used as a source of fatty-acid-derived energy to fuel cancer growth. It is thought that this occurs due to upregulation of adipocyte Protein 2 (a fatty-acid carrier protein) in omental metastases compared to primary ovarian tumours.2 Ovarian cancer cells co-cultured with primary human omental adipocytes also express high levels of the fatty-acid receptor, CD36, which imports fatty acids into the cell for use.1

These findings taken together, suggest that ovarian cancer cells, when migrated to areas with a relative abundance of adipocytes (like the omentum) can induce adipose tissue to release fatty-acids and that this can be used efficiently as a fuel.

Anatomical illustration from Sobotta’s Human Anatomy (1908) showing the omentum.

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