Molybdenum (Mo)

Chris Masterjohn has just sent out an email about Mo. I noted that we don’t actually have a topic about it. Hence I thought I would put up some info.

A few years ago I found a particular salad sold by a shop called Marks and Spencers (3 bean salad) particularly helped my sleep. I Identified the black turtle beans as the active ingredient and I have noted that they are high in Mo.

I intend, therefore, experimenting to see if I can determine any effect from a small amount of Mo supplementation. There are potentially conflicts between Mo and Cu so AIUI Mo needs to stay below 0.5mg per day. Chris Masterjohn makes a valid point that Mo dependent enzymes are important and it might be that a slight deficiency is not obvious, but fixing it makes a noticeable difference. Obviously this will vary as some people live in areas with higher levels and some in areas with lower levels.


Molybdenum is one of the ingredients in O.N.E. Multivitamin by Pure Encapsulations (75mcg).


Also, Life Extension’s “Two-Per-Day” multivitamin contains 100 mcg of Molybdenum (as molybdenum amino acid chelate)…

My NOW NAC (600 mg) comes bundled with Molybdenum and Selenium. I take one of those a day along with 3 g of NOW NAC tablets.

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Chris Masterjohn has put another email out about Molybdenum which I copy below.

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Does Molybdenum Lengthen Lifespan?

Here are some hints that it may.

Chris Masterjohn, PhD
Mar 1 40x40

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In order to be useful, molybdenum has to be incorporated into the molybdenum cofactor (“MoCo”) protein.

The first two enzymes involved in the synthesis of MoCo are coded for by the gene MOCS1.

Researchers were investigating an mTOR (or just “TOR” in this case)-related aging hypothesis in the fruit fly Drosophila and accidentally stumbled their way into the finding that increasing MOCS1 lengthens lifespan in females. The MOCS1 gene was being unintentionally influenced in their original experiment, so they repeated the experiment in a controlled manner to investigate the role of MOCS1.

Because fruit flies mainly express MOCS1 in the nervous system, and because the brain may regulate lifespan in response to nutrient sensing, they engineered the flies to specifically over-express this enzyme in their neurons.

The degree to which increasing MOCS1 expression lengthened lifespan is signified by the degree to which the blue line in the graphs separates itself to the right of the other lines:


It had no effect in males, but it lengthened lifespan 6-12% in females.

The sex-specific effect is largely a mystery, but it makes sense that females have higher molybenum requirements than males, because estrogen increases hydrogen sulfide production.

Fruit flies don’t have “estrogen” but they have estrogen-like hormones, and regardless of whether the mechanisms are the same, females have much higher expression of the first one or two (depending on the strain) enzymes of involved in converting homocysteine to hydrogen sulfide.

That doesn’t necessarily mean that female fruit flies have a higher sulfite burden than males, but it would enable it, and that would make female fruit flies similar to female humans, who experience greater sulfite production during estrogen peaks of monthly cycles, when using birth control or plan B, when pregnant, or when using HRT.

This also can be easily reconciled to a whole other body of evidence that restriction of the sulfur amino acid methionine lengthen lifespan in fruit flies and rodents. The major paradigm for interpreting this is that S-adenosyl-methionine (SAMe) activates the mammalian target of rapamycin (mTOR), so restricting methionine reduces mTOR’s role in aging. However, glycine supplementation activates mTOR and lengthens lifespan. Genetic evidence favors the hypothesis that glycine lengthens lifespan through glycine N-methyltransferase (GNMT), which absorbs extra methyl groups from SAMe, and, when everything needed from proper buffering capacity is in place, allows them to be scavenged in between meals so that the methyl group supply stays relatively stable.

Rapamycin is the namesake of mTOR, and it inhibits MTOR and lengthens lifespan in mice. However, it also scars their hearts, raises their glucose, fattens their liver, and shrinks their testicles.

These findings are usually not witnessed in glycine/methionine studies, and usually these outcomes are improved rather than hurt in those studies. (Although methionine restriction does lead to fatty liver in the context of simultaneous choline restriction and the addition of sugar, alcohol, or fat).

While I will not argue the mechanisms involved could be many and varied, I will point out that the trans-sulfuration pathway is strongly activated by SAMe, and SAMe will rise far more pronouncedly if glycine and GNMT are not serving as a buffer. Thus, an excessive ratio of methionine to glycine (read how to balance them here) should lead to more sulfite accumulation, and thus a higher molybdenum requirement.

Thus, ALL of the above evidence can be reconciled in a model where sulfite — which is toxic across the board, destroys thiamin and B6, tanks testosterone, destroys sperm, drives the nausea, vomiting, and even in many cases hallucinations of pregnancy — also shortens lifespan, which implies that meeting the requirement of molybdenum to convert that sulfite to sulfate should be a critical component in everyone’s longevity toolbox.

While women most likely require more molybdenum than men, men are no less vulnerable to sulfite toxicity and should be no less concerned about meeting their molybdenum requirement.

I have several resources on meeting your personal molybdenum requirement: the Molybdenum Vitamins and Minerals 101 lesson, A Simple DIY Home Test for Molybdenum Deficiency, and Missing From the Databases: Molybdenum, which covers how to get enough molybdenum from food.

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Incidentally I have started supplementing with a small amount (under a milligram daily) of molybdenum. I have noticed an improvement in alcohol metabolism - which would not be surprising. There may also be other changes, but I need some time to develop sufficient data to be certain.

It does imply, however, that enzyme creation was held back by limited availability of Mo.

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Reading up a bit more on this. Molybdenum absorption can conflict with copper absorption and hence it might be sensible to supplement with copper on a different day to Molybdenum. Also molybdenum can increase the metabolism of purines to urate. High urate can cause gout.


I thought I should add to this that I stopped taking any Molybdenum so I could review the effect on urate. It may have put urate up by about 10-20%, which is an expected result. However, as the turnover is not that high I want to see how quickly it goes back down again before restarting.

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I now have seen a couple of blood tests since stopping Molybdenum. The problem with urate is that it varies a certain amount anyway and is affected by things such as drinking beer. However, what I can say is that it does seem to have peaked now, but I will wait a while before trying any more.

These are the recent results (by week, in micromoles per litre)
330 328 330 301.3 355.3 311 349.8 330
start molybdenum (about half a milligram per day)
stop molybdenum
368 365.4 381 342.3

Because the supplementary Mo increases the levels of Mo dependent enzymes (of which there are at least 4 human enzymes) it will increase the rate at which urate is created for a while and stopping supplementing won’t enable the figure to drop back immediately. To me it appears now that I have the 342.3 figure that it is going back down again. However, I am still going to wait a few weeks before trying it again.

It looks like it took something like 3 weeks for the direction of travel to shift.