My most recent episode of Diabetics for Diabetics Radio was centered around the growth hormones testosterone, insulin-like growth factor 1 (IGF-1) and human growth hormone (HGH). I covered each hormone, what it does and where it comes from and how it could potentially impact beta cell health. We also talked about natural ways to influence growth hormone levels to potentially put beta cells in a better position to regeneration and thrive.
In my sharing and promoting the episode on TikTok, some viewer questions filtered through that really got me thinking. One of them was related to polycystic ovarian syndrome (PCOS). In the particular TikTok video I had talked about the role of testosterone (or the lack thereof) in altering iron metabolism in people with T1D. Testosterone works opposite the iron regulatory protein hepcidin in controlling iron's retention intracellularly and its circulation to be used for growth and development. This in turn shapes insulin signaling in developing bodies. A follower of mine questioned how testosterone levels and their effect on iron and insulin might influence PCOS.
I am only vaguely familiar with PCOS, a condition that leads to the accumulation of fluid-filled cysts in women's ovaries, so I didn't have much to offer. PCOS impacts hormonal balance, fertility and metabolic efficiency, but I couldn't tell you more than that. While it has ties to insulin resistance, and thus seems to align with our observations on testosterone, how might testosterone imbalances impact women differently than men?
So here we are: Exploring the intricacies of altered iron utilization, insulin signaling, testosterone levels and the gender-specificity of how these variables impact our metabolisms.
First, let's start with PCOS.
PCOS and Excess Testosterone Leading to Excess Circulating Iron
A. Hyperandrogenism and Low Hepcidin
High Testosterone → Suppressed Hepcidin
Similar to men with high androgens, women with PCOS often exhibit lower hepcidin and relatively increased iron availability.
Studies have shown that some women with PCOS have elevated ferritin, which can indicate higher iron stores, though ferritin can also be an acute-phase reactant in inflammation.
DHEA-S Overproduction (Adrenal PCOS)
Some women with PCOS have high DHEA-S instead of high testosterone.
DHEA-S is an adrenal androgen, and excess amounts indicate chronic stress or HPA-axis dysfunction.
Insulin Resistance Factor
Many women with PCOS have insulin resistance, which itself can lower hepcidin production, further increasing intestinal iron absorption and raising serum iron levels.
This insulin resistance may be the result of alternative sources of inflammation (nutrient deficiencies, environmental toxins etc.)
This interplay of insulin, androgens, and iron can create a feedback loop that exacerbates PCOS pathophysiology.
Traditional knowledge would tell you that testosterone increases insulin sensitivity. How could having too much lead to insulin resistance? Is there something women are doing differently than men?
It lies in the female body's ability to use that testosterone, its downstream impacts on estrogen production, iron accumulation, nutrient imbalances and those variables' effects on inflammatory responses.
My first question was: What are women missing that prevents them from properly converting testosterone to estrogen?
Factors That Negatively Impact Aromatase Activity in Women (and May Contribute to PCOS & High Testosterone)
Aromatase is the enzyme responsible for converting testosterone into estrogen. If aromatase activity is too low, testosterone levels can become elevated, leading to hormonal imbalances, symptoms of PCOS, and fertility issues.
1. Nutrient Deficiencies That Inhibit Aromatase Activity
A. Zinc Deficiency
🔻 Why it’s important:
Zinc is needed for hormonal balance, but too much zinc can inhibit aromatase activity, lowering estrogen production.
Zinc also plays a role in insulin regulation, which affects androgen balance in PCOS.
🔹 Sources: Oysters, pumpkin seeds, beef, lentils
B. Magnesium Deficiency
🔻 Why it’s important:
Magnesium regulates insulin, and insulin resistance is a key driver of PCOS.
Low magnesium can increase testosterone production while lowering estrogen conversion.
🔹 Sources: Dark leafy greens, avocado, nuts, cacao
C. Vitamin D Deficiency
🔻 Why it’s important:
Vitamin D activates aromatase, increasing estrogen levels.
Many women with PCOS have low vitamin D, which is linked to higher androgens and insulin resistance.
🔹 Sources: Sunlight, fatty fish, cod liver oil, supplementation with D3/K2
D. Boron Deficiency
🔻 Why it’s important:
Boron boosts aromatase activity and increases estrogen production.
It also helps reduce excess androgens.
