Post-Finasteride Syndrome (PFS): Symptoms, Causes, Testing, and Treatment for Finasteride Users

Post-Finasteride Syndrome (PFS) is a relatively recent term that describes a set of symptoms observed in certain men following the discontinuation of finasteride therapy. Finasteride is a type II 5α-reductase inhibitor, an enzyme responsible for converting testosterone into dihydrotestosterone (DHT).

To date, Post-Finasteride Syndrome has been documented exclusively in men, as finasteride is prescribed almost exclusively to males for the treatment of androgenetic alopecia (hereditary hair loss) or benign prostatic hyperplasia. Post-Finasteride Syndrome is characterized by persistent physical, neurological, and sexual disturbances that continue for months or even years after stopping the medication, without any other apparent cause.

The most common symptoms include:

• Sexual dysfunction, such as loss of libido, erectile dysfunction, and reduced orgasmic sensation.
• Neuropsychiatric disturbances, such as depression, anxiety, reduced concentration, emotional numbness, and sleep disorders.
• Physical symptoms, such as chronic fatigue, muscle weakness, and pain in the testicles or pelvic region.
   

Although Post-Finasteride Syndrome has not yet been officially included in international diagnostic manuals such as the DSM-5 or ICD-11, its presence is widely acknowledged in medical publications and pharmacovigilance databases, with growing support from scientific groups worldwide calling for its inclusion due to the high volume of reported cases. Finasteride is often prescribed to young men for cosmetic purposes, as thinning hair and hair loss significantly impact self-image and psychological well-being. However, its long-term effects are not yet fully understood. For the safe use of this medication and to prevent adverse effects, it is essential to understand and recognize Post-Finasteride Syndrome.

Mechanisms Behind Post-Finasteride Syndrome: DHT, Neurosteroids, and Epigenetic Factors

The pathogenesis of Post-Finasteride Syndrome remains the subject of intensive investigation, as there is still no universally accepted mechanism that explains the diversity and persistence of symptoms appearing after discontinuation of finasteride. However, contemporary literature has proposed several biochemical and neuroendocrine pathways that appear to be involved in this phenomenon.

The Role of Dihydrotestosterone (DHT): Finasteride inhibits the enzyme 5α-reductase type II, which converts testosterone into dihydrotestosterone (DHT), a much more potent androgen. The reduction in DHT levels through finasteride administration is associated with slowing hair loss and reducing prostate size. However, DHT is not solely responsible for the development of androgenic traits. It also participates in specific physiological axes that may be adversely affected by the abrupt and prolonged inhibition of DHT:

• In neuroprotection, by regulating neurosteroid homeostasis in the brain.
• In psychosexual function, by influencing areas such as the hypothalamus and hippocampus.
• In muscle function, via receptors present in muscle tissues.
   

Androgen Receptors (AR): Studies of tissue samples from patients with Post-Finasteride Syndrome, particularly skin and brain tissue, have shown abnormalities in androgen receptor expression. Specifically, chronic DHT suppression may lead to impaired receptor recalibration, resulting in:

• Hyporesponsiveness to physiological androgens
• Increased sensitivity to cellular stress
• Disruption of intracellular signaling pathways
   

Neurosteroids and GABA Interaction: DHT is not the only molecule affected by finasteride use. This inhibitor also inhibits the synthesis of neurosteroids, such as allopregnanolone and tetrahydrodeoxycorticosterone (THDOC). These molecules regulate the activity of GABA, the brain’s primary inhibitory neurotransmitter. Changes in their concentration may lead to neuropsychiatric symptoms commonly reported by individuals with Post-Finasteride Syndrome, such as increased anxiety, sleep disturbances, depression, and emotional numbness.

Possible Epigenetic Mechanisms: It has been proposed that finasteride may also alter gene expression through epigenetic mechanisms, including DNA methylation, histone H3K9 methylation, and microRNA activity. Alterations in such biological pathways may have a long-term character, disrupting the physiological function of tissues and systems even long after the drug is discontinued.

Potential Predisposition: It is worth noting that not all finasteride users develop Post-Finasteride Syndrome. This suggests that a genetic or individual predisposition may exist, making specific individuals more vulnerable to the drug’s adverse effects. Combined with the syndrome’s multifactorial nature, this highlights the need for a personalized medical approach to both diagnosis and treatment.

