Hereditary hair loss, pattern baldness, female-baldness, and other terms are used to describe androgenetic alopecia. But what exactly is this ailment? To begin with, it is genetic. That isn’t to say you can’t do something about it.

Androgenetic alopecia (AGA) is the most common form of alopecia, affecting up to 80 percent of men and 50 percent of women in the course of their life. AGA is caused by a progressive reduction in the diameter, length and pigmentation of the hair.


Although illnesses that cause hereditary hair loss, such as androgenetic alopecia, might affect people in different ways, there are a few signs that males seem to share. The first symptom of androgenetic alopecia is a receding hairline in men. This is commonly followed by hair thinning around the crown and temple area, which can last until bald patches appear on either side of the head.

It’s vital to remember that everyone with hereditary hair loss has a different experience, so don’t compare yourself to others if you’re dealing with androgenetic alopecia.

Androgenetic alopecia, in addition to its outer qualities, can occasionally be a sign of additional internal health issues. Androgenetic alopecia in men has been linked to other medical disorders such as diabetes, coronary heart disease, and hypertension.


Let’s take a deeper look at how biology plays a role in androgenetic alopecia now that we know what it is and how it frequently occurs. While there are a number of environmental and genetic factors that might influence the onset and severity of androgenetic alopecia, it all comes down to your genes and family history.

Hair thinning results from the effects of the testosterone metabolite dehydrotestosterone (DHT) on androgen-sensitive hair follicles. This is how DHT functions. It’s a hormone created from testosterone (a male sex hormone) that helps men’s overall health and development, especially during puberty, in appropriate proportions. DHT levels that are extremely high, on the other hand, might cause hair loss. As more DHT enters your bloodstream, it can easily bind to receptors on your scalp’s hair follicles, causing them to shrink.


DHT isn’t a terrible thing in and of itself. It is, in reality, a natural hormone that aids in healthy growth during puberty. It can, however, worsen inherited hair loss diseases such androgenetic alopecia in excessive doses. Understanding the typical hair growth cycle is helpful in understanding how DHT causes hair loss.

A follicle surrounds each strand of hair on your body. Consider hair follicles to be small capsules that offer critical sustenance to each hair while also securely anchoring it to the epidermis. Each follicle’s hair passes through a growth cycle that lasts between 2 and 6 years (even if you cut or shave your hair). Each hair enters a resting period at the end of each cycle, after which it comes out a few months later. The empty follicle then generates a new hair. So, where does DHT fall into this?


As previously said, hair grows, matures, and finally falls out before being replaced by another hair within a typical, healthy hair growth cycle. However, if the body converts too much testosterone into DHT, the hair development cycle may encounter some difficulties.

Higher levels of DHT have been shown to shrink hair follicles, which can cause hair to seem thinner and more prone to breaking while also shortening the entire growth cycle. Worse, DHT might make it more difficult to grow new hairs once the old ones have fallen out.


Yes, to put it succinctly. Although there are several methods for treating or perhaps reversing the consequences of androgenetic alopecia, it is a lifelong problem.

While you may have been born with a genetic predisposition to hereditary hair loss problems like androgenetic alopecia, there are a few things you can do to prevent DHT from wrecking your hair.




To rule out other causes of hair loss, such as telogen effluvium, a thorough medical history is required (TE). Chronic hair loss with thinning mostly in the frontal, parietal, or vertex areas are the most common complaints. Pruritus and trichodynia may also be present.

  • Hair loss in maternal and paternal relatives should be questioned about their genetic heritage and hormones.


  • Metabolic syndrome has been linked to male-pattern hair loss in the past.


  • Women with a history of polycystic ovarian disease should be evaluated for androgen sensitivity.
  • Protein powder consumption: Inquire about the patient’s use of pre- and post-workout protein shakes, such as whey isolate powders. Anabolic steroids are known to be included in several items.


  • Age of onset, illness progression, and smoking are all significant factors that should be investigated. The first two are crucial indicators for distinguishing between TE and AGA.



The pattern of hair loss is the telltale indication, and the history and pattern of hair loss are generally enough to make a diagnosis. The expansion of the hair parting in women should be checked. Part width anisotrichosis is revealed by a difference in part width in the affected area compared to normal part width in the unaffected area. Baldness is visible in the frontotemporal region of males.

A trichoscopy should be used to distinguish chronic alopecia areata incognita from patterned alopecia incognita.

During the progression of AGA, most patients experience spikes in hair loss.

Hair-pull tests, trichoscopy, and dermoscopy are some of the clinical tests that can aid in the diagnosis. Dermoscopy reveals yellow specks and varying hair shaft diameters (anisotrichosis). Scarring alopecia, not AGA, is indicated by perifollicular scaling. To diagnose coexisting TE, a hair-pull test may be used. It’s also a good idea to look at the terminal-to-vellus hair ratio.


