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DiscussionLet's talk about it: The science of itIron Deficiency and Morley Robbin …

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Iron Deficiency and Morley Robbins “Root Cause Protocol”

#1 · March 16, 2020, 5:24 pm

Hi everyone! 😁

So I got my iron tested recently, and these were my results (out of range results in red):

ferritin (blood) 9 (reference range 13-150 ug/L)
iron 6 (reference range 6-35 umol/L)
TIBC 46 (reference range 41-77 umol/L)
saturation 0.13 (reference ranges 0.15-0.50)
Hgb 132 (reference range 116-159 g/L)

I was prepared to get iron injections or infusions (because supplements never raised my ferritin levels in the past—I had similar levels 15 years ago, and only managed to raise them to 86 after getting iron injections), HOWEVER a friend in a facebook group who had a bad experience with iron infusions (even though she was truly anemic), suggested I look into the work of Morley Robbins (of the “Magnesium Advocacy Group” and the “Root Cause Protocol”).

Robbins has the idea that “Anemia of Chronic Inflammation” occurs when five markers are present, which are:

1) LOW Mag RBC

2) LOW or HIGH Ceruloplasmin

3) LOW serum Iron

4) LOW % Sat

5) LOW Ferritin

He thinks this indicates the presence of stored iron, that the body can’t utilize, due to copper and magnesium deficiency.

He thinks vitamin D is dangerous because it depletes retinol. He likes retinol for some reason (something to do with the copper/iron balance, but I forget what).

ANYWAY, I have yet to read the studies he mentions in this video, but it gives a good introduction to his ideas: https://therootcauseprotocol.com/a-birthday-gift-from-morley-to-you/

I know bludicka has seen improvements from taking copper, and I wonder how all of this connects to the vitamin A detox.

Needless to say, I am reconsidering getting iron injections or infusions this time...

Any thoughts?

#2 · March 17, 2020, 1:18 am

Okay, so here is a study about the retinol/iron connection:

”Our results suggest that iron deficiency inhibits mobilization of vitamin A stores and may decrease the absorption and irreversible utilization of vitamin A.”

— Kinetic analysis shows that iron deficiency decreases liver vitamin A mobilization in rats: https://www.ncbi.nlm.nih.gov/pubmed/10801932

And another:

”Iron deficiency may cause changes in liver and plasma VA that are refractory to VA intake, and thus a benefit may be derived from combining iron and VA supplements during nutrition interventions.”

— Iron deficiency in young rats alters the distribution of vitamin A between plasma and liver and between hepatic retinol and retinyl esters: https://www.ncbi.nlm.nih.gov/pubmed/10356091

In that one, it was interesting to see that the food restricted rat group stored the most retinol in the liver (even more than the rats given the exact same food, with the exact same amount of iron, who were allowed to eat as much as they wanted, and thus grew larger).

Lynne has reacted to this post.

#3 · March 17, 2020, 1:44 am

Quote from puddleduck on March 17, 2020, 1:44 am
Hmm, so this paper references the second study I linked above, and one other study as well. But I think they are potentially misinterpreting things (I split it into three paragraphs because it was hard to read):

“The two following examples are based on the fact that iron deficiency impairs both vitamin A and iodine metabolism, and can therefore limit the effectiveness of vitamin A and iodine intervention programs. In rat models, iron deficiency lowers serum retinol, and vitamin A accumulates in the liver as retinyl esters, probably due to impaired activity of hepatic acid retinyl ester hydrolase, an iron dependent enzyme (12). Consistent with the data from these animal studies, long-term supplementation with iron caused large increases in serum retinol in Mexican children (13).

“Preschoolers (n = 219) were provided with zinc (20 mg/d), iron (20 mg/d) or zinc + iron supplements (20 mg of both minerals) for 12 mo. As illustrated in the left panelof Figure 1, in zinc deficient children (plasma zinc <10.7 μmol/L), zinc supplements significantly increased plasma retinol, whereas iron supplements did not, but providing zinc plus iron increased plasma retinol even more than zinc alone. Thus, predictably, in children with no evidence of zinc deficiency, iron supplements alone improved plasma retinol. Supplements containing iron alone increased plasma retinol in iron deficient children (plasma ferritin <12 μg/L), but not in those with adequate iron stores (Fig. 1, middle panel). Finally, for children with low plasma retinol (<0.70 μmol/L) at baseline, but not normal values, plasma retinol concentrations were increased by either zinc or iron supplements.

