Iron the primary driver of aging?


Not long ago I wrote an article about how iron accumulation, that is, body stores of iron, could be an important cause of the maladies of aging. I set forth quite a bit of evidence in that article, but I’ve been revisiting this topic and am becoming more convinced that excess iron may be one of the most important drivers of aging. This article will set forth further evidence.

What is aging?

First of all, to see how iron could be important to aging, we need to ask what aging is. Aging is a loss of homeostasis such that the organism is unable to bring its biochemical and physiological systems into proper balance. Aging means that rejuvenation and repair of systems, so important to maintaining health, deteriorate. Rates of disease increase with age, as the organism cannot repair its systems nor fight off infections and cancer as well.

In aging, we see a progressive increase in inflammation, oxidative stress, mitochondrial dysfunction, and a loss of autophagy intensity. These processes normally rise and fall together, so that an improvement or deterioration in one means the same for the others. One reason I’ve emphasized autophagy so much on this blog is because simple interventions like fasting and certain supplements can readily increase autophagy to youthful levels, leading to an improvement in all aspects of aging.

Could iron be the cause of these important aspects of aging? I believe that they could.

Consider insulin resistance, which increases with age and is strongly related to many disease states, including heart disease, cancer, and sarcopenia (1), not to mention diabetes. Insulin resistance features elevated levels of inflammation, oxidative stress, mitochondrial dysfunction, and decreased autophagy, making it an archetype of aging.

In insulin resistance, serum ferritin, the most important measure of body iron status, is strongly correlated with glucose tolerance.(2) The correlation coefficient was 0.73, i.e. high. Ferritin also correlated with blood pressure.

In men, a high serum ferritin, >300, was associated with a 5-fold increased risk of being diagnosed with diabetes.(3)

Many of these studies control for body mass index (BMI), but consider that visceral and subcutaneous fat both also correlate with ferritin.(4)

Metformin is a drug commonly used to treat diabetes, and in contrast to other diabetic drugs, actually extends lifespan in lab animals.(5) There have been suggestions that diabetics treated with metformin may actually live longer than non-diabetics without metformin, leading to the idea that metformin is a true anti-aging drug. Some people are now taking metformin for the purpose of lifespan extension.

How does metformin work? In a cell culture model in which metformin protects against damage from chemotherapy, it was found that the mechanism is restoration of iron homeostasis.(6) Without going too deep into the biochemistry, the body keeps iron under tight control, and metformin restores that control.

Metformin is also effective on non-alcoholic fatty liver, and the mechanism may be decreased iron absorption.(7)

The Mediterranean diet

The Mediterranean diet has been extolled because those living around the Mediterranean have much lower rates of heart disease than elsewhere. There are many confounding factors, however, including red wine, sunshine (vitamin D), social patterns, etc.

Could iron levels have anything to do with better health in the Mediterranean? Yes. A study was done to look at markers of oxidative stress in men in Crete versus men in the Netherlands (Zutphen).(7) Men in Crete had half the level of ferritin in their blood than the men of Zutphen, 69.8 vs 134.2. This data point might be able to account completely for the difference in health between the two populations.

The Cretan men may have lower serum ferritin through less consumption of red meat and through drinking of red wine; iron fortification of food could play a role (not sure whether they do that in Crete), as well as a diet high in fiber, which inhibits iron absorption.

Iron is involved in the pathology and toxicology of everything

A scientist by the name of Douglas Kell, who is at the University of Manchester in England, has written a magnum opus of an article on how iron could be involved as a central mechanism in the pathology and toxicology of nearly everything: “Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples”.(8)

Growth hormone, fasting, and hepcidin

Growth hormone is the focus of much study in aging, as it appears to promote aging. Calorie restriction, which reliably increases lifespan in animals, is thought to work at least in part by lowering levels of IGF-1, which is produced in the liver by the action of growth hormone; prolonged fasting also lowers IGF-1 levels. (For more, see Fasting-mimicking diet slows aging.)

