The Diet that Nobody Needs
Cachexia (pronounced ka-kek-sia)
is involuntary weight loss that occurs in cancer patients even with
apparently adequate nutritional intake. Its symptoms
may include anorexia, debility, and malnutrition, or they may consist
solely of weight loss. The quantity of weight lost has
no correlation with size, location, or type of tumor.
A diminutive tumor can substantially affect the weight of the host;
tumor release of mainly undetected soluble factors is thought to
be responsible for this startling potency.
Almost one-half of hospitalized adult cancer patients have lost at least 10 percent of their body weight. One-quarter of these patients have lost 20 percent or more. Virtually all patients with disseminated (scattered and abundant) metastasis show evidence of cachexia.
Cachexia varies in severity; there is metabolic dysfunction even when cachexia does not strip the weight. The direct cause of lost weight is often difficult to determine, and can be complicated by factors such as tumor location and therapeutic measures taken. Loss of appetite may also be an indirect effect of depression. But cancer itself may secrete contributing factors. Tumors implanted in animals and causing anorexia sometime resolve when the tumor is removed. Survival of some with certain forms of cancer can be more accurately predicted from the severity of the cancer cachexia than from the type of therapy received, as cachexia and anorexia mean that prognosis is poor. Carbohydrate Metabolism Changes with Cancer
Ordinarily, you eat carbohydrates to produce energy. But when a body has cancer, carbohydrates may actually drain that body of energy to feed the tumor.
A person showing signs of cachexia may feel better, and avoid nourishing the tumor, if he or she avoids foods and liquids containing simple carbohydrates, such as sugar, honey, and milk products.
Cachexia is often accompanied by anorexia, malabsorption, energy expenditure, and humoral factors. In less than a majority but nevertheless a significant number of patients, taste is affected, and is reported to pertain most often to sweet flavors, followed by salt and sour.(8) Some develop an aversion to meat. Certain food aversions are attributable to an association being formed between that food and the nauseating therapy, and can to some extent be combated with the introduction of novel foods when nausea is absent. Protein Metabolism in Cancer
In cancer cachexia, both patient and tumor have the same protein requirements, but cancer cells generally have a higher growth rate, and therefore demand--and obtain--more protein. This may cause the breakdown of protein for patient and tumor to exceed the amount that comes into the body. When that happens, the cancer causes the body to begin breaking down its own muscle tissue to meet its protein requirements. Insufficient protein supply can affect immune response, gastrointestinal function, and healing.
High-quality protein contains the amino acids from which the body reconstructs its own protein.
So that cancer patients get enough protein to meet increased bodily needs, they may benefit from increasing the amount of protein they eat.
Appetite and food intake is heavily influenced by the hypothalamus, a tiny but critical structure at the base of the brain; in turn, the hypothalamus is affected by substances borne in the blood.(3,5) These humoral or blood-borne factors, including hormones, peptides, and amino acids, are often afflicted in advanced stages of cancer. Peptide and hormone levels affected by tumor cells are likely to influence feeding.
Glucagon, for example, suppresses appetite and has been modestly elevated in cachectic patients.
Levels of the transmitter serotonin in the brain relate inversely to appetite—more serotonin means less hunger.
Tryptophan, the precursor to serotonin, is elevated in brains of anorectic cancer patients and not in food-deprived and tumor-free animals, further aligning serotonin with appetite loss; yet serotonin antagonists do not dispel the anorexia.
Insulin increases feeding and weight gain in cancer-free animals and has thus been enlisted to combat anorexia. But cachectic patients do not respond normally to insulin; their tissues lose sensitivity to it. When insulin does increase feeding in tumor-bearing animals, it does not seem to prolong survival. Even forced feeding seems incapable of prolonging survival.
Lipid Metabolism in Cancer
Most of the weight loss in humans and animals with cancer comes from loss of fat. Even this has a drawback. The dissolved fat puts undesirable substances such as cholesterol into the bloodstream.
The food that is ingested by cancer patients may not be adequately absorbed.
Intestinal malabsorption is sometimes, but not always, attributable to such direct influences as fistula, surgery, or therapy. The reason for malabsorption in patients with no obvious reason for it is relatively unexplored. Longstanding cancer can increase metabolic rate, thus contributing to energy expenditure and weight loss in the patient, but this finding is not consistent.
Because the quantity of tumor tissue in hypermetabolic patients is insufficient to account entirely for the amount of weight these patients lose, other hypotheses, such as cancer-induced futile biochemical cycles, have been proposed. Anaerobic glucose metabolism and increased protein synthesis, discussed more completely elsewhere, account for part of the energy lost. There is evidence that tumor cells secrete factors, and cause its host to secrete factors, that induce such effects as angiogenesis and proteolysis. Other factors released may simply diminish the desire for food.
The best treatment for cancer cachexia is removal of the malignancy. When that cannot be accomplished, at least the devastation of cachexia can be contested.