Molybdenum, Hard To Pronounce, Harder Still To Obtain

Discussion in 'Diet' started by Morning Star, Sep 6, 2016.

  1. Jennifer

    Jennifer Member

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  2. Amazoniac

    Amazoniac Member

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    I wasn't aware of the thread when the abstract was posted on the previous page here.
    Thank you for details, Richard.

    Some interesting bits:

    "The Food and Nutrition Board of the NAS/NRC states that a safe adequate intake of molybdenum is 75 to 350 μg/day for adults and 25 to 75 μg/day for children aged 1–6 years (4)."

    "Little information is available on molybdenum metabolism in humans; data for intestinal absorption ranging from 50–70% during long term balance studies were reported by Tipton and co-workers (6) and Robinson and co-workers (7). In a recent work, Turnlund and co-workers (8) and Cantone and co-workers (9) report intestinal absorption values around 90% and 85%, respectively. In humans molybdenum is contained principally in the liver, kidneys, fat, and blood. Of the approximate body total of 9 mg of molybdenum, most is concentrated in the liver, kidneys, adrenals, and omentum (10). More than 50% of molybdenum in the liver is in a nonprotein cofactor bound to the mitochondrial outer membrane and can be transferred to an apoenzyme transforming it into an active enzyme molecule (11). More than half of the excreted molybdenum via urine. Molybdenum is considered to be rapidly excreted, mainly as molybdate. An excess may also be excreted through the bile, particularly the hexavalent forms. Experimental studies showed that injected radio-molybdenum increased the liver and kidney levels, and that the endocrine glands and the brain had an exceptionally high molybdenum content (12)."

    "Copper prevents accumulation of molybdenum in the liver and may antagonise the absorption of molybdenum from food (14). The antagonism of copper depends on the dietary sulphate (15). It has been suggested that copper and sulphate may displace molybdate in the body (16, 17)."

    "The toxic effect of molybdenum lies in the inhibition of the activity of the sulphide oxidase system and in the formation of thiomolybdate from molybdate and endogenous sulphides. Sulphate ions activate the enzymic system oxidising sulphide and thiomolybdate, restraining thus the formation of thiomolybdate and accelerating the oxidation of thiomolybdate into the less toxic molybdate (19)."

    "Heavy metal damage to the brain is well documented for mercury, manganese, lead, and cadmium. Even the term Lucor manganicum (manganese madness) has been coined. This is the first case of acute human molybdenum poisoning which demonstrated that molybdenum is a new and unwelcome member of the Lucor metallicum family. Otherwise, molybdenum toxicity does not distinguish itself from other heavy metals (21) except, perhaps, in the specific impairment of bone collagen which resembles lathyrism (22)."

    "The increased acidity promotes the absorption of molybdenum from the stomach into the bloodstream (23). Indeed, the fractional absorption of molybdenum from the gastrointestinal tract was almost 100% when administered in diluted HCl and 50% in infant formula (24)."

    "When molybdenum or some other heavy metal is deposited in the grey matter of the brain, it will inhibit the nerve transport, increase the breakdown of various neurotransmitters, and stimulate the production of harmful proteins (22). The consequences of molybdenum deposits can include seizures, decreased learning ability, impaired motor coordination, memory loss, and even psychotic reactions. That sequence of events might explain the persistence of psychiatric symptoms in the patient and the later development of brain sequelae at the time when his blood molybdenum was already normal as revealed by SPECT. The brain is rich in fat tissue and molybdenum has shown preference for depositing in the fat tissue (10). Molybdenum in plasma appears to reflect the »hide-and-seek« situation where molybdenum is rapidly disappearing from plasma and accumulating in the fat tissue of the brain, or elsewhere. Therefore, molybdenum plasma concentrations would not be a good indicator of molybdenum intoxication, not even shortly after exposure to high doses of that metal."

    "De Stasio and co-workers (29) found a much larger uptake of aluminium and molybdenum in neurone cultures than that of other elements, indicating higher neurone cell affinity for molybdenum. We too, found specific predilection for environmental radon daughters of the proteins and lipids in patients with the Alzheimer’s Disease and Parkinson’s Disease, respectively (30)."