“These observations strongly support the hypothesis that the low plasma retinol concentrations seen in 29% of these children at baseline were in fact caused by iron deficiency and/or zinc deficiency, rather than vitamin A deficiency. Iron supplements increased plasma retinol by ∼0.65 μmol/L, which is a remarkably large increase considering that the cut-off values for vitamin A deficiency are <0.35 μmol/L (severe) and <0.7 μmol/L (mild). If similar results are found in other locations, they may reveal that we have overestimated the global prevalence of vitamin A deficiency and underestimated the benefits of iron supplementation.”

— Iron Supplements: Scientific Issues Concerning Efficacy and Implications for Research and Programs https://academic.oup.com/jn/article/132/4/813S/4687233

Couldn’t the bolded above indicate that kids with poor nutrition (like the rats on a restricted diet) store their vitamin A in their liver instead of “detoxing” it (like how Dr. Smith has seen serum retinol levels increase AFTER starting the detox)? I don’t know, but it seems possible.

Hmm, so this paper references the second study I linked above, and one other study as well. But I think they are potentially misinterpreting things (I split it into three paragraphs because it was hard to read):

“The two following examples are based on the fact that iron deficiency impairs both vitamin A and iodine metabolism, and can therefore limit the effectiveness of vitamin A and iodine intervention programs. In rat models, iron deficiency lowers serum retinol, and vitamin A accumulates in the liver as retinyl esters, probably due to impaired activity of hepatic acid retinyl ester hydrolase, an iron dependent enzyme (12). Consistent with the data from these animal studies, long-term supplementation with iron caused large increases in serum retinol in Mexican children (13).

“Preschoolers (n = 219) were provided with zinc (20 mg/d), iron (20 mg/d) or zinc + iron supplements (20 mg of both minerals) for 12 mo. As illustrated in the left panelof Figure 1, in zinc deficient children (plasma zinc <10.7 μmol/L), zinc supplements significantly increased plasma retinol, whereas iron supplements did not, but providing zinc plus iron increased plasma retinol even more than zinc alone. Thus, predictably, in children with no evidence of zinc deficiency, iron supplements alone improved plasma retinol. Supplements containing iron alone increased plasma retinol in iron deficient children (plasma ferritin <12 μg/L), but not in those with adequate iron stores (Fig. 1, middle panel). Finally, for children with low plasma retinol (<0.70 μmol/L) at baseline, but not normal values, plasma retinol concentrations were increased by either zinc or iron supplements.

“These observations strongly support the hypothesis that the low plasma retinol concentrations seen in 29% of these children at baseline were in fact caused by iron deficiency and/or zinc deficiency, rather than vitamin A deficiency. Iron supplements increased plasma retinol by ∼0.65 μmol/L, which is a remarkably large increase considering that the cut-off values for vitamin A deficiency are <0.35 μmol/L (severe) and <0.7 μmol/L (mild). If similar results are found in other locations, they may reveal that we have overestimated the global prevalence of vitamin A deficiency and underestimated the benefits of iron supplementation.”

— Iron Supplements: Scientific Issues Concerning Efficacy and Implications for Research and Programs https://academic.oup.com/jn/article/132/4/813S/4687233

Couldn’t the bolded above indicate that kids with poor nutrition (like the rats on a restricted diet) store their vitamin A in their liver instead of “detoxing” it (like how Dr. Smith has seen serum retinol levels increase AFTER starting the detox)? I don’t know, but it seems possible.

Lynne and Viktor2 have reacted to this post.

#4 · March 17, 2020, 2:56 am

Quote from puddleduck on March 17, 2020, 2:56 am
Oh man guys, the second study referenced in the quote above is super interesting: Iron and zinc supplementation improves indicators of vitamin A status of Mexican preschoolers https://academic.oup.com/ajcn/article/71/3/789/4729207

I’ll pick out some quotes.

“The coexistence of multiple micronutrient deficiencies is increasingly recognized as a widespread public health problem in developing countries (1–4). In Mexico, iron deficiency is highly prevalent (1, 5) because of the low bioavailability of iron in the plant-based, high-phytate diets consumed habitually in rural areas. We showed previously that the rural Mexican diet significantly impairs absorption of both iron and zinc (6) and has a low vitamin A content (7).”

