EVERYONE Will Get Finasteride Side-Effects Eventually

Feelsbadman

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That is something you set for yourself and wishes can come true
??
im already ugly and baldin wouldn't suit me at all

ill take my chances with finasteride
your tissue is already grown in adult hood finasteride cant reduce the size of your dick
 

Feelsbadman

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i don't understand how it redues your dik size?
i take supplements and eat a diet full of nitrates, een with finasteride i get throbbing erection and have huge veins in my c***
 

Jeju

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i don't understand how it redues your dik size?
i take supplements and eat a diet full of nitrates, een with finasteride i get throbbing erection and have huge veins in my c***
Are you okay, mate? You posted earlier that you miss having a sex drive but now you’re saying you have a throbbing erection with huge veins.
 

Pigeon

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Another interesting piece about FDA:


"The bar for “safe” is equally low, and over the past 30 years, approved drugs have caused an epidemic of harmful side effects, even when properly prescribed. Every week, about 53,000 excess hospitalizations and about 2400 excess deaths occur in the United States among people taking properly prescribed drugs to be healthier.


Prescription drugs are the 4th leading cause of death.


This evidence indicates why we can no longer trust the FDA to carry out its historic mission to protect the public from harmful and ineffective drugs. Strong public demand that government “do something” about periodic drug disasters has played a central role in developing the FDA.2 Yet close, constant contact by companies with FDA staff and officials has contributed to vague, minimal criteria of what “safe” and “effective” mean."
 

Pigeon

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Found some very interesting studies about the importance of DHT:




DHT is an estrogen (receptor) antagonist​


A neat little study, and in-vivo at that, which demonstrates that DHT is a direct estrogen receptor (ER) antagonist. According to the study, so are testosterone, nandrolone and a few other steroids with demonstrated therapeutic effects on ER-positive breast cancer (BC). However, all of the other steroids mentioned by the study are aromatizable and as such suboptimal as anti-estrogens compared to DHT. This is probably one of the reasons that back in the 1960s when synthetic steroids for treatment of BC were first developed, only DHT derivatives such as Proviron and Masteron eventually made it to clinical trials and got approval for this condition. None of the aromatizable synthetic androgens (or testosterone for that matter) made it through the clinical trials despite being much more widely used (experimentally) for BC at the time. When we also consider the fact that DHT (and other 5-AR derives steroids) are also aromatase inhibitors, it becomes clear that DHT is right up there with progesterone in terms of importance for estrogen antagonism, and perhaps the main anti-estrogen in males. Another interesting finding of the study was that the anti-estrogenic effects of DHT were independent from its role as an androgen agonist. However, androgen agonists are well-known known to have anti-estrogenic effects of their own, so the effectiveness of DHT as an anti-estrogen is actually amplified by its role as a strong androgen. Finally, the study provide some information on what a physiological dose of DHT would be, which is subject to much debate in the literature and in the blogosphere. As the study states, healthy males produce about 45 mcg estrogen daily and DHT amounts need to be about 50 times higher in order to fully block the effects of a given amount of estrogen. This means that a daily physiological dose is about 2mg for healthy adult males, and that dose may need to be increased with increasing age or pathological conditions resulting in elevated estrogens such as liver disease, diabetes, prostate cancer, etc.

