Doctors/anyone please... Testosterone and neurotranmitters

[T Man]

My Doctors at a very good research University for Anxiety and mood disorders are asking for your inputs. They are requesting any information on Testosterone use and Neurotransmitter response. Or I should say overuse/abuse of Testosterone/Anabolic hormones. Papers or studies etc.

What is and how are Neurotransmitters affected by Testosterone usage? By this we mean is Dopamine primarily elevated by T or is there others at play also. We are trying to figure out why Testosterone would aggravate anxiety and by what mechanism. I am currently using Remeron which is a SSNRI.

As Dr John knows, (hello) last year I came off a mixed cycle of Test and Anabolics and all hell broke loose with me. My system at the moment will not tolerate any more than a 2.5 mg Androderm patch a day, which puts me at just about 400 ng/dl at 10 am. When I try to increase by even very small amounts I get hyper and anxiety sets in. My Docs just want to get me up in the high normal range for better mood and energy. I fatigue very easily after coming off of this cycle. It really had lasting effects on my hormone/brain chemistry. Any help would greatly be appreciated.

 

[T Man]

Sorry for the typo in the heading..... should be "Neurotransmitters".... Input or experiences would be appreciated. Thanks

 

[marianco]

Speculation (in reality the situation is even more complex and I continue to research the matter):
1. Testosterone can increase dopamine levels in the brain.
2. Increasing dopamine levels may reduce serotonin levels - since their production is inversely related.
3. Serotonin help reduce perceived stress and helps reduce anxiety symptoms.
4. Reduction in serotonin level may increase the likelihood of perceived stress and anxiety.
5. Increased perceived stress and anxiety may cause the brain to increase Adrenocorticotropic Hormone (ACTH) release.
6. The ACTH signal is received by the adrenal glands, which in turn starts the stress response (including increasing cortisol, norepinephrine, epinephrine production, among the 50 hormones produced by the adrenals).
7. Increased perceived stress may activate the sympathetic nervous system, which then increases output of norepinephrine from the brain as part of the fight-or-flight reaction.
8. Increased testosterone may also lead to aromatization of testosterone to estradiol/estrone (estrogens).
9. Estrogens have multiple effects including behavioral effects such as increasing anxiety, irritability, hyperactivity and aggression.
10. Estrogen increases the expression of receptors and other associated proteins for neurotransmitters including serotonin, norepinephrine, and dopamine.
11. Reduction in serotonin level from increased dopamine levels may affect thyroid hormone conversion in the liver from T4 to T3 via the cytochrome P450 2D6 enzyme.
12. Reduction in active thyroid hormone may destabilize mood - perhaps contribute to anxiety, hyperactivity
13. Estrogen itself may compete with thyroid hormone at the thyroid hormone receptor site - creating a virtual hypothyroid state - perhaps also contributing to anxiety - despite normal thyroid hormone levels.
14. Remeron's mechanism of action includes increasing serotonin release, increasing norepinephrine release (at higher doses), and by blocking histamine receptors (accounting for sleepiness and weight gain at lower doses).
15. Remeron, in my experience, does not work well to reduce anxiety.
16. Increased norepinephrine levels from Remeron makes a person more likely to have anxiety when norepinephrine is further increased and serotonin decreased - from other causes - such as those written above.
17. The higher the dose of Remeron, the higher the increase in norepinephrine, the higher the likelihood of anxiety.
18. One of testosterone's functions is to reduce stress by reducing ACTH production from the brain and by directly reducing adrenal gland hormone production (i.e. reducing cortisol production).
19. Should the adrenal gland, from long term exposure to anabolic steriods, become tolerant to the effects of testosterone, testosterone may not be able to reduce stress and anxiety.
20. Adrenal insufficiency may occur from long term anabolic steriod use - where the adrenals cannot make adequate cortisol and other hormones as needed when stressed to handle stress.
21. Adrenal insufficiency/fatigue results in intolerance of stress, fatigue, chronic sleepiness, irritability, anxiety.
22. Tolerance to testosterone's effects in the brain may occur with long term anabolic steriod use.
23. Testosterone usually has a calming effect. This may not occur if tolerance occurs to testosterone.
24. With adrenal fatigue, progesterone levels are reduced.
25. Progesterone is being shunted to create more cortisol in adrenal fatigue.
26. Progesterone has a mood stabilizing, calming, antidepressant, sleep-promoting effects through several mechanisms of action.
27. Progesterone increases seroronin, norepinephrine, GABA, dopamine activity in the brain. Progesterone blocks NMDA Glutamate receptors. Progesterone promotes myelination of nerves to improve signal transmission. Progesterone increases Estrogen receptor sensitivity. Progesterone promotes thyroid hormone activity.
28. Low progesterone levels may lead to increased anxiety, insomnia, tension, and mood instability.
29. Low testosterone levels and high cortisol levels (as a result), may lead to insulin resistance.
30. Insulin resistance not only predisposes one to diabetes, it impairs neuron signal transmission, and directly reduces testosterone production.
31. Insulin resistance may increase the likelihood of mood instability, anxiety, depression.
32. A serotonin-reuptake inhibitor (a group of medications with many members) increases serotonin more specifically than other effects.
33. Increasing serotonin has a calming effect.
33. Increasing serotonin excessively, however, causes a reduction in dopamine production.
34. Excessive serotonin, and subsequent reduction in dopamine causes a motor movement disorder called akathisia.
35. Akathisia has symptoms including anxiety, panic attacks, insomnia, irritability, restlessness, hyperactivity, agitation (to the point of suicide attempts by some people).
36. When attempting to balance or optimize the effects of one hormone/neurotransmitter, one may have to balance or optmize the effects of others to obtain the desired state. Testosterone, Estrogen, Progesterone, Cortisol, Insulin, Thyroid Hormone, Dihydrotestosterone, the metabolites of progesterone, Norepinephrine, Epinephrine, Serotonin, Dopamine, GABA (gamma amino butyric acid), Glutamate, Histamine, etc. are highly interlinked in their effects - with the endpoint of allowing a person to maintain balance between health and the stress the person faces.

