A Low or a High Protein Diet for Cancer ? The evidence

Many allopathic oncologists and even alternative practitioners believe that a high protein diet, including with meat and other animal sources, is healthy, especially for a cancer patient. In this perspective, “paleo” meat-eating scientists often invoke a study from the Journal of Cancer research that purports to support the theory that a high protein diet in the form of animal foods is an anti-cancer diet, one which strengthens the immune system and reduces malignant growth. This study states, in pertinent part:
” We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein.” Cancer Res; 71(13); 4484–93.  (Source)  (EXHIBIT A).
The problem with this study is that humans are not mice, humans have different digestion tracts from rodents, different anatomies (See “comparative anatomy” picture below) with different functions and abilities etc, (EXHIBIT B). Among many other differences,  rodents  can make their own vitamin C that humans can’t make and humans have under 3 percent protein in mother’s milk while rodents much more.
Furthermore, this study included low carbs, a piece of the diet which may have been more decisive in getting results, much more than the high protein element, especially for rodents. We already know that cancer thrives on sugar and that a low carbs diet  lowers glucose level and the insulin and IFG-1 hormones. We also don’t know all of what went into this “high protein-low carb” diet, for example, if the experimenter inserted turmeric in the diet, this ingredient would have had a beneficial impact with a high protein diet.  (EXBIBIT C).
On the other hand, there is plenty of hard evidence that a low protein diet promotes cancer control and lowers risks from contracting cancer.  Fontana et al (2) have shown a strong effect of a low-protein, low-calorie diet and endurance running on circulating concentrations of several growth-promoting hormones (including, but not limited to IGF-1) and other clinical biomarkers, thanks to  which low dietary protein (ie around 9% of dietary calories) has been shown to  decrease cancer risk.
Campbell et al showed that a protein diet greater than 10 percent of calories is a risk factor for cancer.  Campbell’s work  began after an observation of an association between primary liver cancer and animal protein consumption in Filipino children (4), which coincided with the findings of a  supportive experimental animal study in India (5). This led to a series of experimental research investigations and publications over the next 30 years concerning the association of animal protein consumption with primary liver cancer, its mechanisms, and its implications for human cancer at many sites.  Campbell et al also  showed that tumor growth in rats was greatly enhanced by diets containing over 10% animal protein (casein) and was completely repressed with either 5% animal protein or 20% plant protein (6).
On of the mechanisms of action that explain these results from a low protein diet is based on the weakening of a key enzyme complex which is  responsible for carcinogen activation (7) and for the subsequent and dominant promotion of preneoplastic clones and their sequelae (8), the life-long development of full-blown tumors (9) The experimenters  could turn on and off tumor development, both in its early (10) ) and late (11) stages of development.
In other words, animal foods greater than 5 percent acted like a cancer fertilizer, a switch that either fueled or  enhanced the development of malignancy with a high protein diet and diminished its inflammatory growth with a low protein diet.
In the Science of Medicine, findings often do not withstand the passage of time, what is known today is shown inexact or flawed tomorrow and the conclusions inferred therefrom are often exaggerated for self-serving purposes. Be that as it may, ACRI’s own experience and other findings corroborate the American “vegan squad” (12)  expert’s recommendations that a  low protein plant-based diet is better than a high protein animal diet to lower cancer risks and to help with the control and regression of malignancies.
(1). Another piece of evidence from a study that showed  Laron syndrome patients fare better on most modern chronic diseases (ie, reduced prevalence rates in diabetes, cancer and other diseases). Laron syndrome patient carry mutations in the growth hormone receptor (GHR) gene that lead to severe congenital IGF-1 deficiency with decreased insulin/IGF-1 signaling (IIS).  Western diets with high intake of hyperglycemic carbohydrates and insulinotropic dairy over-stimulates IIS. The reduction of IIS in Laron subjects unmasks the potential role of persistent hyperactive IIS mediated by Western diet in the development of diseases of civilization. Cf. Melnik BC1, John SM, Schmitz G., Over-stimulation of insulin/IGF-1 signaling by western diet may promote diseases of civilization: lessons learnt from laron syndrome, Nutr Metab (Lond). 2011 Jun 24;8:41.
(2). Fontana L, Klein S, Holloszy JO. Long-term low-protein, low-calorie diet and endurance exercise modulate metabolic factors associated with cancer risk. Am J Clin Nutr 2006;84:1456–62.
(3). Campbell TC, Campbell TM II. The China Study: startling implications for diet, weight loss, and long-term health. Dallas, TX: BenBella Books, Inc, 2005.
(4). Madhavan TV, Gopalan C. The effect of dietary protein on carcinogenesis of aflatoxin. Arch Pathol 1968;85:133–7.
(5). Dunaif GE, Campbell TC. Relative contribution of dietary protein level and aflatoxin B1 dose in generation of presumptive preneoplastic foci in rat liver. J Natl Cancer Inst 1987;78:365–9.
(6). Youngman LD, Campbell TC. Inhibition of aflatoxin B1-induced gamma-glutamyl transpeptidase positive (GGT+) hepatic preneoplastic foci and tumors by low protein diets: evidence that altered GGT+ foci indicate neoplastic potential. Carcinogenesis 1992;13:1607–13
(7). Hayes JR, Campbell TC. Effect of protein deficiency on the inducibility of the hepatic microsomal drug-metabolizing enzyme system. III. Effect of 3-methylcholanthrene induction on activity and binding kinetics. Biochem Pharmacol 1974;23:1721–32 (Among other studies).
(8). Youngman, op. cit.
(9). Appleton BS, Campbell TC. Inhibition of aflatoxin-initiated preneoplastic liver lesions by low dietary protein. Nutr Cancer 1982;3:200–6
(10). Youngman LD, Campbell TC. High protein intake promotes the growth of preneoplastic foci in Fischer #344 rats: evidence that early remodeled foci retain the potential for future growth. J Nutr 1991;121:1454–61
(11). Youngman LD. The growth and development of aflatoxin B1-induced preneoplastic lesions, tumors, metastasis, and spontaneous tumors as they are influenced by dietary protein level, type, and intervention. PhD dissertation. Cornell University, Ithaca, NY, 1990.
(12). In addition to Professor Campbell, this squad is made up of the following physicians, all best-sellers. Dr Dean Ornish, Dr Caldwell Esselstyn, Dr John McDougall, Dr Neal Barnard, Dr Joel Fuhrman.
(13). ACRI’S anti-cancer diet recommendations differs. No all vegan diets are equal. ACRI recommends a low calorie, low carb, high fat, nutrients dense, superfoods rich vegan diet with at least 80 percent raw and sprouted foods.
Journal of Cancer Research (2011) Source
A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation
Victor W. Ho1, Kelvin Leung1, Anderson Hsu1, Beryl Luk1, June Lai1, Sung Yuan Shen1, Andrew I. Minchinton3, Dawn Waterhouse4, Marcel B. Bally4, Wendy Lin5, Brad H. Nelson5, Laura M. Sly2, and Gerald Krystal1
Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction–induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets.
Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu–induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression.