Of interest here is the hormone hepcidin, which was discovered only 15 years ago.(9)

Hepcidin, a peptide hormone made in the liver, is the principal regulator of systemic iron homeostasis. Hepcidin controls plasma iron concentration and tissue distribution of iron by inhibiting intestinal iron absorption, iron recycling by macrophages, and iron mobilization from hepatic stores.… Synthesis of hepcidin is homeostatically increased by iron loading and decreased by anemia and hypoxia. Hepcidin is also elevated during infections and inflammation, causing a decrease in serum iron levels and contributing to the development of anemia of inflammation, probably as a host defense mechanism to limit the availability of iron to invading microorganisms. At the opposite side of the spectrum, hepcidin deficiency appears to be the ultimate cause of most forms of hemochromatosis, either due to mutations in the hepcidin gene itself or due to mutations in the regulators of hepcidin synthesis. The emergence of hepcidin as the pathogenic factor in most systemic iron disorders should provide important opportunities for improving their diagnosis and treatment.

Hepcidin controls iron levels through raising and lowering the amount that is absorbed from the gut. It bears repeating that the body has no way to rid itself of excess iron; it can only detect when iron levels are sufficient and then decrease its rate of uptake from the gut.

It turns out that growth hormone decreases hepcidin, and prolonged fasting increases it.(10)

Our results indicate that in humans, hepcidin-25 exhibits diurnal changes that can be altered by prolonged fasting, which increases hepcidin-25 concentrations approximately 3-fold after 3 days of fasting, possibly owing to a suppression of erythropoiesis that may occur during the fasting state to preserve tissue iron concentrations. In contrast, GH administration decreased hepcidin-25 concentrations by approximately 65%, presumably by stimulating erythropoiesis. These results indicate that circulating hepcidin-25 concentrations display much more dynamic and rapid variation than might have been anticipated previously.

From a mechanistic point of view, this makes complete sense. Tissue growth requires iron, so stimulation of growth by HGH causes hepcidin to decrease, which increases intestinal iron absorption. Fasting promotes an anti-aging state in which growth is suppressed, so hepcidin increases, and intestinal iron absorption decreases.

The effect of fasting on the iron-regulatory hormone hepcidin. The effect of supplemental growth hormone on levels of the iron-regulatory hormone hepcidin.

What I’m saying here is that the effects of fasting on aging (slowing it) and the effects of growth hormone on aging (accelerating it) may be completely explainable by their respective effects on iron levels. Exercise even has an iron component to its healthful effects: it increases hepcidin.(11)

If that sounds outrageous, consider that we know that excessive levels of iron (ferritin) are a major risk factors for all of the diseases of aging, whether heart disease, cancer, dementia, even sarcopenia. We also know that growth hormone (through its influence on IGF-1) and fasting are reliable interventions in aging, one promoting it, the other decreasing it.

Therefore iron may be a major mechanism of aging, and could be added to Douglas Kell’s list above.

Obviously iron is not the only promoter of aging, since even with a low ferritin level, you won’t live forever. But the fact that is accumulates throughout the lifespan, correlating with chronological age, and that it can induce oxidative stress, insulin resistance, inflammation, and mitochondrial dysfunction, is highly suggestive. It appears that excess iron, by promoting the production of lipofuscin, also reduces autophagy.(12)

Gordon Lithgow of The Buck Institute for Research on Aging agrees.

“We fed iron to four day-old worms, and within a couple of days they looked like 15 day-old worms,” said Lithgow. “Excess iron accelerated the aging process.” Lithgow says excess iron is known to generate oxidative stress and researchers expected to see changes in the worm based on that toxicity. “Instead, what we saw looked much more like normal aging,” said Lithgow. “The iron was causing dysfunction and aggregation in proteins that have already been associated with the aging process. Now we’re wondering if excess iron also drives aging. ”[…]

Lithgow says the work has implications for the aging research field. “Maintaining the proper balance of metals is key to good health throughout the lifespan, and it’s pretty obvious that this delicate balance can go off-kilter with age,” he said. “This is a phenomena that has not been extensively studied by aging researchers and it’s an area that has potential for positive exploitation.”