 

[HeadDoc]

succinct and informative. Thank you.

 

[T Man]

I can't thank you enough for your insight and info. This is a must read for everyone!

 

[rocintl]

Very useful. Thank you!

 

[marianco]

I read your fantasic reply about T and neurotransmitters. You mentioned that Remeron was not good for anxiety. It seems that I can't tolerate SSRI's. They activate me and aggravate my anxiety/panic. Especially prozac and celexa. Zoloft gave me anxiety attacks after only a few days. Paxil made me get the shakes after a week. Also got the zaps when I went off the very low dose of 5 mgs. Remeron @ 7.5mg is having some calming affects on my GAD compared to before taking it. It has also helped my depression after crashing from the anabolic cycle last year. I am very sensitive to all medications and usually need to take low doses.

In your opinion what is a safe alternative route? For now The Univ Docs want me to stay on the Remeron and try Buspar with it. They really want me to take .5 Klonopin daily. But, I am fighting them on this because addictions run in my family and I am afraid of possible long term side effects. Am I being foolish and misinformed about Klonopin? I use .25mg of Klonopin 1 or 2 times a week sometimes less as needed.

They also mentioned Nardil which I really want to avoid. That seems like scary stuff with all its restrictions and side effects.

The Docs at the Univ don't want to touch the Endocronology issues. They want to only address the anxiety disorder and let my Endo treat the pituitary problem with HRT. My Endo's listen but know much about HRT or anxiety issues.

Any thoughts would be greatly appreciated.

Its interesting to me, as I have become more adept at psychiatric neuroendocrinology - the branch of psychiatry I am currently developing intensely, how much each specialty has deliberately limited their knowledge and abilities - each specialty is an island - with the consequence of promoting chronic illness and partial responses to treatment.

Off my soapbox,...

At a very low dose, the bulk of Remeron's effect is due to its ability to block histamine receptors (an antihistamine effect) - which causes sedation, reduction in anxiety, and increase in appetite. This becomes outweighed at higher doses by its ability to increase serotonin, then at even higher doses, its ability to increase norepinephrine. Antihistamines (such as Vistaril) have been used as mild anxiolytic medications. They are limited because at high doses they cause oversedation. Many also have an anticholinergic effect - which can increase dopamine, but if dosed too high can cause an agitated confused state, as well as a potentially fatal irregular heart beat - thus the clinician has to be careful.

