Iron Toxicity Post Index

Iron Toxicity Post Index

Scroll through the entire list of Iron Toxicity Posts from this single page.

Iron Toxicity Post #1: Menstruation does not automatically mean Iron Deficiency Anemia!

Iron Toxicity Post #2: Things that go ‘bump’ in the night.

Iron Toxicity Post #3: The underlying pathogenic event in oxidative stress is cellular iron mismanagement. 

Iron Toxicity Post #4: It’s the bookends of iron that will kill your metabolism.

Iron Toxicity Post #5: A deficiency of Ceruloplasmin (Cp) is one of the earliest manifestations of Copper deficiency.

Iron Toxicity Post #6: Magnesium deficiency and abnormal iron metabolism.

Iron Toxicity Post #7: All manner of pathogens – fungal, viral, mycotoxin etc., MUST have iron to flourish and grow!

Iron Toxicity Post #8: Why Morley has ‘lost it’ and is obsessing over iron and the proper management of iron.

Iron Toxicity Post #9: Bioavailable copper is essential to reduce iron induced hydroxyl radical (*OH)!

Iron Toxicity Post #10: OK, know anybody who’s struggling with Arrhythmias?

Iron Toxicity Post #11: If the Sun is the ‘center’ of our Universe, I’m coming to regard Ceruloplasmin as the ‘Sun’ of our universe of metabolic activity.

Iron Toxicity Post #12: Find out what the TRUE source of most, if not all, chronic disease especially neurodegenerative conditions.

Iron Toxicity Post #13: STOP using iron-enriched, iron supplements and ignoring your ceruloplasmin status!

Iron Toxicity Post #14: For those who doubted my post on iron overload as the cause of osteoporosis!

Iron Toxicity Post #15: For those who are or know someone who is struggling with Endometriosis

Iron Toxicity Post #16: A ‘primer’ on the TOTAL relationship of Copper and Iron Metabolism

Iron Toxicity Post #17: Could ‘Folate deficiency’ be an EPI-genetic deficiency of bioavailable copper?

Iron Toxicity Post #18: Most on this planet are dealing with ‘Subclinical Iron Overload’

Iron Toxicity Post #19: Start connecting the dots on how magnesium deficiency is tweaked by iron

Iron Toxicity Post #20: Iron dysregulation and magnesium deficiency are at the heart of most, if not all, chronic conditions.

Iron Toxicity Post #21: We are ‘Dead Flies Walking’

Iron Toxicity Post #22: There is a difference between ‘Iron Deficiency and ‘Iron Dysregulation’!

Iron Toxicity Post #23: Iron shavings in processed food!

Iron Toxicity Post #24: Diabetes is NOT a medical disease!

Iron Toxicity Post #25: Iron movement, not iron storage! 

Iron Toxicity Post #26: Red Blood Cell metabolism is by inference Iron metabolism

Iron Toxicity Post #27: On the Iron-ic ignorance of blood testing

Iron Toxicity Post #28: Stop allowing ferritin only blood test!

Iron Toxicity Post #29: Irregular iron blood markers especially low ferritin is code for more magnesium, ceruloplasmin and B2

Iron Toxicity Post #30: How blood pressure gets tweaked.

Iron Toxicity Post #31: When iron is out of control, it has a profound effect on magnesium status!

Iron Toxicity Post #32: How oxidative stress created by iron causes metabolic changes.

Iron Toxicity Post #33: Lyme has a relationship with Iron dysregulation!

Iron Toxicity Post #34: Iron dysregulation causes cancer.

Iron Toxicity Post #35: Mother Nature intends iron to be moving not stored.

Iron Toxicity Post #36: You are not anemic!  

Iron Toxicity Post #37: There’s no such thing as heart failure!

Iron Toxicity Post #38: Why Vitamin D and iron is not a good idea!

Iron Toxicity Post #39: Excess unbound iron is very bad! Get properly tested.

Iron Toxicity Post #40: Medication can cause iron induced oxidative stress!

Iron Toxicity Post #41: Anemia of Inflammation and how it relates to anemia

Iron Toxicity Post #42: Keep it simple searchers!

