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Antidepressant Effects and Steroids

Vision

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Get Shredded!



Introduction


Today’s world can be painstakingly stressful, People are in a rush to compete or get somewhere, with a self appointed deadline.. With this being said ,many people are turning to medication, as large phrama tends to peddle medication and dispense it down our throats (It seems that everyone now suffers from some sort of mental aliment)..There was a study performed in 2005 as it showed that 27 million Americans were taking antidepressants (This is just America alone), almost double by 2010, and steadily increased up until 2015 this represents roughly 25% of the population at this time, and this number has certainly expected to rise as studies show antidepressant usage has been on a continual increase. Unfortunately enough its been proven that usage continues to rise significantly among young/adult men.


Let’s begin the discussion and what this article pertains to,and about is users taking antidepressants and how they affect anabolic steroid, post cycle therapy, testosterone levels and in general building muscle.


This discussion has taken place on are numerous internet panels, thousands of questions/concerns regarding antidepressant usage and anabolic steroid cycles..


To keep on point and avoid going off topic on the details about how these antidepressants effect depression and anxiety,we will merely only discuss how they affect bodybuilding and steroid usage.
_____________________________


SSRI (Selective serotonin reuptake inhibitor)


Below are the five of the most common and popular SSRI products.
Lexapro
Celexa

Paxil

Zoloft

Prozac



SNRI (Serotonin-norepinephrine reuptake inhibitor)Below are the three of the most common and popular SNRI products.
Effexor
Cymbalta

Pristiq



SexAgeMedicationASECS scorefree T (pg./ml.)
M35venlafaxine1623.4
M36sertraline215.2 *
M43paroxetine1813.5 *
M45venlafaxine1716.3 #
M46venlafaxine2013.2 *
M46paroxetine/mirtazepine2013.4 *
M47citalopram1929.0
M47fluoxetine2217.6 #
M50sertraline176.2 *
M53nefazodone2511.1 *
M54bupropion217.4*
M74venlafaxine245.6 *
F20citalopram291.7
F31venlafaxine210.50*
F37paroxetine230.70 *
F41paroxetine191.5
F44sertraline160.40 *
F45bupropion/trazodone160.50 *
F47fluoxetine200.50*
F52bupropion160.40

STRONG INHIBITORS
Generic NamesBrand Names
BupropionWellbutrin
FluoxetineProzac
ParoxetinePaxil
QuinidineCardioquin
MODERATE INHIBITORS
Generic NamesBrand Names
DuloxetineCymbalta
SertralineZoloft
DiphenhydramineBenadryl
ThioridazineMellaril
AmiodaroneCordarone
TrazodoneDesyrel
CimetidineTagamet
SSRIS AND SNRIS THAT ARE NOT INHIBITORS
Generic NamesBrand Names
VenlavaxineEffexor
CitalopramCelexa
EscitalopramLexapro
Testosterone Levels





Competitive athletes, sport fitness buffs, serious lifters, and bodybuilder know the importance of testosterone and it’s pivotal role is to the male body/Endocrine system..


In recent times there have been some numerous studies studies that supporting that SSRI’s in particular can cause reduced testosterone levels,as well as effect female hormonal levels.. Below is a study supporting these notions!


Antidepressant-Induced Sexual Dysfunction Associated with Low Serum Free Testosterone.





Alan Jay Cohen, M.D.


Private Practice and Assistant Clinical Professor of Psychiatry, UCSF


SUMMARY




In the course of an evaluation for treatment of antidepressant-induced


sexual dysfunction (ASD) with a new agent, an unforeseen pattern emerged


in the pre-treatment laboratory assessment. Free serum testosterone


levels in both men and women study subjects were found to be below the


normal ranges in 75 percent of subjects in this small study. There were


no other consistent laboratory findings that could account for such a


high percentage correlation.


Further inquiries into the possible causes for decreased serum


testosterone and its association with ASD seems warranted.





INTRODUCTION





Antidepressant-induced sexual dysfunction (ASD) is a well recognized


complication of treatment for mood and anxiety disorders, (Gitlin 1997).


Recent discoveries have helped to provide effective remedies for this


significant obstacle to patient compliance and successful treatment


outcome(Cohen 1997, Gitlin 1997, Bartlik 1995). However, no remedy is


100% effective. In addition, there is no fully satisfactory theory that


explains the physiologic mechanisms responsible for the varied aspects


of sexual dysfunction observed. In the course of an


evaluation of treatment for ASD in a community office-based research


setting, a striking pattern emerged in the laboratory screening


protocol. Free testosterone levels were found to be subnormal in 15 of


20 patients. No other consistent laboratory value nor physical


examination finding could account for this observation. Causes for


reduced free testosterone and its effect on sexual function are


discussed with implications for future research and treatment


strategies.





METHODS AND AIMS





Twenty subjects, ages 35 to 74 years, were evaluated for a double blind


placebo controlled trial of a dietary supplement combination for the


treatment of ASD. All of the subjects were using medication for the


treatment of mood disorder (DSM IV Criteria) included SSRI’s, SNRI’s,


bupropion, trazodone and mirtazipine. Screening physical exams and


laboratory studies included CBC, TSH, Prolactin, serum free


Testosterone, Serum Chemistries, and Urinalysis were done. The Arizona


Sexual Effects Change Scale (ASECS) was used as part of the clinical


assessment of ASD. In the course of the evaluation process, low serum


free testosterone was noted in 15 patients.





RESULTS




Twelve men and eight women were evaluated. Eight men had subnormal free


testosterone levels, two additional men had borderline low levels. Six


women had subnormal levels of free testosterone. The average age of male


subjects was 50.5 years. The male ASECS mean score was 20 with a mean


free Testosterone of 13.5 pg/ml. The laboratory range of free


Testosterone was 16 – 33 pg/ml. The average age of female subjects was


39.6 years; female ASECS score was 20, and the mean free Testosterone


level was 0.8 pg/ml. (normal range 0.8 – 3.0 pg/ml). (Laboratory ranges


were modified according to standardized norms for age; average free


testosterone levels decline slightly with increasing age.) Table #1


summarizes the data on all of the subjects in the study.


Prolactin levels were above normal in only two subjects (one male, one


female), both of whom were also found to have below normal levels of


free testosterone.





All of the other subjects had normal Prolactin levels. Thyroid


stimulating hormone was found to be normal in all subjects.


Table 1.







(*denotes subnormal fT levels, # denotes borderline low free T levels)


ASECS score range is 5-30 , 5 is maximal sexual function, 30 is minimal score.





DISCUSSION





This report is the first known documentation of reduced free


testosterone levels associated with ASD. Prior reports have mentioned


SSRI-induced prolactin elevations but none have described effects on


testosterone levels(Amsterdam 1997).





Certainly, drugs can play a role in decreasing testosterone levels.


Ketoconazole, megestrol, cimetidine, and spironolactone have all been


reported to lower testosterone levels(De Coster 1985, Griffin and Wilson


1998). Methadone and other opiates can suppress testosterone by reducing


LH levels centrally(Griffin and Wilson 1998) Anticonvulsants have been


associated with reduced free testosterone although epilepsy itself is also known to exhibit this effect (Herzog, 1992).





Carbamazepine may increase metabolic clearance of testosterone and reduce LH levels. The P-450 CYP3A3/4 system is involved in the metabolism of testosterone (Griffin and Wilson, 1998).


