Of relevance to this topic from
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Mitigating Chemotherapy Side Effects with Intermittent Fasting
Fasting induces an array of biochemical and physiological changes that may delay aging and the onset of chronic degenerative diseases, including cancer (Lee 2011; Brandhorst 2015; Stipp 2015; Safdie 2012). Some forms of fasting or caloric restriction may also protect animals and cancer patients from some chemotherapy side effects and sensitize cancer cells to the effects of chemotherapy (Lee 2011; Brandhorst 2013; Horne 2014; Stipp 2015; Safdie 2012). Interestingly, preliminary reports suggest that fasting for several days followed by normal food consumption may protect patients against chemotherapy toxicity without causing long-term weight loss (Lee 2011).
In a randomized early-stage trial, a 48-hour fast reduced chemotherapy immunotoxicity in women with breast cancer. Thirteen women with HER2-negative stage II or III breast cancer participated in the study. Seven women fasted for 24 hours before and after receiving neo-adjuvant chemotherapy, while the remaining women ate normally. The women received a chemotherapy regimen that included docetaxel, doxorubicin, and cyclophosphamide. Laboratory studies of subjects’ blood 30 minutes after chemotherapy revealed significantly less DNA damage in lymphocytes and monocytes in blood samples from the fasting women compared with those from the women who ate normally. This protective effect was still detectable seven days after chemotherapy treatment (de Groot 2015).
There are several potential mechanisms by which fasting may interfere with tumor progression and protect healthy cells against chemotherapy toxicity, but reductions in levels of glucose and insulin-like growth factor-1 (IGF-1) are often cited as important mediators of these benefits (Lee 2010; Hine 2014; Safdie 2009; Cheng 2014; Brandhorst 2013). In a chemotherapy toxicity study, one group of mice underwent a 48-hour fast, while another group underwent a 48-hour fast but also received injections of IGF-1. Both groups received injections of the cytotoxic agent doxorubicin. In the fasting-only group, the survival rate after injection of doxorubicin was 100%; in the group who fasted and received IGF-1 injections, the survival rate was only 38% (Lee 2010).
Fasting triggers healthy cells to switch into a “protected mode” that confers resistance to toxins, including chemotherapy. In cancer cells, pro-cancer genes called oncogenes prevent this switch. In other words, under fasting conditions, healthy cells are protected against toxicity from chemotherapy but cancer cells are not. This phenomenon has been called differential stress resistance (Raffaghello 2010).
In a report on 10 cases, subjects with various types of cancer voluntarily fasted for 48–140 hours before receiving chemotherapy and/or 5–56 hours after chemotherapy. Six of the patients underwent chemotherapy in both a fed and a fasted state at different times; they reported reduced fatigue, weakness, and gastrointestinal side effects while fasting. The other four subjects underwent all of their chemotherapy treatments while fasting; the severity of most side effects was reported to be low relative to typical experience. In cases in which cancer progression could be assessed, fasting did not reduce the efficacy of chemotherapy (Safdie 2009).
Abundant preclinical evidence indicates fasting itself may retard cancer growth. A series of studies in cancer cell lines showed cycles of fasting were as effective as chemotherapy in delaying the progression of various tumors. Moreover, fasting increased the ability of chemotherapy to kill several types of cancer cells. The researchers who conducted this investigation concluded “These studies suggest that multiple cycles of fasting promote differential stress sensitization in a wide range of tumors and could potentially replace or augment the efficacy of certain chemotherapy drugs in the treatment of various cancers” (Lee, Raffaghello 2012).