Almanac A1C

Intermittent Fasting and Hair Loss: Molecular Mechanisms and Protective Countermeasures to Preserve Hair Follicle Regeneration

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dr. Karunia Valeriani Japar

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Introduction

Intermittent fasting (IF) has emerged as a prominent intervention for metabolic optimization, disease prevention, and longevity, with research supporting its role in enhancing cardiovascular health, improving insulin sensitivity, and promoting stem cell rejuvenation in tissues such as muscle, intestine, and hematopoietic systems. Practiced by millions worldwide, IF encompasses protocols such as time-restricted feeding (TRF) and alternate day fasting (ADF), both of which have demonstrated beneficial systemic effects. Yet, amid the enthusiasm for IF, recent findings reveal an unexpected tissue specific consequence like the suppression of hair follicle regeneration through the apoptotic depletion of hair follicle stem cells (HFSCs). Studies employing both animal models and human cohorts have identified a mechanistic link between fasting-induced metabolic alteration, specifically increased lipolysis in skin fat, and hormonal cascades that elevate oxidative stress within the HFSC niche. This result in slowed hair regrowth, marked reduction of stem cell reserves, and with chronic exposure, focal hair loss or baldness. These observations compel a reevaluation of the universally positive narrative surrounding IF, urging scientist and clinicians to recognize its adaptive trade-offs. Delving into these nuanced effects, this review collates the latest evidence on fasting mediated HFSC attrition, elucidates the underlying metabolic and endocrine mechanisms, and explores emerging interventions aimed at mitigating fasting-related hair loss without compromising overall metabolic health and longevity benefits [1,2] .

Hair Follicle Stem Cells- The Engine of Hair Growth

Hair follicles represent one of the most dynamic regenerative tissues in mammals, undergoing continuous cyclical growth throughout an individual’s lifetime. This regenerative capacity is orchestrated by a specialized population of multipotent stem cells known as hair follicle stem cells (HFCSs), which serve as the biological engine driving hair regeneration, maintenance, and repair. Understanding the biology of HFSCs and their regulatory microenvironment is essential for comprehending how systemic metabolic perturbations, such as IF, can influence hair growth dynamics [3,4].

The hair growth cycle consists of three distinct, highly regulated phases: anagen (active growth), catagen (regression), and telogen (rest). During anagen, which typically last three to ten years in humans, the hair follicle undergoes active proliferation and produces the hair shaft through coordinated epithelial-mesenchymal interactions. This phase is followed by catagen, a brief two-to three-week transitional period characterized by apoptosis-driven regression, during which the hair follicle loses approximately one-sixth of its diameter and forms a club hair. The cycle concludes with telogen, a three-to four-month resting phase when the hair follicle remains quiescent before re-entering anagen to initiate a new growth cycle. Over a normal human lifetime, each hair follicle3 completes this anagen-catagen-telogen cycle approximately 10 to 20 times [5,6,7].

Figure 1. Hair Follicle Stem Cells Can Generate Various Cell Types Within The HF [3]

HFSCs reside primarily in a specialized anatomical compartment known as the buldge, located between the sebaceous gland opening and the attachment site of the arrector pili muscle. This bulge region functions as stem cell niche, a distinct microenvironment that integrates systemic signals such as hormones, nutrients, and metabolic cues with local molecular factors to regulate HFSC behaviour. Within this niche, HFSCs exist predominantly in a quiescent, slow cycling state during telogen, characterized by their capacity to retain DNA labels over extended periods, earning them the designation of label-retaining cells. This quiescence is maintained through a delicate balance of inhibitory and activating signaling pathways, most notably bone morphogenetic protein (BMP) signaling, which promotes HFSC quiescence, and Wnt/ b- catenin signaling, which drives HFSC activation and proliferation [3,4,8,9,10,11,12,13,14].

Upon initiation of a new hair cycle, quiescent bulge HFSCs undergo activation in a spatially and temporally coordinated manner. The transition from telogen to anagen begins when activating signals, particularly Wnt ligands secreted from the dermal papilla (DP), a mesenchymal signal within the bulge microenvironment. Activated HFSCs proliferate and generate a rapidly dividing population of transit-amplifying cells (TACs) located in the hair matrix, the proliferative zone surrounding the dermal papilla at the proximal end of the hair follicle. These TACs undergo multiple rounds of division before committing to terminal differentiation, giving rise to all inner hair follicle lineages, including the hair follicle lineages, including the hair shaft, inner root sheath, cuticle, and companion layer [2,4,6,15].

The self-renewal capacity of HFSCs is fundamental to their function as tissue stem cells. During each hair cycle, a subset of activated HFSCs undergoes symmetric self-renewing divisions to replenish the bulge stem cell pool while others generate daughter cells that commit to differentiation pathways. This balance between self-renewal and differentiation is tightly regulated by cell-intrinsic transcription factors including and differentiation is tightly regulated by cell-intrinsic transcription factors, including Sox9, Lhx2, Runx1, Nfatc1, and FOXC1, as well as by epigenetic modifiers that control chromatin accessibility and gene expression programs. Disruptions of these regulatory mechanisms can lead to premature HFSC depletion, impaired hair follicle regeneration, and ultimately hair loss [3,4,13,14,16,18].

Importantly, HFSC activity is highly responsive to systemic metabolic status and stress signal. The HFSC niche integrates inputs from diverse sources, including circulating hormones (such as glucocorticoids and catecholamines), metabolic substrates (including glucose, fatty acids, and amino acids), and paracrine signals from adjacent cell. Populations such as adipocytes, immune cells, and nerve fibers. This metabolic sensitivity positions HFSCs as particularly vulnerable to perturbations in whole body energy homeostasis, such as those induced by fasting or caloric restriction. Recent evidence demonstrates that under conditions of nutrient stress, HFSCs can undergo metabolic reprogramming that alters their proliferative capacity, oxidative stress levels, and survival that ultimately affecting hair follicle regeneration outcomes [1,2,3,8,9,20].

