Does Finasteride use cause Vitamin B12 deficiency ?

Hey Brain Bug,

Cheers for the info. I understand your sick and tired of theorizing, iā€™m just curious,i donā€™t know how this all works but as i mentioned in my posts earlier,does tissue containing 5AR2 becomes inflammed because my scalp,balls,liver experienced some form of pain, because some people get brainfog, is it possible as i mentioned below that 5AR1 gets supressed also and brain tissue becomes inflammed?. Also as this theory has not been proven, is it possible that a homornal imbalance can cause this inflamation much like what women experience with menopause.

Thanks man just curious.

INHIBITING DHT VIA 5AR2 ----> STOP DRUG ---->DHT COMES FLOWING BACK ā€”> 5AR2 AND/OR 5AR1 (BECAUSE THEY BOTH RELATE TO DHT) DOWNREGULATE AND SUPRESSES ITā€™S ACTION TO REDUCE INFLUX OF DHT ----> ANY DHT INCREASE SUPRESSES THE ENZYME MORE? THATS WHY WE GET EXCESS ESTROGEN? BECAUSE 5AR2 IS NOT CONVERTING TEST TO DHT AT THE RATE OF REDUCING ESTROGEN?

HENCE WHY SOME GET MENTAL SIDES TO BECAUSE 5AR1 GETS SUPRESSED POSSIBLY INFLAMMED BRAIN TISSUE?

Hey,

while taking fin the DHT is much lower.
DHT relgulates togehter with E the relase of LH and FSHā€¦the Testo levels go up.
Because the body thinks the is less DHT. But whle on the drug, the cell need still DHT so he trys to adjust on a other levelā€¦until a point where the signaling of the AR gets to high. this is when people on the drug starts getting sides. When you stop the drug DHT comes back very fast and the cells are not able to adjust back so quick. The signaling of the AR gets so high, thats why some get a hugh libido boost and things strats to improve even more. until this critical Point when the cells tryes to protect them, by the hypersignaling. This can the cells do by many things like Histons or posttranslational modifikations and many other things.
Once the Modification is done, the cells are hypersensitiv and all the time you give them even more of a androgen it will produce the proteins, that are encoded on ARGĀ“s. But the signaling will be getting much higher and so the body will shut even more downā€¦ but this also depends on the individual epigentik. As i said AR and 5AR are exrpessed by ARGĀ“s and controled by its owen Product, its not so simple, because many other enzymes are involed. Yes, LAck of androgen action, lack of 5AR, lack of 3a-diol-g that ā€œprotectsā€ the cells from estrogenic effects
Mental sides, because fin also inhibits the 5AR1 and Allopregnenolone is also synthesized by 5ARā€¦same damageā€¦
Even the AR signaling is not so easy, here is a lil overview, what is knowen about the signaling:

[i]Structurally, AR can be subdivided into four functional domains: the NH2-terminal transactivation domain (or A/B domain), the DBD (DNA-Binding Domain), hinge region, and the LBD (Ligand-Binding Domain). An NH2-terminal AF1 (Activation Function-1), functions in a ligand-independent manner when artificially separated from the LBD, creating a constitutively active receptor. A ligand-dependent AF2 function is located in the LBD, which is responsible for an optimum transcriptional activation in response to the ligand (Ref.3). The unbound AR forms a complex with HSPs (Heat-Shock Proteins). The binding of androgens to AR induces dissociation of the AR from the HSPs and subsequent receptor dimerization and translocation into the nucleus, facilitating the ability of AR to bind to its cognate response element, and recruit coregulators to promote the expression of target genes. The transcriptional activity of AR is greatly modulated by coregulatory proteins. Coactivators such as ARA70 (Androgen Receptor Coactivator, 70-Kd) and ARA55 stabilize the process of ligand binding to AR. The ability of AR to be translocated to the nucleus is regulated by several coregulators, for example, the F-Actin binding protein: Filamin. Inside the nucleus, AR interacts with DNA by targeting specific nucleotide palindromic sequences termed ARE (Androgen Response Element) (Ref.2).

