Psych0naut said:
You should try hypnotics instead. Anxiolytics generally do a poor job in helping you fall asleep unless you're very sensitive to them or take them in high doses(much higher doses than their equivalent doses of a hypnotic). Taking anxiolytics in high doses as a sleep aid will cause much more negative effects like a drowsy, tired feeling the next day, and having a lot of trouble getting out of bed. In the long term but even in a relatively short period they'll cause a much larger rise in tolerance and worse physical dependancy compared to taking hypnotics for insomnia, because they are much more effective sleep aids, and so need much lower equivalent doses.
Hypnotics are generally a lot more physically addictive than equivalent doses of anxiolytics, this is due to their much stronger effects, because they bind differently to the GABA-benzodiazepine receptors than anxiolytics. This is also why hypnotics have much higher acute toxicity than anxiolytics. A lethal overdose on anxiolytics by themselves(without any other CNS depressants) is almost impossible, but a lethal overdose on hypnotics by themselves(without any other CNS depressants) is much more real, and a very real possibillity with the strongest intermediate acting hypnotics like Rohypnol, Loramet, and Normison, and the short acting hypnotics like Dormicum, Dormonoct and Halcion. But still, taking a lot lower dose of a hypnotic is much more effective and beneficial than taking a high dose of an anxiolytic.
All of that is fact, and is what I have been saying (and bringing scientific studies to back up all the claims that the hypnotics are on another level, a level more akin to barbiturates). However, a few posters (one of which was the narutokin - a prebuscent kid with severe mental issues and a fetish for needles, he'd IV his piss if he thought there was some kind of metabolite in it, thinks that I am "wrong" LMAO).
Benzodiazepines produce a range of effects from depressing to stimulating the CNS via modulating the GABA(A) receptor, the most prolific inhibitory receptor within the brain. The GABA(A) receptor is made up from 5 subunits out of a possible 19, and GABA(A) receptors made up of different combinations of subunits have different properties, different locations within the brain, and different activities relative to pharmacological and clinical effects.
Benzodiazepines bind at the interface of the α and γ subunits on the GABA(A) receptor. Benzodiazepine binding also requires that alpha subunits contain a histidine amino acid residue, (i.e., α1, α2, α3 and α5 containing GABA(A) receptors).
In order for GABA(A) receptors to be sensitive to the action of benzodiazepines, they need to contain both an α and a γ subunit, where the benzodiazepine binds at the interface. Once bound, the benzodiazepine locks the GABA(A) receptor into a conformation where the neurotransmitter GABA has much higher affinity for the GABA(A) receptor, increasing the frequency of opening of the associated chloride ion channel and hyperpolarizing the membrane. This potentiates the inhibitory effect of the available GABA, leading to sedatory and anxiolytic effects.
As mentioned above, different benzodiazepines have different affinities for GABA(A) receptors made up of different collection of subunits. For instance, benzodiazepines with high activity at the α1 (BZ1 or omega 1 receptor) are associated with sedation, hypnosis, amnesia, toxicity, motor impairment, cognitive impairment, whereas those with higher affinity for GABAA receptors containing α2 and/or α3 subunits have good anti-anxiety activity. Benzodiazepines also bind to glial cell membranes.
There are two central benzo receptor subtypes, as described above, (BZ1 and BZ2), and one peripheral Benzo receptor has been identified and well studied and researched.
Diazepam, alprazolam, bromazepam, lorazepam, prazepam, oxazepam, clonazepam, and clorazepate are strong BZ - 2 receptor (omega 2 receptor) agonists. Omega 2 receptors mediate moderate to strong anxiolysis and some anticonvulsant activity.
Triazolam, temazepam, nitrazepam, flutoprazepam, nimetazepam, flunitrazepam, and lormetazepam are strong BZ - 1 receptor (omega 1 receptor) agonists. BZ - 1 receptors mediate hypnotic effects, anxiolysis, powerful sedation, amnesia, anticonvulsant activity, euphoriant activity, motor-impairment, cognitive impairment, and ataxia.
However, ALL benzodiazepines have affinity to both omega 1 and omega 2 receptors and all benzos bind to both, just that some bind to BZ1 much more strongly (the hypnotics) and some bind more strongly to BZ2 (the anxiolytics).
The "Z" hypnotics are BZ1 or omega 1 selective, but they bind to a subgroup of the BZ1 (omega 1 receptors). They don't bind to what temazepam, flunitrazepam, nimetazepam, nitrazepam or flutoprazepam bind to - oh hell no!!