In summary, hair follicle stem cells represent a highly dynamic, metabolically sensitive stem cell population that orchestrates the lifelong cyclical regeneration of hair follicles. Their quiescence activation, self-renewal, and differentiation are governed by an intricate interplay of cell-intrinsic genetic programs and cell-extrinsic niche signals, including systemic metabolic cues. This metabolic integration renders HFSCs uniquely susceptible to dietary and lifestyle interventions such as IF, which can profoundly influence hair growth through mechanisms that are only now beginning to be elucidated [1,2,3,9,20].

Intermittent Fasting and Stem Cell Apoptosis- What the Data Show

Impaired Hair Follicle Regeneration Under Common IF Protocols

The groundbreaking study by Chen and colleagues, published in Cell in 2024, systematically evaluated the impact of commonly practiced intermittent fasting regimens on hair follicle biology using murine models. Two widely adopted IF protocols were implemented: time restricted feeding (TRF), characterized by an 8-hour feeding window and 16-hour fasting period daily (16:8), alternate day fasting (ADF), involving complete 24-hour fasting cycles alternating with ad libitum feeding days. Mice were shaved at postnatal day 21 to synchronize hair follicle entry into anagen, and hair regrowth was monitored over time. Remarkably, which control mice with unlimited access to food (ad libitum, AL), exhibited near-complete hair regrowth by day 30 post-shaving, both TRF and ADF groups demonstrated only partial hair regrowth even after 96 days. This dramatic impairment in hair follicle regeneration occurred despite metabolic improvements, including enhanced glucose tolerance and insulin sensitivity, confirming that the effect on hair growth was independent of overall metabolic health benefits [1,2,21].

Histological and immunofluorescence analyses revealed that hair follicles in fasted mice remained predominantly in the telogen (resting phase, falling to progress through the normal anagen (growth) phase that drives hair shaft production. These observations provided the first direct evidence that intermittent fasting, while metabolically advantageous, exerts a potent inhibitory effect on tissue regeneration in peripheral organs such as the skin [1,2].

Selective Induction Of Apoptosis In Activated HFCS

To elucidate the cellular mechanism underlying fasting-induced hair follicle dysfunction, the research team employed lineage tracing, flow cytometry, and immunohistochemical staining for apoptotic markers. Strikingly, they observed a marked increase in active caspase-3-a definitive marker of apoptotic cell death, specifically within activated HFSCs during and following fasting periods. In contrast to control mice, where HFSCs transitioned smoothly from quiescence to activation around day 20 post-shaving and remained viable throughout anagen, fasted mice exhibited a cyclical pattern: HFSCs were activated during feeding windows, only to undergo programmed cell death during subsequent fasting periods. This repetitive cycle of activation followed by apoptosis resulted in progressive depletion of the HFSC pool over time [1,2].

Flow cytometry quantification demonstrated a significant reduction in both the proportion of EdU-positive (proliferating ) HFSCs and the total number HFSCs in fasted animals compared to controls. Importantly, this apoptotic response was selective for activated HFSCs, epidermal stem cells (EpiSCs), which maintain the epidermal barrier and possess higher intrinsic antioxidant capacity, remained unaffected by intermittent fasting. This tissue-specific vulnerability highlights the unique metabolic fragility of HFSCs in the context of nutrient stress [1,22,2,23].

Dose-Response Relationship Between Fasting Duration and HFSC Loss

One of the most compelling findings from this research was identification of a clear dose-response relationship between fasting duration and the severity of HFSC apoptosis. To test whether fasting duration correlated with stem cell death, researchers subjected mice to varying lengths of fasting, ranging from 8 hours to 24 hours, and quantified apoptotic signals in hair follicles. After 8 hours of fasting, minimal apoptotic activity was detected. However, as fasting duration increased to 16 hours, numerous apoptotic HFSCs appeared, with further escalation observed at 24 hours of fasting. Apoptotic signals diminished following refeeding, indicating that HFSC death was dynamically linked to the fasting state itself rather than permanent cellular damage [1,21,23].

Importantly, the dose-response effect extended to different IF regimens: more aggressive protocols, such as 20:4 TRF (20 hours fasting,4 hours feeding) or prolonged ADF cycles, produced more pronounced hair growth impairment compared to milder 16:8 TRF schedules. This graded response underscores that the metabolic stress imposed by extended fasting periods directly determines the extent of HFSC vulnerability and hair follicle dysfunction [21,23]

Chronic IF Exposure: HFSC Depletion And Hair Follicle Degeneration

A critical question addressed by the study was whether repeated exposure to intermittent fasting would allow for adaptive resilience in HFSCs, potentially mitigating the detrimental effects over time. Unfortunately, long-term experiments revealed the opposite outcome. Mice subjected to chronic intermittent fasting for 8 months developed regions of complete baldness on their dorsal skin, accompanied by histological evidence of hair follicle degeneration. Detailed examination of these hair follicles showed a significant reduction in HFSC number, hair follicle length, and HFSC compartment size, all hallmarks of stem cell exhaustion and tissue atrophy [1,21,23].

Rather than adapting to the metabolic challenge, HFSCs underwent repetitive cycles of activation during feeding periods and apoptosis during fasting periods, culminating in irreversible depletion of the stem cell niche. This progressive loss of regenerative capacity ultimately manifested as hair follicle miniaturization and baldness, demonstrating that chronic IF can drive stem cell-driven tissue degeneration in skin appendages [1,2,23].

