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Why You Need to Manage Your Iron Status and How to Do It

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Chris Masterjohn., PhD shared some points on Why You Need to Manage Your Iron Status and How to Do It

In episode 32, I tell the story of my personal struggle with iron overload, and weigh in on the proper use of blood tests and strategies to manage anemia, hemochromatosis, and everything in between. It's important to realize that these are the extremes, and there is a large middle space where we need to not only manage how much iron we accumulate, but how we direct it away from its disease-promoting roles and into its health-promoting roles.

This is a great primer on iron as well as a source of insights you may not have encountered elsewhere, such as the importance of oxidative stress as an independent regulator of ferritin, and the potential dangers of supplements designed to protect against oxidative stress like milk thistle, Protandim, sulforaphane, and green tea extract, for people at risk of anemia.

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This is part of a series on managing nutritional status where all of the episodes are collated on the shownotes page for the introductory post, What Makes a Good Marker of Nutritional Status?

This episode is also brought to you by Kettle and Fire bone broth. I use their 24-hour simmered bone broth as a source of glycine-rich collagen and other nutrients that slowly release from the bones and the marrow inside them. A team of chefs designed the recipe, so it’s delicious to the max.  And the state-of-the-art packaging makes it the only bone broth on the market that is cooked in the traditional way and has no additives or preservatives, yet stays shelf-stable for up to two years, making it easily available at a moment’s notice. Head to kettleandfire.com/chris to get $10 off your first order.

This episode is brought to you by US Wellness Meats. I use their liverwurst as a convenient way to make a sustainable habit of eating a diversity of organ meats. They also have a milder braunschweiger and an even milder head cheese that gives you similar benefits, as well as a wide array of other meat products, all from animals raised on pasture. Head to grasslandbeef.com and enter promo code “Chris” at checkout to get a 15% discount on any order that is at least 7 pounds and is at least $75 after applying the discount but under 40 pounds (it can be 39.99 lbs, but not 40). You can use this discount code not once, but twice!

Show Notes for Episode 32 on Managing Iron Status

In this episode, you'll find all of the following and more:

  • 0:33 Cliff Notes.
  • 10:30 Introduction.
  • 13:12 My personal story with iron overload.
  • 30:12 The physiological roles of iron: hemoglobin, myoglobin, nitric oxide synthase, iron-sulfur clusters in the cytochromes of the electron transport chain, guanylyl cyclase, thyroid peroxidase (TPO), myeloperoxidase (MPO), oxygen transport, energy and ATP production, cellular regulation, thyroid hormone production, immunity.
  • 38:20 Iron as a source of oxidative stress: free iron, hydrogen peroxide, and the hydroxyl radical, oxidative stress as an independent regulator of ferritin.
  • 41:10 Regulation of iron status.
    • Ferritin, long-term storage, protector against pathogens, protector against oxidative stress.
    • Transferrin, short-term iron storage.
    • Hepcidin, master coordinator of iron metabolism.
    • HFE, communicator between transferrin and hepcidin.
  • 49:10 Regulation of dietary absorption of plant and animal iron.
  • 51:00 Measuring and assessing iron status: complete blood count (MCH, MCV, RDW, CHr), full iron panel, sensitivity and specificity of transferrin saturation versus ferritin, differential interpretation of ferritin as a marker of iron overload, inflammation, or oxidative stress.
  • 1:11:43 What to do for anemia: differentiate potential causes, iron in foods (heme, nonheme, vitamin C, polyphenols, phytate, calcium), iron in supplements (iron-saturated lactoferrin, heme iron, liposomal iron), avoid Nrf2-stimulating supplements (like Protandim, sulforaphane, milk thistle, green tea extract), importance of followup measurements of ferritin.
  • 01:21:03 What to do for iron overload: blood donation, dietary management, phlebotomy, chelation, importance of followup.

Iron Foods and Supplements

The first way to improve iron status is to eat iron-rich foods such as clams, liver, and red meat.

Various unrefined plant foods contain iron, with legumes, greens, seaweed, and potatoes towards the top of the list, and whole grains, nuts, seeds, beets, and many other foods containing small but meaningful contributions. The iron is less bioavailable because it is often in its oxidized state and must be reduced by an intestinal enzyme before absorption. The activity of that enzyme can be limiting, but taking vitamin C can solve the problem by increasing the reduction of the iron while still in the GI tract. Phytate and polyphenols inhibit nonheme iron absorption through means that cannot be overcome by vitamin C, making the bioavailability of plant iron worse than that of animal iron across the board and subject to large variation.

Refined grains are usually fortified with iron, but this is inorganic iron that, while making a contribution to iron status, is not the ideal form and is likely to promote oxidative stress in the intestines and perhaps feed undesirable bacteria.

If foods are not adequate to improve anemia, it is important to use supplements. Inorganic iron is likely to cause gastrointestinal side effects. 30% Iron-saturated lactoferrin is a great way to overcome this, but I have not found a source. If you know of one, please post it in the comments. Plant-derived iron supplements are likely to help with this, but to be less bioavailable and less effective at improving iron status.

Iron Smart liposomal iron and Proferrin ES heme iron provide iron in forms that are likely to be better absorbed without causing as many gastrointestinal side effects.

Iron Status Links and Research

The iron chapter of Modern Nutrition in Health and Disease is a great starting place for anyone who is scientifically inclined. This is one of the few textbooks I was required to purchase in school and found so useful I kept as a cherished reference. When the most recent edition came out, I bought the Kindle version, which is incredibly easy to navigate and take notes from compared to the hardcover version of the previous addition that I also still have.

Although the absorption of heme iron is poorly understood compared to the absorption of plant iron, iron status regulates one of the proteins believed to be involved in absorbing heme (HCP1) to the same degree as it regulates the proteins involved in absorbing plant iron (DcytB, DMT1, ferroportin, hephaestin).

Global prevalence of HFE variants.

Proven: The causative role of homozygous H63D mutation in hereditary haemochromatosis. I don't like the word “proven” in the title, but this letter collects some of the key studies documenting the ability of the H63D allele to contribute to hemochromatosis without the C282Y allele.

Nrf2 is the central gene controlling the response to oxidative stress. HFE is a central gene in the regulation of iron metabolism that is disrupted in hemochromatosis. In mice, loss of these genes synergize to produce an oxidative nightmare.

