- Reaction score
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So I am not sure if this iinfo has already been shared here already but I thought it's worth reading:
Alan Jacobs, MD
(http://blog.alanjacobsmd.com/)
Clinical Experience in the Evaluation and Treatment of 300 cases of Post Finasteride Syndrome
In April 6, 2010 I blogged here on A Neuroendocrine Approach to Finasteride Side Effects in Men. Now I am reporting on how we've done over the past 3 years caring for around 300 men sufferring from Post Finasteride Syndrome (PFS).
First, the group of 300 + men presenting with sexual dysfunction while on finasteride, or recently or not-so-recently off it, did all show a similarly abnormal hormonal profile called hypogonadotropic hypogonadism or HH, which means low testosterone along with low LH and FSH, the pituitary hormones that stimulate the gonads. However, the group was otherwise not monolithic. In fact, I found three groups into which these men could be separately categorized.
10% of the the guys actually had a different reason to have HH, completely unrelated to the finasteride. For example, they had a benign pituitary tumor or some other related pituitary condition partially blocking its function in the hypothalamic-pituitary-gonadal (HPG) axis, so they could not make LH and FSH, and thus their testicles stopped making testosterone.
50% of the guys came with a family history, or genetic load, for emotional conditions such as anxiety and depression. Then when the finasteride caused big-time sexual problems, they were so distressed that their mental anguish itself appearred strong enough to suppress their HPG axis such that they had a separate reason to not be able to raise their LH and FSH when their testosterone declined, presumably initially from the finasteride. This mechanism is no different than the dancers and marathon-running women who loose their menstrual cycles. Such huge stressors, whether physical or mental, cause the higher brain centers in the temporal lobes to put the brakes on fertility, as if it were not a good time to have kids if your own internal stiuation is so hectic to begin with. The emotional parts of the brain inhibit the HPG axis directly, again blocking LH and FSH from responding to the low sex hormones. In this situation it was unclear whether the finasteride, their emotional brains, or both were impeding these guys' ability to get better.
Then there were the 40% of guys who had no other reason than PFS to have HH, and to be sexually impaired, physically perturbed and mentally distraught - the pure post finasteride syndrome.
The first group of guys got treated in the appropriate neurosurgical setting, or reassured that there was no treatment needed except to normalize their testosterone levels. The second group presented more of a problem as they needed to be shaken out of their despair first in order for their HPG axis to be released from the grip of their higher emotional brian centers and be able to start making appropriate amounts of LH and FSH, leaving the only variable left to deal with the finasteride. The best way to do this was to raise their testosterone levels directly and aggressively such that they felt great and trusted their bodies to be normalizable. Also, in many cases anti-anxiety medications were added and were very helpful. Gradually these guys' minds eased and they were eventually given the option to taper off the hormone after 6-12 months to see if they would stay normal on their own, though very few have as of yet wanted to. The third group could most often be treated successfully by using medications to raise LH and FSH directly and letting their testicles follow suit and make more testosterone. Sometimes LH and FSH would not budge enough and direct testosterone replacement was necessary and did the trick as long as the dose was pushed high enough and estradiol was kept from rising, due to peripheral conversion (aromatization) of the testosterone, with a different medication.
PFS is an troublesome condition, however, my experience is that it is well worth applying the neuroendocrine approach to caring for these guys since it has been most often beneficial to them.
Alan Jacobs, MD
(http://blog.alanjacobsmd.com/)
Clinical Experience in the Evaluation and Treatment of 300 cases of Post Finasteride Syndrome
In April 6, 2010 I blogged here on A Neuroendocrine Approach to Finasteride Side Effects in Men. Now I am reporting on how we've done over the past 3 years caring for around 300 men sufferring from Post Finasteride Syndrome (PFS).
First, the group of 300 + men presenting with sexual dysfunction while on finasteride, or recently or not-so-recently off it, did all show a similarly abnormal hormonal profile called hypogonadotropic hypogonadism or HH, which means low testosterone along with low LH and FSH, the pituitary hormones that stimulate the gonads. However, the group was otherwise not monolithic. In fact, I found three groups into which these men could be separately categorized.
10% of the the guys actually had a different reason to have HH, completely unrelated to the finasteride. For example, they had a benign pituitary tumor or some other related pituitary condition partially blocking its function in the hypothalamic-pituitary-gonadal (HPG) axis, so they could not make LH and FSH, and thus their testicles stopped making testosterone.
50% of the guys came with a family history, or genetic load, for emotional conditions such as anxiety and depression. Then when the finasteride caused big-time sexual problems, they were so distressed that their mental anguish itself appearred strong enough to suppress their HPG axis such that they had a separate reason to not be able to raise their LH and FSH when their testosterone declined, presumably initially from the finasteride. This mechanism is no different than the dancers and marathon-running women who loose their menstrual cycles. Such huge stressors, whether physical or mental, cause the higher brain centers in the temporal lobes to put the brakes on fertility, as if it were not a good time to have kids if your own internal stiuation is so hectic to begin with. The emotional parts of the brain inhibit the HPG axis directly, again blocking LH and FSH from responding to the low sex hormones. In this situation it was unclear whether the finasteride, their emotional brains, or both were impeding these guys' ability to get better.
Then there were the 40% of guys who had no other reason than PFS to have HH, and to be sexually impaired, physically perturbed and mentally distraught - the pure post finasteride syndrome.
The first group of guys got treated in the appropriate neurosurgical setting, or reassured that there was no treatment needed except to normalize their testosterone levels. The second group presented more of a problem as they needed to be shaken out of their despair first in order for their HPG axis to be released from the grip of their higher emotional brian centers and be able to start making appropriate amounts of LH and FSH, leaving the only variable left to deal with the finasteride. The best way to do this was to raise their testosterone levels directly and aggressively such that they felt great and trusted their bodies to be normalizable. Also, in many cases anti-anxiety medications were added and were very helpful. Gradually these guys' minds eased and they were eventually given the option to taper off the hormone after 6-12 months to see if they would stay normal on their own, though very few have as of yet wanted to. The third group could most often be treated successfully by using medications to raise LH and FSH directly and letting their testicles follow suit and make more testosterone. Sometimes LH and FSH would not budge enough and direct testosterone replacement was necessary and did the trick as long as the dose was pushed high enough and estradiol was kept from rising, due to peripheral conversion (aromatization) of the testosterone, with a different medication.
PFS is an troublesome condition, however, my experience is that it is well worth applying the neuroendocrine approach to caring for these guys since it has been most often beneficial to them.
