in this article:
The importance of the trichological examination at a young age, even before the first symptoms of thinning appear, is essential to receive appropriate information on the most suitable products for your hair type. In recent years trichology (the science that studies the anatomy, the physiology of hair and hair) has made numerous steps forward and can now offer numerous solutions that can block or counter the fall. As well as for one’s physical well-being, it is necessary to choose a qualified graduate school science professional and with the appropriate professional certifications, even the choice of the trichologist must fall on qualified professionals specialized in dermatology.
Attention therefore to the false experts, able to exploit economically the psychological drama of those who are losing their hair. In this article we will focus on symptoms, causes and treatments for hair loss by type.
Hair loss from the point of view of medicine: an overview
In special literature, hair loss is referred to as alopecia: from the Greek ‘alopex’ = fox, term used to emphasize the similarity with this animal, which loses the hair twice in a year. The life cycle of the hair involves the alternation of three phases, one of growth, one of rest, and one of fall. The average duration of this cycle varies from 2 to 7 years. It is therefore estimated that each follicle produces about 20 hairs during its lifetime.
The number of hairs fallen during the day varies and depends on numerous factors such as:
- sex (the fall is greater in men than women)
- season (in autumn and spring the fall increases)
- health conditions (the use of certain drugs and some diseases can accelerate the fall)
- washing and brushing (the mechanical trauma facilitates the detachment of the hair)
- hair density (the more hair you have and the greater the fall in absolute terms)
- genetics (some subjects are genetically predisposed to fall).
For information purposes only, without this being a rule, a fall of more than 100 hairs a day that lasted for a few weeks is an indication of the suffering of the hair. In these cases it is advisable to contact a specialized doctor who can assess and resolve the situation.
The remedies used to combat hair loss are numerous and range from the use of simple lotions to the administration of real drugs (finasteride, minoxidil). Massages, laser therapies, phototherapies and cryotherapies are some examples of the many techniques available today in modern trichological centers. When the problem is particularly marked and as such irreversible, modern hair transplantation techniques are able to offer aesthetic results of all respect.
Prevention, however, continues to play an essential role against hair loss. Briefly, we say that it is important to follow a series of hygiene rules, such as avoiding drastic diets and eating healthy, protecting hair from the sun and tanning lamps, not smoking and also avoiding passive smoking. Finally, washing the hair often (at least 3 times a week, but also more often if they are fat) does not accentuate, but often even prevents, the fall.
Hair loss stages and classification
In 1951, Dr. James B. Hamilton elaborated a scale for the classification of androgenetic hair loss, subsequently taken up and adapted by Norwood.
As can be seen by observing the various images, androgen type hair loss progressively affects first of all genetically predisposed areas.
However, there are cases in which androgen tic hair loss homogeneously affects a large area of the scalp. Ludwig elaborated a three-stage scale to describe this phenomenon, more frequent in female subjects.
There are two main types of alopecia, telogenics and androgen. The first involves, usually in a short time, a limited or generalized fall of the hair, in response to a strong physical or psychological stress. This type of alopecia, which can affect both men and women, is reversible. Between the two, it therefore represents the ‘beneficial’ form.
The other type of alopecia is called androgenic, to underline that it affects mainly, but not exclusively, men. In these cases, the term ‘lose hair’ is not entirely correct, as the hair follicles, although undergoing a gradual process of involution, which leads the hair to lose the terminal appearance and to acquire the characteristic traits of the fleece (hairs) very thin, soft and depigmented), they remain numerically the same. Contrary to what is said for the telogenic form, androgenic alopecia is irreversible.
Symptoms, causes and treatment of androgenic hair loss (androgenic alopecia)
With age, physiologically, the hair follicles on the forehead and temples undergo a gradual process of involution, with the consequent thinning of the hair present in these areas. This phenomenon is valid both for men and for women, where the problem, although less evident, is accentuated after menopause.
Androgen alopecia can also affect women of childbearing age, almost always due to major hormonal changes. In many cases there is indeed a level above the norm of typically male hormones, first of all the dihydrotestosterone.
The etiology of androgenic alopecia has not been clarified, even if some things now seem certain. For example, it has been demonstrated that the presence of androgens is necessary for it to occur; for this reason a child will never suffer from androgenic alopecia. It has also been observed that in men predisposed to hair loss the activity of 5-α-reductase is greater than normal. The same enzyme, which promotes the transformation of androstenedione into dihydrotestosterone, stimulates the secretion of the sebaceous glands. An excess of sebum (see greasy hair) tends to weight and subtract vitality to the hair, but does not directly atrophy the follicles. For this reason the term seborrheic alopecia has now fallen into disuse.
