Have you asked yourself why upper limit of Manganese is 11mg/day?


I struggled today with balancing the oats and maltodextrin mixture of my Soylent. The reason is that grains like oats have quite a bit of Manganese. With 100g of oats (a very reasonable amount per day), this accounts for about 5mg. Combine with a multivitamin, adding another 5mg, and I was now teetering over the edge of the upper limit listed by Soylent (later edit: this was a mistake; the figure is from the USDA, but for us DIYers, we commonly associate the two)

At this point, I wondered, how, exactly are they coming up with this 11mg/day figure.

Here is what I realized:

  1. Maganese toxicity from foods has not been reported in humans. (a more rigorous reference to come).

  2. So how are they getting that figure of 11mg/day? See the article here by Greger (you may need an academic proxy):

One reason for the difficulty in recommending optimal intakes of manganese is that scientists really are not sure of typical manganese intakes. Daily food composites prepared on the basis of the FDA’s Total Diet Study menus contained on average 2.2 mg Mn for women and 2.7 mg Mn for men (Pennington et al. 1989). The average intakes of adults eating Western-type and vegetarian diets in various surveys ranged from 0.7 to 10.9 mg Mn/d (Freeland-Graves 1994, Gibson 1994).

  1. A more detailed summary of this is given in this article by Ljung and Vahter (apologies for the length). Note that NOAEL refers to “no observed adverse effect level”. Amusingly, I want you to notice that the guy who’s study is used to determine the 11mg/day limit was the same guy above who said “scientists really are not sure…”

How the NOAEL for manganese was established

In the background document for the WHO drinking-water guidelines (WHO 2004), the use of 11 mg as a NOAEL is based on a review by Greger (1999) and on a report on dietary reference values for manganese published by the Institute of Medicine in 2000 (IOM 2001):

 A review of typical Western and vegetarian diets found average adult manganese intakes ranging from 0.7 to 10.9 mg/day (Greger 1999; Institute of Medicine [IOM] 2002 [sic]). The upper range manganese intake value of 11 mg/day from dietary studies is considered a NOAEL. It is not believed that this amount of manganese in the diet represents an overexposure to the element (IOM 2002 [sic]). (WHO 2004)

The IOM in turn, also refers to Greger (1999):

A NOAEL of 11 mg/day of manganese from food was identified based on the data presented by Greger (1999). Greger (1999) reviewed information indicating that people eating Western-type and vegetarian diets may have intakes as high as 10.9 mg/day of manganese [. . . .] Because no adverse effects due to manganese intake have been noted, at least in people consuming Western diets, 11 mg/day is a reasonable NOAEL from food. (IOM 2001)

However, the article by Greger (1999) did not focus on manganese intake from different diets but rather on potential biomarkers of manganese in human nutrition and toxicology. In the introduction section on manganese exposure she stated that “the average intakes of adults eating Western-type and vegetarian diets in various surveys ranged from 0.7–10.9 mg Mn/day,” with reference to Gibson (1994) and Freeland-Graves (1994). However, no mention of these values is made in Gibson (1994), whose article is a review on trace elements in vegetarian and omnivorous diets, with a concern for deficiencies in vegetarian diets. The Freeland-Graves (1994) article is also a review published in a book on risk assessment of essential elements by the International Life Sciences Institute. The intake values of 0.7–10.8 mg Mn/day were observed for Canadian women in a study carried out by Gibson and Scythes in 1982. These values were also cited in the Freeland-Graves (1994) review and presented in a table of daily manganese intakes compiled from several studies.

The values used for setting the NOAEL thus originate from one study, where 100 Canadian women aged 30 ± 6.1 years were asked to complete dietary protocols of all consumed foods and beverages (including drinking water) in their own homes for 3 consecutive weekdays (Gibson and Scythes 1982). The authors present both calculated and analyzed intake values. The calculated daily manganese intake ranged from 0.7 to 10.8 mg, where 90% of the women ingested < 5 mg/day, and almost half the women (40%) ingested < 2.5 mg/day. The average daily manganese intake was calculated at 3.1 ± 1.5 mg. The analyzed manganese intake from duplicate portions provided a slightly lower average daily manganese intake of 2.4 mg/day. The analyzed maximum intake was not presented. The slight discrepancy between the calculated and the analyzed manganese intakes was explained by the authors to be a result of an overestimation in portion size (Gibson and Scythes 1982).