    "Apparently, depressed people accumulate molybdenum in the body by excreting less molybdenum via the urine (31). Acute molybdenum toxicity affects male gonads and leads to testicular atrophy (13) (correspondence Haywood–Shelton from 9 March 1999), as evidenced by the patient’s low testosterone and the improvement of his depression after the testosterone patch therapy."

    -
    "A male health practitioner in his late thirties (the patient), apparently in full health, wanted to be even the healthier. His colleague suggested that he should try a molybdenum supplement (Molybdenum Chelated, 100 μg molybdenum per tbl., Nutriwest Co., Douglas, WY) to cure his »allergy« to perfume of his patients. That far he had had a remarkably empty medical record and was outstanding in his educational curriculum. According to his wife’s testimony, he was »easy going, doesn’t get angry often, and it takes a lot to rattle him«. The patient consumed a HCl supplement for »indigestion«, and other non-noxious nutriceuticals (Table 1) before he started to take molybdenum on 1 July 1997. The manufacturer’s recommendation read: »One tablet per day, or as directed«. Instead, the patient followed the recommendation from his physician »Take as needed« and consumed an average of 7 to 8 tablets of molybdenum per day (700–800 μg). He did not start with 700 μg; he started with about 300μg a day, and then gradually increased the intake over a period of 18 days. On day 7 he showed the first signs of anxiety and agitation. On day 14 he became mildly psychotic and experienced visual and auditory hallucinations. He also exhibited excessive craving for salt; so much so that he woke his spouse up at 2:00 a.m. to get him salt from a grocery store. On day 18 he could »smell the molybdenum all around him« and he abandoned molybdenum supplements. The smell was like the one of salt water, distinctive but mild. By the time the patient stopped taking molybdenum, he had already consumed a total cumulative dose of 13.5 mg of molybdenum. On day 19 he had severe psychosis with strong audio and visual hallucinations, insomnia, intense craving for salt, diarrhoea, and painful and cold extremities. On day 22 his hallucinations were accompanied by petit mal seizures and on day 24 he tried to take his life with a knife and, »chased by the devil«, he ran through a plate glass window and jumped headlong off a six-metre wall. The flight ended up with multiple body contusions and difficulties in movement. He struggled with an officer when the police picked him up, as he thought that they were trying to hurt him."

    Nice. This is what a true detox phase should look like.​

    I'm not too worried about it, he was taking a lot of other stuff that could've created a favorable environment for trace mineral toxicity. As always, most of these reports involve people taking more than necessary, insisting despite bad reactions for too long, and including a cocktail of other questionable compounds.

    Effect of molybdenum on other trace elements - iodine, manganese and tungsten, arsenic and selenium

    --
    Phenols , PST and Sulphur Metabolism
    @Daniel - some things there might interest you.
     
  3. Amazoniac

    Amazoniac Member

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    Trace Elements in Human et Animal Nutrition (vol. 2) - Walter Mertz
    "As is the case for many other elements, silicon availability is also probably affected by excess amounts of certain other mineral elements in the diet, which may result in a diminution of silicon absorption through a reduction in the production of soluble silicon. Molybdenum is an example of such an element; an interrelationship between silicon and molybdenum has been established (20). A marked interaction was demonstrated with both semisynthetic and amino acid diets. Plasma silicon levels were strongly and inversely affected by molybdenum intake; silicon-supplemented chicks on a liver-based diet (molybdenum 3 ppm) had a 348% lower plasma silicon level than chicks on a casein diet (molybdenum 1 ppm). Molybdenum supplementation also reduced silicon levels in those tissues examined. Conversely, plasma molybdenum levels are also markedly and inversely affected by the inorganic silicon intake. Silicon supplementation of an amino acid diet reduced the plasma molybdenum levels of the silicon-supplemented chicks by 280% and the red blood cell molybdenum by 425% compared to the low-silicon group. Reduction in molybdenum tissue retention by silicon also occurred."
     
  4. Amazoniac

    Amazoniac Member

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    Worth reading:
    Molybdenum for Candida albicans Patients and Other Problems

    The claw crane machine is not operating right now. Here are the key terms:
    Acetic acid, NAD, FAD (not Candida, the coenzyme), threonine, thiamine, acetone/aldehyde/ammonia/bleach sniffing, sulfite/sulfate, sulfur-containing amino acids metabolism, glutathione, selenium, iron metabolism/anaemia, oxygenation, reasonable supplementation (copper intake must be adequate).

