Thread revival...
High-Fat Ketogenic Diet to Control Seizures Is Safe Over Long Term, Study Suggests
ScienceDaily (Feb. 17, 2010) — Current and former patients treated with the high-fat ketogenic diet to control multiple, daily and severe seizures can be reassured by the news that not only is the diet effective, but it also appears to have no long-lasting side effects, say scientists at Johns Hopkins Children's Center.
"Despite its temporary side effects, we have always suspected that the ketogenic diet is relatively safe long term, and we now have proof," says senior investigator Eric Kossoff, M.D., a pediatric neurologist and director of the ketogenic diet program at Hopkins Children's. "Our study should help put to rest some of the nagging doubts about the long-term safety of the ketogenic diet," he adds.
http://www.scienceda...00216163531.htm
I've not seen any plausible reason to believe a ketogenic diet is harmful in the long-run. I hope more studies, like this one, back this up.
And as I've been saying, the ketogenic diet is a profoundly potent tool to be used among the first line of treatments for any cancer and any brain degenerative condition. If I had cancer--boom!--keto all the way. Starve those cancer cells of glucose, and insure the lowest systemic inflammation possible, since cancer requires fertilizer-like inflammation to spread itself like weeds in a garden.
And brain disorders especially respond well to keto diets.
The key is to eat healthy fats, of which most doctors are entirely misguided on. But that's been covered in other threads.
Interesting thread.
I came to this thread after seeing my fasting glucose levels to go up after a 6 month period in a paleo diet. I started at mid-eighties and I am now in upper nineties. Peter at hyperlipid wrote an excellent
post about this.
What is happening? Well, the first thing is that LC eating rapidly induces insulin resistance. This is a completely and utterly normal physiological response to carbohydrate restriction. Carbohydrate restriction drops insulin levels. Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non esterified fatty acids. These are mostly taken up by muscle cells as fuel and automatically induce insulin resistance in those muscles. There are a couple of nice summaries by Brand Miller (from back in the days when she used her brain for thinking) here and here and Wolever has some grasp of the problem too.
In the context of my disease (mitochondrial myopathy), ketogenic diet seems beneficial.
Ketogenic diet slows down mitochondrial myopathy progression in mice
Sofia Ahola-Erkkilä1, Christopher J. Carroll1, Katja Peltola-Mjösund1, Valtteri Tulkki1, Ismo Mattila2, Tuulikki Seppänen-Laakso2, Matej Orei2, Henna Tyynismaa1 and Anu Suomalainen1,3,*
1 Research Program of Molecular Neurology, Biomedicum-Helsinki, University of Helsinki, Helsinki 00290, Finland, 2 VTT Technical Research Centre of Finland, Espoo FI-02044 VTT, Finland and 3 Department of Neurology, Helsinki, University Central Hospital, Helsinki, Finland
* To whom correspondence should be addressed at: Biomedicum-Helsinki, r.C523B, Haartmaninkatu 8, 00290 Helsinki, Finland. Tel: +358 947171965; Fax: +358 919125610; Email: anu.wartiovaara@helsinki.fi
Received November 12, 2009; Accepted February 16, 2010
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 (KD), 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 mouse, a disease model for progressive late-onset mitochondrial myopathy, accumulating mtDNA deletions during aging and manifesting subtle progressive respiratory chain (RC) deficiency. We found that these mice have widespread lipidomic and metabolite changes, including abnormal plasma phospholipid and free amino acid levels and ketone body production. We treated these mice with pre-symptomatic long-term and post-symptomatic shorter term KD. 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 RC 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 wild-type 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 KD can slow down progression of the disease in mice. These results suggest that KD may be useful for mitochondrial late-onset myopathies.
Mechanism of action seems to be an increase in mitochondrial biogenesis. This is also the hypothesis in the treatment of epilepsy
Mitochondrial Biogenesis in the Anticonvulsant Mechanism of the Ketogenic Diet
Bough KJ, Wetherington J, Hassel B, Pare JF, Gawryluk JW, Greene JG, Shaw R, Smith Y, Geiger JD, Dingledine RJ.
Ann Neurol 2006;60:223–235. [PubMed]
OBJECTIVE
The full anticonvulsant effect of the ketogenic diet (KD) can require weeks to develop in rats, suggesting that altered gene expression is involved. The KD typically is used in pediatric epilepsies, but is effective also in adolescents and adults. Our goal was to use microarray and complementary technologies in adolescent rats to understand its anticonvulsant effect.
METHODS
Microarrays were used to define patterns of gene expression in the hippocampus of rats fed a KD or control diet for 3 weeks. Hippocampi from control- and KD-fed rats were also compared for the number of mitochondrial profiles in electron micrographs, the levels of selected energy metabolites and enzyme activities, and the effect of low glucose on synaptic transmission.
RESULTS
Most striking was a coordinated upregulation of all (n = 34) differentially regulated transcripts encoding energy metabolism enzymes and 39 of 42 transcripts encoding mitochondrial proteins, which was accompanied by an increased number of mitochondrial profiles, a higher phosphocreatine/creatine ratio, elevated glutamate levels, and decreased glycogen levels. Consistent with increased energy reserves, synaptic transmission in hippocampal slices from KD-fed animals was resistant to low glucose.
CONCLUSION
These data show that a calorie-restricted KD enhances brain metabolism. We propose an anticonvulsant mechanism of the KD involving mitochondrial biogenesis leading to enhanced alternative energy stores.
I have just orderered a HbA1c test. If the results are normal I rather prefer to stay in mild ketosis, even with a FG in the upper nineties.
Note that my overall energy levels have sky-rocketed after switching to Paleo and after going through a difficult 10-week period of ketoadaption. This is relevant, as one of my symptoms was a low, CFS like, energy level.