On the etiology of alopecia numerous hypotheses have been put forward, let’s have a look at two of them. Some hypothesize that in the follicles of subjects predisposed to hair loss, there is an accumulation of a substance with an inhibiting action, which accelerates the frequency of growth cycles. This substance would be produced during the anagen phase and would imply a rapid transition from the growth phase to the telogen phase. Because of this phenomenon, the size of the follicle would be reduced cycle by cycle, making the hair more fragile and thinner.
A second hypothesis presupposes that at the base of alopecia there is an inflammatory process at the level of the bulbs. In response to this phenomenon autoantibodies would form, which would block the activity of the matrix, that is, of that group of cells that, by dividing, allows hair growth. The production of these autoantibodies would be genetically dictated.
The various types of alopecia can be distinguished in:
- non-cicatrizial forms (temporary forms of alopecia with transient functional inhibition of the papilla of the hair). Examples include androgenetic alopecia, post-gravidic, from undernutrition, from psychophysical trauma, alopecia areata, traction alopecia, iatrogenic (from drugs), etc.;
- cicatricial forms (forms of definitive alopecia with disappearance of follicle and germinating papilla). Examples are scleroderma, discoid lupus erythematosus, lichen planus, decliving folliculitis, mycoses, neoplasms.
Androgenetic alopecia is the main cause of progressive thinning of the scalp. Over 80% of the male population and 50% of the female population are affected. The spread of androgenetic alopecia is therefore such as to justify the appellation of ‘common hair loss’ and to be able to consider it, within certain limits, an absolutely physiological condition. Although not a real disease, androgenetic alopecia is often experienced as a profound discomfort, with negative repercussions on the psychological and social level.
The greater frequency of androgenetic alopecia in men than in women is due to its double origin, underlined by the terms ‘andro’ and ‘genetic’. On the one hand, in fact, the presence of androgens, typically male, is necessary, while on the other hand a genetic predisposition of the hair follicles is necessary to undergo the involutional stimuli. Not by chance, as early as the 4th century BC Aristotle noted that neither eunuchs (castrated males) nor children were affected by hair loss, sensing a correlation between the secretion of male hormones and hair loss. These hypotheses were confirmed by Hamilton in 1940. For this reason, hair loss has been, and is still erroneously related to a greater degree of virility and sexual potency.
However, testosterone levels (the male sex hormone par excellence) are not necessarily high in androgenetic alopecia; often there is a decrease in the total quota and an increase in the free fraction. Even more relevant are the values of one of its most powerful androgen derivative, dihydrotestosterone; this hormone is also formed at the level of hair follicles starting from the testosterone precursor, thanks to the intervention of an enzyme called 5-alpha-reductase type 2.
As a result of dihydrotestosterone, the hair becomes increasingly short and thin, until it cannot adequately cover the scalp; this because the anagen phase (of growth) is progressively reduced in favor of that of involution (catagen) and of rest (telogen). Moreover, follicles assume increasingly synchronized growth cycles, such as those of an animal’s fur: this is why the possibilities of telogen effluvium (hair loss numerically very high and qualitatively homogeneous) are also raised. In an advanced phase, due to the typical saving of the nape and the temples (ormono-independent zones), androgenetic alopecia determines the so-called ‘crown’ hair loss. The hairs necessary for the ‘famous’ hair transplant will be taken from these areas.
In addition to the increase in follicular activity of 5α-reductase, androgenetic alopecia may be due to an increase in the number or affinity of androgen receptors, a decrease in SHGB (androgen transport proteins in the blood) or a decrease in follicular aromatases (enzymes that convert testosterone into estrogen, with a strengthening effect on the hair).
The higher the concentrations of the enzyme 5-alpha-reductase type 2 in the hair follicle and the greater the possibilities of miniaturization. During experimental studies it was possible to find a greater activity of this enzyme in man than in women and, in both sexes, in the frontal region compared to the occipital one.
However, genes that predispose to hair loss are still misunderstood; this is why androgenetic alopecia is considered a polygenic disease, that is, caused by many different genes. For example, the androgen receptor gene is located on the X chromosome and is therefore inherited in the male on the maternal side; it has been clearly seen that a particular polymorphism of this gene predisposes to an early onset of androgenetic alopecia. Other genes have been discovered recently and research in this field continues to be particularly active.
For now, we must limit ourselves to considering that the chances of developing a real androgenetic alopecia are related to the number of first or second degree relatives who are affected by this condition; we are obviously talking about probabilities and not absolute certainties.
The clinical manifestations of androgenetic alopecia are different in both sexes. In man, the disease causes a progressive thinning of the fronto-temporal area (the so-called receding hairline) and of the vertex, while in the woman the ‘hair loss’ saves the temples and mainly affects the vertex and the frontal region, just behind the ‘hanging. The term hair loss has been marked by the quotes because the androgenetic alopecia does not determine a real fall, but a progressive miniaturization of the hair up to make it invisible to the naked eye.
