Molybdenum, Hard To Pronounce, Harder Still To Obtain

Morning Star

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Well not really. A host of natural foods are rich in this element. Oats, lentils navy beans, chickpeas. Problem of course is that these items are horribly estrogenic if one were to eat them in quantities sufficient to obtain a proper amount of Mo.

Following a peat inspired diet will invariably lead to a deficiency. Although Peat has some contrarian ideas regarding the desirability of transition metals in nutrition, iron especially, given its steady accumulation with age, and the attendant metabolic inefficiency. I would not, however rush to conflate these two, Mo and Fe. Undoubtedly some of it is needed to preserve the integrity of the human organism. How much is needed though is unclear to me. Should one just bite the bullet and occasional consume the least worst option among these offenders,in the manner of liver and shellfish, Or supplement. Thoughts?
 

Ras

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Well not really. A host of natural foods are rich in this element. Oats, lentils navy beans, chickpeas. Problem of course is that these items are horribly estrogenic if one were to eat them in quantities sufficient to obtain a proper amount of Mo.

Following a peat inspired diet will invariably lead to a deficiency. Although Peat has some contrarian ideas regarding the desirability of transition metals in nutrition, iron especially, given its steady accumulation with age, and the attendant metabolic inefficiency. I would not, however rush to conflate these two, Mo and Fe. Undoubtedly some of it is needed to preserve the integrity of the human organism. How much is needed though is unclear to me. Should one just bite the bullet and occasional consume the least worst option among these offenders,in the manner of liver and shellfish, Or supplement. Thoughts?

Chickpeas are not very estrogenic.
 

paymanz

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fruits are also a good source of the element ,per unit of weight they seem low on Mo(because of high water content) but with big servings of fruit they are good source.

white rice also is not bad 79mcg/100g raw Dietary intake of minerals and trace elements in rice on the Jamaican market

and whole milk around 40-70 mcg /L http://www.journalofdairyscience.org/article/S0022-0302(51)91818-8/abstract
Cream from the cows on the control ration
contained 263 y per liter,......
Analysis of composite samples of cream and skimmilk showed that most of the
molybdenum in "control" mill¢~ or in those from cows receiving a molybdenum
supplement was concentrated in the cream fraction.
http://www.imoa.info/HSE/environmental_data/human_health/molybdenum_uptake.php
There was no influence of age on the Mo concentration Specific effects of different food and beverage intakes could not be demonstrated, with the exception of a positive correlation between butter consumption and Mo concentration
vegetables around 30-100 mcg/100g Mineral contents of some plants used in Iran (this table is on dry basis)
 
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paymanz

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Liver is probably best source,

Also notice high level in fat tissue next to liver, probably proves it is a fat soluble mineral and can be found in butter too.

Molybdenum levels in humans
 
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Amazoniac

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Essential trace metals in man: Molybdenum - ScienceDirect

"MOLYBDENUM, atomic number 42, is the only metal in the second transitional series which is essential for mammals. Insofar as is known, there are only two mammalian enzymes dependant upon molybdenum as a co-factor; both are dehydrogenases and both are molybdoflavoproteins. Xanthine oxidase found in liver, kidney and milk, oxidizes xanthine, hypoxanthine, some other purines and aldehydes, whereas aldehyde oxidase, found in liver, oxidizes aldehydes to acids [1]."

"[From the available] data it appears that molybdenum goes with copper, zinc and manganese, and with related silver and cadmium in those tissues where both are found frequently."

"[From an analysis, the] richest sources were meats, grains and legumes; the poorest vegetables, fruits, sugars, oils and fats. In fact, molybdenum was not detected in 11 of 25 vegetables other than legumes, and occurred in low concentrations (< 0.1 microg/g) in ten others. Spinach, a yam, canned soup, three syrups, cocoa, mustard, wheat germ and sunflower seeds contained fairly sizeable amounts."
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"Molybdenum, like other essential trace elements, is one of the key substances upon which life on this planet depends. Organisms concerned with the nitrogen cycle, such as blue-green algae, Azotobacter, Rhizobium and others require molybdenum. Because nitrogen-fixing bacteria in sea and soil require molybdenum, without it there would be little protein, only that derived from those soil bacteria which use vanadium for this purpose; and from stored nitrates in rocks. The fixation of atmospheric nitrogen is the initial step in the synthesis of protein. Furthermore, molybdenum is essential for molds and bacteria which reduce nitrate nitrogen, and which decompose dead organic matter into simple compounds which can be used again for organic synthesis. It is also required for Nitrosomonas which oxidize ammonia to nitrates; and for Nitrobacter which oxidize nitrite to nitrate [2]."

