Biomolecules of Fermented Tropical Fruits and Fermenting Microbes as Regulators of Human Hair Loss, Hair Quality, and Scalp Microbiota

Abstract

Plant-derived secondary metabolites (polyphenols/terpenes/alkaloids) and microbial exometabolites/membrane components of fermented tropical fruits are known as highly bioavailable biomolecules causing skin and hair improvement effects (wound healing, anti-inflammatory, antioxidant, antidiabetic, antiacne, skin/hair microbiota balancing, hair growth-promoting, and hair loss-inhibiting). Caffein is considered as a hair growth promoter. A randomized placebo- and caffein-controlled clinical trial on the efficacy of fermented papaya (FP) plus fermented mangosteen (FM) towards human hair quality and loss was conducted. Shampoo and lotion hair care products containing FP, FM, and caffein as active agents were developed and applied to 154 subjects of both sexes with clinically confirmed androgenic or diffuse alopecia for 3 months. Their clinical efficacy was assessed subjectively by questionnaires filled in by dermatologists/trichologists, and by the objective trichomicroscopical calculations. Hair and scalp skin quality was determined by microbiota pattern and ATP, SH-groups, protein, and malonyl dialdehyde quantification. Comparative clinical data showed that the experimental hair care cosmetics significantly inhibited hair loss, increased hair density/thickness, and improved hair follicle structure versus placebo and caffein controls. The cosmetics with FP and FM substantially normalized the microbiota pattern and increased ATP content in hair follicle, while inhibiting lipid peroxidation in the scalp skin, and SH-group formation in the hair shaft.

Keywords: ATP; MDA; SH-groups; alopecia; caffeine; clinical trial; fermented papaya/mangosteen; hair loss; pre-/probiotics; skin microbiota.

Figure A1

Microphotographs of hair density before and after the trial in the patient K-va of the experimental Group 1. (a) Hair density on the frontal area before the trial; (b) hair density on the frontal area after the trial; (c) hair density on the occipital area before the trial; (d) hair density on the occipital area after the trial.

Figure A1

Microphotographs of hair density before and after the trial in the patient K-va of the experimental Group 1. (a) Hair density on the frontal area before the trial; (b) hair density on the frontal area after the trial; (c) hair density on the occipital area before the trial; (d) hair density on the occipital area after the trial.

Figure A2

Microphotographs of hair density before and after the trial in the patient Ko-va of the placebo control Group 2. (a) Hair density on the frontal area before the trial; (b) hair density on the frontal area after the trial; (c) hair density on the occipital area before the trial; (d) hair density on the occipital area after the trial.

Figure A3

Microphotographs of hair density before and after the trial in the patient I-va of the caffeine control Group 3. (a) Hair density on the frontal area before the trial; (b) hair density on the frontal area after the trial; (c) hair density on the occipital area before the trial; (d) hair density on the occipital area after the trial.

Figure 1

Determination of hair density. One cm² is bordered by the orange line. Magnification ×60.

Figure 2

The determination of a single hair diameter was conducted under ×200 magnification lenses. The numbers in yellow squares indicate the hair diameter in μm.

Figure 3

Determination of the hair follicle diameter and lipid/water mantel conditions: (a) hair root/follicle; (b) lipid mantel and hydration conditions were performed under ×200 magnification.

Figure 4

Preparation of hair follicles for the ATP measurements in the hair follicles: (a) hair plucking; (b) separated hair follicles.

Figure 5

Hair diameter (μm) distribution before and after the trial: (a) Experimental Group 1; (b) Placebo Control Group 2; (c) Caffeine Control Group 3. Small boxes—median values; large boxes—median values ± standard error of median (SEM); whiskers—median values ± 1.96 SEM. p < 0.05.

Figure 6

Hair density (n/cm²) distribution before and after the trial: (a) Experimental Group 1; (b) Placebo Control Group 2; (c) Caffeine Control Group 3. Small boxes—median values; large boxes—median values ± standard error of median (SEM); whiskers—median values ± 1.96 SEM. p < 0.001.

Figure 7

Thick hair presence (%) before and after the trial: (a) Experimental Group 1; (b) Placebo Control Group 2; (c) Caffeine Control Group 3. Small boxes—median values; large boxes—median values ± standard error of median (SEM); whiskers—median values ± 1.96 SEM. p < 0.01.

Figure 8

Medium hair presence (%) before and after the trial: (a) Experimental Group 1; (b) Placebo Control Group 2; (c) Caffeine Control Group 3. Small boxes—median values; large boxes—median values ± standard error of median (SEM); whiskers—median values ± 1.96 SEM. p< 0.05.

Figure 9

Thin hair presence (%) before and after the trial: (a) Experimental Group 1; (b) Placebo Control Group 2; (c) Caffeine Control Group 3. Small boxes—median values; large boxes—median values ± standard error of median (SEM); whiskers—median values ± 1.96 SEM. p < 0.05, p < 0.01.

Figure 10

Relationship between ATP content in hair follicles and labile protein leakage from the hair shaft in patients with two types of alopecia (n = 154). Blue dots represent values for the individual person. Red line is a correlation curve.

Figure 11

Sources of oxidative stress in different types of alopecia.