Scientific research has established a clear connection between diet and hair loss. Can the Western diet contribute to the development of Androgenetic Alopecia, and if so, what factors play a role in this process? Is it possible to prevent hair loss through a more balanced lifestyle? This article aims to address these important questions.
Diet and Hair Loss: Increased Androgen Production as a Key Correlating Factor
Individuals with Androgenetic Alopecia (AGA) or Female Pattern Hair Loss (FPHL) exhibit a “dysregulation” in androgen production and response, presenting higher levels of bioavailable Testosterone, Dihydrotestosterone (DHT), and weaker androgens.
This increased androgen production can be triggered by elevated cortisol levels, which in turn may be caused by stress, obesity, high intake of animal proteins and fats in the diet, and lifestyle factors such as alcohol consumption and smoking.
Addressing these factors through dietary modifications and lifestyle changes can reduce serum androgen levels and potentially influence the progression of Androgenetic Alopecia/FPHL.
To effectively impact the course of Androgenetic Alopecia through diet, one must intervene in one or more of the underlying pathophysiological parameters of AGA. At least three recognized factors must be present simultaneously for an individual to develop Androgenetic Alopecia:
- Genetic predisposition
- Hormonal response of the hair follicles
- Inflammation in the perifollicular area
As understood, the first factor—genetic predisposition—is not modifiable. While promising, gene therapy does not currently offer a solution to this aspect of the “equation,” as will be discussed further in the relevant section. Regarding perifollicular microinflammation, it remains unclear whether it is a necessary and sufficient condition for AGA development, a causal factor, or simply a secondary phenomenon; the extent of follicular damage attributable to inflammation has not yet been quantified.
Moreover, since local microinflammation can only be treated pharmacologically—either topically or systemically—there is limited hope for dietary interventions to influence this parameter.
The hormonal aspect of AGA, however, is partially controllable by the individual without the need for medication, as diet and lifestyle can influence several stages of androgen metabolism.
The biochemical steps involved in androgen production and action in AGA include:
- Androgen production (gonads, adrenal glands, sebaceous glands)
- Androgen transport via the bloodstream
- Production and conversion of androgens by extra-glandular tissues (skin)
- Metabolism within target cells
- Cellular response to androgens
Among these, natural interventions can target the first three steps, while the latter two remain beyond direct control. Therefore, dietary and lifestyle changes can primarily affect androgen production and transport within the body.
In the following section, we will examine how lifestyle and diet elevate serum androgen levels and how natural strategies can reduce this production. As we will see, androgen production by the glands is influenced by dietary fat content, the production of androgen-binding molecules in serum is regulated by insulin, and the conversion of Testosterone to DHT in the skin is associated with subcutaneous fat levels, diet, and lifestyle.
Από τους παραπάνω παράγοντες μπορεί κανείς να επέμβει με φυσικά μέσα στους τρεις πρώτους και δεν μπορεί να επέμβει στους δύο τελευταίους. Από τις παραμέτρους της ΑΑ, μπορούμε λοιπόν να επέμβουμε μόνο στην ορμονική και συγκεκριμένα μόνον στην παραγωγή και μεταφορά των ανδρογόνων στο σώμα.
Στην παρακάτω ενότητα θα δούμε πως αυξάνονται τα ανδρογόνα στον ορό μέσω του τρόπου ζωής και διατροφής και πως μπορεί κανείς με φυσικά μέσα να μειώσει την παραγωγή αυτή. Όπως θα δούμε, η παραγωγή των ανδρογόνων από τους αδένες επηρεάζεται από την περιεκτικότητα της διατροφής σε λιπαρά, η παραγωγή μορίων που μεταφέρουν τα ανδρογόνα στον ορό ρυθμίζεται από την ινσουλίνη,
ενώ και η μετατροπή της Τ σε DHT στο δέρμα σχετίζεται με το ποσοστό του υποδόριου λίπους, τη διατροφή και τον τρόπο ζωής.
Are Androgen Levels Elevated in Androgenetic Alopecia?
Testosterone (T) and Dihydrotestosterone (DHT)
Studies have been conducted in both genders to determine whether serum androgen levels differ between individuals with androgenetic alopecia (AGA) or female pattern hair loss (FPHL) and those with normal hair density. While the production rate and serum levels of testosterone (T) generally remain within normal ranges in men with AGA, this is not the case for dihydrotestosterone (DHT).
In a study by Vierhapper et al., it was found that the hepatic production rate of DHT in individuals with AGA was on average 300% higher, while the renal clearance rate of DHT was approximately 50% lower compared to the control group.1 As a result, although serum testosterone levels remained normal, DHT levels were significantly elevated. Similar findings had been reported earlier by Demark-Wahnefried et al.2.