The NOAEL of 11 mg/day thus is based on calculated daily intakes of manganese and not on actual measurements of manganese intakes. No mention is made of the subjects’ health statuses or why it seems unfounded to draw any conclusions on a “no observed adverse effect level” of daily manganese intakes at 11 mg. In fact, several studies from different countries have reported daily manganese intakes after 1982, when the Gibson and Scythes study was published. Table 1 shows manganese intake data from an array of countries and ages. Children’s average manganese intake from omnivorous diets was reported to be about 2 mg/day (mean values range from 1.3 to 3.6 mg/day), whereas adult omnivorous diets resulted in a slightly higher intake of about 2.7 mg/day (mean range 1.5–3.9 mg/day). This value is similar to the analyzed intake value of 2.4 mg/day reported by Gibson and Scythes (1982). Both children and adults with a vegetarian diet have reportedly higher values of daily manganese intake than those with an omnivorous diet, which can be explained by the higher manganese concentration in plants than in meat and fish. The daily intake also seems to differ with country of residence, likely because of differing diets. None of the studies found intakes as high as 11 mg/day.

I have bolded some of the text.

I realize this was a bit long, so let me summarize for you what this indicates: the figure of 11mg/day was based on a single survey of 30-year old Canadian women in which they approximated how much Maganese was consumed in an average diet. These figures ranged from 0.7-10.9mg/day. Based on the fact that these people were “healthy”, they concluded that 11mg should be the recommended upper limit.

What this means is that if you are a Canadian woman who consumes 0.7-10.9mg of Manganese per day, then you should be fine. What is the upper limit of Manganese for other people? Is 15mg/day okay? Is 20mg/day okay? We have no freakin’ idea.

My warning to all of you DIY Soylenters is to understand that there is a lot we don’t understand about diet and recommendations, and the more you dig into these recommendations, the more questions you find. This is why, as a scientist, Rob’s blog post struck me the wrong way:

Epistemic arrogance – Elemental analysis has given us a finite, complete list of the elements our bodies are made of. This doesn’t tell us the different chemical configurations required, such as vitamins, but patients have lived for many years on synthetic diets in a medical setting. It was premature in the 19th century, but it’s overdue today. Again, beware of zero-risk bias. How nutritionally complete is the average western diet already?

There is a sense of epistemic arrogance in following certain food intake guidelines that you’ve come to realize are based on singular studies and very limited data. How many other ‘recommended intakes’ are based on limited data and somewhat sketchy conclusions? I personally like the idea of Soylent, but just be careful.

And as for the Manganese issue? Now that I understand where this 11mg figure is coming from, I’m not going to freak out if I exceed this value.

High Manganese in whey / use in High protein soylent
New keto recipe... and it's yummy :)
Oat flour:Maltodextrin Ratio

It’s not something Soylent came up with, they get the 11mg/day limit from the USDA. That doesn’t mean that it’s absolutely right, but there’s nothing wrong with erring on the side of caution, which is why I believe it exists. The upper limits and recommended intakes are estimated to be safe for 97% of the population. On webmd they state:

More than 11 mg per day might not be safe. Excess manganese can cause serious side effects, including symptoms resembling Parkinson’s disease, such as shaking (tremors). People who have trouble getting rid of manganese from the body, such as people with liver disease, may experience side effects when taking less than 11 mg per day.

(emphasis added)

So ultimately, as long as we’re aware and careful, I think @ThSGM is right. Doctors will often suggest supplementing past the USDA upper limits for certain nutrients, depending on your circumstance. When in doubt, consult your physician.


I’m sorry, you’re absolutely right that Soylent did not come up with this figure. I didn’t mean to make that impression.

This isn’t meant to be a slant against the average physician, but I’m doubtful a physician would know any more than this short literature search reveals. What you need is a specialist. That’s the difficulty with these diet-related questions. Most people in the general population are asking general questions about diet, and these are answerable by a general physician or nutritionist.

