The Overlooked Link Between Iron Deficiency and Hair Loss
Iron deficiency is the world’s most prevalent nutritional disorder, yet its role in hair follicle biology remains underrecognized by both patients and general practitioners. While androgenetic alopecia dominates public attention due to its hormonal and genetic origins, iron deficiency represents one of the few reversible contributors to hair thinning—particularly among women.
Hair is a non-essential tissue in survival terms, meaning the body will prioritize iron supply to vital organs like the heart, liver, and brain during times of deficiency. As a result, the scalp is often one of the first places to manifest subclinical micronutrient deficits. For those experiencing diffuse thinning or sudden increases in shedding, especially without clear genetic predisposition, iron deficiency should be a front-line investigation.
This becomes even more critical in women of childbearing age, vegetarians or vegans, patients with gastrointestinal disorders like celiac or IBD, or individuals who have undergone bariatric surgery. All of these populations are at elevated risk for iron deficiency—making targeted intervention both necessary and potentially transformative for hair restoration outcomes.
By understanding how iron directly influences follicular metabolism, clinicians and patients alike can shift from symptom management to root-cause resolution. Let’s explore how iron acts as a biochemical fuel for the scalp’s mini-organ: the hair follicle.
The Role of Iron in Hair Biology
Iron’s significance in the human body extends beyond oxygen transport—it plays a direct regulatory role in follicular stem cell function, DNA replication, mitochondrial activity, and keratinocyte differentiation. In the context of hair, these roles converge to determine whether a follicle thrives, stagnates, or regresses.
Oxygen Transport and Follicle Proliferation
Iron enables the synthesis of hemoglobin, the oxygen-carrying protein within red blood cells. Hair matrix keratinocytes—the rapidly dividing cells at the base of the follicle—require constant, high oxygen delivery to sustain mitotic activity. In iron-deficient states, reduced hemoglobin impairs oxygenation, triggering a shift from the active growth phase (anagen) to the resting phase (telogen), thereby precipitating telogen effluvium.
This starvation of oxygen also impairs the production of ATP within follicular mitochondria, compounding the metabolic slowdown and leading to thinner, weaker hair shafts.
Ferritin Storage and Follicle Resilience
Within the dermal papilla and surrounding follicular sheath, iron is stored in the form of ferritin, a protein complex that buffers the supply during times of systemic shortfall. However, ferritin levels in the hair bulb decrease before serum ferritin drops below clinically anemic thresholds. This is why hair loss can precede any other symptoms of iron deficiency.
When iron stores dip below approximately 30 ng/mL, the body begins reallocating ferritin to core tissues—leaving the follicle depleted, fragile, and prone to miniaturization. This makes serum ferritin a critical biomarker in the diagnostic workup of unexplained alopecia.
Iron as a Cofactor in DNA Synthesis
One of iron’s most underappreciated functions in the hair cycle is its role as a cofactor for ribonucleotide reductase, the rate-limiting enzyme in DNA replication. This is especially important during anagen, when keratinocytes are dividing rapidly to build the hair shaft.
Inadequate iron impairs this enzymatic pathway, halting cell division and follicular regeneration. As Trost et al. (2006) emphasized, without sufficient iron, the follicle’s mitotic machinery grinds to a halt, resulting in follicular dormancy or loss.
Additional Iron-Dependent Enzymatic Functions
Cytochrome P450 enzymes, which contribute to steroid metabolism, are iron-dependent. Disruption here may amplify androgenic sensitivity in predisposed patients, compounding hair loss patterns.
Iron-sulfur clusters, involved in mitochondrial electron transport, are crucial for energy production in the follicular bulb. Mitochondrial dysfunction has been linked to both aging-related and telogen effluvium-type hair loss.
Together, these roles confirm that iron is not just a supportive nutrient, but a core element of the follicle’s operational integrity.
Recognizing Iron Deficiency Hair Loss
Increased Daily Shedding
One of the earliest and most noticeable symptoms of iron-deficiency hair loss is a sudden uptick in daily hair fall. Patients often report strands collecting in the shower drain, accumulating on the pillow, or coming out more easily while brushing. Unlike alopecia areata or male-pattern baldness, this shedding is diffuse and non-scarring. The scalp may not show obvious bald spots in the early stages, which can delay diagnosis. However, if hair fall exceeds 150–200 strands per day consistently, it warrants clinical evaluation.
