Depression while on cycle? Let's talk about why and some remedies
Posted: Sat Aug 08, 2020 12:30 pm
I need to be just come out say this in the opener sentence, I'm very much against antidepressants and large pharma.
Ok, before I lose you here, please bear with me; Yet at the same time this statement makes me a hypocrite because I have Incorporated them in my life when need be (when needed).. Personally I'm an advocate with exhausting all resources possible before using antidepressants, antidepressants are pushed down people's throats too frivolously, nevertheless at the same time some people do in fact need them, that is the reality, mental health issues are very real and sometimes needs medication..
Cycling and depression: What's the best options to assist with such symptoms?
I personally feel using natural supplements before considering any meds. 5-HTP comes to mind, DHEA, Injection Vitamin B, Gaba and even L-tryptophan. L-trytophent is an amino acid, a protein building block that can be found in many plant and animal proteins. L-tryptophan is called an “essential” amino acid because the body can’t make it. It must be acquired from food.
5-HTP, GABA and L-tryptophan could be used for treating insomnia, sleep apnea, depression, anxiety, facial pain, a severe form of premenstrual syndrome called premenstrual dysphoric disorder (PMDD), smoking cessation, grinding teeth during sleep (bruxism), attention deficit-hyperactivity disorder (ADHD), Tourette's syndrome, and to improve athletic performance. The list goes on.
FYI, I have tourette's/Ticks and this truly has provided comfort and a sense of calm, removing the dreaded anxious feeling that comes along with having ticks.
How does it work?
L-tryptophan is naturally found in animal and plant proteins. L-tryptophan is considered an essential amino acid because our bodies can't make it. It is important for the development and functioning of many organs in the body. After absorbing L-tryptophan from food, our bodies convert it to 5-HTP (5-hyrdoxytryptophan), and then to serotonin. Serotonin is a hormone that transmits signals between nerve cells. It also causes blood vessels to narrow. Changes in the level of serotonin in the brain can alter mood.
I'm not a licensed medical practitioner therefore I can't give any medical advise, although I will give some suggestions based on personal experience.
Ok, now that we've talked about a "few" natural alternatives, let's take a deeper look into meds and how they can be very detrimental with AAS use.
Let's leap frog here real fast, scroll down and read the study in the read title labeled as "SSRI's and Gear", scan that over and return back here
and we shall continue.
*
*
*
*
*
*
*
Welcome back
For myself I have always resorted to Wellbutrin and/or Busparin (Buspar). Just an FYI, buspar can act muck like cabergoline when assisting with delayed ejaculations or inability to have an orgasm. Click here to learn more about buspar and sexual dysfunctions from AAS or medications (https://pubmed.ncbi.nlm.nih.gov/1035003 ... 0in%20men.
Let's get right into it with AAS and how some compounds can in fact be used as antidepressants like drugs during a cycle/blast. And - How some compounds can in
fact be the culprit for depression, tiredness, lethargy and loss of sense of well being.
AAS (androgens) especially Halo because it's extremely aggressive can result in a decrease peak of plasma corticosterone concentrations by way of potentially disabling HSD-11B or 11B-HSD which are hosts of enzymes that catalyze the conversion of cortisone to active cortisol.. Almost inducing a state of adrenal fatigue by other methods of action, basically inducing adrenal fatigue like symptoms..You can experience this while on most AAS "especially" Trenbolone, drol and some pro-hormones (MT1/SD), there can be a slew of rather aggressive sides not only from it's toxicity to the liver but through this other indirect course of action yielding a slew of undesired sides in "some" users....
I suggest adding some DHEA with some sublingual vitamin b12 complex and take it from there.. Try and cut back on caffeine, actually I would suggest extracting it from your daily life for a bit if someone is experiencing adrenal like symptoms.
An other suggestions, you may want to add some low to a moderate dose of GHRP-6 and/or Hexarelin, these peptide both act in a similar mechanisms and have been known to increase the release of ACTH which can improve the serum plasma levels with cortisol, restoring it to a health functional state, hindering any "halotestin or AAS" related sides that may be present by way of adrenal fatigue like symptoms..