If we examine with a magnifying glass the scalp a subject with advanced androgenetic alopecia, we can see that the apparently hairless areas (the bald areas to be clear) are actually covered by a thin hair. Often, androgenetic alopecia is accompanied by seborrhea and furuncular desquamation; however these conditions are not always associated.
Androgenetic alopecia, also called androgenetic hair loss, can be countered by using specific drugs. Currently, only two medicines have been approved by the FDA for the treatment of this condition. The first, minoxidil, is used for topical use, is more effective in the area of the vertex and has a mechanism of action still unclear. The second one, called finasteride, is taken by os and fights the androgenetic alopecia, preventing the action of the enzyme 5-alpha-reductase type 2. In both cases the treatment cannot prove effective before a certain time interval (usually it takes at least 3-6 months).
Such drugs have a certain effectiveness when androgenetic hair loss is still in an intermediate stage; in an advanced phase it is possible to intervene successfully only through the surgical redistribution of hair bulbs (hair transplantation) or through alternative thickening techniques, possibly patented and certified by companies operating in the sector for many years.
Female androgenetic alopecia: signs, causes, therapies
In women, the loss of hair, although generally more attenuated than in men, often involves psychological consequences far more dramatic and devastating, related to the perception of considerable damage to their image. Fortunately, the treatment of female androgenetic alopecia offers more and more effective therapeutic opportunities, with a lower incidence of side effects.
An essential element in all forms of androgenetic alopecia is – as the name itself recalls – the presence of androgens. In fact, in the absence of these hormones – as can be appreciated in precociously castrated males – hair loss does not occur.
In the article dedicated to the relationship between androgens and hair, however, we explained how the hormone levels are very similar in men bald compared to the general population. Therefore, male androgenetic alopecia is generally not related to excess of androgens, but rather to the excessive sensitivity of hair follicles to their action. In fact, since birth, some hair is genetically predisposed to incorporate the ‘miniaturizing’ stimulation of androgens.
It is no coincidence that androgenetic alopecia is a slow phenomenon that – by increasingly shortening the growth phases and lengthening those of rest prior to the fall – involves the gradual transformation of the terminal hair into elf hair (thin, depigmented, very short and almost imperceptible).
As explained, women suffering from hyperandrogenism (excess of androgens) are clearly more susceptible to alopecia, even if the two conditions are not always and necessarily correlated. Women suffering from acne, seborrhea, hypertrichosis and hirsutism (suggestive but not pathognomic signs of hyperandrogenism) are therefore more likely to suffer from female alopecia.
In women, the majority of cases of hyperandrogenism are due to polycystic ovary syndrome (PCOS), which on a clinical level manifests itself through anovulatory cycles, menstrual changes, hirsutism and sometimes obesity. This last condition is often correlated, either as a consequence, or as a triggering element, to hyperandrogenism, probably favored by the variable degree of insulin resistance correlated to it. The cases of hyperandrogenism linked to the presence of androgenic secreting neoplasms are rarer.
The levels of estrogen, hormone that, in contrast to androgens, is typical of women, especially during their fertile age, influence – this time positively – the health of hair. Moreover, at the level of the hair and hair-like bulbs there can be variable concentrations of enzymes acting on androgens and estrogens, which transform them into derivatives capable of influencing the life of the hair to a much greater extent. The best known of these enzymes is called 5-alpha-reductase and acts on testosterone transforming it into dihydrotestosterone, the real responsible for hair involution and consequent thinning.
The aromatase enzyme, on the other hand, converts androgens into estrogens, prolonging the life of the hair and counteracting hair loss; a similar action is also performed by the 3-alpha-steroid dehydrogenase and 17-beta-hydroxysteroid dehydrogenase enzymes. For this reason, female androgenetic alopecia can be noticed for the first time, or become more evident, after menopause, a period in which a generalized decrease in estrogens is observed with a variation in the percentage ratio between ovarian and adrenal steroids.
Without prejudice to the always necessary genetic predisposition, the same circumstance can therefore manifest itself in coincidence of hormonal changes, due, for example, to a birth or to the initiation or interruption of estrogen-progestin treatments (including those for contraception.
The hereditary component is another hallmark of androgenetic alopecia; as a consequence, it is much more probable to accuse the problem when it has already become manifestly evident in parents, grandparents, uncles or brothers.
Female androgenetic alopecia is distinguished from the male one by a later appearance of thinning, which is generally known for the first time between 30 and 40 years, and due to its different location. In fact, while in man the problems of hair loss affect the fronto-occipital area, in the woman they involve a more diffused region, in particular the vertex or in any case the zones behind the fronto-temporal line. Another distinctive feature is the greater gradualness with which female alopecia manifests itself in relation to what happens in man.