So a lot of the kids in the study had anemia:

“Mean hemoglobin concentrations were below normal, whereas mean ferritin, zinc, and retinol concentrations were within the normal range. At baseline, the mean prevalence of anemia in all groups was 73%, that of low plasma ferritin was 51%, that of low plasma zinc was 25%, and that of low plasma retinol was 29%.”

But the researchers point out that we don’t really know how much stored retinol they have in their livers.

“Zinc deficiency is commonly associated with low plasma concentrations of vitamin A, even when hepatic vitamin A stores are normal, suggesting that there is a defect in mobilization of vitamin A rather than in its absorption or transport to the liver.”

These are the supplements that were given.

“Children in each of the 4 groups received 20 mL/d of a beverage containing 20 mg Fe as ferrous sulfate, 20 mg Zn as zinc methionine, 20 mg Zn plus 20 mg Fe, or placebo.”

They mixed the minerals into a beverage with citric acid, so I don’t know if that would’ve affected anything at all.

“The changes in plasma retinol, RBP, and transthyretin after 6 mo of supplementation with zinc, iron, or both are shown in Table 3. The increase in plasma retinol and TTR, but not in RBP, was significantly higher in the zinc group than in the placebo group. Supplementation with iron alone significantly increased retinol, RBP, and transthyretin. Supplementation with zinc plus iron significantly increased retinol but had no significant effect on RBP or transthyretin. Iron supplementation was associated with a higher increase in retinol and RBP than supplementation with zinc or zinc plus iron.”

I wonder if TTR (transthyretin) is more protective than RBP alone, because I read that low TTR levels indicate that you are sicker and more likely to die from your illness, while RBP shows up in a lot of inflamed/sick parts of the body—also John posted images of how TTR covers the exposed end of the retinol in the RBP, which made me think the retinol is “wrapped up better” when in TTR, but I don’t know much about it and am not a scientist. ANYWAY, zinc is needed to make alcohol/aldehyde enzymes.

If even anemic children on a low vitamin A diet have retinol stored in their livers, it must be pretty hard to develop a vitamin A deficiency? So I don’t know why Morley Robbins uses these studies to support cod liver oil consumption. Most of us probably have enough retinol in our livers to last us quite a long while... And if we eat retinol in the diet, how would we ever run out?

I guess I need to look into the idea that vitamin D supplements deplete retinol aspect next.

There is a facebook group around the idea that vitamin D3 supplements can cause osteoporosis and acute hypercalcemia:
https://www.facebook.com/groups/517807781731760/

Oh man guys, the second study referenced in the quote above is super interesting: Iron and zinc supplementation improves indicators of vitamin A status of Mexican preschoolers https://academic.oup.com/ajcn/article/71/3/789/4729207

I’ll pick out some quotes.

“The coexistence of multiple micronutrient deficiencies is increasingly recognized as a widespread public health problem in developing countries (1–4). In Mexico, iron deficiency is highly prevalent (1, 5) because of the low bioavailability of iron in the plant-based, high-phytate diets consumed habitually in rural areas. We showed previously that the rural Mexican diet significantly impairs absorption of both iron and zinc (6) and has a low vitamin A content (7).”

So a lot of the kids in the study had anemia:

“Mean hemoglobin concentrations were below normal, whereas mean ferritin, zinc, and retinol concentrations were within the normal range. At baseline, the mean prevalence of anemia in all groups was 73%, that of low plasma ferritin was 51%, that of low plasma zinc was 25%, and that of low plasma retinol was 29%.”

But the researchers point out that we don’t really know how much stored retinol they have in their livers.

“Zinc deficiency is commonly associated with low plasma concentrations of vitamin A, even when hepatic vitamin A stores are normal, suggesting that there is a defect in mobilization of vitamin A rather than in its absorption or transport to the liver.”

These are the supplements that were given.

“Children in each of the 4 groups received 20 mL/d of a beverage containing 20 mg Fe as ferrous sulfate, 20 mg Zn as zinc methionine, 20 mg Zn plus 20 mg Fe, or placebo.”

They mixed the minerals into a beverage with citric acid, so I don’t know if that would’ve affected anything at all.

“The changes in plasma retinol, RBP, and transthyretin after 6 mo of supplementation with zinc, iron, or both are shown in Table 3. The increase in plasma retinol and TTR, but not in RBP, was significantly higher in the zinc group than in the placebo group. Supplementation with iron alone significantly increased retinol, RBP, and transthyretin. Supplementation with zinc plus iron significantly increased retinol but had no significant effect on RBP or transthyretin. Iron supplementation was associated with a higher increase in retinol and RBP than supplementation with zinc or zinc plus iron.”

