Does SSRI's (anti-depressants) lower test levels?

[joltman]

Or is it something else with thoose drugs that decreases sexdrive?

 

[KoRn01ForLife]

Selective Serotonin Reuptake Inhibitors (SSRI's) pose a risk of lowering libido. The mechanism of action through which this occurs is independent of the testosterone levels in the body. Test levels will not be affected by SSRI's. The effect on the limbic system is thought to be responsible for the effects on sex drive, although I believe there is an effect on the hypothalamus because of the bodies' response to the presence of the drug (other NT"s are up/down regulated to maintain homeostasis). I believe norepinephrine and dopamine levels change to compensate and sex drive may be impacted upon because of activty change at the hypothalamus.

 

[KoRn01ForLife]

hypothalamus or hypocampus now I forget

 

[b1ewsw32]

hypothalamus or hypocampus now I forget

It's the hypothalamus..the master control switch and thermostat that regulates activity of vital functions and seves to keep the body in homeostatis. Functions such as hormonal regulation,apetite,thirst and sleep.

It acts like a thermostat in the sense that it reads levels of hormones and chemicals in the blood that will circulate and latch on to various receptors in the hypothalamus...these are feedback mechanisms.Then it will make appropiate adjustments via releasing hormones to the pituitary gland. ie. too litle and hypothalm. will signal pituitary in an effort to produce more. Too much and hypothalm will instruct pituitary to slow down or stop production.

The hippocampus is the main cpu wich receives various information and stimuli from different regions of the brain and then consolidating them into long-term memories.

Some SSRI's down-regulate hypothalamic dopamine which can cause decrease in sexual vigilance and also cause an increase in prolactin levels, which further decrease sexual functioning.

If one is not any exogenous testosterone than the reduction of hypothalamic dopamine with a co-responding rise in prolactin will cause decreases in testosterone levels over time.

B32

 

[KoRn01ForLife]

It's the hypothalamus..the master control switch and thermostat that regulates activity of vital functions and seves to keep the body in homeostatis. Functions such as hormonal regulation,apetite,thirst and sleep.

It acts like a thermostat in the sense that it reads levels of hormones and chemicals in the blood that will circulate and latch on to various receptors in the hypothalamus...these are feedback mechanisms.Then it will make appropiate adjustments via releasing hormones to the pituitary gland. ie. too litle and hypothalm. will signal pituitary in an effort to produce more. Too much and hypothalm will instruct pituitary to slow down or stop production.

The hippocampus is the main cpu wich receives various information and stimuli from different regions of the brain and then consolidating them into long-term memories.

Some SSRI's down-regulate hypothalamic dopamine which can cause decrease in sexual vigilance and also cause an increase in prolactin levels, which further decrease sexual functioning.

If one is not any exogenous testosterone than the reduction of hypothalamic dopamine with a co-responding rise in prolactin will cause decreases in testosterone levels over time.

B32

Has this notion of dopaminergic down-regulation indirectly causing a decrease in testosterone via the increase in prolactin been substantiated in the literature? I may be wrong; I am certainly open to new ideas, but I still believe that changes in testosterone levels and the actions of SSRI's are mutually exclusive.

 

[KoRn01ForLife]

BTW, I am rather tired at the moment so if I reread this tomorrow and it makes no sense, I apologize

 

[b1ewsw32]

Has this notion of dopaminergic down-regulation indirectly causing a decrease in testosterone via the increase in prolactin been substantiated in the literature? I may be wrong; I am certainly open to new ideas, but I still believe that changes in testosterone levels and the actions of SSRI's are mutually exclusive.

Yes it has....and as you will see the effect is at the hypothalamic-pituitary level but not at testicular levels..as response to HCG is not impaired in conditions of hyperprolactinemia.

1: Pharmacol Res Commun. 1986 Jul;18(7):601-9. Related Articles, Links


Further acquisitions on gonadal function in bromocriptine treated hyperprolactinemic male patients.

Zini D, Carani C, Baldini A, Cavicchioli C, Piccinini D, Marrama P.

