Greetings,
I am a new member and i plan to stick around in hopes of curing my condition. I have been a lurker here for some days but i have been reading a lot about depersonalization and derealization in another forum. The reason i didnt make the connection and came here immediately is because i do not have taken any medication that justify me having pfs symptoms. The only phenomenon i dont understand here in this forum is the crash, because i never experienced any crash. My symptoms simply started as a mild depression accompanied with panic and anxiety attacks triggered not by hormones by by real life events and possibly exacerbated due to low testosterone. Some days i would stay awake for 3 days not being able to sit down just walking up and down. I also suffered from vitamin deficiency due to very unhealthy diet and sleeping patterns. I had little exposure to the sun so i probably had vitamin D deficiency and definitely had vitamin C deficiency because i got scurvy (gums bleeding horribly, cramps) which resolved shortly after i started consuming lemon. I slowly started to lose interest in real life and was interested only in gaming and porn. After a while i started to lose interest in those things too. Consuming only pizzas and fast food and a lot of sweets i became obese. Thing is that i didn’t become all around fat but belly fat possibly due to the excessive sugar consumption and metabolic issues that sugar causes, i was like a pregnant woman. Now i weight as much as back then but dont look fat because my fat is better distributed. After a year of being like this i started to notice more symptoms. My balls got smaller propably due to low LH and brain not signaling them to function properly and my body hair started to become thin and unnoticeable.Later i started dieting and powerlifting and my condition got much better. I still suspected that my testosterone was low and this is a reason why i am experiencing these foggy dereliazation feelings accompanied with anhedonia and reduced libido. I got tested and my testosterone was at 450 with range of 300 to 1100 and my E2 was at 50 with range 20 to 50 an LH was low I think that i also found DHT was low but back then i was of the uneducated opinion that DHT doesnt do anything important . I figured my estrogen was low so i took an aromatase inhibitor and retook the testosterone test the next morning. My T was at 1200 and LH high. I didnt take any further tests and continued the protocol of 2,5mg of letrozole once every week as happened in a study that i read in which letrozole was used to treat obesity related hypogonadism. 54% of men that took letrozole reported loss of libido and unsurprisingly i had the same results so i stopped taking letrozole. To me there seem to be one correct way to treat my condition. Lose weight decrease aromatase and increase T and DHT and if that fails use TRT. If TRT doesnt improve my condition it means i got PFS or some psychiatric induced hormonal problem. Sorry for not filling the questionnaire but ticking doesnt work when i click it.
If you haven’t taken any antiandrogenic substances its very unlikely you have PFS in my opinion. Do you have sexual side effects?
Yes as i mention in the post i have low libido, anhedonia, lack of motivation, depression, fatigue, and brain fog/ depersonalization. I dont use ssris and i find a medication used for bipolar disorder very uplifting as my doctor promised. I have found a neurologist and a urologist that both take my symptoms seriously unlike many people experienced here. My urologist was very skeptical since i had symptoms even if i was in range of low T. He was willing to perscribe me TRT but i never visited him again cause his office is far.
Yeah I’ve read the whole post now. Its awful that this is happening to you friend, I’d recommend trying TRT and if it doesn’t work I’d say it could possibly be PFS induced by the deficiencies if all bloods are in range.
Thing is the gradual symptoms of low T started even before the adoption of the unhealthy lifestyle and maybe it is these symptoms that led to my adopting this easy lifestyle. Doctor said that this gradual increase in symptoms is characteristic of low T. I should run some tests and update probably. The only strange thing is that T is low but not horribly, and the feeling of derealization, brain fog is very close to pfs. Thing is that many men with low T also complain of brain fog and it is listed as one of the symptoms of low T.
Personally I think you’ll have good results from TRT.
PFS is basically all low T symptoms because T isn’t working right or androgen receptors or some shit but you can also obviously get low T symptoms the simple lovely way, from low T.
Anyone else can help?
Hi @hairy_scalp,
Firstly, thanks for sharing your story. I noted your observation in another topic that it is increasingly recognised that antiandrogenic products have lasting consequences, and we obviously do our best to further the recognition of this issue and bring further useful investigations to fruition. Talking of fruition, congratulations on managing to get scurvy in this day and age…I’ll skip the lifestyle factors you’re clearly aware probably don’t help matters.