Serotonin Reuptake Inhibitors (SSRIs - such as Prozac, Paxil, Zoloft, Luvox, Celexa, and Lexapro) simultaneously reduce dopamine levels while increasing serotonin levels. The reduced dopamine levels (depending on the person's genetic predisposition), cause a mental/motor movement disorder called Akathisia. Akathisia at the extreme causes severe agitation, a high distress level that makes someone want to jump out of their skin. Some people end up committing suicide as a result. At lower levels, akathisia can manifest as panic attacks, irritability, anxiety, insomnia, physical discomfort that causes people to move frequently - e.g. to pace, squirm in their seats, toss and turn in bed.

Besides increasing serotonin and blocking histamine, other psychiatric medication mechanisms of action which may reduce anxiety include:
1. increasing GABA (e.g. benzodiazepines or some anticonvulsants),
2. blocking norepinephrine (e.g. beta-blockers such as propranolol or atenolol),
3. reducing norepinephrine output (e.g. alpha-2 adrenergic blockers such as clonidine or tenex).
4. increasing dopamine in the frontal cortex, reduction of dopamine in limbic system (e.g. low dose antipsychotic medications - an old tactic, though with many side effects)
5. The anticonvulsants have numerous mechanisms of action - too numerous to list. They, in general, are useful options for reducing anxiety. Except for Depakote, Gabapentin, and Zonegran, the other anticonvulsants, however, speed up the liver and reduce levels of progesterone, possibly the other steroid hormones, thus complicating birth control - and hormone replacement therapy. This needs to be taken into account and appropriate adjustment made (e.g. raising hormone dose) when the anticonvulsants and hormones are used together.

Additionally, depending on the person and the deficiency involved, restoring activity of testosterone, progesterone, estrogen, and thyroid hormone (all of which affect neurotransmitter activities through various mechanisms) can reduce anxiety.

Some supplements such as Valerian, theanine also affect GABA and other neurotransmitters in reducing anxiety. Theanine (extracted from green tea) is particularly useful since it doesn't have a sedative effect, though it appears to work at least by increasing GABA production in the brain - thus promoting a calm wakefulness.

When a person is afraid of addiction, I usually explain the difference between "addiction" and "dependence". Dependence happens with all substances when used for a long time. The body develops a partial opposing force/activity to the substance which becomes uncovered when the substance is abruptly stopped. Dependence even happens with aspirin - causing a withdrawal migraine. In short, dependence is the presence of a potential withdrawal effect from the use of a substance. When a medication is effective in improving a person's ability to function (such as the medical use of a substance), I do not consider it addiction. Addiction is quite different. Addiction is the non-medical use of a substance, which results in the development of impairment in function. Impairment in function is the important concept.

Aside from hormone treatment, the most effective medications (for their indications) in psychiatry are the stimulants and the benzodiazepines. Despite years of drug company ads touting the effectiveness of serotonergic medications for anxiety and the stigma of their potential for addiction and dependence, the benzodiazepines are still the most used subtances for the treatment of anxiety. For good reason - they work more often than not. Long term use of benzodiazepines is possible because full tolerance does not develop - there is still a residual effect which may be enough for the patient to adequately reduce anxiety.

Klonopin is generally safe for long-term use. However, I generally check the liver (liver function panel) twice a year to reduce the risk of developing liver inflammation - a fairly rare event. In more than 16 years of experience with the use of benzodiazepines in the treatment of anxiety, I have had to stop Klonopin twice and Ativan once due to the development of liver enzyme elevations. The primary long-term problem with benzodiazepines, particularly the longer-acting ones is that metabolism slows as we age. Thus, some benzodiazepines (such as Valium), end up lasting for days, effectively saucing the brain, reducing cognitive functioning. This can be treated by reducing the dose or shifting to a shorter acting medication (which is longer acting in a senior citizen).

I rarely use MAOIs these days. They primarily act by increasing serotonin. But the Serotonin reuptake inhibitors are safer - having much fewer interactions with foods and other rmedications. I keep them as an option when other medications fail - particularly for depression.

Tricyclic antidepressants - which work by increasing serotonin and norepinephrine and by blocking histamine - are useful for treating anxiety. They are limited by weight gain, oversedation, anticholinergic side effects. I avoid them in potentially suicidal patients since they are the most lethal medications I prescribe, when in overdose.