The antioxidant response element (ARE), which is regulated by Nrf2, regulates ferritin expression. This means that oxidative stress regulates ferritin independently of iron status. It also means that supplements designed to stimulate Nrf2 to increase antioxidant defenses could aggravate the risk of anemia in someone with deficient or suboptimal iron status.

Insertion of even one H63D allele of the HFE gene into mice is sufficient to contribute to iron accumulation and oxidative stress in the brain, though there are many protective responses that kick into gear to mitigate the effect.

Although some studies have associated HFE polymorphisms with Parkinson's, others have not, and there is no association in meta-analysis. That doesn't mean it doesn't aggravate the risk when combined with other more important factors, so more research is needed on those nuances.

The C282Y allele is associated with the risk of Alzheimer's disease when combined with a mutation in the transferrin receptor. Despite the fact that the C282Y allele is far more strongly associated with hemochromatosis than the H63D allele, the H63D allele is far more strongly associated with the risk of Alzheimer's, perhaps resulting from effects of the mutations independent from iron overload, or perhaps from differences in the tissue distribution of iron overload.

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114 Comments

  1. Hi. Thanks for the great info.
    My recent blood counts – previous years readings in brackets.
    Ferritin = 91 (27)
    Calculated TIBC 53 (65)
    Transferrin Sat 53% (34%)
    Transferrin 2.1 (2.6)
    Compared to many my Ferritin is low, although jumped up from previous year.
    My Transferrin Sat seems very high?
    My doctor said everything was fine. I asked whether testing for Hemochromatosis was needed, he said Ferritin was too low for it.
    I’m an Irish female.
    Any advice/thoughts would be very appreciated. Thank you

  2. wow wow wow, this “educated” lecturer does not know that ferritin in the blood contains very little to no iron. It’s an empty shell that has spilled its iron because of Fenton reaction. Read Douglas B. Kell (knighted for his work on iron) articles about that.
    Also, an hour of talk about iron, and no mention of copper or ceruloplasmin. This is really really such a low level of insight.
    Feroportin does not work or almost does not work without ceruloplasmin, and yet you did not say the word ceruloplasmin or copper even once.
    There is no iron metabolism. There is only copper/iron metabolism. This lecture was not even a waste of time. It was plain misleading.
    Chris, eat your ego, and do watch (and rewatch), and read (and reread) Morley Robbins interviews and articles. Because if you don’t talk about copper and ceruloplasmin, it seems like Morley is the only one out there talking about it, and that’s absolutely depressing
    Hepcidin is not a “master regulator” of iron. In the words of Morley Robbins, iron is a 4 year old with a hammer, and hepcidin is a teenage brother who locks the 4 year old in a room, so he doesn’t do any more damage. Ceruloplasmin is the mother of 4 year old, who when present will take the 4 year old by the hand and guide it where it needs to go, so the house is orderly and peaceful. But Chris did not mention the mother, how sad.

    1. My total iron is high (200), Ferritin low (33), Saturation (65%) and copper is within higher safe range…. I don’t think it’s that easy as to increase copper.
      Get Gene tested …everyone is different there is no one mineral that can correct iron overload.

      I think Chris did a great job at a high level but again I agree he missed information.

  3. Hi Chris,

    Thank you for all of the great information in this episode! What I can’t seem to find an answer to is if you can simultaneously have low ferritin and iron overload? I too am homozygous for the H63D variant, but did not know this until recently. The strange thing is that I have struggled with low ferritin for a couple years (lowest was 10, highest was 25 after months of supplementing) without anemia. My doctor recently did a complete iron panel for me:

    Iron- 235 ug/dL
    TIBC- 391 ug/dL
    Saturation- 60%
    Ferritin- 12 ng/mL

    I had not been taking any supplemental iron for over a year, but had been eating a diverse and healthy diet. Is it possible to have iron overload and not be storing any iron?? Of course this makes me panic that iron is taking over my brain and organs and aging me rapidly…any thoughts would be very much appreciated!

    Thank you!
    Jill

    1. Jill,

      You have the same issue I do, and I can find NOTHING online in terms of an answer. I can only think to do a retest due to a possibility of hemolysis in the lab or before the lab. Frustrating that there are no answers.

      1. Olivia- yes! It is so frustrating. Has your doctor suggested any treatment? Mine seems unconcerned, meanwhile I’m in constant anxiety about oxidative stress, ha! And from everything I’ve read, ferritin levels that low are just too low and would likely present symptoms of fatigue, etc. It’s very confusing!! My only thought is that it’s just early on in the presentation of hemochromatosis, and eventually ferritin will rise. I have no explanation as to why my ferritin has been almost nothing for years. No bleeding to speak of, good iron rich diet, no evidence of gut issues yet it won’t budge. Just curious, have you also had any thyroid issues? Thanks!

    2. I have the same issue – I eat no iron at all and I still have high iron low Ferritin and low Hemoglobin- I cannot get phlebotomies it is very frustrating.

  4. If it ever fits into your plan, I would love to hear more causes of chronic low ferritin.

    I have a 20 year old boy with an athletic build and eats primal + some grains but has been low for years, with no clear causes. Slightly low white blood cell count but hematologist said he must run low because all looks good. May not be related, but his Oura ring shows like 8 wake spikes per night, though he does not remember them. Thanks…

  5. what about iron infusions, one month apart before dna that shows i am POSITIVE: The patient is heterozygous positive for both the Cys282Tyr and
    His63Asp mutations. This genotype is associated with an increased risk for the
    development of hereditary hemochromatosis. it has been a year since the infusions. anemia is gone. ferretin level is now 28 n/ml from 5 when i had the infusions. scared. thought you should have these as well.
    Component Your Value Standard Range
    Iron (FE) 117 mcg/dL 50 – 170 mcg/dL
    Transferrin 213 mg/dL 163 – 382 mg/dL
    Total Iron Binding Capacity, Calculated 298 mcg/dL 250 – 425 mcg/dL
    % Transferrin Saturation, Calculated 39 % 15 – 50 %

  6. Thanks for all your great work. I hope you will find my case interesting as it does not seem to fit typical iron panel results, and I hope you will be able to shed some light on it.