    @Jennifer @Travis

    --
    http://journals.sagepub.com/doi/abs/10.1177/00220345710500013401
     

    Attached Files:

  5. Travis

    Travis Member

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    A mineral for Candida albicans? . . A Bloody Mineral!

    I have read about many things, but I haven't read about that. Did you know that C. albicans has a Δ¹²-desaturase and also a cyclooxygenase-type enzyme giving it the ability of create prostaglandin E₂ de novo, from glucose, without prior assimilation of any ω−6 fatty acid? In Candida albicans: prostaglandin E₂ serves as a morphogenic factor transforming the yeast into the invasive—and more immunoresistant—mycelial, fungal, and hyphal form. If you were to think that a cyclooxgenase inhibitor would limit Candida transformation, they you'd be right! Aspirin is a powerful antifungal agent:


    And as you know: macrophage-engulfed C. albicans can potentially escape from said immune cell making this process, paradoxically, a pathological process; In the pursuit of destroying a pathogen the macrophage only serves to disseminate it. The killing power of the macrophage is depending on many things, not the least being the plasma arginine concentration. In sepsis: circulating L-arginine—and yes, stereochemistry actually matters here because D-arginine is not an iNOS substrate—can be found ranging from about 40·μM to 50·μM, representing low killing-power (and demonstrating its importance), while its normally found at around 70·μM to 90·μM. However! the maximum macrophage killing-power of C. albicans isn't achieved until an L-arginine concentration of 200·μM is reached. For this reason I do recommend taking 1200·mg of L-arginine in the morning when TNFα is at its cirdadian peak, and hence iNOS is also its circadian peak; this amount expected to raise the plasma L-arginine concentration roughly 50·μM, hopefully killing all macrophage-engulfed pathogens while confounding Candida's attempt at dissemination.


    Molybdenum could be important, but so is . . . iron! Besides the cloud of free-radical or otherwise reactive small molecules such as nitrogen dioxide, superoxide, and hypochloric acid [sic], emitted in a pathogen-directed manner by neutrophils, this immune cell also secretes lactoferrin. This is done ostensibly to bind iron and keep it from the invading pathogen, perhaps analogous to how tryptophan pyrrolase limits circulating indoles. If you'd think that iron overload was a risk factor in candidemia, and perhaps even infections of all types, then you would be correct:

    Abe, F. "Experimental candidiasis in iron overload." Mycopathologia (1985)

    Also secreted by the neutrophil is transcobalamin I. As its name implies, this protein binds vitamin B₁₂ with apparent analogous intent. (If you had thought intrinsic factor was our only B₁₂-binding protein you'd be, in fact, very wrong indeed.) The simple fact that transcobalamin is expressed in the human colon where vitamin B₁₂-producing bacteria can be found puts a serious dent in vitamin B₁₂ omnivore mythology. Instead: I propose that vitamin B₁₂ deficiency is merely the result of bacterial dysbiosis, a conclusion that gets support from the fact that other frugivores/herbivores get along just fine. ('Copraphagia' is merely a mindless, stupid, and disparaging attempt to get around this obvious fact.) Should a person like to argue this, then perhaps they should find just one study of experimentally-induced vitamin B₁₂ deficiency where antibiotics hadn't been used prior.

     
  6. tca300

    tca300 Member

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  7. Amazoniac

    Amazoniac Member

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    From what I read, cow's milch has on average 50 mcg/L. We don't know how much is good and if more than the current recommended intakes (75-250 mcg/d) can be beneficial. The person would need to consume copious amounts of milk to serve as the main source of molybdenum to get to the higher of the ends. It's also possible that a great deal is lost when you remove the cream (paymanz, 2016).

    Molybdenum - Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc - NCBI Bookshelf

    "A human study involving doses up to 1.5 mg/day showed no adverse effects on copper utilization (Turnlund and Keyes, 2000)."

    But:
    "Individuals who are deficient in dietary copper intake or have some dysfunction in copper metabolism that makes them copper-deficient could be at increased risk of molybdenum toxicity. However, the effect of molybdenum intake on copper status in humans remains to be clearly established."​

    To be fair, I think molybdenum has to be at the bottom when it comes to a priority list of possible deficiencies. It isn't too safe either to experiment with trace minerals if you have persistent vitamin deficiencies because those will tend to lodge.

    tyw used to believe that a dose of at least 500 mcg at a time was needed for a therapeutic effect (if I remember it right). He has various post on it. Personally, I wouldn't feel with the comfortables going that high, but it's still below the current upper of the limits (estimated to be 2000 mcg/d).
     