I wonder if TTR (transthyretin) is more protective than RBP alone, because I read that low TTR levels indicate that you are sicker and more likely to die from your illness, while RBP shows up in a lot of inflamed/sick parts of the body—also John posted images of how TTR covers the exposed end of the retinol in the RBP, which made me think the retinol is “wrapped up better” when in TTR, but I don’t know much about it and am not a scientist. ANYWAY, zinc is needed to make alcohol/aldehyde enzymes.

If even anemic children on a low vitamin A diet have retinol stored in their livers, it must be pretty hard to develop a vitamin A deficiency? So I don’t know why Morley Robbins uses these studies to support cod liver oil consumption. Most of us probably have enough retinol in our livers to last us quite a long while... And if we eat retinol in the diet, how would we ever run out?

I guess I need to look into the idea that vitamin D supplements deplete retinol aspect next.

There is a facebook group around the idea that vitamin D3 supplements can cause osteoporosis and acute hypercalcemia:
https://www.facebook.com/groups/517807781731760/

Lynne has reacted to this post.

#5 · March 17, 2020, 5:20 am

Okay, I finally figured out that Morley Robbins read Matt Stone’s blog post on vitamin A and responded to it for his followers:

https://therootcauseprotocol.com/iron-toxicity-post-74-formerly-itp75/

Robbins is obsessed with retinol, Weston A. Price, and Cod Liver Oil. He makes the appeal to nature fallacy, saying that only sources of synthetic retinol (supplements and fortified foods) might be a problem, because natural retinol is essential for the utilization of iron and of copper.

He references this review, “The anemia of vitamin A deficiency: epidemiology and pathogenesis:”
https://www.nature.com/articles/1601320

It suggests that vitamin A deficiency leads to anemia. I would like to look into their evidence for this more at some point.

But since I really can’t see how I would’ve completely depleted my retinol stores in only 16 months, I’d like to move on to look at what he says about copper and magnesium, in case those minerals are affecting my iron levels.

Lynne has reacted to this post.

#6 · March 17, 2020, 5:48 am

Do you finally understand why I despise hormone-D so much? That obnoxious, synthetic, toxic supplemental hormone that is completely misunderstood by scientists, clinicians and the masses kills retinol, the very metabolic backbone for making this vital ferroxidase enzyme.

— Morley Robbins, EYE-Ironic Origin of Alzheimer’s Disease (Iron Toxicity Post #61)

He is suggesting that both Alzheimer’s Disease and Parkinson’s Disease are the consequence of copper and iron dysregulation, which is caused by a deficiency of the of ferroxidase enzyme ceruloplasmin.

#7 · March 17, 2020, 5:54 am

Hey @puddleduck are you regularly eating beef and beans?

#8 · March 17, 2020, 5:58 am

Quote from Orion on March 17, 2020, 5:54 am

Hey @puddleduck are you regularly eating beef and beans?

Hey @orion ! 🙂 Yes, I eat beef (or sometimes chicken) at least one meal every day (and have done this pretty much the entire detox), and beans for one meal every day as well. I am trying to increase my bean intake at the moment, because of Karen Hurd’s information.

All my other blood markers (except for vitamin D, which is low) are normal. So I don’t think it’s an absorption issue.

#9 · March 17, 2020, 6:08 am

What symptoms do you have that believe the low iron is the issue? I wonder if over more time it would balance on its own? I know literature is always back and forth, but I always assumed iron in supplement form was bad...

#10 · March 17, 2020, 6:30 am

Quote from Orion on March 17, 2020, 6:08 am

What symptoms do you have that believe the low iron is the issue? I wonder if over more time it would balance on its own? I know literature is always back and forth, but I always assumed iron in supplement form was bad...

Thanks @orion ! I have CFS/POTS symptoms (primarily fatigue, which isn’t new but is worse, and an excessive increase in heartbeat when standing upright vs. lying down, which seems to have gotten worse, too).

Yeah, a few days ago I was going to request iron injections or infusions from my doctor, but now I’m starting to think even supplemental iron might not be the best idea. 😝 You might be right that this could improve on its own. Since my hemoglobin is fine, the “wait and see” approach doesn’t seem unreasonable, eh?

Iron Deficiency and Morley Robbins “Root Cause Protocol”

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