It is possible that antidepressants may be inducing the CYP3A3/4 isoenzyme with resultant enhanced metabolic clearance of testosterone and reduction in free hormone levels. Changes


in sex hormone binding globulin levels can influence the quantity of


circulating free testosterone (Griffin and Wilson


1998). Certain medical conditions; cirrhosis, renal failure, HIV infection etc. have been associated with lower levels of testosterone (Griffin and Wilson, 1998).


Even being a sports enthusiast may adversely effect testosterone levels (if the fan is on the losing side) (Bernhardt 1998).


Studies investigating testosterone levels and mood disorders have shown


conflicting results (Seidman1998, Levitt, 1998). Levels of testosterone in 12 depressed males were


compared to age-matched normal controls by Levitt and Joffe in 1988.


No significant differences were noted between the two


groups. Clearly, more research is needed to elucidate what role, if any, testosterone plays in the evaluation and treatment of antidepressant-induced sexual dysfunction.


Further studies should take into account diurnal variations in hormone level, total and free levels of hormone as well as pre-and post-antidepressant levels.


This report isn hindered by the limitations of a small number of subjects, lack of a control group, and no information on the testosterone level of subjects prior to the onset for antidepressant use.


Further studies should also include measurement of total testosterone levels as well as concomitant SHBG levels.





CONCLUSION





This is the first description of an association between low testosterone levels and antidepressant-induced sexual dysfunction known to this author.


Further research is needed to evaluate this relationship in greater detail. It does open avenues of exploration regarding treatment of ASD utilizing hormone replacement.





REFERENCES


1.) Amsterdam J. et al (1997) Breast enlargement during chronic


antidepressant therapy J Affective Disorders Nov.;46(2):151-156.


2.) Bartlik B et al (1995) Psychostimulants apparently reverse sexual


dysfunction secondary to selective serotonin reuptake inhibitors. J Sex


Marital Ther. 21, (4):264-271.


3.) Bernhardt PC et al (1998) Testosterone changes during vicarious


experiences of winning and losing among fans at sporting events. Physiol.


Behav Aug.;65(1):59-62.


4.) Cohen AJ and Bartlik B (1998) Ginkgo biloba for


antidepressant-induced


sexual dysfunction J Sex Marital Ther Apr-Jun 24:2 139-143.


5.) De Coster R et al (1985) Effect of a single administration of


ketoconazole on total and physiologically free plasma testosterone and 17


beta-oestradiol levels in healthy male volunteers. Eur J Clin Pharmacol


29(4):489-493.


6.) Gitlin M. (1997) Sexual side effects of psychotropic medications, in


Psychiatric Clinics of North America:Annual of Drug Therapy, pg.61-90.


7.) Griffin J and Wilson J (1998) Disorders of the testes and the male


reproductive


tract in :Williams Textbook of Endocrinology 9th ed. W.B. Saunders Co.


pgs.845-861.


_8.) Herzog AG (1995) Hormonal changes in epilepsy Epilepsia


Apr;36(4):323-326.


9.) Levitt A and Joffe R (1988) Total and free testosterone in depressed


men Acta Psychiatr Scand Mar;77(3)346-348.


10.) Sternbach H (1998) Age-associated testosterone decline in men:clinical


issues for psychiatry Am J Psychiatry Oct, 155:10,1310-1318.


11.) Seidman S and Rabkin J (1998) Testosterone replacement therapy for


hypogonadal men with SSRI-refractory depression. J Affect. Disord


Mar;48(2-3):157-161.


__________________________________________________ ______________________





Now at this point is obvious that it should be generalized that an SSRI/SNRI’s can potentially affect Free Test levels/Test!





Post Cycle Therapy





Here is where the facts get interesting..Now if your well rounded or even done your research you should and understand about running a PCT or what it is.


PCT - Post cycle therapy/ drugs to help recovery and assist with natural production..





Tomaxifien is one of the drugs used by many not only during a cycle, it's more favored for PCT, Tomaxifien is also known by its trade name - Nolvadex (Tamoxifen Citrate).





Nolvadex (Tamox) uses an enzyme "CYP2D6" to convert itself into a more useful form that our bodies can use. Unfortunately many antidepressants also use this same CYP2D6 enzyme, therefore you have two medications competing for the same pathway. This may happen with many different drugs.


The problem? Antidepressants have priority on the CYP2D6 enzyme therefore can render Nolvadex to be nearly useless, which could cause serious side effects during our PCT such as Gynecomastia. If you’re on an antidepressant and plan on using Nolvadex as part of your PCT, it’s important for you to know which antidepressants will cause issues or if your on an antidepressant that will inhibit Nolvadex from being functional, a great alternative would be Clomid or toremifene if you have issues and can not use tamox (Toremifene Citrate) for your PCT. Below is a list provided by BreastCancer.org showing which SSRI & SNRI are strong to moderate inhibitors and those that are not.













Here is some more research on another very popular (repetitively newer) SNRI namedPristiq (Desvenlafaxine) it’s independent of CYP2D6 enzyme therefore shouldn’t negatively interact with Nolvadex.




Weight Gain

One of the largest issues in particular with some SSRI’s is unwelcome weight gain, while some bodybuilders would welcome some additional help putting on weight, the majority of this weight comes in the form of fat particularly in the stomach, chest and back areas. The evidence is conclusive that the majority of SSRI’s can and will cause some form of weight gain, studies have shown that SSRI’s can/will reduce a users metabolism to some degree, however as to why SSRI’s slow down a bodies metabolism remains unknown. Even an active healthy adult that eats a balanced diet can experience weight gain. In some cases weight gain in upwards of 30+ lbs is experienced on longer term SSRI usage. SNRI’s on the other hand have a much less likely chance of causing unwelcomed weight gain, in the event SNRI’s cause weight gain it’s typically significantly less than with an SSRI.Prolactin Levels


There is significant medical information that ‘some’ SSRI’s handily increase prolactin levels, prolactin is certainly something users want to keep under control especially on cycle as high prolactin levels can cause an on set of Gyno-puffyness/swelling of breast tissue, lactating breasts is not welcomed by any male! (Get bloods checked,getting a full blood panel pre-cycle/mid/post is crucial)





Study below:





Changes in plasma prolactin during SSRI treatment: evidence for a delayed increase in 5-HT neurotransmission.


Cowen PJ1, Sargent PA.


Author information





Abstract





We studied the effect of the selective serotonin reuptake inhibitor (SSRI), paroxetine, on basal plasma prolactin concentrations in 11 healthy subjects. Subjects were tested before paroxetine, and after 1 and 3 weeks of treatment (20 mg daily). On each test occasion prolactin levels were sampled before and following administration of a placebo capsule, for a total of 4 h. After 3 weeks paroxetine treatment plasma prolactin levels were significantly higher than those seen either pre-treatment or after 1 week of treatment. In contrast, 1 week of paroxetine treatment did not significantly increase prolactin concentrations over pre-treatment values. Plasma concentrations of paroxetine did not differ between 1 and 3 weeks of treatment. The secretion of plasma prolactin is, in part, under the tonic regulation of serotonergic pathways and the present results therefore support animal experimental data suggesting that SSRIs produce a delayed increase in some aspects of brain serotonin neurotransmission.





Conclusion





In this discussion we should have learned what compounds may have an interaction and what compounds to have concerns with..