Is iron the primary driver of aging?

When I recently checked, my ferritin level was 137, which is too high, so I’m interested in lowering it. Blood donation or therapeutic phlebotomy are the best ways to lower iron stores, since 70% of body iron is contained in red blood cells.

It’s not hard to find advice about iron levels, and yet, as part of a standard anti-aging program, I’ve never seen it recommended to keep them in the low normal range. It could be one of the most important anti-aging interventions available.

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  1. Simon says:

    Great post, fascinating stuff.

    Working under the assumption all of the above is true, it should therefore be possible to supplement with TRT (which increases red blood cell count) and HGH, whilst letting blood regularly, and retain all the benefits of both with little of the risks.

    • P. D. Mangan says:

      Thanks, Simon. Right, assuming it’s true, you might be able to largely counteract deleterious effects of HGH through phlebotomy.

      • Steve Johnson says:

        Or blood donation.

        Anyone ever study regular blood donors?

        Obviously there are going to be confounding factors if you take into account who would sell plasma but if you restricted the study to people who consistently donate blood and compared them to people who consistently gave to charity in some other form you might be able to find something out.

        • P. D. Mangan says:

          Steve, my previous post ( discussed several studies on blood donors as well as a RCT of therapeutic phlebotomy, and disease risk is indeed way lower, 88% lower for heart attacks for instance in one study. Donors to charity is a great choice of control group, don’t know if that’s been done. One study was adjusted for coronary risk factors, age, and so on, but not for SES or IQ, which I think could be important. If we can take these studies at face value, donating blood probably even exceeds exercise for lowering disease risk.

          • Jared says:

            Except that blood donors vs non blood donors is a terribly biased sampling. There’s no way to control for biased sampling unless you already know exactly what the bias is… which we don’t.

          • P. D. Mangan says:

            There’s a study somewhere that compared frequent donors to non-frequent donors, so that would presumably eliminate a number of confounds, like donors being healthier. Also, the study that found donors had lower disease risk controlled for age, BMI, smoking, etc.

  2. Bruce Bowen says:

    Bloodletting in the old days most likely DID relieve a lot of chronic ailments. Funny how modern medicine mocks it.

    • P. D. Mangan says:

      Absolutely, Bruce. Bloodletting is the main reason that you often hear that “physicians did more harm than good until the 20th century”. I would say that’s nonsense and assumes that everyone before our time was an idiot. They could see what worked and what didn’t, and blood letting can be effective for lots of things, including infections.

  3. P says:

    What I’m reading here seems to indicate that working out, building muscle, and eating high amounts of calories to sustain the muscle will lead to aging faster by increasing iron in the body. And that being a weak herb will lengthen my lifespan by decreasing iron. But why would you want to live longer as a wimp when being stronger and fit increases your quality of life? Or am I reading this all wrong?

    • P. D. Mangan says:

      Well, the weak herb is just as if not more likely to have high iron levels. Sugar, for instance, increases iron absorption a lot. Anything made with flour in the US (and a lot of other places) is iron fortified. Exercise reduces iron levels.

      As for protein, not all is the same and it’s not protein per se but heme iron that is the concern. Fish, chicken, dairy products are all low in iron. Red meat contains lots. Therefore one should use iron chelating substances at meals that have meat, green tea and red wine mainly. Or avoid red meat (and flour and sugar), or donate blood regularly.

      • mike says:

        I thought that p’s questioning was spot on because that’s the immediate thing that I took away from your article. Great piece, btw. The regulation and uptake of iron in response to exercise and muscle hypertrophy is indeed logical. Wouldn’t this new cache of iron that is absorbed be shuttled to new cellular development and not continue to circulate in the blood? Furthermore, as it all relates to life span, it’s been known that lean muscle is a fairly decent indicator of organ reserve status or basically, the condition of our vital organs. Many correlative results have been found there.