Noticeable Reduction in Density
Over time, as more follicles shift into the telogen phase and fewer re-enter anagen, the scalp begins to appear less covered—especially under overhead lighting or in photographs. This reduction in density typically presents across the top of the scalp, along the part line, and around the temples. The hair becomes thinner as a whole, giving a “see-through” appearance rather than sharply demarcated balding zones. The change may be subtle at first but can progress significantly if left unaddressed.
Altered Hair Quality
Iron deficiency doesn’t just affect the quantity of hair—it impacts quality as well. Individual strands often become more fragile, coarse, and brittle. Hair loses its natural luster and elasticity due to impaired keratin synthesis, as the follicles struggle to produce structurally sound shafts without adequate nutrients. Split ends and breakage become more frequent, and even normal styling or brushing can result in visible damage. In many cases, patients report their hair feels limp or “lifeless,” which often accompanies slower growth.
Delayed Regrowth After Shedding
In a healthy hair cycle, telogen hairs are replaced by new anagen-phase growth within 1–2 months. In iron-deficient individuals, however, that regrowth window is significantly delayed. The scalp may remain sparse even after shedding subsides, and any regrowth that does occur may be finer, shorter, or lighter than before. This is due to the follicles’ impaired ability to re-enter the active growth phase without sufficient iron reserves to support cell division and matrix development.
Accompanying Systemic Symptoms
Unlike purely hormonal or genetic hair loss, iron-deficiency-related alopecia frequently coexists with broader systemic symptoms. Fatigue, low energy, poor concentration, and shortness of breath are common. Patients may also complain of feeling cold more often or experiencing irritability and dizziness. On physical exam, classic signs of prolonged depletion may include pallor of the skin or lower eyelids, glossitis (a smooth, inflamed tongue), angular cheilitis (cracks at the corners of the mouth), and koilonychia (spoon-shaped nails). These findings often precede overt hair loss and serve as valuable diagnostic clues.
Diagnostic Implications
When patients present with any combination of these symptoms—particularly diffuse shedding without clear patterning—ferritin testing should be prioritized. Normal hemoglobin levels do not rule out iron-related hair loss. Ferritin values below 30 ng/mL are highly suggestive of telogen effluvium, and in many cases, a threshold of 70–100 ng/mL is necessary to support robust follicular activity. Identifying and correcting low iron stores early can prevent long-term miniaturization and make full recovery far more achievable.
Why Women Are More Vulnerable to Iron-Related Hair Loss
Iron deficiency disproportionately affects women—especially during the years of menstruation, pregnancy, and postpartum recovery. Unlike men, whose iron demands remain relatively constant after adolescence, women face cyclical and episodic iron loss that places their hair follicles at greater risk.
Key Contributing Factors:
1. Menstrual Blood Loss
On average, women lose 30–40 mL of blood during each menstrual cycle, equating to a loss of approximately 15–20 mg of iron monthly. However, in cases of menorrhagia (heavy menstrual bleeding), iron losses may exceed 80 mg per cycle—far surpassing the typical dietary intake of 10–20 mg per day.
Over time, this cumulative loss depletes iron stores, even in women with otherwise normal hemoglobin. It’s often the first unrecognized cause of hair thinning in young women.
2. Pregnancy and Lactation
Iron requirements double during pregnancy, reaching 27 mg/day to support fetal development, placenta formation, and increased maternal blood volume. If this demand isn’t met with supplementation, maternal ferritin levels drop rapidly, leading to both anemia and postpartum hair loss that may extend far beyond the typical telogen effluvium window.
Breastfeeding mothers also lose iron through milk secretion and prolonged amenorrhea, which may mask symptoms until fatigue or hair changes become apparent.
3. Dietary Preferences and Deficiencies
Many women restrict red meat—often the richest source of heme iron, which is absorbed 2–3x more efficiently than non-heme iron found in plants. Vegetarian and vegan diets, while ethically and environmentally popular, often lack the iron density and absorption efficacy needed for follicular health.
Common dietary inhibitors such as calcium, phytates (in grains and legumes), and polyphenols (in tea and coffee) can further reduce iron uptake by up to 60% when consumed around meals.
4. Underdiagnosis and Misattribution
Hair loss in women is frequently dismissed as cosmetic, hormonal, or age-related. Yet studies show that up to 20% of premenopausal women are iron-deficient without overt anemia (American Society of Hematology, 2017). Many don’t receive proper ferritin testing until advanced hair loss prompts dermatological referral.