Getting bloods and consulting with your physician is very important, keep in mind that keeping an open honest trust policy with your GP will go a long way and it could avoid any unwanted side effect by listening to suggestions and having situational awareness.





If you suffer from anxiety or depression,you should know the risk with using AAS..


(Some of these articles have been shared/modified for easier understanding, and research has been add or removed to further support the topic at hand)





 
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MiSh

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Intresting point on nolva on pct. Wasn't aware that antidepressants and nolva was not good mix. I don't use nolva, just my belief. Good read. Hope some other readers take to point.


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Vision

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Intresting point on nolva on pct. Wasn't aware that antidepressants and nolva was not good mix. I don't use nolva, just my belief. Good read. Hope some other readers take to point.


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One of the first things I ask when someone mentions issues and PCT and such, I question other med intakes.. there is a vast about of meds that cause a conflict of interests with AAS, not per say AAS but the hormone levels and fluctionations
 

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NSAID and certain autoimmune diseases don't go hand in hand. From experience I'm speaking of.


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Vision

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NSAID and certain autoimmune diseases don't go hand in hand. From experience I'm speaking of.


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Experience is science as well brother, if you care to elaborate more that would be very beneficial to this entire post...
 

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I have Cielac Disease. Found out about 3 years ago. Also allergic to milk and all milk by products. Can't have any balsamic or reg vinegar, no probiotics, any ciders of any sort, no whey or stuff like that. Soy is starting to bother me. Anything processed in same plant as milk, wheat and list goes on. Certain alcohol I can drink, which is mismal. I stopped for 8 months. Night Vegetables bother me and certain fruit. Aspirins bother the hell out of me. I'm on strict Paleo diet, because of something. That's why i use injectable instead of orals, I don't know what fillers or crap that's inside that could damage me more. Vitamins I take quite a bit and a lot of Veges. And my levels are pretty normal , my dr says what ever I'm doing keep it up. We have to understand our body and what we put inside. When we understand ourselves then we can heal ourselves naturally in our positive mind. To learn something new daily, it's a blessing for me. I love to learn. So hope this long speech was useful in some aspect.


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Vision

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I have Cielac Disease. Found out about 3 years ago. Also allergic to milk and all milk by products. Can't have any balsamic or reg vinegar, no probiotics, any ciders of any sort, no whey or stuff like that. Soy is starting to bother me. Anything processed in same plant as milk, wheat and list goes on. Certain alcohol I can drink, which is mismal. I stopped for 8 months. Night Vegetables bother me and certain fruit. Aspirins bother the hell out of me. I'm on strict Paleo diet, because of something. That's why i use injectable instead of orals, I don't know what fillers or crap that's inside that could damage me more. Vitamins I take quite a bit and a lot of Veges. And my levels are pretty normal , my dr says what ever I'm doing keep it up. We have to understand our body and what we put inside. When we understand ourselves then we can heal ourselves naturally in our positive mind. To learn something new daily, it's a blessing for me. I love to learn. So hope this long speech was useful in some aspect.


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First off, Im sorry to hear that your going through this, I know you must have really made some huge sacrifices in your lifestyle, cutting out favorites and such..I too began having slight sensitive to certain foods and products as I get older, but nowhere near the scale as you.. Im no to familiar when it concerns Cielac, and the slew of issues it posses, I have read somethings here and there, but rather by chance compared to researching..

Let me ask you.. What level of fitness do you consider yourself at, your goals and such, and how does the limitation and restrictions effect your training and lifestyle? Do carbs have a direct negative influences as well? I worked with a fellow once that had cielac, he was a reg dude, and every once in a blue moon he would vanish and call out, for days on end.. He would return and talk about nightmarish episodes while out in RnR.. He would come back all normal, then again, shit would hit the fan and he's out.. I thought it was just an excuse, but a dude that knew an other dude who knew this dude found out it was in fact legit! it was crippling the kid... Seems food and products effect it all the way around?!?

You mentioned drinking, he would show us pics now and then of him having a micro or 2, or 3, so I taking it alc is no biggy?
 

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Alcohol carries gluten, barley, hops, wheat , potato extract in vodka. List goes on. Corn shouldn't bother certain people but it bothers me because it's genetically modified. Anything in foods or drinks that's been modified bothers me. Effects of eating something I shouldn't , lethargy like crazy , joint pain it's like tendinitis, cramps in stomach, my legs shut down and I can barly walk, I have to lay down and sleep for rest of day. I can only have jasmine rice and sweet potato only for carbs. That's it. I work out 3 days a week only now. Processed coffee bothers me. It's a nitemare. Xanthum gum and certain preservative effect me. Pure maple sugar bothers me. I go fishing and hunting in Alaska 2 to 3 times a year. I buy from local farms certain meats that are not feed pellets but with organic foods that are raised on their farm or I raise them. The list is forever. Just have to understand your body and its process. Certain chemicals that are used in ug's labs bother me and elevate my pancreas in just 4 weeks. Blood work is key. Knowledge is indispensable.


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ldog

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I really enjoy these discussions that bring AAS use in touch with real life.
 

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so which one is better for us juicers the SSRI or SNRI??



reguards,
BACKSTAR
 

MiSh

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Most labs I see here, no one takes in consideration of their pancreas. Levels of their amylase and lipase. It regulates both endo and exocrine cells. In return of insulin and glucagon. Also it works with the liver and kidney. Pancreas to me is very important. Guicol can damage pancreas levels over time and even alcohol.


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sneedam

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To be honest, I have been on an SSRI for a long time and mine is Pexeva. That is the brand name or (peroxetine) my doctor recently told me that I could switch to paxil, with the main ingredient peroxitene with a different delivery system.nI am skeptical to switch it up but he said it also had less sexual side effects. I have done my research and it seems peroxitene is peroxitene but until you make the switch you just do not know for sure. It is a coin toss. My main reason is for extreme anxiety, yeah I know hard for a guy to admit sometimes but it is not under my control as of yet....... So I take it so I can deal.... I have also just been put on a beta blocker and that has me F'ed up in the sex department??? Why???? Anyway am swithcing to paxil this week and am enjoying this thread so far.... Usually test makes me shine in all areas but this time I am missing the most important area!!!!!!!
 

Vision

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To be honest, I have been on an SSRI for a long time and mine is Pexeva. That is the brand name or (peroxetine) my doctor recently told me that I could switch to paxil, with the main ingredient peroxitene with a different delivery system.nI am skeptical to switch it up but he said it also had less sexual side effects. I have done my research and it seems peroxitene is peroxitene but until you make the switch you just do not know for sure. It is a coin toss. My main reason is for extreme anxiety, yeah I know hard for a guy to admit sometimes but it is not under my control as of yet....... So I take it so I can deal.... I have also just been put on a beta blocker and that has me F'ed up in the sex department??? Why???? Anyway am swithcing to paxil this week and am enjoying this thread so far.... Usually test makes me shine in all areas but this time I am missing the most important area!!!!!!!

This is why I enjoy posting reads and studies, you really get to hear authentic person to person experiences and feedback.. I too suffer from anxiety, some self induced but for the most more its been a battle since I was a child.Ive been off and on medications throughout my life span thus far, with some great experiences and others were-well a learning curve so to speak.. I can entirely related to the matter concerning MISSING the most desired effect!