        In addition and at least to my knowledge, autophagy and fasting states also intiate HGH secretion in a muscle sparing process. How would you reconcile this considering that HGH lowers regulating hepcidin?

        • P. D. Mangan says:

          Mike, thanks. Iro isn’t the problem, but excess iron. If an older man (such as me) were to grow muscle, he doesn’t necessarily need more iron, since he can take it from his already abundant iron stores in the body.

          There does seem to be a paradox re HGH and hepcidin. Why fasting increases hepcidin while at the same time producing a growth hormone burst, while exogenous HGH decreases hepcidin, I can’t answer – maybe no one can. I would speculate that other factors are involved, such as adequate calorie intake.

      • Steve says:

        I believe an egg at each meal help prevent iron absorption.

  4. Ross says:

    PD, great stuff. The interaction with sugar is a double whammy. Thanks for doing this!

    So, this all got me researching, too. Took a blood test, and darned if my ferritin levels aren’t essentially the same as yours (roughly same age….) Disturbing! I have just done my first donation to rectify this, but want to drive my levels down to optimal (30-60 ng/ml say some). What are your goals, and other than blood donation, how will you approach?

    All this said, NHANES II disagrees on (statistical) significance of effect:

    I think that’s 40 year old data from people with lower ferritin levels, but…what’s your reading of it? Why did this study miss the association?

    Thanks again PD. Keep on rockin’!

    • P. D. Mangan says:

      Thanks, Ross. I think I came across that report when I was researching my article, and after looking around a bit and thinking about it, I find I’m unable to explain it. There are so many reports contradicting it in terms of disease risk and mortality, so I don’t know. For example: Elevated Serum Transferrin Saturation and Mortality and see this graph: However, they state that those with transeferrin sat that high are (only) about 2% of the population. That’s plenty of people, enough for doctors to be on the alert, but maybe that wouldn’t be reflected in overall mortality statistics.

      This paper: states that a combination of high transferrin sat and high LDL is associated with an almost 4-fold greater mortality rate.

      Both these papers are among many written by this man:

      For us anti-aging aficionados, we understand that doing everything like everyone else might get us into our 80s, only 20 years away for me. And an average iron level is part of that. I want mine to be probably 50 to 70, as there are reports of non-anemic iron deficiency at around 50 ferritin.

      As for what I’m going to do about it, well, I was turned down by the blood bank. My alt doc, the same one who prescribes my aromatase inhibitor, might be willing to do a therapeutic phlebotomy, which might cost $150 or thereabouts. I’m also considering adding IP6, an iron chelator, to my supplement regimen. Beyond that:

      Added: This report is a solid summary of the state of the evidence regarding iron and health: In it the author cites a study that showed that average ferritin level of a 60 year old man was 150, that of a 90 year old man was 80, the difference being due to increased mortality among men with higher ferritin levels.

  5. Dennis,

    I’ve found many studies that do not find a ferritin-CHD link. See here, here, and here for example. The latter study is interesting for the comments about the hemochromatosis gene Cys282Tyr mutation. Since the costs of genetic testing have fallen by orders of magnitude since those studies were done I’d like to find a newer study that tested for the Cys282Tyr mutation and perhaps other hemochromatosis mutations. There are at least 5 genes which have hemochromatosis mutations: HFE, HJV, HAMP, TfR2, or SLC40A1 and occur in low double digit percentages of white populations. Their interactions are complex and they vary greatly in severity.

  6. Malcolm Klein says:

    Great info, thanks. I became aware of this myself recently and tested myself and was at 132 ng and after two blood donations got it down to 37! Need to retest soon to see if it is stable on my current diet. I’ve read that as low as 20 is even better- my hemoglobin is still fine. Its amazing how many foods are supplemented with iron- basically anything with wheat, corn, rice and oats! That paper on the link between excess lysosomal iron and lipofuscian formation and reduced autophagy is especially fascinating. Thanks again for all your posts.