Figure 2. Under fed conditions, HFSCs undergo proper activation and hair follicles transition from telogen to anagen. In contrast, fasting triggers dermal adipocyte lipolysis, releasing FFAs into the surrounding niche to be utilized by HFSCs. This metabolic reprogramming induces apoptosis in HFSCs, inhibit hair follicle regeneration [2]

Mechanistic Independence From Caloric Restriction And Circadian Disruption

To exclude confounding variables, the researchers meticulously examined whether the observed effects were attributable to reduced caloric intake or alterations in circadian rhythm, both factors commonly associated with intermittent fasting. Metabolic cage analysis revealed that mice on TRF and ADF regimens consumed equivalent total daily calories compared to control mice, as fasted animals compensated by increasing food intake during feeding windows. This finding ruled out caloric restriction as the underlying cause of HFSC apoptosis [1,2].

Similarly, experiments comparing daytime versus nighttime fasting schedules, designed to dissect circadian influences, yielded comparable levels of HFSC activation followed by apoptosis regardless of timing. Additionally, genetic ablation of TSC2 (a negative regulator of mTORC1, the master cellular nutrient sensor) in HFSCs did not rescue fasting-induced apoptosis, excluding mTORC1 signaling as a mediator of this effect. Collectively, these control experiments established that HFSC apoptosis during intermittent fasting arises from a distinct metabolic mechanism independent of overall energy balance, circadian disruption, or canonical nutrient-sensing pathways [1,2].

Translation To Human Growth: Clinical Trial Evidence

To assess the translational relevance of these findings, the research team conducted a randomized clinical trial (NCT05800730) involving 49 healthy young adults. Participants were randomized to either a time-restricted diet involving 18 hours of fasting per day or a control group compared with unrestricted eating patterns, and hair growth rates were measured over a 10-day period. The results demonstrated an 18% reduction in the average speed of hair growth in the fasting group compared to controls. While this reduction was statistically significant, it was notably milder that the effects observed in mice, consistent with the slower human metabolic rate, lower hair growth velocity, and higher intrinsic antioxidant capacity in human HFSCs compared to their murine counterparts [1,2,24,25].

Despite the modest magnitude of the effect, the clinical trial provided critical proof of principle evidence that intermittent fasting can inhibit human hair growth through mechanisms analogous to those identified in animal models. The authors emphasized that larger, longer-duration studies are necessary to fully characterize the extent, variability, and clinical significance of fasting-induced hair growth suppression in diverse human populations [1,2,23].

In summary, rigorous preclinical and early clinical evidence demonstrates that commonly practiced intermittent fasting regimens, including 16:8-time restricted feeding and alternate day fasting, significantly impair hair follicle regeneration by selectively inducing apoptosis in activated hair follicle stem cells. This effect exhibits a clear dose-response relationship, with longer fasting durations producing greater HFSC loss and hair growth impairment. Chronic application of intermittent fasting results in progressive HFSC depletion, hair follicle degeneration, and baldness in animal models. Human clinical trial data corroborate these findings, revealing an 18% reduction in hair growth speed with daily 18 hour fasting. Importantly, these effects are independent of caloric restriction, circadian rhythm alterations, or mTORC1 signaling, pointing to a distinct metabolic vulnerability of HFSCs under intermittent fasting conditions.

Mechanistic Insights- Fat Fueled Cascade and Hormonal Adaptations

Interorgan Communication: The Adrenal Gland-Dermal Adipocyte Axis

The discovery that intermittent fasting selectively induces HFSC apoptosis prompted Chen and colleagues to investigate the upstream regulatory pathways responsible for this tissue-specific vulnerability. Initial hypotheses centred on canonical nutrient-sensing mechanisms, such as mTORC1 signalling, which plays a central role in coordinating cellular metabolism with nutrient availability. However, genetic ablation of TSC2, a negative regulator of mTORC1, did not rescue fasting-induced HFSC apoptosis, ruling out this pathway as a primary mediator. Similarly, experiments controlling for caloric restriction and circadian rhythm disruption failed to account for the observed phenotype, indicating that a distinct metabolic mechanism was at play [1,2,26,27].

Attention then turned to the dermal adipocyte layer , a critical component of the HFSC niche that undergoes dynamic remodelling in response to systemic metabolic demands. The researchers discovered that fasting triggers interorgan communication between the adrenal glands and dermal white adipose tissue (dWAT), establishing a previously unrecognized hormonal axis that directly impacts HFSC survival. Specifically, fasting activates the adrenal glands to secrete elevated levels of the stress hormones corticosterone (the primary glucocorticoid in rodents, analogous to cortisol in humans) and epinephrine adrenaline). These hormones act on dermal adipocytes via glucocorticoid receptors (GR) and beta-3-adrenergic receptors (ADRB3), respectively, to stimulate lipolysis, the enzymatic breakdown of stored triglycerides into free fatty acids (FFAs) and glycerol [1,2,26,28,29,30].

Critically, this fasting-induced lipolysis in dermal adipocytes was directly correlated with both the duration of fasting and the appearance of apoptotic HFSCs. Short fasting periods (8 hours) produced minimal lipolysis and negligible HFSC apoptosis, whereas longer fasting durations (16–24 hours) resulted in robust lipolysis and extensive stem cell death. Importantly, refeeding rapidly halted adipocyte lipolysis and prevented further HFSC apoptosis, demonstrating that this process is dynamically and reversibly linked to the nutritional state [2].