AAS, love-hate relationship with many trade-offs!
Anavar, Masteron, Proviron, Testosterone..
The paradox with 3 of the 4 hormones mentioned (test,mast and proviron) they are essentially the most favored when it concerns that "feel good effect" that we look for when running compounds.
Let's look at your supra-physiological dosages of Testosterone (which has 3 mechanisms of action,1-testosterone, 2-conversion to estro, 3-conversion to DHT) and your other compounds like mast/proviron..Basically, your reaction with these compounds/hormones by way of exogenous sources along with their aggressiveness as a potent hormone (DHT) and interplay's with E2 (by was of test conversion) all these can significantly decrease the corticosterone and ACTH response through its pathways, by initiating a response via the hypothalamus..
(Anavar is known to be outstanding for blocking cortisol levels from having excessive dumps).
I'll include a study that explains more on how Dihydrotestosterone and it's derivative can potentially display some cross-reactivity that will disrupted corticolsteroids which may possess blocking properties of cortisol..In a nut shell, DHT's could possibly act somewhat as a cortisol "blocker" in sensitive users..End result, adrenal fatigue like symptoms!
Just my take, I'm no specialist..I'm just looking at things from a different approach, it may not be the most popular belief.
(study)
J Neurosci. 2006 Feb 1;26(5):1448-56.
The androgen 5alpha-dihydrotestosterone and its metabolite 5alpha-androstan-3beta, 17beta-diol inhibit the hypothalamo-pituitary-adrenal response to stress by acting through estrogen receptor beta-expressing neurons in the hypothalamus.
Lund TD1, Hinds LR, Handa RJ.
Author information
Abstract
Estrogen receptor beta (ERbeta) and androgen receptor (AR) are found in high levels within populations of neurons in the hypothalamus. To determine whether AR or ERbeta plays a role in regulating hypothalamo-pituitary-adrenal (HPA) axis function by direct action on these neurons, we examined the effects of central implants of 17beta-estradiol (E2), 5alpha-dihydrotestosterone (DHT), the DHT metabolite 5alpha-androstan-3beta, 17beta-diol (3beta-diol), and several ER subtype-selective agonists on the corticosterone and adrenocorticotropin (ACTH) response to immobilization stress. In addition, activation of neurons in the paraventricular nucleus (PVN) was monitored by examining c-fos mRNA expression. Pellets containing these compounds were stereotaxically implanted near the PVN of gonadectomized male rats. Seven days later, animals were killed directly from their home cage (nonstressed) or were restrained for 30 min (stressed) before they were killed. Compared with controls, E2 and the ERalpha-selective agonists moxestrol and propyl-pyrazole-triol significantly increased the stress induced release of corticosterone and ACTH. In contrast, central administration of DHT, 3beta-diol, and the ERbeta-selective compound diarylpropionitrile significantly decreased the corticosterone and ACTH response to immobilization. Cotreatment with the ER antagonist tamoxifen completely blocked the effects of 3beta-diol and partially blocked the effect of DHT, whereas the AR antagonist flutamide had no effect. Moreover, DHT, 3beta-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN. Together, these studies indicate that the inhibitory effects of DHT on HPA axis activity may be in part mediated via its conversion to 3beta-diol and subsequent binding to ERbeta.
"SSRI's and Gear"
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
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.
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.
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.
STRONG INHIBITORS
Generic Names Brand Names
Bupropion Wellbutrin
Fluoxetine Prozac
Paroxetine Paxil
Quinidine Cardioquin
MODERATE INHIBITORS
Generic Names Brand Names
Duloxetine Cymbalta
Sertraline Zoloft
Diphenhydramine Benadryl
Thioridazine Mellaril
Amiodarone Cordarone
Trazodone Desyrel
Cimetidine Tagamet
SSRIS AND SNRIS THAT ARE NOT INHIBITORS
Generic Names Brand Names
Venlavaxine Effexor
Citalopram Celexa
Escitalopram Lexapro
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)
Ok, before I lose you here, please bear with me; Yet at the same time this statement makes me a hypocrite because I have Incorporated them in my life when need be (when needed).. Personally I'm an advocate with exhausting all resources possible before using antidepressants, antidepressants are pushed down people's throats too frivolously, nevertheless at the same time some people do in fact need them, that is the reality, mental health issues are very real and sometimes needs medication..
