As mentioned above, this product uses a ketone called BHB. BHB is short for Beta-hydroxybutyrate, which your body makes naturally. It’s supposed to increase your energy and burn fat simultaneously. There are no studies, however, that verify these claims. Keto Pills attempt to simulate this process, but there is little evidence right now that corroborates these theories. There is some promising research for exogenous ketones. For example, this study concludes that exogenous ketone drinks effectively achieve ketosis. It should be mentioned that Keto Pills are not the same thing, so the comparison is a little unclear. Ketosis, by the way, is just a way of referring to the metabolic process of burning fat instead of carbohydrates for energy.
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While the effects of leptin on seizure susceptibility and its relationship to KD-induced weight loss are intriguing, there are as yet no direct data supporting leptin as an anticonvulsant mediator of the KD. Certainly, the clinical implications of the study by Xu et al. (2008) are intriguing, namely, that intranasal administration of leptin might be efficacious in aborting acute seizure activity. And if the clinical effects of the KD are due in part to increased leptin levels, then accelerated development and validation of leptin as a novel anticonvulsant medication would be warranted.
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Given these findings, it is not surprising that investigators have studied the effects of dietary supplementation with PUFAs alone, to determine whether these substrates can render an anticonvulsant effect. Early case reports suggested that seizures might be better controlled with this approach (Schlanger et al., 2002). However, a recent randomized trial in adult patients with epilepsy failed to demonstrate superiority of a PUFA supplement (EPA) plus DHA, 2.2 mg/day in a 3:2 ratio) over placebo (Bromfield et al., 2008). Thus, the jury is still out as to whether PUFAs alone can mirror the clinical effects of the KD.
So, if the KD acts principally to enhance glutathione levels in the brain, then would taking glutathione supplements (which are commercially available) be sufficient to protect against seizure activity? The answer is negative since available glutathione formulations are largely digested before they can get into the bloodstream, let alone to the brain. The only supplement that effectively raises glutathione levels in the body is N-acetyl-L-cysteine (NAC) which has traditionally been used to treat liver toxicity induced by toxic levels of acetaminophen. Would NAC be a suitable substitute for the KD? The clinical experience to date has been mixed, with some patients with progressive myoclonic epilepsies improving on NAC supplementation (Hurd et al., 1996; Edwards et al., 2002)