    TL;DR

    My blood tests showed normal transferrin saturation (at first 45%, then consistently 31-35%) but elevated ferritin (580). Liver disease and inflammation seem unlikely given the rest of my blood results and overall health status. I donated blood, and over the next two months ferritin dropped to 128. After 10 months, ferritin is back at 550. Is the fact that the ferritin level dropped in response to the blood donation enough to conclude that it is indeed iron overload? Or can the ferritin level respond this way even if the underlying cause is something other than iron overload?

    Long version:

    I started following the paleo diet in 2011, strict, low-carb with plenty of vegetables. In April 2018, I decided to give the carnivore diet a try, hoping to improve minor acne (which turned out to be a success as I have been 100% acne free ever since). After eating almost exclusively beef for a month, I had a comprehensive blood work done.

    Below are the iron panel results:
    May 2018
    Iron 126 [33-193]
    Transferrin 2.16 [2.0-3.6]
    TIBC 278 [228-428]
    UIBC 152 [112-346]
    Transferrin Saturation 45.4 [20.0-45.0]
    Ferritin 588 [30-400]

    All other results were good, including C-reactive protein and liver enzymes. I am 34yo, slim, athletic, have no serious health conditions, and feel great.

    I immediately stopped eating red meat and switched to eating exclusively fish and chicken. After 14 days, a new iron panel was done. It showed the same numbers except that Transferrin Saturation dropped to 33. Additionally, soluble transferrin receptor was tested and it was at 2.82 [1.79-4.63].

    Next, I donated blood once and maintained the fish and chicken diet. An iron panel after a month showed ferritin dropped to 377 while other number stayed the same. Then again at two months since the blood donation, the ferritin dropped farther to 128.

    DNA testing has never been done (I am going to have it done now though).

    I got busy with work and stopped monitoring the issue. With regards to my diet, I stayed mostly carnivore but reintroduced beef, keeping a balance between beef, fish, and chicken. I also introduced liver (since I noticed vitamin A deficiency symptoms; 30g per day) and strawberries (for vitamin C). I also eat 8 eggs daily. Based on Cronometer, I hit 100%+ for everything except vitamin E (78%), calcium (45%), magnesium (65%), potassium (80%).

    Fast forward 10 months, a recent blood work showed that, similarly to a year ago, transferrin saturation is normal and ferritin is elevated again:
    April 2019
    Iron 18 [11-34]
    Transferrin 2.09 [2.00-3.30]
    TIBC 52 [50-83]
    Transferrin Saturation 0.35 [0.13-0.50]
    Ferritin 557 [22-275]

    Is it possible to have iron overload despite normal transferrin saturation? Is donating blood a good idea?

  7. Hi Chris,

    Is supplementing with vitamin c ill-advised if you are susceptible to iron overload?

    For example, how would supplementing with 1 g of vitamin c (ascorbic acid) daily with food affect iron accumulation in the body?

    Also, how much would you expect ferritin and transferrin saturation to lower with each pint of blood donated?

    Thanks,
    IronMan

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  9. Hi doctor Masterjohn! What is the Hb target for a H63D homozygout patient?
    Does Hemoglobin important or not?
    Thanks for your attention.

  10. Hey chris!

    Also have found out i’m homozygous H63D

    I would love to give blood but I was living in the UK for 3 months from 1992-1996 and it’s illegal here. Anything else you could recommend?

    I haven’t had an Iron Test yet, but that’s next for me.

  11. Hello Chris,
    I´ve read is several Lactoferrin product informations that LF is a protein binding iron to make it available for the body so it helps for Iron deficiency as well as for iron overload.
    So would it be a good alternative for spending blood?

  12. small typo below
    So because iron has such incredible roles to have these two faces, the health face and the disease face, we need a sophisticated system to regularly how much we absorb regulate

    Is there a correspondence between hemoglobin and ferritin? i.e. if hemoglobin goes down from say 16 to 15 does that mean ferritin goes down too in a corresponding amount? thanks. ralph

  13. Hi Chris ,I sent you a
    Cumulative iron study but forgot to include my email
    Iron 15umol/L. (10-33)
    Tibc 55umol/L. (45-70)
    Saturation. 27o/o (16-50)
    Ferritin. 491 ug/L. (25-320)
    Did a blood test for hemo but was negative
    I would really appreciate you’re thoughts on these results and do you think I should give blood to reduce the ferritin level
    Thanks karlos

      1. Hi Chris. Would you have any idea why my vitamin D has doubled in the last 6mths ,I haven’t taken any vitamin D supplements at all
        Thanks karlos

  14. Hi I live in Australia ,
    My cumulative iron studies were
    Iron 15 umol/L (10-33)
    TiBC 55 umol/L. (45-70)
    Saturation 27 o/o (16-50)
    Ferritin. 491ug/L. (25-320)
    I would appreciate you’re thoughts on these results ,I did a blood test for hemocromatosis but come back neg
    Thanks karlos

  15. Hi Chris,
    Thank you so much for the detailed information. So glad I ran across your podcast. Amazing work! My situation is the reverse (at least I thinks so, based on no medical background), low ferritin (9). I have been struggling with fatigue, leg / muscle pain, dizziness, not recovering from workouts etc. My Dr noticed my platelet count was going up slightly year over year and asked for more blood work. I also had a bone marrow biopsy which came back negative. Its really frustrating as I have not been able to work out (which is a huge stress relief). It looks like my ferritin and saturation % are really low. What would be the ideal range?

    Platelet count 579
    IRON, TOTAL – 44 (Reference Range: 40-190 mcg/dL)
    IRON BINDING CAPACITY 337 (Reference Range: 250-450 mcg/dL (calc))
    % SATURATION 13 (Reference Range: 11-50 % (calc))
    Ferritin – 9

    My total iron is 44 which is above the range but its right on the border. Also, started taking ferrasorb 36mg of iron, 1x day but have not noticed any changes except for an upset stomach. I am eating organ meats, drinking broth to help with my gut and eating lots of greens. Any help, thoughts you can share would be much appreciated.

