Restricting and/or Eliminating Dietary Protein

The following is an email letter from John Baird, Sr. VP, Chief Legal Officer (CLO) and Director of Corporate Affairs for the pH Miracle Center and Young pHorever, Inc. concerning my theory on restricting dietary protein. =============================================================== In the appended article, once again, we see research validating one of your primary theses… that is – protein dietary restriction. Coming from a performance athletic background, your low protein diet admonition was a hard sell for me. I used to take protein supplements by the hand full, and I consumed protein bars constantly in addition to taking Creatine and other protein building supplements. You have conclusively shown that muscle mass can be just as easily be built and maintained on a low protein vegetarian diet as on a high animal protein diet. It’s all in the quality of the blood. The attached article points out how high-energy protein synthesis at the cellular mitochondrial level works. Our bodies produce more of a “high energy” protein (d4EBP) in the mitochondria when the ingestion of protein is restricted. The article is silent on whether the beneficial effects of a low protein diet, still hold up IF all ingested protein is vegetarian in origin. You certainly seem to be correct again, when you say that we should avoid ALL animal protein. BUT….I wonder if it is also necessary to avoid vegetarian protein as well? The population of Loma Linda, CA is statistically one of the longest-lived in the world. It is thought that the reason for this statistical variance is that most inhabitants of Loma Linda are Seventh Day Adventists, who are largely vegetarian. Yet Adventists don’t intentionally restrict vegetarian protein… and still the added longevity shows up in the statistical evidence. This Loma Linda statistical variance may indicate that it is not necessary to restrict vegetarian protein to get the the enhanced d4EBP mitochondrial activity to which the appended article refers. Regards, John Baird Sr. VP, Chief Legal Officer (CLO) Director of Corporate Affairs pH Miracle Center Young pHorever, Inc. ————————–Referenced Article——————– ‘Anti-Atkins’ Diet Extends Life in Flies October 5, 2009 (Ivanhoe Newswire) — Flies fed an “anti-Atkins” low protein diet live longer because their mitochondria function better, according to a new study from the Buck Institute for Age Research in California. The research shows that the molecular mechanisms responsible for the lifespan extension in the flies have important implications for human aging and diseases such as obesity, diabetes and cancer. Mitochondria act as the “powerhouse” of the cells. It is well known that mitochondrial function worsens with age in many species, and especially in humans with Type II diabetes and obesity. “Our study shows that dietary restriction can enhance mitochondrial function, hence offsetting the age-related decline in its performance,” Buck faculty member Pankaj Kapahi, PhD, lead author of the study, is quoted as saying. The research calls into question the health benefits of the high-protein diets often used to lose weight. Kapahi said that while the long-term impacts of such diets have not been examined in humans, he believes they are likely to be harmful. “In flies, we see that the long-lived diet is a low protein diet and what we have found here is a mechanism for how that may be working,” he said. The researchers reported that while there is a reduction in protein synthesis with the low protein diet, the activity of specific genes involved in generating energy in the mitochondria are increased. That activity — conversion of RNA to protein — is important for the protective effects of dietary restriction, said Kapahi. “There have been correlative studies that show mitochondria change with dietary restriction, [and] this research provides a causal relationship between diet and mitochondrial function.” The study describes the mechanism by which mitochondrial genes are converted from RNA to protein by a particular protein (d4EBP). Flies fed a low protein diet showed an uptick in activity of d4EBP, which mediates cell growth in response to nutrient availability. The research showed that d4EBP is necessary for lifespan extension. When the activity of the protein was genetically “knocked out” the flies did not live longer, even when fed the low protein diet. When the activity of d4EBP was enhanced, lifespan was extended, even when the flies ate a rich diet. The Buck Institute study provides a significant advance in understanding the role of 4EBP, said Kapahi, and implies an important role for 4EBP and mitochondrial function as excellent targets to explore their role in lifespan extension in mammals. SOURCE: Cell, October 2, 2009 Reference:

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