  8. Amazoniac

    Amazoniac Member

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    - Role of Vitamin A Metabolism in IIH: Results from the Idiopathic Intracranial Hypertension Treatment Trial (Figure 1)

    [​IMG]

    - Molecular Cloning of Retinal Oxidase/Aldehyde Oxidase cDNAs from Rabbit and Mouse Livers and Functional Expression of Recombinant Mouse Retinal Oxidase cDNA inEscherichia coli - ScienceDirect

    "Retinal oxidase (EC 1.2.3.11) is a molybdenum-containing flavoenzyme with high enzymatic activity as to retinoic acid synthesis."​

    - The Impact of Single Nucleotide Polymorphisms on Human Aldehyde Oxidase

    "Aldehyde oxidase (AO) is a complex molybdo-flavoprotein that belongs to the xanthine oxidase family. AO is active as a homodimer, and each 150-kDa monomer binds two distinct [2Fe2S] clusters, FAD, and the molybdenum cofactor. AO has an important role in the metabolism of drugs based on its broad substrate specificity oxidizing aromatic aza-heterocycles, for example, N1-methylnicotinamide and N-methylphthalazinium, or aldehydes, such as benzaldehyde, retinal, and vanillin."​

    - https://febs.onlinelibrary.wiley.com/doi/abs/10.1016/0014-5793(93)80818-F

    :hattip gbolduev
     
  9. Amazoniac

    Amazoniac Member

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    One more figure showing the metabolism of vitamin A and the dependence on proper oxidation of retinal.

    The Roles of Vitamin A in the Regulation of Carbohydrate, Lipid, and Protein Metabolism
    [​IMG]

    As Travisord would say, the more deficient in molybdenum you are, the more likely it is that some parts might be compromised, becoming retinull.
     
  10. Amazoniac

    Amazoniac Member

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    For those that suspect a deficiency and just can't get enough from diet but are not willing to supplement it due to concerns of imbalances (which I believe is legit), there are desiccated kidneys available. However I don't have any experience with it.

    --
    Risk assessment
    Assessment of Molybdenum Toxicity in Humans (explaining how the tolerable intake got defined)

    Random unrelated parts:

    "[..]sulphate alleviates molybdenum toxicity in monogastric animals (except when they are copper deficient, in which case it can intensify the toxic symptoms) and exacerbates it in ruminants."

    "Histological examinations of animals following acute doses generally show damage to the liver and kidney and sometimes to the adrenals and spleen."

    "Possible reasons for the low degree of toxicity are the facts that molybdenum is a necessary trace element in the body, functioning in conjunction with some flavoprotein enzymes (xanthine oxidase, aldehyde oxidase, sulphite oxidase), and it is rapidly eliminated in the urine.31–34 Because molybdenum toxicity is associated with copper intake or depleted copper stores in the body, humans who have an inadequate intake of dietary copper or some dysfunction in their copper metabolism that makes them copper deficient, could be at greater risk of molybdenum toxicity."

    "An effect that is shared by a number of species involves bone or joint abnormalities[.]" "Aching joints and symptoms resembling gout have also been reported from areas of Armaenia where the population has a high intake of molybdenum via food."
     
  11. Amazoniac

    Amazoniac Member

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  12. Amazoniac

    Amazoniac Member

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    Molybdenum is quite interesting. Its inclusion in intravenous nourishment corrected issues with sulfur-containing amino acids:

    Amino acid intolerance during prolonged total parenteral nutrition reversed by molybdate therapy | The American Journal of Clinical Nutrition | Oxford Academic

    "Molybdenum has been known to have a functional role in the enzymes xanthine oxidase, aldehyde oxidase, and sulfite oxidase. It has been shown that molybdenum is incorporated into the apoprotein of these enzymes rendering them active (4). Xanthine oxidase functions in the disposal of the purine and pyrimidine metabolites in mammals (5). Sulfite oxidase is essential in the handling of cystine and methionine, the sulfur-containing amino acids in the diet (6). Aldehyde oxidase is important in the oxidation of a wide variety of nitrogen containing heterocycles [such as niacin] that are either abundant in nature or are manufactured in man (7)."

