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Oud 5 november 2020, 08:47   #121
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Effect of androgen deprivation on penile ultrastructure

Abstract

Aim: To investigate the ultrastructural changes of penile corpus cavernosum and tunica albuginea in rats treated with castration or finasteride.


Methods: Eighteen male Sprague-Dawley rats of nine weeks old were randomly divided into three groups with 6 rats each. Group A served as the control, Group B was castrated and Group C, treated with finasteride. Four weeks later, rats were anesthetized and blood samples obtained for the determination of serum testosterone (T) and dihydrotestosterone (DHT) levels; penile tissues were taken for scanning electron microscopy.


Results: The T, free T and DHT levels in Group B and the DHT level in Group C were significantly lower than those in Group A (P<0.05). The tunica albuginea was significantly thinner in Group B than that in Group A (P<0.05), but there was no significant difference between Group C and Group A (P>0.05). Elastic fibers in the tunica albuginea of Group A were very rich and arranged regularly and undulatedly, but in Group B, most of the elastic fibers were replaced by collagenous fibers. In Group C, the tunica albuginea was mainly composed of thick and irregular-arranged collagenous fibers. In Group A, there were abundant smooth muscle fibers in the trabeculae of corpus cavernosum, but they were much less in Group C and scarce or even disappeared in Group B. In Groups B and C, the diminished/disappeared smooth muscle fibers were replaced by irregularly arranged collagenous fibers.


Conclusion: In rats, androgen is essential for maintaining the normal structure of penile tunica albuginea and corpus cavernosum.



https://pubmed.ncbi.nlm.nih.gov/12647000/


The corpus cavernosum after treatment with dutasteride or finasteride: A histomorphometric study in a benign prostatic hyperplasia rodent model


Abstract

Erectile dysfunction is a common side effect of finasteride and dutasteride treatments. The objective of this study was to investigate the structural changes in the penis using a benign prostatic hyperplasia (BPH) rodent model treated with dutasteride or finasteride. Sixty male rats were divided into the following groups: C, untreated control rats; C + D, control rats receiving dutasteride; C + F, control rats receiving finasteride; H, untreated spontaneously hypertensive rats (SHRs); H + D, SHRs treated with dutasteride; and H + F, SHRs treated with finasteride. Treatments were performed for 40 days, and penises were collected immediately thereafter. The organs were analyzed using histomorphometric methods to determine the cross-sectional penile area, as well as the surface density (Sv) of smooth muscle fibers, connective tissue, elastic system fibers, and sinusoidal spaces of the corpus cavernosum. The results were compared using a one-way ANOVA with Bonferroni's posttest. Groups C + D and C + F had a significantly smaller penile cross-sectional area, but more elastic system fiber Sv compared to Group C. Group C + D showed less smooth muscle Sv, and Group H showed more connective tissue but a smaller sinusoidal space Sv in the corpus cavernosum compared to Group C. Groups H + D and H + F had less smooth muscle Sv than Group H. Group H + D also had more connective tissue and elastic system fiber Sv than Group H. Both dutasteride and finasteride promoted penile modifications in the control rat penis, although this affect was greater in Group H animals. In this rodent model, dutasteride was the drug that most affected the corpus cavernosum.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6116690/

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Oud 15 november 2020, 10:27   #122
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November 11, 2020
Investigation of Suicidality and Psychological Adverse Events in Patients Treated With Finasteride



Findings This pharmacovigilance case-noncase study of 3282 users of finasteride used VigiBase, the World Health Organization’s global database of individual case safety reports, and found a disproportional signal of suicidality, depression, and anxiety associated with finasteride use for alopecia in patients younger than 45 years. No such signal was associated with drugs that had different mechanisms of action but similar indications or with drugs that had similar mechanisms and adverse effect profiles.


https://jamanetwork.com/journals/jam...stract/2772818
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Oud 16 november 2020, 00:33   #123
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Oorspronkelijk geplaatst door Pionier Bekijk bericht
and found a disproportional signal of suicidality, depression, and anxiety associated with finasteride use for alopecia in patients younger than 45 years.]
Ik zou het persoonlijk best interessant vinden als er een vergelijkbare studie zou zijn (voor zover die er niet is) onder een grote populatie kalende mannen onder de 45 die fina niet slikt en gewoon kaal wordt. Angst, depressie en zelfs zelfmoordneigingen zijn ongetwijfeld ook in die groep hoger.