A number of coregulators themselves perform enzymatic activities such as phosphorylation or acetylation, modifying either the chromatin surrounding the promoter of the target gene or other coregulators. The prototypic coactivators of this type that possess acetyltransferase activity include, CBP (CREB Binding Protein), the closely related p300 and other nuclear receptor coactivators: p/CAF (p300/CBP Associated Factor), SRC1 (Steroid Receptor Coactivator-1), and SRC3 (Ref.3). PIAS [Protein Inhibitor of Activated Signal Transducer and Activator of Transcription (STAT)] family of proteins and ANPK (Androgen Receptor-Interacting Nuclear Kinase) also interact with and coactivate AR. Transcriptional activation by AR ultimately requires the recruitment of RNA Pol II (RNA polymerase-II) to the promoter of target genes. RNA Pol II recruitment is mediated through the assembly of GTFs (General Transcription Factors) to form the preinitiation complex, the first step of which is the binding of TBP (TATA box-Binding Protein) near the transcriptional start site. TBP is part of a multiprotein complex, TFIID (Transcription Factor-IID), which also contains general and promoter-specific TAFII (TBP-Associated Factors) proteins. TBP binding induces DNA bending, bringing sequences upstream of the TATA element in closer proximity, presumably enabling interaction between GTFs and steroid receptor-coregulator complexes. TFIIB binds directly to TBP and functions to recruit the TFIIF-RNA Pol II complex. TFIIF domains, in addition to interacting with TFIIB and RNA Pol II, apparently also serve in transcription initiation and elongation. The ATPase and kinase TFIIE and the helicase TFIIH are then recruited to RNA Pol II to facilitate DNA strand separation before transcription initiation. TFIIE and TFIIF recruitment to RNA pol II are acetylated by p300 and p/CAF (Ref.2). Ubiquitin ligase activity has been identified for two AR coactivators, ARA54 and E6-AP. The coactivators with ubiquitin ligase activity contribute to nuclear receptor transcription through targeting the degradation of corepressors. AR can also interact with a number of transcription factors including Activator Protein-1, SMAD3 (Sma and Mad Related Family), NF-KappaB (Nuclear Factor-KappaB), SRY (Sex-determining Region-Y), and the Ets family of transcription factors.

Transcriptional corepression of androgen-bound AR can be attributed to three corepressors: cyclin-D1, calreticulin and HBO1. Cyclin-D1 inhibits AR transactivation through a mechanism independent of its function in cell cycle regulation (Ref.4). The calcium-binding protein calreticulin is localized to the endoplasmic reticulum and nucleus and has also been characterized as a corepressor of AR. The AR corepressor HBO1 is a member of the MYST protein family that is characterized by a homologous zinc finger and carries an acetyltransferase domain. Although AR is normally thought to function as a homodimer, it has been found to heterodimerize with other nuclear receptors including the ER (Estrogen Receptor), GR (Glucocorticoid Receptor) and TR4 (Testicular Orphan Receptor-4) and in each case result in a decrease in AR transcriptional activity.

In addition to the transcriptional or genomic mode of action by steroids, androgens, can also exert rapid, nongenomic effects. Nongenomic steroid activity typically involves the rapid induction of conventional second messenger signal transduction cascades. Nongenomic action of androgens can occur through multiple receptors. Androgens can activate cAMP and PKA through the SHBG (Sex Hormone Binding Globulin)/SHBGR complex (Ref.1). Androgens also stimulate an elevation in intracellular Ca2+ through a GPCR (G-Protein Coupled Receptor) by activating an influx through nonvoltage-gated Ca2+ channels. The elevation of intracellular calcium activates signal transduction cascades, including PKA (Protein Kinase-A), PKC (Protein Kinase-C), and MAPKs (Mitogen-Activated Protein Kinase), that can modulate the activity of the ARs and other transcription factors. AR also interacts with the intracellular tyrosine kinase c-Src, triggering c-Src activation. One of the targets of c-Src is the adapter protein SHC (SH2 Containing Protein), an upstream regulator of the MAPK pathway. The activity of AR and AR coactivators are influenced by direct phosphorylation by MAPK (Ref.3). AR phosphorylation by ERK2 is associated with enhanced AR transcriptional activity and an increased ability to recruit the coactivator ARA70. The SRC family of transcriptional coactivators: SRC1, SRC3, and TIF2 (Transcription Intermediary Factor-2) are targets of MAPK phosphorylation that results in an increased ability of these coactivators to recruit additional coactivator complexes to the DNA-bound receptor. The nongenomic, rapid stimulation of second messenger cascades by androgens may ultimately exert biological effects through modulation of the transcriptional activity of AR or other transcription factors. Such modulation may occur through direct phosphorylation of transcriptional activators or their coregulators (Ref.1). The AR can also be activated in the absence of its cognate ligand, androgen by signaling pathways initiated by various growth factors.