We’re asking much more specific questions, which debate the exact recommendations from, e.g. the USDA. What you need is someone who does research in this area, and knows the current state of the literature. I would also recommend a thorough search of current literature, as I never made any effort to distinguish between pre-90s literature and post-90s.

I was going to suggest contacting Greger herself, but it appears she’s emeritus.


I suggest taking a look at the Linus Pauling Institute. They usually match the USDA guidelines, although they do deviate on some nutrients. The more important part is they tend to give a detailed, well cited, review of the evidence available. They also mention potentially useful considerations, e.g. that manganese and iron may be absorbed/transported from food via shared pathways. It is obviously difficult to balance a fully compliant nutrient set on a day to day basis without many ingredients. That being said, for my part, I’m not willing to have my primary soylent recipe blow the door off any of the USDA UTLs. So far I’ve had the best luck by skipping the multi and getting everything via food (or supplemented food) sources. YMMV.


Thank you for the useful website. As you say, it’s a complicated issue, and we should be guided by the USDA recommendations. However, that being said, some of us (myself included) are so dependent on the USDA UTLs that we fight to reduce our recipe from say, 11.5mg/day to 10.5mg/day.

And yet, at the end of the day, as I pointed out, that 11mg/day figure was more or less obtained arbitrarily.

That was my main point.


That is a good point to make. Nutrition science in regards to human is still surprisingly weak. I think my favorite UTLs to ignore are Niacin and Vitamin A.

The Linus Pauling Institute points out the Niacin UTL is set to avoid the Niacin flush. However, initially uncomfortable, the flush isn’t bad and is linked to improvements in HDL. I also know that repeated exposure to higher than flush-threshold niacin may reduce the magnitude of that ‘side effect’.

Vitamin A is only dangerous at the UTL when it is in a form that is going to be bioavailable regardless. However, Beta Carotene (the primary naturally occurring form of Vitamin A in vegetables) only becomes bioavailable as needed. What is even more fun is that the IU for Vitamin A are a total train wreck because of the differences in bioavailablity of various sources.

Actually a whole thread about such things would probably be really useful if it doesn’t already exist. Does it exist? I’m kind of new here.


Sorry for grave-digging this old thread. I’m doing some research into manganese, since my recipe was a little over the threshold.

Turns out, according to an uncited statement on the NIH page for manganese, excess manganese can inhibit iron absorption, especially in those with iron-deficiency anemia. I was recently diagnosed with low levels of iron and hemoglobin, so I’m going to lower the level of manganese (most from oat powder) in the recipe.

Hopefully this provides healthy contrast to @Sintax’s observation that usually more is better.


For a well-cited discussion, you should review the LPI page on Manganese (which @drknexus mentioned above). You’ll find:

Although the specific mechanisms for manganese absorption and transport have not been determined, some evidence suggests that iron and manganese can share common absorption and transport pathways (10). Absorption of manganese from a meal decreases as the meal’s iron content increases (7). Iron supplementation (60 mg/day for four months) was associated with decreased blood manganese levels and decreased MnSOD activity in white blood cells, indicating a reduction in manganese nutritional status (11). Additionally, an individual’s iron status can affect manganese bioavailability. Intestinal absorption of manganese is increased during iron deficiency, and increased iron stores (ferritin levels) are associated with decreased manganese absorption (12). Men generally absorb less manganese than women; this may be related to the fact that men usually have higher iron stores than women (13). Further, iron deficiency has been shown to increase the risk of manganese accumulation in the brain (14).


I’d caution you to be more careful, here. In this case, the nutrition science and medical science are very good… we know quite a lot about the potential harm of manganese, because of incidents of environmental exposure (like welders) or people with a lot of manganese in the water supply (either natural, or because of contamination.) Regardless the cause, we know we see high rates of neurological problems, and we know this is because manganese accumulates in the brain, which is very hard to address.

To quote the LPI page:

Due to the severe implications of manganese neurotoxicity, the Food and Nutrition Board (FNB) of the Institute of Medicine set very conservative tolerable upper intake levels (UL) for manganese

So while we know we don’t need very much, we also know that this is a clear case where too much is quite dangerous. So the search for a tolerable upper limit was not about going as high as we can until we know any more is unsafe; rather, it was about keeping it down at a level which we can be fairly sure is relatively safe. When it comes to something that accumulates in your brain over time, you don’t want to consume more than you have to.