These results were further confirmed by Bang et al., who observed markedly increased serum DHT levels in AGA patients (mean 71.84 ng/ml; range 20.50–221.08 ng/ml) compared to individuals without AGA (mean 1.41 ng/ml; range 0.45–2.40 ng/ml, p < 0.001), while testosterone levels did not differ significantly between the two groups. Additionally, the DHT/T ratio—which reflects the activity of the 5α-reductase enzyme system—was on average 18.54 in women with FPHL versus 0.48 in control subjects (p < 0.005).4
Choi et al. conducted a study measuring serum and follicular levels of testosterone, dihydrotestosterone, and their ratios in 35 men with AGA (aged 28–55) and their sons (aged 8–16), as well as 55 men without AGA and their sons. The findings were notable: sons of fathers with AGA exhibited approximately 300% higher serum T/E (testosterone/estradiol) ratios (mean 35.83, range 30.37–42.54) compared to controls (mean 10.47, range 6.39–15.95, p < 0.001). The difference was even more pronounced between fathers with AGA and those without, showing nearly a 500% increase in the T/E ratio in men with AGA (mean 46.41, range 32.99–68.34) compared to controls (mean 9.17, range 6.34–11.41, p < 0.001).5
A study by Poor et al., comparing androgen metabolites in the urine of men with AGA and controls, found increased excretion of testosterone metabolites, specifically androsterone and etiocholanolone, but not cortisol metabolites.
Regarding women with FPHL, Vierhapper et al. found elevated serum testosterone but normal DHT levels. Women with FPHL often present with clinical signs of androgen excess, such as acne, hirsutism, and seborrhea, as well as systemic virilization symptoms like irregular menstruation and infertility. However, in 60–70% of these women, testosterone, dehydroepiandrosterone sulfate (DHEA-S), and other endocrine parameters have been found within normal ranges in some studies. Conversely, Juricskay et al., in a study comparing urinary androgen metabolites between women with FPHL and controls, reported significantly elevated levels in the FPHL group.
In the remaining 30–40% of women with FPHL, there is often an underlying systemic disorder. Increased androgen production in these cases is most commonly associated with polycystic ovary syndrome (PCOS), which reportedly accounts for over 80% of FPHL cases. Less frequently, adrenal hyperplasia and very rarely androgen-secreting malignant tumors are implicated
SHBG (sex hormone binding globulin)
SHBG (sex hormone binding globulin) is the primary carrier protein for androgens in the bloodstream and serves as the main “reservoir” of testosterone (T), with albumin playing a secondary role. Of the total circulating testosterone (total T), approximately 2% is bioavailable as free testosterone (free T), about 44% is bound to SHBG, and the remainder is bound to serum proteins, mainly albumin. Some studies suggest that free T may constitute around 10%, as SHBG binds approximately 70% and albumin about 19% of total T under normal physiological conditions. However, testosterone bound to SHBG and albumin is biologically inactive; only the fraction of free T in the serum remains active.
As previously noted, total testosterone levels do not appear to differ significantly between healthy men with or without androgenetic alopecia (AGA) and healthy women with or without female pattern hair loss (FPHL). However, SHBG levels are lower in AGA patients of both genders. Cipriani et al. reported that although serum testosterone levels were similar between men with AGA and control groups, salivary testosterone levels were elevated in individuals with AGA. This suggests that bioavailable free testosterone is likely higher in AGA patients, a finding further supported by Arias-Santiago et al. in 2010, who compared cardiovascular risk factors in men and women with FPHL, as will be discussed below.
Consequently, a greater proportion of testosterone exists in its free, bioavailable form in the serum of AGA patients. However, subsequent studies by Georgala et al. in postmenopausal women and by de Ronde et al. involving 400 adult men indicated that serum SHBG levels do not appear to significantly affect testosterone bioavailability.
Other Androgens in Serum
In the 1991 study by Schmidt et al., involving 65 men with androgenetic alopecia (AGA), serum levels of androstenedione were found to be 20-30% higher compared to normal reference levels. Additionally, DHEA-S levels were reported to be increased by up to 250% in a small-scale study by Pitts on 18 young men with AGA. A similar study by Moltz involving 125 women with female pattern hair loss (FPHL) concluded that 67.2% exhibited mild hormonal imbalances unrelated to polycystic ovary syndrome (PCOS). In these women with FPHL, both DHEA and androstenedione were found to be elevated.
DHEA and androstenedione are direct adrenal derivatives, produced via enzymatic conversion from cortisol. While DHEA is a weak androgen, DHEA-S is a stronger androgen and recent evidence has shown that it can be directly converted into dihydrotestosterone (DHT) within the hair follicle, specifically in the cells of the dermal papilla.
From the above, it is evident that patients with AGA and FPHL do not typically have demonstrably elevated total testosterone levels under normal conditions. However, most studies agree that free testosterone and DHT are increased, SHBG levels are decreased, and weaker androgens are elevated in the serum of individuals with AGA. Given that these androgens are directly implicated in the development of AGA, it is important to explore how lifestyle and diet may influence the serum concentrations of these androgens
Nutrition and Hair Loss: What Generally Causes an Increase in Androgen Production?
Androgen secretion from the adrenal glands depends on the release of ACTH from the pituitary gland, with androgen levels closely following cortisol secretion. Therefore, increased cortisol secretion is accompanied by a rise in the production of DHEA and androstenedione from the adrenal glands, as well as elevated DHT levels in the hair follicles. Patients with androgenetic alopecia (AGA) or female pattern hair loss (FPHL) often present with increased serum levels of weaker androgens, associated with heightened adrenal activity and concurrent hypercortisolemia, which may potentially influence the progression of AGA.