The diurnal variation of plasma total and free testosterone (tT and fT) and the gonadotropinemic response to LH-RH were evaluated in a group of hyperprolactinemic impotent males with pituitary microprolactinoma before and during therapy with bromocriptine, a well known dopamine agonist drug. Before treatment, basal levels not only of tT but also of fT were decreased and the diurnal variation of both tT and fT was absent. Moreover, the LH-RH test showed a delay in the LH response peak, together with normal basal levels of LH. Bromocriptine therapy caused normalization of both the secretion response of LH to LH-RH and of the secretion pattern of tT and of fT (basal levels and diurnal variation) besides a significant decrease in PRL levels and an improvement in sexual function. The possible effects of high plasma levels of PRL at various levels of the hypothalamus-pituitary-testicular axis are discussed.

Clin Endocrinol (Oxf). 1979;11(2):217-23. Related Articles, Links


Hyperprolactinaemia and hypogonadism in men: response to exogenous gonadotrophins.

Luboshitzky R, Rosen E, Trestian S, Spitz IM.

Three male patients with pituitary tumours and marked hyperprolactinaemia were investigated. Their prolactin (PRL) levels ranged from 210 to 2500 ng/ml. The subjects had clinical and laboratory characteristics of hypogonadotrophic hypogonadism. All were treated with human chorionic gonadotrophin (HCG) and in one subject human menopausal gonadotrophin (HMG) was given in addition. In all three patients, despite the persistence of hyperprolactinaemia, serum testosterone had risen to normal levels within 4--17 days after starting HCG. Despite the normal testosterone level, impotence persisted in two patients and the third had persistently decreased libido. The hypogonadism in these patients may be related to an absolute reduction in gonadotroph number secondary to destruction by tumour mass. Alternatively, hyperprolactinaemia may inhibit the synthesis or release of the gonadotrophins or LHRH. Despite hyperprolactinaemia, pharmacological doses of HCG induced testosterone secretion in all these three subjects.


Here's an interesting one...
: J Clin Endocrinol Metab. 1977 Oct;45(4):825-8. Related Articles, Links


Hyperprolactinemia as a cause of delayed puberty: successful treatment with bromocriptine.

Koenig MP, Zuppinger K, Liechti B.

An 18-year-old male patient was referred because of galactorrhea and delayed puberty. There was no gynecomastia, but a white milky secretion could easily be expressed from each breast. The chest and skull X-rays were normal. The plasma prolactin was increased to 58 ng/ml and rose to 97 ng/ml after 200 microgram TRF iv. The patient was treated for one year with testosterone; his voice deepened, body hair developed, libido and sexual function became overt, and bone age advanced from 14 1/2 to 17 years, but the galactorrhea increased. After a satisfactory stage of pubertal development was reached, the testosterone was stopped. tthe galactorrhea then decreased to its pretreatment intensity; however, sexual potency diminished, sexual hair growth decreased, and the plasma prolactin levels rose to 246 ng/ml. After a 5-month interval without treatment, bromocriptine was given and brought about an impressive improvement. Virilization and general well being were superior to that during testosterone treatment, the galactorrhea vanished, plasma prolactin decreased, testosterone rose to normal values, and a normal semen analysis was recorded.

Although the possibility of slight elevation of prolactin with SSRI treatment would be incapable of rendering a hyperprolactinemic condition, like those demonstrated above, the occurence would be at the central(hypothalm-pituitary) level.

However IMHO any elevation of prolactin up and beyond upper normal levels will effect HPTA to some degree,sexual potency and may induce gynecomastia and a drug like dostinex is recommended as adjunctive HPTA therapy with clomid/tamoxifen once initial HCG administration is completed.

I also believe that it should be added to SSRI treatment in order to mitigate dopamine-down-regulation in order to preserve Libido, work-out vigilance and prevent the possible SSRI induced gyno, which BTW I always get on zoloft(sertraline).

B32

 

[KoRn01ForLife]

Well, you learn something new every day

 

[joltman]

Yes it has....and as you will see the effect is at the hypothalamic-pituitary level but not at testicular levels..as response to HCG is not impaired in conditions of hyperprolactinemia.

1: Pharmacol Res Commun. 1986 Jul;18(7):601-9. Related Articles, Links


Further acquisitions on gonadal function in bromocriptine treated hyperprolactinemic male patients.

Zini D, Carani C, Baldini A, Cavicchioli C, Piccinini D, Marrama P.

