I’m NOT asking for medical advice, just input from other Dopers who may have similar experiences/pharmacology wisdom.
I recently switched from Ambien (not covered by insurance) to Restoril/Temazepam (covered by insurance). The doctor promised it would knock me out and all the PDR information cites it as a very powerful sleep aid.
It does absolutely nothing to me. The dr. doubled the dose . . . still nothing. She tripled the dose and told me to make sure I was near my bed when I took it. It does absolutely nothing!
Different meds have different effects on different folks.
Restoril would likely be less effective if one had developed a tolerance for other drugs in its class, such as valium, xanax, or others.
The benzodiazepines work by increasing the tendency of GABA A receptors to bind Gamma-Amino Butyric Acid.
One should take into consideration other drugs that might be in one’s system, like alcohol, opiates, stimulants, or any chemical that activates the microsomal enzyme oxidating system (MEOS). They could alter the effect of Restoril on GABA receptors.
I don’t take any other meds, save an occasional aspirin, and I don’t drink alcohol or caffeine. I have never taken valium, xanax, or other anti-anxiety meds. Is it possible that the drug just doesn’t work with my chemistry? All the literature on it seems emphatic about its powerful effects.
Well, it’s certainly not working in its standard fashion with you. Benzos are known to have a paradoxical stimulatory effect in a significant number of folks.
That’s one of the reasons I don’t prescribe sleep meds.
Temazepam is metabolized by an enzyme coded for by the CYP 3A4 gene. Pharmakokinetic studies are still being performed on the 3A4 enzyme, and it appears that single point mutations (SNPs) in the gene do not always have predictable changes in the enzyme’s drug metabolic ability the way they do in other drug metabolizing genes such as CYP 2C9, 2C29, 2D6, 1A2, MTHFR, etc. It is possible, though rare, that you have two copies of 3A4, making you a super metabolizer. This Wikipedia article gives an overview of 3A4’s activity and inducers that will decrease metabolism of other drugs. If you continue to have problems, talk to your MD about pharmacogenetic testing to see if you posess any SNPs that will alter your drug metabolic capabilities. You can use that information to select a drug that will fit your needs and biochemistry.
Thanks, both, for the informed replies. There have been other drugs that don’t seem to work well either, perhaps there is a genetic reason. I’ll ask about a pharmacogenetic test.
I have a sort of related question. If a person used vicodin or other pain killers excessively (I’m thinking of my SIL with chronic back problems) and then stopped using them for a long period of time, does their resistance drop down to normal levels or will they always be highly resistant to their effects?
(I realize our OP said she’d never used those drugs…I’m just curious.)
After a few weeks (for vicodin anyway, longer for other long acting stuff like methadone), their tolerance for the drug will go away and they’ll respond more normally.
That’s how a number of drug abusers have died. After a long period of abstinence from heroin, they go back to it, and shoot up the same amount that they did when they were still using.
After a relapse following prolonged abstinence, many opiate users find their drug intake rapidly escalates to as high as or higher than it was before, however.