<http://en.wikipedia.org/wiki/Amisulpride#Pharmacology>
Now this is news to me.
"
Amisulpride functions primarily as a D2 and D3 receptor antagonist. It
has high affinity for these receptors with dissociation constants of 2.8
nM and 3.2 nM, respectively. Although standard doses in the 400 to 1200
mg a day range used to treat psychosis inhibit dopaminergic
neurotransmission, low doses in the 50 to 200 mg range preferentially
block inhibitory pre-synaptic autoreceptors. This results in a
facilitation of dopamine activity, and for this reason, low dose
amisulpride has also been used to treat clinical depression.
"
What a funky drug. In low doses it facilitates dopamine activity but in
high doses it inhibits it.
When major tranquilisers were first introduced the psychiatric community
thought they would increase levels of depression. I wonder if at the
time they even had a dopamine hypothesis or just guessed but based on a
different understanding, a truthful one that the drugs were just like a
chemical straitjacket (and produced a similar docility-inducing effect
to a lobotomy).
PErhaps I'm simplifying brain neurochemistry too much in assuming that
because this drug is used to treat clinical depression when it's used as
a dopamine facilitator the opposite effect which it produces when it's
used as a tranquiliser might cause depression. After all, it's a
serotonin hypothesis for depression and a dopamine one for psychosis
which justifies the entire biomedical model of treatment...but that
myth's been dispelled so many times now that it's not correct to call
mental illness an illness unless the use of words to describe things
unrelated to fundamental concepts is considered an acceptable use of
language.
Anyway, I'm sure I'm oversimplifying this but perhaps it's worth noting
that antipsychotics are now being used in the treatment of depression.
In America there are new drugs being licensed for treatment resistant
depression which combine antidepressants and antipsychotics in a single
pill. I don't know if it's antipsychotics used to promote dopamine or
inhibit dopamine which is how these new drugs attempt to work with
treatment resistant depression.
I just began taking amisulpride (50 mg) for depression 10 days ago (in addition to the Celexa and cymbalta I was already taking, but, I suspect, was no longer working).
ReplyDeleteThe positive effect was immediate. I have long suspected based on my experience with depression and the volumes of research I have done over the years, that the dopamine connection was the way to go (for me anyway).
Yet because amisulpride is an "anti-psychotic" I was so afraid of taking it after a bad experience with zyprexa years ago that it sat on my bedside table for a month before I decided trying it might be an alternative to suicide.
Clearly for many of us out here, dopamine is the missing ingredient. Why aren't the pharmaceutical houses on this big time? Too competitive with the SSRI's perhaps?
I've always been and always will be grateful to big pharma for saving my life more than once, but something is not right with this picture...
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Amisulpride is an interesting chemical. It works like an antipsychotic on dopamine receptors but it also works on serotonin receptors as well. I think at low levels the antipsychotic element is small.
ReplyDeleteI've never tried the drugs you're taking. I've taken high doses of Sodium Venlaflaxine. If it's treatment-resistant depression then that used to be the best. Google and you can find out more. It helps release the same neurotransmitter released by smoking as well as serotonin.
Antipsychotics in low doses are being combined with antidepressants for new ways to treat treatment-resistant depression. I was treated for bipolar and schizoaffective:bipolar type. I took high doses of antipsychotics, mood stabilisers and antidepressants for treatment resistant depression every day for a few years. I was too tired to kill myself. That's what the antipsychotics did. The antidepressant got me high and the mood stabiliser limited my emotional range.
These drugs took everything I valued and I found I could get better drugs. I use cannabis and alcohol. I've heard good reports about MDMA too. LSD is being experimented with at John Hopkins for the treatment of depression in terminal cancer. Ketamine is proving positive for depression in bipolar. Search the blog for links to the research.
Dopamine isn't the missing ingredient. The dopamine hypothesis is bollocks. Herbal cannabis with high CBD content performs as well as atypical antipsychotics but has a different neurochemical mechanism. They both chill people out though without sending them to sleep. Do you find you're a little bit more relaxed on the new drug?
Dopamine is also involved in creativity, having more sexual partners and schizotypy traits. Before the sexual revolution people considered having many sexual partners a good thing society changed. They used promiscuity as an unwritten diagnostic factor for schizophrenia. They still unofficially use it now. Dopamine is involved in all that too.
Sex and mental health have strong correlations. Basically sex releases endrophines - the same neurotransmitter released by chocolate, chillies and intense exercise. You might think it'll be a strange day when a doctor tells you to have sex to feel happier...but 200 years ago that's exactly what the did.
An official treatment for hysteria was a paroxial orgasm or some medical term like that. Basically doctors would masturbate their female patients to relieve the symptoms of hysteria. The vibrator was invented because doctors arms were getting tired. Seriously. It was a steam powered medical device to make women orgasm.
So there are many non-pharmacological or illegal pharmacology options too.
What's not right is your doctor isn't telling you that you're getting narcotics little different from the illegal ones. There's a new book called the Myth of the Chemical Cure.
What's also relevant is there are other things you can do to seek happiness. If you unmedicalise it you might be able to find better answers for yourself. It can take time but it's worth it.
Please, help me if you could. I have read that you know a lot about brain chemistry. Please help. I have some form of muscle atrophy. Sistemic, by me. Doctors dont know exactly. I was prescribed corticosteroids for some other disease and it was excellent for my muscles. I have no idea how it helps, but it does. Because of long taking of oral prednizone, I have a very bad depression. But, when I am taking antidepressants( zoloft, paroxetin, trazodone or any other my symptoms with muscles getting worse. Very, very bad. So, I found that corticosteroids making serotonin and dopamine level low, but antidepressants are making it higher. Something in between is struggle for my neurotransmitters among steroids and antidepressants and my musles go into atrophy very fast, even after 3 tablets! I know that amilsulprid in low doses reacts as antidepressant and I was presribed it but I didnt have courage to try it because of very bad atrophy( lungs are also affected). Here I ask, because of strange activity of amilsulprid, is it better for me to take higher or lower dose? Thank you very much for any answer, I am desperate
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ReplyDelete