Hormonal Drivers of dermal Adipocyte Lipolysis

To establish the causal role of adrenal hormones in mediating fasting-induced HFSC apoptosis, the research team employed a series of elegant genetic and pharmacological interventions. First, they performed complete adrenalectomy (surgical removal of both adrenal glands) in mice prior to subjecting them to intermittent fasting regimens. Strikingly, adrenalectomized mice exhibited neither dermal adipocyte lipolysis nor HFSC apoptosis during fasting, and their hair regrowth remained comparable to control animals. This definitive experiment established that adrenal gland signalling is essential for fasting-induced HFSC death [1,2].

To dissect the relative contributions of corticosterone versus epinephrine, the investigators generated adipocyte-specific conditional knockout mice lacking the glucocorticoid receptor, effectively blocking corticosterone signalling in dermal adipocytes. Additionally, they pharmacologically inhibited beta-adrenergic signalling using propanolol, a non-selective beta-blocker that prevents epinephrine from activating ADRB3 receptors on adipocytes. Both interventions significantly attenuated fasting-induced lipolysis in dermal adipocytes and reduced HFSC apoptosis, indicating that both corticosterone and epinephrine contribute synergistically to the adipocyte to HFSC signalling cascade [23,31].

Importantly, direct injection of equivalent concentrations of corticosterone or epinephrine into adipocyte-lipolysis-deficient mice (Lacking the rate-limiting lipolytic enzyme ATGL) did not induce HFSC apoptosis, confirming that these hormones exert their effects indirectly via adipocyte lipolysis rather than through direct toxic effects on HFSCs. Collectively, these findings establish a clear hormonal axis: fasting → adrenal activation → corticosterone + epinephrine secretion → dermal adipocyte lipolysis → FFA release → HFSC metabolic disruption [1,2,3].

Free Fatty Acid Overload and Metabolic Disruption in HFSCs

The surge of free fatty acids released from dermal adipocytes during fasting represents a critical metabolic challenge for activated HFSCs. Under normal fed conditions, HFSCs rely primarily on glucose oxidation to meet their energy demands. However, during fasting, the systemic shift toward lipid mobilization results in a marked increase in FFA concentrations within the HFSC niche. While many cell types possess robust enzymatic machinery to efficiently catabolize FFAs via fatty acid oxidation (FAO) activated HFSCs exhibit a critical metabolic vulnerability: they lack the appropriate metabolic machinery to safely process the influx of FFAs [2,32].

To directly test whether FFAs mediate HFSC apoptosis, the researchers employed multiple complementary approaches. First, they generated HFSC-specific conditional knockout mice lacking CPT1A (Lhx2^CreER^; Cpt1a^fl/fl^), the rate-limiting enzyme required for transporting long-chain fatty acids into mitochondria for FAO. Genetic blockade of FAO in HFSCs significantly reduced apoptosis during fasting, demonstrating that FFAs must enter the FAO pathway to exert their toxic effects. Conversely, exogenous administration of FFAs (such as palmitate or oleate) directly into the skin or into cultured HFSCs was sufficient to induce apoptosis even in the absence of fasting, confirming that FFAs alone are necessary and sufficient to trigger HFSC death [2,32].

RNA sequencing of HFSCs isolated from fasted mice revealed a dramatic transcriptional shift toward lipid metabolism and oxidative stress pathways. Genes associated with fatty acid uptake, FAO enzymes, and mitochondrial dysfunction were significantly upregulated, while genes involved in glucose metabolism and antioxidant defence were downregulated. This metabolic reprogramming characterized by forced engagement of FAO machinery that HFSCs are poorly equipped to handle culminates in mitochondrial overload and cellular stress [1,2,32].

Oxidative Stress, Reactive Oxygen Species, and Mitochondrial Dysfunction

The metabolic switch from glucose to fatty acid oxidation in HFSCs results in a catastrophic accumulation of reactive oxygen species (ROS), the primary executioner of fasting-induced HFSC apoptosis. ROS are highly reactive molecules including superoxide anion, hydrogen peroxide, and hydroxyl radicals that are generated as byproducts of mitochondrial respiration, particularly when electron transport chains are overloaded or dysfunctional. Under normal physiological conditions, cells maintain ROS homeostasis through a robust antioxidant defence system comprising enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase, as well as non-enzymatic antioxidants like glutathione and vitamins E and C [1,33].

However, activated HFSCs possess inherently lower antioxidant capacity compared to other skin stem cell populations, such as epidermal stem cells (EpiSCs). This differential antioxidant capacity explains the selective vulnerability of HFSCs to fasting-induced oxidative stress: while EpiSCs remain unaffected by intermittent fasting due to their robust ROS-scavenging machinery, HFSCs succumb to oxidative damage when forced to metabolize FFAs [1,2,23].

Mechanistic studies employing fluorescent ROS probes, transmission electron microscopy, and mitochondrial function assays confirmed that fasting dramatically elevates ROS levels specifically within activated HFSCs. These elevated ROS levels were accompanied by ultrastructural evidence of mitochondrial dysfunction including swollen mitochondria, cristae disorganization, and loss of membrane potential, all hallmarks of oxidative damage. Furthermore, markers of oxidative DNA damage, lipid peroxidation, and protein carbonylation were significantly elevated in fasted HFSCs, indicating widespread cellular injury [1,23,33].

The oxidative stress-induced damage ultimately activates intrinsic apoptotic pathways, as evidenced by increased expression of pro-apoptotic proteins (such as BAX and activated caspase-3) and decreased expression of anti-apoptotic proteins (such as BCL-2). The execution of apoptosis is irreversible, resulting in the permanent loss of activated HFSCs from the niche and progressive depletion of the stem cell pool with repeated fasting cycles [1,23].