🔹 Sources: Apples, avocados, raisins, nuts
2. Chronic Inflammation & High Cortisol Levels
Inflammation and high stress hormones (cortisol) suppress aromatase activity, leading to low estrogen and high testosterone.
A. Chronic Inflammation Lowers Estrogen
Inflammatory cytokines (TNF-alpha, IL-6) interfere with aromatase function.
Gut dysbiosis, leaky gut, or chronic infections increase systemic inflammation, worsening hormone imbalances.
🔹 Fix It With:
Omega-3 fatty acids (salmon, flaxseeds) to reduce inflammation.
Curcumin & resveratrol as natural anti-inflammatories.
Gut health support: Prebiotic fiber, fermented foods, and probiotics.
B. High Cortisol Suppresses Aromatase
🔻 Why it’s important:
Chronic stress increases cortisol, which lowers aromatase activity and estrogen production.
High cortisol also triggers insulin resistance, making hormonal imbalances worse.
🔹 How to Lower Cortisol Naturally:
✅ Prioritize deep sleep (melatonin helps).
✅ Reduce over-exercising (chronic cardio worsens cortisol).
✅ Ashwagandha & Rhodiola help modulate stress response.
3. Toxin Exposure That Lowers Aromatase
Environmental toxins known as endocrine disruptors can block aromatase activity and interfere with hormone balance.
A. Plastics & BPA Exposure
Bisphenol A (BPA) and phthalates found in plastics mimic estrogen but block aromatase activity.
🔹 Solutions:
✅ Use glass or stainless steel instead of plastic.
✅ Avoid canned foods (BPA linings).
✅ Switch to non-toxic skincare (no parabens, sulfates).
B. Pesticides & Heavy Metals
Glyphosate (found in non-organic produce) is linked to hormonal imbalances and aromatase inhibition.
Heavy metals (lead, mercury, cadmium) interfere with estrogen metabolism.
🔹 Solutions:
✅ Eat organic produce when possible.
✅ Support liver detoxification (cruciferous vegetables, NAC, glutathione).
There is this whirlwind of inflammatory factors disarming aromatase's ability to create estrogen from testosterone. This excess testosterone is furthering the imbalances being experienced by altering the body's iron balance, encouraging additional inflammation and taxing our body's recovery mechanisms.
One thing that comes to my mind as I put this together is the order of operations or timeline of this development in the body. Is there a tripwire in all this that creates this inflammatory inertia? It's clear that a lack of aromatase puts the body in a high testosterone state that promotes iron overload, but is there a single factor that is disarming the aromatase?
Maybe? But probably not. Let's think about mineral deficiencies.
Mg/Zn/B/Vit. D deficiency -> Decreased aromatase -> High Testosterone -> Iron overload -> More inflammation
And with more inflammation comes a greater strain on the nutrients we're taking in, furthering the deficiencies and imbalances that started the sequence in the first place.
But in truth, any source of inflammation could initiate this feedback loop. Whether it be stress, toxins or nutrients:
Stress/Toxins/Nutrients -> No aromatase -> High testosterone -> Iron overload -> Inflammation -> More Stress/Greater Demand for Nutrients/Greater Vulnerability to Toxins
And so the loop continues.
With this iron imbalance and handicapped estrogen conversion in the back of our minds, what about insulin resistance? PCOS is commonly marketed as a byproduct of hyperinsulinemia resulting from the body's loss of insulin sensitivity. With what we know about the relationship between testosterone, tissue building and insulin use (more Test, better sensitivity) you might think this to be counterintuitive. But think about what it took to arrive at this elevated testosterone level, namely the loss of estrogen.
The Normal Role of Estrogen in Women's Metabolism & Insulin Sensitivity
Estrogen is not just a reproductive hormone; it plays a central role in energy metabolism and insulin signaling. Here's how:
A. Estrogen Enhances Insulin Sensitivity
Estrogen (especially estradiol, E2) increases insulin receptor expression on cells, making them more responsive to insulin.
It helps regulate glucose uptake in muscles, liver, and fat cells, preventing excess sugar from circulating in the blood.
Estrogen improves the function of GLUT4 (glucose transporter protein), which allows glucose to enter cells efficiently.
B. Estrogen Reduces Fat Storage Around Organs
Estrogen promotes subcutaneous fat storage (hips, thighs, and breasts), which is metabolically protective.
