Hair Mineral Testing

[aprilk1869]

I've been doing research into how a riboflavin deficiency can tie in with iron problems, here's what I've come up with so far. Please note I'm not an expert and welcome comments.

From what I can understand, Flavoenzymes reverse the oxidation of hemoproteins such as hemoglobin. If this doesn't happen then methemoglobin levels increase meaning oxygen can't get into the tissues so you end up with symptoms of fatigue etc. Methemoglobinemia can also be caused by various substances such as antibiotics and nitrates. Those with Methemoglobinemia can be treated with riboflavin.

Oxidative Stress
Flavoenzymes participate in protection of erythocytes and other cells against oxidative stress. This included the support of intracellular levels of reduced glutathione via glutathione reductase and the direct reduction of oxidized forms of hemoproteins by methomoglobin reductases.
http://books.google.co.uk/books?id=...wCQ#v=onepage&q=flavoproteins vitamin&f=false

Methemoglobinemia
Methemoglobinemia (or methaemoglobinaemia) is a disorder characterized by the presence of a higher than normal level of methemoglobin (metHb) in the blood. Methemoglobin is an oxidized form of hemoglobin that has a decreased affinity for oxygen, resulting in an increased affinity of oxygen to other heme sites and overall reduced ability to release oxygen to tissues. The oxygenhemoglobin dissociation curve is therefore shifted to the left. When methemoglobin concentration is elevated in red blood cells, tissue hypoxia can occur.

Symptoms
Signs and symptoms of methemoglobinemia (methemoglobin >1%) include shortness of breath, cyanosis, mental status changes (~50%), headache, fatigue, exercise intolerance, dizziness and loss of consciousness. Arterial blood with elevated methemoglobin levels has a characteristic chocolate-brown color as compared to normal bright red oxygen-containing arterial blood.[6]

Severe methemoglobinemia (methemoglobin >50%) patients have dysrhythmias, seizures, coma and death (>70%).[6] Healthy people may not have many symptoms with methemoglobin levels < 15%, however patients with co-morbidities such as anemia, cardiovascular disease, lung disease, sepsis, or presence of other abnormal hemoglobin species (e.g. carboxyhemoglobin, sulfehemoglobin or sickle hemoglobin) may experience moderate to severe symptoms at much lower levels (as low as 5-8%).

Acquired methemoglobinemia
Exposure to exogenous oxidizing drugs and their metabolites (such as benzocaine, dapsone and nitrates) may accelerate the rate of formation of methemoglobin up to one-thousandfold, overwhelming the protective enzyme systems and acutely increasing methemoglobin levels.

Other classical drug causes of methemoglobin include antibiotics (trimethoprim, sulfonamides and dapsone[2]), local anesthetics (especially articaine and prilocaine[3]), and others such as aniline dyes, metoclopramide, chlorates and bromates. Ingestion of compounds containing nitrates (such as the patina chemical bismuth nitrate) can also cause methemoglobinemia.

Treatment
This is achieved by providing an artificial electron acceptor (such as methylene blue, or flavin) for NADPH methemoglobin reductase (RBCs usually don't have one; the presence of methylene blue allows the enzyme to function at 5x normal levels[5]) The NADPH is generated via the hexose monophosphate shunt.

http://en.wikipedia.org/wiki/Methemoglobinemia

Comparison of methylene blue, riboflavin, and N-acetylcysteine for the reduction of nitric oxide-induced methemoglobinemia.
In vitro, NO-induced methemoglobin formation is significantly decreased by medium (1 microM) and high (10 microM) concentrations of MB [methylene blue] and partially by high riboflavin concentrations (120 microM). NAC and low concentrations of riboflavin do not alter methemoglobin formation.
http://www.ncbi.nlm.nih.gov/pubmed/10809266

 

[aprilk1869]

"Despite normal levels of reduced glutathione, which may have been due to the size of the sample, there were signi?cantly increased levels of methemoglobin in CFS (mean = 1.26%) compared with controls (mean = 0.55%) ( p <0.005), indicating oxidative damage to the hemoglobin molecule."

www.cfids-cab.org/rc/Richards-2.pdf

 

[Lou]

"Despite normal levels of reduced glutathione, which may have been due to the size of the sample, there were signi?cantly increased levels of methemoglobin in CFS (mean = 1.26%) compared with controls (mean = 0.55%) ( p <0.005), indicating oxidative damage to the hemoglobin molecule."

www.cfids-cab.org/rc/Richards-2.pdf

Anyone here care to make this somewhat more understandable to the lay person? Thanks.This in reference to her previous post as well.

 

[adreno]

Justy lead me on to some studies in another thread.

Here's a study showing that riboflavin deficiency causes iron loss, in rats. The iron was lost in the feces, not accumulated in the liver:

Riboflavin deficiency in the rat: effects on iron utilization and loss.