A Distinct Metabolic Adaptation, not a Simple Nutritional Deficit

A critical insight from this work is that fasting-induced HFSC apoptosis represents a biologically adaptive response to nutrient stress rather than a pathological side effect of caloric deprivation or circadian disruption. Several lines of evidence support this interpretation. First, metabolic cage analyses demonstrated that intermittent fasting mice consumed equivalent total daily calories  as control mice, as they compensated by eating more during feeding windows, thereby ruling out chronic energy deficiency as the underlying cause. Second, the timing of fasting (day versus night) had no impact on HFSC apoptosis, excluding circadian rhythm alterations as a confounding variable. Third, the effect was independent of mTORC1 signalling, the canonical cellular nutrient sensor [1,2].

Instead, fasting-induced HFSC apoptosis arises from a distinct, evolutionarily conserved metabolic adaptation designed to prioritize energy allocation during periods of unstable nutrient supply. Under conditions of nutrient scarcity, the body strategically reallocates resources away from non-essential regenerative processes—such as hair growth—toward vital functions required for survival, such as maintaining cardiac, hepatic, and neurological function. The selective elimination of activated HFSCs during fasting can thus be understood as a programmed trade-off: the organism sacrifices hair regeneration capacity to conserve energy and metabolic substrates for critical organ systems [1,2].

This interpretation is further supported by the observation that fasting enhances stem cell function in other tissues, including intestinal, hematopoietic, and muscle stem cells, which possess robust FAO machinery and higher antioxidant capacity. These stem cell populations thrive under fasting conditions precisely because they are metabolically equipped to efficiently utilize FFAs as an energy source, whereas HFSCs—lacking this metabolic flexibility—are eliminated. Thus, the differential response of stem cell populations to fasting reflects tissue-specific metabolic adaptations rather than a uniform systemic effect [1,2],.

The mechanistic basis of fasting-induced HFSC apoptosis involves a multi-step cascade initiated by adrenal gland activation during nutrient deprivation. Elevated corticosterone and epinephrine levels stimulate lipolysis in dermal adipocytes, triggering the rapid release of free fatty acids into the HFSC niche. Activated HFSCs, lacking the metabolic machinery to efficiently process FFAs, undergo forced engagement of fatty acid oxidation pathways, resulting in mitochondrial overload, excessive ROS production, oxidative damage, and ultimately apoptosis. Critically, this response is independent of caloric restriction, circadian rhythm alterations, or mTORC1 signalling, representing instead a distinct metabolic adaptation that prioritizes energy allocation under nutrient stress. The selective vulnerability of HFSCs, compared to other stem cell populations with higher antioxidant capacity, underscores the tissue-specific nature of fasting’s effects on regeneration.

Human Evidence- Clinical Trials and Translational Relevance

Clinical Trial: 18% Slower Hair Growth in Humans

To test whether fasting affects human hair growth, researchers conducted a randomized clinical trial with 49 healthy adults. Participants were divided into two groups: one practiced 18-hour daily fasting (eating only during a 6-hour window) while the control group ate normally. After just 10 days, the fasting group showed an 18% reduction in hair growth speed  compared to controls [1,22].

This finding confirmed that intermittent fasting does slow human hair growth, though the effect was much milder than what researchers observed in mice. The difference is likely due to several factors: humans have slower metabolism, longer hair growth cycles, and better antioxidant defences in their hair follicle stem cells compared to mice. Scalp biopsies from fasting participants showed some dying hair follicle stem cells, but many survived, explaining why humans experience slowed growth rather than complete hair loss [1].

Dr. Bing Zhang, the study’s lead author, explained: “Mice have a very high metabolic rate compared with humans, so fasting has a more severe effect on mouse hair follicle stem cells. We see a milder effect in humans—there are still some dying stem cells, but many survive. So there is still hair regrowth; it’s just a little bit slower than usual” [34].

Study Limitations and Need for More Research

While this trial provided important evidence, it had several limitations. The study was small (only 49 people), short (just 10 days), and included only healthy young adults. This means we don’t yet know [34,35,36]:

  • How different people respond (older adults, people with health conditions, different ethnicities)
  • What happens with longer-term fasting (months or years)
  • Whether certain fasting schedules are safer for hair than others
  • Who is most at risk for fasting related hair loss

Researchers emphasized the need for larger, longer studies to answer these questions and develop guidelines for safe fasting practices that protect both metabolic health and hair growth.

Real World Observation: Hair Loss During Fasting and Weight Loss

Beyond clinical trials, doctors have observed hair loss in people practicing various forms of fasting and rapid weight loss. Common scenarios include:

  • Ramadan Fasting: During Ramadan, Muslims fast from dawn to sunset for one month. Dermatologists in countries with large Muslim populations report increased cases of telogen effluvium, a temporary form of hair loss during or shortly after Ramadan. This type of hair loss is reversible, with hair typically regrowing once normal eating resumes [37,38,39].
  • Rapid Weight Loss: Studies from the 1970s documented hair loss in patients who lost significant weight quickly (12-25 kg over 2-5 months) through strict dieting. These patients showed increased numbers of hair follicles entering the resting phase, leading to temporary hair shedding [40].
  • Bariatric Surgery: Up to 57% of patients who undergo weight-loss surgery experience temporary hair loss, typically starting 3-6 months after surgery and lasting 6-12 months. While surgery involves additional factors like nutrient malabsorption, the pattern of hair loss is similar to what’s seen with fasting [41].

Clinical Perspective: A Known but Underrecognized Effect

Medical experts note that hair loss during weight loss is common in clinical practice, though the underlying mechanisms weren’t well understood until recently. Dr. Hans Schmidt, a bariatric surgeon, stated: “We frequently see some degree of hair loss in patients during rapid weight loss, regardless of which method they use”. He emphasized that this new research shows the effect is independent of calorie reduction, meaning it’s specifically about fasting patterns, not just eating less [42].