When estrogen is low, women are more likely to store visceral fat (belly fat), which is associated with insulin resistance.
C. Estrogen Reduces Inflammation & Oxidative Stress
Estrogen has anti-inflammatory effects and reduces oxidative stress, both of which improve insulin sensitivity.
Chronic inflammation is a major driver of insulin resistance in PCOS.
D. Estrogen Protects Against Lipotoxicity
Lipotoxicity (fat buildup in organs like the liver and pancreas) contributes to metabolic syndrome.
Estrogen helps prevent fat accumulation in the liver, reducing the risk of non-alcoholic fatty liver disease (NAFLD), which is common in insulin-resistant PCOS.
Women naturally have lower testosterone levels than men, so when it becomes excessively high, it overwhelms estrogen’s metabolic benefits. In a state of testosterone dominance in the female body, testosterone interferes with estrogen's insulin signaling.
And no matter where you start in this cascade of inflammatory responses, each ensuing reaction furthers the imbalances being experienced elsewhere. All roads seem to lead to inflammation. All roads from inflammation seem to deplete specific resources that stand to create another inflammatory response. Insulin resistance is the inevitable result.
Once insulin resistance takes hold, it creates widespread metabolic dysfunction in women:
Chronic Hyperinsulinemia (High Insulin Levels)
The pancreas overproduces insulin to compensate for resistance.
High insulin triggers even more testosterone production from the ovaries.
Increased Blood Sugar & Type 2 Diabetes Risk
Glucose uptake is impaired, leading to high blood sugar (hyperglycemia).
Over time, this exhausts beta cells in the pancreas, increasing the risk of type 1 & type 2 diabetes.
Fatty Liver Disease (NAFLD)
Insulin resistance increases fat accumulation in the liver.
Many women with PCOS develop non-alcoholic fatty liver disease (NAFLD), further impairing metabolism.
Chronic Low-Grade Inflammation
High insulin and androgens stimulate pro-inflammatory cytokines (TNF-alpha, IL-6).
This worsens metabolic dysfunction and perpetuates insulin resistance.
Increased Cortisol & Stress Response
PCOS women often have higher cortisol levels, which also contributes to insulin resistance and weight gain.
Chronic stress worsens inflammation and makes hormone balance even more difficult.
So what can we do about it?
How to Restore Hormonal Balance & Improve Insulin Sensitivity in PCOS
Since excess testosterone is directly linked to insulin resistance, improving insulin sensitivity can lower androgens and restore estrogen balance. Here’s how:
A. Regulate Blood Sugar & Insulin
✅ Myo-Inositol & D-Chiro-Inositol: Improve ovarian insulin sensitivity and lower androgens.
✅ Berberine: Reduces insulin resistance as effectively as metformin.
✅ Strength Training & Walking After Meals: Increases GLUT4 activation for glucose uptake.
B. Support Estrogen Metabolism
✅ Cruciferous Vegetables (Broccoli, Kale, Cauliflower): Support estrogen metabolism and detoxification.
✅ Flaxseeds & Spearmint Tea: Naturally help balance androgens.
✅ Magnesium & Zinc: Support aromatase function to convert testosterone into estrogen.
C. Reduce Inflammation
✅ Omega-3s (DHA & EPA): Reduce systemic inflammation and support insulin sensitivity.
✅ Curcumin & Resveratrol: Lower inflammatory cytokines linked to insulin resistance.
✅ Adequate Sleep & Stress Management: Lowers cortisol, which worsens insulin resistance.
A key for me in understanding the testosterone/estrogen/insulin balancing act is the difference between the sexes. I was coming into the topic of PCOS with a male-centric view of testosterone. But as nature continues to demonstrate, there is nuance and context everywhere you look.
Testosterone plays a key role in metabolism, but its effects on insulin sensitivity are vastly different between males and females due to hormonal balance, fat distribution, and receptor sensitivity.
In men, testosterone is generally insulin-sensitizing and helps with muscle glucose uptake and fat metabolism.
In women, while testosterone (in much smaller quantities) increases lean muscle mass, libido, cognitive function and energy, excess testosterone (as seen in PCOS) is linked to insulin resistance, inflammation, and metabolic dysfunction.
