I had a haircut today. The lady that cut my hair said that she started to come off antidepressants a couple of weeks ago. She halved the dose but had bad withdrawal symptoms. Her doctor said to stop them outright as there will be repercussions anyway so just go the whole hog.

She seemed so much happier than I've seen her over the last couple of years.

I don't know what the medication was, as I felt it might be too intrusive to ask.

Whatever, did they work? Was it time for her to resume her "native" serotonin again? Did the treatment leave her with elevated serotonin levels? What about the length of treatment anyway? Are there long term treatment scenarios in patients that could be terminated but aren't? What about side-effects versus benefits? ... What's going on? ...

It's good to know that she can quit and be happy. I would have assumed, knowing the pharmaceutical companies, that there would be hell to pay.

several sites cover this topic eg....
http://bjp.rcpsych.org/cgi/reprint/179/42/s4.pdf

I have been taking AD's for 19 years now adn haevt'n scene ayn bda seid efex.

I think that odd cases of unsuspected experiences will always arise and think that, in any case, attempts to manage without medication should be tried perhaps every 6 months under the GP's control (usually with a gradual removal of the drugs).

too bad that most people wont follow the regimen the way it's directed.

realistically, the reason why drug companies profit so much is because there is no follow-through...either on the side of the patient or the provider.

not everyone who needs help has access to reliable treatment because of financial status or health coverage or ignorance.

it's just my opinion that a majority of people seeking help through antidepressants won't get the correct treatment, and there are plenty of ways to function efficiently without that route.

if one cares to know, I believe the goal of the regimen is to initiate personal choice....and I'd be willing to prove it if anyone disagrees

you are totally wrong, "antidepressants" have never helped any true-depressive no matter what way they are used, after no matter how many years, after no matter what combinations. I got out of bed at 7:00 PM today. I had 11 doctors over 14 years. Following "regimens" does not work at all and never has. I have never once gotten any relief from any "antidepressant", save for dozens of stablon tablets having a MINIMAL effect that allows me to leave my home for a bit but still not do much in pain and suffering. No one else like me has ever gotten any help from any medical establishment but there is a black-out on this and people with Pseudo-depression are covered instead, because going from 'feeling fine and cocky', to feeling 'fine and cocky' (no change) can be lied about as "the drugs worked".

no doubt that it won't work for everyone.
i was referring to how much money is really made off of the way the medical system is set up(especially in the context of anti-depressants).

the way things are going, i hope that things are developed for those who are in more extreme conditions.

they dont work for anyone with real depression, just a placebo effect on false depression thats then reported as a percentage success rat. the real rate is zero, just like aspirin would help zero percent of people with a ruptured spinal disc.

I sympathise with your condition.

I wondered if you could provide a list of all depression patients and the medication they are/were on so that I could appraise their situation. As your statement suggests you know them all I thought it might be good to take advantage of your insights.

Tone does not apparently have depression, or maybe he has not tried the right antidepressant yet. (I tried about 15). They certainly changed my life significantly!!

New research reports a better understanding of how AD's work - at least some of them.....

http://www.physorg.com/news185727145.html

Nope, people don't really have any idea how this shit actually works. No one knows how consciousness works, so knowing how monoamines function in perception is not possible. Look, in the not so near future, for a new class of antidepressants that act on VMAT rather than the traditional reuptake route. The preliminary work is showing lots of promise for antidepressant treatment, and Parkinson's treatment as well.

Why would you consider vesicular monoamine transporter modifiers to be superior in vivo to any other antidepressants?

Is all of this because you are a reserpine fan? It of course is known as a VMAT inhibitor.

Why would you target reuptake? Just a different way to impact neurotransmitter release. There are basically 3 different neurotransmitter pools, and changing concentrations in the different pools can have a significant impact. For Parkinson's it is thought that a part of the problem is that dopamine is oxidized in the cytoplasm, so getting more dopamine into vesicles prevents this oxidation from taking place. The idea is actually almost the exact opposite of Reserpine, which causes an assload of problems, because neurotransmitters need to be packaged in order to be released. Reserpine follows the same line of thinking as the other forms of treatment--to inhibit.

A major advantage of this system over targeting reuptake, is to target specific modalities of release (synaptic vesicles vs. large dense core vesicles). Another advantage, is that rather than inhibiting like MAOIs SSRIs etc. you are optimizing efficiency. If someone is deficient in serotonin, it doesn't make sense to me to inhibit the patients body further, but rather to enhance.

You'll have to explain the mechanisms underlying the modification of VMAT physiology more clearly for the antidepressant effect that you think are so advantageous. I don't see enough info from you on the various affected transmitters and their modulation mechanisms (specifically for the antidepressant application). And also, what do you think about the side-effects, bearing in mind that the previous, OK inhibitory, VMAT modulators had catastrophic side-effects and issues, as Ernest Hemingway's curtailed genius demonstrates. (Hint: an historical perspective could be worth investigating for any so-called 'new' drug or drug category).

What are the physiological bases for clinical depression, in your opinion?

I don't think anyone knows the physiological bases for clinical depression--I certainly don't. I just happen to know this is a project that is being worked on because Kantz is a professor of mine. As far as side effects, that has to be explored. This is a new novel approach. The side effects will be nothing like Reserpine, because that type of drug functions in a completely different direction. Of course blocking neurotransmitters from entering vesicles is going to cause serious problems; this means they can never be released. Increasing the efficiency of VMAT means that you can get more neurotransmitter release (proven in fruit flies) when the body wants to release it, as opposed to reuptake in which you keep the transmitter in the synapse longer than it normally would be, which could potentially impact timing of transmission.

http://www.ncbi.nlm.nih.gov/pubmed/1850781...m&ordinalpos=13

http://www.ncbi.nlm.nih.gov/pubmed/2005398...um&ordinalpos=2

http://www.ncbi.nlm.nih.gov/pubmed/1076903...ogdbfrom=pubmed

This is a really interesting discussion friend, but I can't respond any further tonight. I just thought I'd let you know in case you thought you'd convinced me!

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