Here is another one to think about with respect to the protective aspects of a low carb / primal / paleo diet (I know it is mice and we are not mice....but still worth thinking about):
Ketogenic diet slows down mitochondrial myopathy progression in mice
Ketogenic diet slows down mitochondrial myopathy progression in mice
Mitochondrial dysfunction is a major cause of neurodegenerative and neuromuscular diseases of adult age and of multisystem disorders of childhood. However, no effective treatment exists for these progressive disorders. Cell culture studies suggested that ketogenic diet, with low glucose and high fat content, could select against cells or mitochondria with mutant mitochondrial DNA (mtDNA), but proper patient trials are still lacking. We studied here the transgenic Deletor mice, a disease model for progressive late-onset mitochondrial myopathy, accumulating mtDNA deletions during aging and manifesting subtle progressive respiratory chain deficiency. We found that these mice have wide-spread lipidomic and metabolite changes, including abnormal plasma phospholipid and free amino acid levels and ketone body production. We treated these mice with presymptomatic long-term and post-symptomatic shorter term ketogenic diet. The effects of the diet for disease progression were followed by morphological, metabolomic and lipidomic tools. We show here that the diet decreased the amount of cytochrome-c-oxidase negative muscle fibers, a key feature in mitochondrial respiratory chain deficiencies, and prevented completely the formation of the mitochondrial ultrastructural abnormalities in the muscle. Furthermore, most of the metabolic and lipidomic changes were cured by the diet to wildtype levels. The diet did not, however, significantly affect the mtDNA quality or quantity, but rather induced mitochondrial biogenesis and restored liver lipid levels. Our results show that mitochondrial myopathy induces widespread metabolic changes, and that ketogenic diet can slow down progression of the disease in mice. These results suggest that ketogenic diet may be useful for mitochondrial late-onset myopathies.
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APOE-4: The Clue to Why Low Fat Diet and Statins
may Cause Alzheimer's
by Stephanie Seneff
Have you seen this essay? I think it deserves some attention. This section got my attention;
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Amyloid-beta (also known as "abeta") is the substance that forms the famous plaque that accumulates in the brains of Alzheimer's patients. It has been believed by many (but not all) in the research community that amyloid-beta is the principal cause of Alzheimer's, and as a consequence, researchers are actively seeking drugs that might destroy it. However, amyloid-beta has the unique capability of stimulating the production of an enzyme, lactate dehydrogenase, which promotes the breakdown of pyruvate (the product of anaerobic glucose metabolism) into lactate, through an anaerobic fermentation process, with the further production of a substantial amount of ATP.
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So maybe interventions that lower amyloid plaque by lowering the resistance to its effects on lactate metabolism would be protective, while simply blocking its production would be dangerous.
According to Dr Bernstein, amyloid is also put out by the pancreas when insulin is produced, and reduces hunger for carbohydrate. He sometimes prescribes the drug Amylin to deal with this.
If it promotes the proper use of carbohydrate, this makes sense; constant glycolysis followed by gluconeogenesis being a rather inefficient way to produce the energies of life.
http://endo.endojournals.org/cgi/content/abstract/en.2008-0770v1
"Amylin-Mediated Restoration of Leptin Responsiveness in Diet-Induced Obesity: Magnitude and Mechanisms"
I've come to believe that the most important function of leptin is ensuring the availability of ketone-family metabolites to tissues like the brain that need them. Leptin normally decreases the appetite for carbohydrate; a person deficient in the ability to use lactic acid might be expected to be resistant to this effect; brain cells need glucose, or ketones, or lactic acid; if they can't use lactic acid, but enough glucose has been consumed to suppress ketosis, the paradoxical situation where consuming carbohydrate actually increases carbohydrate hunger instead of satisfying it might arise.
Secondly, Dr. Eva, the word is 'lose' not 'loose'.