November 16, 2016
Iron Toxicity Post #43: The ‘gestation and birth’ of iron toxicity

Today is my Natal Day! Let me first thank the many folks who’ve taken the time to reach out and celebrate with me. I’m most grateful to this loving and giving community, and I’m also grateful to my parents, especially my Mom, for allowing this little life to exist.

My Mom’s Dad, John M. deLashmutt, Jr. had an annual tradition of giving a gift to his family on his natal day. That always left a big impression on me. So given that Magnesium Advocacy Group (MAG) is a second family of sorts for me, well here’s my gift to you all. 

It’s a bit complicated, a bit convoluted, and also a bit counter-conventional.

I realize that I have been an incessant bore this year with my non-stop posts about iron toxicity.  Well, we are not done yet. Today’s post is intended to drill into how this iron chaos starts, from the very inception of life. 

I am piggybacking on a recent post by a member who shared some illuminating research recently (Steer, et al, 1995), but only four people noted its existence last week. 

I believe this contemporary issue of “anemia of pregnancy” is completely out of control. It is completely misleading by clinical training as well as understanding of basic mineral metabolism especially as it relates to haemoglobin (Hgb) & red blood cells (RBC). 

It turns out that among the most important aspects of early life, as a mammal, is creating and managing our red blood cells.

Fraser, S.T., et al. (2011). “Heme Oxygenase-1: A Critical Link between Iron Metabolism, Erythropoiesis, and Development.”

An important quotation from the very beginning of this article was:

“The first mature cells to arise in the developing mammalian embryo belong to the erythroid [Red Blood Cell] lineage. This highlights the immediacy of the need for red blood cells during embryogenesis and for survival.”

For those that have been following my incessant posts these past twelve months, you will know that every facet of red blood cell formation and metabolism is copper dependent. It not about iron status, as we know.

Fox, P.L. (2003). “The copper-iron chronicles: The story of an intimate relationship.” (No full text available now)

I would encourage you to read this classic article as it explains how and why this has become so confusing.  What the Fraser (2011) article also highlights is yet another aspect of Hgb metabolism is copper dependent, which is heme oxygenase-1 (HO-1) protein that is the rate-limiting enzyme in the breakdown of haemoglobin.

Ideally, these RBCs that carry the Hgb that carry the oxygen are supposed to live, on average around 120 days and then they get recycled. As it turns out, that is when in copper deficiency state, the amount of HO-1 increases thus causing an increase in the rate of Hgb turnover.

Johnson, W.T., et al. (2004). “Increased heme oxygenase-1 expression during copper deficiency in rats results from increased mitochondrial generation of hydrogen peroxide.”

This is not an insignificant fact about RBC/Hgb metabolism.

I would go so far as to state that the research that the member brought to our attention especially the Steer, et al., 1995 in BMJ, is among the most powerful studies to explain how and why society is being methodically exposed to excess iron.

Steer, P., et al. (1995). “Relation between maternal haemoglobin concentration and birth weight in different ethnic groups.”

The magnitude of this article is that Hgb in a pregnant woman, especially in the second half of the pregnancy is supposed to drop to 8.5-9.5 mg/L. 

This is a critically important fact and set of studies that challenges the conventional clinical paradigm of where iron levels are supposed to be during the course of a healthy pregnancy.

What they also found is that as Hgb drops, birth weight of the infant rises. High Hgb is a sign of potential premature birth and pregnancy risk.

What is the big deal about adding iron to a woman who’s Hgb appears low?

  • It’s a clear signal that more likely than not that the pregnant woman and the babino are copper deficient.
  • It increases the chances of undermining the production and metabolism of ceruloplasmin that is key for proper healthy copper metabolism.
  • It increases the chances for oxidative stress in both the Mom and developing foetus.  A particularly poignant and penetrating look at this dynamic was outlined by Keyer & Imlay (1997):

Keyer, K., Imlay, J.A. (1997). “Inactivation of Dehydratase [4Fe-4S] Clusters and Disruption of Iron Homeostasis upon Cell Exposure to Peroxynitrite*”

This research should send a chill down the spine of those taking iron supplements and those getting iron infusions. 

I encourage any who are pregnant, or planning to get pregnant to read and study this research carefully. Please share it liberally with your Obstetrician, Midwife, etc. and do not be surprised that they may not know these issues, understand these implications, nor practice in a way to avoid iron impacts.

I would encourage you to have the Full Monty Iron panel and have it properly interpreted.

A votre sante!

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