New research indicates that fasting, including intermittent fasting and low-calorie diets, could significantly enhance cancer treatments by bolstering the immune system and altering tumor environments. Experts suggest this approach may be on the verge of a major shift in cancer care.
A 2024 study published in the journal Immunity found that fasting strengthens natural killer (NK) cells, a type of immune cell crucial for destroying tumors. In experiments with mice implanted with human colon and melanoma cancer cells, a fasting regimen of 24 hours twice a week led to tumors that were up to 70 percent smaller compared to mice that ate freely. During fasting periods, NK cells adapted to use fatty acids as an energy source instead of glucose, which cancer cells typically consume. This shift optimizes their ability to infiltrate and survive within tumors.
Furthermore, fasting appeared to increase the migration of NK cells to the bone marrow, where they become primed to produce interferon-gamma, a substance that boosts immune response. This effect is believed to be beneficial across various cancer types and could be particularly effective when combined with immunotherapy.
Hormonal and Cellular Changes
Fasting also influences hormone levels that can drive tumor growth. The absence of food intake reduces insulin release from the pancreas. Since many oncogenes, which promote uncontrolled cell growth, are activated by insulin, lowering insulin levels can help inhibit cancer progression. For estrogen-sensitive breast cancers, fasting appears to directly affect cancer cells. Current treatments like tamoxifen aim to block estrogen receptors, but cancer cells can develop resistance. Research in mice with human estrogen-positive breast cancers demonstrated that a 48-hour weekly fast, in conjunction with tamoxifen, increased stress hormones like cortisol. This activated glucocorticoid receptors within tumor cells, triggering genes that inhibit tumor growth while reducing those that promote multiplication. Consequently, tumors shrank, and tamoxifen remained effective.
Studies involving humans on low-calorie diets designed to mimic fasting also showed similar increases in cortisol and activation of tumor-inhibiting genes. These diets also led to lower levels of cancer-promoting hormones such as leptin and insulin-like growth factor-1.
Potential Drug Mimicry and Challenges
While fasting shows promise, its application in clinical settings faces challenges. Maintaining very low-calorie diets can be difficult, and for patients experiencing cachexia (severe weight and muscle loss), fasting could be detrimental. Researchers are exploring drugs that can replicate the effects of fasting. Dexamethasone, a steroid used to manage chemotherapy side effects, has been shown to activate the same glucocorticoid pathways as fasting in mice. Combining dexamethasone with tamoxifen in mice delayed tumor growth without causing the weight loss associated with fasting. Dexamethasone also reduced liver metastases and prolonged survival in certain cancers.
However, dexamethasone's effectiveness may vary by cancer type. In non-hormonal breast cancers like triple-negative and HER2-positive types, activating glucocorticoid receptors could potentially worsen the cancer. This contrasts with hormone-negative cancers where typical chemotherapy doses of dexamethasone do not appear to negatively impact treatment.
Future Directions and Caution
Other strategies under investigation include time-restricted eating, such as extending overnight fasting to at least 13 hours, which has been linked to a reduced risk of cancer recurrence. Additionally, GLP-1 drugs like Mounjaro are being considered for their potential to mimic fasting's effects.
Despite encouraging findings, experts caution that research is still in its early stages. More data from extensive patient trials are needed before fasting-based interventions can be widely adopted. Patients are advised to consult their oncologists and maintain a balanced diet, as some supplements, like high doses of vitamins C and E, may potentially encourage cancer spread in certain contexts.