Ketogenic-diets and other low-carb diets seem to mimic the hormonal state found in type-1 diabetes. Since diabetics cannot utilize glucose as fuel, due to insulin-resistance, the body begins to oxidize fats for energy to stay alive and while this causes a temporary weight-loss, it doesn’t mean the person is getting healthier, but rather they are wasting away due to insulin-deficiency. Ketogenic diets also promote unhealthy amounts of lipid-peroxides which deplete our endogenous antioxidants (like glutathione and vitamin-e).
Quite the contrary. The following are appropriate ketogenic diet studies, not studies on diabetes.
The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. We sought to determine whether the KD improves mitochondrial redox status. Adolescent Sprague-Dawley rats (P28) were fed a KD or control diet for 3 weeks and ketosis was confirmed by plasma levels of beta-hydroxybutyrate (BHB). KD-fed rats showed a twofold increase in hippocampal mitochondrial GSH and GSH/GSSG ratios compared with control diet-fed rats. To determine whether elevated mitochondrial GSH was associated with increased de novo synthesis, the enzymatic activity of glutamate cysteine ligase (GCL) (the rate-limiting enzyme in GSH biosynthesis) and protein levels of the catalytic (GCLC) and modulatory (GCLM) subunits of GCL were analyzed. Increased GCL activity was observed in KD-fed rats, as well as up-regulated protein levels of GCL subunits. Reduced CoA (CoASH), an indicator of mitochondrial redox status, and lipoic acid, a thiol antioxidant, were also significantly increased in the hippocampus of KD-fed rats compared with controls. As GSH is a major mitochondrial antioxidant that protects mitochondrial DNA (mtDNA) against oxidative damage, we measured mitochondrial H2O2 production and H2O2-induced mtDNA damage. Isolated hippocampal mitochondria from KD-fed rats showed functional consequences consistent with the improvement of mitochondrial redox status i.e. decreased H2O2 production and mtDNA damage. Together, the results demonstrate that the KD up-regulates GSH biosynthesis, enhances mitochondrial antioxidant status, and protects mtDNA from oxidant-induced damage.
The ketogenic diet increases mitochondrial glutathione levels.This is a
nice summary of
this study (PDF):
The researchers wanted to determine whether increased levels of βOHB actually reduced oxidative stress in vivo. To do this, they implanted mice with a subcutaneous βOHB pump, which supplied a steady release of βOHB. Researchers then injected a chemical, paraquat, which induces build up of reactive oxygen species. Compared to control mice (with no βOHB pump), βOHB mice had an impressive 54% reduction in reactive oxygen species.
Researchers also evaluated a maker of oxidative stress in these mice, 4-hydroxynonenal (4-HNE). 4-NHE is a product of polyunsaturated lipid degradation and accumulates in response to oxidative stress. The control mice had a three-fold increase in 4-NHE, indicating high levels of oxidative stress. This increase was completely suppressed in βOHB mice, indicating that high levels of βOHB protect against oxidative stress.
The level of BHB used in the study yeilded a blood ketone level of about 1.2 mm, which is toward the lower end of the nutritional ketosis range.
Ketogenic-diets focus on burning fatty-acids as fuel, that is how the person is suppose to lose weight on that diet. Ketosis and diabetes are so closely related that uncontrolled diabetes would eventually lead to ketosis itself and then if still left untreated, it would lead to ketoacidosis.
If you are not a type I diabetic, you will produce enough insulin to inhibit ketogenesis. In a healthy individual, ketones and fatty acids inhibit the uptake of glucose on a ketogenic diet. This is a good thing otherwise your blood sugar would drop to coma-inducing levels. The title of a recent study says it all.. almost:
Impaired glucose tolerance in low-carbohydrate diet: maybe only a physiological state.One of the largest failures of most diets is that they are catabolic in nature; they focus of losing “weight” instead of adipose. What I think we should be doing is to become more anabolic, but make sure we shuttle energy into lean tissues rather than adipose. I believe this is done with starch.
Ketogenic diets spare protein. Muscle-building branched-chain amino acids are increased by 50% on a ketogenic diet vs a high carb diet, vis a vis calories and protein.
The effects of a 4-day isocaloric isoprotenic dietary replacement of carbohydrate by fats were studied in six healthy subjects, the experimental diet being preceded and followed by a 3-day period of balanced diet. During the ketogenic regimen, the concentrations of fat derived substrates (free fatty acids, glycerol and 3-hydroxybutyrate) rose significantly and glucose levels decreased by 16.5 +/- 3.2% (mean +/- SEM). The hormonal pattern switched towards a catabolic mode with a fall in insulin levels (-44.0 +/- 6.3%) and a rise in glucagon concentration (+39.0 +/- 10.4%). A significant fall in triiodothyronine and rise in reverse triiodothyronine were observed, while thyroxine levels remained unchanged. The average levels of the most important gluconeogenic amino acids (alanine, glutamine, glycine, serine and threonine) were reduced by 8-34% while those of the branched chain amino acids increased by more than 50%. Since these changes reproduce those observed after a few days of total fasting, we suggest that it is the carbohydrate restriction itself which is responsible for the metabolic and hormonal adaptations of brief fasting.
Hormonal and metabolic changes induced by an isocaloric isoproteinic ketogenic diet in healthy subjects.This may be in part due to protein recycling or
autophagy. This is also most likely why people who are starving to death do not die of protein deficiency. Dr. McDougall has written about
this.
Starving People Die of Fat, Not Protein, Deficiency In 1981, 10 Irish prisoners from the Republican Army (IRA) went on a hunger strike. Nine out of 10 of these men died between 57 and 73 days (mean of 61.6 days) of starvation after losing about 40% of their body weights (the remaining striker died of complications of a gunshot wound).16,17 This experience gave doctors a chance to observe first hand the metabolic changes that occur during starvation. Protein stores were generally protected during starvation, with most of the energy to stay alive being derived from the men’s fat stores. It was estimated that the hunger strikers had lost up to 94% of their body-fat levels, but only 19% of their body-protein levels at the time of death.16 They died when they ran out of fat. Since fat is more critical than protein, people should be asking, “Where do you get your fat (on any diet)?
By the way, BCAA supplementation has been found to extend life in mammals.
Recent evidence points to a strong relationship between increased mitochondrial biogenesis and increased survival in eukaryotes. Branched-chain amino acids (BCAAs) have been shown to extend chronological life span in yeast. However, the role of these amino acids in mitochondrial biogenesis and longevity in mammals is unknown. Here, we show that a BCAA-enriched mixture (BCAAem) increased the average life span of mice. BCAAem supplementation increased mitochondrial biogenesis and sirtuin 1 expression in primary cardiac and skeletal myocytes and in cardiac and skeletal muscle, but not in adipose tissue and liver of middle-aged mice, and this was accompanied by enhanced physical endurance. Moreover, the reactive oxygen species (ROS) defense system genes were upregulated, and ROS production was reduced by BCAAem supplementation. All of the BCAAem-mediated effects were strongly attenuated in endothelial nitric oxide synthase null mutant mice. These data reveal an important antiaging role of BCAAs mediated by mitochondrial biogenesis in mammals.
http://www.ncbi.nlm....pubmed/20889128
