where does dht come from?
- Green tea. Derived from the Camellia sinensis plant, green tea is one of the most popular drinks worldwide.
- Coconut oil. Coconut oil comes from the kernel or meat of coconuts.
- Onions (and other foods rich in quercetin) .
- Turmeric.
- Pumpkin seeds.
- Edamame.
Testosterone converts to DHT by the action of the 5 alpha-reductase enzyme at these target tissues. [1] This isolated synthesis at a specific target tissue makes DHT primarily a paracrine hormone. [2] As it is produced mainly in the liver, only small amounts are present in the systemic circulation.
DHT plays a critical function in the sexual development of males, beginning early in prenatal life. The role of DHT differs as males progress through the different stages of development. It has various impacts on their physiology during childhood, puberty, and even throughout adult life.
Prenatal
During sexual development, various embryological structures develop under the influence of a variety of genes and hormones. A specific and unique environment of hormones results in male or female differentiation of structures. In males, testosterone, anti-mullerian hormone (AMH), and DHT act in concert to inhibit female differentiation and promote the development of the male phenotype. DHT is essential for the formation of the male external genitalia. The testicular Leydig cells produce testosterone under the influence of placental human chorionic gonadotropin by around day 60 of prenatal development. The luteinizing hormone (LH) from the fetal pituitary takes over testosterone production by roughly week 16. The peripheral 5-alpha-reductase type 2 converts circulating fetal testosterone to DHT, which is responsible for proper male differentiation of the urogenital sinus, the genital tubercle, urogenital fold, and labio-scrotal folds. This activity leads to the formation of the penis, scrotum, and prostate. DHT, along with insulin-like factor 3 (INSL3), helps stimulate gubernacular growth required for testicular descent. The absence of DHT may lead to ambiguous male external genitalia and undescended testis. Sex steroids accumulate from testicular production of testosterone in the male fetus and placental production of estrogen in both sexes, causing negative feedback on fetal pituitary, which helps control gonadotropin levels in the womb.
Childhood
After birth, the loss of placental estrogen removes negative feedback on the hypothalamic-pituitary-gonadal (HPG) axis, which results in a transient increase in its activity in both sexes for the first few months of life. In males, this promotes a rise in testosterone levels and, therefore, DHT. The negative feedback on the HPG axis recovers by six months of age and the levels of sex hormones remain low until adrenarche.
Adrenarche typically occurs around six years of age in both sexes. The adrenal gland develops a new layer, the zona reticularis. This layer of the adrenal gland produces androgens, including testosterone, which increases systemic testosterone, leading to the development of sebaceous and apocrine glands, contributing to the development of minor acne and body odor. Testosterone production continues to increase as the zona reticularis continues to mature. There is enough peripheral conversion of testosterone into DHT by age 10 to result in pubic hair development. These events of adrenarche are distinct from puberty though they often coincide.
Puberty
An increase in the activity of the HPG axis characterizes the onset of puberty. Hypothalamic secretion of gonadotropin-releasing hormone (GnRH) increases, stimulating pituitary LH secretion, which increases testosterone production from the testes. The increase in systemic testosterone is associated with a significant conversion to DHT at its target tissues. This DHT promotes further growth and maturation of the penis and scrotum. DHT is also the primary androgen responsible for facial hair, body hair, pubic hair, and prostate growth. The circulating level of DHT in the blood is only 10% of the circulating level of testosterone. However, the DHT level can be as much as ten times greater than testosterone due to its isolated production in peripheral tissues.
DHT (dihydrotestosterone) is a hormone that plays a key role in the sexual development of people assigned male at birth (AMAB). More specifically, DHT is an androgen — a hormone that stimulates the development of male characteristics.
DHT affects the sexual development of people AMAB throughout their lives, beginning as early as in fetal development. The role of DHT changes as people AMAB progress through different life stages. Scientists aren’t sure if and how DHT affects people assigned female at birth (AFAB), but they think it may play a role in body hair and pubic hair growth.