In women, the precociousness of diagnosis and therapeutic intervention is very important to stop the process of involution of the follicles, making the hair reacquire the original splendor before the problem becomes irreversible. The key examination for the diagnosis of female alopecia is trichogram, naturally accompanied by the inevitable anamnesis and the evaluation of the clinical picture. In particular, the familiarity of alopecia, the use of contraceptive or cortisone pills, the possible use of anabolic steroids and the regularity of the menstrual cycle will be evaluated, looking for possible signs of hyperandrogenism (lowering of the voice, diffused hair in typically male areas, obesity, acne etc.).
To confirm or exclude what emerges from the anamnestic data and the objective examination, it is necessary to perform laboratory endocrinological screening, during which we will evaluate the blood concentrations of androgens, cortisol, thyroid hormones, TSH, SHBG, estrogens, progesterone and gonadotropins (LH, FSH), also in relation to the various phases of the menstrual cycle. Only in this way will it be possible to intervene pharmacologically on the delicate hormonal balance of the woman, improving the therapeutic efficacy of the treatment and minimizing the side effects.
The pharmacological therapeutic options for female androgenetic alopecia, largely impracticable in humans, must first be distinguished in topical and systemic. The first group includes drugs to be applied directly to the scalp, such as the famous minoxidil or estrone sulphate. Also effective is the topical administration of hydroalcoholic solutions of natural progesterone or its 17-hydroxylated derivatives, associated or not with spironolactone. There is also the possibility of counteracting the activity of the enzyme 5-alpha-reductase by topical application of azelaic acid.
The systemic pharmacological therapy of female androgenetic alopecia is indicated in cases of hyperandrogenism on a dysfunctional basis, as in the case of PCOS; while in hyperandrogenisms supported by organic causes (for example, by androgen-secreting neoplasms) it is necessary to remove the cause itself by means of surgical intervention. Among these drugs we remember the spironolactone which – to limit the side effects associated with the therapy (amenorrhea, mastodynia, chloasma) – must be taken systemically from the 16th to the 25th day of the cycle, preferably combined with an estroprogestinic to ensure contraception. In the case of a progestogen deficiency, however, the administration of systemic synthetic progestogens is indicated.
The most commonly adopted therapeutic solution remains however the combined administration of estrogens and progestins, in particular of ethinylestradiol and of cyproterone acetate (endowed with important antiandrogenic activities). This therapeutic intervention is exploited not only in the treatment of female androgenetic alopecia, but also in the treatment of the manifestations of hyperandrogenism in women.
Beard hair loss – beard alopecia (alopecia barbae)
Beard hair loss – also known as alopecia barbae – is a particular form of alopecia areata that affects the beard. This disorder can manifest itself either as an event in itself, or in association with scalp alopecia. In fact, it has been estimated that, when alopecia affects only the beard, within a year it will also affect the scalp in at least 50% of cases. Although beard alopecia is a benign phenomenon that does not cause serious consequences from a physical point of view, it can negatively affect the patient on a psychological level. Naturally, beard alopecia occurs in male patients, but with a greater incidence in young individuals between the ages of 30 and 40.
Beard hair loss is a form of alopecia areata that affects the beard and, as such, is considered an autoimmune pathology. The fall of the hair, in fact, happens because the immune system attacks the hair follicles, thus hindering its normal activity and preventing the hairs from growing normally.
The beard alopecia is characterized by the loss of beard hair in well-localized areas, more or less extensive and with a rounded shape. The formation of these spotted hairless can take place anywhere in the beard, so they can appear in the area of the whiskers, neck, chin, cheeks, or sides. Usually, beard hair loss begins with the appearance of a single patch of variable size that, with the passage of time, tends to expand. At this first spot they can add others in different areas of the beard.
Often, before the appearance of the glabrous patches, or just before their extension, the patient feels sensations of itching or burning, which can be associated with a slight inflammation of the skin. These symptoms, however, can also occur when the patches have already manifested themselves. In some cases we can witness the regrowth of hairs in the affected areas, but often they are hairs that no longer have the initial color and that, instead, are white.
It is therefore clear that a benign ailment which is the alopecia of the beard can turn into a real nightmare for different men, who see their altered appearance. This can create psychological harm in the patients affected and can have serious repercussions on their social life. As mentioned, patients suffering from other autoimmune diseases are more likely to undergo beard alopecia.
For this reason, it is not unusual for a patient suffering from this disorder to be affected by other diseases, such as:
- Atopic dermatitis;
- Crohn’s disease;
- Hyperparathyroidism or other thyroid disorders.
Fortunately, in many cases, beard alopecia tends to regress spontaneously within a few months. However, this does not mean that the disorder is permanently resolved. In fact, alopecia can return to strike the patient’s beard even after a short time from its resolution, giving rise to a continuous succession of regrowth phases and phases of hair loss. In other patients, however, alopecia may not manifest itself for years, only to reappear when the individual least expects it.
