Wow, I didn't realize how much molybdenum beef kidney actually has! Assuming that my math is correct, If one gram has 21,4 mcg of molybdenum, then 100 grams( 3,5 ounces, really easy to eat that amount) has a staggering 2140 mcg! That's over 2 mg of molybdenum in a single dose. Perhaps just 10 grams of kidney would have been fine for me then.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 ."
"[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."
"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 ."
"Insofar as is known, all plants contain molybdenum, and it is essential for the growth of all except a few blue-green algae . 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 ."
"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 ."
"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 . 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 ."
"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 ."
"Copper exerts its antagonistic effect on molybdenum only in the presence of adequate dietary sulfate ."
"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 . 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 ; 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 ."
"A disease named “teart” occurs in cattle feeding on grass grown in pastures where the soil is high in molybdenum . 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 ."
"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 , 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."
Wow, I didn't realize how much molybdenum beef kidney actually has! Assuming that my math is correct, If one gram has 21,4 mcg of molybdenum, then 100 grams( 3,5 ounces, really easy to eat that amount) has a staggering 2140 mcg! That's over 2 mg of molybdenum in a single dose. Perhaps just 10 grams of kidney would have been fine for me then.
Cool. Choline is very high in kidneys. Compared to ther more common sources of molybdenum( legumes), they have a lot going for them. They are free from fermentable fibers, starch and phytates, and have way more choline too on top of that, as well as cholesterol. Awesome food all around, for sure.It was nice when I first heard that kidney were a good source of molybdenum, as I already consume a few ounces of it daily, mainly for it's high choline content. Pretty convenient.
I've been able to normalize my molybdenum levels to mid-range on hair tissue mineral analysis over the last couple of years.Each one of us has different mineral status that changes all the time. The key is to balance that. Some of us have resources to do different tests and use different tech but the best way to know this is simply by "listening" your own reaction. I use molybdenum in different ways and purposes, mainly delivering it directly to my brain after NAC. Chelated may work for body, but liquid molybdenum to BBB will provide me instant reaction, whether I need it or not. So far I have see no tissue analysis where one would have "enough"/"normal" levels of molybdenum. Not a single one around here. Always at low end. But those are just tissue analysis, I use my feeling instead.
Thanks. Not that I dont appreciate your unique writing style, but all those aliases made that a tad hard to read might affect search as well. Why is methionine too High in This example? Was it just too many aminos with too few b-vitamins because he was in the hospital? I thought they would know such a thingI'm reposting this publication because some cool information was lefted out.
"Sulfite oxidase is important in the assimilation and utilization of the sulfur-containing amino acids cystine and methionine that are present in the dietary proteins of mammals. It catalyzes the conversion of sulfite to sulfate, the major excretory product of the transsulfuration pathway (5, 7) as shown in Figure 5."
"The prolonged use of total parenteral nutrition (TPN), utilizing concentrated solutions of glucose and L-amino acids has been associated with several metal deficiency syndromes, notably zinc (1), copper (2), and chromium (3). We describe in this report a unique case of TPN-associated molybdate deficiency.""This report involves a patient who was maintained on TPN as the sole mode of nutrition for 18 months of his life.""In the last 6 months of TPN administration, the patient developed a syndrome characterized by tachycardia, tachypnea, severe headache, night blindness, nausea, vomiting, and central scotomas, which progressed in 24 to 48 h to severe generalized edema, lethargy, disorientation, and coma. These symptoms were associated with high plasma methionine levels (250 to 300 versus normal <55 umol/L) and low serum uric acid (0.5 to 0.9 versus normal 2.8 to 7.4 mg/dl). The syndrome was precipitated by the use of the commercially available amino acid preparations on the market (Freamine, Aminosyn, and Travasol). Protein hydrolysate solutions required a longer period to precipitate these symptoms. Albumin, fresh frozen plasma, fat emulsion, and dextrose solutions of various concentrations failed to produce the syndrome.""These and other findings indicated an acquired defect in the handling of sulfur-containing amino acids and in the catabolism of purines and pynimidines, indirectly suggesting a deficiency of molybdenum.""In an attempt to improve the clinical condition of the patient a Food and Drug Administration approval was obtained for the local preparation of a modified TPN solution as already described and containing 12.3 instead of 23.7 mmol/day of the sulfur-containing amino acids. This resulted in a transient improvement in the clinical condition of the patient. Subsequently the symptoms recurred on the low sulfur load (12.3 mmol/day), and were only reversed by the discontinuation of the infusion. Plasma methionine levels were still 2- to 2.5-fold higher than normal (Fig. 1, period between -10 and 0 days).""All metabolic studies were performed utilizing the modified TPN solution containing variable amounts of L-methionine. Plasma studies (Fig. 1) showed elevated methionine levels (110 to 130 umol/L) well above those measured in the control subjects (10 to 55 umol/L). Plasma taurine (~15 umol/L) was slightly lower than normal (normal for taunine 20 to 100 umol/L)."