    Thank you!
    Elena

      1. Thanks Chris! ProFerrin worked like freaking magic. I felt better within a week. Because of my high platelets I am getting blood drawn once every two months and just got Ferritin pulled and it went up to 36 in 6 weeks (from 9). To caveat I was eating organic chicken liver 1x week and supplementing with Vitamin C. So cool. Thank you for the recommendation. Also, I was just diagnosed with essential thrombocythemia (age 38) Which explains my cbc and high platelets. Any podcasts, MPN hematologist, books, blogs on the topic you can share would be much appreciated. I am on the watch regimen and have to take a baby aspirin every day (which I am not too excited about). Just trying to find proactive ways outside of diet, exercise that I can ensure my blood disorder/cancer does not evolve into MF or something more serious. Chris Kresser has an interesting podacast on it. If you know of any other resources please let me know. THANK YOU!

        1. That’s great to hear Elena. I don’t have any info on on thrombocythemia right now though, unfortunately.

          1. Proferrin has talc and food coloring in it. I’m confused as to why you would recommend this product?

  16. I don’t know if Chris will allow this incredibly long comment… it’s actually a copy and paste, but I believe it’s valuable information.

    FOR NON-RESPONDERS [IRON HEALTH]
    Many of our customers successfully improve their iron status with our Liver product because it naturally provides the cofactors that support endogenous iron production (vitamin A, B12, zinc, copper, etc) along with a moderate amount of heme iron. For this reason, liver should be considered as a first line supplement option to manage iron status. It’s important to know that adding more dietary iron to the equation doesn’t always work… if that’s not the root cause of the issue.

    That being said, sometimes inadequate dietary iron IS indeed the root cause of the issue, in which case, our Spleen product should be considered due to a totally different mechanism of action and the high heme iron content (5Xs more than liver) either in combination with the Liver (or) as a stand alone product. The spleen plays a critical role in hemoglobin health. When the bone marrow is injured or impaired, cell production is damaged. The incredible thing is that the spleen works as a compensatory organ and takes over to generate the blood cells the marrow was producing. It sometimes swells to 5 times its normal size to accommodate this new activity. It’s one of the many ways that our body can adapt and change to overcome injury and disease… it’s amazing how smart our bodies are! In these instances, the spleen needs all the help and nourishment it can get. Like supports like… it’s grounded in science! For this reason, Liver plus Spleen should be considered as a second line supplement option to provide the cofactors that support endogenous iron production, the compensatory support and it’s significant and meaningful amount of dietary heme iron.

    Unfortunately, there will remain a few non-responders if the root cause is a struggling thyroid which is often the case. A struggling thyroid creates a cascade of struggling metabolic processes including struggling digestion and inadequate nutrient assimilation. If a struggling thyroid is the root of the issue, natural desiccated thyroid support should be considered when FREE T3 levels are not in the functional medicine range (i.e. 3.0 – 4.0 pg/mL) and / or reverse T3 (rT3) are elevated. Our Thyroid product provides 30mg of natural thyroid glandular with 470mg of Liver per capsule for those seeking targeted support in harmony with nature — the old fashioned way, the way that our early ancestors did.

    There’s a very good chance that one’s iron status will improve with the Liver product alone… if it does not, consider adding in the Spleen product which provides a totally different biological mechanism and it supplies over 500% more heme iron per serving (12.5 MG). Lastly, if iron status remains unimproved, one’s thyroid status should be evaluated. If indeed a struggling thyroid is at play, consider a natural desiccated thyroid product like this one as an option to naturally balance, nourish and support thyroid health.

    UPDATE:
    There are a few other mechanisms that can contribute to low iron health / blood markers. The most common are as follows:
    -Not adequate digestion and assimilation… think thyroid status and downstream pancreatic enzymes, stomach acidity, bile production.
    -Not adequate digestion and assimilation… think lectins, phytates and other anti-nutrients in the diet.
    -Not adequate immune response… think anemia of chronic disease; Thymus and / or BTC may need to be considered in addition to diet and lifestyle changes.

    Many gut and digestive issues have a deficiency characteristic such as low stomach acid (80% of Americans), low pancreatic enzymes, low bile and/or low liver function. I’m not saying that all do, just a lot!

    Low Acid — Restrict liquids with meals… most Americans actually have LOW stomach acid so stop diluting it with water during dinner… if that’s you, also consider adding Betaine HCL and/or Apple Cider Vinegar to produce adequate stomach acid to get the job done right. A ketogenic / paleo / primal diet can help address the root cause.

    Low Enzymes — Consider eating pancreas or supplementing with pancreatic enzymes to help… a struggling thyroid, heavy metal exposure and pancreatic insufficiency can all suppress enzymes. A ketogenic / paleo / primal diet can help address the root cause.

    Low Bile — Our early ancestors used bile from the gallbladder… it was sprinkled on the meat and used as a condiment as we might use mustard today. Word has it that bile did a lot for the taste of liver. If you can’t do this, consider supplementing with ox bile. A ketogenic / paleo / primal diet can help address the root cause.

    Low Liver — Most Americans have non-alcoholic fatty liver that causes a sluggish liver and sluggish bile… supporting your own liver health with lots of choline from egg yolks and eating grass fed liver will do wonders. A ketogenic / paleo / primal diet can help address the root cause.

    TOP [14] THINGS TO IMPROVE IRON & FERRITIN HEALTH
    In summary, go after the root cause so that you can provide targeted support; however, biological systems are complex and people are lazy. With that said, feel free to throw the kitchen sink at it. Here’s a list of literally everything that I know…
    1. Grass Fed Liver – works for most people
    2. Grass Fed Spleen – different mechansim of action plus tons of hem iron
    3. Grass Fed Bone Marrow – red blood cell production
    4. Grass Fed Thyroid – thyroid affects everything
    5. Grass Fed Thymus and / or Grass Fed BTC – if one suspects it’s anemia of chronic disease… these will support and boost immune health.
    6. Grass Fed Pancreas – supports pancreatic health and provides digestive enzymes
    7. Grass Fed Gallbladder (w/ Ox Bile & Liver) – gallbladder with ox bile to absorb the fat soluable vitamins
    8. Increase acid by restricting liquid with meals, add betaine HCL and consider apple cider vinegar (ACD) with meal too.
    9. Love on the egg yolks for the choline… like Chris Masterjohn says “choline is king.”
    10. Get sensible sunshine, wild fish eggs or add a vitamin D3 supplement
    11. Get fermented veggies like kimchi, sauerkraut and nattō or add a vitamin K complex supplement
    12. Mind your magnesium orally as well as transdermally
    13. Go paleo / primal (< 150g of carbs / day)
    14. Go to our "About Us" page and do EVERYTHING on that list EXCEPT for #8… don't do this if you're not ready for it!

