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Does anyone know what effect a high fat die has on Benzos as their fat lipid?


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I'm on Diazepam mid taper and doing the PKD ( Paleo Keto Diet) Which is very high diet fat 2:1 fat to protein ratio, or even higher again in fat in some cases , and am concerned as people on all types of medication have reported the Ketogenic, PKD , Carnivore/ Z/C diets have effected the strength  oF their medication.

 

In some cases they've had to cut the dose or were able, or had to to get off the med completely very quickly as the Ketogenic, PKD , Carnivore/ Z/C diets  made the medication  effects  a lot stronger ,  where as others reported feeling as if they were in sudden  withdrawal or had up-dosed and were having side effects  from their medication, as per the title does anyone know what effect  the high fat  has on Benzos as their fat lipid?

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  • 6 months later...

I'm wondering the same thing. I haven't started my taper yet and am in Ketosis. Have you learn't anything new about this.

I am thinking about stopping my Keto diet but am scared to throw my system off because I only started Valium 8. Desember.

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Doing research right now on ways to lower glutamate (excitatory brain chemical) and aid GAD (enzyme that converts glutamate to GABA). Found interesting things about diet.  The modified Paleo-Keto may be the answer, minus any high glutamate foods.  Authors advise including these veg and fruit in your diet, but only occasionally. Some high offenders are milk casein (butter, cream), tomatoes, peanuts, and broccoli. Also leave out fermented things, Parmesan and Roquefort cheeses, and any soy products. NO aspartame!!

https://nutritionforseizures.com/low-glutamate-foods-can-reduce-the-excitotoxicity-in-the-brain/

 

Since the gut is often misbehaving during wd, betaine to raise stomach acid and bile extracts/lipases, etc. may be a good addition to break down the food properly.

 

There is a hospital diet that was developed for seizing children, who got no results from meds, that is a strict Keto diet.  There's a Meryl Streep movie about it called,"First, Do No Harm." https://www.youtube.com/watch?v=HyeC9IiFKpw    Most who try it get results, and those who do the diet for 2 years never seizure again. It has also been shown that glutamate is primarily involved in these cases, especially the severe Rasmussen's encephalitis. For RE they take out half the kid's brain to stop the seizures.

 

Molybdenum and vitamin C aid the GAD enzyme and help at the GABA binding sites. If you're gluten intolerant or have Hashimoto's thyroiditis, then it's likely your GAD is genetically impaired.

 

The reason people sometimes crave high sugar as comfort foods is because the glucose temporarily raises GABA.  This is done at a cost.

 

Will write more as I dig through the literature.

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So are we dealing with low GABA problem or GABA receptor malfunction? Because I totally understand how keto diet can help produce GABA from the citric cycle but I am also hearing that we might just have receptor damage, not necessarily less GABA.. I’m confused atm..
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Confused about the diet:  The keto type diets increase GABA in the cerebrospinal fluid.  They aren't sure exactly how but hypothesize it's by using intermediate pathways as ketones are used as fuel versus glucose.

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940242/

Glucose is ordinarily the sole fuel for the human brain; fatty acids cannot be used because they do not cross the blood-brain barrier. Ketone bodies do enter the brain, in proportion to the degree of ketosis. Ordinarily, utilization of ketones by the brain is minimal. During the ketogenic diet, however, ketone bodies partly replace glucose as fuel for the brain. The ketone bodies are converted to acetyl-CoA by D-β-hydroxybutyrate dehydrogenase, acetoacetate-succinyl-CoA transferase, and acetoacetyl-CoA-thiolase and then enter the Krebs cycle within brain mitochondria, leading to the production of adenosine triphosphate (ATP) (Fig. 2).

 

Although animal studies have failed to demonstrate affects of the ketogenic diet on brain GABA levels in the absence of amino acid loading, a recent study on cerebro-spinal fluid amino acid levels before and during the ketogenic diet found evidence of increased cerebrospinal fluid GABA [45]. GABA levels were higher in responders than in nonresponders, and, in the best responders, GABA levels were significantly higher at baseline as well as during the diet. In that study, children under 5.5 years of age had higher cerebrospinal fluid GABA levels during the diet than did older children.

 

Why low GABA in withdrawal?

Your body works on negative feedback loops: It turns off GABA production as there's no reason to make it as you externally supply it. Since you take the drug daily, you may bind up most of the available sites. Again, no reason to grow new ones as constant sedation.  When the drug stops, now you have to make your own GABA and all the associated enzymes. Previously all the sites were bound, so now need to grow new ones. This takes time.

 

Since glutamate and GABA are in opposition to balance one another, if you stop GABA drug, you get too much glutamate. High glutamate damages receptors. If your GAD enzyme works well, it will begin to convert some glutamate to GABA. High glutamate has been discovered in patients with seizures, schizophrenia, etc. Glutamate also works on NMDA receptors which can produce hallucinations.  May be why some get depersonalization and derealization.

 

 

 

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The keto type diets increase GABA in the cerebrospinal fluid. 

 

So maybe it is not good to be on it before you start tapering?

It sounds like if you are already on the KETO diet and taking some benzos, then quitting the keto diet may even throw you into withdrawal. Does that make sense to you? Does anyone have any experience with that?

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