So, why does testosterone improve insulin sensitivity in men but impair it in women with PCOS? Let's break it down.
Differences in Hormonal Balance: The Estrogen-Testosterone Ratio
The key difference between men and women is how testosterone interacts with estrogen and other hormones.
A. Men: Balanced Testosterone to Estrogen Ratio Enhances Insulin Sensitivity
Men naturally have more testosterone and lower estrogen.
Testosterone in men improves insulin sensitivity by:
✅ Increasing muscle mass, which enhances glucose uptake.
✅ Stimulating GLUT4 transporters, which improve cellular glucose uptake.
✅ Reducing visceral fat, which lowers systemic inflammation.
In men, a small amount of testosterone converts to estrogen via aromatase, maintaining balance.
❌ Estrogen dominance in men leads to excess body fat (chest + belly), loss of muscle mass and decreased libido/erectile dysfunction.
B. Women: High Testosterone & Low Estrogen Promote Insulin Resistance
In women with PCOS, testosterone is too high, and estrogen conversion is impaired.
Since estrogen normally improves insulin sensitivity, low estrogen levels worsen metabolic health.
High testosterone in women:
❌ Increases visceral fat, which promotes insulin resistance.
❌ Reduces SHBG (Sex Hormone Binding Globulin), leaving more “free” testosterone circulating.
❌ Disrupts insulin signaling pathways, leading to higher blood sugar and higher insulin levels.
Women’s glucose metabolism is more dependent on estrogen, so when testosterone dominates, metabolic function declines.
Testosterone's Effect on Muscle & Fat in Men vs. Women
Testosterone has different effects on muscle and fat distribution in men and women.
A. In Men: Testosterone Increases Lean Muscle Mass & Insulin Sensitivity
✅ Testosterone promotes muscle growth, and muscle is highly insulin-sensitive.
✅ More muscle means more glucose uptake, reducing insulin resistance.
✅ Testosterone in men reduces visceral fat, lowering inflammation and metabolic dysfunction.
❌Estrogen dominance increases visceral fat and decreases lean muscle mass
B. In Women: Testosterone Shifts Fat to the Belly & Increases Inflammation
❌ Testosterone in women promotes visceral (belly) fat storage, which is associated with insulin resistance. Remember that estrogen promotes subcutaneous fat storage away from the belly (hips, thighs, breasts).
❌ Higher visceral fat increases inflammatory cytokines (IL-6, TNF-alpha), which block insulin signaling.
❌ Testosterone disrupts adiponectin, a hormone that normally improves insulin sensitivity.
In short:
In states of high testosterone, men store fat in a more metabolically neutral way (subcutaneous fat), while women with PCOS store it in an insulin-resistant way (visceral fat).
Testosterone in men builds insulin-sensitive muscle. In women, excess testosterone leads to insulin-resistant fat storage.
Testosterone & Mitochondrial Function: Energy Efficiency Differences
Testosterone regulates mitochondrial function, the powerhouse of the cell responsible for energy metabolism.
A. In Men: Testosterone Improves Mitochondrial Efficiency
✅ Enhances ATP production, supporting muscle function and metabolism.
✅ Improves mitochondrial respiration, reducing oxidative stress.
✅ Increases insulin receptor sensitivity, helping glucose metabolism.
B. In Women: Excess Testosterone Impairs Mitochondria
❌ Excess testosterone in women can impair mitochondrial function, leading to oxidative stress.
❌ This oxidative stress further reduces insulin sensitivity and increases inflammation.
❌ Poor mitochondrial function leads to metabolic sluggishness and inefficient glucose metabolism.
The Role of SHBG: Free vs. Bound Testosterone
Testosterone can exist in two forms in the body:
Bound testosterone (attached to SHBG - Sex Hormone Binding Globulin)
Free testosterone (circulating and biologically active)
A. In Men: SHBG Maintains Balance
✅ In men, SHBG levels are higher, keeping testosterone properly regulated.
✅ This prevents excess testosterone from disrupting insulin signaling.
B. In Women with PCOS: SHBG is Too Low, Leading to More "Free" Testosterone
❌ High insulin levels suppress SHBG, leading to more free testosterone.
❌ Free testosterone directly interferes with insulin signaling, causing high blood sugar and weight gain.
❌ Lower SHBG worsens symptoms of PCOS by amplifying androgen dominance.