Inmy 20's when I was cycling back to back, no brake, I noticed my depression was elevated, or stress/anxiety was fluctuating,almost like PMS so to speak..Never understood, thinking it was AAS.. In essence it was,but I was also on antiD's for a bit.. I was also taking AI's and yet I was having undesired effects of estro and gyno:hmm:..

After discontinuing the use of antidepressants (not by choice, by chance) the effects subsided substantially..Hmm, bloods were better (estro was elevated during by not earth shattering),sense of well being increased/improved, and I felt more "ALPHA" compared to just in a cloud or unproductive and lackadaisical with anything from thoughts to physicals activities or even motivation..

This is when I really dialed in and did research, I found info about females and estro, but I compared (as we are still humans) and to my surprise the antiD's greatly effected and competed with intensity to binding sites..

as AAS improves the CNS and neurotransmitters with signaling, you would think it would amplify the effect of antidepressants concerning the high concentration of dopamine and serotonin,wrong..

Its been years since I used any Antidepressants, i utilized Proviron now and it seems to be the mecca and the most pronounced agent I have ever used with my issues, and it works and compliments other andros,, in fact its used at some clinics thought-out thew world for anxiety and depression disorders..

when was your last blood work, can you post a pic? Id like to see your thyroid levels..
 

Vision

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so which one is better for us juicers the SSRI or SNRI??



reguards,
BACKSTAR

First off Id like to say "welcome to ASF" On behalf of PSL, I wish BlackStar labs a successful and prosperous journey..

In regards to you questions, both have there drawbacks, however that doesnt mean SOL... Proviron is a great option to utilize for a slight AI, but mostly for a antidepressant..I swear by it..

I literally have a warm fuzzy feeling all day!
 

sneedam

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Interesting Vision,
I have in the past been diagnosed with hypothroidism but it is now well within the normal range <2.0 and I have been on anti'Ds for so long I do not even remember what a normal functioning person is supposed to feel (to an extant).....I will look to see if I have any thyroid tests I have had and will post if I can find but I do know the latest labs were below what the GP said were normal so that is good and I am off synthroid.....Give me a bit and I will see if I can come up with some past labs..... Interesting about Provy....I might need to do a little or maybe a lot of research because I hate being so attachd to this medication......
Thanks Vision....
 

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Provi.. I'm going to look into that also. What dosages are minimal for Provi that limit depression? I understand body type and weight are in variables and dosage can be adjusted. Put ur experience and input would be great.


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Vision

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Provi.. I'm going to look into that also. What dosages are minimal for Provi that limit depression? I understand body type and weight are in variables and dosage can be adjusted. Put ur experience and input would be great.


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Here is a thread I made in regards to provirons and the effects!

I hope it finds you well in regards to this whole topic.thread..

A fellow brother recently had a thread going with concerns with his "first tren cycle". The discussion soon turned into how to combat or hinder sides.

So lets talk about this shall we?

Tren is the compound that's well known for having a love hate relationship with most users. Most will deem it a necessary evil. But, in fact it doesn't have to be classified as evil after all.

Allow me to intro some clinical studies that have been conducted with a compound most commonly known as Proviron-trade name (Mesterolone).This agent posses some amazing characteristics with Antidepressant properties, as well Antianxiety.
It works by also metabolizing and being recognized through the endocrine as (other) a neurosteroid,effectively functioning as a so-called proneurosteroid (
testosterone is also recognized as one).. These steroids synthesized in the brain (Proviron especially) and have effects on brain function,In addition to their actions on neuronal membrane receptors,improving the quality of the channels that cells use to communicate and interact.

Proviron(mesterolone) will exert inhibitory actions on neurotransmission, acting as potent positive allosteric modulator of the GABA receptor (This is crucial concerning Tren-Insomnia as healthly function levels of GABA will produce a stable sleep state/environment for rest) and possess, in no particular order, antidepressant,sress-reducing, feeling warm/fuzzy/rewarding,pro-social, antiaggressive(huge consider tren sides),prosexual,sedative/prosleep,cognitive-memory improvement..The list goes on!

(Where does this apply with Tren? It can aid all the way around with individuals how are sensitive or not.From the social aspect,overwhelming sense of anxiety,lack of sleep,basically every stated above that may apply with the usage of tren and the onset of its unwanted side)

In addition to this information, an individual can also utilized
masteron(Drostanolonein) in conjunction with Proviron, running both concurrent may yield a great synergenic effect,each compound will compliment one an other.

Below is a image illustrating the neurotransmitter/receptor and how it functions, also I will include some real actual studies conducted with proven results expressing the benefits of this compound (proviron)
Keep in mind that these doses may seem extreme,its been proven time and time again that such significant dosages are not needed to yield the effect. Merely a daily intake of 50-100 will suffice for almost anyone!


Citation
Database: PsycINFO
[ Journal Article ]
A comparison of the antidepressant effects of a synthetic androgen (mesterolone) and amitriptyline in depressed men.
Vogel, William; Klaiber, Edward L.; Broverman, Donald M.
Journal of Clinical Psychiatry, Vol 46(1), Jan 1985, 6-8.

Abstract

  1. 26 depressed male outpatients were randomly assigned to 14 wks of treatment with either mesterolone or amitriptyline in a double-blind parallel treatment design. Ss completed the Hamilton Rating Scale for Depression and a symptom checklist each week. Findings reveal that the drugs were equally effective in reducing depressive symptoms. Mesterolone produced significantly fewer adverse side effects than amitriptyline and did not produce hypomania or tachycardia, recognized side effects of amitriptyline. (10 ref) (PsycINFO Database Record (c) 2013 APA, all rights reserved)
Methods Find Exp Clin Pharmacol. 1984 Jun;6(6):331-7.
The effects of mesterolone, a male sex hormone in depressed patients (a double blind controlled study).
Itil TM, Michael ST, Shapiro DM, Itil KZ
.
Abstract
Based on computer EEG (CEEG) profiles, in high doses, antidepressant properties of mesterolone, a synthetic androgen, were predicted. In a double-blind placebo controlled study, the clinical effects of 300-450 mg daily mesterolone were investigated in 52 relatively young (age range 26-53 years, mean 42.7 years) male depressed outpatients. During 6 weeks of mesterolone treatment, there was a significant improvement of depressive symptomatology. However, since an improvement was also established during the placebo treatment, no statistically appreciable difference in the therapeutic effects of mesterolone was established compared to placebo. Mesterolone treatment significantly decreased both plasma testosterone and protein bound testosterone levels. Patients with high testosterone levels prior to treatment seem to have had more benefit from mesterolone treatment than patients with low testosterone levels. The degree of improvement weakly correlated to the decrease of testosterone levels during mesterolone treatment.
 
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MiSh

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I take gaba for sleep prescribed by Dr. Sometimes I like to take to much during the day to make me happy happy. Provi, mast and gabbapentine would be a great synergy then. I know gabba makes u on top of the world at high doses for me. I'm going to put all 3 compounds in next cycle with Tren and see what outcome is. Does it also release dopamine?


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Vision

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I take gaba for sleep prescribed by Dr. Sometimes I like to take to much during the day to make me happy happy. Provi, mast and gabbapentine would be a great synergy then. I know gabba makes u on top of the world at high doses for me. I'm going to put all 3 compounds in next cycle with Tren and see what outcome is. Does it also release dopamine?


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brother the gaba goes great with some ADD meds as well, it actually improves your ability to comprehend things...