Laatst gewijzigd door minten; 16 november 2020 om 00:39
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Oud 16 november 2020, 09:02   #124
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Oorspronkelijk geplaatst door minten Bekijk bericht
Ik zou het persoonlijk best interessant vinden als er een vergelijkbare studie zou zijn (voor zover die er niet is) onder een grote populatie kalende mannen onder de 45 die fina niet slikt en gewoon kaal wordt. Angst, depressie en zelfs zelfmoordneigingen zijn ongetwijfeld ook in die groep hoger.

Akkoord.


Dit is van het Reuters artikel:


  • Merck exaggerated the safety profile of propecia. Merck also omitted the experiences of several subjects who had sexual dysfunction symptoms and didn't include the experiences of men who didn't finish the study.
https://www.reuters.com/investigates...recy-propecia/


Dit is nieuw voor mij, Merck is echt ver gegaan....


  • Merck created a fake "peer-reviewed" journal, the "Australasian Journal of Bone and Joint Medicine," in which to publicize pro-Vioxx articles.
https://www.cbsnews.com/news/new-mer...ass-reporters/

Laatst gewijzigd door Pionier; 17 november 2020 om 10:40
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Oud 18 november 2020, 15:30   #125
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Dual-5?-Reductase Inhibition Promotes Hepatic Lipid Accumulation in Man



Context:
5?-Reductase 1 and 2 (SRD5A1, SRD5A2) inactivate cortisol to 5?-dihydrocortisol in addition to their role in the generation of DHT. Dutasteride (dual SRD5A1 and SRD5A2 inhibitor) and finasteride (selective SRD5A2 inhibitor) are commonly prescribed, but their potential metabolic effects have only recently been identified.



Objective:
Our objective was to provide a detailed assessment of the metabolic effects of SRD5A inhibition and in particular the impact on hepatic lipid metabolism.



Design:
We conducted a randomized study in 12 healthy male volunteers with detailed metabolic phenotyping performed before and after a 3-week treatment with finasteride (5 mg od) or dutasteride (0.5 mg od). Hepatic magnetic resonance spectroscopy (MRS) and two-step hyperinsulinemic euglycemic clamps incorporating stable isotopes with concomitant adipose tissue microdialysis were used to evaluate carbohydrate and lipid flux. Analysis of the serum metabolome was performed using ultra-HPLC-mass spectrometry.



Setting:
The study was performed in the Wellcome Trust Clinical Research Facility, Queen Elizabeth Hospital, Birmingham, United Kingdom.

Main Outcome Measure:
Incorporation of hepatic lipid was measured with MRS.



Results:
Dutasteride, not finasteride, increased hepatic insulin resistance. Intrahepatic lipid increased on MRS after dutasteride treatment and was associated with increased rates of de novo lipogenesis. Adipose tissue lipid mobilization was decreased by dutasteride. Analysis of the serum metabolome demonstrated that in the fasted state, dutasteride had a significant effect on lipid metabolism.



Conclusions:
Dual-SRD5A inhibition with dutasteride is associated with increased intrahepatic lipid accumulation.


https://academic.oup.com/jcem/article/101/1/103/2806602
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Oud 20 november 2020, 18:29   #126
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Nieuwe studie;


The Potential Involvement of Cholinergic System in Finasteride Induced Cognitive Dysfunction

Highlights

•Repeated finasteride (100?mg/Kg, s.c.) administration impairs memory
•Finasteride (100?mg/Kg, s.c.) decreases sociability and social preference
•Reduced AChE activity in discrete brain regions after finasteride administration