"Insofar as is known, all plants contain molybdenum, and it is essential for the growth of all except a few blue-green algae [2]. Molybdenum may not be found in all parts of plants (see Table 5), but undoubtedly occurs in their seeds and roots. Marine plants have 0.45 ppm, land plants 0.9 ppm, with less in gymnosperms and more in those growing on molybdenum rich soils. Leguminous and seed crops accumulate molybdenum, and can be used as indicator plants for biogeochemical prospecting [21]."

"Plankton concentrate molybdenum to 25 times that of sea water, and brown algae to 11 times."

"In mammals, molybdenum is found mainly in liver, kidney and blood. The amounts depend upon the intake, and tissues normally deficient can be made to accumulate this metal when it is fed in large amounts [14]."

"There are only three, or possibly four, metalloenzymes known which are dependent upon molybdenum, and all of them are molybdoflavoproteins. Two are mammalian O2 oxidoreductases, found where molybdenum occurs in liver and kidney: xanthine oxidase, which catalyzes the oxidation of hypoxanthine to xanthine and xanthine to uric acid, as well as some other purines, pterins and aldehydest, and aldehyde oxidase, which catalyzes the oxidation of aldehydes to acids, as well as quinoline and pyridine derivatives. Both contain four atoms of iron, one atom of molybdenum and one mole of flavin adenine dinucleotide per mole of enzyme."

"Because most aldehydes are vasodilators, aldehyde oxidase is essential for circulatory homeostasis, and because hypoxanthine is nephrotoxic, xanthine oxidase is essential for the integrity of the kidney. In cattle, xanthine calculi occur where molybdenum is deficient [14]. Therefore, molybdenum has only a few specialized functions in the human body, insofar as is known. In experimental animals, levels of tissue xanthine oxidase were in direct proportion to the intake of molybdenum [14]."

"Molybdenum is apparently distributed throughout the liver cell, with little accumulation in nuclear DNA, unlike copper, which is concentrated in mitochondria, and zinc, concentrated in nuclei and in DNA. In view of its association with purines, one might expect it to be chelated by nucleic acids, and it is obviously linked to flavin.
Dietary copper and sulfate are antagonistic to molybdenum in sheep and cattle, and molybdenum in excess produces deficiency of copper [14]."

"Copper exerts its antagonistic effect on molybdenum only in the presence of adequate dietary sulfate [24]."

"Inhibition of molybdenum toxicity by sulfate could be explained by mass displacement of molybdate by sulfate, both being hexavalent and both belonging to the same periodic group. There is no other hexavalent ion in the body present in sufficient quantities to displace molybdate."

"The relationship of sulfate intake to molybdenum content of liver and total body of sheep is illustrated by the work of **** quoted by Underwood [14]. When the ratio of the intakes of molybdenum to sulfate was altered from the normal of 1: 3000 to 1: 21,000, molybdenum content of liver was decreased to 30.3 per cent of the initial value, and of the whole body to 18.2 per cent. When the ratio was altered from a high intake of molybdenum of 1: 47 to 1: 300, liver content declined to 33.3 per cent and whole body to 9.4 per cent. By increasing sulfate intake seven times, tissue molybdenum was depressed by factors of 5.5 and 10.6."

"Soluble hexavalent molybdenum compounds are readily absorbed from the gastrointestinal tract into liver. Molybdenum is found in blood, especially in red cells, and is excreted mainly in the urine, but to some extent in bile, thus producing an hepato-intestinal cycle, which also occurs in manganese metabolism. Excretion is rapid and efficient, but little is known of mechanisms for renal retention in the presence of deficiencies. It is excreted largely unconjugated as molybdate. Apparently there is no mechanism for rejection of hexavalent molybdenum in the gastrointestinal tract, but the liver probably acts as a barrier to adsorption of slight excesses, excreting them in bile."

"Under usual conditions the minimal requirements of mammals for molybdenum are very small. The rat needs more than 0.5 microg/day [2]; at 300 g body weight, this amount would compare with 120 microg/day for a 70 kg man. Thus, it is possible that diets composed largely of refined foods may provide marginal intakes of molybdenum."