Iron Toxicity Post #43: The ‘gestation and birth’ of iron toxicity

Iron Toxicity Post #44: Iron Elephant

Iron Toxicity Post #45: Brain aging and Alzheimer’s  

Iron Toxicity Post #46: The “Reader’s Digest” version of what causes mitochondrial dysfunction

Iron Toxicity Post #47: The truth about the cause of mitochondrial dysfunction (as least as I see it)

Iron Toxicity Post #48: Dealing with cancer

Iron Toxicity Post #49: IP-6 offers a compelling solution to iron overload 

Iron Toxicity Post #50: The Iron-ic deceit of Hormone D

Iron Toxicity Post #51: The Deceit of ‘Anemia’

Iron Toxicity Post #52: Are you still anemic? 

Iron Toxicity Post #53: You were not born with a ‘Red Light’ deficiency!

Iron Toxicity Post #54: A Tale of Two Cities

Iron Toxicity Post #55: Ferritin is NOTHING, Hemosiderin is EVERYTHING!

Iron Toxicity Post #56: How Anemia of Inflammation is misdiagnosed!

Iron Toxicity Post #57: The very source of this Iron-c crisis that is pandemic on this planet

Iron Toxicity Post #58: Toto is my HERO!

Iron Toxicity Post #59: A Tale of two irons and the hepcidin peptide that regulates them

Iron Toxicity Post #60: ‘Am I really anemic?’ or said another way: ‘Not known because not looked for’

Iron Toxicity Post #61: EYE-ronic origin of Alzheimer’s disease

Iron Toxicity Post #62: You do NOT have a Candida Infection, you DO have an Iron Infestation!

Iron Toxicity Post #63: Setting the story straight about iron homeostasis

Iron Toxicity Post #64: Ferroxidase blocks the Hydroxyl Radical (OH*)

Iron Toxicity Post #65: There is NO such thing as ‘Iron Metabolism’.  There is ONLY Copper<>Iron Metabolism

Iron Toxicity Post #66: ‘Iron and the RBC (Red Blood Cell): Is this where the assault begin?

Iron Toxicity Post #67: There is 5 TIMES MORE IRON in breast cancer cells than normal cells

Iron Toxicity Post #68: It’s really the iron, especially in gluten!

Iron Toxicity Post #69: Retinol-A is an absolute requirement for building blood and especially hemoglobin.

Iron Toxicity Post #70: The Iron-ic truth of osteoporosis

Iron Toxicity Post #71: There is no iron deficiency anemia on planet earth, but there is a pandemic of anemia adiponectin deficiency

Iron Toxicity Post #72: Iron deficiency is associated with RESISTANCE to infection

Iron Toxicity Post #73: Why I detest hormone-D supplementation.

Iron Toxicity Post #74: Will the REAL Vitamin-A step forward

Iron Toxicity Post #75: PROOF that Copper Deficiency is the CAUSE of so-called ‘anemia’

Iron Toxicity Post #76: ‘Hypoferremia’ (Low Serum Iron) occurs in ANY Inflammatory state

Iron Toxicity Post #77: Iron Metabolism is REGULATED via intake – NOT excretion!

Iron Toxicity Post #78: ALS is caused by the over-expression of SOD (because Copper is MIA and Iron is STUCK)

Iron Toxicity Post #79: Is Stored Iron Safe?

Iron Toxicity Post #80: Cholesterol is an Anti-Oxidant? HUH?

Iron Toxicity Post #81: If you’re 6-9 months Pregnant, YOU ARE NOT “Anemic!!!!”

Morley and Kristan’s first LIVE Q & A (members only) – Ascorbic Acid and our ceruloplasmin

Morley and Kristan’s first LIVE Q & A (members only) – Ascorbic Acid and our ceruloplasmin

MEMBERS WEBINAR!

On Monday afternoon, 14th January 2019, at 4pm CST (7am Tuesday 15th January Brisbane Australia time), website members can join Morley and Kristan for a LIVE webinar on the topic of Ascorbic Acid.