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Nutr Res. 2015 Aug;35(8):726-35.
Curcumin ameliorates the tumor-enhancing effects of a high-protein diet in an azoxymethane-induced mouse model of colon carcinogenesis.
Byun SY1, Kim DB1, Kim E2.
An increasing number of reports suggest that a high-protein diet (HPD) is associated with an increased risk for colorectal cancer (CRC). One of the proposed mechanisms is that an HPD increases the delivery of protein to the colon and generates various toxic metabolites that contribute to colon carcinogenesis. Curcumin was shown to exert significant preventive properties against CRC. We therefore hypothesized that curcumin can reverse the tumor-enhancing effects of an HPD. This study examined the effects of curcumin on the development of azoxymethane (AOM)-induced colorectal tumors in HPD-fed mice. A total of 30 female Balb/c mice were randomly divided into 3 groups: those fed a normal diet (20% casein), those fed an HPD (HPD; 50% casein), and those fed an HPD supplemented with curcumin (HPDC; 0.02% curcumin). The mice were subjected to an AOM-dextran sodium sulfate colon carcinogenesis protocol. Mice in the HPDC group exhibited a significant (40%) reduction in colorectal tumor multiplicity when compared with those in the HPD group. The expression of colonic inflammatory proteins (cyclooxygenase-2 and inducible nitric oxide synthase), the levels of plasma inflammatory markers (nitric oxide and tumor necrosis factor-α), fecal ammonia, short- and branched-chain fatty acid levels, and the rate of colonocyte proliferation were significantly lower in the HPDC than the HPD group. In conclusion, curcumin inhibited the development of colorectal tumors in an AOM-induced mouse model of colon carcinogenesis by attenuating colonic inflammation, proliferation, and toxic metabolite production. Curcumin might be useful in the chemoprevention of CRC in individuals consuming an HPD.

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Copyright (c) Advanced Cancer Research Institute and agents.
DISCLAIMER.  This post is educational and its information should not be construed as medical advise.

Advanced Cancer Research Institute’s Director, Christian Joubert, has contributed in the coming and edification of a needed spiritual civilization by working as a professor of international public law in France and at Gonzaga Law School as well as in holistic medicine and other disciplines in different universities and institutes for most of his adult life. In association with his activities in clinical practice, organic agriculture, eco-development, community building, he has also actively participated via litigation and education in the legal protection of internationally recognized human rights, focusing on the protection of fundamental health rights and medical freedoms. He is presently working on a documentary and a book on Holistic Oncology, both of which have been designed to promote the necessary paradigm shift that will forever replace today's outdated, dogmatic, ideological and bankrupted conventional oncology model with progressive, evidence-based, sustainable and resilient holistic standards of care that are much more efficient, safe and cost-friendly than what persists in today's mainstream. See link on mission for more details.

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