Diagnosis of Post-Finasteride Syndrome: Laboratory Testing and Functional Evaluation

Post-Finasteride Syndrome is currently diagnosed only after ruling out other organic or psychiatric causes for the patient’s symptoms. There is no standardized diagnostic test. However, in conjunction with thorough medical history and psychosexual assessment, specific laboratory tests can significantly assist in excluding other pathologies and in understanding the biological basis of the symptoms:

• Total Testosterone (TT): Essential for evaluating androgen status. Low levels may contribute to sexual dysfunction or fatigue.
• Free Testosterone (FT): The bioavailable form of testosterone. Often more indicative than total testosterone for detecting functional deficiency.
• Dihydrotestosterone (DHT): The primary hormone blocked by finasteride. Measuring it provides insight into 5α-reductase activity.
• Pregnenolone: A precursor hormone involved in the production of neurosteroids. Its measurement offers indirect information on allopregnanolone availability, whose deficiency has been linked to neuropsychiatric symptoms in patients with Post-Finasteride Syndrome.
• Neurotransmitter Profile: Provides insight into neurochemical pathways. Disturbances in GABA and serotonin levels are associated with the psychiatric symptoms of Post-Finasteride Syndrome.
• Adrenal Function Test - AdrenalScan®: Allows dynamic monitoring of hormonal rhythms throughout the day, crucial for evaluating the HPA axis (hypothalamus–pituitary–adrenal), which is often disrupted in Post-Finasteride Syndrome.
   

These tests provide essential information about the hormonal, neurosteroid, and psychoneurological function of the body. Other tests, such as gonadotropins (LH, FSH), a full thyroid panel, and gut microbiome analysis (EnteroScan®), can also be valuable when specific symptoms are present. Still, they are not always necessary during the initial phase of investigation.

In addition to laboratory tests, the diagnostic approach to Post-Finasteride Syndrome may also include, when clinically indicated, imaging or psychometric techniques. These include brain MRI to exclude organic lesions in key areas of the brain, scrotal triplex ultrasound to evaluate potential inflammation or a varicocele, psychometric tests such as BDI, SHIM, and HADS to assess mood and sexual function, and prostate ultrasound to help differentiate from benign prostatic hyperplasia.

Post-Finasteride Syndrome Treatment: Medical Therapies, Supplements, and Supportive Nutrition

The management of Post-Finasteride Syndrome is multifactorial, as there is currently no established treatment protocol. The choice of therapeutic approach depends on symptom severity, age, hormonal profile, and the patient's psychological state.

In patients with confirmed hypogonadism (low free or total testosterone), testosterone replacement therapy (TRT) may be applied, aiming to restore sexual function and energy balance. In cases where testosterone is excessively converted to estrogens, and only upon clinical suspicion supported by specialized laboratory testing, aromatase inhibitors may be used. Finally, although they do not address the root cause, medications for erectile dysfunction, as well as antidepressants or anxiolytics, may be prescribed on a case-by-case basis to manage severe symptoms of Post-Finasteride Syndrome.

In addition to the above pharmaceutical interventions, which are implemented only in specific cases, several natural strategies can help address Post-Finasteride Syndrome. These strategies aim to restore internal physiological balance through dietary and lifestyle optimization, and to support this with supplements or herbs with neuroendocrine activity.

Nutrition: Nutrition can profoundly affect hormonal balance and the composition of the gut microbiome. By supporting proper gut and liver function, a well-structured diet can indirectly facilitate the restoration of neurotransmitters and neurosteroids, supporting the endocrine axis through:

• Foods rich in cholesterol (e.g., egg yolks, butter, liver), as cholesterol is a precursor molecule for steroid hormones.
• Intake of fatty acids (omega-3 from fatty fish, walnuts, flaxseed), which support neuronal membrane function.
• Foods containing probiotics and prebiotics (yogurt, kefir, fermented products, green bananas), which strengthen the gut microbiome.
• Avoiding excessive consumption of sugar, caffeine, alcohol, processed foods with preservatives, and trans fats.
   

Lifestyle: Daily routines and environmental factors play a critical role in regulating the hypothalamic-pituitary-adrenal (HPA) axis and restoring psycho-neuroendocrine balance.

• Sleep: Consistent sleep schedule, no exposure to screens after 21:00, and adherence to the natural day–night rhythm. Melatonin influences neurosteroid synthesis.
• Exercise: Moderate intensity, 30-45 minutes daily. Resistance training (weights) boosts testosterone production and insulin sensitivity.
• Sun exposure: At least 20 minutes daily without sunscreen. Supports vitamin D production, which is essential for overall hormonal balance.
• Stress management: Breathing exercises, meditation, psychotherapy, as chronic stress disrupts the production of DHEA and cortisol.
   