The appropriate regulation of androgen activity is necessary for a range of developmental and physiological processes, particularly male sexual development and maturation. However, excessive production of adrenal androgens can cause premature puberty in young boys and their hypersecretion in females, may produce a masculine pattern of body hair and cessation of menstruation (Ref.4). Their mis-regulation is also implicated in the formation and progression of prostatic adenocarcinoma (Ref.3). Therefore, the removal of testicular androgens by castration has long been recognized to result in tumor regression, and surgical or pharmacological androgen ablation remain the predominant form of treatment for advanced prostate cancer. Androgen ablation therapy is often combined with treatment with nonsteroidal antiandrogens, such as hydroxyflutamide, to block residual adrenal androgen action. Androgen Replacement Therapy has been in use for over 60 years to treat, with proven efficacy and safety, on patients with male hypogonadal disorders and/or failure of sexual development. Apart from that, the last decade has witnessed a wider therapeutic role of androgens for nonclassical indications. These include male contraception; aplastic anemia; and sarcopenic, osteopenic, and depressive states frequently associated with an expanding variety of chronic systemic conditions (characterized by reduced circulating testosterone) such as AIDS, rheumatoid arthritis, chronic renal failure, chronic obstructive airways disease, and physiological aging[/i]

Cheers Brainbug. Itā€™s all starting to become a bit more clear now. Now to find the reset button!

Is it possible that our prostates got inflammed(shut-down) also, that would explain hypogondal levels? Can reducing inflammation fix this?

I know we donā€™t know the answers, but it would clear my head a bit.

I wrote that all before, lack of androgen action on the cells----->cells dont make the need proteins, dont work corectly or will die. Dead cells will be cleaned away by the immunsystem.
Even the bloodflow to the Penis and Prostata is controled by androgen action in the brain.
I think you get a few things very wrong. The Prostata is not responsible for hypogonadal level.
Because the Prohormones are Produced in the testical and the adrenal glands. The cells convert it to the more functional DHT when its needed.
the relase of he LH and FSH comes from the brain, to make it simple. just google the HPTA you will see how it works.
But!!! There are also AR on the pituitray gland. So when cells are hypersensitiv, (some can be more some can be less) even the Rezeptors in the P.gland are hypersensitv and ā€œthinkā€ there is to much DHT but there isnt, so it slows down the release of LH and FSH wich is responsible for the relase of T as a Prohormon. But also higer Estrogens control the relase of those hormon. Anyway there are many many more things like the pulsing of GnRH etc. Its not so simple.
Also here i wrote before, can the lack of androgenaction cause a inflammation YES, is this the toot of the Problem? NO. so do you think treating a inflammation will help? NO.
What causes all the Problems? higher Estrogens and and and. the lack of androgen action on the cells, and missing Proteins and celldeath.
Have a look at awors treat about the studies, they will show us a lot. This will show us, which Androgen responsive gens are over or under expressed.

"The problem appears to be the testosterone to DHT conversion. This may be caused by and imbalance between thyroid hormones and cortisol, damage to the 5AR Type 2 enzymes or simply reduced amount of enzymes due to prostate and penile atrophy. "

Can we establish that estrogen domiance is a problem? Due to the lack of testosterone to DHT production hence low 3-adiol G? [Size=4]3-Adiol-G increases with Andractim. So That says a lot.[/size]
What about Androgen Sensivity Syndrome?

Our bodies still react to androgens. Facial hair - Errectile function. Refer to above. Just look at the guys who took steroids. Why didnā€™t it last or work for long, steroids increase estrogen. There facial hair growth still increases which suggests an increase in androgen activity ,which is true.

Look at the guys who took anti-estrogens. They had temporary recoveries. But with the lack of 5ar2 activity and/or imbalance between thyroid hormones and cortisol you go back to square one. Itā€™s like trying to fix a something with sticky tape, eventually itā€™s going to happen again unless you go get it fixed.