The diurnal variation of plasma total and free testosterone (tT and fT) and the gonadotropinemic response to LH-RH were evaluated in a group of hyperprolactinemic impotent males with pituitary microprolactinoma before and during therapy with bromocriptine, a well known dopamine agonist drug. Before treatment, basal levels not only of tT but also of fT were decreased and the diurnal variation of both tT and fT was absent. Moreover, the LH-RH test showed a delay in the LH response peak, together with normal basal levels of LH. Bromocriptine therapy caused normalization of both the secretion response of LH to LH-RH and of the secretion pattern of tT and of fT (basal levels and diurnal variation) besides a significant decrease in PRL levels and an improvement in sexual function. The possible effects of high plasma levels of PRL at various levels of the hypothalamus-pituitary-testicular axis are discussed.

Clin Endocrinol (Oxf). 1979;11(2):217-23. Related Articles, Links


Hyperprolactinaemia and hypogonadism in men: response to exogenous gonadotrophins.

Luboshitzky R, Rosen E, Trestian S, Spitz IM.

Three male patients with pituitary tumours and marked hyperprolactinaemia were investigated. Their prolactin (PRL) levels ranged from 210 to 2500 ng/ml. The subjects had clinical and laboratory characteristics of hypogonadotrophic hypogonadism. All were treated with human chorionic gonadotrophin (HCG) and in one subject human menopausal gonadotrophin (HMG) was given in addition. In all three patients, despite the persistence of hyperprolactinaemia, serum testosterone had risen to normal levels within 4--17 days after starting HCG. Despite the normal testosterone level, impotence persisted in two patients and the third had persistently decreased libido. The hypogonadism in these patients may be related to an absolute reduction in gonadotroph number secondary to destruction by tumour mass. Alternatively, hyperprolactinaemia may inhibit the synthesis or release of the gonadotrophins or LHRH. Despite hyperprolactinaemia, pharmacological doses of HCG induced testosterone secretion in all these three subjects.


Here's an interesting one...
: J Clin Endocrinol Metab. 1977 Oct;45(4):825-8. Related Articles, Links


Hyperprolactinemia as a cause of delayed puberty: successful treatment with bromocriptine.

Koenig MP, Zuppinger K, Liechti B.

An 18-year-old male patient was referred because of galactorrhea and delayed puberty. There was no gynecomastia, but a white milky secretion could easily be expressed from each breast. The chest and skull X-rays were normal. The plasma prolactin was increased to 58 ng/ml and rose to 97 ng/ml after 200 microgram TRF iv. The patient was treated for one year with testosterone; his voice deepened, body hair developed, libido and sexual function became overt, and bone age advanced from 14 1/2 to 17 years, but the galactorrhea increased. After a satisfactory stage of pubertal development was reached, the testosterone was stopped. tthe galactorrhea then decreased to its pretreatment intensity; however, sexual potency diminished, sexual hair growth decreased, and the plasma prolactin levels rose to 246 ng/ml. After a 5-month interval without treatment, bromocriptine was given and brought about an impressive improvement. Virilization and general well being were superior to that during testosterone treatment, the galactorrhea vanished, plasma prolactin decreased, testosterone rose to normal values, and a normal semen analysis was recorded.

Although the possibility of slight elevation of prolactin with SSRI treatment would be incapable of rendering a hyperprolactinemic condition, like those demonstrated above, the occurence would be at the central(hypothalm-pituitary) level.

However IMHO any elevation of prolactin up and beyond upper normal levels will effect HPTA to some degree,sexual potency and may induce gynecomastia and a drug like dostinex is recommended as adjunctive HPTA therapy with clomid/tamoxifen once initial HCG administration is completed.

I also believe that it should be added to SSRI treatment in order to mitigate dopamine-down-regulation in order to preserve Libido, work-out vigilance and prevent the possible SSRI induced gyno, which BTW I always get on zoloft(sertraline).

B32

WTF you get bitch tits from zoloft, Im on that and the list of sideeffects doesnt say anything about gyno.
What do you suggest? THat I talk to my doc about getting steroids?

 

[Hacksquats]

Hey great stuff guys, very, very impressive knowledge, awesome links too.
I think its worth mentioning that SSRI's do stress the liver. This in and of itself could cause a small reduction in T-Levels too. I heard that alcholol stresses the liver to the point that estrogen is not broken down - thus causing bitch tits. Could this be the case with SSRI's too?

I know the research claims they are great, but I think Testosterone is the number one anti-depressant and life accelerator known to man. Unless you're bed ridden or have unmanagable OCD stay the hell away from SSRI's. I wanna puke when I see that Zoloft commercial - total bs. Actually I'm just pissed because I put on 30lbs of fat while on it.