The Vicious Cycle of High Testosterone & Insulin Resistance in PCOS
In PCOS, a self-reinforcing loop is created where outside inflammatory sources decreases aromatase activity and induces insulin resistance which increases testosterone, and testosterone further increases insulin resistance:
1️⃣ Insulin resistance leads to high insulin levels.
2️⃣ High insulin stimulates the ovaries to produce more testosterone.
3️⃣ Excess testosterone reduces estrogen conversion and worsens metabolic health.
4️⃣ More testosterone causes visceral fat gain, increasing inflammation.
5️⃣ Inflammation further blocks insulin sensitivity, making the cycle worse.
This is why PCOS treatment often focuses on improving insulin sensitivity—because breaking this cycle can reduce testosterone levels naturally.
How to Restore Insulin Sensitivity in Women with High Testosterone (PCOS)
To counteract the insulin-resistant effects of high testosterone, the focus should be on:
✔ Lowering insulin resistance
✔ Reducing inflammation
✔ Supporting estrogen balance
A. Improve Insulin Sensitivity
✅ Myo-Inositol & D-Chiro-Inositol – Help lower insulin levels & reduce testosterone.
✅ Berberine – A natural alternative to metformin for insulin resistance.
✅ Strength training & walking after meals – Helps increase glucose uptake.
B. Reduce Androgen Levels Naturally
✅ Spearmint Tea – Lowers free testosterone levels.
✅ Zinc & Magnesium – Support proper hormone metabolism.
✅ Cruciferous Vegetables (Broccoli, Cauliflower, Kale) – Help convert testosterone into estrogen.
C. Balance Hormones & Reduce Inflammation
✅ Omega-3s (EPA/DHA) – Reduce inflammatory cytokines.
✅ Curcumin & Resveratrol – Improve insulin sensitivity & support estrogen balance.
✅ Adrenal support (Rhodiola, Holy Basil) – Helps lower stress-driven testosterone.
Final Takeaway: Why Testosterone Acts Differently in Men vs. Women
Men: Testosterone improves insulin sensitivity because it builds muscle, enhances mitochondria, and reduces visceral fat.
Women with PCOS: Excess testosterone worsens insulin resistance by increasing belly fat, reducing estrogen, and promoting inflammation.
So the roles of estrogen and testosterone are opposite in each sex. Estrogen dominance ensures insulin sensitivity and proper body composition in women, while testosterone accomplishes that in males. Testosterone decreases inflammation and maintains hormonal balance in males, while increasing inflammation and disrupting balance in women.
While it may be a bit confusing at first, given the different trajectories of each sex, it seems we both end up at the same symptoms.
Men: Low testosterone (and possibly elevated estrogen), excess iron retention, insulin resistance
Women: High testosterone, low estrogen, excess iron retention, insulin resistance
We've demonstrated that women's state of excess testosterone can lead to an overabundance of iron in circulation. This would match the expected pathology of hemochromatosis. Too much iron being mobilized and absorbed into systems unequipped to handle iron en mass. Inflammation and the classic symptoms of iron overload result.
But with men and their lowered testosterone, excess iron in circulation wouldn't make sense. Testosterone increases iron circulation. So what's happening in the male body?
Hypogonadism in Males and Iron Retention
A. Testosterone, Hepcidin, and Iron Uptake
Testosterone Suppresses Hepcidin
Under normal circumstances, testosterone can reduce hepcidin production, promoting greater iron absorption and mobilization.
Higher testosterone generally correlates with lower hepcidin, higher serum iron, and more RBC production (erythropoiesis).
Hypogonadism = Lower Testosterone
If testosterone is chronically low, we might expect hepcidin to rise (or at least not be as suppressed).
Higher hepcidin typically blocks intestinal iron absorption and sequesters iron in storage sites (e.g., within ferritin in the liver or macrophages).
B. Could This Lead to “Over-Retention” of Iron?
Increased Hepcidin → Decreased Iron Export
Hepcidin reduces the activity of ferroportin (the iron exporter on gut enterocytes and macrophages). This leads to reduced release of iron into circulation, but it also can increase stored iron in tissues if dietary or stored iron is abundant.
Potential Tissue Iron Accumulation?