So the Canadian study was not about a level over which we’re unsafe, but to validate a level under which we’re pretty sure is still safe… and given that most dietary sources of manganese are otherwise generally healthy foods (almonds, whole grains, spinach…), you can’t very well recommend that people avoid those foods. If people eating healthy diets get up to 11mg and are generally healthy, you should not set the upper limit lower than that. But is 20mg safe? Probably not… some studies found people in areas where the level of manganese in the water is about about 2mg per liter, and who eat local produce raised on that same water, showed higher rates of neurological diseases in the elderly (who had a lifetime to accumulate manganese in the brain.)

All of this suggests taking a conservative approach.

I use even more oat flour in my DIY than you do, but I also use a high-end multivitamin which uses only 1 mg of manganese, so my total counts are lower.

I recommend you reconsider your choice of multivitamin. If you use your soylent as a substantial portion of your diet, the multivitamin is probably not the best place to cut corners, and if an otherwise good multivitamin nevertheless is a bad fit with a diet high in oats, I’d consider changing the multi.


@MentalNomad: I am not trying to be deliberately obtuse here, but apart from your argument that, we should take the conservative approach (which I don’t disagree with), you quote a study that tells me very little of the original question.

Unfortunately, I don’t have a subscription to the journal with the the study that you quote (the one about 2mg/litre in Greece). They do not provide figures of Manganese intake in the diet, so I do not understand how the 2mg/litre estimate relates to the the diet quantities we are discussing. It is recommended that we drink something like 2 litres of water per day. So if I were to play the game of recommending limits, I’d say anything about 4mg of Manganese is toxic, no?

Your statement is

But is 20mg safe? Probably not…

but I have no idea where you’re pulling that claim. Why 20mg? Why is 11mg safe (which was, as I pointed out, pretty arbitrarily decided based on a typical female diet in a single Canadian study), and not 15mg? Why not 18mg or why not 25mg? Somehow, you’ve come to the conclusion that 20mg is “probably not” safe. But why?

I don’t mean to pick on your post, but as far as I’ve read, you haven’t said anything new. At the end of the day, your point is: “Nobody knows. So play it safe.”

In that case, I would argue that not just this issue of Soylent (in regards to Manganese) is contentious, but the entire premise of Soylent is in doubt. If one is put off by the uncertainty of a strict upper/lower limit for Manganese, I shudder to think how much we understand of the required contents of the rest of the Soylent ingredients. If this is true, then playing it safe entails not consuming Soylent at all.


This statement is unfounded and erroneous. In the U.S. 1 out of 200 people have hemochromatosis, as I do. I keep my ferritin at 25ngto 50ng and serum iron at 80ng to 120ng. I cna control serum iron, ferritin, hct/hgb with exacting precision.


My Mn after 1 year of Swanson’s Manganese chelate derived from TRAACS manganese glycinate chelate did not move the red blood cell level into range. I am at 7.5 with a range of 11-33 per labcorp.

Mn is grossly overlooked and even more grossly misunderstood. I have a hypothesis I briefed the director or AI research at MIT who is about to publish a very important white paper on Mn. She had to pass me off to a collegaue who said I must of read his papers. The fact is I read no ones papers. I tested and experimented on myself.

I am going to try the citation from Walter Last and see if the Mn sulfate form gets me in range. Everyone in this thread needs to realize that all of your guessing games at mg dosing is just that, guessing. Try a chelate form and test. Get in range and either cease or try to find a miantenance dose.


AI research? Like artificial intelligence? How does that relate to manganese? If there are relevant papers you could link them here; most everything is online nowadays, even if it is behind a paywall.

It’s fine for you to experiment on yourself, but I don’t know if we can take that seriously, or even what the implication is. You say your “red blood cell level” is at 7.5 with a range of 11-33; I don’t understand how that’s related to manganese or even what units those are. You say you have a hypothesis but you don’t say what it is (or I missed it).

I had to look up hemochromatosis and I found this helpful tip: “Iron can be dropped to safe levels by regularly removing blood from your body.” So those bloodletters were on to something!