It’s been a HOT topic for a long time – why exactly ascorbic acid is not recommended here, and why we suggest whole food vitamin c instead.

We have already had an introductory discussion for everyone to see on our Facebook page here.

The recorded video from the full session is available lower down in the thread here (below the 30 minute video).

How to get there?

  • Login to your member account (or register to join us if you aren’t yet a member!)
  • Head to the ‘Musings by Morley’ section
  • Look for the ‘January Q & A’ post (from January 2019!)
  • Connect to us via the link included.

We can’t wait to have more people joining us in this session and asking questions live – being a webinar, we can have you live with us, or chatting with us via the chat.

See you there!

Kristan and Morley

PS. Don’t forget to stop by and watch all the other amazing videos that are available within the membership area – Morley and Dr Ben in the RCP101 video course, and more within ‘Musings by Morley’ part of the forum.

PPS. A recording will be available after the event, for those who can’t join in live. It’s always fun to join the energy of the conversation LIVE though. 🙂

Iron Toxicity Post #70: The Iron-ic truth of osteoporosis

Iron Toxicity Post #70: The Iron-ic truth of osteoporosis

(The following was originally posted on Facebook Magnesium Advocacy Group on May 13, 2018) Iron Toxicity Post #70: The IRON-ic TRUTH of Osteoporosis and it’s Origin…[A special thanks! to my colleague Kristan Kershaw who took a sow’s ear of a draft post and turned it into a most amazing and timely post for the Moms out there! Kudos to KK for all your efforts!]In many countries, this weekend includes a celebration of Mother’s Day. To the many women out there who are Mothers, and to the many who perhaps are not, this post is for all of you. And to the many MAG-pies and MAG-nets who have elderly parents they care for, or are worried about, or others they care for who are ‘at risk’ of osteoporosis, this post is for you, too!

Recently there’s been a bit of discussion around osteoporosis – it’s time to set things straight based on the research out there, not assertions on a website.

Do you know what osteoporosis actually is? Your understanding of Osteopenia and/or Osteoporosis would not be enhanced by reading this post (https://therootcauseprotocol.com/wp-content/uploads/2022/09/Osteoporosis-Prevention-and-Natural-treatment.pdf) by a well-meaning MAG-pie.

Do you think it is calcium loss?

Needing to drink more milk?

Are hormones not in proper balance?

‘Just in your genes’?

Actually no. ‘It is caused by an imbalance in bone remodeling, where bone resorption by osteoclasts exceeds bone formation by osteoblasts.” (Christenson RH. 1997 and also supported by Zarjou A et al, 2010)

Unlike the ‘Stop autoimmunity’ website assertion that ‘there is a limited time that we can increase our bone mass’, we are continuously regenerating new bone. The bones we grow as children and young adults do not suddenly stop cellular growth and repair when we hit our 30s and 40s. Beyond continual repair and regeneration of bone, the bone marrow provides us with ongoing supplies of red blood cells and immune cells.

There’s Yamasaki K, Hagiwara H. 2009 study, which is titled “Excess iron inhibits osteoblast metabolism” – well, that’s fairly self-explanatory isn’t it? They talk about how their results give an indication that iron overload might give rise to osteoporosis by inhibiting osteoblast proliferation and differentiation.

What one of the studies presented below raises, is that if we are struggling to make bone marrow, then perhaps our capacity to make new blood cells may be hindered. What do you think could be the underlying reason for this hindrance?

First, I want you to start thinking about what the other 69-iron toxicity posts and numerous other discussions covered about how excess, unbound iron fuels the aging process. What happens to our iron levels as we get to around 40?

If we look at Figure 1 (slightly adjusted from the ‘Stop autoimmunity’ original source), we notice women’s bone density suddenly appears to decrease from the 40-50 age range.

What do we know happens in the 40’s and 50’s for women? Menopause.

So Osteoporosis and menopause – what’s the link?

What does this mean in the context of metabolism in the body? Suddenly women are accruing iron, not bleeding every month, the iron building up in their body is causing changes in the osteoblasts, which prevents them from maintaining density. What does excess unbound iron cause in the body? Oxidative Stress.