Abstract

Iron absorption and daily loss of Fe were measured in riboflavin-deficient (B2-) Norwegian hooded rats and controls (B2+). Animals were fed on a test meal extrinsically labelled with 59Fe and whole-body radioactivity measured for 15 d. Riboflavin deficiency led to a reduction in the percentage of the 59Fe dose absorbed and an increased rate of 59Fe loss. All post-absorption 59Fe loss could be accounted for by faecal 59Fe, confirming that the loss was gastrointestinal. Fe concentrations and 59Fe as a percentage of retained whole-body 59Fe were higher in the small intestine of riboflavin-deficient animals than their controls, 14 d after the test meal. A separate experiment demonstrated that riboflavin deficiency was associated with a significant proliferative response of the duodenal crypts of the small intestine. These observations may explain the enhanced Fe loss in riboflavin deficiency.

PMID 1878361

 

[adreno]

In this study, iron stores in the livers of riboflavin deficient rats were measured, and found to be significantly lower than controls:

The influence of riboflavin deficiency on absorption and liver storage of iron in the growing rat.

Abstract

1. Iron absorption was measured in weanling riboflavin-deficient (RD) rats or weight-matched (WM) controls fed on appropriate diets for 7 weeks. Concentrations of radio-Fe (59Fe) in plasma were monitored every 30 min for 4 h following intragastric administration. 2. Total Fe absorption in RD rats was significantly lower than that in WM controls, and the tissues of the stomach and small intestine of RD rats retained significantly (P less than 0.001) more 59Fe by comparison with WM groups. 3. In a separate experiment, ferritin-Fe concentrations were measured in the livers of four groups of rats (ad lib. (C), pair-fed (PF) and WM controls and RD) at day 0, and subsequently at days 14, 21, 28, 35 and 49. 4. Liver ferritin-Fe concentration was significantly lower (P less than 0.05) in RD rats than in all other controls after 3 weeks on the respective diets and remained lower for the remainder of the experiment.

PMID 3676194

 

[garcia]

Anyone here care to make this somewhat more understandable to the lay person? Thanks.This in reference to her previous post as well.

I'll give it a go.
From what aprilk1869 has posted, ME/CFS patients have increased levels of methemoglobin. Methemoglobin is an oxidized form of hemoglobin (the protein in red blood cells that helps transport oxygen) which has a decreased affinity for oxygen, resulting in a reduced ability of blood to release oxygen to tissues.

Luckily this can be treated with riboflavin which reverses the oxidation of hemoglobin.

High levels of Methemoglobins may be causing some of our symptoms:

Signs and symptoms of methemoglobinemia (methemoglobin >1%) include shortness of breath, cyanosis, mental status changes (~50%), headache, fatigue, exercise intolerance, dizziness and loss of consciousness.

 

[Lou]

Figuring all this out becomes 'curiouser and curiouser'. So if it turns out our iron loss is not via accumulation in the liver does this change the cascade of nutritional events proposed by Christine? Or does her theory work just as well?

Comments? Thanks.

Here's a study showing that riboflavin deficiency causes iron loss, in rats. The iron was lost in the feces, not accumulated in the liver:

Riboflavin deficiency in the rat: effects on iron utilization and loss.

Abstract

Iron absorption and daily loss of Fe were measured in riboflavin-deficient (B2-) Norwegian hooded rats and controls (B2+). Animals were fed on a test meal extrinsically labelled with 59Fe and whole-body radioactivity measured for 15 d. Riboflavin deficiency led to a reduction in the percentage of the 59Fe dose absorbed and an increased rate of 59Fe loss. All post-absorption 59Fe loss could be accounted for by faecal 59Fe, confirming that the loss was gastrointestinal. Fe concentrations and 59Fe as a percentage of retained whole-body 59Fe were higher in the small intestine of riboflavin-deficient animals than their controls, 14 d after the test meal. A separate experiment demonstrated that riboflavin deficiency was associated with a significant proliferative response of the duodenal crypts of the small intestine. These observations may explain the enhanced Fe loss in riboflavin deficiency.

PMID 1878361

 

[justy]

Here's a study showing that riboflavin deficiency causes iron loss, in rats. The iron was lost in the feces, not accumulated in the liver:

Riboflavin deficiency in the rat: effects on iron utilization and loss.

