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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 5 of 5. This is the beginning of the thread.
Posted by turalizz on August 2, 2002, at 15:53:44
Posted by Squiggles on August 2, 2002, at 16:47:02
In reply to Dopaminergic Mechanisms in Depression and Mania, posted by turalizz on August 2, 2002, at 15:53:44
Is DA dopaminergic? I am sorry but i'm
very bad with medical acronyms.tx
Squiggles
Posted by Chloe on August 2, 2002, at 20:48:58
In reply to Re: Dopaminergic Mechanisms in Depression and Mania » turalizz, posted by Squiggles on August 2, 2002, at 16:47:02
> Is DA dopaminergic? I am sorry but i'm
> very bad with medical acronyms.
>
> tx
>
> SquigglesHi Squiggles,
DA=dopamine antagonistHope you are feeling better...
Chloe
Posted by Shawn. T. on August 3, 2002, at 3:30:16
In reply to Dopaminergic Mechanisms in Depression and Mania, posted by turalizz on August 2, 2002, at 15:53:44
DA stands for dopamine. I believe that it is important to note that a very wide range of neurotransmitters and other substances play a role in depression. To argue that one particular system in the body is unaffected by changes in other systems is a losing cause. Depression is so difficult to pin down because it really involves such a wide range of systems within both the brain and body. Environmental factors can also play a powerful role. If I were so inclined, I could make a very strong case for a role for both acetycholine and its receptors (both nicotinic and muscarinic) in depression, mania, and anxiety disorders. An additional example is that a substance P inhibitor can relieve depressive symptoms in some people, although that does not signal that substance P plays a primary role in depression.
My personal definition of depression is that it is a state of enhanced immune function and decreased ability to experience pleasure (anhedonia) in response to chronic stress, either internal or external, that has any number of effects on both the brain and body. The realm of the internal can include sickness, injury, and a wide range of other factors. External issues can include any effects that an environment has upon a person. Internal and external issues may overlap; the world of depression is certainly not black and white.
While reductionism has resulted in a diverse set of more and more focused explanations of depression, its results considered by themselves are ultimately unable to paint an entire portrait of a depressed individual. One must take note of systems within the body and brain on many different levels, ionic, molecular, hormonal, immunological, and tissular. That list does not even encompass anything close to the number of factors that must be taken into account. Interdisciplinary approaches have begun to be the norm in many scientific fields; I cannot see why this should not be so in the field of medicine. Only after looking at the issue of depression from a series of different angles can a person begin to understand exactly what effects an antidepressant or therapeutical approach should have. Not even then is it possible to suggest a certain approach that will work best for everyone.
My personal suggestion is that a 5-HT-moduline antibody would be a more ideal antidepressant. I am aware, however, that such a drug would not be ideal for everyone. Some people, such as those who have a form of cancer, would not want to take a drug that decreases immune system function. Someone that has multiple sclerosis or an autoimmune disorder, however, would be more likely to benefit from a drug that suppresses certain functions of the immune system. Note that a number of antidepressant options with a wide range of immunological and analgesic effects are currently available. A broad consideration for health, mindset, and social factors will have to be taken under account if and when there comes a day when a person or team of people has a number of optimized pharmacological or therapeutical options available.
I'm currently trying to relate my ideas on the effects of 5-HT-moduline to the effects that it has upon immune system function. I am definitely of the opinion that many present and future antidepressant drugs will be someday used for much more than treating major depression or anxiety disorders. Some, of course, already are being used to treat other health problems, but I often find that they cause a broad set of other health problems unrelated to the one under treatment consideration.
Anyone that is interested in learning about depression from a viewpoint that is not overwhelmingly concerned with neurotransmitter functions will likely want to check out some of Dr. Bruce Charlton's work involving depression. Interestingly enough, his views often coincide with the ones that I have developed while trying to figure out depression from a mostly neurotransmitter biased approach.
http://www.hedweb.com/bgcharlton/
I'll go ahead and post a rough framework of ideas that I would like to further develop regarding a link between neurotransmitter function and immune system function. I believe that the ideas that I have previously posted regarding 5-HT-moduline along with the following information should help to illuminate the connection between depression and the sickness behavior that Dr. Charlton describes.My explanation of the link between antidepressants and cytokines is that antidepressant drugs increase activation of 5-HT2 serotonergic receptors, which results in an increase in cortisol secretion (Maes and Meltzer 1995). Initially (in a stress free individual at time T = 0), cortisol seems to inhibit the excretion of certain cytokines. After perhaps three weeks of chronic unpredictable stress, increased levels of cortisol will have led to cells more resistant to the inhibitory effects of glucocorticoids on the immune system. At this time, the 5-HT2 receptors will have become less sensitive, and a decrease in cortisol secretion should occur. Thus, after 3 weeks or so, the body will experience a sharp increase in immune function.
Here is some information on the relation between cytokines and depression: http://users.skynet.be/crc.mh/hottopics2.html
Furthermore, SSRI's potentiate the effects of 5-HT upon cortisol levels: http://www4.infotrieve.com/newmedline/detail.asp?NameID=9534832&loggedusing=M&Session=&SearchQuery=cortisol+and+ssri&count=12
For information on the relation to cytokines, see
http://biopsychiatry.com/immunesystem/index.html
The following link illustrates the link between stress and cytokines:
http://www.marquiswhoswho.net/MMAES/myimages/PLOTNI.pdf
Shawn
Posted by turalizz on August 3, 2002, at 4:06:26
In reply to Re: Dopaminergic Mechanisms in Depression and Mania » turalizz, posted by Squiggles on August 2, 2002, at 16:47:02
> Is DA dopaminergic? I am sorry but i'm
> very bad with medical acronyms.
>
> tx
>
> SquigglesHi Squiggles,
DA = Dopamine
NE = Noradrenaline = Norepinephrine
5-HT = Serotonin
This is the end of the thread.
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