As an adult, your body converts about 10% of your testosterone (the main androgen) into DHT each day. This takes place in the genital skin and prostate in people AMAB and in the skin in people AFAB. It also happens in other parts of your body, such as your liver.
Levels of DHT are naturally much higher in people AMAB than in people AFAB because they naturally have more testosterone.
DHT has different roles in different life stages for people AMAB — mainly during fetal development and puberty.
Unlike testosterone, DHT doesn’t play a significant role in maintaining male physiology in adulthood. Effects mainly include prostate enlargement and male pattern hair loss in adulthood.
During fetal development, a specific and unique environment of hormones results in male or female differentiation of sexual anatomy. In males, DHT acts with other hormones (including testosterone) to block the formation of the female anatomy and to promote the development of the male anatomy.
DHT is essential for the formation of the male external genitalia, including the penis and scrotum, in a fetus. DHT also helps with the formation of the prostate.
During puberty for children AMAB, DHT promotes further growth of the penis and scrotum. It’s also the main androgen that’s responsible for:
Certain health conditions are associated with high levels of DHT, including:
Benign prostatic hyperplasia (BPH) is a condition in which your prostate grows in size. It’s very common in people AMAB over the age of 50.
Your prostate can produce large amounts of DHT. This local DHT production stimulates normal prostate activity but also commonly leads to prostate growth. BPH can cause difficulty with peeing and sexual dysfunction.
People who have prostate cancer usually have an increase in DHT levels. An increase in DHT activity in your prostate, in addition to certain genetic mutations that cause prostate cells to grow uncontrollably, leads to prostate cancer.
Androgenic alopecia is commonly known as male pattern hair loss. The hair loss usually happens on the top and frontal regions of your scalp, causing your hairline to recede over time.
Increased DHT activity at your hair follicles is partly responsible for this hair loss, in addition to other factors, including genetic ones. High levels of DHT can shrink your hair follicles and shorten the hair growth cycle, resulting in hair loss.
Polycystic ovarian syndrome (PCOS) is a hormonal imbalance that affects people AFAB. It happens when their ovaries create excess androgens, including testosterone, which leads to increased DHT levels. This causes a variety of symptoms, including irregular periods, excessive hair growth (hirsutism) and acne.
Certain conditions are associated with low levels of DHT, including:
Lower-than-normal DHT levels mainly affect people AMAB. Some scientists think low DHT levels in children AFAB may delay the start of puberty.
5-alpha reductase is an enzyme that helps convert testosterone to DHT. A genetic mutation (change) that affects the production of the enzyme can cause low or no levels of DHT. This is called 5-alpha reductase deficiency. People inherit this condition in an autosomal recessive pattern.
5-alpha reductase deficiency affects the sexual development of genetically male (XY chromosomes) fetuses. Males born with the deficiency typically have:
In cases of severe 5-alpha reductase deficiency, genetically male babies with XY chromosomes have external genitalia that appear female. Low DHT doesn’t affect the development of the testicles (they can still produce sperm) and internal sexual organs and structures. This is different from androgen insensitivity syndrome. People with this condition have normal testes with normal to high testosterone levels — they just lack androgen receptors. This causes them to not have secondary sexual characteristics and to have infertility.
During puberty, children who are genetically male with 5-alpha reductase deficiency experience a lack of facial hair growth. Because their body still makes testosterone, they still experience voice deepening, muscle mass increase and penis enlargement.
As your body converts testosterone to DHT, if you have low levels of testosterone, you’ll have lower-than-normal levels of DHT as well. Another name for low testosterone is male hypogonadism.
There are two main types of male hypogonadism: classical (congenital or acquired) and late-onset. Male hypogonadism can cause different issues depending on your age.
If you think you or your child may have a condition related to low DHT or excess DHT, talk to your healthcare provider. They can order some tests or refer you to a specialist, such as an endocrinologist.