"Molybdenum has a low order of toxicity [26]."
"A disease named “teart” occurs in cattle feeding on grass grown in pastures where the soil is high in molybdenum [14]. It is characterized by diarrhea, anemia, poor coats and poor condition. When pasture grass contained 20-100 ppm molybdenum, dry weight, this disease was likely to occur; normal grass contains 3-5 ppm. Presumably alfalfa and clover are the accumulator plants.
This disorder can be treated by excess copper in the diet, or by increasing dietary sulfate. Adequate copper apparently prevents accumulation of molybdenum in liver, in the presence of adequate sulfate, and antagonizes absorption of large amounts from food. Removal of affected animals from such pastures results in rapid recovery as molybdenum is readily excreted in the urine."

"Renal calculi are not uncommon in cattle feeding on molybdenum-deficient pastures." "The relation of marginal intakes of molybdenum to renal xanthine calculi is not known, but presumably such intakes could decrease the body’s xanthine oxidase, especially if the copper intake were elevated from corrosion of copper pipes by soft, acid water [47]."

"Because molybdenum is so intimately concerned with xanthine oxidase, which itself is concerned with the formation of uric acid from hypoxanthine and xanthine as end points of purine metabolism, it is possible that in some way hyperuricemia may be affected by excesses or deficiencies in the diet. Gout represents an inborn error of purine metabolism [43], and theoretically there is adequate xanthine oxidase; deficiency of molybdenum could be expected to reduce the formation of uric acid."

"The major sources of caloric energy, carbohydrates and fats, contain adequate molybdenum only in the whole grain products. Refined sugars contained little or no molybdenum (the “raw” sugars we analyzed were partly refined) and it was found in molasses, a product of refining sugar."

"Unlike other essential trace metals, mean concentrations of molybdenum in liver and kidney were relatively low in the newborn, rising to a peak in the second decade of life and declining slightly thereafter."
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Amazoniac

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Other Ingredients
Microcrystalline cellulose, hypromellose (derived from cellulose) capsule, leucine, silicon dioxide.
I contacted Thorne to find out why on their website they claim that their molybdenum glycinate doesn't contain silicon dioxide, contrary to many vendors. They replied that it's no longer manufactured with it.
@impuritiespersecutor
 

tara

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So there might be a reason to eat kidneys every once in a while. :)
 

Amazoniac

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Kale is (apparently) a great source of molybdenum, 38mcg for each 100g. @Travis - You consume 5x that, correct?

I suspect my coffee intolerance can be related to the coffee inducing a deficiency. I can't think of anything else that could be responsible right now.


"Accutane is an active vitamin A, it is retinoic acid. it bypasses all the regulations in retinoid pathway. Now go and see what is in retinoic pathway, ZINC takes retinol and converts to retinal, then you need NAD then you need aldehyde enzymes to convert it further down to retinoic acid. Accutane bypasses all of this. This tanks your Zinc, NAD, b2, molybdenum, Magnesium, B6. Same exact things needed for 3 beta HSD. Retinoic acid is what produces Progesterone."

"Acne will be cleared with an active retinoic acid. To make that acid in your body, you don’t take ACCUTANE. You take Zinc, NAD, B6, Magnesium and then Manganese(might not be needed) molybdenum and b2. that is all."

"Never take end of the pathway products, they will kill all the minerals and cofactors in the pathway. If you see some claim that some product cures something. Just look at the pathway and feed the pathway."

"You see claim Accutane cures acne. Boom, you just open retinoic metabolism and feed the cofactors from the beginning. Zinc, then NAD, then B6 then molybdenum and b2"

"Like to make Progesterone you need retinoic acid and 3 beta HSD. You just need to feed the cofactors for that pathway, and never the end product, since if you feed the end product it kills all the cofactors in the pathway."

"Liver does not have active vitamin A. Liver has retinol. active vitamin A is accutane which is retinoic acid, which is the end product of retinol metabolism. to get retinoic acid from retinol you need 5 steps and these steps include Zinc, NAD, B6 etc. so if you feed accutane, body lowers Zinc NAD, etc. You can eat liver no problem."

"NAD ribose, active B6, Zinc, Magnesium molybdenum plus active b2 would be my stack for the symptoms."​
To release iron from the liver you need xanthine oxidase which runs on vitamin B2 and molybdenum

B2 and molybdenum = AO

NAD= ALDH


Caffeine: A vitamin-like nutrient, or adaptogen. Questions about tea and coffee, cancer and other degenerative diseases, and the hormones.

"To talk about caffeine, it’s necessary to talk about uric acid. Uric acid, synthesized in the body, is both a stimulant and a very important antioxidant, and its structure is very similar to that of caffeine. A deficiency of uric acid is a serious problem. Caffeine and uric acid are in the group of chemicals called purines.