 

[bullmastiff]

Testosterone and Neurotransmitters- Parnate

I realize the short comings of Maois with their drug interactions and dietary
restrictions. However I've heard some good things about the effectiveness of parnate (maoi) on another board. It increases Dopamine quite a bit in addition to serotonin and norepenephrine. So you get a balance of all the neurotransmitters. Therefore you tend not to get a decrease in testosterone and one male on it said his went up quite a bit while on it. Also many patients report an increase in libido while on it as opposed to the decrease which is very common on the ssris. They're coming out with a selegeline patch soon which may alleviate some of the dietary retrictions of the other maois. The patch will be in doses that will inhibit both mao-a and mao-b like the traditionsl maois.

 

[Sonny]

Lithium's mechanism of action?

marianco: How does lithium work to augment the effect of antidepressants? Over the years, I have seen this strategy commonly used in treatment resistant cases.

Lithium has been useful to me as an anxiety medication. It does not "hit" with the same intensity as a benzo...it's a lot more subtle, but very effective and it's long-term efficacy has been excellent for me.

IMO, lithium is about as "natural" as you can go in terms of psychiatric medicine. It is an element already found in your body. Throughout history, civilizations that consumed trace amounts of lithium (usually in water) had far lower occurrences of mental distress.

Cheers,
Sonny

 

[marianco]

Re: Lithium's mechanism of action?

marianco: How does lithium work to augment the effect of antidepressants? Over the years, I have seen this strategy commonly used in treatment resistant cases.

Lithium has been useful to me as an anxiety medication. It does not "hit" with the same intensity as a benzo...it's a lot more subtle, but very effective and it's long-term efficacy has been excellent for me.

IMO, lithium is about as "natural" as you can go in terms of psychiatric medicine. It is an element already found in your body. Throughout history, civilizations that consumed trace amounts of lithium (usually in water) had far lower occurrences of mental distress.

Lithium and other mood stabilizing medications have extremely complex mechanisms of action. One result is to increase serotonin levels - which may have an anxiolytic effect.

Mechanisms of action for Lithium include:
1. Stabilization of the inactive conformation of G-Protein
2. Inhibition of Adenylate Cyclase
3. Up-regulation of some Adenylate Cyclase subtypes
4. Uncompetitive inhibition of inositol-1-phosphatase - leading to a reduction in neuronal myo-inositol levels.
5. Supressing the phophatidyl inositol pathway
6. Reduction of Protein Kinase C activity by down-regulating selective PKC isozymes
7. Reducing intracellular calcium levels via the intracellular signaling pathways - leading to the regulation of synthesis and release of neurotransmitters, neuronal excitability, cytoskeletal remodeling, and neuroplasticity
8. Reduction in the turnover rate of archidonic Acid (part of the omega-6 fatty acid pathway)
9. Down-regulation of arachidonic acid-specific phospholipase A12 protein
10. Inhibition of glycogen synthase kinase-3 by competing with magnesium for a binding site
11. Increase in the Extracellular Signal-Related Kinase signaling pathway activity (such as in the frontal cortex and hippocampus).
12. etc., etc.

Which ones are most important for pharmacologic function is not clear - though the sum total is probably the case - which each patient having individual differences in response.

Lithium is NOT a natural part of the body. Excessive doses, such as in the 1950s when cardiologists thought it would make a good salt substitute, led to cardiac arrhythmias, confusional states, and deaths.

Lithium has interactions with common medications such as Ibuprofen and other Non-steroidal Antiinflammatory Agents - which block the excretion of lithium in the kidneys, leading to sometimes excessive concentrations in the blood.

Lithium is unique medication in that the effective dose is extremely close to the toxic and lethal dose. It is thus not a medication to play with. More is not necessarily better because it may also be fatal. The physician has to be highly careful with its use.

 

[supwiz]

Re: Lithium's mechanism of action?

Lithium and other mood stabilizing medications have extremely complex mechanisms of action. One result is to increase serotonin levels - which may have an anxiolytic effect.