If a man with low testosterone continues to ingest normal or high amounts of iron—and if hepcidin is high—free iron may accumulate within cells (e.g., liver, macrophages, pancreas, gonads) rather than circulating normally. Over time, this can contribute to a degree of tissue iron overload or abnormal distribution, though the classic presentation of iron overload is more commonly linked to low hepcidin (as in hemochromatosis or testosterone dominance in women) or repeated transfusions.
Anemia vs. Overload
Clinically, many hypogonadal men actually lean toward anemia or borderline low iron in circulation, but “functional” iron deficiency can coexist with increased stored iron locked away intracellularly.
Hence, it’s possible to see a mixed picture: low serum iron (less RBC formation, mild anemia) and increased iron retention in storage compartments.
Men experiencing low testosterone are over-storing iron. In states of excess iron, which the standard western diet promotes, inflammatory free iron is being stowed away in organs and glands that aren't equipped to handle the highly volatile molecule. But because of our current medical standards for measuring iron, IE serum ferritin, low-T males are testing as being iron deficient. Confusion results.
Based on the blood tests, standard western medicine recommends increasing iron intake but fails to recognize that it's simply feeding iron to a system already overloaded. We would need to regulate the imbalances holding iron out of circulation before becoming concerned with the iron in circulation.
Similar Symptoms via Different Mechanisms
Overlap in Symptoms
Both male hypogonadism and female hyperandrogenism may present with fatigue, metabolic issues, mood changes, and other systemic symptoms.
In men, the root cause is low testosterone leading to high hepcidin, potential “hidden” iron retention, and lower RBC production.
In women, excess testosterone leads to low hepcidin, higher circulating iron, and potential oxidative stress—yet can still manifest in overlapping metabolic/inflammatory phenotypes.
Putting It All Together
Men with Hypogonadism
Low testosterone → less suppression of hepcidin → increased intracellular iron retention and potentially higher ferritin stores, but lower circulating iron for RBCs. This can manifest as mild anemia with paradoxically high tissue iron.
Women with PCOS (Hyperandrogenic)
High testosterone → suppressed hepcidin → more intestinal iron absorption → higher circulating iron and ferritin.
When combined with insulin resistance and inflammation, this can worsen oxidative stress and endocrine dysregulation.
Despite different testosterone statuses (low in men, high in women), both scenarios can lead to “iron mismanagement,” inflammation, and metabolic distress. The end result may overlap symptomatically (fatigue, mood changes, metabolic issues) but arises from opposite ends of the androgen spectrum.
Key Takeaways and Future Considerations
Testosterone–Hepcidin Axis
Testosterone typically reduces hepcidin, but the net effect on total body iron can differ drastically depending on whether testosterone is low (risking hidden iron sequestration) or high (risking increased iron circulation).
Acknowledging the Iron-Hiding Response in states of outside inflammation
Our body has a natural reflex to increase hepcidin and store iron away in times of infection and acute inflammation. Might this be furthering the iron-induced inflammation cycles?
Individual Variation
Genetics, diet, and comorbidities influence how each person handles iron. Not everyone with hypogonadism or PCOS will present with abnormal iron biomarkers, but it’s a possible link worth exploring.
Clinical Implications
Monitoring ferritin, transferrin saturation, and hepcidin levels in patients with either PCOS or hypogonadism could offer insights into their iron status and guide potential interventions (e.g., phlebotomy, iron supplementation, or dietary modifications).
Hyperandrogenic State in Women
Often multifactorial, with insulin resistance and aromatase dynamics playing significant roles. Nutritional and inflammatory factors also modulate androgen production and clearance.
Areas for Further Research
Prospective trials examining how correcting testosterone imbalances (in either direction) influences iron parameters, and vice versa, could clarify causal relationships.
Investigating whether manipulating iron levels might help manage PCOS or male hypogonadism symptoms would also be valuable.
Bottom Line
In male hypogonadism (low T), hepcidin may be higher, leading to abnormal iron trapping in storage sites.
In female hyperandrogenic states (like PCOS), hepcidin is often suppressed, promoting excessive iron loading in circulation.
Both conditions can share symptoms of metabolic dysfunction and inflammation, but through opposite hormonal pathways. Understanding the testosterone–iron–hepcidin interplay can open doors for new diagnostic or therapeutic strategies in reproductive and metabolic disorders.
References and Citations
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Hepcidin and Iron Regulation
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