However, if beard alopecia is not resolved by itself and if the disorder becomes disabling from a psycho-social point of view for the patient, the doctor may decide to intervene by pharmacological treatment. However, it is important to point out that not all patients respond equally to therapy for beard alopecia; therefore, what can be effective for an individual, on the other hand, can turn out to be completely useless for another.
Below we will briefly illustrate the main characteristics of the therapeutic strategies and of the drugs most used in the treatment of beard alopecia. Corticosteroid drugs are potent anti-inflammatories that act by suppressing the activity of the immune system and, for this reason, are useful in the treatment of autoimmune disorders, including beard alopecia. In the treatment of this form of alopecia, corticosteroids can be administered either locally or systemically. Normally, the first therapeutic approach involves the intralesional administration (ie injection directly in the areas affected by the disorder) of corticosteroids, such as triamcinolone.
Corticosteroids for topical use, on the other hand, do not seem to be among the best therapeutic strategies, since – especially when used for long periods – they are often the cause of folliculitis. Finally, in severe cases it is possible to resort to systemic corticosteroids, although it seems that this type of alopecia areata is not particularly effective.
The role of minoxidil in the treatment of beard alopecia is still doubtful. In fact, while its use seems to be useful in some patients, in others it seems not to have significant therapeutic effects. According to some studies conducted on patients with beard alopecia, the use of phototherapy performed with different types of lasers (excimer laser, Erbium fractional laser) would be able to induce the – sometimes complete – re-growth of hairs in correspondence with the areas affected by disorder.
The treatment of alopecia areata involves the use of topical corticosteroid drugs, because of their side effects, in fact, it is preferable to avoid administering them systemically. However, in the most severe cases of alopecia areata, the doctor may consider it necessary to use the above-mentioned corticosteroids intramuscularly, or may decide to resort to the use of immunosuppressive drugs. Minoxidil-based lotions, on the other hand, have proved to be quite effective in the symptomatic treatment of the disease. Finally, P-UVA phototherapy is also commonly used for the treatment of alopecia areata.
The following are the classes of drugs most used in therapy against alopecia areata and some examples of pharmacological specialties; It is up to the doctor to choose the active ingredient and the dosage most suitable for the patient, based on the severity of the disease, the health status of the patient and his response to treatment.
As mentioned, the pharmacological treatment of alopecia areata involves the administration of corticosteroids for topical use. Except for very serious cases, where it may be necessary to resort to parenteral administration of these same drugs. Among the active ingredients that can be used there can be named the following medications:
Generally, it is recommended to apply the minoxidil solution on the affected area twice a day, for a period of not less than 3-4 months. In any case, you must always follow the directions given by your doctor. Furthermore, it should be remembered that the treatment based on minoxidil for topical use should not be interrupted abruptly, as it would risk returning to the pre-treatment situation within a few months.
Immunosuppressive drugs can be used in the most severe cases of alopecia areata. In fact, thanks to their activity, these drugs reduce the attack of the immune system against the hair follicles.
Among the various active ingredients that can be used, we mention cyclosporine (Sandimmun, Ciqorin). It is available in various pharmaceutical formulations suitable for different routes of administration, including oral and parenteral. When used to treat alopecia areata, the dose of ciclosporin to be administered should be determined by the physician on an individual basis for each patient.
Hair loss diagnosing: trichogram
Trichogram is the microscopic examination of the hair. This semi-invasive procedure allows to follow the hair’s life cycle, assessing its state of health and helping the dermatologist to identify the underlying causes of any alopecia. Trichogram, by itself, is a rather simple procedure, which nevertheless requires compliance with certain procedural standards to increase the reliability of the results. For example, to avoid interpretative errors, the patient is asked not to wash the hair for at least a week before the test. In view of trichogram, fractions and cosmetic treatments such as undulations or permanent dyes should also be avoided for at least two weeks.
Trichogram begins with the removal, by tearing, of 50-100 hairs; also in this case the procedure must comply with very precise rules. The tear, for example, must be rather decisive and carried out in the direction of hair growth; otherwise it may cause structural deformations of the roots, thus invalidating the results of the test.
In case of diffuse alopecia, the tear should be performed at the site of greater thinning, while in front of cases of alopecia areata it should be performed on the edge of the patch and in the contralateral zone. In both cases, however, it is a good rule to proceed to a further tear from a control area, generally at the occipital level. In fact, for example, in the case of male androgenetic alopecia, the increase in the percentage of hair in telogen affects only the fronto-occipital areas, while in the case of effluvium in telogen the phenomenon is widespread throughout the scalp.
In the event that the patient suffers from seborrhea and / or hyperhidrosis, the withdrawal must also be performed in the temporal zones. If, on the other hand, the patient suffers from dandruff, the hair removal can be done only in the area of the nape.