https://pubmed.ncbi.nlm.nih.gov/6542571/

“…Estrogen treatment to such mice stimulates breast growth and as in other species increases the amount of progesterone receptor in the breast. Both effects of estradiol can be inhibited by dihydrotestosterone. We concluded that this might be an adequate model system for investigating the mechanism of the antiestrogenic action of androgen, and we designed experiments to assess two mechanisms that have been proposed for this action, namely that androgen acts at the genomic level via its own receptor to block estrogen action or that androgen acts as a pharmacological antagonist and/or weak estrogen agonist by competing with estradiol for the estrogen receptor. The findings in these experiments favor the latter possibility. Indeed, the fact that dihydrotestosterone was equally effective in blocking estrogen effects in tfm/Y and control mice suggests that this action of androgen is not mediated by the androgen receptor. If this interpretation is correct, then this effect of androgen is different than the antiestrogenic effect of the hormone in the embryonic mouse breast (11) and in the uterus (12). Dihydrotestosterone binds weakly to the estrogen receptor in mouse breast and like some other antiestrogens appears to anchor the estrogen-receptor in the nucleus of the cell. These effects have only been studied with pharmacological amounts of hormone, but the fact that the relative binding affinities of dihydrotestosterone, 313-androstanediol, testosterone, and Sfdihydrotestosterone correlate with their capacities to inhibit induction of the progesterone receptor is in keeping with the finding in MCF7 tumor cells (10) that androgens bind to the estrogen receptor. Unlike the situation in MCF7 cells, however, we were unable to demonstrate any estrogen-like effects of dihydrotestosterone on the mouse breast.”
“…If androgen prevents the development of gynecomastia in normal men by acting as a direct antiestrogen at the level of the estrogen receptor, this is the first androgen action recognized that is not mediated by the androgen receptor.”
“…Normal men produce ~45 mcg of estradiol each day, a sixth of which is secreted by the testes and the remainder of which is derived from the extraglandular aromatization of circulating androgens (1). Extraglandular estradiol formation takes place by two mechanisms, one from the direct conversion of testosterone to estradiol and the other from androgens of adrenal origin by the sequence of androstenedione – estrone – estradiol. The function of estradiol in normal men is unknown, but feminization, commonly manifested by gynecomastia, ensues under conditions of relative or absolute estrogen excess (2)….By this estimate estradiol binds to the estrogen receptor with an affinity that is approximately fifty times greater than that of dihydrotestosterone.”







Low DHT can cause hypogonadism symptoms even in eugonadal men​


Seemingly contradictory title, but the study findings are pretty clear. Namely, even in males with normal testosterone levels there is a direct inverse relationship between DHT levels and symptoms of hypogonadism such as sexual dysfunction and “aging male” syndrome. For every 10% increase in DHT levels there was a 4.67% decrease in hypogonadism symptoms of eugonadal males. So, once again, this is evidence that testosterone (T) is little more than a pro-hormone produced in the gonads and peripheral tissues and that its metabolite DHT is the primary androgen responsible for health of males.

https://pubmed.ncbi.nlm.nih.gov/33811609/

“…Results: Serum total/free T as well as dihydro-T (DHT) was associated with IIEF-EF and AMS scores in the overall population using univariate analyses. Multivariate approaches revealed DHT concentrations in subjects with normal T levels (n = 416, Total T > 12 nmol/L) to be significant predictors of AMS scores. A 0.1 nmol/l serum DHT increase within the eugonadal range was associated with a 4.67% decrease in odds of having worse symptoms (p = 0.011). In men with biochemical hypogonadism (Total T < 12 nmol/L), total and free T rather than DHT were associated with AMS results. This association was not found for IIEF-EF scores. Indirect effects of age and BMI were seen for relations with hormone concentrations but not questionnaire scores. Conclusion: DHT can be associated with symptoms of hypogonadism in biochemically eugonadal men. Serum DHT measurement might be helpful once the diagnosis of hypogonadism has been ruled out but should not be routinely included in the primary diagnostic process.”
 

Pigeon

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DHT, not T, likely the “active” androgen in heart and brain​



Interesting study, done on baboons (so should have good relevance for humans), demonstrating that the cardiovascular system (CVS) exclusively accumulates and recognizes (at the receptor level) DHT, instead of testosterone (T). In fact, the androgen receptor in CVS is so structurally different it apparently cannot even bind T. Recent studies with ALS patients suggest the same may be true in humans, not only in the CVS but in the nervous system as well. Namely, ALS patients tend to have high (circulating) T but lower DHT levels, especially in their brains. The hypothesis for a unique role of DHT in tissues is further corroborated by animal ALS studies demonstrating that administration of DHT is therapeutic, while multiple studies with T have produced null or negative effects. Aside from suggesting once again that DHT, instead of T, is the true tissue-active androgen in humans (and most animals) it also suggests that administration of 5-AR drugs such as finasteride / dutasteride may play a direct causative role in CVD and lethal neurodegenerative conditions such as ALS. Such ALS link has already been established for statins, and considering statins’ decimating effects on DHT levels, the risks from finasteride / dutasteride use are likely to be much higher.

