Hair loss is one of the things that worries us the most, both men and women since it is mixed.
It is true that there is a clear prevalence of it occurring more in men.
This type of baldness is usually androgenic alopecia and, as is our custom, we will start at the beginning, explaining the causes and at the end we will offer a possible solution.

Androgenic alopecia, what is it?

Androgenic alopecia is a hormone-associated disorder that affects 30-50% of men by the age of 50 and can climb up to 80% of men by the age of 80.
The synonym “male pattern hair loss” highlights the fact that hair loss occurs in a defined and reproducible pattern.

This particular type is the most common cause of alopecia and occurs due to a hormonal imbalance. Dihydrotestosterone (DHT), an androgenic hormone, is a sex steroid produced in the gonads.
The target sites of DHT are similar to those of testosterone, and it attaches easily by staying bound for 53 minutes compared to 35 minutes for testosterone.
Excess DHT causes the miniaturization of the hair by reducing the anagen phase and increasing the telogen phase causing its subsequent loss.

Normally, up to ten percent of the testosterone in the body is irreversibly converted to DHT by the action of the enzyme 5α-reductase.
Inadequate blood flow to the scalp can also be another reason for hair loss due to the lower oxygen and nutrient arrival.
As we said earlier in our statement, androgenic alopecia affects both sexes, however, in men, it leads to great hair loss. https://doi.org/10.1111/jocd.12930

In general, androgens stimulate bone and muscle development while also promoting significant hair growth in areas such as the beard or chest hair.
However, androgens also induce hair transformation into sensitive hair follicles in the frontal or vertex area.
While the receptors are present in the dermal papilla cells of androgen-sensitive hair follicles, the testosterone that reaches the dermal papilla cells of the beard hair follicles, frontal area, and vertex is converted into DHT, which acts as a much more potent androgen, through the action of 5α-reductase type II.

DHT-bound androgen receptors induce growth factors or other similar factors in the beard, resulting in anagen prolongation.
Conversely, DHT-bound androgen receptors in androgen-sensitive hair follicles in the frontal or vertex area induce the action of transforming growth factor-b or other factors that inhibit the proliferation of hair matrix cells, resulting in a shortening of the anagen cycle. https://doi.org/10.1111/j.1087-0024.2005.10107.x

What effects does it entail?

Hair loss results in reduced self-esteem, loss of confidence, and anxiety in affected men.
The disorder has a negative effect due to visible hair loss on social perceptions.
More importantly, androgenic alopecia is usually experienced as a moderately stressful condition that decreases satisfaction with body image.

In addition to the above, androgenic alopecia is increasingly identified as a risk factor for arterial stiffness and cardiovascular disease.
Familial tendency and racial variation in prevalence are recognized, with heredity accounting for approximately 80% of the predisposition.
Normal levels of androgens are sufficient to cause hair loss in genetically susceptible individuals.
The key pathophysiological features of this type of alopecia are alteration in the development of the hair cycle, miniaturization and follicular inflammation.

Here, the anagen phase decreases with each cycle, while the duration of the telogen phase remains constant or is prolonged.
Ultimately, the duration of the anagen phase becomes so short that the growing hairs do not reach the skin’s surface long enough, leaving an empty follicular pore. Miniaturization of the hair follicle is the histological hallmark of androgenic alopecia. Once the erector hair muscle, which attaches circumferentially around the primary follicle, has separated from all secondary follicles and the primary follicles have miniaturized and shed, hair loss is likely irreversible.
PMID: 25905192.

How can it be treated?

There are different therapeutic variants on the market to treat androgenic alopecia.
Among the most commonly used and most effective are minoxidil and 5α-reductase inhibitors.

In this article we will refer to the use of enzyme inhibitors, due to the speed and efficacy demonstrated in different papers.
Within this therapeutic group, there is a well-known pharmacological formulation, finasteride.

Finasteride was the first 5α-reductase inhibitor to receive clinical approval for the treatment of benign human prostatic hyperplasia and androgenic alopecia.
These clinical applications are based on finasteride’s ability to inhibit the type II isoform of the enzyme 5α-reductase, which is the predominant form in the human prostate and hair follicles, and the concomitant reduction of testosterone to DHT.

Twenty-five studies investigating the efficacy of finasteride in male patients with androgenic alopecia met the inclusion criteria of medically accepted treatment guidelines.
A level of evidence of type 1 can be attributed to this treatment.

In all included trials, daily intake of 1 mg finasteride resulted in a significant increase in total hair count compared to placebo.
Long-term results were available at 24, 36, 48, 60 and 120 months.
Mean changes from baseline were statistically significantly greater at all time points compared to placebo. https://doi.org/10.1111/j.1527-3458.2006.00053.x

If we talk about non-synthetic inhibitors, we must include Serenoa repens.
This extract is produced from the berries of the saw palmetto.
This plant is native to the West Indies and is grown in abundance on the southeastern Atlantic coast of North America.
The purified extract of serenoa repens contains 85-90% fatty acids and sterols, with an abundance of carotenoids, lipases, tannins, sugars and fatty acids such as caprylic acid, palmitic acid, oleic acid and beta sitosterol.
The combination of saw palmetto lipopoly extract (LSESr) and beta sitosterol has been claimed to improve androgenic alopecia.
DOI: 10.4103/0974-2077.53097

A study that aimed to test plant-derived 5α-reductase inhibitors, specifically Serenoa repens lypoposteric extract (LSESr) and β-sitosterol, in the treatment of androgenic alopecia, included men aged 23 to 64 years of age, in good health, with mild to moderate androgenic alopecia.
The report showed that 60% of study subjects (6/10) who received the dose of the active study formulation improved at the final visit. https://doi.org/10.1089/107555302317371433

In another study, with 50 male volunteers between the ages of 20 and 50 who received topical products from Serenoa repens for 24 weeks, the average hair count and terminal hair count increased at weeks 12 and 24 compared to baseline. https://doi.org/10.1111/ajd.12352

Active Capilar

Active Capilar is a dietary supplement formulated based on vegetable oils and extracts, biotin, zinc and selenium, indicated to help recover the health of the scalp that has been affected by an imbalance and deterioration in its physiology, causing abnormal fragility and fall.

Its formula based on plant oils and extracts such as NaturSYNTM Oil (linseed oil, wheat germ oil, borage oil, saw palmetto oil, pine bark extract, rye extract), help regulate hormonal imbalances causing hair loss and sebum accumulation in the hair follicle and improve capillary microcirculation.
All this favors the growth, increase of thickness and density of the hair.

Therapeutic amounts of biotin, vitamin E, selenium, and zinc have been added to the formula.

Taken regularly as 1 capsule daily with breakfast, it offers visible results in the medium term.

Conclusion

As we can see, androgenic alopecia can be responsible for hair loss (in men it is the most common cause).

Although it is true that there are other factors that can damage the scalp and promote its loss, such as:

• Stress
• hypothyroidism or hyperthyroidism
• pregnancy, postpartum and menopause
• Drug treatments

As for androgenic alopecia, Active Capilar would act as an inhibitor of the enzyme 5α-reductase without the intervention of synthetic drugs.