Winding back a bit further, Reactive Oxidative Species (ROS) such as superoxide and that pesky ‘oxidative problem child’ H2O2 (Hydrogen Peroxide) should be neutralized by our natural antioxidant enzyme systems – however in mineral dysregulated bodies, which are high in unbound iron, low in bioavailable copper and magnesium, and with little antioxidant support in the body (let’s think of our ever-busy Ferroxidase and Superoxide Dismutase (SOD)) if we do not have enough of the components in our antioxidant systems, we cannot neutralize these ‘accidents’, that are called ‘oxidants’ that are also called, Reactive Oxidative Species.

Cellular changes start to happen, let’s say, osteoblasts cannot keep up with recycling of the bones, and our bones get weaker and less able to stay in balance.

What should make you all uneasy about this is that there are few, if any, articles that are published which note the changes and challenges in iron metabolism and its known and well chronicled impact on bone health and bone replacement – why is this not routine? Why is this not shared or tested for?

How many MAGpies or MAGpie family members/friends have had their iron investigated when also investigating osteoporosis?

There is overwhelming evidence in the research presented in Jia et al, 2012, “Ferric Ion Could Facilitate Osteoclast Differentiation and Bone Resorption through the Production of Reactive Oxygen Species”.

They present strong evidence around the diagnosis of Osteoporosis being clinically to be from oxidative stress in the Bone Recycling Program. More papers are listed in the reference list below.

↑ Iron = ↑ Oxidative stress = ↓ OsteoBlast regrowth = ↓ Bone Density = ↑ Chance for Osteopenia/Osteoporosis

Osteoporosis and Estrogen/Hormones – what’s the link?

We already know from several past iron toxicity posts that hormones are ruled by enzymes that RELY on minerals for activation in the body – so, if our adrenals aren’t working effectively (stress anyone?), the body goes into a ‘backup mode’ and changes happen in the hormones (Estrogen Dominance so often rolls on in! What is now known is that the estrogen is not low, but simply not bioavailable. Sound familiar?)

And what’s underlying these habitual, and all-too-common hormonal changes? Once again, excess, unbound iron!

There is discussion in the paper by Jian J, Pelle E, Huang X., 2009, about the involvement of hormones, including estrogen, in osteoporosis.

“……In addition to Estrogen deficiency, abnormally high iron is a key cause of postmenopausal osteoporosis.”

So, are you telling me that if we have women experiencing Estrogen deficiency, then abnormally high iron is a key player in osteoporosis as a result? What? Hormones are related to bone density?

How many more MAG members just pricked up their ears?

I would suggest considering the other ‘book end’ of Estrogen Dominance having an involvement there, too – as has been talked about extensively in past iron toxicity posts/discussions in MAG. Instead of obviously high Iron by the definitions commonly used, we know that iron stores are building, while the amount of ‘available’ and ‘usable’ iron is dropping; bioavailable copper and magnesium are bottoming out. The true iron levels are not obvious particularly because of the testing generally done by conventionally trained practitioners.

Underlying the Estrogen Dominance – there is still excess, unbound iron wreaking havoc in the woman’s body, preventing bone regeneration and seeing bone density dropping rapidly, especially when women become post-menopausal.

(Which leads to ↑ Iron via supplementation in allopathic and other conventional practitioner circles and ↑ estrogen, and ↑ risk for Osteoporosis!)

More iron loading, more Estrogen Dominance problems, more drugs and synthetic hormones added to their body to ‘fix’ the problem (i.e. ‘treat the seats’ of symptoms) and the sicker female folks get.

Huo Y et al, 2012 comment within their article “Excess iron is associated with various diseases including osteopenia and osteoporosis, which are closely related to the alternation of the endogenous estrogen level”. They talked about creating a mouse model by removing ovaries and then monitoring hemoglobin and serum iron (both decreased) yet the iron level in the liver and spleen tissue increased. Hepcidin was elevated in these mice too.