Also you talk about dosing with manganese but we’re really trying to avoid ingesting too much manganese in food and water. Or at least trying to figure out how much is too much. I wouldn’t experiment on myself with something that is toxic in small doses; it can affect your brain and body.


Yes, artifical intelligence. She happens to be in the MIT AI department. She is an expert in biosciences. Look up the ?Mercola interview of Stephanie Seneff.

Of course I have to experiment on myself, conventional medicine has damn near killed me on mulitple occasions. I beat death in Sept. 2004, I get it. When it comes to endocrinology I am better versed than 90% of the endocrinologists in the United States, I have to be it is a matter of survival.

Regarding Hemochromatosis - Yes, I cited that with a bit of assuming on my part. The take away for you is this:

  1. 1 out of 200 have hemochromatosis, making it fairly prevalent. The number of carriers of just one of the mutations makes it even more substantial and prevelant in our society. It is the #1 genetic mutation in the U.S.
  2. Iron, copper, magnesium and calcium are all manganese antagonists.
  3. the blood letting phlebotomies you cited not only level down the iron they also dump the other elements cleaving to the iron to include manganese.
  4. The lab results cited are from Labcorp. I track all available elements of my red blood cells. Instead of guessing how many mg’s everyone should be taking as referenced in this thread, which is not very intelligent since everyone has differences in thier biologics and since citations such as hemochromatosis are game changers, it is wiser to not try to apply one set of standards to everyone when everyone has more variances to their genetics than can be counted. The unit of measure is ng/mL
  5. If Swanson vitamins proffers a 46mg daily dose of chelated Mn and if others are proffering 400mg of Mn sulfate, then maybe you should be paying attention to the post that cites how the RDA was concluded on a weak at best cllinical trial of women in Canada.
  6. MnSOD and the SOD II gene are at the center of cardiac health not to mention the key element to eNOS. Ignoring this fact is plain ignorant.
  7. Testing on self in a controlled way, smal incremental titration with frequent testing is intelligent and prudent and responsible and and and…
  8. Ignoring this very important element is simply wrong.

Now how to get there: There is bunches of data on Mn, but few site the various types of chelated forms and the significance of the chelate variant, such as glycinate or citrate or sulfate.

There has been some expository from Walter Last that at least brings some identificaiton as to what chelate to use. http://www.health-science-spirit.com/myasthenia.html

Test using labcorp, define baseline
ingest water infused with Mn Sulfate as identified in the linked article
two weeks
test with a 50% mid range target
most other levels target 66% or 75% of upper range
in this instance 50% is prudent
you test and treat in small increments until in the sweet spot
beyond the numerics - how oyu feel has equal weight
then you either stop dosing or find a maitenance dose that sustains and
enables backing off the testfrequency to monthly or better yet quarterly

Mn has a direct affect on A1C and many belive is at the center of the type II diabetes discussion

It is key essential and is an absolute if you want health and longevity.

Also the FDA and their RDA’s …I mean really?

The FDA the butchers and sellouts of the government who have fortification and enrichment programs that promote the use of iron that is not bioavailable and that kills beta cells. Only a fool would rely on a government standard.


Ironman, I’m sorry you suffer from hemochromatosis . I carry a gene mutation for HFE-related hemochromatosis , but I also have one normal copy, and I do not have any indications of dysfunction. I have, however, looked into hemochromatosis more than most people. Hereditary hemochromatosis accounts for the majority of cases.

Among Europeans like myself, about 1 in 10 carry at least one copy of one of the several gene mutations for one of the several types of hemochromatosis. People like me are fortunate that it takes more than one mutation to lead to iron accumulation or iron overload.

You said,

I beg to differ - my only statement was simply that the LPI page on Manganese was a reputable source. I guess you’re calling the quote from the LPI page unfounded and erroneous, but it is, in fact, well-written and based on multiple citations of the medical literature. However, the LPI information is based on the general population, not on people suffering from full-blown hemochromatosis, so it may not apply to your particular case! That does not make it incorrect for the majority of readers. There will always be exceptions.