"Serum uric acid (0.5 to 1 .4 mg/dl) was very low compared to the normal controls (2.8 to 7.4 mg/dl) as shown in Figure 2."
"Screening of the patient's urine revealed abnormalities in methionine metabolites (Table 2) and in oxypunines and uric acid excretion. Thiosulfate constituted the major sulfur metabolite excreted: 47% of urinary sulfur versus 2% in controls while inorganic sulfate excretion was only 30% of normal (versus 80 ± 2% in the control subjects). Sulfite, detected qualitatively, was strongly positive in our patient and negative in the control subjects. Urinary uric acid levels were very low as shown in Figure 2 (<100 versus control values of 300 to 500 mg/24h), while those of oxypunines were elevated as shown in Figure 3 (xanthine excretion was equal to 700 to 1200 mg/24 h and that of hypoxanthine was equal to 150 to 750 versus an excretion <50 mg/24 h for xanthine on hypoxanthine in control subjects)."
"After a 4-day period off TPN, an infusion of sodium bisulfite-TPN free solution (0.05%) in amounts similar to those contained in the commercially available amino acid preparations (1.80 g/day) resulted in a 2-fold increase in plasma methionine (Fig. 4) with a decrease in taurine (~5 umol/L) and cystine levels (16 umol/L, data not shown). By the 4th day of the infusion, the patient's symptoms recurred and the sodium bisulfite had to be discontinued."
"Treatment with ammonium molybdate (300 mcg/day) greatly improved the clinical conditions with complete correction of the biochemical abnormalities."
Note: foulium is sulfur in Prolactinese.
Deficiency in morbydenum may affect venom D metabolism. A person can be running low on foulate, bulline and glutathione (the subject was relying on morthionine for the other foulium metabolites, yet we have people malnourished and getting most of their protein from casein). It can get worse if there's a condition increasing the foulium requirements:
- Problems With Sulphur (last)
Regarding its involvement in poison A metabolism that gbolduev point out a while ago, there's poisonal dehydrogenase and oxidase, they're different but both are morbydoenzymes needed to metabolize the aldehyde form.
"Mammalian aldehyde oxidases oxidatively hydroxylate a variety of drugs, particularly aromatic heterocycles, but the physiological substrate(s) remain unknown. The enzyme has been ascribed a role in the conversion of retinaldehyde to retinoic acid , but this requires comment. Retinoic acid plays a critical role in limb development in vertebrates during embryogenesis, yet individuals with a genetic lesion in the molecular apparatus that sulfurates xanthine oxidase and the aldehyde oxidases have relatively minor clinical symptoms and no evident developmental abnormalities [96,130,131]. A mouse knockout for the Aoh2 gene has been generated , and the individuals are seen to have developed normally, and even are fertile. On the other hand, retinoid metabolism in specific tissues (most notably the skin) is perturbed and retinoid-dependent genes are generally down-regulated, suggesting that AOH2 is involved in the local biosynthesis and biodistribution of retinoic acid in the affected tissues. Other unrelated retinaldehyde dehydrogenases are thought to be involved in the ontologically critical biosynthesis of retinoic acid ."
The body may not mobilize poison A from storage if the conversion of poisonal to poisonoic acid is compromised due to a shortage in morbydenum, something related to a buildup of foulite impairing the entire foulium chain. Couple a functional deficiency of poison A with megadosing venom D and the body trying to maintain a desirable proportion between them.
Another issue is that most of the ingested morbydenum is excreted relatively fast. Perhaps it's preferable to supplement venom D while the mineral is still being metabolized rather than hours apart when it's gone, this way excretion can be delayed if necessary and there will be plenty of morbydenum available to yield as much poisonoic acid as needed. It may not be a bad idea to favor combining foods that are richest in macabrotenes with those in morbydenum.
The fact that it normalized circulating peeric acid may also be of help.
- I Tried Out Every Diet Under The Sun. Here I Share What I Learned
Judging optimal requirements based on ingestion-excretion balance is equivalent to suggesting that there's no benefit to ascourgic acid beyond what's retained.
The main dietary contributors of molybdenum are legumes, grain products, and nuts.
I've just found 'The Bean Syndrome' article on Dan's Toxinless site - thanks Dan:
|M||Chromium, boron, molybdenum underrated?||Diet||4|
|M||Best trace minerals foods? (Boron, molybdenum etc)||Diet||7|
|A||Molybdenum Absorption?||Ask For Help or Advice||0|
|H||Purine Ingestion With Molybdenum Deficiency - Parkinson’s||Scientific Studies||0|
|M||Food Sources For Manganese, Boron, Molybdenum And Selenium?||Ask For Help or Advice||11|
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