Dr. Jennifer Cheng, an endocrinologist, added: “As intermittent fasting is commonly used for weight loss, we should be aware of potential side effects. More studies in humans are needed to see if the information from mice fully applies to people” [34].

Importantly, experts stress that fasting-related hair loss should not discourage people from intermittent fasting, given its proven metabolic benefits. Dr. Zhang noted: “We don’t want to scare people away from intermittent fasting because it’s associated with many beneficial effects—it’s just important to be aware that it might have some unintended effects [34,42].

Why Some People Are More Affected Than Others

Not everyone who practices intermittent fasting experiences noticeable hair loss. Several factors may explain why some people are more vulnerable [34,35]:

  • Nutritional status: people with existing vitamin or mineral deficiencies (iron, zinc, biotin) may be more susceptible
  • Metabolism: those with faster metabolic rates may experience stronger effects
  • Genetics: individual differences in antioxidant systems and fat metabolism likely play a role
  • Fasting intensity: longer fasting windows and more frequent fasting days increase risk
  • Age and hormones: hormonal changes with age or medical conditions may amplify effects
  • Stress levels: additional physical or emotional stress may worsen the impact

Future Directions

Scientist have outlined several important research priorities [1,34,35]:

  1. Larger, longer studies tracking hair health in diverse populations over months to years
  2. Identifying who is at risk through genetic or metabolic testing
  3. Testing protective strategies like antioxidant supplements or specific nutrients
  4. Finding the optimal fasting schedules that preserves metabolic benefits while protecting hair
  5. Developing topical treatments that protect hair follicles during fasting

Biological Adaptation, Not Flaw- Implications for Health and Longevity

Intermittent fasting (IF) triggers distinct tissue-specific responses that represent evolutionary trade-offs designed to optimize survival during nutrient scarcity. The finding that fasting induces apoptosis in hair follicle stem cells (HFSCs), thereby slowing hair regeneration, has been shown to be an adaptive mechanism, not a biological flaw. Under conditions of metabolic stress, such as fasting or significant caloric reduction, the body strategically allocates available energy and repair resources to vital organs and essential physiological processes. While non-vital functions like hair growth are temporarily suppressed, IF actually enhances the regenerative capacity of somatic stem cells in organs crucial for survival, including the intestine, skeletal muscle, and hematopoietic (blood-forming) systems. For example, fasting boosts intestinal stem cell (ISC) function via increased fatty acid oxidation, improves muscle stem cell renewal capacity, and promotes self-renewal and stress resistance in hematopoietic stem cells, contributing to tissue rejuvenation and longevity. Meanwhile, transient suppression of HFSC activity spares energy and metabolic substrates, which may be rapidly redirected in periods of energy abundance. This tissue-prioritization strategy highlights the sophisticated adaptations underlying fasting responses: metabolic pathways shift to protect essential organs, while reversible hair growth inhibition is a calculated trade-off that favours long-term organismal fitness and resilience. Thus, the impacts of IF on hair follicles should be viewed in the broader context of health optimization and evolutionary biological wisdom, not as a fundamental flaw of fasting regimens [43,44,45,46,47,48].

Counteracting the Effects – Potential Protective Strategies

Experimental Interventions: Blocking Hormonal and Adipocyte-Mediated Pathways

The elucidation of the adrenal-adipocyte-HFSC axis as the central mechanism driving fasting-induced hair loss has opened new avenues for targeted interventions aimed at preserving hair follicle regeneration without compromising the metabolic benefits of intermittent fasting. To establish proof-of-concept for therapeutic protection, Chen and colleagues employed a series of elegant genetic, surgical, and pharmacological interventions in their murine models [1,2].

  • Surgical Adrealectomy- the complete removal of both adrenal glands prior to initiating intermittent fasting regimens completely abolished dermal adipocyte lipolysis and prevented HFSC apoptosis, resulting in normal hair regrowth despite ongoing fasting. This definitive experiment established that adrenal hormone secretion is both necessary and sufficient for fasting-induced HFSC death, identifying the adrenal glands as a potential therapeutic target. However, given the critical systemic roles of glucocorticoids and catecholamines in stress responses, glucose homeostasis, and immune function, complete adrenal suppression is not a viable clinical strategy [2].

More refined approaches focused on selectively blocking adrenal hormone signalling specifically within dermal adipocytes. Adipocyte-specific conditional knockout of the glucocorticoid receptor significantly attenuated fasting-induced lipolysis and reduced HFSC apoptosis, thereby partially rescuing hair regrowth. Similarly, pharmacological beta-adrenergic blockade using propranolol, a non-selective beta-blocker that prevents epinephrine from activating ADRB3 receptors on adipocytes, also mitigated lipolysis and protected HFSCs during fasting. These findings suggest that localized hormonal modulation within the HFSC niche, rather than systemic hormone suppression, may represent a viable strategy for hair protection [2].

Additionally, genetic ablation of adipose triglyceride lipase (ATGL),  the rate-limiting enzyme catalysing the first step of lipolysis—in dermal adipocytes completely prevented fasting-induced FFA release and HFSC apoptosis, demonstrating that blocking adipocyte lipolysis itself is highly protective. While genetic manipulation is not clinically translatable, these experiments validate adipocyte lipolysis as a key therapeutic target and suggest that pharmacological inhibitors of lipolytic enzymes, if developed with tissue-specific delivery mechanisms, could offer hair protection during fasting [1,2].