  17. Glanbia makes Bioferrin:
    https://www.glanbianutritionals.com/en/bioferrin
    Their site advertises it as a safe source of iron with “superior and better tolerated delivery of iron to the body.” But, what really confuses me, is Life Extension’s APO-Lactoferrin is Bioferrin!
    So, is Bioferrin Apo- or Holo-Lactoferrin? Or, are there two kinds of Bioferrin?
    I’ve been taking Jarrow’s Lactoferrin 3x250mg/day and it doesn’t seem to be increasing my ferritin (which I thought was the brand used in the pregnancy study). I get tested often and the last test was 19ng/mL. So, I’m desperately trying to find the right Lactoferrin for increasing ferritin.

  18. Hi Chris
    My daughter tells me she has low iron in her body (as opposed to in her blood).
    Can you suggest how she may build up her iron levels in her body?
    Fay Groves

    1. How does she know it’s low in the body? Usually low in the blood means high in the tissues. Blood work can appear “anemic” all the while someone has iron toxicity. Iron is supposed to circulate in the body (reticuloendothelial system), not go into storage. Iron dysregulation is linked to low bio-available copper. Certain labs would bear this out. I get my ceruloplasmin checked, copper & zinc, and RBC magnesium. We have to address the liver’s ceruloplasmin and make sure we get enough retinol (cod liver oil for one thing) and not rely on Ferritin as any kind of iron health indicator. Blood donations will help pull out the toxic iron, and nudge the body into absorbing the iron it needs as ceruloplasmin/ferroxidase enzyme increases.

      https://www.med.unc.edu/medselect/files/anemia2.pdf

  19. Note the recommended supplement, Iron Smart liposomal Iron, contains folate (folic acid) – not good for someone with an MTHFR C677T gene mutation.

    1. 1) It is a bit of a stretch to say that folic acid is “not good” for someone with an MTHFR C677T gene mutation. That polymorphism *may* make it more difficult to utilize folic acid but this is not a given. Especially if you are heterozygous.

      2) One capsule contains only 175mg folic acid – that is a fairly low quantity and should be safe for basically anyone.

      1. 1) I get my information from Ben Lynch who is an expert on this subject – I am not. He recommends limiting with heterozygous and avoiding more seriously with homozygous. If you want to argue the validity of that statement you can argue it with him, but for now I’m going to go with the much more public and distinguished figure than the mysterious “Zoltan.”

        2) First of all it’s 175 micrograms not 175 milligrams. Secondly, the recommendation in Chris’s article is to take 3 tablets. That is 525 mcg per day or 131% the RDA already without considering other sources. It would seem to me that that’s plenty to start causing problems, especially if someone is homozygous.

        All I’m saying is someone with MTHFR SNP’s may want to go with Proferrin ES heme iron over the Iron Smart liposomal iron due to the folic acid content.

  20. Love your work! I’ve seen various sources online (https://www.ncbi.nlm.nih.gov/pubmed/19475341 and http://nutritiondata.self.com/facts/beef-products/3476/2) that show that it’s spleen that’s the king of heme iron as opposed to liver. It appears that beef spleen has up to 5 X’s more heme iron than beef liver. I am a huge uptick in people buying our Grassfed Liver And Grassfed Spleen supplement in an effort to support iron status.

    Is this accurate? Is spleen king when it comes to iron? Please share your thoughts. Thank you.

  21. HI Chris,
    What do you recommend for resolving high ferritin (230 ng/mL) in pregnancy?
    I am in my first Trimester and currently awaiting results of genetic testing for the HFE gene. My brother is compound heterozygote…..
    Is blood donation an option in pregnancy or am I better to wait until after the birth?
    Thank you

  22. Hi, Chris!

    This article was very helpful, since I’ve been struggling with low Hb and ferritin.

    The two brands Chris Kresser recommended are difficult to order online to where I’m at, so what do you think about MegaFoods Blood Builder? It’s a food state iron and multivitamin formula with 60mg vit C, 40mg Folate, 6mg vit B-12, 26mg iron, and 125mg beet root powder.

    Is it worth investing in something like this, or should I simply stick with an iron chelate like Ferrochel (18mg or 26 mg)?

    Thanks

  23. Hi Chris,

    I commented above a while back that I was diagnosed via liver biopsy that I have hemochromatosis and recently I have been experiencing lots of fatigue and joint pain. It had been awhile since I had an iron panel run and decided to check it out. Lo and behold, I am actually anemic. Ferritin is 15 and iron serum is 64. Saturation was on the lower side of 20.
    Not looking for a diagnosis or anything like that, but I am curious if you have seen or heard of this before? Someone who has hemochromatosis becoming anemic?
    Thank you

  24. I had bone marrow biopsy that showed high iron stores but blood was normal . I also have Factor X 1 deficiency – bleeding disorders. Can you please reciprocate on this strange phenomenon. Thank You.

  25. Hi Chris,
    Thank you for this in depth report. I have finally gotten my low ferritin up to a measly 17
    ( I’m also hypothyroid and I suspect the two conditions agrivate each other) unfortunately iron supplements are destroying my digestion. Would colostrum perhaps offer the same benifits as the elusive iron saturated lactoferrin supplement?
    Thaks,
    Christy

  26. Hi, Chris.

    What about high ferritin levels and high transferrin saturation, but no mutations in C282Y and H63D? My ferritin has been pretty high for some time, reaching 630 ng/mL last month, while my transferrin is at 51%. And after genetic testing I know I have no mutations in the aforementioned alleles.

    Just so you know, I don’t have a very high dietary iron intake (and I don’t use supplements that contain iron). At most about 8 mg/day, which is the RDA for adult males. And also, my inflammation seems to be under control, with normal CRP levels.

    Are there cases of hemochromatosis in the absence of mutations in C282Y and H63D? Or could this be a different problem of iron overload? Do you have any idea of what might be going on? Any suggestions on what can I do?

    I hope you can shed some light. And thanks for another great episode!