https://onlinelibrary.wiley.com/doi/abs/10.1002/ar.1092230410

“…This study, along with our previous studies (McGill et al., 1980; McGill and Sheridan, 1981; Sheridan et al., 19811, allows us to compare the in vivo nuclear uptake and retention of 3H-androgen in the cardiovascular system after the injection of 3H-testosterone or 3HDHT. This comparison, along with our biochemical data and the data published in the literature, has led us to two main conclusions to be discussed in detail below. First, we interpret the aggregate data to indicate that the main androgen acting on the cardiovascular system of the baboon is circulating DHT. Second, we believe that the androgen receptor in the baboon cardiovascular system is a physically different androgen receptor from that found in the kidney of a number of species and from the androgen receptor found in certain areas of the developing rat brain.”
“…In summary, after comparing the uptake and retention and metabolism of 3H-steroid in the cardiovascular system of baboons following the injection of 3H-testosterone in the present study and 3H-DHT in previous studies (McGill et al., 1980; McGill and Sheridan, 1981; Sheridan et al., 1981), we interpret the data to suggest that the physiological important androgen for the cardiovascular system is circulating DHT, not testosterone, even though there is approximately ten times more circulating testosterone than DHT. In addition, in comparing our autoradiographic data, indicative of in vivo nuclear uptake and retention of 3H-androgens, with the published biochemical data dealing with the in vitro binding characteristics of cytosolic receptor, we interpret the discrepancy between in vivo nuclear uptake and retention of unmetabolized testosterone in the kidney and lack of in vivo nuclear uptake and retention of unmetabolized testosterone (DHT is accumulated) in the myocardium to be indicative of separate receptors for testosterone and DHT.”





DHT better (and safer) than testosterone for improving blood pressure, insulin levels​



A great human study on the beneficial effects of androgens for a variety of metabolic biomarkers associated with insulin resistance and diabetes II. The only gripe I have with this study is that they claim it was conducted with “healthy” men when in reality all men had low plasma total testosterone (PTT), which of course makes them anything but healthy considering the broad negative effects low gonadal function (of which total T is a sign of) has on systemic health. One of the strengths of the study is that the androgen doses used as treatment were physiological – estimated absorbed steroid amounts were about 12mg for T and 3.5mg for DHT daily. Thus, it demonstrates that restoring normal concentrations of androgens in men has a number of positive effects on biomarkers that are currently considered more of a genetic than environmental origin, and most certainly not due to an endocrine dysfunction. Another strong point of the study was that it lasted only 3 months, yet the benefits were quite robust, and happened without ANY changes to dietary or exercise habits. Finally, my favorite finding of the study – DHT was more effective than T at improving those biomarkers, despite the almost 4-fold lower dose used! So, if you are a male above 35 and have a few extra inches around your midsection, you should probably politely decline your doctor’s offer of metformin and instead request a steroid panel combined with a DHT script Oh, and last but not least – while one subject in the T group developed (benign) prostatic nodules, none of the DHT subjects developed any prostate issues. Another (mild) issue of possible concern is that some of the subjects in the T group had increased hemoglobin and hematocrit. The medical literature keeps warning about increased hematological risks as a result of androgen therapy, but as it turns out once again those risks are mostly associated with aromatizable androgens.

