Posted by desolationrower on March 30, 2011, at 20:38:06
In reply to Re: has anyone done ketogenic diet + antidepressants, posted by morgan miller on March 26, 2011, at 23:58:32
So back on what I posted about before:
as morgan said, coconut has MCT which are more easily converted to ketone bodies. Ketosis can have beneficial effects on the brain, most known in epilepsy (i'm not sure the alzheimer's and mitochondria stuff is related to this. it might be a separate benefit, showing up as mental energy or something, especially if you are older or something). Anyway, just low-carb probably won't have this effect at all, since ketones don't occur in large amounts unless you eat less than about 50grams a day, and keep protein levels to moderate/low levels. But the effects on cortisol would be present.
If it is related to the beneficial effect, then perhaps ketosis should be considered like ssris, as opposed to TCAs and bupropion which tend to be proconvulsive.
This: antiepileptic drugs (seems to be ones used for mood disorders) are potentiated by acetone, the main ketone. others aren't:
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Pharmacodynamic and pharmacokinetic interactions between common antiepileptic drugs and acetone, the chief anticonvulsant ketone body elevated in the ketogenic diet in mice
SummaryPurpose:  Acetone is the principal ketone body elevated in the ketogenic diet (KD), with demonstrated robust anticonvulsant properties across a variety of seizure tests and models of epilepsy. Because the majority of patients continue to receive antiepileptic drugs (AEDs) during KD treatment, interactions between acetone and AEDs may have important clinical implications. Therefore, we investigated whether acetone could affect the anticonvulsant activity and pharmacokinetic properties of several AEDs against maximal electroshock (MES)induced seizures in mice.
Methods:  Effects of acetone given in subthreshold doses were tested on the anticonvulsant effects of carbamazepine (CBZ), lamotrigine (LTG), oxcarbazepine (OXC), phenobarbital (PB), phenytoin (PHT), topiramate (TPM) and valproate (VPA) against MES-induced seizures in mice. In addition, acute adverse effects of acetoneAEDs combinations were assessed in the chimney test (motor performance) and passive avoidance task (long-term memory). Pharmacokinetic interactions between acetone and AEDs were also studied in the mouse brain tissue.
Results:  Acetone (5 or 7.5 mmol/kg, intraperitoneally [i.p.]) enhanced the anticonvulsant activity of CBZ, LTG, PB, and VPA against MES-induced seizures; effects of OXC, PHT, and TPM were not changed. Acetone (7.5 mmol/kg) did not enhance the acute adverse-effect profiles of the studied AEDs. Acetone (5 or 7.5 mmol/kg, i.p.) did not affect total brain concentrations of the studied AEDs. In contrast, VPA, CBZ, LTG, OXC, and TPM significantly decreased the concentration of free acetone in the brain; PB and PHT had no effect.
Conclusions:  Acetone enhances the anticonvulsant effects of several AEDs such as VPA, CBZ, LTG, and PB without affecting their pharmacokinetic and side-effect profiles.
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Long-term Effects of a Very Low-Carbohydrate Diet and a Low-Fat Diet on Mood and Cognitive FunctionBackground Very low-carbohydrate (LC) diets are often used to promote weight loss, but the long-term effects on psychological function remain unknown.
Methods A total of 106 overweight and obese participants (mean [SE] age, 50.0 [0.8] years; mean [SE] body mass index [calculated as weight in kilograms divided by height in meters squared], 33.7 [0.4]) were randomly assigned either to an energy-restricted (approximately 1433-1672 kcal [to convert to kilojoules, multiply by 4.186]), planned isocaloric, very low-carbohydrate, high-fat (LC) diet or to a high-carbohydrate, low-fat (LF) diet for 1 year. Changes in body weight, psychological mood and well-being (Profile of Mood States, Beck Depression Inventory, and Spielberger State Anxiety Inventory scores), and cognitive functioning (working memory and speed of processing) were assessed.
Results By 1 year, the overall mean (SE) weight loss was 13.7 (1.8) kg, with no significant difference between groups (P = .26). Over the course of the study, there were significant time x diet interactions for Spielberger State Anxiety Inventory, Beck Depression Inventory, and Profile of Mood States scores for total mood disturbance, anger-hostility, confusion-bewilderment, and depression-dejection (P < .05) as a result of greater improvements in these psychological mood states for the LF diet compared with the LC diet. Working memory improved by 1 year (P < .001 for time), but speed of processing remained largely unchanged, with no effect of diet composition on either cognitive domain.
Conclusions Over 1 year, there was a favorable effect of an energy-restricted LF diet compared with an isocaloric LC diet on mood state and affect in overweight and obese individuals. Both diets had similar effects on working memory and speed of processing.
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