Cycling and depression: What's the best options to assist with such symptoms?
I personally feel using natural supplements before considering any meds. 5-HTP comes to mind, DHEA, Injection Vitamin B, Gaba and even L-tryptophan. L-trytophent is an amino acid, a protein building block that can be found in many plant and animal proteins. L-tryptophan is called an “essential” amino acid because the body can’t make it. It must be acquired from food.
5-HTP, GABA and L-tryptophan could be used for treating insomnia, sleep apnea, depression, anxiety, facial pain, a severe form of premenstrual syndrome called premenstrual dysphoric disorder (PMDD), smoking cessation, grinding teeth during sleep (bruxism), attention deficit-hyperactivity disorder (ADHD), Tourette's syndrome, and to improve athletic performance. The list goes on.
FYI, I have tourette's/Ticks and this truly has provided comfort and a sense of calm, removing the dreaded anxious feeling that comes along with having ticks.
How does it work?
L-tryptophan is naturally found in animal and plant proteins. L-tryptophan is considered an essential amino acid because our bodies can't make it. It is important for the development and functioning of many organs in the body. After absorbing L-tryptophan from food, our bodies convert it to 5-HTP (5-hyrdoxytryptophan), and then to serotonin. Serotonin is a hormone that transmits signals between nerve cells. It also causes blood vessels to narrow. Changes in the level of serotonin in the brain can alter mood.
I'm not a licensed medical practitioner therefore I can't give any medical advise, although I will give some suggestions based on personal experience.
Ok, now that we've talked about a "few" natural alternatives, let's take a deeper look into meds and how they can be very detrimental with AAS use.
Let's leap frog here real fast, scroll down and read the study in the read title labeled as "SSRI's and Gear", scan that over and return back here
and we shall continue. *
*
*
*
*
*
*
Welcome back
For myself I have always resorted to Wellbutrin and/or Busparin (Buspar). Just an FYI, buspar can act muck like cabergoline when assisting with delayed ejaculations or inability to have an orgasm. Click here to learn more about buspar and sexual dysfunctions from AAS or medications (https://pubmed.ncbi.nlm.nih.gov/1035003 ... 0in%20men.
Let's get right into it with AAS and how some compounds can in fact be used as antidepressants like drugs during a cycle/blast. And - How some compounds can in
fact be the culprit for depression, tiredness, lethargy and loss of sense of well being.
AAS (androgens) especially Halo because it's extremely aggressive can result in a decrease peak of plasma corticosterone concentrations by way of potentially disabling HSD-11B or 11B-HSD which are hosts of enzymes that catalyze the conversion of cortisone to active cortisol.. Almost inducing a state of adrenal fatigue by other methods of action, basically inducing adrenal fatigue like symptoms..You can experience this while on most AAS "especially" Trenbolone, drol and some pro-hormones (MT1/SD), there can be a slew of rather aggressive sides not only from it's toxicity to the liver but through this other indirect course of action yielding a slew of undesired sides in "some" users....
I suggest adding some DHEA with some sublingual vitamin b12 complex and take it from there.. Try and cut back on caffeine, actually I would suggest extracting it from your daily life for a bit if someone is experiencing adrenal like symptoms.
An other suggestions, you may want to add some low to a moderate dose of GHRP-6 and/or Hexarelin, these peptide both act in a similar mechanisms and have been known to increase the release of ACTH which can improve the serum plasma levels with cortisol, restoring it to a health functional state, hindering any "halotestin or AAS" related sides that may be present by way of adrenal fatigue like symptoms..
AAS, love-hate relationship with many trade-offs!