When was the last time your doctor tested your hepcidin levels if they were worried about anemia?

Stick with me here a bit longer here-  if Estrogen contributes to iron homeostasis, and we have a stressed out population of women who have been misled and misfed information about what is really in their food, what is in their birth control pills, they have led a low-fat (i.e. low Retinol-A, low-bioavailable copper) diet, eaten less and less of the foods their parents (Mothers) and grandparents (grand-Mothers) ate potentially more laden with sprays and processed food than previous generations.

You mean to tell me that when post-menopausal, there are signs that it’s likely more Iron will be stored via Hepcidin in the organs, while the amount of iron in their hemoglobin and serum drop. What? Does this sound familiar to any of you reading along?

Not to mention that we have a population where more and more women are having symptoms of or labels applied of estrogen dominance – so many either being thrown into surgical menopause (often not keeping ovaries too!) or due to other imbalances.

Now let’s build our list…

↑ Excess Iron = ↑ Oxidative stress = ↓ osteoblast regrowth = less bone density

↑ Excess, unbound iron = ↑ Estrogen = ↑ Iron stored into the Liver via Hepcidin + ↓ levels of Hemoglobin + Serum Fe

Osteoporosis and retinol – how can it help?

I have recently discussed the critical importance of Retinol in our bodies to help get the body moving Iron where it needs to go, getting our Bioavailable Copper increased, and so much more.

We know that new blood cells are made within the bone marrow (or the cascade of cell creation is started there at a minimum). We are learning today that when there is high oxidative stress as iron increases in the body, that the regeneration of bone cells (osteoblast regeneration) is reduced.

What else do the osteoblasts need to carry out the repair and regeneration? Three key Ingredients:

Retinol-A (Vitamin A), Bioavailable copper and Magnesium

Bloem, 1995 stated that ‘repletion with vitamin A was followed by regeneration of the bone marrow, disappearance of the Hemosiderin from the spleen and liver, and erythroblastic activity.’ That’s a BLOCKBUSTER SHIFT in the dynamics of bone activity, btw.

We have established above that there’s more iron getting stored into many women’s livers and spleens from hormone imbalances, that with increased oxidative stress, there’s less osteoblast regrowth in the bones and less bone density and now we are saying that retinol (vitamin a) intake from food causes regeneration of bone marrow, reduction in the loading of iron in the spleen and liver, and increased cell production?

No way?

What’s compounding these changes? ‘Stressors!’ (From our very stressful modern day life, from the chemicals put into our bodies, food, inherited from our mothers/ grandmothers, from blue light bombardment, from expectations of mothers to be everything to everyone 24/7, from excess, unbound iron, the never-ending process of creating oxidative stress keeps chugging it out!)

Back to our list…

↑ Excess, unbound Iron = ↑ Oxidative stress = ↓ Osteoblast regrowth = LESS bone density

↑ Excess iron = ↑ Estrogen = ↑ more Iron stored into the Liver via Hepcidin + ↓ Hemoglobin + Serum Fe

↑ Retinol-A (via food repletion) = ↑ bone marrow regeneration = ↑ Osteoblasts (maintain bone density) + ↑ new blood cells = ↑ Ferroxidase activity = ↓ Excess, unbound iron = ↓ Oxidative Stress

Vitamin D, zinc and calcium supplementation – why aren’t these critical to bone strength as we keep getting told?

We are already starting to see a picture on how come the RCP (Root Cause Protocol) ties in with reducing the chances of osteoporosis, reduce excess unbound iron, decrease oxidative stress via adrenal support and magnesium, increase bioavailable copper and retinol through food/whole food supplements, and we have our bases covered for the true osteoporosis risk factors.

So how about the Vitamin D (Hormone-D!), K2, zinc and calcium side of things?

These have been addressed – ad nauseum — by previous posts, but here’s a quick summary.

– We get K2, zinc and calcium from eating an ancestral diet, which is as wide and varied as possible.

– We get Hormone-D from sunlight and foods such as eggs and cod liver oil (both great sources of retinol – who would have thought??).

