Cachexia is the silent killer. It is usually cachexia that kills you, not the cancer. The body is literally eating itself. The top killer for cancer / AIDS patients is organ failure.
When cachexia exists, your body is essentially cannibalizing itself. Because you are not getting enough nutrition, and the cells are being deprived of what they need to function, your body starts using healthy tissue to feed the cells. This causes the loss of lean muscle mass, and the longer the condition lasts, the more your body will use healthy tissue to feed on. Your metabolic rate will actually increase significantly, speeding this terrible process.
People who have cancer do not do well with surgery to remove cancerous tumors. It is important to note that when cachexia is present, the cancer patient’s chances of surviving the cancer are greatly diminished, which is why it has to be treated as soon as possible.
Cachexia
Cachexia describes a syndrome of progressive weight loss, anorexia, and persistent erosion of host body cell mass in response to a malignant growth. Although often associated with preterminal patients with disseminated disease, it may also be present in the early stages of tumour growth before any signs or symptoms of malignancy.
It is present in approximately 50% of cancer patients during treatment, and nearly 100% of treated cancer patients at death.1 It accounts for at least 20% of deaths in neoplastic patients.
Cachexia impairs quality of life and response to therapy, increasing morbidity and mortality of cancer patients.
Mediators of anorexia and associated abnormalities are unknown. Cachectin/TNF or other host-derived cytokines (produced as a defense against malignancy) have been implicated as signal molecules in cachexia, based upon similar metabolic derangements produced by these cytokines in other chronic wasting illnesses.
Raised resting energy expenditure is typical of cachexia, but not starvation. However, this is not the cause of weight loss because it is compensated for by a reduction in energy used for voluntary activity, which further adds to loss of skeletal muscle from immobility.
Nutritional support is effective in maintaining body weight of cachectic cancer patients, but ineffective in maintaining lean body mass. Cachexia has repeatedly been associated with adverse clinical outcomes.
The patient is likely frustrated with their own fraility, the family is upset at the poor nutritional state of their loved one, but the healthcare provider should be the most concerned. This clinical presentation without a prior diagnosis is worrisome, and if the patient does have an underlying etiology, this likely represents progression.
Caring for the cachectic patient presents a frustrating and recurring dilemma. Cachexia is defined as ongoing weight loss, often with muscle wasting, associated with a long-standing disease. In cachexia, refeeding often does not induce weight gain. Anorexia, excluding the willful avoidance of eating, usually occurs in conjunction with cachexia (1).
Pathophysiology
The causes of cachexia and anorexia are only now beginning to be elucidated. Research has shown the important role of cytokines causing metabolic abnormalities in chronic illnesses, such as cancer, chronic obstructive pulmonary disease (COPD), HIV-associated wasting syndrome, cardiac disease, and some rheumatologic diseases (1). Cytokines are elevated in pro-inflammatory states and have been found to cause an activation of proteolysis and lipolysis (2, 3). Many tumors are known to produce their own cytokines, which were found to cause a decreased appetite and weight loss in animal models (4). The activity of the various cytokines involved produces a net negative energy balance in the patient suffering from a chronic disease.
There are several other implicated hormonal factors that may induce cachexia. Decreased testosterone levels, seen in the aging and those with disease may lead to cachexia. Testosterone normally inhibits macrophage release of pro-inflammatory cytokines, and low levels of the hormones is associated with lipolysis and anorexia (5, 6). Studies have also found alterations in insulin-like growth factor (IGF)-1, which normally works to increase muscle protein synthesis (4). However, low concentrations are found in malnourished individuals. Elevated glucocorticoid levels are also seen in cachectic patients; these hormones are known to suppress cell transporters involved in amino acid and glucose uptake (6).
Cachexia represents the clinical consequence of a chronic, systemic inflammatory response. The changes seen in cachexia are complex and highly co-ordinated. It is characterised by an accelerated loss of skeletal muscle, often accompanied by loss of appetite and altered taste.
- Muscle wasting is the principal cause of function impairment, fatigue and respiratory complications, mainly related to a hyperactivation of muscle proteolytic pathways.
- There is also an increase in the synthesis of proteins involved in the response to tissue injury; the so-called ‘acute-phase response’.
- Pathological changes occur in response to the body’s acute-phase response to tissue damage, including synthesis by the liver of large amounts of proteins, e.g. C-reactive protein, complement factors, fibrinogen and many others.
- This response consumes large amounts of energy and amino acids which are obtained by breaking down skeletal muscle.
- In acute conditions this is an effective response, as skeletal muscle can be replaced later.
In a chronic condition, it adds to morbidity and can prove fatal.
Raised resting energy expenditure is typical of cachexia, but not starvation. However, this is not the cause of weight loss because it is compensated for by a reduction in energy used for voluntary activity, which further adds to loss of skeletal muscle from immobility.
Prognosis
The prognostic sign of cachexia is alarming. In cancer patients, weight loss documented prior to initiating chemotherapy predicts a shortened survival than those who had maintained weight (7). In nursing home residents, long-term patients losing 5% or more of his or her body weight have a 10-fold increase in mortality over 6 months compared to those who gain weight over a 1 month period (8). This indicates that if any intervention can be effective to reverse or stop weight loss, the physician should employ them early. Unfortunately however, a meta-analysis found that nutritional supplementation alone does little to decrease mortality or complications (1).
Patients with cachexia require small, nutritious, combinations of foods and meals with high doses of sprouts – (see our smoothie recipe; liquidise foods for easy absorption and less strain on the digestive system) every 20 – 30 minutes to sustain organ function until body is stronger again for solid foods
References
- Thomas DR. Guidelines for the use of orexigenic drugs in long-term care. Nutr Clin Pract 2006; 21:82-7.
- Kotler DP. Cachexia. Ann Intern Med 2000; 1333:622-34.
- Mitch WE, Goldberg AL. Mechanisms of muscle wasting. The role of the ubiquitin-proteasome pathway. N Engl J Med 1996; 335:1897-1905.
- Jatoi A. Weight loss in patients with advanced cancer: effects, causes, and potential management. Curr Opin Support Palliat Care 2008; 2:45-8.
- D’Agostino P, Milano S, Barbera C, et al. Sex horome modulate inflammatory mediators produced by macrophages. Ann NY Acad Sci 1999; 876:426-9.
- Morley JE, Thomas DR, Wilson MG. Cachexia: pathophysiology and clinical relevance. Am J Clin Nutr 2006; 83:735-43.
- Jatoi A. Pharmacologic therapy for the cancer cachexia/weight loss syndrome: a data-driven, practical approach. J Support Oncol 2006; 4:499-502.
- Ryan C, Bryant E, Eleazer P, Rhodes A, Guest K. Unintentional weight loss in long-term care: predictor of mortality in the elderly. South Med J 1995; 88:721-4.