    "Our patient manifested severe neurological abnormalities when stressed with a sulfur load. The relevant biochemical abnormalities included low inorganic sulfate excretion (<30% of normal) with elevated cxcretion of sulfite and the abnormal sulfur metabolite, thiosulfate. Two differences are, however, worth noting in our patient. The first is the absence from the urine of the abnormal amino acid, S-sulfocystine, and second the persistent hypermethioninemia observed before molybdate supplementation."

    upload_2018-9-20_19-45-32.png

    "The elevated methionine levels in our patient must have resulted primarily from a deficiency of sulfite oxidase precipitated by a prolonged inadequate molybdenum intake. In effect decreasing the sulfur load in the TPN solution infused did not improve methionine clearance and did not lower the plasma methionine levels except when supplemented with ammonium molybdate (Fig. 1). In addition we can postulate that the hypermethioninemia could partially be secondary to a block of methionine conversion to cystine, possibly as a result of accumulated sulfite. This would explain the low levels ofcystine and tauninc noted before molybdate therapy as well as the hypcrmcthioninemia and subnormal cystine and taunine levels seen with a separate infusion of sodium bisulfite."

    "The mental disturbances and occasional coma seen with this patient are likely related to the deficiency of sulfite oxidase, since the few subjects reported to have xanthine oxidase deficiency have no associated neurological abnormalities ( 15, 16). It is not clear, however, how the deficiency of the enzyme leads to these neurological problems. Animals depleted of tissue sulfite oxidase were significantly more susceptible to neurological toxicity from injected sulfite (22). It is conceivable that the excess sulfite accumulating in the plasma could lead to the observed symptoms by a direct action on the central nervous system or through the formation of S-sulfonates which are toxic to the brain (23, 24). Low circulating levels of cystine (25) or inorganic sulfate (26) are other possible causes. In addition, hypermethioninemia cannot be ruled out (27). Recently Steele and Benevenga (13, 14) have shown that the transaminative pathway of methionine catabolism can lead to the formation of hydrogen sulfite and methanethiol, two compounds that are extremely toxic (14)."
     
  13. Elephanto

    Elephanto Member

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    High dose Molybdenum is the only way I know of to chelate inorganic/free copper (usually from copper plumbing) that is found high in Alzheimer's, certain other mental conditions and hypothesized to play a role in male pattern baldness. I know that a protocol of a few weeks made a long-lasting change to my hair, seems to afford almost unconditional protection against further regression (well that and resplenishing Zinc, which is low in all types of hair loss). The "Candida" perspective is new to me, but it could also explain the results it achieved as shared in a hair loss guide where complete regrowth was achieved. It was 3 x 450mcg a day. Low doses don't interfere with Copper levels in studies.

    On another note, I don't supplement with it apart from the few past protocols I did, I eat Adzuki beans and lentils anyway, but this is because I can feel it raising Nitric Oxide with moderately high doses.
    Nitric Oxide Mediates Molybdenum-Induced Antioxidant Defense in Wheat under Drought Stress

    Nitrite-dependent nitric oxide synthesis by molybdenum enzymes. - PubMed - NCBI
     
  14. Amazoniac

    Amazoniac Member

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    Your posts are great, thanks for the input.
    @Wagner83
     
  15. Waynish

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  17. mujuro

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    Wow. Re manganese, I had a sweet potato phase a few weeks ago where I was eating 1kg or more per day, and found that my coffee tolerance went waaay up. I was drinking up to 3 cups, which is insane for me. So I’m guessing it was the manganese, because I don’t get much manganese from anywhere else.
     
  18. Amazoniac

    Amazoniac Member

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  19. Mauritio

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    Interesting!

    Were you able to reproduce those effects ?
     
  20. Amazoniac

    Amazoniac Member

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    Nitric Oxide, Nitrates, Nitrites, And Fluoride, KMUD, 2015

    - Environmental Effects of Molybdenum on Caries [here it's a 'no (Wagner, 2018)'.]
    - Jenkins GN[Author] molybdenum - PubMed - NCBI

    @Liubo (Sebi's work might also interest you)
     
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