    • P. D. Mangan says:

      Malcolm, thanks for the comment. Lower ferritin does seem to be better; on the other hand, I’ve read of some cases of non-anemic iron deficiency at somewhat higher levels. In other words, it appears that the first manifestations of iron deficiency are not in lower hemoglobin, but could be manifested as fatigue or other symptoms. Two donations sounds about right, one donation cases a ferritin drop of up to 50 ng. Also, the lower your ferritin gets, the more iron your body will want to absorb.

      Iron enrichment is everywhere, as you note, hard to avoid.

  7. Time Travler says:

    This is all very interesting but you left out another factor that effect ferritin levels (maybe because it’s not common in the US) – namely “g6sp”, which is an enzyme deficiency that effect red blood cells. A deficiency that lead to high ferritin (300+) and low hemoglobin levels on the other hand. Anyone who has it, is caught between the rock and and a hard place as phlebotomy is out of the question on account of being anemic at the same time. Unless, he or she were screened for “g6sp” in time. Then the safest way to stay clear is to avoid certain foods; like fava beans for instance…so much for the Mediterranean diet….

    What are your thoughts on this?

    • P. D. Mangan says:

      One of the few things I remember about G6PD deficiency is that fava beans can set off an attack, but I wasn’t aware of high ferritin levels. That does make sense, because if you don’t make enough hemoglobin, the iron has to go somewhere else. This deficiency is more common in people of Italian and (I think) Greek origin.

      • Time Travler says:

        There are different levels of sensitivities; some can’t as much as smell fava beans (especially fresh), while others can eat them and be unaware that they are endangering themselves. But that is only the trigger, while lacking the enzyme is the root cause. For all I know, mine could have been triggered after taking antimalarial medication prior to a safari trip to Africa; or by stress. Either way, once inflicted, there’s no cure as the enzyme deficiency cause a destruction of red blood cells that’s called hemolysis and the resulting anemia is called a hemolytic anemia. The disorder found mostly in people of African, Asian, Middle Eastern and Mediterranean decent.

        I came seeking answers and ended up providing info… (-:

  8. Time Travler says:

    there was a’s “g6pd”

  9. Ben V says:

    It is tough to say that iron is essential, leading to very bad things when deficient and when no new sources are available (fasting) your body quickly locks it down, I assume, to preserve what is left.

    It is like your body isn’t so worried about excess iron, which is supported by the fact that we store excess at some level. It almost panics when it is potentially low.

    It would be interesting to repeat the hepcidin during fasting test with the increase in hepcidin per sample normalized for starting ferritin level. I’d assume someone with plenty of ferritin stores wouldn’t need to increase hepcidin so quickly to conserve what is left.

    Of course we didn’t evolve for longevity, so our system, which supports youth and growth for reproduction, Isn’t best for longevity.

    • P. D. Mangan says:

      Hi Ben, I think your last sentence sums it up. The force of natural selection declines with age, so things that help us increase reproduction, but which harm us at older age, like iron excess, are not selected against.

  10. mike says:

    Hi. Nice article. I have a question about ferritin levels; you said that your level of 137 was too high but I’ve seen that “normal” numbers are between 24 and 336 micrograms per liter. I am presuming that yours was also based upon micrograms per liter. How would 137 be considered “high” then?

    • P. D. Mangan says:

      With ferritin, normal levels that labs used have a ridiculously wide range. Labs calculate normal levels of anything by running samples from “healthy” people and finding the range that 95% of people fit into. But in the case of ferritin, I think that risk probably increases linearly from a level of perhaps 50 or so. For instance, fertile women have low ferritin levels, typically around 50, and have the lowest risks of heart disease and cancer compared to men of the same age (about 1/4 the amount) and lower than post-menopausal women. That’s why I say my ferritin of 137 is too high. The optimal range is necessarily speculative, but it seems likely that you want the minimal amount of iron and no more, which might correspond to a ferritin of 50. (There are some reports of non-anemia iron deficiency at that level, with fatigue as a symptom, clearing up with iron supplementation. Others have found that you need to go much lower, say below 20, to have a deficiency.) My interviewee in a previous post, Dr. Weinberg, has a ferritin of 43, is in good health and is 93 years old.