Conclusion

Our study provides evidence that repeated administration of finasteride decreases social interaction and results in cognitive deficits, potentially through a cholinergic mechanism. Further studies are required to understand the exact link between the cognitive effects and the cholinergic system. A deeper probe of the current findings holds promise for the development of novel neurosteroid-based therapeutics to treat affective and cognitive disorders.


https://www.sciencedirect.com/scienc...04893?via=ihub
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Oud 23 november 2020, 13:02   #127
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https://men-elite.com/2020/09/29/the...esearch-shows/

The truth on DHT: what the research shows



DHT is an essential male hormone, not just for libido, or feeling manly, but for general health as well.
DHT is synthesized from:
  • Testosterone through the enzyme 5 alpha reductase (5AR)
  • 17-hydroxypregnenolone and 17-hydroxyprogesterone in what is termed the “backdoor” pathway
  • 5?-androstane-3?, 17-?-diol (dihydroandrosterone/3?-diol) via the intracrine reverse synthesis pathway (3?-hydroxysteroid dehydrogenase (3?-HSD))
DHT is 2.5-10 times more potent than testosterone and here’s why:
  1. DHT has a 4 time higher affinity to AR (androgen receptor) than testosterone.
  2. Binding of DHT to the AR transforms the AR to its DNA-binding state.
  3. DHT upregulates AR synthesis and reduces AR turnover.
  4. The dissociation rate of testosterone from receptors is 3-5 fold faster than DHT (meaning DHT exerts a much more powerful effect on AR than testosterone)
However, circulating DHT is usually only about 10% or less that of testosterone and high concentrations of intracellular T can shift androgen receptor binding away from DHT by mass action (R).
Furthermore, in the blood, SHBG binds with 5 times higher affinity and for more than 3 times longer to DHT compared to testosterone.
To maximize the androgenic benefits of DHT, we want to maximize 5-AR and inhibit the binding of DHT to SHBG. You can download my guide/PDF on how to do that below.
This article is to show you what happens when men have high DHT or when they are dosed with supra-physiological amounts.
DHT is essential for libido and sexual function

It’s probably well known that DHT is very important when it comes to libido and sexual function.
According to this study, serum DHT concentration was the only independent hormonal predictor of the frequency of orgasms. An increase in concentration of 1.36 nmol/l corresponded to an average increase of one orgasm a week (R). This shows that DHT directly opposes the anti-libido effects of prolactin.
Inhibiting DHT synthesis impairs corpus cavernosum growth and trabecular smooth muscle relaxation, endothelial function and increases connective tissue deposition. This all contributes to erectile dysfunction, even in the presence of physiological levels of total testosterone (R).
DHT is also critical for activating gene expression of neuronal and endothelial nitric oxide synthases, which are critical physiological mediators of penile erection (R).
Furthermore, DHT is essential for spermatogenesis and thus fertility (R).
Estrogen is thought to be essential for sexual function in men, however, administrating high doses of DHT lowers estrogen dramatically and doesn’t reduce sexual function.
There were no spontaneous complaints, or discontinuations for, adverse effects on sexual function during the study. DHT administration had no effects on any of 33 measures of sexual function and mood, apart from a mild, but significant decrease in overall sexual desire, which was reversible after cessation of treatment… DHT treatment increased serum DHT with complete suppression of serum T, luteinizing hormone, follicle stimulating hormone, and estradiol throughout the 24-month study resulting in reduced spinal bone density.
Reference
DHT isn’t just neutral towards sexual function as shown above, but is essential for it.
As to the clinical effects, the only statistically significant effect was an improvement in early morning erections and ability to maintain erections.
Reference
And also:
Administration of dihydrotestosterone to eugonadal men led to a transient increase of nocturnal sexual dreams and erections and irritability, waning after 3–4 weeks of dihydrotestosterone administration.
Reference
The effects waned after 3-4 weeks, so taking 1-2 weeks off every 4 weeks from DHT (if you’re using it) might enable you to maintain those benefits.
DHT doesn’t cause prostate cancer