The hair sample is then placed on a slide coated with Peru balsam, with hairs arranged parallel to each other. It covers the coverslip and proceeds with the examination under an optical microscope or polarized light. Thanks to the optical enlargements the dermatologist can evaluate in which growth phase the uncorked hair is found, observing the structure with particular attention at the root level.
Briefly, let us recall that the life cycle of a hair consists of three contiguous phases:
- Anagen: it is the growth phase, which affects at the same time variable percentages between 80% and 90% of the hair; its duration, of several months or even years, tends to decrease in the presence of androgenetic alopecia.
- Catagen: it is the hair fall phase and lasts about two weeks.
- Telogen: it is the resting phase of the hair that precedes the fall (catagen), and lasts about 100 days. The length of this period tends to increase in the presence of androgenetic alopecia, up to the inversion of the temporal relationship between anagen and catagen.
Once the roots of the preparation have been examined, trichogram foresees the meticulous counting of the number of hair present in the various phases, followed by the calculation of the relative percentages.
According to the classical dictates, in the normal trichogram the hair percentages in the various phases correspond roughly to the following values:
- Anagen: 80-90% of the hair.
- Catagen: 1-2% of the hair.
- Telogen: 10-20% of the hair.
Whatever the percentages of reference (variable depending on the equipment used, the experience of the operator, the time spent between taking and microscopic examination, etc.), in pathological trichograms there is a variation with respect to the standard values. This datum, together with the clinical picture and the anamnesis, is a precious help in the formulation of a correct diagnosis. In alopecia areata, for example, the roots have a dystrophic appearance in an easily recognizable anagen phase, while in the androgenetic alopecia the roots in the telogen phase are clearly higher than the norm.
Trichogram is a very reliable test that allows you to get accurate information on the state of health of the hair, allowing you to identify any anomalies and alterations in the normal life cycle of the same. Thanks to the information obtained from this examination it is therefore possible to identify the causes of a hair loss, discriminating whether it is effluvium or drainage and whether this thinning is taking place in the anagen or telogen phase. Below, the main characteristics of these different forms of hair loss will be described.
Once established the type of thinning that afflicts the patient through the help of trichogramma, the doctor can prescribe further tests and analyzes in order to evaluate the cause of hair loss. Only in this way will it be possible to undertake the pharmacological and non-pharmacological treatment that is best suited to each patient.
Effluvium in anagen
It is characterized by hair loss of several hundreds, or even thousands of units, in anagen phase (of growth). This condition occurs classically a few days after a particularly stressful event, such as poisoning, aprotoxic diet, chemotherapy, exposure to ionizing radiation or febrile diseases. In predisposed subjects, these stressful events cause alopecia areata, which is characterized by a heavy effluvia in anagen. In any case the fall is self-limiting and in general the lost hair grows back spontaneously if the stressful event does not reoccur.
Effluvium in telogen
It is possible to distinguish two different forms of effluvium in telogen, the acute one and the chronic one.
Effluvium in acute telogen
It is also caused in this case by stressful and short-lived events, which nevertheless took place a few days, but about three months before the effluvium. The massive loss of hair can be the consequence of surgery, bleeding, loss or feverish illnesses. The phenomenon is self-limiting and tends to autorisolversi, but in some cases, the dermatologist can still decide to prescribe a therapy based on corticosteroids.
Effluvium in chronic telogen
In the chronic form of the telogen effluvium one appreciates an important and relatively constant hair loss over time. More frequent in women, it is generally linked to a chronic disorder of hair growth, often without a tendency to spontaneous resolution. Among the main causes of chronic telogen we remember frequent donations of blood, serious mental illnesses, distiroidisms, chronic systemic diseases or prolonged use of some drugs (retinoids, interferon, heparin, some oral contraceptives, allopurinol, etc.). The treatment of this form of effluvium involves the administration of corticosteroids topically or orally, depending on the severity of the clinical picture.
Defluvium in anagen: it is characterized by a hair loss above the norm, but without the dramatic characters of the effluvium. The thinning is due to the progressive loss of follicles, secondary to their destruction. It is typical of scarring alopecia and may represent the consequence of diseases such as lichen planus, discoid erythematosus cutaneous lupus, alopecia folliculitis, linear scleroderma (morphea), Broq pseudo-area, tricomalacia and radiation scarring alopecia.
Defluvium in telogen
In most cases, hair loss is characterized by a drain into telogen. Indeed, this is the characteristic manifestation of androgenetic alopecia, a condition linked to the activity of androgens in a genetically predisposed soil. As anticipated, this disease is characterized by a moderate fall of the hair, accompanied by their gradual involution (they become increasingly thin, short and depigmented). Unlike the drainage in anagen, in the androgenetic alopecia the follicle is preserved, but it becomes more and more superficial.