https://care.diabetesjournals.org/content/24/12/2149

“…Men with low levels of PTT (confirmed by two measurements) were selected from a large occupation-based population. The inclusion criteria were as follows: 1) either PTT ≤3.4 ng/ml [5th percentile value of PTT distribution in the 1,718 men of the TELECOM Study (7)] from 1985 to 1987 and <4.0 ng/ml (13th percentile value) from 1992 to 1993 (3) or PTT <4.0 ng/ml from 1992 to 1993 and <4.0 ng/ml a few days before inclusion; 2) no history of vascular thrombosis or ischemic heart disease; 3) no treatment by androgens, anti-androgens, and antidiabetic or antithrombotic drugs; 4) normal values of plasma prolactin, estradiol, and thyroxin; 5) no current prostatic disease and a normal PSA value. A total of 18 healthy men with stable low plasma androgens (Table 1) and a range of PTT from 1.4 to 3.7 ng/ml at baseline were included. The 18 selected men were randomly assigned to one of three treatment groups: testosterone, DHT, or placebo. The randomization code was known only to the study manager. Treatment was a gel administered every morning by percutaneous route. The daily dose during the first weeks was 125 mg for the testosterone and 35 mg for the DHT treatment groups. The adaptation of treatment doses between days 10 and 20 aimed at obtaining a trough level of PTT between 4 and 10 ng/ml for the testosterone group and a trough level of plasma DHT between 4 and 10 ng/ml for the DHT group. To maintain the double blinding, the study manager also sometimes changed the dose of placebo. The subjects were asked not to change their dietary and physical activity. Compliance to treatment was assessed by interview and by measuring sex hormones and gonadotropins at the end of the trial.”
“…At baseline, the three treatment groups were similar with respect to age, BMI, waist-to-hip ratio (WHR), blood pressure, plasma glucose, lipids, insulin, leptin, androgens, and sex hormone–binding globulin, as well as hemoglobin, hematocrit, coagulation, and fibrinolysis parameters (data not shown). At the end of the trial, a significant difference was shown for the variation of fasting plasma insulin (P < 0.05), fasting plasma insulin–to–fasting plasma glucose ratio (P < 0.01), and HOMA index (P < 0.05), which all decreased under androgens. The two-by-two comparisons showed a significant improvement only for DHT compared with placebo (P < 0.01 for all of these indexes of insulin sensitivity). No significant differences were observed for 2-h plasma glucose and insulin among the three groups (data not shown), whereas plasma leptin significantly decreased under androgen treatment (P < 0.05), mainly with DHT (P < 0.05 for DHT vs. placebo). Systolic blood pressure increased in the placebo group (P = 0.052) (Table 1). The only serious event was the discovery of a prostatic nodular hyperplasia, benign at biopsy, in a subject treated by testosterone. A trend for an increase in weight was observed under androgen treatment (P = 0.09), mainly with testosterone (Table 1), without any modification of waist circumference and WHR (data not shown). No change was observed on the ECG recordings. No significant difference was shown among the three groups for lipids (Table 1), PSA, hepatic enzymes, coagulation, and fibrinolysis parameters, but hemoglobin and hematocrit increased under androgens (P < 0.05 and P < 0.01, respectively), mainly with testosterone (data not shown).”
“…This randomized, controlled, double-blind trial provides evidence that in healthy men, androgen treatment, particularly DHT, improves insulin sensitivity and decreases plasma leptin level without notable side effects. The three treatment groups were quite identical at baseline concerning glucose tolerance status. In the placebo group, one subject was diabetic according to 2-h plasma glucose (227 mg/dl, with fasting plasma glucose at 85 mg/dl), and none had impaired glucose tolerance (IGT) or impaired fasting glucose (IFG). In the DHT group, one subject had IGT, and none had diabetes or IFG. In the testosterone group, all of the subjects had normal glucose tolerance. The primary differences at baseline concerned bioavailable testosterone with a trend for a higher level in the DHT group, which should have blunted (not increased) the response to DHT treatment and blood pressure, probably explaining the nearly significant improvement of systolic blood pressure under androgens by a regression to the mean phenomenon in the placebo group. On the contrary, the parallel decrease in fasting plasma insulin and leptin and the improvement in insulin sensitivity under androgens appear very consistent. Our study may appear limited because of the sample size (half of that planned), enjoining the use of conservative nonparametric tests, and causing the final statistical analysis to be equivalent to a planned intermediary analysis. Indeed, to have confirmed the a priori hypotheses in these conditions of weak statistical power emphasizes the effect of androgens, mainly DHT, to improve insulin sensitivity and to decrease leptin concentrations in healthy men with low PTT. Very few side effects were observed, including a tendency for weight increase and an increase in hemoglobin and hematocrit, although these were reversible a few months later (data not shown), thus indicating good patient compliance to the allocated treatment, also confirmed by hormone measurements.”
“…The decrease in plasma leptin concentration is also probably explained by the supposed reduction in adipose tissue mass (11), but the influence of androgens on leptin could also be mediated by a stimulation of the splanchnic β-adrenoceptors (12) or by a direct suppressive effect on ob gene expression (13). Nevertheless, our data clearly demonstrate the role of androgens to decrease leptin levels in healthy men, as previously suggested (5). In conclusion, this clinical trial demonstrates that androgens improve insulin sensitivity and decrease leptin levels in adult men. We recruited healthy subjects ranked in the lowest 10 percentiles of the PTT distribution from a large occupation-based population by systematically measuring PTT. Therefore, these data can most likely be extrapolated to healthy men in the first decile of the PTT distribution. The pathways through which androgens exert their inhibiting effects on insulin and leptin in humans deserve further fundamental research. In parallel, as low levels of testosterone are predictive of the development of insulin resistance and type 2 diabetes (14), and as type 2 diabetic patients are known to have a lower level of PTT than nondiabetic men (15), larger studies on androgen treatment in insulin-resistant nondiabetic subjects and in type 2 diabetic patients are necessary.
 