Anavar, Masteron, Proviron, Testosterone..
The paradox with 3 of the 4 hormones mentioned (test,mast and proviron) they are essentially the most favored when it concerns that "feel good effect" that we look for when running compounds.
Let's look at your supra-physiological dosages of Testosterone (which has 3 mechanisms of action,1-testosterone, 2-conversion to estro, 3-conversion to DHT) and your other compounds like mast/proviron..Basically, your reaction with these compounds/hormones by way of exogenous sources along with their aggressiveness as a potent hormone (DHT) and interplay's with E2 (by was of test conversion) all these can significantly decrease the corticosterone and ACTH response through its pathways, by initiating a response via the hypothalamus..
(Anavar is known to be outstanding for blocking cortisol levels from having excessive dumps).
I'll include a study that explains more on how Dihydrotestosterone and it's derivative can potentially display some cross-reactivity that will disrupted corticolsteroids which may possess blocking properties of cortisol..In a nut shell, DHT's could possibly act somewhat as a cortisol "blocker" in sensitive users..End result, adrenal fatigue like symptoms!
Just my take, I'm no specialist..I'm just looking at things from a different approach, it may not be the most popular belief.
(study)
J Neurosci. 2006 Feb 1;26(5):1448-56.
The androgen 5alpha-dihydrotestosterone and its metabolite 5alpha-androstan-3beta, 17beta-diol inhibit the hypothalamo-pituitary-adrenal response to stress by acting through estrogen receptor beta-expressing neurons in the hypothalamus.
Lund TD1, Hinds LR, Handa RJ.
Author information
Abstract
Estrogen receptor beta (ERbeta) and androgen receptor (AR) are found in high levels within populations of neurons in the hypothalamus. To determine whether AR or ERbeta plays a role in regulating hypothalamo-pituitary-adrenal (HPA) axis function by direct action on these neurons, we examined the effects of central implants of 17beta-estradiol (E2), 5alpha-dihydrotestosterone (DHT), the DHT metabolite 5alpha-androstan-3beta, 17beta-diol (3beta-diol), and several ER subtype-selective agonists on the corticosterone and adrenocorticotropin (ACTH) response to immobilization stress. In addition, activation of neurons in the paraventricular nucleus (PVN) was monitored by examining c-fos mRNA expression. Pellets containing these compounds were stereotaxically implanted near the PVN of gonadectomized male rats. Seven days later, animals were killed directly from their home cage (nonstressed) or were restrained for 30 min (stressed) before they were killed. Compared with controls, E2 and the ERalpha-selective agonists moxestrol and propyl-pyrazole-triol significantly increased the stress induced release of corticosterone and ACTH. In contrast, central administration of DHT, 3beta-diol, and the ERbeta-selective compound diarylpropionitrile significantly decreased the corticosterone and ACTH response to immobilization. Cotreatment with the ER antagonist tamoxifen completely blocked the effects of 3beta-diol and partially blocked the effect of DHT, whereas the AR antagonist flutamide had no effect. Moreover, DHT, 3beta-diol, and diarylpropionitrile treatment significantly decreased restraint-induced c-fos mRNA expression in the PVN. Together, these studies indicate that the inhibitory effects of DHT on HPA axis activity may be in part mediated via its conversion to 3beta-diol and subsequent binding to ERbeta.
"SSRI's and Gear"
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
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.
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.
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.
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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.
STRONG INHIBITORS
Generic Names Brand Names
Bupropion Wellbutrin
Fluoxetine Prozac
Paroxetine Paxil
Quinidine Cardioquin
MODERATE INHIBITORS
Generic Names Brand Names
Duloxetine Cymbalta
Sertraline Zoloft
Diphenhydramine Benadryl
Thioridazine Mellaril
Amiodarone Cordarone
Trazodone Desyrel
Cimetidine Tagamet
SSRIS AND SNRIS THAT ARE NOT INHIBITORS
Generic Names Brand Names
Venlavaxine Effexor
Citalopram Celexa
Escitalopram Lexapro
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)