Prive odesnt release anything, it will assist will signaling and pathways with firing and such...its much like a amplifier!
 

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Good deal.. Thanks for input.


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Vision

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Get Shredded!
Interesting Vision,
I have in the past been diagnosed with hypothroidism but it is now well within the normal range <2.0 and I have been on anti'Ds for so long I do not even remember what a normal functioning person is supposed to feel (to an extant).....I will look to see if I have any thyroid tests I have had and will post if I can find but I do know the latest labs were below what the GP said were normal so that is good and I am off synthroid.....Give me a bit and I will see if I can come up with some past labs..... Interesting about Provy....I might need to do a little or maybe a lot of research because I hate being so attachd to this medication......
Thanks Vision....


I figured maybe there was a T4 issue with the way you described thing. turns out you in fact had an issue.. but get me those bloods when you can... also, I swear by the proviron.. the best stuff outside anabolics,, its a staple for me year round
 

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Guys

There seems to be much interest in this topic. I'm going to focus my efforts on this and dig for more information. Stay tuned.
 

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Listed below are some fascinating notes which all should find interesting. One thing that I did come across and Vision spoke to this in the article above is the correlation between Anti-Depressants and increased Prolactin levels. We all know what out of range Prolactin levels can cause. It seems to make sense that if you have low-medium testosterone and you take an Anti-Depressant which results in increasingly high Prolactin levels then one could have poor erections,loss of libibo and be a prime target for Gyno issues. With that said, I would caution anyone that is taking an Anti-Depressant to avoid any AAS that could possibly increase your Prolactin levels...such as Deca-Durabolin. References below via Wiki as.

Prolactin


Prolactin (PRL), also known as luteotropic hormone or luteotropin, is a protein that in humans is best known for its role in enabling female mammals to produce milk; however, it is influential over a large number of functions with over 300 separate actions of PRL having been reported in various vertebrates.[SUP][1][/SUP] Prolactin is secreted from the pituitary gland in response to eating, mating, estrogen treatment, ovulation, and nursing. Prolactin is secreted in a pulsatile fashion in between these events. Prolactin also plays an essential role in metabolism, regulation of the immune system, and pancreatic development.
Discovered in non-human animals around 1930 by Oscar Riddle [SUP][2][/SUP] at Cold Spring Harbor Laboratory on Long Island, New York, and confirmed in humans in 1970 by Henry Friesen [SUP][3][/SUP] prolactin is a peptide hormone, encoded by the PRL gene. [SUP][4][/SUP]
Although often associated with human milk production, prolactin plays a wide range of other roles in both humans and other vertebrates. (For example, in fish—the oldest known vertebrates—an important function is probably related to control of water and salt balance.) Prolactin also acts in a cytokine-like manner and as an important regulator of the immune system. It has important cell cycle related functions as a growth-, differentiating- and anti-apoptotic factor. As a growth factor, binding to cytokine like receptors, it also has profound influence on hematopoiesis, angiogenesis and is involved in the regulation of blood clotting through several pathways. The hormone acts in endocrine, autocrine, and paracrine manner through the prolactin receptor and a large number of cytokine receptors.[SUP][1][/SUP]
Pituitary prolactin secretion is regulated by endocrine neurons in the hypothalamus, the most important ones being the neurosecretory tuberoinfundibulum (TIDA) neurons of the arcuate nucleus, which secrete dopamine (aka Prolactin Inhibitory Hormone) to act on the D[SUB]2[/SUB] receptors of lactotrophs, causing inhibition of prolactin secretion. Thyrotropin-releasing factor (thyrotropin-releasing hormone) has a stimulatory effect on prolactin release, however Prl is the only adenohypophyseal hormone whose principal control is inhibitory.
Several variants and forms are known per species. Many fish have variants prolactin A and prolactin B. Most vertebrates including humans also have the closely related somatolactin. In humans, three smaller (4, 16, and 22 kDa) and several larger (so called big and big-big) variants exist.[SUP][not verified in body][/SUP]
Contents





EffectsEdit

Prolactin has a wide range of effects. It stimulates the mammary glands to produce milk (lactation): increased serum concentrations of prolactin during pregnancy cause enlargement of the mammary glands of the breasts and prepare for the production of milk. Milk production normally starts when the levels of progesterone fall by the end of pregnancy and a suckling stimulus is present. Sometimes, newborn babies (males as well as females) secrete a milky substance from their nipples known as witch's milk. This is in part caused by maternal prolactin and other hormones. Prolactin also has been found to play an important role in maternal behavior.[SUP][5][/SUP]

Prolactin provides the body with sexual gratification after sexual acts: The hormone counteracts the effect of dopamine, which is responsible for sexual arousal. This is thought to cause the sexual refractory period. The amount of prolactin can be an indicator for the amount of sexual satisfaction and relaxation. Unusually high amounts are suspected to be responsible for impotence and loss of libido (see hyperprolactinemia symptoms).

Highly elevated levels of prolactin decrease the levels of sex hormones — estrogen in women and testosterone in men.[SUP][6][/SUP] The effects of mildly elevated levels of prolactin are much more variable, in women both substantial increase or decrease of estrogen levels may result.

Prolactin is sometimes classified as a gonadotropin[SUP][7][/SUP] although in humans it has only a weak luteotropic effect while the effect of suppressing classical gonadotropic hormones is more important.[SUP][8][/SUP] Prolactin within the normal reference ranges can act as a weak gonadotropin but at the same time suppresses GnRH secretion. The exact mechanism by which it inhibits GnRH is poorly understood although expression of prolactin receptors (PRL-R) have been demonstrated in rat's hypothalamus, the same has not been observed in GnRH neurons.[SUP][9][/SUP] Physiologic levels of prolactin in males enhance luteinizing hormone-receptors in Leydig cells, resulting in testosterone secretion, which leads to spermatogenesis.[SUP][10][/SUP]
Prolactin also stimulates proliferation of oligodendrocyte precursor cells. These cells differentiate into oligodendrocytes, the cells responsible for the formation of myelin coatings on axons in the central nervous system.[SUP][11][/SUP]
Prolactin also has a number of other effects including contributing to pulmonary surfactant synthesis of the fetal lungs at the end of the pregnancy and immune tolerance of the fetus by the maternal organism during pregnancy.
Prolactin delays hair regrowth in mice.[SUP][12][/SUP]
Prolactin promotes neurogenesis in maternal and fetal brains.[SUP][13][/SUP][SUP][14][/SUP]

Production and regulationEdit

In humans, prolactin is produced at least in the pituitary, decidua, myometrium, breast, lymphocytes, leukocytes and prostate.[SUP][15][/SUP][SUP][16][/SUP]
Pituitary PRL is controlled by the Pit-1 transcription factor and ultimately dopamine, extrapituitary PRL is controlled by a superdistal promoter and apparently unaffected by dopamine.[SUP][16][/SUP] The thyrotropin-releasing hormone and the vasoactive intestinal peptide stimulate the secretion of prolactin in experimental setting, however their physiological influence is unclear. The main stimulus for prolactin secretion is suckling, the effect of which is neuronally mediated.[SUP][17][/SUP]
In decidual cells and in lymphocytes the distal promoter and thus prolactin expression is stimulated by cAMP. Responsivness to cAMP is mediated by an imperfect cAMP–responsive element and two CAAT/enhancer binding proteins (C/EBP).[SUP][16][/SUP] Progesterone has been observed to upregulate prolactin synthesis in the endometrium but decreases it in myometrium and breast glandular tissue.[SUP][18][/SUP] However breast and other tissues may also express the Pit-1 promoter in addition to the distal promoter.
Extrapituitary production of prolactin is thought to be special to humans and primates and may serve mostly tissue specific paracrine and autocrine purposes. It has been hypothesized that in other vertebrates such as mice a similar tissue specific effect is achieved by a large family of prolactin like proteins controlled by at least 26 paralogous PRL genes not present in primates.[SUP][16][/SUP]
Vasoactive intestinal peptide and peptide histidine isoleucine help to regulate prolactin secretion in humans, but the functions of these hormones in birds can be quite different.[SUP][19][/SUP]