Pigeon

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Lowering DHT synthesis causes severe hypothyroidism, despite higher T levels​



Just a quick post in regards to one of the most controversial steroids out there – dihydrotestosterone (DHT). Mainstream medicine has vilified this steroid for decades and has blamed a host of male and female pathologies on it – i.e. baldness, prostate enlragement (BPH), prostate cancer (PC), PCOS, diabetes, obesity, dementia, osteoporosis, etc. One of the most popular prescription drugs in the last two decades was the 5α-Reductase (5-AR)) inhibitor finasteride, which is the drug of choice for “treating” male baldness, BPH, PC, and even PCOS. Unfortunately, a large number of finasteride users develop the so-called post-finasteride syndrome (PFS), which is so debilitating that many people with PFS commit suicide. Doctors, pharma companies producing finasteride and related drugs, public health officials, and even mainstream media continue to deny that PFS exists, despite over 1,300 individual lawsuits (see link on PFS above) brought by patients against the drug makers the vast majority of which were either settled out of court or won by the plaintiffs. There have been multiple studies on PFS and the opinion on the exact cause(s) varies, but the consensus is that the pathology is at least partially caused by the drop in androgenic tone as a result of lower DHT levels as well as reduced 5-AR expressions in virtually all tissues that express the enzyme. Upon reviewing the symptoms of PFS it quickly becomes apparent that they significantly overlap with the symptoms of hypothyroidism. Mainstream medicine and pharma executives vehemently deny that finasteride (and other 5-AR inhibitors such as dutasteride) affects thyroid function or causes hypothyroidism but there are multiple studies demonstrating elevated prolactin, cortisol, cholesterol, and blood glucose as a result of using 5-AR inhibitors, and those are classic symptoms of hypothyroidism. And now the study below states it is apparently known in medical circles that inhibition of DHT synthesis causes severe hypothyroidism, despite the elevated levels of testosterone (T). The normal, or even elevated, levels of T in PFS patients have repeatedly been used as an argument by finasteride defenders that the drug does not amount to a “chemical castration” because T is the main steroid responsible for the male phenotype, so the higher T levels should compensate for the drop in DHT. Well, apparently, yet another “expert opinion” bites the dust…

Be that as it may, if using a 5-AR inhibitor indeed causes (severe) hypothyroidism, it would easily explain most of the manifestations of PFS and suggests a rather straightforward approach to treating it (e.g. administration of thyroid supplement). And of course, this study once again underscores the fact that DHT is far from pathological – it is in fact vital for (male) health and the campaign against it may very well gown down in history as one of the longest-lasting, most widespread, state-sanctioned, male-focused iatrogenic atrocities of our times.

