Conflicts of interest: The author declares no conflicts of interest.
Dr. Frances O. A. Ajose, MRCP(UK), FRCP(LOND) Consultant Physician Dermatologist, Lagos State University Teaching Hospital, PO Box 1723 Surulere, Lagos, Nigeria E-mail: email@example.com
Background African hair in its natural state poses tenacious grooming challenges; consequently a large portion of the African cosmetic industry is focused on means to relax the tight curls of African hair to make the hair more manageable. In malnourished and hypoproteinemic states, African hair straightens in an uncomplimentary manner. Recently, we observed that in certain diseases African hair changes to a desirable silky wavy texture.
Method To identify the diseases that turn African hair silky and their parameters we examined 5612 dermatology patients at a tertiary hospital in Nigeria. We then studied the clinical and basic laboratory parameters of those patients whose diseases were accompanied by the silky hair change.
Result Silky hair change similar to the hair of the African neonatal child was observed in five diseases, namely AIDS, rheumatoid arthritis, systemic lupus erythematosus, pulmonary tuberculosis with cachexia, and Behçet’s disease.
Conclusion Our study identified retrogression of African hair to the neonatal structure in five diseases. Anemia of chronic illness, high erythrocyte sedimentation rate, and mild hypocalcemia were significant laboratory parameters. This is an important observation, which should excite and advance research into the nature and structure of African hair. The causes of structural hair changes should include these five diseases.
Hair, especially scalp hair, is imbued with greater social and psychological significance than with biological importance.1
Human hair is categorized into three broad groups, namely, African, Caucasian, and Asian based on morphological variations but without major biochemical differences.1 The structure of African hair2 is a flattened ellipse, with several small twists and inconsistent cuticle and fiber diameter. It is brittle, tightly coiled, spring-like, and has the slowest growth rate.3 In comparison, Asian hair is circular in cross-section, straight, thicker, with the highest tensile strength and fastest growth rate while Caucasian hair is oval, straight to wavy with medium diameter and tensile strength.3
Furthermore, African hair has the least moisture and lipid content, hence the lackluster appearance that requires greasy pomade to make it shine.
Consequently, African hair in its natural state poses tenacious grooming challenges.4 Most individuals with the African hair type are dissatisfied with their hair in its natural state. Considerable labor and cost is expended to make African hair more manageable.5
African hair grooming practices4 over the years have included thermal straightening, chemical straightening, permanent waving, hair weaving and extensions, natural afro styles, braids, twists, and locks. All grooming practices apart from the virgin state render African hair even more brittle and prone to damage.6
Chemical relaxing and hair styling services currently account for 80% of African salon business.7 The “Jheri curl”5 was a popular chemical hair relaxing style, which gave the wearer a glossy loosely curled hair. The two-part process consisted of a rearranging chemical, to straighten out the tight curls followed by another chemical to set the curls loosely. Reapplication of the chemicals is required at the rate the virgin hair grows from the scalp. This process caused the African hair to become extremely brittle and dry and intense labor and cost was required to maintain the style.
This Jheri curl type of hair structure is what we have observed in the disease states under study.
However, the majority of African babies are not born with springy tight curls, the African child at birth is either bald or has silky loose curls (Fig. 1) similar to the Jheri curls. The springy tight curls develop within the first year of life but a few negroid Africans retain their silky hair type for life.
The present study was to identify diseases that turn African hair silky and understand their basic clinical and laboratory parameters.
This was a prospective cohort study of 5612 patients attending the adult skin clinic at the Lagos State University Teaching Hospital, Lagos Nigeria (LASUTH) between 2004 and 2009, who consented to participate.
Demographic data were collected. All patients were naked for examination by the author to assess hair structure. Investigations included retroviral infection status, full blood count, erythrocyte sedimentation rate (ESR), basic serum chemistry, hair microscopy, skin biopsy, and the CD4 count of patients that were positive for retroviral infection.
The study was approved by the hospital ethics committee.
Five chronic diseases were found to be associated with silky hair change in our cohort, namely acquired immune deficiency syndrome (AIDS) (Fig. 2a,b), rheumatoid arthritis (RA) (Fig. 3a,b), systemic lupus erythematosus (SLE) (Fig. 4a,b), pulmonary tuberculosis with cachexia (PTBc) (Fig. 5), and Behçet’s disease (BD).
