Tricyclic Antidepressants

Immune system vs bipolar disorder

Question:

Addendum:  I think psychologically seeing what it meant to be "hospitalized" made me realized that I want to avoid that place like the plague again. This may have had the indirect effect of strengthing my immune system to prevent me from a physical illness causing me to  wind up there again. -Rob

– Hide quoted text — Show quoted text -> I used to get sick a lot. > Then I had my first hospitalization for bipolar in 1996. > Since then, I don’t think I’ve even had a fever.  That’s more than 4 years, > when I often became sick for at least 1 week (about 4-5 days) a year. > Does that say anything significant?  I’m not sure, but it is interesting.. > I’ve never given it serious consideration. > -Rob > > I’m a newcomer on this site. can anyone direct me to some information on > the > > relation between manic depression and the immune system. > I was having a problem with a staph infection that had flared up for years > and had my immune system fully *tested*…… it turns out I have a hell > of > an immune system! > Hope it helps… at least comparatively….. > EileenB

Response:

I’m not sure I’ve seen anything on Manic Depression specifically, but I know that depression (and hence the depression side of manic depression) can certainly weaken your immune system. One good website for all sorts of information on Bipolar (including links to hundreds of related sites) is http://bipolar.about.com -Rob

– Hide quoted text — Show quoted text -> I’m a newcomer on this site. can anyone direct me to some information on the > relation between manic depression and the immune system.

Response:

> I’m a newcomer on this site. can anyone direct me to some information on the > relation between manic depression and the immune system.

I was having a problem with a staph infection that had flared up for years and had my immune system fully *tested*…… it turns out I have a hell of an immune system! Hope it helps… at least comparatively….. EileenB

Response:

>the depression side of manic depression)

What does the manic side do to the immune system?  I had a rash disappear when h-manic in 1994 Ralph V. Dammit Jim, I’m a Bike Courier, not a Doctor

Response:

Hi, Pierre… Just passing through here myself. I have a whole catalogue of mental/psychological symptoms:  bi-polar, depression, anxiety, panic, ADHD, obsessive-compulsive, chronic fatigue, brain fag, brain fog, short and long term memory loss, loss of comprehension…have I missed anything? I get these symptoms upon exposure to chemicals in the air and a number of foods.  (Suicidal depression with just a taste of wheat, brain fog, neurotic upon exposure to auto exhaust, psychotic ranting with exposure to combustion products of natural gas–and it goes on and on and on and on.) I’m moving shortly to a country with clean air…!? I have been symptom-free.  It’s possible (at least for me)(and others, I am sure but I’m not going to preach {too much}). I wonder how many of us here have concommitant problems with allergies and sensitivities and immune system disorder?  Raise your hands!  Yes, you in the back hiding under the chair, too…. How about seasonal ebb and flow of symptoms? TM Check out the case studies in this book which is probably available in the library: An Alternatative Approach to Allergies Theron G. Randolph, M.D. & Ralph W. Moss, Ph.D. > I’m a newcomer on this site. can anyone direct me to some information on > the > relation between manic depression and the immune system. mune system!

Before you buy.

Response:

>the depression side of manic depression) > What does the manic side do to the immune system?  I had a rash disappear when > h-manic in 1994 > Ralph V.

in brief, mania is associated with higher than normal levels of adrenaline (norepinephrine and epinepinephrine).  In prescription form, epinephrine is given for allergic/immune reactions which might be severe enough to require an emergency room visit (ex bad reactions to bee stings).  I;ve noticed personally, that my allergies (and pain, for that matter) improve when I;m manic.  regards, julie

Response:

I used to get sick a lot. Then I had my first hospitalization for bipolar in 1996. Since then, I don’t think I’ve even had a fever.  That’s more than 4 years, when I often became sick for at least 1 week (about 4-5 days) a year. Does that say anything significant?  I’m not sure, but it is interesting.. I’ve never given it serious consideration. -Rob

– Hide quoted text — Show quoted text -> I’m a newcomer on this site. can anyone direct me to some information on > the > relation between manic depression and the immune system. > I was having a problem with a staph infection that had flared up for years > and had my immune system fully *tested*…… it turns out I have a hell of > an immune system! > Hope it helps… at least comparatively….. > EileenB

Response:

I’m a newcomer on this site. can anyone direct me to some information on the relation between manic depression and the immune system.