https://genesandnutrition.biomedcentral.com/articles/10.1186/s12263-017-0555-5

“…ETU is a common environmental contaminant, metabolite, and degradation product of the fungicide class of ethylenebisdithiocarbamateas, such as mancozeb and zineb [89]. They are used to prevent crop damage in the field and to protect harvested crops from deterioration in storage or transport [90]. Toxicological data show the thyroid gland as the primary target of ETU through the interference with thyroid peroxidase activity [91]. In addition, pre- and post-natal exposures to low doses of ETU are associated to effects on development and on the reproductive hormone profile in rats [89]. In particular, the reproductive hormone profile showed significantly reduced levels of serum DHT in male rats at ETU 0.3 mg/kg body weight/day, which corresponded to the dose at which the hypothyroid status was more evident. Severe hypothyroidism has been demonstrated to be associated with the inhibition of T conversion to DHT by 5α-reductase, with a consequent increase in serum T concentration.”





Drop in androgen levels causes Parkinson Disease (PD), DHT reverses it​



Yet another study demonstrating that many of the so-called chronic, degenerative and above all “mysterious” conditions often have quite a simple cause and, potentially, treatment. There is no need for mutated genes or complex interactions of genes with environment that nobody can decipher. Chronic stress leads to metabolic and endocrine changes that alone are sufficient to cause virtually all “named” pathologies we have on the books. Just as importantly, endogenous chemicals that have been declared “evil” for more than a century, now turn out to be among the most protective substances available to medicine. Case in point – the study demonstrated that all it takes for PD to develop in males is a sudden drop in androgen levels. While the study mentions both testosterone (T) and DHT as key players, the treatment regimen in this study for reversing PD used DHT instead of T. Yes, that same “evil” DHT that we have been told causes prostate cancer, baldness, obesity, PCOS, osteoporosis, etc. /s
All it took to reverse the symptoms of PD in these castrated rodents was DHT supplementation with HED of ~2mg/kg daily, for 30 days. This dose of DHT is high, but in extreme (and sudden) cases such as castration much higher doses of an androgen may be needed to reverse severe brain pathologies. Other rodent studies have shown that DHT at a HED of 5mg-10mg daily also has robust neuroprotective effects. Interestingly, the drop in androgen levels caused a massive increase in nitric oxide (NO) synthesis. This elevation in NO resulted in destruction of dopamine-producing neurons, as well as a drop in the brain-anabolic factor GDNF. DHT administration reversed all of these pathological changes. Speaking of androgen-depleting events – physical or chemical castration is not the only possible cause. Chronic stress, emotional trauma, radiation exposure (X-rays anyone?), endocrine disruptors, infectious disease, endotoxin, SSRI drugs, PPI drugs, statins, PUFA, etc all count as “castration” events that can potentially cause such PD-inducing drop in androgen levels. Speaking of PUFA, cholesterol and castration, I posted something on that very topic just a few weeks ago.

Btw, the reason the study authors used DHT instead of T was that they were concerned about T aromatizing easily to estrogen, considering the negative effects estrogen has on brain pathologies like PD in males. In fact, the role of estrogen in PD pathology is acknowledged to the point that aromatase inhibitors are proposed as promising candidates for treating PD.

https://www.ncbi.nlm.nih.gov/pubmed/28770670/

Well, if androgen drop causes PD, androgen administration reverses it, and estrogen administration worsens it then the only conclusion is that DHT is the main protective factor here. T, aside from its conversion into estrogen, has only one other pathway it can go towards – conversion into DHT. Actually, it can convert back into androstenedione but that pathway is minor and also leads to estrogen. Finally, DHT lowers estrogen but T does not (it even increases it). So, it is fair to say that loss/decline of potent androgenic steroids can cause PD and supplementation with the most potent endogenous non-aromatizabe androgen (DHT) can reverse it. Considering the causative role elevated NO and lower dopamine (and as such higher prolactin) play in prostate cancer, the whole approach with chemical castration starts to look even more absurd. If anything, this study suggests that DHT should be used to treat prostate cancer