Variance in levelsEdit

There is a diurnal as well as an ovulatory cycle in prolactin secretion. In many mammals, there is also a seasonal change in prolactin release.
During pregnancy, high circulating concentrations of estrogen and progesterone increase prolactin levels by 10- to 20-fold. However, at the same time, estrogen, as well as progesterone, inhibit the stimulatory effects of prolactin on milk production. It is the abrupt drop of estrogen and progesterone levels following delivery that allows prolactin — which temporarily remains high — to induce lactation.[SUP][verification needed][/SUP]
After childbirth, prolactin levels fall as the internal stimulus for them is removed. Sucking by the baby on the nipple then promotes further prolactin release, maintaining the ability to lactate. The sucking activates mechanoreceptors in and around the nipple. These signals are carried by nerve fibers through the spinal cord to the hypothalamus, where changes in the electrical activity of neurons that regulate the pituitary gland cause increased prolactin secretion. The suckling stimulus also triggers the release of oxytocin from the posterior pituitary gland, which triggers milk let-down: Prolactin controls milk production (lactogenesis) but not the milk-ejection reflex; the rise in prolactin fills the breast with milk in preparation for the next feed.
In usual circumstances, in the absence of galactorrhea, lactation will cease within one or two weeks of the end of demand breastfeeding.
It has also been found that compared to un-mated males, fathers and expectant fathers have increased prolactin concentrations.[SUP][20][/SUP]
High prolactin levels can also contribute to mental health issues.[SUP][citation needed][/SUP]
Prolactin levels peak during REM sleep, and in the early morning. Levels can rise after exercise, high-protein meals,[SUP][21][/SUP] sexual intercourse, breast examination,[SUP][21][/SUP] minor surgical procedures,[SUP][22][/SUP] following epileptic seizures[SUP][23][/SUP] or (occasionally) due to physical or emotional stress,[SUP][21][/SUP][SUP][24][/SUP] In a study on female volunteers under hypnosis, prolactin surges resulted from the evocation, with rage, of humiliating experiences, but not from the fantasy of nursing.[SUP][24][/SUP]
Prolactin levels have also been found to rise with use of the drug MDMA (Ecstasy), leading to speculation that prolactin may have a role in the post-orgasmic state as well as decreased sexual desire. [SUP][25][/SUP]
Hypersecretion of prolactin is more common than hyposecretion. Hyperprolactinemia is the most frequent abnormality of the anterior pituitary tumors, termed prolactinomas. Prolactinomas may disrupt the hypothalamic-pituitary-gonadal axis as prolactin tends to suppress the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus and in turn decreases the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, therefore disrupting the ovulatory cycle in females.[SUP][26][/SUP] Such hormonal changes may manifest as amenorrhea and infertility in females as well as impotence in males. Inappropriate lactation (galactorrhoea) is another important clinical sign of prolactinomas, which may be treated with the administration of bromocriptine, which is an agonist of the dopamine D[SUB]2[/SUB] receptor.

Structure and isoformsEdit

The structure of prolactin is similar to that of growth hormone and placental lactogen. The molecule is folded due to the activity of three disulfide bonds. Significant heterogeneity of the molecule has been described, thus bioassays and immunoassays can give different results due to differing glycosylation, phosphorylation, sulfation, as well as degradation. The non-glycosylated form of prolactin is the dominant form of prolactin that is secreted by the pituitary gland.
There are mainly three different forms of prolactin in regard to size:

  • Little prolactin is the predominant form.[SUP][27][/SUP] It has a molecular weight of appxoximately 22-kDa.[SUP][27][/SUP] It is a single-chain polypeptide of 198 amino acids, and is apparently the result of removal of some amino acids.
  • Big prolactin of approximately 48 kDa.[SUP][27][/SUP] It may be the product of interaction of several prolactin molecules. It appears to have little, if any, biological activity.[SUP][28][/SUP]
  • Big big prolactin of approximately 150 kDa.[SUP][27][/SUP] It appears to have a low biological activity.[SUP][29][/SUP]
The levels of larger ones are somewhat higher during the early postpartum period.[SUP][30][/SUP]
Pit-1 is a transcription factor that binds to the prolactin gene at several sites to allow for the production of prolactin in the pituitary gland. A key regulator of prolactin production is estrogens that enhance growth of prolactin-producing cells and stimulate prolactin production directly, as well as suppressing dopamine.
Human prolactin receptors are insensitive to mouse prolactin.[SUP][31][/SUP]

Prolactin receptorEdit

Main article: Prolactin receptor
Prolactin receptors are present in the mamillary glands, ovaries, pituitary glands, heart, lung, thymus, spleen, liver, pancreas, kidney, adrenal gland, uterus, skeletal muscle, skin, and areas of the central nervous system.[SUP][32][/SUP] When prolactin binds to the receptor, it causes it to dimerize with another prolactin receptor. This results in the activation of Janus kinase 2, a tyrosine kinase that initiates the JAK-STAT pathway. The activation of the prolactin receptor also results in the activation of mitogen-activated protein kinases and Src kinase.[SUP][32][/SUP]

Diagnostic useEdit

Prolactin levels may be checked as part of a sex hormone workup, as elevated prolactin secretion can suppress the secretion of FSH and GnRH, leading to hypogonadism, and sometimes causing erectile dysfunction in men.
Prolactin levels may be of some use in distinguishing epileptic seizures from psychogenic non-epileptic seizures. The serum prolactin level usually rises following an epileptic seizure.[SUP][33][/SUP]