There was a period of time (a few decades) where DHT was thought to promote prostate cancer, however, that thinking is luckily starting to change. It’s about time, since there has been research for over 2 decades showing that DHT doesn’t promote prostate cancer.
There isn’t a correlation between circulating DHT and intraprostatic DHT. The prostate regulates it’s own DHT levels, which is about 10 times higher than circulation.
Giving testosterone might cause issues, since it can convert to estrogen, but giving DHT directly can actually help to shrink the prostate as it can lower estrogen. It’s actually estrogen and prolactin that drives prostate cancer.
Quite a few studies found that high (supraphysiological) serum DHT levels, DHT gel treatment did not significantly increase total, central, or peripheral prostate volumes, as measured by ultrasonography, nor was serum prostate-specific antigen (PSA) elevated. Additionally, International Prostate Symptom Scores (IPSS) remained unchanged in men treated with DHT gel for 6-24 months (R, R, R).
This 1.8 years survey of 37 men aged 55-70 years treated with daily percutaneous DHT treatment suggested that high plasma levels of DHT (> 8.5 nmol/l) effectively inducing clinical benefits while slightly but significantly reducing prostate size (R).
There is an association in some studies between short telomere length and prostate cancer, but the effects of DHT on leukocyte telomere length may not reflect what occurs in prostate tissue. However, in prostate biopsies from men in the Prostate Cancer Prevention Trial, shorter telomere length was associated with higher odds of prostate cancer (225). Because the concentration of DHT is very high in the prostate, one may hypothesize that if DHT stimulates telomere lengthening in prostate, it may paradoxically play a protective role in some cells.
Reference
DHT for metabolic syndrome

Metabolic syndrome is a cluster of conditions that increase the risk of heart disease, stroke and diabetes. Metabolic syndrome includes high blood pressure, high blood sugar, excess body fat around the waist and abnormal cholesterol levels. The syndrome increases a person’s risk of heart attack and stroke.
Insulin sensitivity

This randomized, controlled, double-blind trial provides evidence that DHT specifically (and to a much lesser extent, testosterone), improves insulin sensitivity and decreases plasma leptin level without notable side effects (R). Testosterone treatment caused prostatic nodular hyperplasia, benign at biopsy, whereas DHT didn’t.
Androgens, especially DHT, upregulate insulin receptor expression and activity and increase glycogen synthesis and cholesterol uptake in the liver (R).
Low DHT or lowering DHT with a 5-AR inhibitor, such as finasteride or dutasteride, is associated with an increase in blood glucose and glycosylated hemoglobin A as well as the risk of type 2 diabetes (R, R, R).
5-AR is necessary to inactivate cortisol, so blocking 5-AR increases cortisol, which promotes insulin resistance and liver disorders, such as NAFLD, steatosis, etc. (R, R).
Heart, liver and kidney function

DHT therapy in men with coronary artery disease (CAD) decreased myocardial ischemia and improved left ventricular diastolic function (R).
This in vitro study found:
In summary these in vitro data show that the T and DHT (via their anti-inflammatory effects) preserve endothelial cell function and prevent synthesis of cell adhesion molecules and release of proinflammatory cytokines.
Reference
The findings above could explain some of the previously described clinical observations of the relationship between low T and DHT and peripheral vascular disease and the anti-ischemic effects of acute infusion of testosterone in men with CAD and similar effects by DHT gel treatment (R).
A few more facts:
  • 5-AR inhibition may result in the development of kidney dysfunction (R).
  • Dutasteride, a 5-AR inhibitor, treatment increased activities of liver alanine aminotransferase and aspartate aminotransferase, suggesting dysregulation of liver metabolism (R).
  • DHT is a biomarker for reduced risk of stroke, which means that DHT is inversely correlated with stroke (R).
  • Higher DHT was associated with lower ischemic heart disease mortality in older men (R).
Vascular function