http://www.jbc.org/content/288/29/20843


“…To find out whether the observed pathological changes are due to castration-related loss of male sex hormone, we performed this experiment. However, testosterone may be converted into estrogen by aromatase. Therefore, to avoid the complexity, castrated male mice received DHT pellets (30-day release), which were implanted subcutaneously in the scapular area of the neck of castrated male mice on the day of castration (Fig. 8A). It is interesting to see that DHT supplementation protected nigral TH (Fig. 8, B and C) and preserved striatal DA (Fig. 8D) in 4–5-week-old castrated male mice. Accordingly, DHT supplementation also improved rotarod performance (Fig. 8E), horizontal activity (Fig. 8F), total distance (Fig. 8G), movement time (Fig. 8H), number of movement (Fig. 8I), and stereotypy (Fig. 8J).”
“…On the other hand, NO has also been implicated in several CNS disorders, including inflammatory, infectious, traumatic, and degenerative diseases (18, 3638). There is considerable evidence for the transcriptional induction of iNOS (the high output isoform of NOS) in the CNS that is associated with degenerative brain injury (18, 35, 37, 38). NO is potentially toxic to neurons and oligodendrocytes that may mediate toxicity through the formation of iron-NO complexes of iron-containing enzyme systems (39), oxidation of protein sulfhydryl groups (40), nitration of proteins, and nitrosylation of nucleic acids and DNA strand breaks (41). Here, we have described a new mechanism by which iNOS-derived NO may couple nigrostriatal degeneration (summarized in Fig. 12I). Whereas castration increased the expression of iNOS in the nigra, the level of GDNF went down drastically in the nigra after castration. ”
“…”While scientists use different toxins and a number of complex genetic approaches to model Parkinson’s disease in mice, we have found that the sudden drop in the levels of testosterone following castration is sufficient to cause persistent Parkinson’s like pathology and symptoms in male mice,” said Dr. Kalipada Pahan, lead author of the study and the Floyd A. Davis endowed professor of neurology at Rush. “We found that the supplementation of testosterone in the form of 5-alpha dihydrotestosterone (DHT) pellets reverses Parkinson’s pathology in male mice.” “In men, testosterone levels are intimately coupled to many disease processes,” said Pahan. Typically, in healthy males, testosterone level is the maximum in the mid-30s, which then drop about one percent each year. However, testosterone levels may dip drastically due to stress or sudden turn of other life events, which may make somebody more vulnerable to Parkinson’s disease. “Therefore, preservation of testosterone in males may be an important step to become resistant to Parkinson’s disease,” said Pahan. Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Parkinson’s disease. Nitric oxide is an important molecule for our brain and the body. “However, when nitric oxide is produced within the brain in excess by a protein called inducible nitric oxide synthase, neurons start dying,” said Pahan.”
 

georgman

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Topical Cetirizine is probably one of the more popular/affordable ways of inhibiting PGD2 (I believe it also releases PGE2), I assume if it goes systemic, it could give you whatever sides are associated with it, such as drowsiness, nothing nearly as bad as a 5AR inhibitor.

Castor Oil is good for PGE2, however, there is evidence that it lowers testosterone in rats, so I don't personally use it, not orally anyway.
I couldn't find the study about castor oil lowering testosteron, could you link it for me please or if not possible do you know how it does that?
 

uzzzzzzzi

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I wonder if the sexual side effects are reversible as the manual says? It's 100% going to change, even if I stop using it.
 

rippedgenius

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does this also apply to ru?
 

JaneyElizabeth

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I wonder if the sexual side effects are reversible as the manual says? It's 100% going to change, even if I stop using it.
Most people have no sides. If you do, in fact, have real ones and not BS ones, then you can either be bald or take the pill but I won't beg you to keep your hair. You're the balding competition and since I am short, we need hair say Ileists all.
 

uzzzzzzzi

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Most people have no sides. If you do, in fact, have real ones and not BS ones, then you can either be bald or take the pill but I won't beg you to keep your hair. You're the balding competition and since I am short, we need hair say Ileists all.
Thank you for your advice, but I don't think so. It must matter. The question is whether it matters to the extent that I can detect it. I wondered if the effect would go away if I stopped taking the drug, or if it would change my body permanently.
 