  27. Hi, Chris.

    Great episode! I was wondering if you could help me. What can you say about high ferritin and high transferrin saturation, but no mutations in C282Y and H63D? My last blood tests showed 630 ng/mL for ferritin and 50% for transferrin saturation…

    Are there other types of iron overload other than hemochromatosis? Or is it possible to be hemochromatosis even in the absence of the C282Y and H63D mutations?

    In any case, is there anything to do besides blood donation? Do you think restricting iron from the diet could be helpful?

    Thank you.

  28. Thanks. It is an injectible PCSK9 antibody that attempts to replicate a mutation found in Dallas African American men with abnormally low LDL levels despite negative environmental factors.

  29. Thanks to your post for making this easy to understand. Since 23andme unmasked, I discovered I’m H63D heteroz. but with average range Ferritin and Transferrin # (in addition to being heteroz. familial cholesterolemia. I’m on Praluent because statins impaired brain function, irritability, and concentration greatly, while Praluent “only” impairs math computation on days 3-5 after injection. I have read that statins may reduce iron levels, which may contribute to the reduction in MIs, although not sure about Praluent.)

    My question is on alcohol (3oz of red wine/day) and whether it drives up iron intake in a way that may impair liver function and cause an increase in glucose levels or whether glucose is simply related to alcohol tolerance in an HFC individual’s liver like mine.
    ————————-
    Here is the scenario: I had elevated liver & uric acid 2 days post-fever and hours after a Praluent injection, so my Dr. suggested I eliminate oxalate and phytic acid containing foods, slash animal protein, eliminate tea, 91% dark chocolate & wine. These foods comprised nearly 100% of my diet. After switching, my numbers returned to normal – and remained normal after reintroducing all foods, except for abstaining from alcohol and dark chocolate and keeping animal protein to 3x3z/day. Meanwhile, my blood glucose dropped to lifetime lows and have stayed low: 103 to 94, vitamin D levels have increased to normal, and Praluent seems to affect computation less.

    P.S. You may recall me from the 1st AHS, I had the poster on tripling HDL.

    1. Hi Jonathan. I’m not familiar with that medication. I don’t think alcohol will drive up iron, but it can contribute to oxidative stress, which is more dangerous in the presence of iron and hyperlipidemia.

  30. Love your work!!

    I own and run Ancestral Supplements… our second most popular item is our Grass Fed Beef Liver supplement… it comes from cows that are pasture raised in NZ… grass fed / grass finished.. all the good stuff.

    Seems that more and more customers are turning to our liver as a source of heme iron in an effort to improve their iron status. I image the copper and B6 may potentially play a role in the success that people are seeing. In one serving, 6 capsules provides about 2mgs of heme iron (doesn’t seem like a whole lot). Some people do well with 6 caps, others double the dose for a few weeks. The overwhelming majority of our customers are doing amazing… I’m quite sure that it has a lot to do with the nutrient density of liver (vitamin A, choline, folate, B12, etc), not just the additional iron.

    My question is this… some customers don’t do so well at first. It seems that maybe 1/15 to 1/20 experience an unusual side effect (e.g. bloating, extreme fatigue, diarrhea, joint pain, etc). We 3rd party test all batches for microbes before shipping… and since our product is freeze dried, there’s less than 1% moisture… seems highly unlikely that it could be a contamination issue.

    One of my customers who experienced diarrhea wrote “this could be a sign or symptom of normal detoxing. For most people, your liver supplement is the first time that they are introducing real, preformed vitamin A (retinol) into their body. Since vitamin A is absolutely essential for detoxing, immune health and methylation, some individuals experience detox symptoms… ” Is this plausible?

    Any idea what could be happening (or) advice… So far, we have encouraged these customers to do this:

    Swallow the capsule with plain water, and that’s it. Wait at least an hour before consuming other foods (be sure to do this earlier in the day rather than at night). Allow plenty of time for digestion and stomach emptying if you want to gauge how it will make you feel.

    The dosing protocol is one capsule a day during week 1… Increase to two capsules a day for week 2… three capsules a day for week 3 and so on… until you make it to six capsules a day.

    Would love any explanation, advice or suggestions that you could offer. BTW, our philosophy is whole foods first, supplements second.

  31. Chris,
    I just wanted to say a huge “thank you” for this podcast episode. I’ve been questioning my iron status for years and, because my iron and ferritin levels were only slightly above the lab reference range, my primary physician reported that I did not show signs of hemochromatosis (although my iron saturation was near 90%!!) After hearing this podcast and your reference to different lab values I decided to order the genetic testing on my own. I found out that I had two copies of C282Y and now am seeing a hematologist to help manage my levels. I can’t imagine how long I would have gone and the potential damage to my liver/organs if it wasn’t for this podcast.

    1. Kate, it is absolutely infuriating to hear that this was dismissed with an iron saturation of 90%. That is profoundly irresponsible. I’m glad you’ve been able to get on the right track.

      1. Kate and Chris can you please guide me on how you lower tsat. My tsat is high but ferritin at normal range. Doctors seem to blow off questions about tsat being high. Thanks for any advice.

  32. I got ferritin tested but it’s transferrin that wasn’t tested.

    I have normal hemoglobin but low ferritin and higher iron serum and Saturation.

    Not sure what it means.

    I have a yellow color to my skin that I hate, and I’m not sure if it’s from hypothyroidism or iron.

  33. Privatemdlab offers Iron, Comprehensive Panel, 52.26 with discount of 15% . All other labs exclude ferritin.

    1. No they don’t. You can get iron panels with ferritin from directlabs.com and healthccheckusa.com.

  34. Thanks for your answer, Chris.

    My tests actually showed that my iron levels aren’t that wonderful – ferritin was 37.5 and transferrin saturation was 27.58. I’m still trying to work out why I have the weird reactions I do, but copper deficiency is the next thing on my list to investigate. I have problems with histamine and even more so with tyramine and I’ve already ruled out most of the other nutrients which affect MAO function, so copper seems like a reasonably likely suspect.

    Thanks so much for your whole site – it has really helped me understand some of my family’s ongoing health issues, and lots of other people on one health group I use refer to your articles and discuss them. It must have been a lot of work to put it all together, and we’re really grateful for the way it helps so many people.