Why Standard Blood Tests Aren’t Enough: Lab Work for Hair Loss Evaluation
When evaluating hair loss, many primary care physicians rely solely on hemoglobin or hematocrit levels. While useful in diagnosing anemia, these values often remain normal even in the presence of severe iron depletion. This is especially problematic in telogen effluvium, where hair shedding can be an early or isolated symptom of low iron.
To determine if iron deficiency is compromising follicular activity, a comprehensive iron panel must be ordered. This deeper analysis helps differentiate between absolute iron deficiency (true depletion) and functional deficiency (impaired availability).
Serum Ferritin
Ferritin is the single most informative biomarker of iron storage, mirroring tissue reserves—including those that feed the scalp. Values below 30 ng/mL correlate strongly with chronic telogen effluvium, while readings under 15 ng/mL confirm iron-deficiency anemia. For optimal hair regrowth, many dermatologists target 70 – 100 ng/mL, particularly in women with diffuse shedding (Rushton et al., 2002).
Serum Iron
This test quantifies circulating iron bound to transferrin. Levels fluctuate throughout the day and can swing after meals, so morning, fasting samples provide the most reliable snapshot of immediate iron availability.
Total Iron-Binding Capacity (TIBC)
TIBC gauges how much transferrin is available to bind iron. When iron stores fall, the liver increases transferrin production and TIBC rises—often serving as an early biochemical clue to depletion before anemia appears.
Transferrin Saturation
Calculated from serum iron and TIBC, transferrin saturation shows the percentage of transferrin actually carrying iron. Values below 20 % indicate early deficiency, and levels under 15 % are common in anemia driven by chronic disease or systemic inflammation.
Complete Blood Count (CBC) with Hemoglobin and Hematocrit
A full CBC rules out overt anemia and reveals red-cell morphology. Microcytic, hypochromic erythrocytes (small, pale red cells) point to longstanding iron deficit and help distinguish it from other causes of hair shedding.
C-Reactive Protein (CRP) or Erythrocyte Sedimentation Rate (ESR)
These inflammatory markers identify hidden systemic inflammation. Because ferritin is an acute-phase reactant, inflammation can falsely elevate ferritin readings and mask true iron deficiency—making CRP or ESR essential when the clinical picture and labs don’t align.
Optional Add-Ons:
Reticulocyte hemoglobin content (CHr) for early functional iron deficiency
Soluble transferrin receptor (sTfR) to differentiate anemia of inflammation vs. iron deficiency
Correcting the Deficiency: Iron Supplementation Strategies That Work
Once iron deficiency is confirmed—especially in the context of hair loss—treatment should address both the underlying cause and the most effective replenishment strategy. Iron repletion is not a one-size-fits-all protocol; it must be adapted based on individual tolerance, absorption capacity, and severity of depletion.
Oral Iron Therapy
For most patients, iron repletion begins with oral tablets because they are inexpensive, widely available, and effective when taken correctly. The three standard preparations are ferrous sulfate, which provides about 65 mg elemental iron per 325 mg tablet; ferrous gluconate, which delivers roughly 35 mg elemental iron per 325 mg tablet; and ferrous fumarate, which contains about 106 mg elemental iron per 325 mg tablet. Each of these salts can restore ferritin if taken consistently over several months and adjusted to the individual’s tolerance.
Dosing and Absorption
A typical regimen starts with one tablet per day and, if gastrointestinal comfort allows, progresses to twice-daily dosing. Because iron competes with many dietary constituents, clinicians advise taking tablets on an empty stomach and pairing them with 250–500 mg of vitamin C—orange juice works well—to enhance absorption. Patients should avoid swallowing iron within two hours of calcium supplements, dairy products, tea, coffee, or high-fiber meals, since these bind or block iron in the gut. Common side-effects include transient nausea, constipation, dark stools, and abdominal cramping; most people can mitigate these by switching among iron salts, spacing doses, or using a gentle laxative.
Advanced Oral Options
When standard ferrous salts prove too irritating—or when adherence falters because of GI distress—newer formulations offer a useful alternative. Polysaccharide-iron complexes contain non-ionic iron that releases slowly and causes fewer gastric symptoms. Liposomal iron encloses the mineral in a phospholipid membrane, allowing it to pass through the intestinal lining with minimal contact and irritation. Heme iron polypeptide, derived from animal sources, enters enterocytes via a different pathway and is highly bioavailable without generating the oxidative stress associated with free ferrous ions. Although these preparations cost more than traditional salts, their superior tolerability often translates to better long-term compliance and faster recovery.