In addition to male and female alopecia, in women the defluvium in telogen is also associated with hyperprolactinemia, anorexia nervosa and all forms of alopecia related to hyperandrogenism (polycytosis ovary syndrome, androgenic secreting neoplasms, etc-) and / or hypoestrogenism (menopause, post-partum, suspension of oral contraceptives, etc.).
Hormones and hair loss
Sex hormones and GH heavily affect the growth of our hair. In particular, their evolution from hair to elf to terminal hair is regulated by the somatotropic hormone (GH), while the involution depends on the activity of androgens. In man, in particular the hairs of the vertex and of the frontal areas are more sensitive to the action of androgens, while in women this sensitivity is more widespread.
These hormones, typical of males but present in minor concentrations even in females, can slowly miniaturize the hair, which becomes thinner and thinner until it gives the impression of being ‘fallen’. Without androgen, therefore, there cannot be alopecia; however, it is said that greater androgenic concentrations correspond to a greater ‘loss of hair’. For this to happen, in fact, androgens must act on genetically engineered soil; in fact, since birth, a part of our hair is genetically predisposed to suffer the negative influence of androgens. It is in particular the intracellular metabolism of testosterone to heavily influence the life cycle of hair.
Testosterone is the androgen hormone par excellence, secreted by the testes and to a lesser extent by the adrenal gland; the latter also produces other types of androgens, such as androstenedione, dehydroepiandrosterone (DHEA) and androstenediol (in women there is a very small synthesis of androgens even at the ovarian level). Upon reaching the target organs, these hormones can be metabolised to testosterone, which in turn undergoes the action of the 5-α-reductase enzyme turning into dihydrotestosterone. By contrast, all androgens, including testosterone, can also be transformed into estrogens (typically female sex hormones) by the enzyme aromatase.
While estrogens have a positive effect on hair (proliferative signal), testosterone, and in particular its metabolite dihydrotestosterone, play a crucial role in the thinning process (antiproliferative signal). The true androgen active at the level of the piliferous and capillary matrix is therefore dihydrotestosterone. To this hormone we owe the growth of the sexual hairs on the face, on the chest, on the back and on the shoulders, both the fall of the hair in subjects and in predisposed areas. It is therefore not surprising that the 5-α-reductase activity – to which the aforementioned conversion of testosterone to dihydrotestosterone is due – is particularly marked in the frontal region of the bald subjects.
Dihydrotone binds to a specific cytoplasmic receptor of a protein nature; the complex thus formed migrates to the nucleus, where it binds to specific receptors by regulating protein synthesis. In particular, at the piliferous level, binding to nuclear receptors activates the transcription processes with messenger RNA synthesis, which at the ribosomal level represses (in predisposed subjects) the synthesis of structural hair and hair proteins.
The SHBGs, to which testosterone is bound tenaciously, increase their concentration in relation to the increase (physiological, pathological or iatrogenic) of estrogens and thyroid hormones. On the other hand, SHBG levels decrease in response to the increase in plasma androgens; in this case, there is an increase in the free fraction of testosterone. As a consequence, 5-α-reductase enzymes will have more substrate (free testosterone) available for the synthesis of dihydrotestorene.
Estrone is a female sex hormone (estrogen) secreted by the ovary and produced at the peripheral level, especially in the adipose tissue, by conversion of androstenedione by the enzymearomatase. Estrone can also be synthesized starting from estradiol by the enzyme 17β-hydroxysteroid dehydrogenase. This hormone is involved in numerous physiological processes, fundamental for the whole organism. Estrone exerts its action by interacting with the estrogen receptors, thus activating a cascade of chemical signals that – depending on the case – leads to different biological responses.
The levels of estrone present in the female organism vary over time depending on the stage of life in which the same woman is located. During the woman’s fertile age, the concentrations of estrone are lower than those of diestradiol, which also predominates in terms of the power of action; during pregnancy, estriol, placental steroid with very low estrogenic activity, prevails. Estrone becomes predominant only after lamenopause, due to the blockage of ovarian production of estradiol, with passage to average estrogenic plasma concentrations of 10 pg / ml, against 100 pg / ml of the fertile period.
The concentration of estrone prevails over that of estradiol even before the time of expiration. Because of its origin dependent on androstenedione, estrone levels tend to be elevated in women suffering from hyperandrogenism, resulting for example ovarian apolicistosis, use of testosterone derivatives or androgen-secreting tumors.
As mentioned, estrone can be produced starting from androstenedione, as it can be synthesized starting from estradiol. Estrone, in its turn, can be converted into estrone sulfate, a derivative endowed with a rather prolonged half-life, which acts as a reserve of estradiol and estrone (originated at the cellular level by the steroid sulfatase).