High blood pressure
DHT increases the synthesis of nitric oxide through eNOS phosphorylation thus improving circulation and vascularity (R).
The following in vitro study shows that DHT has anti-inflammatory and protective effects in the vascular system:
DHT inhibited the tumor necrosis factor-? and lipopolysaccharide-induced expression of vascular cell adhesion molecules (VCAMs) and intercellular adhesion molecules (ICAMs). In addition, DHT inhibited messenger RNA (mRNA) expression of IL-6, PAI-1, and Cox-2 and the release of cytokines and chemokines such as growth-regulated oncogene proteins (GRO), granulocyte-macrophage colony-stimulating factor, and tumor necrosis factor in endothelial cell culture.
Reference
Cholesterol
DHT:
  • Reduces lipid accumulation and cholesterol synthesis via increasing expression of carnitine palmitotyltransferase1 (CPT-1) and phosphorylation of 3-hydroxy-3-methyl-glutaryl-CoA reductase (R).
  • Inhibits ox-LDL–induced foam cell formation and atherosclerosis (R).
DHT administration for up to 2 years in normal men, didn’t cause any thrombotic events or detrimental shifts in total cholesterol, HDL and LDL cholesterol, or triglycerides. Nor were exceptionally high levels of DHT associated with a change in right carotid intima-media thickening (R, R).
Inhibiting 5-AR with dutasteride resulted in increased total cholesterol, and low-density lipoprotein cholesterol levels (R). Georgi (Haidut) posted a while ago that “inhibition of DHT synthesis causes severe hypothyroidism, despite the elevated levels of testosterone (T)“. Although the study was in rats, it could still be applicable to humans. I’ve seen quite a few test results from men a few weeks after quitting finasteride who experienced thyroid storm, which is most likely the rebound happening due to the suppression from finasteride.
Mitochondrial function and energy production

Androgens, especially DHT:
  • Stimulate lipolysis and down-regulates lipoprotein lipase activity and increases the expression of fatty acid-binding protein leading to an increase in fatty acid oxidation and in oxidative phosphorylation.
  • Increase the expression of pyruvate dehydrogenase, which increases the production of oxaloacetate and acetyl-CoA leading to a stimulation of the tricarboxylic acid (TCA) cycle.
  • Increase the expression of succinate dehydrogenase and aconitase, also upregulating TCA and increasing oxidative phosphorylation.
  • Increase the expression of cytochrome c oxidase, which leads to an increase in oxidative phosphorylation. The increase in oxidative phosphorylation leads to a decrease in reactive oxygen species and an increase in insulin sensitivity (R).
Fat loss

DHT:
  • Inhibits preadipocyte proliferation and adipocyte differentiation, which prevents the excess formation of fat cells (R).
  • Stimulates lipolysis (R).
  • Stimulates lipid disposal (R).
  • Downregulates lipogenesis, which reduces the conversion of carbs to fat (R).
  • Prevents the downregulation of the leptin receptor (R).
Extras