Intravenous Iron Infusions
If oral therapy fails—because of severe deficiency, malabsorption, inflammatory bowel disease, prior bariatric surgery, or simply lack of time to replete stores—intravenous (IV) iron becomes the treatment of choice. Formulations such as ferric carboxymaltose (Injectafer®), iron sucrose (Venofer®), and iron dextran (INFeD®) deliver large doses directly into the bloodstream, bypassing the gastrointestinal tract entirely. IV iron replenishes ferritin rapidly, often in one or two sessions, and eliminates the nausea or constipation many patients experience with tablets. Because infusions carry a small risk of hypersensitivity or hypotension, they must be administered in a monitored medical setting.
Duration and Monitoring
In the context of hair loss, clinicians usually plan three to six months of iron therapy, whether oral or intravenous, to rebuild scalp and systemic stores. Ferritin and hemoglobin should be re-checked every eight to twelve weeks; an increase in ferritin of at least 20 ng/mL within the first month indicates that therapy is on track. Even after laboratory normalization, treatment continues for roughly three additional months to saturate tissue reserves and support follicular recovery. Stopping early invites relapse and a return of shedding. Patients should also remember that cosmetic improvement lags behind biochemical correction: shedding often subsides by weeks 6–8, yet visible regrowth may not appear until months 3–6 because hair follicles must complete an entire growth cycle before new density becomes evident.
Rebuilding from the Inside: Iron-Rich Diet and Nutrient Absorption
While iron supplements play a crucial role in correcting deficiencies, long-term success in preventing hair loss relies heavily on daily nutrition. The human body regulates iron absorption based on current demand, which means that after repletion, maintaining adequate intake through food becomes essential. For hair follicles—one of the most metabolically active tissues—consistent access to bioavailable iron supports ongoing cell turnover and prevents future shedding episodes.
Heme vs. Non-Heme Iron in the Diet
Dietary iron is classified into two forms: heme and non-heme. Heme iron, found in animal-based foods, is more readily absorbed, with a typical uptake rate of 15–35%. Non-heme iron, present in plant sources, is less bioavailable, with absorption rates ranging from 2–20% depending on other factors in the digestive tract. For individuals susceptible to hair loss, prioritizing heme-rich foods is especially beneficial.
Top Iron-Rich Foods for Hair Health
- Red meat (beef, lamb, bison)
- Organ meats (liver, kidney)
- Shellfish (clams, oysters, mussels)
- Poultry (especially dark meat)
- Lentils and chickpeas
- Tofu and tempeh (preferably fermented)
- Dark leafy greens (spinach, kale, swiss chard)
- Iron-fortified cereals, breads, and oats
- Pumpkin seeds, hemp seeds, quinoa
- Dried fruits (apricots, raisins, prunes)
These options include both heme and non-heme sources, making them valuable whether you eat animal products or follow a plant-based diet. When paired strategically, even non-heme sources can make a meaningful contribution to ferritin restoration.
Nutrient Synergy for Enhanced Absorption
The body’s ability to absorb iron from food is not just about what you eat, but how you combine it. Vitamin C is the most powerful enhancer of non-heme iron absorption. It chemically reduces iron to a form that is more easily absorbed in the small intestine. Smart pairings—such as lentils with lemon juice, spinach with strawberries, or tofu stir-fried with bell peppers—can significantly improve iron bioavailability.
Beta-carotene-rich foods like carrots, sweet potatoes, and squash may also help increase iron uptake, possibly by modifying intestinal pH or through direct synergy in the absorption pathways.
Foods and Substances That Inhibit Iron Absorption
Several common dietary components can block iron absorption if consumed simultaneously with iron-rich meals. Calcium competes directly with iron at absorption sites, which is why dairy products or calcium supplements should be spaced at least 1–2 hours away from meals that contain iron. Tannins found in tea and coffee are potent inhibitors of non-heme iron uptake, reducing absorption by up to 60%. Similarly, phytates in whole grains, legumes, and nuts bind iron in the gut and make it unavailable. Fortunately, phytate impact can be mitigated by traditional food prep methods such as soaking, sprouting, or fermenting.
The Role of Cookware in Iron Intake
Even the tools used in cooking can influence iron status. Preparing food in cast iron cookware can subtly increase the iron content of acidic or moist dishes—particularly tomato-based sauces or stews—by up to 2–3 mg per serving. While not a standalone solution, this technique can complement broader dietary strategies for iron maintenance.