– Calcium carbonate supplements (most commonly suggested) require 12 steps to metabolize them into a form we can actually use. Other than many of the population not having the energy/mineral reserves to deal with that, many of us are going to grind to a halt (think cement = calcium) if calcium is supplemented from anything except food

– Supplemental Hormone D kills retinol/retinoic acid in our liver, eyes (see iron toxicity post #62) and elsewhere in the body, preventing it from being able to facilitate cellular regeneration, repair and renewal, leading to a weakening in bone strength and repair.

– Excess hepatic iron disrupts the 25(OH) enzyme (also mag dependent) – if we have excess iron in our liver and we don’t have enough magnesium, we can’t carry out the transfer of Hormone D within the body – so it’ll test ‘low’.

– What’s the biggest reason for insufficient zinc in the body? Excess unbound iron.

– Did you know: Magnesium from food and suggested supplemental sources helps the calcium to go where it’s needed?

We need bioavailable copper (Evans et al, 1970) and retinol to synthesize ceruloplasmin – And it turns out that Retinol-A is absolutely critical to loading that ^^^^ Copper to ensure Ferroxidase (FOX) enzyme function (Barber & Cousins, 1987)

If we have insufficient Retinol-A, and a lack of magnesium and a lack of Bioavailable Copper, what happens? We don’t have enough ferroxidase function, and we are faced with Iron that is dysregulated and prone to act out!

What else happens when we don’t have enough ferroxidase function?

We build up excess stored iron, yet apparent low blood Iron (because the body wants to protect us from the massive oxidative stress that high or hiding Iron in the blood represents) our adrenals get stressed out, we start to get any number of metabolic ‘conditions’ kicking in – hormonal imbalances, autoimmune conditions, diabetes, arthritis, depression, Alzheimer’s, our healthcare practitioners tend to dish out more iron, Vitamin-D and any number of other medications which only compound and confuse these conditions!

Now the way the RCP (Root Cause Protocol) looks at these things is dramatically different.

Look at our expanded list now!

↑ excess Iron = ↑ Oxidative Stress = ↓ Osteoblast regrowth = LESS bone density

↑ excess Iron = ↑ Estrogen = ↑ more Iron stored into the Liver via Hepcidin + ↓ Hemoglobin + Serum Fe

↑ Retinol (via food repletion) = ↑ Bone Marrow Regeneration = ↑ Osteoblasts (maintain bone density) + ↑ New blood cells = ↑ Ferroxidase enzyme function = ↓ Excess, unbound iron = ↓ Oxidative Stress

↑ Magnesium + Bioavailable Copper + Retinol-A = ↓ Oxidative Stress including ↓ Excess, unbound Iron = less chance of osteoporosis/osteopenia (and the added bonus that Hormone-D will stabilize, too, in general!)

What does all this really mean? Just tell me how to reverse this osteoporosis risk.

The research behind the RCP (Root Cause Protocol) has always been encouraging the consumption of whole foods to obtain whole food vitamin c (to help with bioavailable copper), magnesium and adrenal support (to reduce stress on the body and provide important components for making Mg-ATP (energy)) and retinol (vitamin A).

The research shared today is emphasizing that this is the right path, and that if you want strong bones, low risks of fractures, and to reduce the chance of getting osteoporosis. Do the protocol!

 Reduce your oxidative stress (from food, physical/mental stress, get plenty of sleep, etc).

 Increase your retinol-A, Bioavailable Copper and Magnesium to give you more energy, reduce inflammation and give your body a chance to heal itself

 Release stresses of the past and emotions, which may be holding you, back from progressing.

¬ Reduce your iron load (when ready – support your body before donating blood!)

RCP = ↓ oxidative stress + ↑ via Bioavailable Copper, Mag, Retinol-A = ↓ Excess, unbound Iron = ↓ chance for osteoporosis AND better mineral flow throughout the body as well as ↑ positive health outcomes (= DEC ↓ “Stress!”)