Gynecomastia
Gyno is known to be due to high estrogen and prolactin and low DHT and DHT treatment can reverse it.
Intramuscular injection of 200 to 400 mg DHT-hp every 2 to 4 weeks for 16 weeks was associated with a 67% to 78% decrease in breast size in adolescent boys with gynecomastia; no regrowth was observed for up 15 months post treatment… There was no change in testicular volume… There was no change in liver or renal function.
Reference
Brain & cognition
DHT promotes stress resiliency. Blocking 5-AR enhances cortisol release during stress, whereas DHT blunts it, most likely through CRH suppression (R, R).
DHT promote spatial memory (R).
DHT protects against neurodegeneration, by antagonizing TGFbeta (R). In this case study, someone with a demyelinating disease, Charcot-Marie-Toot 1, was able to induce neuroregeneration with 20mg/day of Anavar (oxandrolone) (R).
Lastly:
DHT treatment (in mice) promoted expression of synaptic plasticity markers [namely, cAMP-response element binding protein (CREB), postsynaptic density protein 95 (PSD95), synaptophysin (SYN), and developmentally regulated brain protein (Drebrin)], positively modified synaptic structure, and significantly delayed cognitive impairment.
Reference
DHT is needed for blood flow
Lower T or DHT levels, but not E2, is associated with symptoms of intermittent claudication in older men (R).
Bone
High doses of DHT can completely shut down LH and testosterone production and cause a major drop in estrogen. This might be a concern for some people because it’s mainly estrogen that’s been thought to be beneficial for bone, however, there is evidence that estrogen isn’t needed for bone strength/growth (R).
Furthermore, Finasteride increases the risk of fractures, which indicates that it weakens muscle strength and bone quality (R).
Eyes
DHT is needed to keep the eyes moist and prevent dry eyes. 5-AR inhibition may result in the development of dry eye disease (R). Androgen deficiency produces pathophysiological changes manifested in the reduction of tear production and evaporative dry eye conditions.
Suppression
DHT doesn’t have a suppressive effect on testicular steroidogenesis, similar to estrogen. DHT actually suppresses testicular aromatase. DHT inhibits steroidogenesis on a hypothalamic level, and doesn’t affect LH secretion at a pituitary level (R).
Anabolism/catabolism
DHT isn’t very anabolic, however, DHT derivatives, such as Anavar or Masteron are much more anabolic than DHT, and this is partly due to much slower clearance through the liver.
Apart from it not being very anabolic, DHT is anti-catabolic. This study found that people who experience muscle wasting from AIDS, retained more muscle mass if their DHT was normal, compared to those with low DHT (R). Anavar, a DHT derivative, is used to preserve muscle mass in people with wasting disease and to help them add more muscle for recovery (R). Even 5mg was enough to stop catabolism, whereas higher doses such as 15mg daily were needed for muscle growth in these patients.
Furthmore, DHT up-regulates androgen receptors (R).
Serotonin excess and cancer
DHT downregulates tryptophan hydroxylase 1 (TPH1; the rate-limited enzyme in serotonin synthesis in the body), thus protecting against the formation of tumors. Serotonin is also potent inflammatory and causes vasoconstriction, so DHT protects against that as well (R).


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Oud 23 november 2020, 19:13   #128
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Finasteride-induced secondary infertility associated with sperm DNA damage

Conclusion(s)

The significant reduction in DFI within 3 months of finasteride cessation and continued improvement suggests a causal link between finasteride and sperm DNA damage. We hypothesize that low-dose finasteride may exert a negative influence on sperm DNA integrity, resulting in increased pregnancy losses. We suggest that in infertile men using finasteride, sperm DFI should be measured in addition to semen parameters, and a trial of discontinuation of finasteride may be warranted.


https://www.sciencedirect.com/scienc...15028211000161
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Oud 24 november 2020, 11:13   #129
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Altijd lachen om die "bijwerkingen", alles in het leven heeft bijwerkingen.

Natuurlijk kan de ene persoon bijwerkingen krijgen en de andere niet, dat is nou eenmaal de natuur. Moet altijd wel lachen om die schreeuwerds, zus is niet goed, zo is niet goed, maar vervolgens vreten ze wel zakken chips leeg en gieten flessen cola naar achter.

Als je zo bang voor finasteride bent neem je het niet, het is wel het enige middel samen met minoxidil wat werkt.
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Oud 24 november 2020, 11:22   #130
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Altijd lachen om die "bijwerkingen", alles in het leven heeft bijwerkingen.

Natuurlijk kan de ene persoon bijwerkingen krijgen en de andere niet, dat is nou eenmaal de natuur. Moet altijd wel lachen om die schreeuwerds, zus is niet goed, zo is niet goed, maar vervolgens vreten ze wel zakken chips leeg en gieten flessen cola naar achter.

Als je zo bang voor finasteride bent neem je het niet, het is wel het enige middel samen met minoxidil wat werkt.
Spijtig genoeg is fina niet hetzelfde als een aspirientje dat je maar een paar keren neemt. En kijk maar naar mensen die PFS hebben hier, ze zijn gezond en deden aan sport en toch hebben ze na het stoppen van fina nog altijd last, maar ja indien je zou weten hoe belangrijk DHT (en andere derivate hormonen) zijn zou je dat beseffen.



Fina tegen haarverlies is hormoontherapie dat men voor de rest van zijn leven moet blijven slikken. Men houdt de werking van één van de meest belangrijke mannelijke hormonen tegen (en verstoord ook zo de onderliggende afgeleide hormonen).


