Can human chorionic gonadotropin supplements enhance penile growth?

In a recent study published in Scientific Reports, researchers investigated whether human chorionic gonadotropin (HCG) [Food and Drug Administration (FDA)-authorized testosterone-releasing agent without compromising spermatogenesis] supplements could expedite tunica albuginea restructuring to aid penile development.

Study: HCG supplement did not accelerate tunica albuginea remodeling to facilitate penile growth. Image Credit: Prostock-studio/Shutterstock.comStudy: HCG supplement did not accelerate tunica albuginea remodeling to facilitate penile growth. Image Credit: Prostock-studio/


A small penis is often associated with sexual dysfunction, leading to significant psychological issues among couples. Penile development relies on androgen, making testosterone replacement therapy advisable for individuals with micropenis.

In a prior study, the authors demonstrated that lysyl oxidase (LOX) inhibitors (anti-LOX) in combination with a vacuum erectile device (VED) extended the penis by remodeling the tunica albuginea, reducing collagen crosslinking, and ultimately increasing penile length.

About the Study

In this study, researchers explored whether HCG supplementation could enhance tunica albuginea remodeling and increase penile length when combined with LOX inhibitors and VED.

Forty-two four-week-old male Sprague-Dawley (SD) rats were divided into seven groups: anti-LOX, control, VED, HCG, anti-LOX and VED, VED and HCG, and VED+HCG+anti-LOX. Anti-LOX activity was induced through intragastric gavage using a specific LOX inhibitor, beta-aminopropionitrile fumarate, at a dosage of 100 milligrams per kg per day.

HCG was administered intramuscularly thrice per week at 100 international units (IU) per kg. The VED force (aspiration pressure, -300 mm Hg) was applied twice daily on weekdays (five-minute sessions with a two-minute gap) to stretch the penis.

Four weeks after the intervention, all rats' erectile function, exposed penis length, and total penile length were assessed. The maximal ratio of intracavernous pressure (ICP) level in the penile crus to carotid mean artery pressure (MAP) was calculated to measure erectile function. The exposed length of the penis was measured from the corpus cavernosum and urethral bulb junction to the glans cartilage tip.

Blood samples were collected to evaluate testosterone, dihydrotestosterone, and HCG levels using an enzyme-linked immunosorbent assay (ELISA). Additionally, radioimmunoprecipitation assays (RIPA) and Western blot tests were conducted, and the corpus cavernosum of the penis was histopathologically examined.


All treated mice exhibited significantly larger penises than control rats (31 mm). Specifically, anti-LOX (36 mm), VED (35 mm), HCG (33 mm), LOX inhibitor and VED (39 mm), VED and HCG (34 mm), and LOX inhibitor + VED + HCG (38 mm) significantly lengthened the penis by 15% (5.0 mm), 8.0% (2.3 mm), 12% (4.0 mm), 26% (8.0 mm), 10% (3.2 mm), and 22% (7.0 mm), respectively.

Anti-LOX increased the exposed length of the penis and total penile length by 9% and 15%, respectively. Penile lengthening was more pronounced in the LOX inhibitor + VED group (19% and 26%).

While HCG induced an eight percent increase in penile length, it only slightly affected the exposed penile length (three percent). Furthermore, anti-LOX+VED+HCG increased the exposed length of the penis and total penile length by 18% and 22%, respectively, which was comparable to LOX inhibitor and VED treatment (19% and 26%, respectively).

HCG significantly stimulated dihydrotestosterone and testosterone secretion in the presence or absence of LOX inhibitors and VED, and it increased androgen receptor (AR) expression more than other intervention groups. Notably, none of the interventions improved or compromised erectile function.


In summary, the study's findings indicate that HCG supplementation did not synergize with LOX inhibitors and VED to accelerate albuginea remodeling and facilitate penile growth.

While HCG injections extended the penis by increasing dihydrotestosterone and testosterone release, the underlying mechanism remains unknown and requires further research.

Journal reference:
Pooja Toshniwal Paharia

Written by

Pooja Toshniwal Paharia

Pooja Toshniwal Paharia is an oral and maxillofacial physician and radiologist based in Pune, India. Her academic background is in Oral Medicine and Radiology. She has extensive experience in research and evidence-based clinical-radiological diagnosis and management of oral lesions and conditions and associated maxillofacial disorders.


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