Response:

Hi Pierre, Welcome to ASDM. Here is what I found using Metacrawler. > I’m a newcomer on this site. can anyone direct me to some information on the > relation between manic depression and the immune system.

DEPRESSION AND THE IMMUNE SYSTEM http://sulcus.berkeley.edu/mcb165/mcb165sp98tPaper/mcb165sp98R.manuscrip t/_38.html Category: Neurochemistry Term Paper Code: 38 Abstract Depression affects the human body in more than one way. Its physiological effects can be seen in the depressive moods of the person. A general sense of apathy is observed. However, depression more than just affects moods; it also affects the human immune system. The neurotranmsitters responsible for the psychological aspects of depression also exert a physical effect by influencing the endocrine system in the body. These two systems then combine their efforts and modify the immune system. People suffering from depression almost always suffer from some other disease, such as colds. These people are more susceptible to diseases because depression lowered their immune system’s ability to combat the illness. Since the beginning of civilization, depression has plagued the human population. Countless literary classics, art works, and musical masterpieces reflect the artists’ own private battles with one of the major psychiatric disorders of modern times: depression. The Greek physician Galen recorded more than 2000 years ago that people suffering from depression were more susceptible to cancer. However, until recently, depression is not recognized as a psychiatric disorder. With its widespread occurrences in the population, depression is often looked upon as a part of the life experience. Though many experience every once a while depression symptoms such as unhappy mood, hopelessness, loss of energy, weight loss, irregular sleep pattern, and decreased appetite, some experience these symptoms with cyclic regularity. These people are clinically diagnosed as possessing depression as a psychiatric disorder, either as unipolar depression or bipolar illness. For the rest of the population with depression, though the disorder many not impair daily life as much as clinical depression, it handicaps daily life in a more subtle fashion. People in depression have weaker immune systems, allowing them to be susceptible to diseases that their immune systems can normally defeat. For example, college students during periods of final exam often are more likely to catch colds or flu. The lower immunity for disease is undoubtably due to the stress of the bombardment of exams, which has similar effects to depression. The mental state of a being can directly affect his immune system; the brain or the central nervous system (CNS) control the release of hormones, which then act upon the immune system. To understand the exact pathway of how a mental or emotional state such as depression can alter the immune system, the hormone releasing mechanisms and the immune system must be examined along with the neuropathways of depression itself. Depression is an affective disorder that is thought to relate to the functioning of the monoamines, especially serotonin and norepinephrine. There are several hypothesis to the development of depression. The catecholamine hypothesis of affective disorders states that such disorders result from decreased norepinephrine levels. The first generation antidepressants were monoamine oxidase inhibitors and tricyclics. Monoamine oxidases are enzymes which break down monoamines such as norepinephrine, serotonin, and dopamine. With this enzyme blocked, these neurotransmitters will not be metabolized when released into the synpase. Over time, the neurotransmitters will accumulate and increase firing at the monoamine synapses. Tricyclics work in the same fashion as the stimulant cocaine. It prevent the reabsorption of monoamines after they have been released into the synapse. The tricyclics are more selective than MAO inhibitors. They are more effective in increasing norepinephrine levels. Despite their effectiveness in treating depression, MAOIs and tricyclics both have some unwanted side effects. Monoamine oxidase not only destroys monoamines, but also other substances in food such as tyramine. Accumulation of tyramine in the body can cause high blood pressure, headaches, and internal bleeding, leading to stroke or death. Tricyclics block transmission at cholinergic synapses, thus causing anticholinergic effects. These unwanted side effects encouraged the finding of the second generation antidepressants. The drug reserpine depletes monoamines from the brain and causes severe depression. Stimulants, MAO inhibitors, and tricyclics all increase catecholamines and alleviate depression, even inducing some mania. Using these two pieces of data, depression was thought to develop as a result of low levels of monoamines in the synapses. However, tests soon showed that though all three monoamines are