Thyroid Imbalance
Muscle Weakness
Breathlessness
Heart Palpitations
Anxiety
Osteoporosis (in severe cases)
Trembling Hands
Hair Loss
Insomnia
Weight Loss
Fatigue
Heat Intolerance
Increased Bowel Movements

Cortisol Imbalance
Fatigue
Difficulty Falling Asleep
Mood Swings
Feeling of Stress
Abdominal Weight Gain
Decreased Muscle Mass
Thinning Hair/Beard
Erectile Dysfunction
Irritability/Anxiety
Premature Aging
Decreased Libido
Depression
Headaches
Achy Joints

Estrogen Dominance
Low sex drive
Impotency/erectile dysfunction
Infertility
Gynecomastia, or ā€œman boobsā€
Weight gain
Enarged prostate
Prostate cancer
Testicular cancer

Hormonal Imbalance
Difficulty Passing Urine
Impotence
Prostate Inflammation
Headaches / Migraines
Mood swings / Depression
Inability to lose weight
Fatigue
Foggy thinking / Memory loss
Lack of interest in Sex
Water retention / Bloating
Low Blood Sugar
Adult Acne
Reduced Muscular Strength Enlarged Prostate
Erectile Dysfunction
Lowered Libido
Burning Sensation Urinating
Panic / Weeping
Blood Sugar Imbalance
Leg / Muscle Cramps
Feelings of being crazy
Hysteria
Allergies
Swollen feet / ankle
Low Thyroid symptoms
Low Sperm Count Incontinence
Lack of Sex Drive
Prostate Cancer
Breast Enlargement
Rapid Weight loss
Hair loss
Hypoglycemia
Anger / Irritability
Bone loss (Osteoporosis)
Age and Liver spots
Dry aging skin
Insomnia
Diabetes

@ Propeciashiz:

I dont want to be rude, but did you read, what i wrote??? First this is a post about, if fin can causes a B12 deficiency. And please not about some Theories. I just tryed to explain why.
I know my english is not the best, but please read first. Spaming the Forum with all those theories is not the best way.
All I can say, when you think you got it, than test it. You realy get obsessed by it, this is the worst thing that can happen to you, but also this I told you more than 1000 times. I know, we all want a cure of this mess and like I also told you there are many people working on this.
Many people here have seen the best DocĀ“s on the world, if you think its so simple, why do you think we still are suffering? And these are DocĀ“s who know their jobĀ“s.
I wont give you a answer on this, because I did this tooo many times. And I dont have the time to repat everything again and againā€¦ If you want to do something, read about epigenetic, geneexpression and AR sign.
But the best thing i can tell you is, stop driving yourself mad. You need now all your power for recover and stressing youself is the worst thing you can do now. We can spend yours of time to talk about all theories, or we can do someting! Like I said, if you think you know what the Problem is, try it.

Hey Brainbug,

Iā€™m not being disrespectful at all, but did you read my post? iā€™m agreeing with you totally but canā€™t anyone on here be open minded theres been one theory written and itā€™s a good one. But cant you just listen?

"The problem appears to be the testosterone to DHT conversion. This may be caused by and imbalance between thyroid hormones and cortisol, damage to the 5AR Type 2 enzymes or simply reduced amount of enzymes due to prostate and penile atrophy. "

Can we establish that estrogen domiance is a problem? Due to the lack of testosterone to DHT production hence low 3-adiol G? 3-Adiol-G increases with Andractim. So That says a lot.
What about Androgen Sensivity Syndrome?
IF DHT INCREASES 3 - ADIOl - G THAT MAKER IS FINE. THE PROBLEM IS THE CONVERSION OF T TO DHT VIA 5 ALPHA REDUCTASE

Our bodies still react to androgens. Facial hair - Errectile function. Refer to above. Just look at the guys who took steroids. Why didnā€™t it last or work for long, steroids increase estrogen. There facial hair growth still increases which suggests an increase in androgen activity ,which is true.

Look at the guys who took anti-estrogens. They had temporary recoveries. But with the lack of 5ar2 activity and/or imbalance between thyroid hormones and cortisol you go back to square one. Itā€™s like trying to fix a something with sticky tape, eventually itā€™s going to happen again unless you go get it fixed.

@ Brainbug

Yeah sorry dude, I guess this is driving me a bit nuts. I struggle to even perform my job now.

Does anyone else get exhausted when taking B-vitamins? When I take them, its like Iā€™ve taken a benadryl.