Mechanisms of action for Lithium include:
1. Stabilization of the inactive conformation of G-Protein
2. Inhibition of Adenylate Cyclase
3. Up-regulation of some Adenylate Cyclase subtypes
4. Uncompetitive inhibition of inositol-1-phosphatase - leading to a reduction in neuronal myo-inositol levels.
5. Supressing the phophatidyl inositol pathway
6. Reduction of Protein Kinase C activity by down-regulating selective PKC isozymes
7. Reducing intracellular calcium levels via the intracellular signaling pathways - leading to the regulation of synthesis and release of neurotransmitters, neuronal excitability, cytoskeletal remodeling, and neuroplasticity
8. Reduction in the turnover rate of archidonic Acid (part of the omega-6 fatty acid pathway)
9. Down-regulation of arachidonic acid-specific phospholipase A12 protein
10. Inhibition of glycogen synthase kinase-3 by competing with magnesium for a binding site
11. Increase in the Extracellular Signal-Related Kinase signaling pathway activity (such as in the frontal cortex and hippocampus).
12. etc., etc.

Which ones are most important for pharmacologic function is not clear - though the sum total is probably the case - which each patient having individual differences in response.

Lithium is NOT a natural part of the body. Excessive doses, such as in the 1950s when cardiologists thought it would make a good salt substitute, led to cardiac arrhythmias, confusional states, and deaths.

Lithium has interactions with common medications such as Ibuprofen and other Non-steroidal Antiinflammatory Agents - which block the excretion of lithium in the kidneys, leading to sometimes excessive concentrations in the blood.

Lithium is unique medication in that the effective dose is extremely close to the toxic and lethal dose. It is thus not a medication to play with. More is not necessarily better because it may also be fatal. The physician has to be highly careful with its use.

Hi Marianco, Are we to understand that high levels of myo-inositol can lead to anxiety states? I've always thought that we can take supplemental myo-inositol to reduce anxiety levels? Appreciate any comments. Greg B.

 

[JustOne]

Is Akathisia more psychological like anxiety, or more physical like parkinsons?
I think I might of had it before, is loss of apetite and inability to keep food down one of the symptoms?

 

[marianco]

Re: Is it possible - hCG causing panic attacks?

OK, my doctors aren't very helpful in this area. I mentioned that I was feeling very tired after I get my shot. Both doctors I talked with said the same thing "I've never heard of that happening so I don't know what to tell you." Then, I ask if it's possible (Over the las 3 weeks) that because of the hCG (Possible raise in E2) is causing panic attacks? Both have no idea.

Any advice on these 2 issues?

I can't give you advice since you are not a patient.

However, I can give educational information about HCG (Chorionic Gonadotropin).

The issue of HCG and panic attacks is much more complex than what appears on the surface.

A partial account of the metabolic cascades involved is as follows:

HCG acts like LH (Luteinizing Hormone).

LH has several actions, such as:
1. It stimulates testosterone production from the testes
2. It stimulates the production of aromatase enzyme
3. It stimulates the production of Cytochrome P450sc enzyme
4. etc.

Testosterone has several actions, such as:
1. Increasing dopamine production in the brain.
2. Increasing OR Decreasing Thyroid hormone production.
3. Reducing ACTH production.
4. Directly reducing Adrenal hormone production.
5. Becomes Estradiol via Aromatase enzyme.
6. Becomes DHT (Dyhydrotestosterone) via 5-Alpha-Reductase enzyme
7. Promotes insulin sensitivity.
8. Has antiinflammatory signaling functions.
9. Excessive Testosterone can result in an increase in anxiety depending on the metabolic cascades involved.
10. etc.

Aromatase Enzyme:
1. Turns Testosterone into Estradiol
2. etc.

Cytochrome P450sc enzyme:
1. Turns Cholesterol into Pregnenolone
2. etc.

Estradiol (and other estrogens) has multiple actions, including:
1. Acting as a Monoamine Oxidase Inhibitor in the brain
2. Reducing thyroid hormone activity by increasing production of Thyroid Binding Globulin from the liver.
3. etc.

Monoamine Oxidase Inhibitors (such as Estradiol) to varying extents:
1. Increase Serotonin levels
2. Increase Norepinephrine levels
3. Increase Dopamine levels
4. etc.

Serotonin:
1. Reduces the perception of stress - thus has an antianxiety effect.
2. Reduces norepinephrine production from norepinephrine neurons - contributing to its antianxiety effect.
3. Reduces dopamine production from dopamine neurons - if reduced excessively, this can increase anxiety
4. Has antiinflammatory signaling functions
5. etc.