      Long story short, I want to get my ferritin below 80, perhaps lower. Lab normal ranges are way too wide for anyone serious about their health.

  11. AJ says:

    I’m not the most well read guy on this topic, but just reading the article, it seems that Iron / Ferritin correlates with some of the outcomes, but does it establish a causal relationship? Example, I eat carbs , I have high insulin, I also have high ferritin, have high inflammation, metabolic syndrome, high reactive oxygen species and consequent atherosclerosis and higher mortality rate. The ferritin and metabolic syndrome correlate to my risk of mortality but are not the cause. Carb intake, likely, is. So question is, Is the iron / ferritin actually bad or is it an indicator of something bad?

    • P. D. Mangan says:

      Good question. My view is that ferritin is an independent determinant of disease risk. So even if you got high ferritin from eating lots of carbs or becoming obese, the ferritin (more exactly, iron released from ferritin, that is, free iron) causes damage, and much of the damage can be mitigated by lowering iron. This can be seen in the trials in which lowering iron improves insulin resistance. In liver disease, iron overload is frequent, but may be caused by alcohol, hepatitis, or obesity. Nevertheless, lowering iron is an effective treatment.

  12. Steven says:

    So can we safely say that fasting has a desirable effect on iron levels? Perhaps converting unbound iron in tissues to bound ferritin since fasting has improved iron levels of persons diagnosed as having iron deficiency anemia.

  13. Steve says:

    This is quoted from a message I received from The Magnesium Man, Morley Robbins. I think he knows more about this than anyone else and is able to connect all the dots between iron, copper, ceruloplasmin and mineral balance…

    He says…

    “Hepcidin is a Hormone with 25 Amino Acids.

    Ceruloplasmin is an “Enzyme” with 1,046 Amino Acids and 8 Coppers (4 Cu+, and 4 Cu++). It is a TANK compared to that puny tricycle [hepcidin] that Organized Medicine wants you to think “runs” Iron metabolism.

    It is UTTER RUBBISH. That is WHY I do NOT talk about it [hepcidin].

    What is ESSENTIAL is for proper Iron metabolism is to have fluid circulation and movement. That is the JOB of Cp [ceruloplasmin]…

    As you dig DEEPER into this issue, you will find that Hepcidin gets PRODUCED under conditions of Inflammation and that is the VERY MECHANISM that CAUSES Iron storage. (Hepcidin KILLS Ferroportin that DEPENDS On Cp [ceruloplasmin] for proper function…) It’s taken me 2 yrs to FULLY understand this shell game.

    Hope that helps!”

    • P. D. Mangan says:

      Geez, he seems awfully sure of himself. The relative size is irrelevant; hepcidin is a hormone, ceruloplasmin isn’t, and even if they were both enzymes or both hormones, the molecular size doesn’t determine importance. “It is UTTER RUBBISH.” sorry, but that’s the sign of a crank.

  14. Marco says:

    Hi P.D.
    I have a question about the “all meat” diets.

    Lots of people on Twitter seem to think that lowering Ferritin is not good per se, because Ferritin is simply a marker of a dysregulation and that eating iron is not the problem.

    Considering just the iron issue, eating bioavailable iron in pills doesn’t seem to me a safe and healthy practice.

    Why eating four pounds of red meat a day would be?

    Thank you.