I read this, but it realy seems for me you do no understand as often as i told you this and im sorry I dont have the time to explain it to you again and again and again.

This is the last time.
Sure, there is a Problem of the reduction of T to DHT, for some people, some have normal DHT levels some dont. Cause the expression of 5AR depends on a ARG.
Take DHT and see what will happen, but on your owen risk. When there is just a Problem of the reduction of T to DHT, taking DHT and an AI would make everthing fine, but it dont!
Taking a AI will raise DHT, like taking DHT, like taking clomid but for most of the people this is only a short benefit, for some it does nothing and for some it also can make things worse.
Why? because the cells are hypersenstiv and when you push the androgens higher, the cells in some cases will shut down even more. As I explained you many many times.

We have so many Problems, one of it is sure a estrogen dominance and a lack of 3a-diol-g.
3a-HSD converts DHT to 3a-diol-g and 3a-HSD is expressed by an androgen resposiv gene.
This shows that we have a lack of androgen action.
Just for you once again, raising androgens, when cells are hypersensitiv can, a) bring a short live benefit, until the cells shut down even more b) makes nothing

I also explained it many times. Cells get more senitiv, to a point, when they get to sensitiv and the cells shuts down the production of the proteins. This is depending on the tissue the expressin of the AR and the subtypes of the 5AR. Thats why some get brainfog, some not, why some get a bigger dick, there are also people outside who take finasterid, for getting a biger dick, why? because it makes the cells more sensitiv until again the point they become hypersensitiv and shut down. This is why the beard is stilll growing, and why some dont lose muskels and why some get better with the time.

But I told this to you many many times and you still dont get it or dont want to understant. The Problem is not so simple, or do you think, popin a AI and DHT will be the cure? The best thing is. Try to find out, but like I said on your owen risk, there are people who get better with a TRT or taking a AI. But this also depends on how sensitiv their cells are.

Spamming the forum with your theories wont do anything, I even dont know what you want to hear? If you dont listen, or think you know what to do feel free. Mate you are realy getting obsessed by this! I dont know what those discussions should bring? Even this is a treat about the Vit B12.

Hey, no i dont have this. May be you try to lower the dose or the intake timeframe.

brainbugā€¦honest questionā€¦

what are your credentials?

I have the same problem. If I take a vitamin B complex my body reacts strongly in a bad way. I tried 2 different brands with the same result. B Vitamins as part of multivitamins are no problem. But by taking high dose of vitmin B3 I get a lot of benefits. No clue why I react on B Vitamins so stronglyā€¦

Lincoln. honest answer?

care about your own things! This is a open forum and i dont post here what my job is!
What the hell is wrong with some of you guys??? Realy, What do you want to do?
I take my time and try to explian some things. I worte in some other post what i think about some people here and now its realy over!!! I only wanted to help, help with my knowlage, but I also can let it be and dont have to spend me time with, sorry to say that, with some big idiots!

Lincoln, Think what you want! Do what you want. I dont care about that anymore. We all are sitting in the same boat! Why the hell, some idiots always must atack otherr people here???

it causes vit d deficiency for sureā€¦mine hasnt changed a bit!!!

WOW!!! I sincerely did NOT mean to offend you. I dont keep up with usernames here anymore so I might have forgotten that you are involved in research.

I was just asking who you are, ie some sort of doctor or scientist. You could be anybody.

My question was not meant to offend at all, thats why I said ā€œhonest questionā€.

A lot of people are tempremental on here.

yes, fucking hormons! drives us crasy!

They sure do! We will fix this. Weā€™re in the same boat.

My B12 levels were low (304 pg/mL) but still considered ā€œnormalā€ by the lab range.

Several doctors believe the standard range is too wide: ā€œā€¦people with B12 levels between 200 pg/mL and 350 pg/mL ā€“ levels considered ā€œnormalā€ in the U.S. ā€“ have clear B12 deficiency symptoms.ā€
Source: chriskresser.com/b12-deficiency-a-silent-epidemic-with-serious-consequences

My guess is that my low B12 is caused by malabsorption, as I eat plenty of B12 containing foods. A possible cause of the malabsorption is hypochlorhydria (low stomach acid) which can be caused by hormone imbalances.

I plan on doing a test for hypochlorhydria before trying any B12 supplementation.