Units and unit conversionsEdit

The serum concentration of prolactin can be given in mass concentration (µg/L or ng/mL), molar concentration (nmol/L or pmol/L) or in international units (typically mIU/L). The current IU is calibrated against the third International Standard for Prolactin, IS 84/500.[SUP][34][/SUP][SUP][35][/SUP] Reference ampoules of IS 84/500 contain 2.5 µg of lyophilized human prolactin,[SUP][36][/SUP] and have been assigned an activity of .053 International Units of prolactin.[SUP][34][/SUP][SUP][35][/SUP] Measurements that are calibrated against the current international standard can be converted into mass units using this ratio of grams to IUs;[SUP][37][/SUP] prolactin concentrations expressed in mIU/L can be converted to µg/L by dividing by 21.2. Previous standards use other ratios.[SUP][38][/SUP][SUP][39][/SUP][SUP][40][/SUP][SUP][41][/SUP]
The first International Reference Preparation (or IRP) of human Prolactin for Immunoassay was established in 1978 (75/504 1st IRP for human Prolactin) at a time when purified human prolactin was in short supply.[SUP][37][/SUP][SUP][38][/SUP] Previous standards relied on prolactin from animal sources.[SUP][41][/SUP] Purified human prolactin was scarce, heterogeneous, unstable, and difficult to characterize. A preparation labelled 81/541 was distributed by the WHO Expert Committee on Biological Standardization without official status and given the assigned value of 50 mIU/ampoule based on an earlier collaborative study.[SUP][37][/SUP][SUP][39][/SUP] It was determined that this preparation behaved anomalously in certain immunoassays and was not suitable as an IS.[SUP][37][/SUP] However, in the absence of an alternative, it was used. Three different human pituitary extracts containing prolactin were subsequently obtained as candidates for an IS. These were distributed into ampoules coded 83/562, 83/573, and 84/500.[SUP][34][/SUP][SUP][35][/SUP][SUP][37][/SUP][SUP][40][/SUP] On the basis of collaborative studies involving 20 different laboratories, it was concluded that there was little difference between these three preparations. 83/562 appeared to be the most stable. This preparation was largely free of dimers and polymers of prolactin. On the basis of these investigations 83/562 was established as the Second IS for human Prolactin.[SUP][40][/SUP] Once stocks of these ampoules were depleted, 84/500 was established as the Third IS for human Prolactin.[SUP][34][/SUP][SUP][37][/SUP]

Reference rangesEdit

General guidelines for diagnosing prolactin excess (hyperprolactinemia) define the upper threshold of normal prolactin at 25 µg/L for women, and 20 µg/L for men.[SUP][32][/SUP] Similarly, guidelines for diagnosing prolactin deficiency (hypoprolactinemia) are defined as prolactin levels below 3 µg/L in women,[SUP][42][/SUP][SUP][43][/SUP] and 5 µg/L in men.[SUP][44][/SUP][SUP][45][/SUP][SUP][46][/SUP] However, different assays and methods for measuring prolactin are employed by different laboratories, and as such the serum reference range for prolactin is often determined by the laboratory performing the measurement.[SUP][32][/SUP][SUP][47][/SUP] Furthermore, prolactin levels also vary with, for example, age,[SUP][48][/SUP] sex,[SUP][48][/SUP] menstrual cycle stage,[SUP][48][/SUP] and pregnancy.[SUP][48][/SUP] The circumstances surrounding a given prolactin measurement (assay, patient condition, etc.) must therefore be considered before the measurement can be accurately interpreted.[SUP][32][/SUP]
The following chart illustrates the variations seen in normal prolactin measurements across different populations. Prolactin values were obtained from specific control groups of varying sizes using the IMMULITE assay.[SUP][48][/SUP]
ProbandProlactin, µg/L
women, follicular phase (n = 803)12.1
women, luteal phase (n = 699)13.9
women, mid-cycle (n = 53)17
women, whole cycle (n = 1555)13.0
women, pregnant, 1st trimester (n = 39)16
women, pregnant, 2nd trimester (n = 52)49
women, pregnant, 3rd trimester (n = 54)113
Men, 21–30 (n = 50)9.2
Men, 31–40 (n = 50)7.1
Men, 41–50 (n = 50)7.0
Men, 51–60 (n = 50)6.2
Men, 61–70 (n = 50)6.9
Inter-method variabilityEdit

The following table illustrates variability in reference ranges of serum prolactin between some commonly used assay methods (as of 2008), using a control group of healthy health care professionals (53 males, age 20–64 years, median 28 years; 97 females, age 19–59 years, median 29 years) in Essex, England:[SUP][47][/SUP]
Assay methodMean
Prolactin
Lower limit
2.5th percentile
Upper limit
97.5th percentile
µg/LmIU/Lµg/LmIU/Lµg/LmIU/L
Females
Centaur7.921683.357116.4348
Immulite9.251963.547518.7396
Access9.061923.637719.3408
AIA9.52[SUP][49][/SUP]257[SUP][49][/SUP]3.89[SUP][49][/SUP]105[SUP][49][/SUP]20.3[SUP][49][/SUP]548[SUP][49][/SUP]
Elecsys10.52224.158823.2492
Architect10.62254.629821.1447
Males
Access6.891462.745813.1277
Centaur7.881672.976312.4262
Immulite7.451583.307013.3281
AIA7.81[SUP][49][/SUP]211[SUP][49][/SUP]3.30[SUP][49][/SUP]89[SUP][49][/SUP]13.5[SUP][49][/SUP]365[SUP][49][/SUP]
Elecsys8.491803.407215.6331
Architect8.871884.018514.6310
An example usage of table above is, if using the Centaur assay to estimate prolactin values in µg/L for females, the mean is 7.92 µg/L, and the reference range is 3.35–16.4 µg/L.

Conditions associated with elevated levelsEdit

Hyperprolactinaemia, or excess serum prolactin, is associated with hypoestrogenism, anovulatory infertility, oligomenorrhoea, amenorrhoea, unexpected lactation, and loss of libido in women, and erectile dysfunction and loss of libido in men.[SUP][50][/SUP]
1. Physiological

  • Coitus
  • Exercise
  • Lactation
  • Pregnancy
  • Sleep
  • Stress
2. Pharmacological

  • Anesthetics
  • Anticonvulsant
  • Antihistamines (H2)
  • Antihypertensives
  • Cholinergic agonist
  • Drug-induced hypersecretion
  • Catecholamine depletor
  • Dopamine receptor blockers
  • Dopamine synthesis inhibitor
  • Estrogens
    • Oral contraceptives
    • Oral contraceptive withdrawal
  • Neuroleptics
  • Antipsychotics
  • Neuropeptides
  • Opiates and opiate antagonists
3. Pathological

  • Hypothalamic-pituitary stalk damage
    • Granulomas
    • Infiltrations
    • Irradiation
    • Rathke's cyst
  • Trauma
    • Pituitary stalk resection
    • Suprasellar surgery
  • Tumors
    • Craniopharyngioma
    • Germinoma
    • Hypothalamic metastases
    • Meningioma
    • Suprasellar pituitary mass extension
  • Surgery

  • Pituitary
    • Acromegaly
    • Idiopathic
    • Lymphocytic hypophysitis or parasellar mass
    • Macroadenoma (compressive)
    • Macroprolactinemia
    • Plurihumoral adenoma
    • Prolactinoma
  • Systemic disorders
    • Chest-neurologic chest wall trauma
    • Herpes Zoster
    • Chronic renal failure
    • Cirrhosis
    • Cranial radiation
    • Epileptic seizures
    • Polycystic ovarian disease
    • Pseudocyesis
    • Chronic low levels of thyroid hormone


Conditions associated with decreased levelsEdit

Main article: Hypoprolactinemia
Hypoprolactinemia, or serum prolactin deficiency, is associated with ovarian dysfunction in women,[SUP][42][/SUP][SUP][43][/SUP] and arteriogenic erectile dysfunction, premature ejaculation,[SUP][44][/SUP] oligozoospermia, asthenospermia, hypofunction of seminal vesicles, and hypoandrogenism[SUP][45][/SUP] in men. In one study, normal sperm characteristics were restored when prolactin levels were brought up to normal values in hypoprolactinemic men.[SUP][46][/SUP]
Hypoprolactinemia can result from hypopituitarism, excessive dopaminergic action in the tuberoinfundibular pathway, and ingestion of D[SUB]2[/SUB] receptor agonists such as bromocriptine.