There are quite a lot of differences to your clinical situation and PFS. What you describe is also quite in line with symptoms of hypogonadism as you know.
A serum DHT reading is not particularly useful as 5 alpha reductase 2 is a membrane bound protein that reduces the double bond of lipid delta 4 steroids, and is observed to be localised in the endoplasmic reticulum of cells. Low DHT is not particualrly clinically relevant, and millions of men are on finasteride which remarkably reduces DHT without apparent issues. Additionally, men with genetic incapability of metabolism of DHT from T through 5ar2 have neither the issues you or patients here describe.
Our issue is a relatively rare response to the drug. It is not impossible you are someone naturally predisposed to whatever is the underlying genetic/epigenetic difference(s) in PFS patients, and low DHT could therefore hypothetically induce these changes.
However, although I understand you might feel unsupported, this is not a forum for naturally occurring endocrine problems, and unfortunately, although your symptoms have some intriguing clinical overlap and may even ultimately have some mechanistic overlap, we are not yet clear on what causes these problems after antiandrogenic products so there’s little more this forum can offer you at this time. Membership is restricted to those who have used and ceased the drug/substance classes covered by our site: Predominantly 5 alpha reductase inhibitors, antiandrogens, serotonergic drugs, accutane and saw palmetto.
I will suggest you consider whether you believe it to be worth discussing the following with your endocrinologist:
A literature review we have published on our site discusses at length the known relationship between AR CAG repeat polymorphisms androgens. Namely, as the repeat strays from the median length, the tissue response to androgens becomes less efficient. A repeat over 40 denotes SBMA, previously understood as a LMN disease but now known to be a multisystemic disease due to the ubiquitous physiological influence of the AR. A relevant extract from the page linked:
SBMA can manifest in absence of neuromuscular complaints or symptoms, presenting with an endocrine phenotype comprising of symptoms including gynecomastia, testicular atrophy, hypercholesterolemia and diabetes mellitus (Battaglia et al., 2003). Nonclassical symptoms including erectile dysfunction can be cited by patients as amongst their most disabling symptoms (Fratta et al., 2014). Sexual dysfunction across domains including orgasm function, erectile function and satisfaction is commonly reported (Dahlqvist et al., 2019).
This is a slow progressing disease that develops over time, often in middle age, although now it is appreciated in many cases symptoms will begin in adolescence. In one of the most extreme cases recorded:
Grunseich et al. reported a 29-year-old SBMA patient with a long 68 CAG repeat expansion. The patient experienced early onset of multisystemic symptoms. He had been born with penile congenital abnormality. He developed gynecomastia by 16 and muscle weakness, fatigue after exercise, fasciculations, cramping, and tremor by age 18. He experienced ejaculation difficulties, testicular atrophy, burning neuropathic pain and dysesthesia in the feet and fingertips, reduced sweating and decreased facial hair growth. Tongue atrophy was noted, and weakness was observed in the orbicularis oculi and orbicularis oris. He exhibited perioral fasciculations, severe limb weakness bilaterally, difficulty standing on his heels and ankles, and loss of temperature and vibratory sensation in the fingers and toes. Abnormalities were seen on muscle MRI. Evidence of autonomic dysfunction suggestive of small fiber dysfunction was determined, including negligible sweat responses and orthostatic tachycardia without blood pressure changes or symptoms (Grunseich et al., 2014).
Considering the slow progression you describe and low-androgen endpoints without serum explanation, you might want to look at the studies linked in the section above and consider discussing with your clinician the possibility of genetic determination of the CAG polyglutamine tract length in exon 1 of your androgen receptor gene to rule out a polymorphic cause. It’s a relatively simple test nowadays.
All the best in the future
axo
I would like to ask you one question. Does testosterone become dht after it has bound to the androgen receptor? Because if thats the case this would mean that the testosterone in my body doesnt bind with the AR.
No, it is metabolised at the tissue level to DHT by 5ar. DHT binds to the AR as a more potent ligand than T:
Hi @hairy_scalp. I just read your story and also feel you may benefit from ruling out other conditions, like SMBA, that may have resulted in your symptoms.
Best case scenario is that you have something that can be easily diagnosed (relative to PFS) and treated.
I don’t have SMBA. I don’t have any of these symptoms except from a period of low T.
Also depends on the cost.