Antioxidant Strategies: Neutralizing Oxidative Stress in HFSCs

Given that oxidative stress and elevated reactive oxygen species (ROS) are the proximate executors of HFSC apoptosis during fasting, enhancing the antioxidant capacity of HFSCs represents a promising protective strategy. In their study, Chen and colleagues demonstrated that topical application of vitamin E, a potent lipid-soluble antioxidant, twice daily onto the skin of fasted mice significantly improved HFSC survival and partially rescued hair regrowth. Vitamin E neutralizes lipid peroxidation chain reactions initiated by ROS, thereby protecting cellular membranes, mitochondria, and DNA from oxidative damage [49,50].

Importantly, the protective effect of vitamin E was achieved without interfering with the systemic metabolic benefits of fasting, including improved glucose tolerance and insulin sensitivity. This dissociation between metabolic and hair growth outcomes suggests that antioxidant supplementation can selectively protect HFSCs while preserving the health-promoting effects of intermittent fasting [1].

N-acetylcysteine (NAC), a precursor to the endogenous antioxidant glutathione, has also shown considerable promise in protecting hair follicles from oxidative stress-induced damage across multiple contexts. NAC enhances intracellular glutathione synthesis, directly scavenges ROS, inhibits inflammatory pathways (such as NF-κB), and promotes keratinocyte proliferation. In preclinical models, NAC administration has been shown to preserve hair follicle structure, prevent apoptosis, and maintain normal melanin distribution in the setting of chemotherapy-induced alopecia, a condition mechanistically similar to fasting-induced hair loss, as both involve oxidative stress and mitochondrial dysfunction. Clinical trials evaluating NAC supplementation for androgenetic alopecia and lichen planopilaris (a scarring alopecia) have reported significant improvements in hair density, trichoscopic parameters, and reduction of oxidative damage markers [50].

Additional antioxidants with documented benefits for hair health include vitamin C (ascorbic acid), which enhances iron absorption, promotes collagen synthesis, and protects against oxidative damage to hair follicles, and coenzyme Q10 (CoQ10), a mitochondrial antioxidant that supports cellular energy production and reduces oxidative stress. While these antioxidants have not yet been specifically tested in the context of fasting-induced hair loss, their established roles in protecting stem cells and hair follicles from oxidative injury suggest potential efficacy [51].

Micronutrient Supplementation: Addressing Nutritional Vulnerabilities

Emerging evidence suggests that strategic micronutrient supplementation may bolster HFSC resilience during fasting by addressing nutritional deficiencies that exacerbate oxidative stress and impair hair follicle function. Key micronutrients implicated in hair health include [52,53]:

  • Iron : Essential for oxygen transport to hair follicles and cellular energy metabolism. Iron deficiency, particularly low ferritin levels, is strongly associated with telogen effluvium and impaired hair regrowth. Correcting iron deficiency through oral supplementation (150-200 mg elemental iron daily) under medical supervision can restore hair growth over 3-6 months.
  • Zinc : A cofactor for numerous enzymes involved in DNA synthesis, protein synthesis, and antioxidant defense. Zinc deficiency impairs hair follicle proliferation and has been linked to telogen effluvium and alopecia areata. Supplementation with 50 mg zinc gluconate daily for 12 weeks has shown efficacy in clinical trials.
  • Biotin (Vitamin B7): Critical for keratin production, the structural protein of hair. While biotin deficiency is rare, supplementation (3-5 mg daily) may support hair strength and reduce breakage, particularly in individuals with marginal intake or malabsorption.
  • Vitamin D: Plays a role in hair follicle cycling and stem cell differentiation. Low vitamin D levels are associated with telogen effluvium, alopecia areata, and androgenetic alopecia. Supplementation to achieve serum 25-hydroxyvitamin D levels >40 ng/mL may support hair health.
  • Omega-3 Fatty Acids: Support scalp circulation, reduce inflammation, and promote hair follicle health. Found in fish oil, flaxseed, and walnuts, omega-3 supplementation may complement antioxidant strategies.

While micronutrient supplementation alone is unlikely to fully prevent fasting-induced HFSC apoptosis, since the primary mechanism involves FFA-mediated oxidative stress rather than simple nutritional deficiency, optimizing baseline nutritional status may enhance HFSC antioxidant capacity and resilience, thereby reducing vulnerability to fasting-related hair loss.

Topical Treatments: Localized Protection of the HFSC Niche

Topical therapies offer the advantage of delivering protective agents directly to hair follicles while minimizing systemic exposure and side effects. Minoxidil, the most widely used topical agent for hair loss, has been shown to exert unexpected antioxidant and anti-aging effects on hair follicles beyond its canonical role as a potassium channel opener. Long-term topical minoxidil application (5% daily for 4 months) in human scalp tissue xenografted onto mice significantly upregulated key antioxidant enzymes including heme oxygenase-1 (HO-1), peroxiredoxin (PRDX), and glutathione reductase that enhanced mitochondrial function markers (MTCO1, PGC1α, SIRT1), and increased vascular endothelial growth factor A (VEGF-A) expression within hair follicles. These effects collectively improved cellular oxidative stress resistance and hair follicle vitality [54,55].

Given that fasting-induced HFSC apoptosis is driven by oxidative damage and mitochondrial dysfunction, topical minoxidil may offer protective benefits by enhancing the intrinsic antioxidant capacity of HFSCs and improving the metabolic resilience of the hair follicle niche. While this hypothesis remains to be tested in the specific context of fasting, the mechanistic overlap suggests potential utility [54].

Naringenin, a flavonoid with potent antioxidant and anti-inflammatory properties, has demonstrated efficacy in reducing hair loss in murine models when applied topically, either alone or in combination with minoxidil. Naringenin treatment significantly increased total antioxidant capacity in hair follicle tissue, elevated serum VEGF levels, expanded hair follicle diameter, and promoted hair regrowth. Similarly, curcumin-loaded nanoparticles targeting oxidative stress and autophagy pathways in hair follicle cells have shown promise as a novel therapeutic approach for androgenetic alopecia. These findings highlight the potential for developing topical formulations enriched with antioxidants, growth factors, and anti-inflammatory agents specifically designed to protect HFSCs during fasting [56].