involved in mood, serotonin is actually the major neurotransmitter responsible for major depression. This is evident since treatments that effectively relieve depression symptoms have all been shown to change transmission at serotonin synapses. However, this does not indicate that other neurotransmitters are not involved since increase in serotonin levels is know to affect other neurotransmitter levels. For example, low levels of serotonin might lead to lower levels of norepinephrine, making it hard to distinguish which neurotransmitter is actually more responsible for the symptoms of depression. The serotonin hypothesis of depression now states that depression develops mainly as result of low levels of serotonin. In order to treat depression, selective serotonin reuptake inhibitors, or SSRIs, are used in place of monoamine oxidase inhibitors or tricyclics. These drugs are employed to block the reuptake of serotonin at synapses, thus prolonging the availability of serotonin at the synapses. As the reuptake mechanisms are blocked, the level of serotonin at the synapses eventually accumulate and reverse the symptoms of depression. SSRIs are discovered to work only after about two weeks of lag time. This is thought to due to the down-regulation, or reduction, of receptors. It is thought that one of the causes of depression is the oversensitivity of monoamine receptors. Antidepressants might work by reducing the supersensitivity of the receptors by causing down-regulation. Another explanation for why increased levels of serotonin do not cause immediate increase in firing at the synapse is that serotonin synapses may have autoreceptors. When these autoreceptors detect excessive amounts of serotonin, they inhibit the release of more serotonin. Therefore, when SSRIs are first used, these autoreceptors have not yet adjust to the increased amount of serotonin at the synapses. They then naturally prevent more release of serotonin. It is only when these autoreceptors have adapted to the increased levels of serotonin at the synpase that they allow more serotonin to be released. Despite the strong evidence of the serotonin hypothesis, depression may have other causes. The neuroendochrinological hypothesis suggests that circadian cortisol levels may induce depression. According to the hypothesis, the hypothamlamic-pituitary-adrenal cortex may be hyperactive in depressives. Increased levels of cortisol is correlated with depression. Depressives increase their release of ACTH. Since hormones play an important role in the body’s immune system, the increase of ACTH due to depression associates depression with the body’s immune system. The hypothalamus-pituitary-adrenal axis is one of the major hormone systems, or endocrine pathways, involved in depression. The hypothalamus is a region in lower brain which receives information from other parts of the brain and then initiates an endocrine response. The hypothalamus integrates signals from the nervous system with the endocrine system. It contains hormone-releasing cells, which are neurons that release hormones into the blood stream. There are two types of hormone-releasing cell: one releases hormones of the posterior pituitary gland while the other produces releasing hormones that promotes hormone release in the anterior pituitary gland. The pituitary gland is a small gland near the hypothalamus. It is regulated by the hormones of the hypothalamus. While the posterior pituitary gland releases such hormones as oxytocin, a milk-production stimulating hormone, the anterior pituitary gland produces the hormone that is most associated with stress and depression: adrenocorticotropin or ACTH. ACTH is a peptide hormone which stimulates the adrenal cortex to release steroid hormones such as glucocorticoids. While steroid hormones are able to pass through the hydrophobic cell membrane with ease to pass on the chemical signal, peptide hormones such as ACTH can not. They must bind to specific surface receptors on the cell surface in order to activate a second messenger pathway. The receptors they activate actually have enzymatic activity on the cytoplasmic side. They activate another protein called G-protein by exchanging the guanosine diphosphate (GDP) bound on the protein for guanosine triphosphate (GTP). Once the G-protein binds to GTP, its catalytic alpha-subunit dissociates from the beta and gamma regulatory subunits and diffuses laterally across the plasma membrane to activate another enzyme called adenylate cyclase. Adenylate cyclase in turn catalyzes the reaction of converting adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). Cyclic AMP goes on to activate translation factors which initiates translation of certain genes. It is by this pathway that ACTH stimulates the cells of the adrenal cortex to synthesize and secrete corticosteroids such as glucocorticoids. High … read more »

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