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Brain fog with propecia ?


bensk

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Hey fam,

 

I have been on propecia for 7 month and have experienced brain fog quit a few time, it is not permanent but it does happens somedays...

 

Do you guys think it could be related to the propecia ?

 

Thank you,

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Finasteride does induce a state of hypogonadism and inhibits insulin sensitivity. This is probably the cause of brain fog, as a result of insulin being less effective at delivering glucose to brain cells. However, I'm not sure if finasteride has direct neuroactive effects, so this might also be a contributor.

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Ive had the brain fog issue. At first, I thought it couldnt be due to finasteride due to no evidence behind it. then, Merck attached a side effect pamphlet with the pills that explained this could be an issue. it made it evident propecia was the cause. Not sure if it is a long term side effect or just temporary, but few folks have had this occur.

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To correct the above inaccuracy, Dual inhibition of 5αRs, but not inhibition of 5αR2 alone, modulates insulin sensitivity in human peripheral tissues rather than liver. Finasteride blocks R2 whereas Dustasteride blocks both R1 and R2

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To correct the above inaccuracy, Dual inhibition of 5αRs, but not inhibition of 5αR2 alone, modulates insulin sensitivity in human peripheral tissues rather than liver. Finasteride blocks R2 whereas Dustasteride blocks both R1 and R2

 

Thats an interesting perspective.

 

Unfortunately, inhibiting androgen bioactivity by nearly 50% (finasteride) will result in general loss of insulin sensitivity, which is sufficient to precipitate metabolic disorders (e.g., brain fog).

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Do you have a published reference from a legitimate medical journal?

 

Yes sir.

 

Finasteride reduces circulating DHT about 70%. (1) Since DHT is about 3-4x more potent than testosterone as an androgen, this equates to about a 50% drop in total androgen bioactivity. (2) Considering the average testosterone level for an adult male is around 500ng/dL, a 50% drop in total bioactivity would equate to roughly 250ng/dL testosterone level, which can be defined as hypogonadism. (3) Hypogonadism leads to decline in mental function, most notably forgetfulness and fogginess. (4,5)

 

I have the full texts of these references if you want them.

 

 

1. Finasteride in the treatment of men with androgenetic alopecia. Finasteride Male Pattern Hair Loss Study Group

Kaufman KD, Olsen EA, Whiting D, Savin R, DeVillez R, Bergfeld W et al.

J. Am. Acad. Dermatol., 1998

 

2. Serum Androgen Bioactivity During 5a-Dihydrotestosterone Treatment in Elderly Men

Raivio T, Tapanainen JS, Kunelius P, Janne OA

J. Androl., 2002

 

3. Prevalence of hypogonadism in males aged at least 45 years: the HIM study

Mulligan T, Frick MF, Zuraw QC, Stemhagen A, McWhirter C

Int. J. Clin. Pract., 2006

 

4. The male climacterium: clinical signs and symptoms of a changing endocrine environment

van den Beld AW, Lamberts SW

Prostate Suppl., 2000

 

5. Testosterone and cognitive function: current clinical evidence of a relationship.

Beauchet O.

Eur J Endocrinol. 2006 Dec;155(6):773-81.

Edited by EricPotratz
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I haven't had the opportunity to yet read your references but they don't appear to address your comment regarding 5aR2 inhibition and insulin sensitivity. While your statement about androgenic potency may be correct you are neglecting to account for the quantity/quality and location of specific DHT receptors outside of the prostate and hair follicles which might account for a direct relationship between partial inhibition and other clinical manifestations. The role of these receptors are still being studied and are by no means considered "settled science."

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I haven't had the opportunity to yet read your references but they don't appear to address your comment regarding 5aR2 inhibition and insulin sensitivity. While your statement about androgenic potency may be correct you are neglecting to account for the quantity/quality and location of specific DHT receptors outside of the prostate and hair follicles which might account for a direct relationship between partial inhibition and other clinical manifestations. The role of these receptors are still being studied and are by no means considered "settled science."

 

We are talking about the negative mental effects of reduced circulating DHT, not the location of 5a-reductase. The type of 5a-reductase, or its location, doesn't matter in this situation. FYI, the majority of circulating DHT comes from 5a-reductase action in the prostate.

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A hormone must interact with a receptor in order to have an effect. The quantity and location of these these receptors are of paramount importance in the basic understanding of endocrinology. May I ask what your scientific background or degree is?

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A hormone must interact with a receptor in order to have an effect. The quantity and location of these these receptors are of paramount importance in the basic understanding of endocrinology. May I ask what your scientific background or degree is?

 

Hairweare,

 

5a-reductase is not a hormone receptor, its a conversion enzyme. The androgen receptor (AR) is the receptor.

 

The lack of DHT, leads to lack of stimulus on the AR, which leads to lack of glucose uptake and impaired mental function. Doesn't matter where the DHT originally came from.

 

My background is 10 years of male hormone product formulation. You can find more info about me on google.

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Of course, I am referring to DHT and it's receptors. You have offered no evidence that selective partial inhibition of R2 has an effect on insulin sensitivity and central neural function. Again, do you have a science degree or are you just an internet huckster peddling supplements?

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Of course, I am referring to DHT and it's receptors. You have offered no evidence that selective partial inhibition of R2 has an effect on insulin sensitivity and central neural function. Again, do you have a science degree or are you just an internet huckster peddling supplements?

 

Nobody is talking about 5a-reductase isoforms. It has no relevance here. Finasteride flatout cuts circulating DHT by 70%. And both insulin sensitivity and cognitive function are negatively influenced from reduced circulating androgen levels. See post #9 for references.

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You appear to have backed off or changed the subject from your original claim that finasteride affects insulin sensitivity and subsequent central neural function. I would rather rely on credible published medical research than unfounded claims by a supplement salesman with no advanced degree.

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Finasteride is not known to affect insulin sensitivity, however dutasteride is. Secondly, I don't see what insulin sensitivity has to do with brain fog. However, finasteride is known to be neurologically active and may well be the source of the sides.

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Finasteride is not known to affect insulin sensitivity, however dutasteride is. Secondly, I don't see what insulin sensitivity has to do with brain fog. However, finasteride is known to be neurologically active and may well be the source of the sides.

 

Not sure if there is a placebo controlled trial on finasteride based around insulin sensitivity but there plenty of evidence to suggest that a dramatic reduction in circulating androgen is going to negatively affect insulin sensitivity. (see post #9 in this thread) Poor insulin sensitivity, means poor blood sugar control, which could bouts of mental fog. (and of course whatever direct GABAergic effects finasteride or its affected hormones may impart)

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DId you read my link?

 

Yes, good study. I hadn't seen it before.

 

Low androgen levels are generally linked to insulin resistance, so I'm surprised the finasteride didn't show a more negative effect on IR values in that study considering the suppression of DHT.

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