Let’s now examine the conditions that cause hypercortisolemia in healthy adults.
What Causes Hypercortisolemia in Healthy Adults?
The main factors causing an increase in serum cortisol that are not related to pathological conditions (such as diseases, tumors, etc.) are primarily two:
1. Stress
Everyday stress is widely implicated as a contributing factor to hair loss. Cortisol, along with catecholamines, is secreted in response to increased demands for performance and readiness (the “fight or flight” response), both in humans and experimental animals. The correlations between obesity and cortisol, cortisol and testosterone (T), T and androgenetic alopecia (AGA), and other pathological states are not fully understood and— as we will see—sometimes strikingly contradictory.
Two notable, conflicting theories illustrate these complexities:
- Rosmond et al.’s theory suggests that in chronic stress conditions, cortisol secretion eventually decreases rather than increases.
- Drapeau et al.’s theory proposes that central fat accumulation and obesity in men are physiological adaptations to stress, rather than causes of stress.
Based on the classical, evidence-based medical understanding of these correlations—and setting aside these innovative yet currently unproven theories—experimental data demonstrate that during stress, DHEA production increases at the expense of cortisol, which shows reduced serum levels since they share a common biochemical pathway. The elevated DHEA may lead to increased DHT production, with well-known consequences. This finding further supports the link between lifestyle factors and AGA and may help explain Rosmond et al.’s conclusions.
Other pathophysiological mechanisms connecting stress and hair follicles can be found in the section “Stress and AGA” and will not be elaborated here
2. Obesity
Obesity, especially moderate obesity, is another significant factor driving increased cortisol secretion. The additional body mass that obese individuals must carry creates a continuous state of mild biochemical stress. The frequent psychosomatic responses and psychological stress stemming from the “social stigma” often accompanying obesity may further exacerbate the condition.
Findings on how obesity affects androgen production are both interesting and consistent. A study by Tajar et al. involving 3,369 men aged 40-79 across eight European centers showed that obesity is the leading cause of secondary hypogonadism. This conclusion was confirmed by Dhindsa et al. in the Hypogonadism In Males (HIM) study of 1,849 men (1,451 non-diabetics and 398 diabetics), which found that 40% of obese non-diabetic men and 50% of obese diabetic men had free T below normal levels. Numerous other studies confirm these results in adolescents, young adults, and elderly obese men. Similarly, studies on healthy adults under stress (e.g., medical residents, athletes, or individuals awaiting significant exams) show paradoxically decreased T and cortisol levels.
Obesity is almost always accompanied by glucose intolerance, which often leads to chronic hyperinsulinemia. Insulin inhibits hepatic production of sex hormone-binding globulin (SHBG), stimulates androgen production from the ovaries in women, and from the testes in men. According to a study by Tsai et al. involving 221 non-diabetic adults, there is a negative correlation between glucose tolerance and serum free T levels, independent of SHBG levels. These factors result in elevated serum T and androgens in obese women, whereas obese men typically show slightly reduced total T levels, but free T levels comparable to non-obese men. However, aromatization of T to estrogens in increased adipose tissue ultimately raises serum estrogen levels in obese men and, according to a recent publication by Blanchette et al., also increases progesterone.
Therefore, obesity is mainly associated with androgen deficiency in women and possibly below-normal T levels in men. Nonetheless, since adipose tissue also exhibits 5α-reductase activity and converts weaker androgens into more potent ones, it is likely that obese men experience locally increased conversion of T or DHEA-S to DHT in excess adipose tissue compared to non-obese men. Importantly, the hormonal profile changes in obese men have been found to reverse with weight loss and restoration of a normal Body Mass Index (BMI).
Insulin also significantly influences levels of other androgens. High insulin levels following consumption of meals rich in complex carbohydrates or stimulants of insulin secretion (such as coffee and smoking) lead to an increase in all serum androgens.
From the above, it is clear that obesity:
- Increases cortisol and decreases testosterone in men, and lowers SHBG in both sexes
- Increases testosterone in women and possibly enhances local DHT production in men through conversion of weaker androgens in excess adipose tissue
- Elevates insulin, likely through insulin’s inhibitory effect on SHBG production
- Insulin and IGF-1 promote lipogenesis and proliferation in sebaceous glands, increasing sebum production rich in potent androgens, which are reabsorbed by hair follicles and exert negative trophic effects
The trophic effects of hyperinsulinemia on sebaceous glands have been repeatedly demonstrated in individuals with acne and are reversed with healthier dietary habits.
Therefore, addressing obesity should be an integral part of the “therapeutic equation” for managing AGA and FPHL, as restoring healthy anthropometric characteristics normalizes serum T and SHBG levels. Interestingly, a study by Hirsoo et al. on a random sample of 727 men aged 25-34 reported that men with extensive AGA were more likely to be obese, although no explanation was provided.
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