Fasting Schedule Modification: Optimizing Duration and Frequency

A critical insight from the Chen et al. study is that HFSC apoptosis exhibits a clear dose-response relationship with fasting duration. Fasting periods of 8 hours produced minimal HFSC death, whereas 16-hour and 24-hour fasts resulted in progressively greater apoptosis. This finding suggests that modifying fasting schedules to reduce daily fasting duration may mitigate hair loss risk while retaining metabolic benefits [1].

Experimental data from the study demonstrated that mice subjected to a 12:12 time restricted feeding regimen (12-hour eating window, 12-hour fasting window) exhibited nearly normal hair regrowth, despite consuming similar total daily calories as mice on more restrictive 16:8 or alternate day fasting protocols. Conversely, more aggressive regimens, such as 20:4 TRF or extended alternate day fasting produced more severe hair growth impairment. These findings indicate that shorter daily fasting windows (<12 hours) may preserve hair health while still providing circadian rhythm alignment and mild metabolic benefits [1].

Alternative intermittent fasting approaches, such as the 5:2 diet, which involves eating normally for five days per week and restricting calories to <500 kcal on two non-consecutive days—may also reduce cumulative fasting stress on HFSCs compared to daily time-restricted feeding. While formal studies evaluating the impact of different fasting schedules on hair growth in humans are lacking, the dose-response relationship observed in mice suggests that individualized fasting protocols tailored to balance metabolic goals with hair health concerns represent a rational strategy [1].

Genetic and Pharmacological Enhancement of Antioxidant Capacity

Beyond exogenous antioxidant supplementation, enhancing the intrinsic antioxidant defence systems of HFSCs through genetic or pharmacological means represents an emerging frontier. In their study, Chen and colleagues demonstrated that genetic upregulation of antioxidant capacity in HFSCs, achieved by overexpressing key antioxidant enzymes such as superoxide dismutase (SOD) or catalase significantly improved HFSC survival during fasting and rescued hair regrowth. While genetic manipulation is not currently clinically feasible, these experiments establish proof-of-principle that bolstering cellular antioxidant defences can counteract fasting-induced oxidative stress [54].

Pharmacological activators of the NRF2 pathway, a master regulator of cellular antioxidant responses represent a promising translational approach. NRF2 activation upregulates expression of downstream antioxidant enzymes, including HO-1, NAD(P)H quinone oxidoreductase 1 (NQO1), glutathione S-transferase, and glutathione peroxidase, thereby enhancing cellular ROS-scavenging capacity. Topical minoxidil has been shown to activate NRF2 downstream targets in human hair follicles, suggesting that NRF2 activators delivered topically or systemically could protect HFSCs during fasting. Several natural NRF2 activators, including sulforaphane (from cruciferous vegetables) and resveratrol, are currently under investigation for their potential to enhance tissue resilience to oxidative stress [54].

Refeeding Strategies and Nutritional Timing

The observation that refeeding rapidly halts adipocyte lipolysis and prevents further HFSC apoptosis suggests that strategic nutritional timing may influence hair health outcomes during intermittent fasting. While chronic intermittent fasting with repetitive activation-apoptosis cycles depletes the HFSC pool over time, periodic refeeding breaks may allow for HFSC recovery and replenishment, thereby reducing cumulative stem cell loss [2].

One potential strategy involves incorporating periodic “hair-protective refeeding windows” such as one week of unrestricted eating every 4-6 weeks during prolonged intermittent fasting regimens to allow HFSC niche recovery. Additionally, optimizing the macronutrient composition of refeeding meals to prioritize protein (for keratin synthesis), antioxidant-rich foods (to neutralize ROS), and essential fatty acids (to support membrane integrity) may enhance HFSC resilience during subsequent fasting periods [1].

Conclusion

Intermittent fasting (IF) is widely recognized for its significant benefits in metabolic health, disease prevention, and longevity, enhancing stem cell function in vital organs such as the intestine, muscle, and blood. However, recent findings highlight an important tissue-specific trade-off: IF can impair hair follicle regeneration by promoting apoptosis of hair follicle stem cells (HFSCs), leading to slower hair regrowth and, with chronic exposure, even hair loss or baldness. This effect is driven by a fasting-induced metabolic cascade that increased lipolysis in skin fat and hormonal changes elevate oxidative stress within the HFSC niche, selectively depleting activated stem cells. Importantly, the hair-related consequences of IF are independent of total calorie intake or circadian rhythm changes, suggesting a unique metabolic vulnerability in hair stem cells.

Evidence from both animal studies and human trials reveals a dose-response relationship: longer fasting durations result in greater impairment of hair growth. While human impact is less severe than in animal models (e.g., an 18% reduction in hair growth speed after 10 days of daily 18-hour fasting), individual susceptibility varies with genetics, nutrition, metabolism, and stress.

Rather than being a biological flaw, fasting-induced hair changes represent an adaptive response, temporarily prioritizing energy and repair resources for essential organs during systemic stress. Strategies to mitigate this side effect include antioxidant supplementation (vitamin E, NAC), targeted micronutrients (iron, zinc, biotin, vitamin D), topical treatments (minoxidil, antioxidant serums), shorter fasting windows, and optimized feeding schedules. Ongoing research is needed to refine these interventions, personalize fasting regimens, and ensure the safe use of IF while maintaining both metabolic and hair health.

In summary, while intermittent fasting offers substantial metabolic advantages, its impact on hair follicle stem cells underscores the importance of understanding tissue-specific responses and developing protective strategies for comprehensive health.

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