Let’s go with the simplicity of eating real food, whole food supplements and reducing “Stress!” in our life of all forms, rather than getting too lost in the enormity of the deception which has been around us on this and so many other topics we cover in this MAG FB Group (https://www.facebook.com/groups/MagnesiumAdvocacy)! The deception is very real, but the effort to ‘fight it!’ is simply not worth the expended MBR (Mag Burn Rate) associated with that effort!

So here’s to a Happy Mother’s Day to all of the Moms, Mums, Grannies, Grandmothers, etc. that have allowed us all to be here, to be apart of this grand experience called Planet Earth! Most of all, thank you for the love and patience that you have shared and taught us, and may we enrich the lives of those around us – whether related or not — with the mineral truths and insights that are regularly being shared on this MAG FB Group (https://www.facebook.com/groups/MagnesiumAdvocacy).

A votre sante!
MORLEY M. ROBBINS

References within or relevant to Iron Toxicity Post #70

Christenson RH. 1997. “Biochemical markers of bone metabolism: an overview.” Clin Biochem 30:573–593. www.ncbi.nlm.nih.gov/pubmed/9455610

Zarjou A et al, 2010, “Ferritin ferroxidase activity: a potent inhibitor of osteogenesis.” (www.ncbi.nlm.nih.gov/pubmed/19821764 )

Weinberg ED, 2009-July, “Iron Loading in humans: a risk factor for enhanced mortality & morbidity.

”https://www.researchgate.net/publication/232033197_Iron_loading_in_humans_A_risk_factor_for_enhanced_morbidity_and_mortality

Weinberg ED, 2008, “Role of Iron in Osteoporosis” (Abstract ONLY) www.ncbi.nlm.nih.gov/pubmed/19337160

Jia P et al, 2012, “Ferric Iron Could Facilitate Osteoclast Differentiation & Bone Resorption thru ROS” onlinelibrary.wiley.com/doi/pdf/10.1002/jor.22133

Yamasaki K, Hagiwara H. 2009, “Excess iron inhibits osteoblast metabolism” www.ncbi.nlm.nih.gov/pubmed/19735707

Jian J et al, 2009-Dec, “Iron & Menopause: Does Inc Iron Affect the Health of Postmenopausal Women?” www.ncbi.nlm.nih.gov/pmc/articles/PMC2821138/

Cervellati C et al, 2014 “Oxidative Stress and Bone Resorption Interplay as a Possible Trigger for Postmenopausal Osteoporosis”
www.ncbi.nlm.nih.gov/pmc/articles/PMC3913453/

Rossi F et al, 2014-Dec, “Iron overload causes osteoporosis in thalassemia major patients through interaction with transient receptor potential vanilloid type 1 (TRPV1) channels”
www.ncbi.nlm.nih.gov/pmc/articles/PMC4258755/

Xiao W et al, 2015-Sept, “Iron overload increases osteoclastogenesis and aggravates the effects of ovariectomy on bone mass”
https://joe.bioscientifica.com/view/journals/joe/226/3/121.xml

Cervellati C et al, 2014 “Oxidative Stress and Bone Resorption Interplay as a Possible Trigger for Postmenopausal Osteoporosis”
www.ncbi.nlm.nih.gov/pmc/articles/PMC3913453/

Jian J, Pelle E, Huang X. 2009. “Iron and menopause: does increased iron affect the health of postmenopausal women?” Antioxid Redox Signal 11:2939–2943.

Hou Y et al, 2012, “Estrogen Regulates Iron Homeostasis through governing Hepatic Hepcidin expression via an estrogen response element”
https://www.sciencedirect.com/science/article/abs/pii/S0378111912011699

Barber EF & Cousins RJ, 1987, “Induction of Cp Synthesis by Retinoic Acid in Rats–Inf of Dietary Copper & Retinoic” Acid_JrlNutrition www.ncbi.nlm.nih.gov/m/pubmed/3655940/

Guggenbuhl P, Deugnier Y, Boisdet JF, et al. 2005, “Bone mineral density in men with genetic hemochromatosis and HFE gene mutation.” Osteoporos Int 16:1809–1814 (www.ncbi.nlm.nih.gov/pubmed/15928800)

For Facebook Discussion

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