JaneyElizabeth

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Thank you for your advice, but I don't think so. It must matter. The question is whether it matters to the extent that I can detect it. I wondered if the effect would go away if I stopped taking the drug, or if it would change my body permanently.
People allege that it has the opposite sides from raising T and to the extent that any hormone might throw something off if changed, it's not common and the issue for many people is that there's dutasteride too but you pays your money and you takes your chances. Your hair must mean a little to you or you might not be on here researching. People like me, hair is everything and I take finasteride and duta and I dance a jig to the Goddess that we actually have such wonderful treatment options. Guys complain all of the time on here about no treatments. There are amazing treatments compared to 40 years ago, and some can halt baldness and maybe even thicken hair a little but you have to take baldness meds for them to actually work.

Many more guys return saying "oy vey, what was I thinking about?" The sides of baldness are huge and pervasive and they last life long so nothing's free and the price of meager to no treatment is enormous but if you are delving into the sides that might not exist and that you have not in fact experienced, it's not just Janey. All of us answer questions by the woe is me ten years later types and their math and what seems worth what and preference coefficients have change greatly and scientists think it might be related to experience and age because young guys don't know yet what baldness for the next 80 years is for the youngest and they did a poll and people over 100 years of age miss their hair exactly the same as every other age.

Go Figure says Janey. It's as if I wrote that and not Will. Ha!
 

uzzzzzzzi

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People allege that it has the opposite sides from raising T and to the extent that any hormone might throw something off if changed, it's not common and the issue for many people is that there's dutasteride too but you pays your money and you takes your chances. Your hair must mean a little to you or you might not be on here researching. People like me, hair is everything and I take finasteride and duta and I dance a jig to the Goddess that we actually have such wonderful treatment options. Guys complain all of the time on here about no treatments. There are amazing treatments compared to 40 years ago, and some can halt baldness and maybe even thicken hair a little but you have to take baldness meds for them to actually work.

Many more guys return saying "oy vey, what was I thinking about?" The sides of baldness are huge and pervasive and they last life long so nothing's free and the price of meager to no treatment is enormous but if you are delving into the sides that might not exist and that you have not in fact experienced, it's not just Janey. All of us answer questions by the woe is me ten years later types and their math and what seems worth what and preference coefficients have change greatly and scientists think it might be related to experience and age because young guys don't know yet what baldness for the next 80 years is for the youngest and they did a poll and people over 100 years of age miss their hair exactly the same as every other age.

Go Figure says Janey. It's as if I wrote that and not Will. Ha!
I agree with you. I'm actually taking finasteride. But I wanted to understand exactly what the drug was doing to me. A lot of the problems may have occurred long after taking the drug, and people didn't even attribute it to finasteride. I'm not saying it's bad, but I think the more I know about it the more I can overcome it.
 

JaneyElizabeth

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I agree with you. I'm actually taking finasteride. But I wanted to understand exactly what the drug was doing to me. A lot of the problems may have occurred long after taking the drug, and people didn't even attribute it to finasteride. I'm not saying it's bad, but I think the more I know about it the more I can overcome it.
I get that and I always end up defending finasteride but it appears that just for transition, MtF's merit greatly by using Duta and finasteride still and so I take both because I want essentially no DHT due to the excitingly sounding "back door pathway" but Janey says "no" wagging her fingers. Janey don't play that way. The other issue for me is avoiding dermatitis and facial masculinization unless I want that say for my partner that I might not catch up with. So while I haven't lowered dHT by 160 percent (see you add duta with 90 percent reductase power and finasteride with 70 percent that it's mopping up ahem add them together and you get seemingly a number greater than 100 percent and that's not usually allowable in stats.

I support knowledge too, just like you so already I like you, old chap, says Will or should I say old Chad?

Janey asserts that the preceding is all false .
satire and stuff.
signed Janey
 
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