  35. I just got a blood test done and I am having a hard time figuring out what it all means.

    I did it via Labcorp by ordering it myself. I’m guessing it was not a complete test as It did not get transferrin tested. These were the values I got:

    Iron serum 150 ug/dL
    Iron Binding Capcaity(TIBC) 267 ug/dL
    UIBC 117 ug/dL
    Iron Saturation 56%
    Ferritin Serum 33 ng/ml

    Previous test
    Iron serum 140 ug/dl
    Iron Binding Capacity 264 ug/dl
    UIBC 124 ug/dl
    Iron Saturation 54%

    1. Please always include the reference ranges when you post lab results anywhere.

      It looks like your Tf% runs high and ferritin low. I would get your HFE genes checked. Something is a bit amiss, and it could be an early sign of iron overload.

  36. Thank you; this was really informative.

    If you have upregulated ferritin due to excess iron and other causes of inflammation, what happens when you reduce inflammation and so ferritin is reduced a bit – but you still have iron overload? What happens to the iron which was being dealt with by that ferritin? I can see that for someone with anaemia, reducing ferritin would be helpful by taking iron away from long-term storage and making it available for immediate use. But if you have an absolute iron overload, could a reduction in ferritin make symptoms worse in the short term?

    I suspect this might be the case for me – I have negative symptoms from eating iron-rich foods, and also similar negative symptoms from anti-inflammatory supplements / foods, and negative symptoms from lactoferrin too. I have a history of exposure to excess iron and other factors which might indicate iron overload. I’m currently trying to manage the symptoms while I arrange to have labwork done.

    1. Hi Katie, I don’t know the answer to that for sure, but my speculation would be that a phase 2 inducer, or Nrf2 inducer, would help stimulate the protective effects of ferritin. So, milk thistle or something like that.

  37. Thanks for the write-up! One area that I’d be interested in your take on, though, would be the use of iron chelators to intentionally reduce iron absorption or hopefully even reduce total iron stores. For instance, I’ve read that tea can reduce iron absorption quite a bit (at least non-heme iron….heme iron, maybe not?). Also, inositol hexaphosphate (IP6) is reputed to be effective in reducing iron stores. Do you have any take on these?

    My own n=1 experience is that when I drink more green tea, especially along with meals that contain meat, my serum iron goes down significantly.

    1. Joshua, I would reserve these for severe medical conditions and would use them under the supervision of someone who is very well trained in nutrition. They will indeed be effective, but they can induce other nutrient deficiencies.

      1. Not sure what I was thinking when I worded that question. You mentioned that lactoferrin can improve anemia more effectively than inorganic iron supplements. Would the Jarrow product I linked above work?

        1. No, not “lactoferrin.” Iron-saturated lactoferrin, aka holo-lactoferrin, which I can’t find anywhere.

  38. Thanks for the podcast. I believe informing folks about the health issues directly associated with iron overload is crucial.

    I’ve been reading through the many diseased conditions that involve iron deposition, and it includes many. Neurological , infectious, even cancerous conditions often have evidence of iron dyshomeostasis.

    I have iron overload, but not the classic hereditary hemochromatosis. I only have one copy of H63D. I have gotten a genetic test, and have found a good many TFR2 snps, a CP snp, and more.

    Since my family has had many health problems attributable to iron overload, I wonder if having a collection of heterozygous snps. could cause this ?

    I suspect in the future, more will be found about the genetic tendency for iron overload.

    1. Hi Connie, yes it could. Could you please tell me the test you used? 23 and me does not include most of the relevant genes that have rare mutations that can contribute to hemochromatosis apart from the HFE gene.

        1. There are TFR2 SNPs that are on 23andMe and some that are not. Veritas Genetics says they do more but I haven’t looked at it yet.

  39. Great podcast Chris and with fabulous easy translation of the science so that I could understand, thank you.
    What I am not sure of is what to do about having stored iron/ Ferritin of 140 but serum iron is lowish but within range , transferrin saturation of only 18%? My MCHC is always abnormal low – just below range, which I presume means the amount of haemoglobin in red blood cells is low. My doctor states that I am not anaemic because my Estimated Haemoglobin is fine as she sees it although low normal.
    I see it that I have anaemia of chronic disease (Rheumatoid Arthritis – no drugs, try to control with diet, supplements and lifestyle) I have brought my CRP down from 18 over the years to within normal range and last test down to 1.9 but yet still have low available iron and high storage and probably with low absorption kicked in to boot. Should I just continue to eat high iron foods but more so and try to absorb with methods you suggest or will that just push ferritin up higher. I had been under the impression from CKresserthat ferritin above 100 was not desireable and had been considering blood donation but was concerned that with low serum iron incase that would make me ill. I would really value your insight. Thanks so much.

    1. Lynne,

      I would not consider your ferritin high. If your CRP was high, you almost certainly are deficient in iron. You may not be truly anemic, but you’re certainly borderline. I would look out also for reticulocyte hemoglobin as an early indicator. I would try to normalize all CBC values, get TF% up to 30% and not worry about ferritin by iron-rich foods or suppllements if I were you.

      1. Chris,
        In that study you linked above that compared bovine lactoferrin to ferrous sulfate in pregnant women, the researchers stated they used this lactoferrin:
        https://www.dicofarm.com/en/products/infancy/lactoferrin/blf-100/
        It looks like it would be available in Italy to the general public, i.e., not restricted to researchers.

        So, the apolactoferrin that is widely available on Amazon and other websites is iron-free? I am anemic from a chronic inflammatory disease, so I was interested in finding this lactoferrin w/iron. Jarrow has this, but I don’t know if it would be helpful:
        https://www.dicofarm.com/en/products/infancy/lactoferrin/blf-100/

        1. Hi Naomi, thank you for pointing that out. I have emailed the company to ask them about the iron content of that supplement. I would not take a supplement for iron that does not specify its iron content.

          1. Hi Chris
            The Paesano et al papers used Lattoglobina as their 30% iron-saturated lactoferrin*. It appears to be available from Italian pharmacies via eBay.
            My ferritin is 6 and I can’t tolerate any usual forms of iron so I am pretty desperate to order some, but wondered what you thought first?
            Very grateful for your explanation of all this. I was lost!