Abstract

Iron absorption and daily loss of Fe were measured in riboflavin-deficient (B2-) Norwegian hooded rats and controls (B2+). Animals were fed on a test meal extrinsically labelled with 59Fe and whole-body radioactivity measured for 15 d. Riboflavin deficiency led to a reduction in the percentage of the 59Fe dose absorbed and an increased rate of 59Fe loss. All post-absorption 59Fe loss could be accounted for by faecal 59Fe, confirming that the loss was gastrointestinal. Fe concentrations and 59Fe as a percentage of retained whole-body 59Fe were higher in the small intestine of riboflavin-deficient animals than their controls, 14 d after the test meal. A separate experiment demonstrated that riboflavin deficiency was associated with a significant proliferative response of the duodenal crypts of the small intestine. These observations may explain the enhanced Fe loss in riboflavin deficiency.

PMID 1878361

Thanks Adreno for posting this, i flagged it up on another thread about B2. The point i was trying to make is that there is no evidence that i can find that shows that a B2 deficiency will cause iron storage in the liver and that B2 supplementation will cause iron stores to be released into the body. In fact these studies posted above by you show the opposite to be true - B2 deficiency just causes iron deficiency. Of course these studies where in rats not humans, and i would still like to see if there is any published evidence to back up Christines theory on this
All the best, Justy.

 

[adreno]

Luckily this can be treated with riboflavin which reverses the oxidation of hemoglobin.

Methylene Blue was much more effective, though. Low concentrations of riboflavin had no effect, and high concentrations only partially decreased methemoglobin formation.

 

[adreno]

This is interesting, though:

"On the other hand, the iron content of the livers of both pregnant and non-pregnant female rats fell as the manganese level of the diet increased."

Effect of the dietary manganese level on tissue manganese, iron, copper and zinc concentrations in female rats and their fetuses.
http://www.ncbi.nlm.nih.gov/m/pubmed/1152553/

So, it seems manganese can release liver stores of iron. Consequently, maybe we can infer that the opposite is also true: manganese deficiency will lead to higher levels of liver iron.

And finally, riboflavin is needed to utilize the iron.

 

[dannybex]

So, it seems manganese can release liver stores of iron. Consequently, maybe we can infer that the opposite is also true: manganese deficiency will lead to higher levels of liver iron.

And finally, riboflavin is needed to utilize the iron.

Exactly.

It's not just one mineral here or one vitamin there. Everyone has different levels of other imbalances, and we don't know what imbalances may have existed in these rat experiments (which were probably fed a diet of some sort of manufactured, 'chow' enriched with who knows what levels of other vitamins).

I think Christine is definitely on to something, and it's a shame her intentions were completely misinterpreted, and she's left. Who can blame her?

 

[Dreambirdie]

I think Christine is definitely on to something, and it's a shame her intentions were completely misinterpreted, and she's left. Who can blame her?

Actually, Christine has been banned from the forum, "for trying to sell something." I got an email from her this a.m., in which she informed me of this.

I was hoping things btwn her and the mods could be resolved in a more amicable way. I think she and Rich could have had some great discussions about the B vitamins and other nutrients, and how their imbalances affect our health. I am disappointed at how things have turned out.

 

[dannybex]

I totally agree DB. That's really a shame. So much for freedom of speech.

What in the world did she do since she last posted (saying she had quit too!) that caused this banning?

I'd like to know from the mods specifically in which post did she try to sell something? Perhaps they could list it for us?

 

[Lou]

I'm disappointed, too, Dreambirdie. From Aquariusgirl, Brenda, Rand56 and others it certainly seemed this line of investigation held tremendous potential for significant improvement for us.

Perhaps the mods will weigh our interest in this and reconsider. Surely, something can be worked out when potentially so much may be in the balance.

 

[brenda]

removed as expected

 

[Sushi]

I'm disappointed, too, Dreambirdie. From Aquariusgirl, Brenda, Rand56 and others it certainly seemed this line of investigation held tremendous potential for significant improvement for us.

Perhaps the mods will weigh our interest in this and reconsider. Surely, something can be worked out when potentially so much may be in the balance.

Yes, many of us would like to continue this discussion with Christine. We are trying to continue it on our own but she has practical experience that we don't have and her input would make the discussion more fruitful. We don't want an acrimonious discussion, just information that will help us make choices in getting well.

Sushi

 

[Shellbell]

This is so sad as I found Christine's information thought provoking. I would love to hear more. What about the moderator's allowing the people who are interested become a private group, like how Mike Dessin's treatment went to New Day Project? Just a suggestion!

 

[dmholmes]

Actually, Christine has been banned from the forum, "for trying to sell something." I got an email from her this a.m., in which she informed me of this.

Complete BS. Fortunately I'm already on a good path and seeing results due to her work.

 

[aprilk1869]

I was just wondering about iron overload, my parents use enameled iron pots buy Le Creuset. I've read that they're supposed to be good for those who are concerned about the type of pans they use however I'm also wondering about how protective the enamel is against iron. I mean, over time there's bound to be wear and tear, some iron might end up in the food.

Does anyone else use these kinds of pots?

 

[brenda]

I got an email saying the same - banned