Het enige wat echt lachen is, is het feit dat sommige hopeloze kalende mannen zichzelf proberen wijsmaken dat hormoontherapie voor jaren aan een stuk alleen maar effect zal hebben op hun haar.
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Oud 25 november 2020, 16:26   #131
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Trouwens sterk aangeraden om te stoppen met fina als je aan kinderen wilt beginnen. (en best voor je persoonlijke gezondheid om voor altijd te stoppen natuurlijk)


There are warnings from many medical sources NOT to use Finasteride and have unprotected sex should your partner be pregnant.
  1. This information was released by Merck via the FDA in 2011. https://www.google.com/url?sa=t&sour...ognrVif0OszxLF
https://www.accessdata.fda.gov/drugs...MG_MEDR_P1.PDF
"Abnormal male genital development is an expected consequence when conversion of testosterone to 5?dihydrotestosterone (DHT) is inhibited by 5?-reductase inhibitors. These outcomes are similar to those reported in male infants with genetic 5?-reductase deficiency. Women could be exposed to finasteride through contact with crushed or broken PROPECIA tablets or semen from a male partner taking PROPECIA…"


2. The Drugs.com article on Finasteride states: https://www.drugs.com/pregnancy/finasteride.html
"US FDA pregnancy category X: Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in use of the drug in pregnant women clearly outweigh potential benefits…Finasteride is present in semen and therefore may pose a risk to the fetus. Male patients should be instructed to wear a condom during intercourse with women of childbearing potential or discontinue finasteride. The drug should be discontinued in patients wishing to conceive a child."


3. The electronic medicines compendium https://www.medicines.org.uk/emc/pro...044/smpcstates: "Small amounts of finasteride have been recovered from the semen in subjects receiving finasteride 5 mg/day. It is not known whether a male fetus may be adversely affected if his mother is exposed to the semen of a patient being treated with finasteride. When the patient’s sexual partner is or may potentially be pregnant, the patient is recommended to minimise exposure of his partner to semen."


4. An extremely high percentage of post-marketing reports of exposure to Finasteride during pregnancy via Semen resulted in genital birth defects. https://www.medicines.org.uk/emc/product/2194/smpc"
"During continual collection of adverse experiences, post-marketing reports of exposure to finasteride during pregnancy via semen of men taking 1 mg or higher doses have been received for eight live male births, and one retrospectively -reported case concerned an infant with simple hypospadias. Causality cannot be assessed on the basis of this single retrospective report and hypospadias is a relatively common congenital anomaly with an incidence ranging from 0.8 to 8 per 1000 live male births. In addition, a further nine live male births occurred during clinical trials following exposure to finasteride via semen, during pregnancy, and no congenital anomalies have been reported."
NOTE: That's 1 out of 17 reports of paternal exposure resulting in a congenital defect which is extremely high.


5. Handbook of Systemic Drug Treatment in Dermatology edited by Sarah H. Wakelin, Howard I. Maibach, Clive B. Archer. "It is not known whether a male fetus may be adversely affected by in utero exposure to the semen of a man treated with finasteride or duasteride, but condom use is advised."


6. Back in 1997 it was requested Merck test and release the No Observable Effect Level dose for oral administration of finasteride. This was never done or they never released the findings: https://www.accessdata.fda.gov/drugs...1MG_PHARMR.PDF
Thus there is NO proven safe amount of finasteride to be received orally at all by pregnant women that has been proven NOT to cause birth defects, including in semen during oral sex.


7. 'Drug related safety issues affecting pregnancy outcome and concerning risk minimisation measures' by Crijns, Hubertina Johanna Maria Josephina. This states "Presence of drugs in seminal fluid could interfere with embryonic or foetal development because of a direct effect on the uterus or the vaginal mucosa during sexual intercourse during pregnancy." Finasteride directly lowers DHT or Dihydrotestosterone, which is the most critical hormone for male genital development during pregnancy in fetuses.