The beneficial role that estrogens (such as estrone) have on hair has been well known for a long time. Just think, for example, of a pregnant woman, whose body is rich in female sex hormones which, among other things, translates into an increase in the duration of the hair growth phase, decreasing the number of hair entering the telogen phase, therefore, reducing its fall. Estrone – analogously to the other estrogens – acts in this way, that is, it has the capacity to prolong the duration of the hair growth phase (anagen). At the same time, it is able to activate adenylcyclicase and the production of growth factors that govern cell multiplication (HrGF) at the level of the hair matrix.
Given these capabilities, estrone was used in the trichological field by topical way. The preparations based on estrone were thus applied directly on the scalp, in order to stimulate hair growth.
However, the important trans-cutaneous absorption of this hormone – with consequent systemic repercussions – has considerably limited the possibilities for using the topical estrone.
Fortunately, this obstacle has been bypassed by the administration of estrone sulphate, which, as we have seen, is converted into estrone from the pilosebaceous follicle thanks to the action of the enzyme sulfatase. For this reason, local treatment with estrone sulfate may be indicated in the presence of female androgenetic dialectomy. In particular, in the treatment of female androgenetic alopecia, estrone sulphate can be used either alone or in combination with minoxidil.
Ultimately, in order to manifest androgenetic alopecia (responsible for most cases of baldness) there must be a genetic predisposition, which needs a more or less high androgen level to be achieved. If it is true that in the absence of androgens baldness does not occur, the hormonal bald values are generally comparable to those of the general population. In women with androgenetic alopecia, it is not uncommon to find androgen levels above the norm.
Probably, hypophyseal hormones such as the already mentioned GH and prolactin, can regulate the degree of activity of the enzyme 5-α-reductase; just think of puberty acne afflicting boys of a particularly high stature (sign of hypersecretion of GH) or of the defluvium (hair loss) and of the seborrhea of amenorrhoic or hyperprolactinemic women. It is not by a chance then that currently, the most widely used drug in the treatment of male androgenetic alopecia is finasteride, a synthetic 5-α-reductase inhibitor.
Hair loss and smoking
A huge amount of scientific work has shown the negative influence of tobacco smoke on the health of the entire organism. One thing among all reminds us that for every week of smoking (20 cigarettes a day from 25 years of age) one loses one day of life on average.
The negative effects of smoking are also felt at the level of hair and scalp. Just think, for example, of the pro-inflammatory and vasoconstrictive action of nicotine and other substances present in cigarette smoke; all this results in an increased production of free radicals, a lower oxygenation and a lower supply of nutrients to the hair. It is no coincidence that in smokers, hair tends to be more dull and brittle than non-smokers.
We should not forget that the main cause of ‘hair loss’, both in women and in men, is androgenetic alopecia. Some studies (but not all) show that tobacco smoking could be associated with increased levels of androgenic hormones, including DHEA, androstenedione, testosterone and di-hydrotestosterone. The latter, also known as DHT, is the hormone most responsible for androgenetic hair loss; in particular, higher levels of di-hydrotestosterone are associated with a greater incidence of androgenetic alopecia in predisposed subjects.
A study of a sample of 740 Taiwanese men aged 40 to 91 found that in the long run cigarette smoking generally tended to worsen androgenetic alopecia. In fact, smokers presented an approximately twice increased risk of moderate or severe androgenetic alopecia (Norwood type = IV) compared to non-smokers.
Cigarette smoke therefore has a negative effect on hair and increases the chances of hair loss in predisposed subjects. Technically speaking, however, more than hair loss it is correct to speak of miniaturization of the bulb (structure responsible for the synthesis of cells that will form the hair). In androgenetic alopecia, in fact, the bulb becomes smaller and more superficial, giving rise to a hair that is gradually thinner, shorter and partly depigmented.
Drugs that cause hair loss
Several medications can cause temporary hair loss, amplify the existing problem or even cause permanent hair loss. Leaving aside the medicinal preparations (chemotherapy) and the techniques (such as radiation therapy) used in the field of oncology, among the drugs that can cause or accelerate the hair loss we
Each of the aforementioned drugs can cause, favor or accelerate hair loss with its own mechanism of action. In any case, they act by interrupting the natural growth cycle of the hair, favoring its fall. The type of fall (telogen effluvium or anagen effluvium) caused by drugs depends on the active ingredient used, on the dosage to which it is taken and on the sensitivity of each individual to the same drug.
When to see a doctor?
As mentioned, not all patients who take these drugs can go to the hair loss, as this phenomenon depends on a wide variety of factors, including the individual sensitivity to the drug used. Generally, between 40 and 120 hairs are lost during a day; this is considered an absolutely normal phenomenon that is part of the normal life cycle of the hair.
On the contrary, in the moment in which there is a very intense and marked loss of hair, it is necessary to worry about and ask your doctor, or to immediately request a consultation with a specialist. In this regard, it is of fundamental importance to inform the doctor of his state of health, making him participate in the drug therapies that are being followed.