Norepinephrine:
1. Is the primary signal for stress
2. Excessive Norepinephrine can result in anxiety or irritability/anger.
3. Has inflammatory signaling functions.
4. Can increase energy by promoting adrenal hormone production - if the adrenal glands are not fatigued excessively
5. etc.

Dopamine:
1. Promotes a sense of well-being, calmness
2. Deficiency in Dopamine production can cause agitation or anxiety, etc.
3. etc.

Thyroid hormone:
1. Promotes energy production, such as by increasing mitochondria production and thermogenesis.
2. Promotes steroid hormone production - increasing testosterone production - thus lowering thyroid hormone can reduce testosterone production.
3. Promotes IGF-1 production - which does most of the actions of growth hormone
4. Increases serotonine production
5. Promotes insulin sensitivity
6. Has antiinflammatory signaling functions
7. Deficiency in Thyroid hormone can result in anxiety or irritability/anger
8. etc.

Growth hormone/IGF-1 hormone:
1. Can promote a sense of calm and well-being - deficiency of which can result in a higher level of anxiety.
2. Has antiinflammatory signaling functions.
3. etc.

Adrenal Hormone production, includes:
1. Cortisol
2. DHEA
3. Progesterone
4. Testosterone
5. Pregnenolone
6. Adrenal cortex hormone production - particularly Cortisol - promotes energy production
7. etc.

Cortisol:
1. Promotes energy - via gluconeogenesis, etc.
2. Feeds back to the brain to reduce Norepinephrine production - resulting in reduction in anxiety.
3. Deficiency in Cortisol production can result in anxiety
4. etc.

DHEA:
1. Increases Dopamine production in the brain
2. Promotes insulin sensitivity
4. Has antiinflammatory signaling functions
5. Deficiency of DHEA can result in anxiety.
6. etc.

Pregnenolone:
1. Has a stimulant effect.
2. Excessive Pregnenolone production can result in agitation, tension, or anxiety.
3. etc.

Progesterone:
1. Has a calming, mood-stabilizing effect.
2. Deficiency in Progesterone can result in agitation, tension, or anxiety.
3. Has antiinflammatory signaling functions.
4. etc.

Insulin:
1. Excess insulin can reduce testosterone production.
2. Has pro-inflammatory signaling functions.
3. etc. etc. etc.

Immune System:
1. Deficient antiinflammatory signaling may promote anxiety
2. etc. etc.

Nutrition:
1. Certain nutrients are necessary to promote function across the nervous system, endocrine system, and immune system.
2. Deficiency of certain nutrients can promote anxiety in response to HCG as a result of dysfunction in these systems.

Thus, when HCG causes anxiety, the story is actually more complex than just the resulting increase in Estradiol.
1. If HCG increases Testosterone excessively, it can cause a cascade that results in anxiety - e.g. by decreasing thyroid function, decreasing adrenal hormone production, etc - particularly if a person is predisposed to anxiety such as by having hypothyroidism and adrenal fatigue.
2. If HCG increases Estradiol, it can cause a cascade that results in anxiety IF (a big if), Estradiol increases norepinephrine more than serotonin and dopamine, or if it results in significant thyroid hormone reduction (particularly if a person is hypothyroid and has adrenal fatigue).
3. etc. etc. etc.

The solution would involve examining all the involved systems and chemical messengers (neurotransmitters, hormones, etc) rather than just knee-jerk blaming only estrogen and attempting to reduce estrogen levels. The solution involves addressing the problems that are actually present (e.g. hypothyroidism, adrenal fatigue, excessive insulin, etc.) to reduce the risk of anxiety with HCG particularly when one wants to use HCG to preserve testicular size or to use HCG as a replacement for testosterone replacement therapy.

Reducing estrogen levels blindly can increase the risk of multiple problems including anxiety itself - such as when estradiol more strongly increases serotonin than norepinephrine in a person.

Lab tests and an exam would be necessary to help determine where the problem lies. Then solving the problem would not involve so much trial-and-error and guesswork.

Yes, HCG can cause panic attacks in susceptible persons depending on the functioning of the nervous system, endocrine system, and immune system - the sum of which I call 'the mind".

Dr. M

 

[HeadDoc]

thanks again for such a thorough response. Is there a directionality of neurotransmitters to hormones? Do the neurotransmitters control the hormones?