Not routinely recommended

Can be used to differentiate from chronic telogen effluvium



Counseling is essential to address issues such as low self-esteem and poor quality of life, which are particularly prevalent in women. In severe situations, psychotherapy and anxiolytic therapy may be recommended.


There is no conclusive evidence to support the use of amino acids, biotin, zinc, and other micronutrients as a treatment for hair loss of any kind.While starting treatment with minoxidil, nutritional supplements high in amino acids can also be prescribed for 3–4 months. Amino acids, trace elements (Cu, Zn, Iron, and so on) and vitamins, including biotin, are all thought to be advantageous.

Saw palmetto is supposed to have similar effects to finasteride, but there isn’t enough clinical evidence to back it up. Similarly, there is a scarcity of evidence to support the usage of grape seed extracts, green tea, and proanthocyanins.



In males with AGA, minoxidil is still the basis of treatment. According to the expert panel, minoxidil can be used to treat female pattern hair loss (FPHL), although patients must be counselled about the risk of hypertrichosis. Minoxidil should be used as advised. Combining minoxidil with topical medicines like procapil is a good idea.

5-alpha reductase inhibitors

In terms of hair regrowth, finasteride  performs better than minoxidil. Finasteride lowers median DHT levels in scalp. Finasteride should be used for a minimum of 6–12 months. However, if it is well tolerated and has positive results, it could be administered for longer periods of time. The drug should be used on a daily basis, and patients should be informed about the potential negative effects.  Finasteride on alternate days may be given to nervous patients. The response to treatment is evaluated after 6 months, though it may take up to 12 months in certain cases.

Spironolactone and other anti-androgens may be considered.


Hormonal therapy, such as the use of anti-androgens in the treatment of male AGA, has not proven to be very helpful. The use of cyproterone acetate in female patients with clinical and biochemical indications of hyperandrogenism is the only evidence-based indication for the drug.


PRP is an autologous plasma preparation with a high concentration of platelets, which is a new therapy modality. It contains a variety of growth factors and cytokines that help the body’s natural ability to heal and rebuild itself. Acne scars, non-healing wounds, hair loss, and fat graft survival have all been treated with it.

The procedure should not be recommended for all AGA patients. Patient selection is essential. PRP can be a good holding solution for grafts in hair transplants while causing no harm to the patients.

It is unsustainable in the long run and should only be used for 6 months. The panel suggested that PRP be used as an adjuvant to minoxidil/finasteride rather than as a standalone treatment. The growth factors in activated PRP cause dermal papilla cells to proliferate, which is how PRP therapy works. PRP has one major drawbacks: pain during the process. Using local anesthesia creams and vibrators help.


Hair transplantation is a procedure that involves the implantation of hair-follicles

Hair transplantation can be performed on anyone with pattern hair loss, a good donor area, good general health, and reasonable expectations.

It is of 2 types: FUT OR FUE

FUE is commonly practiced now.


FUT/strip involves removing a strip of tissue from the donor location in the back and sides of the scalp and  dissecting individual follicular units using a special microscope. After that, the wound edges are stitched together, producing a single fine scar.

  • It can cover a bigger region because it has a higher number of grafts.


  • For dermatologists, it is currently the gold standard.


  • It offers grafts of good and fine grade.


  • It is considerably more painful.


  • Because of the linear scar, it is inconvenient for the patient.


  • The donor area is limited to the central occipital region.


  • Because of the lower transaction risk, grafts removed by FUT have a higher survival percentage



Small circular incisions are created across a much larger donor region with the FUE process, from which hairs are plucked, producing small, round, light-colored scars.

  • It is less difficult to carry out.


  • It allows the donor region to heal quickly (in 1–2 days).


  • It leaves no scars, is relatively painless, is perfect for patients who prefer short hair, and allows for a quick return to normal activities.


  • It necessitates the selection of a broader donor area.


  • It takes longer to complete.

    Whatever your case of androgenetic alopecia has been, keep in mind that there are things you may do to enhance your hair situation. There are a variety of strategies to combat the consequences of hereditary hair loss and get fuller, thicker hair, from taking hair growth supplements to getting treated at the correct time and creating a better overall hair care regimen.


    1. Mysore V, Parthasaradhi A, Kharkar RD, et al. Expert consensus on the management of Androgenetic Alopecia in India. Int J Trichology. 2019;11(3):101-106.
    2. Cervantes J, Perper M, Wong LL, Eber AE, Villasante Fricke AC, Wikramanayake TC, et al. Effectiveness of platelet-rich plasma for androgenetic alopecia: A review of the literature. Skin Appendage Disord. 2018;4:1–11
    3. Patwardhan N, Mysore V. Dermatosurgery Task Force. Hair transplantation: Standard guidelines of care. Indian J Dermatol Venereol Leprol. 2008;74(Suppl 1):S46–53
    4. Wolff H, Fischer TW, Blume-Peytavi U. The diagnosis and treatment of hair and scalp diseases. Dtsch Arztebl Int. 2016;113:377–86.

    Leave Your Comment

    Your email address will not be published.*