Supplements and Herbal Therapies: Certain supplements and herbal products have been studied in patients with symptoms similar to those of Post-Finasteride Syndrome:

• Ashwagandha (Withania somnifera): An adaptogenic herb that regulates stress and enhances testosterone. Not suitable in cases of hyperthyroidism.
• Magnesium (especially glycinate or threonate): Related to NMDA and GABA receptor function. Improves sleep and reduces muscle tension.
• Vitamin D3: In doses of 2000–5000 IU/day, depending on levels. Caution in patients with hypercalcemia.
• Zinc and selenium: Trace elements involved in testosterone synthesis and antioxidant defense.
   

Before beginning any supplemental treatment, laboratory evaluation and guidance from a qualified health professional are essential.

What Prospective Finasteride Users Should Know Before Starting Treatment

The use of finasteride, like any pharmaceutical agent, comes with potential side effects. Despite generally good tolerability, a small percentage of men develop persistent symptoms after discontinuation, collectively referred to as Post-Finasteride Syndrome. Awareness and preventative evaluation before starting treatment can reduce risk and improve safety.

Step 1: Comprehensive hormonal evaluation before starting
Evaluating the hormonal profile before using finasteride is crucial. The tests, as mentioned earlier, can help identify pre-existing dysfunctions that could worsen. Note that pre-existing hypogonadism or neuroendocrine dysfunction may increase the likelihood of developing Post-Finasteride Syndrome.

Step 2: History of psychological symptoms
A history of depression, anxiety disorder, or post-traumatic stress must be carefully considered, as the neurosteroid changes induced by finasteride may worsen these conditions. Before starting, it is recommended to:

• Undergo psychological or psychiatric evaluation if there is a known history
• Use psychometric tools (such as the BDI test or HADS scale) to map emotional profile
   

Step 3: Consultation with a physician and informed consent
The decision to use finasteride must be based on the patient's informed consent. In some cases, the doctor may recommend a short-term trial period with close monitoring via repeat testing. The physician should provide information about:

• The mechanism of action and potential side effects of the drug
• The possibility of persistent symptoms after discontinuation (even if rare)
• Alternative ways to strengthen hair follicles, such as topical therapies or natural strategies
   

Step 4: Follow-up after initiation
Monitoring should not stop once treatment begins. If changes are observed, immediate adjustment or discontinuation of treatment may be required. Specifically, it is recommended to:

• Repeat laboratory evaluation of the hormonal profile 2–3 months after starting
• Self-monitor: Keep track of changes in mood, libido, and energy, or signs of increased stress or poor sleep quality

Before Finasteride, Prevention Comes First

Finasteride is not a dangerous drug when used appropriately and in the right individual. However, lack of pre-treatment evaluation, long-term use without monitoring, and underestimating early symptoms can pose serious risks.

At Diagnostiki Athinon, we offer advanced functional and hormonal testing to identify individual vulnerabilities. This approach is essential for individuals considering starting finasteride therapy, as well as those who have discontinued use and are experiencing persistent symptoms.

References

1. Stachelek, J., Zwaans, B.M.M., Shtein, R. et al. (2025) Insights into the peripheral nature of persistent sexual dysfunction associated with post-finasteride, post-SSRI and post-accutane syndromes: lessons learned from a case study. Int Urol Nephrol 57, 2387-2394.
2. Traish, A.M. (2018) The Post-finasteride Syndrome: Clinical Manifestation of Drug-Induced Epigenetics Due to Endocrine Disruption. Curr Sex Health Rep 10, 88-103.
3. Melcangi RC, Caruso D, Abbiati F, et al. (2013) Neuroactive steroid levels are modified in cerebrospinal fluid and plasma of post-finasteride patients showing persistent sexual side effects and anxious/depressive symptomatology. J Sex Med. 10(10):2598-2603.
4. Giatti, S., Diviccaro, S., Cioffi, L., & Melcangi, R. C. (2024). Post-Finasteride Syndrome and Post-SSRI Sexual Dysfunction: Two clinical conditions apparently distant, but very close. Frontiers in Neuroendocrinology, 72, 101114.
5. Cilio, S., Tsampoukas, G., Morgado, A. et al. (2025) Post-finasteride syndrome - a true clinical entity?. Int J Impot Res 37, 426–435.
6. Ali AK, Heran BS, Etminan M. (2015) Persistent Sexual Dysfunction and Suicidal Ideation in Young Men Treated with Low-Dose Finasteride: A Pharmacovigilance Study. Pharmacotherapy 35(7):687-695.
7. Cecchin E, De Mattia E, Mazzon G, Cauci S, Trombetta C, Toffoli G. (2014) A pharmacogenetic survey of androgen receptor (CAG)n and (GGN)n polymorphisms in patients experiencing long term side effects after finasteride discontinuation. Int J Biol Markers 29(4):e310-e316.
8. Post-Finasteride Syndrome Foundation (PFSF): https://www.pfsfoundation.org