    • P. D. Mangan says:

      Hi Marco – great question. I see all that stuff on Twitter too. Whether they’re right or wrong, I see so many closed minds who absolutely refuse to contemplate that they might be mistaken. That being said, high ferritin levels do seem to be much more associated with metabolic dysregulation, eating iron-fortified foods, taking iron supplements, eating sugar and refined carbs, than it does with eating meat. The reason is that these factors override the natural iron-regulatory mechanism of the hormone hepcidin and other hormones. If someone has good metabolism, i.e. they’re lean and insulin sensitive, they should be able to regulate the amount of iron they absorb; heme iron (from meat) however is a highly absorbable form as compared to non-heme iron from plant foods.

      Evolution doesn’t care if we live to a ripe old age, only that we reproduce, and therefore has made it so that we don’t rid ourselves of the growth factor iron. Therefore even if someone had great metabolism and was otherwise healthy, I’d be checking my ferritin to be safe. A ferritin above 100 serves no purpose other than iron storage and is associated with worse health.

      I’ve heard from many people who checked their ferritin and found that it was 250, 350, even higher, and they were shocked at this. Presumably the carnivore types would tell them to just eat a steak. But it would take years for a ferritin that high to come down naturally.

  15. Marco says:

    Does the fact that serum ferritin (that is the best indicator of iron status, for what i know…) is ASSOCIATED with metabolic dysregulation aka insulin resistance, guarantee us that metabolic dysregulation is the cause of high ferritin and not the opposite or that they are independent factors simply related to age?

    To be clear:

    a) metabolic dysregulation causes accumulation of iron OR

    b) accumulation of iron causes metabolic dysregulation OR

    c) accumulation of iron AND metabolic dysregulation are INDEPENDENT and both a gift of aging.

    • P. D. Mangan says:

      High ferritin is associated with insulin resistance, and lowering ferritin via phlebotomy improves insulin resistance. Also this paper. So it appears likely that high ferritin causes insulin resistance. How ferritin gets that high is another question; whether the high ferritin came first and causes IR, or whether metabolic dysregulation caused high ferritin and in turn led to IR, well, my guess is that both processes happen.

      Of interest to the meat question, Low iron status and enhanced insulin sensitivity in lacto-ovo vegetarians.

      The efficacy of insulin in stimulating whole-body glucose disposal (insulin sensitivity) was quantified using direct methodology in thirty lacto-ovo vegetarians and in thirty meat-eaters. All subjects were adult, lean (BMI <23 kg/m2), healthy and glucose tolerant. Lacto-ovo vegetarians were more insulin sensitive than meat-eaters, with a steady-state plasma glucose (mmol/l) of 4·1 (95 % CI 3·5, 5·0) v. 6·9 (95 % CI 5·2, 7·5; P=0·0028) respectively. In addition, lacto-ovo vegetarians had lower body Fe stores, as indicated by a serum ferritin concentration (μg/l) of 35 (95 % CI 21, 49) compared with 72 (95 % CI 45, 100) for meat-eaters (P=0·0012). To test whether or not Fe status might modulate insulin sensitivity, body Fe was lowered by phlebotomy in six male meat-eaters to levels similar to that seen in vegetarians, with a resultant approximately 40 % enhancement of insulin-mediated glucose disposal (P=0·0008). Our results demonstrate that lacto-ovo vegetarians are more insulin sensitive and have lower Fe stores than meat-eaters. In addition, it seems that reduced insulin sensitivity in meat-eaters is amenable to improvement by reducing body Fe. The latter finding is in agreement with results from animal studies where, no matter how induced, Fe depletion consistently enhanced glucose disposal.

      Obviously the meat eaters were not carnivore types but were on a mixed diet. Perhaps a combination of processed foods high in refined carbs and sugar, together with heme iron from meat, causes an abnormally high ferritin. Or maybe meat alone would do this (though I tend to doubt it) but who knows? Higher heme iron intake is associated with type 2 diabetes. But again, is it the meat or something else that would interfere with hepcidin function?

  16. robert says:

    I take IP6 the iron cheator on empty stomach to reduce my iron effectively

  17. robert says:

    iron chelator

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