A total of 338 patients aged 16–68 years presented with one of these five diseases over the 5-year study period of which 86 (29.8%) had the silky hair change with a male to female ratio of 2:3 (Table 1).
Table 1. Diagnosis and demographic data of 86 patients with silky hair change seen at a skin clinic in Nigeria, 2004–2009
Patients with silky hair
Infection with human immunodeficiency virus
Pulmonary tuberculosis with cachexia
Systemic lupus erythematosus
Of the patients with AIDS 30% (89 of 295) had CD4 below 100/mm3 at some point in their illness; of this group, 78% (69 of 89) had the silky hair change. Persistence of the neonatal silky hair into adulthood, that was not associated with any chronic ill-health, was observed in 0.5% (30 of 5612) of our cohort.
The hair change was insidious in AIDS and BD, whereas it was dramatic, following a sudden episode of telogen effluvium in RA, PTBc, and SLE. The majority of patients with AIDS and BD observed a sudden ease of combing and thinning of scalp hair but claimed not to have noticed excessive hair loss. Most of them were alarmed at the sudden hair change and opted for an immediate shave but a few exploited the situation and applied baby oil to achieve the Jheri curl look. The cases with RA, PTBc, and SLE experienced a short period of telogen and anagen effluvium before onset of the silky hair growth (Fig. 4b).
The hair change also affected the chest and body hair and in four patients with AIDS, pubic hair was involved.
No scalp abnormality was observed in any of the patients with silky hair change. Hair color, luster, and tensile strength were preserved in the silky hair. The use of highly active anti-retroviral therapy for AIDS did not reverse the hair change but on recovery from tuberculosis, hair structure reverted to normal. There was a female preponderance with a male to female ratio of 2:3.
Histology (Fig. 6a–c) was obtained from one male patient with RA and was reported as “hairy skin with an area of loss of terminal hairs that appear total suggesting scarring alopecia but without inflammation and no clues to suggest aetiology.” Morphology of the hair sample from the same patient showed “No abnormality.”
The hematological indices and serum chemistry of all patients are in Table 2.
Table 2. Mean of basic laboratory results of 86 patients with silky hair change seen at a skin clinic in Nigeria, 2004–2009
Systemic lupus erythematosus
Pulmonary tuberculosis with cachexia
Anemia, Hb < 12 g for
females and < 13.5 g males
Erythrocyte sedimentation rate
WCC, n = 3–10,000
Platelets, n = 100–400,000
> 30% elevation
Total serum protein, n = 6.6–8.7 g/dL
Upper normal (elevated gamma globulin)
Serum calcium, n = 2.5–2.55 mg/dL
The five diseases in question have in common, chronicity, anemia of chronic illness, high ESR, and some degree of immunosuppression.
Telogen effluvium is known to accompany autoimmune diseases but the nature of hair regrowth has not been sufficiently studied.
Straightening of hair has been reported in African patients with AIDS,8–11, but we did not find any reports relating to the other four diseases that we studied. Caucasian hair was also reported by Dawber and Van Neste12 to become kinky following an acute febrile illness in a set of identical twins but it was not stated if this was temporary or permanent.
It has been established that hair curvature is determined at the level of the bulb of the hair follicle13 with active participation of the hair follicle transglutaminase (HFT).14 What factor do these five diseases have in common that alters programming of the curvature of the African hair? From histology,15 it does not appear to be a cellular process. We may have to look into the biochemical processes at the perifollicular dermis of these patients. Perhaps a chemical item is inhibiting the catalytic effect of the HFT. More sophisticated histochemistry than is available to us would be required.
We have identified retrogression of the African hair to the neonatal structure of silky loose curls in AIDS, RA, SLE, BD, and PTBc. Anemia of chronic illness, high ESR, and mild hypocalcemia were significant laboratory parameters. Serum protein level did not appear significant. These diseases should be included in the list of causes of alopecia without scalp abnormality. The etiology of the phenomenon is yet unclear. It is hoped that this observation will excite and advance research into the nature and structure of African hair.
I wish to thank Dr. Eduardo Calonje, Director of Diagnostic Dermatopathology, St John’s Institute of Dermatology, St Thomas’ Hospital, London, for the histology report.