Purines (along with pyrimidines) are components of the nucleic acids, DNA and RNA, but they have many other functions. In general, substances related to purines are stimulants, and substances related to pyrimidines are sedatives.

When the basic purine structure is oxidized, it becomes in turn hypoxanthine, xanthine, and uric acid, by the addition of oxygen atoms. When methyl groups (CH3) are added to nitrogens in the purine ring, the molecule becomes less water soluble. Xanthine (an intermediate in purine metabolism) has two oxygen atoms, and when three methyl groups are added, it becomes trimethyl xanthine, or caffeine. With two methyl groups, it is theophylline, which is named for its presence in tea. We have enzyme systems which can add and subtract methyl groups; for example, when babies are given theophylline, they can convert it into caffeine.

We have enzymes that can modify all of the methyl groups and oxygen atoms of caffeine and the other purine derivatives. Caffeine is usually excreted in a modified form, for example as a methylated uric acid.

One of the ways in which uric acid functions as an “antioxidant” is by modifying the activity of the enzyme xanthine oxidase, which in stress can become a dangerous source of free radicals. Caffeine also restrains this enzyme."​

Cool ps.:
I was searching for tyw's posts on molybdenum, and found this:
the issue with xanthine oxidase is something that I see a lot of. Lots of times people complain that they can't handle coffee or chocolate. Give them molybdenum and manganese, and suddenly all issues go away.
Which is exactly what I was trying to convey with these quotes.
 

Travis

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The funny think about isotretinoin (13‐cis) is that is has very little affinity for RXR and RAR so it probably isn't working through through either of those. Also, all retinoids which bind these receptors have little effect on acne; this makes one seriously doubt that the 'retinoic acid receptor' is mediating this effects. I think perhaps
13‐cis‐retinoic acid is acting through the LXR, despite its name, because of all the retinoids (i.e. 13‐cis, 11‐cis, 9‐cis, alltrans) only 13‐cis really works for this.

Isotretinoin is actually made in body from retinol, among others, so it's actually a completely natural lipid hormone.

Isotretinoin (13‐cis) decreases sebum, and the liver X receptor (LXR) is known to be involved in lipid metabolism. Once a person considers the array of retinoids produced in the body from retinol (i.e. 13‐cis, 11‐cis, 9‐cis, alltrans), and their different binding characteristics, it's hard to see them all as equivalent; you might even stop using the word 'retinoid acid' at all without it being proceeded by an IUPAC prefix designating its stereochemistry—or the location if its 'kink.'

Unlike Thomas Jefferson's hyperdemocratic classification of men, not all retinoids are created equal:

Prostaglandin E₂ and prostaglandin D₂ are actually isomers of eachother yet have radically different effects—you could even say 'opposite' in some cases. Prostaglandin D₂ cannot bind PPARγ until it spontaneously loses H₂O, after which it becomes its most powerful ligand (PGJ₂). Like the prostaglandins, the retinoids appear to be lipid hormones where only very small changes in structure confers radically different biological activities. A similar thing can be said about steroids.

 
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fradon

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Well not really. A host of natural foods are rich in this element. Oats, lentils navy beans, chickpeas. Problem of course is that these items are horribly estrogenic if one were to eat them in quantities sufficient to obtain a proper amount of Mo.

Following a peat inspired diet will invariably lead to a deficiency. Although Peat has some contrarian ideas regarding the desirability of transition metals in nutrition, iron especially, given its steady accumulation with age, and the attendant metabolic inefficiency. I would not, however rush to conflate these two, Mo and Fe. Undoubtedly some of it is needed to preserve the integrity of the human organism. How much is needed though is unclear to me. Should one just bite the bullet and occasional consume the least worst option among these offenders,in the manner of liver and shellfish, Or supplement. Thoughts?

try walnuts...
 