It’s important to note that few people have the hereditary predisposition; I carry the gene, yet I don’t have a predisposition. Of those who do, only some have elevated TS levels. Of those who have elevated TS levels, only a few actually develop elevated ferritin. And of those who have elevated ferritin, only a few actually develop symptoms of hemochromatosis… and of those, only a few have symptoms which rise to clinical significance. This is all a long way of saying two things: it’s surprising more of us don’t know about the disease, since a fair number of us carry the gene - but the actual disease is surprisingly rare, even among those who are genetically predisposed. Also, it’s very hard to put a number on the disease incidence - looking just for TS levels will give a higher estimate than 1% of the population, while people with clinical signs of iron overload are much more rare.

Now, looking back at the information on iron intake and manganese that I cited - the relationship between higher iron intake and lower manganese uptake in people people with normal iron function is strong, making it clear that iron uptake either competes with or impedes manganese uptake. I’d speculate that certain kinds of hemochromatosis seem to bias the body to take up much higher amounts of iron; if your body is attempting to preferentially take up the iron, it may be limiting the potential to take in manganese. Because of your condition, even small amounts of iron may interfere with manganese uptake. Most people would not be well-advised to supplement their manganese. Even people with symptoms of hemochromatosis should take care, because this effect may vary by the type of hemochromatosis (there are at least six different types of hemochromatosis, if I recall properly, and they may affect different stages in the uptake/storage chains, therefore changing how they affect other types of mineral processing.)


General note on a couple of other controversial things brought up in this thread:

The MIT AI researcher Stephanie Seneff… Her focus in Artificial Intelligence was on human auditory processing, understanding human language, and natural language processing. (Her Master’s and EE degrees in Electrical Engineering are from 1980, and she got her PhD in Electrical Engineering and Computer Science in 1985.)

Since 2011, however, she seems to have turned her focus onto glyphosphate, GMO’s, autism, alzheimers, nutrient deficiencies, etc. Some of her papers take the interesting approach of doing natural language searches on medical databases to attempt to find correlations between treatments and conditions. This approach, however, is fraught with bias, and while it may find correlation, it’s very weak on finding causation. Her work and collaborations are not generally taken seriously within the community of scientists knowledgeable about and working within the fields where she is now publishing. Also, the studies in question - which the media often refers to as “MIT Studies” when MIT is not actually associated with them - are published in what most would call bottom-tier journals with “pay to publish” acceptance systems. Her papers are very well received, however, by the anti-biotech crusaders and pseudoscience web sites.

Second, I would not recommend considering Mercola’s web site a reputable source of information - it’s more of a pseudoscience web site run by Joseph Mercola, “an alternative medicine proponent, osteopathic physician, and web entrepreneur, who markets a variety of controversial dietary supplements and medical devices through his website.”


I would take exception to the sidelining of hemochromatosis as being insignificant due to manifestation tiers. The data I am quoting is from the very basic of basic qualifiers of the H63D and C282Y mutations. As you cited there are more mutations that have been and I am sure will be cited with regards to variants and expressions in hemochromatosis. However, my assertions rest on the very most fundemental baseline of the condition/disease.

Also, thank you for the kind words of sympathy, it is an outrageous condition to have to live with and has cause a stroke, via hormonal disruptions and now has caused significant deposits to my pituitary and liver.

I acknowledge your theory that by having hereditary hemochromatosis that the competiton or antagonising of Mn is probably significant.

Also, I want to bring to your attention that from a hereditary perspective the manifestation is actually defined. Reference the epicanter of the condition as Ireland/UK and the documentation of those of us with high iron handling the corpses of the black plague without contammination. I tend to call into light the assertion of neanderthal and being gorded by wild boar and that the mutation is part of some evolution process that spared the iron from the hunters losing so much blood, intuition says bullocks.

As for Mercola, I take him with a grain of salt. He personally has thalassemia and his advice about smaller volume (300cc phlebs) with greater frequency actually translated to helping me cope.

As for Stephanie, she sidelined a hypothesis of mine that is actually a bit more than a hypothesis since it appllies ot my lab results that uric acid increasese in the absences of reasonable Mn levels. The mechanism rests in part in the overlap of the krebs and urea cycle and is also simply a back up antioxidant system to SOD.