            *See page 3 of: http://www.goodlifepharma.be/docs/PaesanoRBiometals2014.pdf

  40. Was diagnosed with Hereditary Hemochromatosis 3 years ago when I was hospitalized with Congestive Heart Disease (also hypothyroid and pre-diabetes). After heart and liver biopsies found blue tissue, an iron panel and HFE DNA test were performed. Homozygous C282Y, with a tsat of 100% and a ferritin of 26,205. Was placed in a coma and on life support. Received chelation of some sort. AV Node ablation and a pacemaker. Left the hospital more than a month later with a tsat of 99% and ferritin of 5,200. After 1.75 years of weekly 450 ml phlebotomies, I entered maintenance – ferritin below 50. I now donate blood every 56+ days at the Red Cross. Ferritin was down to 30 as of last September with tsat at 63%. Last 2 hemoglobin’s prior to donations were 17.3 and 17.2, so no anemia. Due to give blood again in a week. Need to get a new complete iron panel soon. Need to relisten to your podcast several times. Thanks!

      1. I live in the States. I’m in maintenance, so have normal ferritin and hemoglobin. The Red Cross does not ask any questions with regards to Hemochromatosis. Besides, I have AB+ blood which they want. It’s a win, win as far as I’m concerned. I’m thankful that they want my blood because it allows me to stay in front of any further loading.

    1. Wow Mark, that sounds like a terrible experience, thank you for sharing. I’m glad you are in a much better position now.

  41. Due to very low ferritin levels, I take 300 mg of non-heme iron daily, Ferramax. This only slightly helps to raise my iron stores. I’m curious as to what happens to the excess iron that isn’t absorbed in the small intestine. I’ve read that it does not get excreted. Any information would be appreciated. Laura

  42. You have a great understanding of complex subject and are able to convey it in easy to understand manner. It is a pleasure to learn from you. You make biochemistry so interesting.!!!

  43. I was diagnosed with hereditary hemochromatosis over 20 years ago via an iron panel and liver biopsy. If I understand your podcast correctly, the only way to know for sure is through genetic testing. Is this correct?

    1. Sandra,

      The genetic testing tells you the mechanism. Hemochromatosis is diagnosed with biopsy. The information in my podcast allows someone to optimize their iron status years if not decades before they would develop diagnosable hemochromatosis.

    1. Hi Ellie,

      Can you please make your question more specific? You can learn about the Bohr effect in great detail in a book such as “Biochemistry” on the NCBI bookshelf.

      Chris

  44. Thanks, Chris

    This (as usual) is really interesting. My impression is that bloodletting in Europe and the Mediterranean was both more common and involved larger volumes taken than does, for example, bleeding of acupuncture points in TCM.

    I wonder whether the fact that approximately one in three Europeans carry a SNP causing problems with iron handling might underlie this. That would make the persistence of phlebotomy overgeneralization (and erroneous theorizing) from valid observations rather than merely being an error based on an erroneous theory. It’s (still) pretty common that the theory is post hoc and then comes to “explain” the observation; when the theory is debunked, then the observations often get dismissed.

  45. Great episode, Chris. I’ve been donating blood a couple times per year for the last few years. I’ve never had ferritin over 150, and I’ve gotten my ferritin to as low as 30 by donating. But those two donations per year barely get my saturation and TIBC within normal range. I’m often slightly out of range for those numbers, indicating high iron.

    My question: should I donate more even though my ferritin gets low? Would that cause anemic symptoms? Thanks much!

    Chris

    1. Chris,

      That’s a bit strange and I’m not 100% sure what to do about it. But I would find our your HFE status, and I would consider supplementing with Nrf2 inducers to try to raise the ferritin, check other nutritional status, especially copper, and try limiting red meat consumption and get a few hundred mg Ca at every meal. Please make sure to review any of these ideas with your health care practitioner before implementing them.

      Chris

    2. Chris M, if I may comment, here’s what I’d do:

      Donating blood is great, of course, because it stimulates the reticuloendothelial iron recycling system. Iron is not meant to be stored – it’s meant to recycle. So ferritin is just not the issue here.

      But increasing your bioavailable copper is huge. We need it to load copper onto Ceruloplasmin for optimal ferroxidase enzyme function. We cannot regulate iron without enough bioavailable copper, otherwise it goes rogue in the body. Low iron in the blood means HIGH in the tissues and organs, Chris.

      I’ve trained under Morley Robbins in mineral metabolism and always check my clients for signs of copper/iron dysregulation.

      I always suggest a full iron panel, which includes looking at Ceruloplasmin, copper, zinc, Mag RBC, and the other iron markers (serum, TIBC, sat%, transferrin, etc). Ferritin is NOT a true iron marker.

      To increase my own bio-copper, I consume Rosita cod liver oil for the Retinol, grassfed liver, plenty grassfed butter and eggs, and whole food C. The more you donate, the more your iron starts pulling out of the tissues and circulating….also triggers production of new red blood cells.

      If you’re a fast oxidizer, as determined by the hair analysis I do, you may need additional copper via copper liver chelate, but that’s not a suggestion for the general population since most folks are slow oxidizers.

      Please stop focusing on Ferritin. 70% of oxygen is carried in hemoglobin. The other markers will level out as you offload toxic unbound iron in the body via chelation and blood donation. There’s more, but this is pretty important.

      See Sir Douglas Kell, for “Iron Behaving Badly.”
      Also review the Root Cause Protocol by Morley Robbins. Videos are on You Tube as well. And blessings to you.

      1. Thank you Vicki. I agree ferritin is not a specific iron marker on its own. I don’t focus on it to the exclusion of other markers. But I still think it’s a worthwhile marker as part of the panel.

  46. I studied biochemistry from Harper’s Illustrated Biochemistry, by Murray, Granner,Mayes and Rodwell, McGraw hill edition,2003, USA
    There is an extensive discussion on two specific mutations of HFE gene in individuals of hereditary hemochromatosis. As a result of such mutations, there is a loss of regulation of iron absorption in the small intestine. An accumulation of iron occurs in various tissues, primarily in the liver, pancreatic islets, skin and heart muscle. This causes damage such as hepatic cirrhosis, diabetes mellitus, skin pigmentation and cardiac problems. However, in this book I could not find any reference to oxidative stress. There is a table of laboratory tests for assessing patients with iron metabolism disorders.

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