What to Expect: The Timeline of Hair Recovery After Iron Repletion
Correcting iron deficiency is the first and most crucial step toward resolving iron-related hair loss—but it’s only the beginning. Hair follicles follow their own biological timeline. Even after ferritin levels rise and systemic symptoms begin to improve, the visible signs of hair regrowth may take several months to appear. This lag is normal and reflects the complex nature of hair cycling, which requires synchronization of cellular repair, matrix regeneration, and follicular reactivation.
Weeks 0 to 4
In the earliest weeks of treatment, patients typically notice systemic improvements first. Fatigue often begins to resolve, skin tone appears healthier, and general energy levels improve. Internally, serum ferritin levels begin to rise, but no visible changes in hair are expected at this stage. The follicles are still metabolically adjusting and preparing to re-enter the growth phase.
Weeks 4 to 8
Around the second month, many patients observe a reduction in daily shedding. The clumps of hair once found in brushes, drains, or on the pillow begin to decline in frequency and volume. Some early thickening may be felt at the scalp surface, particularly in areas that were diffusely thinned. Improved follicular oxygenation and nutrient delivery support this transition, though visible regrowth is still minimal.
Months 3 to 6
This phase typically marks the beginning of noticeable cosmetic change. Fine, baby-like hairs begin to emerge, especially around the temples, hairline, or central part line. These early regrowth strands may be thinner or lighter in color than the rest of the hair. With continued treatment, the keratinocytes become more productive, leading to shinier, stronger shafts. Texture improves, and volume slowly returns to areas of prior loss.
Months 6 to 12
Most patients reach near-complete recovery of their baseline density by this stage—assuming there are no coexisting causes of hair loss. Hair texture becomes more consistent with the rest of the scalp, elasticity improves, and regrown hairs begin to blend seamlessly with existing strands. In cases where miniaturization had begun to set in, some degree of reversal may be observed as follicles recover from prolonged metabolic starvation.
Important Clinical Note
Hair regrowth always trails behind biochemical correction. Even with optimal compliance, ferritin restoration precedes follicular renewal. It’s also important to maintain iron intake during and after recovery to prevent rebound deficiency. Patients who interrupt supplementation too soon, return to iron-poor eating patterns, or experience continued blood loss (e.g., heavy menstruation) may restart the cycle and experience a second wave of shedding.
When Iron Isn’t the Only Issue
While iron deficiency is a common and correctable cause of hair loss, it is not always the sole factor at play. Some patients normalize their ferritin levels yet experience incomplete regrowth—or find that shedding returns within months. When hair volume fails to recover after six months of optimized iron therapy, clinicians must consider coexisting or overlapping contributors that could be impairing follicular performance.
Androgenetic Alopecia (AGA)
One of the most common confounding factors is androgenetic alopecia, or pattern hair loss. This condition is hormonally driven and presents with recession at the temples, crown thinning, or overall miniaturization of the follicular units. AGA may worsen during iron deficiency due to added metabolic stress, but it does not resolve with iron correction alone. Patients with both iron deficiency and AGA often require additional therapies such as topical minoxidil or oral finasteride to stabilize and reverse follicular shrinkage.
Chronic Inflammatory or Autoimmune Conditions
Systemic inflammation also plays a major role in persistent hair thinning. Autoimmune diseases such as lupus, rheumatoid arthritis, and Hashimoto’s thyroiditis not only disrupt iron metabolism but also directly damage follicles through immune-mediated attack. These conditions can manifest as patchy loss (alopecia areata), diffuse shedding, or even permanent scarring alopecia if inflammation reaches the follicular stem cells. Moreover, chronic inflammation can impair iron absorption and utilization by altering hepcidin regulation and suppressing erythropoiesis, even when dietary intake is sufficient.
Nutrient Synergy and Micronutrient Gaps
Hair follicles do not rely on iron alone. Regrowth requires a highly coordinated supply of vitamins, minerals, amino acids, and coenzymes. Zinc is essential for DNA synthesis and immune function; biotin supports keratin infrastructure; vitamin D influences follicle cycling and dermal stem cell behavior. Protein, including specific amino acids like cysteine and methionine, forms the structural matrix of hair, while vitamin B12 and folate are indispensable for red blood cell production and cellular energy metabolism.
Even mild deficiencies in any of these nutrients—especially when undetected—can blunt the regenerative response, slowing down or halting recovery despite normalized ferritin levels. This is particularly true in patients who follow restrictive diets, suffer from gastrointestinal malabsorption, or have increased nutrient demands due to stress or hormonal imbalances.