What is ultimately driving the issues it that I have developed a protocol to cure atrial fibrillation at least in the lone afibbers group. One has already gone before me and has maintained NSR for 6 months WITHOUT an ablation. The MnSOD and SOD II factors comes into play with the eNOS factor and how proper levels of eNOS, which I have been able to stabilize with amino acid therapy has a greater dispensation of stability when Mn is leveld and super oxidise ie mitigated.

The idea of having scar tissue burned at 212 F to ablate and supposedly correct afib is lunacy. The use of a 6 month benchmark where paroxysmal is 75% and persistent is 50% effective after undergoing a procedure that is more reflective of the dark ages is beyond understanding, until you consider the about of money being made.

I intend on delivering a method/protocol that will take a big bite out of that cash flow and empower the patient. Yet for another thread. My apologies for going off subject, but I wanted to frame it for you. Thank you for your comments.


I want to also convey that during the course of the year where I was taking Mn at 40mg of TRAACS Mn glycinate, I would routinely have phlebotomies that drove my ferritin into single digits and tanked my serum iron <80ng/mL. It had no effect on Mn loading, none. This is counter to the assertions herein that an anemic state lends to accelerated load rates.

What did have an effect on Mn loading was reducing uric acid levels of plus 10 to 5 or 6 via allopurinol where Mn levels would near the low end of range, but still fall short. I have at least a half dozen labs that demonstrate low uric acid, higher Mn and high uric acid and lower Mn.

Yes, this applies to me as part of my profile. However, the possibility and in my opinion probability exists, that there is a corelation.


Well, I’m estimated to be only 2.9% Neanderthal, from a DNA perspective, and that’s above average, even for a European (average 2.7%). What’s more, my sisters is 3.2% Neanderthal… and she has no HFE-related hemochromatosis mutations, at all. (Lucky draw from mom.) Clearly, arguments about Neanderthal inheritance are on thin ice, to begin with.


Please comment on the simulating anemia via phlebotomies and how there were no Mn loading increases. I was able to lock ferritin and serum iron with 80mg/wk (split 40mg doses x2/week) of testosterone, which as a hepcidin antagonist stops and I mean locked down the ferritin and iron from loading. Although, another theory is that the iron then loads into adipose fat and some into ceruloplasmin as a binder to copper. I am going to experiment with Mn sulfate and probably citrate as well and will report back. Thanks again.


I did a bunch of research on this when I was coming up with my own recipe. To start with, most upper intakes from the IOM (Institute of Medicine, which is where the FDA gets their values) are based on common intakes, not observed toxicity. The reason is the ethical problem with clinical trials where you keep increasing doses until toxicity is observed. In short, it would not be ethical to use a more scientific method to find upper limits, so instead, they use the highest observed intakes that are clearly not toxic (in some cases, magnesium I believe, they use the toxicity of elemental magnesium observed in industrial settings; this is a problem, however, because compounds from organic sources tend to be significantly less toxic).

So, here is what I found (I apologize that I no longer have the sources, but it should not be hard to verify this): Supposedly typical vegan diets are very high in manganese. Intakes as high as 22mg have been observed (I don’t know how common these are, but the implication was that it is within the common range). Thus far, no cases of manganese poisoning have been reported related to vegan diets. Given the significant number of vegans in the U.S., it is reasonable to assume that if 22mg was high enough to cause problems in even a small portion of the population, we would see at least some reports of manganese poisoning in the vegan population.

Now, there are two important things to be aware of:

Minerals from synthetic sources tend to have higher toxicity than those from food sources. So, manganese from a multivitamin could be problematic, where larger amounts from food sources would not be.

Second, this is not solid science. It is good reasoning based on the known facts, but it is not proof that 22mg is fine. In fact, it is possible that over the course of many years, this high intake would eventually lead to problems. The probability of this is not very high, but the current brand of veganism that results in this diet has only been big for maybe 20 years. Problems that take 40 years to show up would only show up in the very small population of vegans on this kind of diet from before it got popular. (Still, this kind of long term problem is unlikely.)

I cannot even give you an estimate of where a good balance would be. Be careful, but you can probably get away with a bit more than 11mg, so long as a majority is from food sources.