Dr. Weeks’ Comment:  Cancer alone doesn’t typically kill people.  Cachexia does. Cachexia – from the Greek “kakos” and “hexis”, means “bad conditions” and that, my readers, is an understatement.  Cachexia is NOT simply starvation but a far more complicated lethal process which not only starves but also prevents nourishment.

“Cachexia represents the clinical consequence of a chronic, systemic inflammatory response, with high hepatic synthesis of acute-phase proteins resulting in depletion of essential amino acids. In contrast, in starvation only fat metabolism is increased while the organism tries to conserve lean body mass.”

How to avoid cachexia?  Best to be well nourished but also to reduce inflammation with whole crushed organic non-GMO anti-inflammatory seeds.

And don’t spare the protein – Dr. Gaston Naessans, the creator of the cancer treatment 714X  taught me that cancer is a protein deficiency disease.  The immune system needs protein to function and the cancer needs protein but Dr. Naessans reminded me that “a well-nourished immune system will beat a well-nourished cancer any day of the week“. China Study findings aside,  eating organic non-GMO seed proteins – the highest source of branch chain amino acids in order to avoid the depletion of essential amino acids is essential to health.

Biology of Cachexia

https://academic.oup.com/jnci/article-lookup/doi/10.1093/jnci/89.23.1763

Although cancer cachexia superficially resembles starvation, nutritional intervention alone is unable to reverse the condition. Tremendous progress has been made in the last 10 years in elucidating the role of various factors in host tissue catabolism, and the results of these studies are now being translated into treatment regimens for the benefit of patients with cachexia. Cachexia is an important cause of mortality in cancer patients, accounting directly for between 10% ( 137 ) and 22% ( 138 ) of all cancer deaths, as well as death from other causes such as infection. Thus, an effective therapy for cachexia not only should improve the quality of life of cancer patients, but also may be expected to extend the survival time. In addition, since some tumors may depend on the products from host tissue catabolism for survival, such therapy may also have an antitumor effect. Considering that cachexia is common in those cancers for which therapy is currently limited, this could prove to be of great clinical benefit.

SOURCE   http://molecular-cancer.biomedcentral.com/articles/10.1186/1476-4598-2-36

Cancer cachexia occurs most frequently in malignancy and is associated with more than 20% of cancer deaths [1]. Patients with upper gastrointestinal cancer are especially likely to suffer from substantial weight loss, and patients with pancreatic cancer have the highest frequency of developing a cachectic syndrome. Thus the research groups and physicians dealing with pancreatic cancer are very interested in finding an effective treatment for cachectic patients. But there is still little known about this clinical issue, and our knowledge grows slowly. Much more research and many more clinical trials are needed to increase our understanding of the syndrome and to develop therapeutic strategies for one of the major symptoms of cancer.

The word “cachexia” comes from the Greek words “kakos” and “hexis”, meaning “bad conditions” [2]. Cachexia is a complex metabolic status with progressive weight loss and depletion of host reserves of adipose tissue and skeletal muscle. Cachexia should be suspected if involuntary weight loss of greater than five percent of premorbid weight occurs within a six-month period [3]. Cachexia represents the clinical consequence of a chronic, systemic inflammatory response, with high hepatic synthesis of acute-phase proteins resulting in depletion of essential amino acids [4]. In contrast, in starvation only fat metabolism is increased while the organism tries to conserve lean body mass [5].

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Much research is currently focused on determining the mechanism of the development of cachexia. There are two main theories of the development of cancer cachexia.

The first theory is the pathological alteration of control cycles. Food-intake is regulated through a complex system of hormones and neuropeptides. Inui et al. demonstrated that Neuropeptid Y (NPY), the most potent feeding-stimulatory peptide in this cycle, is deregulated in the hypothalamic orexigenic network, leading to decreased energy intake but high metabolic demand for nutrients [9]. High levels of leptin, a hormone secreted by adipocytes, block the release of NPY. In cachexia the leptin feedback loop seems to become out of control, altering the neuropeptidergic control cycles [9].

The second theory is based on the idea that tumor-derived factors maintain the cachectic syndrome. Tisdale et al. postulated a factor that was extracted from the urine of cachectic patients and which induces protein degradation in skeletal muscle by upregulation of the ubiquitin-proteasome pathway. This proteolysis-inducing factor (PIF) is closely related to weight loss in cachexia, and in a recent study it was shown that PIF is produced in human colon cancer [1, 10, 11].

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Despite the controversial discussion of cachexia-inducing mechanisms uncertainty over what causes cachexia, it is quite clear that proinflammatory cytokines are linked to all pathways that induce cachexia. As mentioned, cachexia is associated with a chronic systemic inflammatory response and the elevation of acute phase proteins. High serum levels of IL-1, IL-6 and INF gamma are present in many cancer patients, and the levels of these cytokines seem to correlate with tumor progression.