My Story: Taking Finasteride during my partner's pregnancy resulted in my son having genital birth defects



https://www.reddit.com/r/finasteride...tm_term=hjn7zh



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Oud 25 november 2020, 18:44   #132
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Oorspronkelijk geplaatst door Pionier Bekijk bericht
Spijtig genoeg is fina niet hetzelfde als een aspirientje dat je maar een paar keren neemt. En kijk maar naar mensen die PFS hebben hier, ze zijn gezond en deden aan sport en toch hebben ze na het stoppen van fina nog altijd last, maar ja indien je zou weten hoe belangrijk DHT (en andere derivate hormonen) zijn zou je dat beseffen.



Fina tegen haarverlies is hormoontherapie dat men voor de rest van zijn leven moet blijven slikken. Men houdt de werking van één van de meest belangrijke mannelijke hormonen tegen (en verstoord ook zo de onderliggende afgeleide hormonen).


Het enige wat echt lachen is, is het feit dat sommige hopeloze kalende mannen zichzelf proberen wijsmaken dat hormoontherapie voor jaren aan een stuk alleen maar effect zal hebben op hun haar.
Je praat hier over hormoontherapie dat men voor de rest vh leven moet blijven slikken.

Hoe zit het dan met topische fina, hoe kijk jij daar tegenaan?
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Oud 25 november 2020, 19:02   #133
PJKG
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Ik zou niet om die vent z'n mening vragen eerlijk gezegd.
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Regime:
- Orale DHT Blokker: Finasteride, 0.5mg 6x pw (07-2019), Dutasteride, 1x pw (09-2020)
- Topische DHT Blokker & Groeistimulant: Essengen 6 Plus (06-2020)
- Shampoo: Afwisselend Regenepure DR (01-2019), Nizoral shampoo (2018-12), en Biotin OGX Shampoo & Conditioner (10-2019)
- Supplementen: Multivitamine complex incl. Biotine, IJzer, Zink en Magnesium afwisselend met Foligain tablets (05-2020)
- Microneedling: 1x per week Dr. Pen Ultima A6 (09-2020)
Gestopt:
- Kirkland 5% Minoxidil Lotion (02-2019 - 05-2020)

- Olie: Castorolie, oraal, 1ml per dag (08-2020 - 02-2021)
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Oud 25 november 2020, 19:12   #134
Haartjes2020
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Ik zou niet om die vent z'n mening vragen eerlijk gezegd.
Waarom niet? Ik ben wel eens toe aan een andere mening dan iedereen die super positief is over topische fina, zonder echte onderbouwing. (inclusief ik zelf)

Wil het dan wel onderbouwd hebben, volgens mij is pionier daar goed in.
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Regime
Biotine 1 x 1000ug pd sinds 10-03-2020
Ketokonazol 3 x pw sinds 10-07-2020
Essengen 6 plus 0.75ml pd sinds 27-07-2020
Dermapen 1,25mm 1 x pw sinds 10-11-2020

Laatst gewijzigd door Haartjes2020; 25 november 2020 om 19:32
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Oud 25 november 2020, 19:25   #135
Pionier
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Waarom niet? Ik ben wel eens toe aan een andere mening dan iedereen die super positief is over topische fina, zonder echte onderbouwing. (inclusief ik zelf)

Wil het dan wel onderbouwd hebben, volgens mij is pioneer daar goed in.
Niet letten op hem, hij is één van de zielige finaslikkers die er niet tegen kan dat ik studies post omdat dat zijn illusie breekt dat fina veilig is.


Nu je vraag, neen ik raad niet echt topische fina aan, alhoewel de kans op bijwerkingen minder is dan oral fina volgens sommige studies. (ik had er een tijd geleden ééntje gepost in mijn andere thread over opkomende middelen)



Wat wel interessant is als je toch een AA wilt gebruiken, is topische duta. Verschillende mensen die dit wel kunnen verdragen maar niet orale of topische fina. De theorie waarom topische duta veiliger zou zijn kan je hier lezen: https://fuehairdoctor.co.uk/topical-...e-dr-lupanzula
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