 

[marianco]

thanks again for such a thorough response. Is there a directionality of neurotransmitters to hormones? Do the neurotransmitters control the hormones?

It is a web of interactions.

Neurotransmitters can control hormones and immune system cytokines.
Hormones can control neurotransmitters and immune system cytokines.
Immune System Cytokines can control neurotransmitters and hormones.

From my point of view, there is actually no difference between a neurotransmitter, hormone, and immune system cytokine. All are chemical messengers of the mind. And the mind is the sum function of the nervous system, endocrine system, and immune system.

 

[marianco]

Is Akathisia more psychological like anxiety, or more physical like parkinsons?
I think I might of had it before, is loss of apetite and inability to keep food down one of the symptoms?

Parkinson's disease is both a physical and mental illness. The mental symptoms of Parkinson's Disease often start much earlier than the physical symptoms. They include depressed mood, lack of motivation, impaired visuospatial thinking, impaired memory, anxiety, impaired concentration, etc. On neuropsychological testing, the impaired visuospatial thinking is most prominent in Parkinson's disease compared to other causes of dementia.

Similarly, akathisia is both a physical and mental condition. It is foremost considered a motor movement disorder just as Parkinson's disease is.

Symptoms of akathisia generally do not include loss of appetite or nausea and vomiting.

 

[hardasnails1973]

If a person has excessive copper similar to wilsons disease but its resulting from imparied adrenals would this build up of copper cause a possbile scenerio similar to estrogen domaince? I research alot of information and elevated histmaines keeps coming back up and only reason I can pin point this is due to an intestinal infection unresolved or that copper is building up in the tissue and causing a defiency in the blood resulting in a DOA deficeincy (enzyme that breaks down histmaines and serotonin) So can estrogen domiance leas into also a decreae of 5hiaa, gaba via urine and posible increases in shbg in the blood. If one is taking cortisol (via salvia testing) and not taking the appropiate dhea could you recieve the benefits from the cortisol, but since you lacking DHEA could the catabolic effects of cortisol be more pronounced (immune suppression, muscle wasting, ect)

 

[hardasnails1973]

If a person has excessive copper similar to wilsons disease but its resulting from imparied adrenals would this build up of copper cause a possbile scenerio similar to estrogen domaince? I research alot of information and elevated histmaines keeps coming back up and only reason I can pin point this is due to an intestinal infection unresolved or that copper is building up in the tissue and causing a defiency in the blood resulting in a DOA deficeincy (enzyme that breaks down histmaines and serotonin) So can estrogen domiance leas into also a decreae of 5hiaa, gaba via urine and posible increases in shbg in the blood. If one is taking cortisol (via salvia testing) and not taking the appropiate dhea could you recieve the benefits from the cortisol, but since you lacking DHEA could the catabolic effects of cortisol be more pronounced (immune suppression, muscle wasting, ect)

Ad to that low homocysteine levels (3.9), low uric acid, low testosterone, low free t, and double normal shbg, low moly on hair, low copper, low ceruoplasm, elevated taurine, sarcosine, all low essential amino acids on urine test.

 

[peterson35]

Epinephrine and Norepinephrine are secreted here. As you remember from Biology
1611, they can be regarded as neurotransmitters (e.g., depolarizing postsynaptic
membranes) or hormones. Normally, both are metabotropic; that is, they increase
the metabolism of many cells including heart and neural cells. NE causes generalized
vasoconstriction to increase blood pressure.NE and Ep cause vasodilation in the heart
and lungs - sympathetic functions. They vasoconstrict in the gut and slow digestion.
Is this a sympathetic function? Ep and NEp are fast acting in the flight/fight response.

http://www.gpc.edu/~jaliff/anaendoc.htm (please see more here)

 

[LowTestosterone38]

I rarely use MAOIs these days. They primarily act by increasing serotonin. But the Serotonin reuptake inhibitors are safer - having much fewer interactions with foods and other rmedications. I keep them as an option when other medications fail - particularly for depression.

The claim that MAOIs work primarily via serotonin is untrue. All expert psychopharmacologists know that irreversible MAOIs such as Parnate, Marplan, Nardil and high dose selegiline target both MAO-A and MAO-B neurotransmitters. Thats a whole lot more than just serotonin. MAOIs are "triple neurotransmitter antidepressants," plus some.

Fred