See alsoEdit



ReferencesEdit




External linksEdit


 
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ldog

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Another good read. Please notice the paragraph showing that Testosterone levels decreased significantly on one particular Anti-Depressant. Anything that decreases Test levels makes me nervous.

New Study Shows the SSRI Paroxetine May Affect Sperm DNA and Male Fertility
Barbara Boughton
June 22, 2009

June 22, 2009 — The selective serotonin-reuptake inhibitor (SSRI) paroxetine (Paxil, GlaxoSmithKline) may affect male fertility through its effects on sperm DNA, according to a small study by Weill Cornell Medical Center researchers. In the study of 35 healthy volunteers without psychiatric disorders, the antidepressant induced abnormal sperm DNA fragmentation in more than 40% of participants.

"Sperm DNA fragmentation is thought to be a very sensitive measure of sperm abnormality, independent of sperm counts or standard sperm tests, and predicts natural fertility as well as fertility with the most advanced forms of assisted reproduction, such as in vitro fertilization," said senior author Peter Schlegel, MD, chair of the department of urology and professor of reproductive medicine at Weill Cornell Medical Center, in New York City. "What the study tells us is that paroxetine could have an effect on fertility that will not show up in standard sperm tests — and cause an increase in genetic damage to sperm," he said.

Their report is published June 10 online in Fertility and Sterility.

Dr. Schlegel noted that because the study did not show any changes in the conventional measures of sperm quality — including sperm volume, concentration, motility, and morphology — their paper suggests that men on SSRIs might have a reduced ability to conceive. "A man could have his fertility affected and still could have what look like normal sperm counts," he said. He advises that men on SSRIs who are interested in conceiving talk to their physicians about other treatment options for depression.


Effects Reversed After Withdrawal

In the study, paroxetine was administered to participants for 5 weeks at escalating doses. Semen analyses were performed at the end of weeks 2 and 4 and again a month after stopping the medication. Sperm DNA fragmentation — defined as missing pieces of code in sperm DNA — was measured with an assay called deoxyuride-50-triphosphate biotin nick end labeling (TUNEL). The men also completed the Brief Sexual Function inventory test at baseline and after the fourth week. Hormonal status, including testosterone levels, was also evaluated in the fourth week after the subjects initiated antidepressant therapy.

In addition to problems in sperm DNA fragmentation, the men also experienced significant sexual dysfunction. At baseline, only 9.7% of patients had a TUNEL score of 30% or less, a cutoff point thought to signal abnormal DNA in sperm. At week 4, however, 50% of patients had a TUNEL score of 30% or less (P = .001). Up to 35% of men in the study also experienced worsening erectile function after starting antidepressant therapy (P < .003), and 47% reported significant declines in ejaculatory function (P < .002). However, normal sexual function as well as normal sperm DNA fragmentation returned 1 month after paroxetine was discontinued.

There was also a significant 28% decrease in testosterone levels in men who took paroxetine (844 ng/dL vs 605 ng/dL; P = .015), although the decreased values remained in the normal range. In healthy men, this decline in serum testosterone levels would have little effect, but for men with compromised fertility, this decline could have negative effects on sperm-cell development, the authors write in their paper.

Coauthor and researcher Cigdem Tanrikut, MD, acknowledged that the study had several limitations. The men were not blinded to the fact that they were taking antidepressants, nor was there any placebo group. Fertility itself was not directly assessed in the study. "Yet the marked changes in sperm DNA integrity strongly suggest a potential negative impact on fertility," said Dr. Tanrikut, adjunct assistant professor of urology and reproductive medicine at Weill Cornell Medical College. In addition, the use of normal healthy volunteers eliminated the chance that the DNA damage — or the sexual dysfunction associated with the antidepressant — might have been caused by comorbid depression or anxiety.

Because sperm DNA returned to normal so quickly, the study suggests that SSRIs may cause problems in sperm transport, rather than production. "If the [DNA] changes were mediated by an effect on sperm production, those changes would have taken months to be reflected in semen analyses," Dr. Tanrikut said. Dr. Schlegel also noted that sperm transmission as well as ejaculation occurs through nerves that can be mediated by serotonin. "Serotonin drives how these nerves work," he said.

Findings "Not Robust"

The authors plan larger-scale randomized placebo-controlled trials with other SSRIs — research that may be necessary to confirm their findings, according to Richard Balon, MD, professor of psychiatry at Wayne State University in Detroit, Michigan, who specializes in research on sexual dysfunction. "These are interesting findings, but they are not robust," he said. As well as the small size of the study, he noted that tests of conventional semen parameters did not show any effect from paroxetine. He also pointed out that many of the men who had abnormal sperm DNA fragmentation were obese, and although the authors could find no correlation in their statistical analysis, it could have possibly influenced the results, Dr. Balon said.


"There are some interesting findings in the study — including the sexual dysfunction found in healthy volunteers taking SSRIs, as well as the decreases in testosterone levels," he said. "But the findings need follow-up and confirmation," he added.

The study was funded by the Frederick J. and Theresa Dow Wallace Fund of the New York Community Trust and the Brady Urology Foundation. Drs. Tanrikut and Balon reported no relevant financial disclosures. Dr. Schlegel is a member of the medical advisory board for Theralogix.

Fertil Steril.2009: Published online June 10, 2009. Abstract



http://www.medscape.com/viewarticle/704701

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sneedam

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Another good read. Please notice the paragraph showing that Testosterone levels decreased significantly on one particular Anti-Depressant.

http://www.medscape.com/viewarticle/704701

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Keep them coming Idog... Very good info... I have had a couple life changing events in the past 2 years and though I have always suffered from debilitating anxiety, in recent I have had to do a lot of soul searching. I am ready to try and get back on track but it is slow and difficult.. I have always been strong but I am being tested...
I am writing this reply in my Dr office waiting for labs... I will update in the other thread and post them as well when I receive the results... Again thanks...
 

ldog

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Brother you are very welcome. I'm here to help. If you ever have any questions or just want a new opinion on things, hit me up on PM.
 

Janoy crevesa

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I'm on prozac. Idk how much it helps but it does help with cravings and appetite.
 

butchsandance77

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Thanks for this information, really quite helpful! Ive been on AntiDs, taking Pristique at 100mg, which is in the SRNI. I hate being on them, I know why I am though, my own decisions last year and I wasn't able to deal with what was going on, took to alcohol and spiraled into anger. Saw a sports psychologist which helped immensely how to deal with stress and exercises to do to centre me back. Unfortunately this is where I really hate being on them, when I run out or forget even one dose, which is this morning, send me over cliff, the world spins, I have nightmares and I know Im in for a bad 24 hrs until my levels come back to normal. And the irrational thought of if I come off the world will collapse.
After reading these studies Im wondering how much my T levels have been affected.
 

Mosam

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Thanks brother I have been looking around for studies about this issue and i found very little information that makes a lot of sense good reading my man
 

XOTG85

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Vision I have been taking 10 mg of citalopram for a few months now and it works great for my depression and anxiety. I’m about to start a Tren Ace run and was thinking of adding .25mg of Pramipexole each night to battle progesterone side affects. With my dose very low for each do I have anything to worry about? I have used prami in the past with great affects but I wasn’t on any anti depressants so I’m not sure how this would affect me. Thanks in advance.
 
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