Antidepressant Effects and Steroids
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.
SNRI (Serotonin-norepinephrine reuptake inhibitor)
Below are the three of the most common and popular SNRI products.
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
TestosteroneAlan Jay Cohen, M.D.
Private Practice and Assistant Clinical Professor of Psychiatry, UCSF
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.
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
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.
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
All of the other subjects had normal Prolactin levels. Thyroid
stimulating hormone was found to be normal in all subjects.
Sex Age Medication ASECS score free T (pg./ml.)
M 35 venlafaxine 16 23.4
M 36 sertraline 21 5.2 *
M 43 paroxetine 18 13.5 *
M 45 venlafaxine 17 16.3 #
M 46 venlafaxine 20 13.2 *
M 46 paroxetine/mirtazepine 20 13.4 *
M 47 citalopram 19 29.0
M 47 fluoxetine 22 17.6 #
M 50 sertraline 17 6.2 *
M 53 nefazodone 25 11.1 *
M 54 bupropion 21 7.4*
M 74 venlafaxine 24 5.6 *
F 20 citalopram 29 1.7
F 31 venlafaxine 21 0.50*
F 37 paroxetine 23 0.70 *
F 41 paroxetine 19 1.5
F 44 sertraline 16 0.40 *
F 45 bupropion/trazodone 16 0.50 *
F 47 fluoxetine 20 0.50*
F 52 bupropion 16 0.40
(*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.
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 ********* cleaarance 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 ********* clearance of testosterone and reduction in free hormone levels.
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 fo antidepressant use. Further studies should also include measurement of total testosterone levels as well as concomitant SHBG levels.
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.
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.
4.) Cohen AJ and Bartlik B (1998) Ginkgo biloba for
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
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
tract in :Williams Textbook of Endocrinology 9th ed. W.B. Saunders Co.
_8.) Herzog AG (1995) Hormonal changes in epilepsy Epilepsia
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
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/seasoned or even done your research you should be you’re a smart to know/use and understand about running PCT’s, Anti’s and other agents for recovery and assistance..
So by now I sure hope that your all to familiar with Nolvadex? That’s correct – (Tamoxifen Citrate).
Nolvadex (Tamox) uses an enzyme ‘CYP2D6***8242; to convert itself into a more useful form that our bodies can use. Unfortunately many antidepressants also use this same CYP2D6 enzyme, thus you have two medications competing for the same pathway.
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 intend on using Nolvadex as your PCT, it’s important for you to know which antidepressants will cause issue and if you’re on an antidepressant that will inhibit Nolvadex from being functional, it’s recommend going with Clomid or Fareston (Toremifene Citrate)instead 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.
Generic Names Brand Names
Generic Names Brand Names
SSRIS AND SNRIS THAT ARE NOT INHIBITORS
Generic Names Brand Names
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.
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)
Below is a study supporting this-
Changes in plasma prolactin during SSRI treatment: evidence for a delayed increase in 5-HT neurotransmission.
Cowen PJ1, Sargent PA.
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.
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,keeping an open honest trust policy will go a long way,and it could avoid any unwated side effect..
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,more information will be added)