In such cases, a comprehensive nutritional assessment and scalp-focused examination are necessary. Identifying and correcting these secondary obstacles is often the key to completing the hair restoration process once iron has laid the foundation.
Medical and Surgical Interventions for Resistant Hair Loss After Iron Repletion
For many patients, correcting iron deficiency results in a clear reduction in hair shedding and a gradual return of scalp coverage. However, when hair volume fails to recover despite optimal ferritin levels and improved nutrient status, clinicians must consider that the underlying hair loss is multifactorial. In these cases, advanced therapeutic approaches may be needed to stimulate regrowth, restore density, or permanently replace lost follicles.
Topical Minoxidil
Minoxidil remains a foundational therapy for both male and female pattern hair loss, but it also serves a vital role in patients who don’t fully respond to nutritional correction. As a vasodilator, minoxidil prolongs the anagen (growth) phase of the hair cycle, increases blood flow and angiogenesis around the follicle, and enhances follicular size and shaft diameter. Its effectiveness extends to individuals with telogen effluvium triggered by iron deficiency, especially when residual thinning persists in high-stress areas like the temples or crown. The 5% concentration, available as a foam or solution, is typically applied once or twice daily and has been shown to improve both density and overall texture in responsive patients.
Low-Level Laser Therapy (LLLT)
LLLT is a non-invasive modality that uses red or near-infrared light—typically in the 630 to 670 nanometer range—to stimulate follicular mitochondria. Devices like the DHRC LaserCap employ photobiomodulation to trigger ATP production, reawaken dormant follicles, and extend the active growth phase. This therapy is particularly valuable for patients recovering from telogen effluvium or those unable to tolerate pharmacological interventions. Clinical studies support its efficacy in both male and female subjects, with consistent use improving hair thickness, strength, and scalp circulation over time.
Hair Transplantation
In patients whose follicles have undergone irreversible miniaturization—often due to long-standing iron depletion compounded by genetic predisposition—surgical intervention becomes the most effective and permanent solution. Hair transplantation offers two primary techniques: Follicular Unit Extraction (FUE), which involves the removal of individual grafts for direct re-implantation, and Follicular Unit Transplantation (FUT), which harvests a linear strip of scalp tissue and extracts units from it for redistribution. While FUE is less invasive and leaves no linear scar, FUT often yields a higher number of grafts and is ideal for cases requiring extensive restoration.
Regardless of technique, surgical outcomes are substantially better when patients enter the procedure with stabilized nutritional and hormonal profiles. Restoring iron levels in advance improves vascular support to the graft site, enhances healing, and increases graft survival rates. For this reason, hair transplantation should only be considered after comprehensive medical optimization—including ferritin repletion, vitamin correction, and control of any inflammatory or autoimmune contributors.
Conclusion: Don’t Let a Fixable Problem Steal Your Hair
Iron deficiency remains one of the most underestimated yet highly reversible causes of hair loss. Its clinical presentation often mimics other types of alopecia, leading to misdiagnosis or delay in treatment. But unlike genetic hair loss, iron-related shedding responds dramatically to targeted intervention—if addressed early and managed thoroughly.
Through proper lab testing, evidence-based supplementation, and long-term dietary optimization, most individuals can regain not just their hair, but their confidence. However, for those who have experienced prolonged deficiency or overlapping causes such as androgenetic alopecia, advanced solutions may be necessary to fully restore scalp density and hair quality.
At DiStefano Hair Restoration Center, we combine medical expertise with cutting-edge technology to diagnose and treat complex hair loss cases—including those rooted in nutrient deficiency. Whether you need custom supplementation, clinical therapies, or surgical restoration, our team is here to guide you toward lasting results grounded in science—not speculation.
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References
Trost LB, Bergfeld WF, Calogeras E. The diagnosis and treatment of iron deficiency and its potential relationship to hair loss. J Am Acad Dermatol. 2006;54(5):824–844.
Rushton DH, Ramsay ID, James KC, Norris MJ, Gilkes JJH. Biochemical and trichological characterization of diffuse alopecia in women. Br J Dermatol. 2002;147(5):982–990.
American Society of Hematology. Iron Deficiency Facts. Accessed 2023.
World Health Organization. Iron deficiency anemia: assessment, prevention, and control. A guide for programme managers. Geneva: WHO; 2001.