Amazoniac

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Molybdenum - Scientific Review on Usage, Dosage, Side Effects
  1. Sardesai VM. Molybdenum: an essential trace element. Nutr Clin Pract. (1993)
  2. Pennington JA1, Jones JW. Molybdenum, nickel, cobalt, vanadium, and strontium in total diets. J Am Diet Assoc. (1987)
  3. Choi MK1, Kang MH, Kim MH. The analysis of copper, selenium, and molybdenum contents in frequently consumed foods and an estimation of their daily intake in korean adults. Biol Trace Elem Res. (2009)
  4. Turnlund JR, Friberg LT. Handbook on the Toxicology of Metals (Third Edition) - Molybdenum. . (2007)
  5. Molybdenum in Drinking-water.
  6. Greathouse DG, Osborne RH. Preliminary report on nationwide study of drinking water and cardiovascular diseases. J Environ Pathol Toxicol. (1980)
  7. Trumbo P1, et al. Dietary reference intakes: vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. J Am Diet Assoc. (2001)
  8. Chan S1, Gerson B, Subramaniam S. The role of copper, molybdenum, selenium, and zinc in nutrition and health. Clin Lab Med. (1998)
  9. Westerfeld WW, Richert DA. A New Dietary Factor Related to Xanthine Oxidase. Science. (1949)
  10. DE RENZO EC, et al. Identification of the xanthine oxidase factor as molybdenum. Arch Biochem Biophys. (1953)
  11. Richert DE, Westerfeld WW. ISOLATION AND IDENTIFICATION OF THE XANTHINE OXIDASE FACTOR AS MOLYBDENUM. J Biol Chem. (1953)
  12. Kessler DL, Rajagopalan KV. Hepatic sulfite oxidase. Identification of the molybdenum center as the site of irreversible inactivation by ferricyanide. Biochim Biophys Acta. (1974)
  13. MAHLER HR, MACKLER B, GREEN DE. Studies on metalloflavoproteins. III. Aldehyde oxidase: a molybdoflavoprotein. J Biol Chem. (1954)
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  16. Percy AK, et al. Sulfite oxidase deficiency: Sulfate esters in tissues and urine. Biochem Med. (1968)
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  20. Johnson JL, Rajagopalan KV, Cohen HJ. Molecular basis of the biological function of molybdenum. Effect of tungsten on xanthine oxidase and sulfite oxidase in the rat. J Biol Chem. (1974)
  21. Cohen HJ, et al. Molecular basis of the biological function of molybdenum: the relationship between sulfite oxidase and the acute toxicity of bisulfite and SO2. Proc Natl Acad Sci U S A. (1973)
  22. Abumrad NN, et al. Amino acid intolerance during prolonged total parenteral nutrition reversed by molybdate therapy. Am J Clin Nutr. (1981)
  23. Turnlund JR1, Keyes WR, Peiffer GL. Molybdenum absorption, excretion, and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Am J Clin Nutr. (1995)
  24. Turnlund JR1, et al. Molybdenum absorption, excretion, and retention studied with stable isotopes in young men during depletion and repletion. Am J Clin Nutr. (1995)
  25. Allaway WH, et al. Selenium, molybdenum, and vanadium in human blood. Arch Environ Health. (1968)
  26. Verseick J, et al. Determination of molybdenum in human serum by neutron activation analysis. Clin Chim Acta. (1978)
  27. Turnlund JR1, Keyes WR. Plasma molybdenum reflects dietary molybdenum intake. J Nutr Biochem. (2004)
  28. Flores CR1, et al. Trace elements status in diabetes mellitus type 2: possible role of the interaction between molybdenum and copper in the progress of typical complications. Diabetes Res Clin Pract. (2011)
  29. Muñiz CS1, et al. Reference values for trace and ultratrace elements in human serum determined by double-focusing ICP-MS. Biol Trace Elem Res. (2001)
  30. Abumrad NN. Molybdenum--is it an essential trace metal. Bull N Y Acad Med. (1984)
  31. Murray FJ1, et al. 90-Day subchronic toxicity study of sodium molybdate dihydrate in rats. Regul Toxicol Pharmacol. (2013)
  32. Hosokawa S1, Yoshida O. Clinical studies on molybdenum in patients requiring long-term hemodialysis. ASAIO J. (1994)
  33. Fungwe TV, et al. The role of dietary molybdenum on estrous activity, fertility, reproduction and molybdenum and copper enzyme activities of female rats. Nutr Res. (1990)
  34. Meeker JD1, et al. Environmental exposure to metals and male reproductive hormones: circulating testosterone is inversely associated with blood molybdenum. Fertil Steril. (2010)
  35. Bompart G1, et al. Mild renal failure induced by subchronic exposure to molybdenum: urinary kallikrein excretion as a marker of distal tubular effect. Toxicol Lett. (1990)
  36. Fuentealba IC1, Haywood S, Foster J. Cellular mechanisms of toxicity and tolerance in the copper-loaded rat. III. Ultrastructural changes and copper localization in the kidney. Br J Exp Pathol. (1989)
  37. Momcilović B. A case report of acute human molybdenum toxicity from a dietary molybdenum supplement--a new member of the "Lucor metallicum" family. Arh Hig Rada Toksikol. (1999)
 
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