Molybdenum, Hard To Pronounce, Harder Still To Obtain

Waynish

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Anyone know the rational mechanistic classification for the metals and minerals that are healthy - and why - and the ones that are not?
 

norseman

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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.
 
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Last time I took molybdenum, it caused terrible dyslexia and memory problems. I slept really well while on it, but woke up very tired, even after sleeping 8 hours+.

The effects on cognition made me wary of trying it again. The form that I used was an amino- acid chelate, so perhaps that's the problem?

It's interesting that I experience a similar situation when I eat beef kidney( it's much less severe, but it still happens). I don't experience that after eating liver( even big amounts of it), so it makes me think that it's more complicated than just molybdenum= cognitive impairment for me.

As for manganese, I've been drinking a cup or two of mate tea( roasted yerba mate basically). This is a commercial brand, so certainly not optimal( it has citric acid and ascorbic acid, both of which are probably not very pure), but it makes for a very convenient way to get a lot of manganese quickly. It's also extremely delicious! I even drank an entire 1,5 L bottle once in one day without even thinking about lol. My skin feels smoother since I started drinking it. Also, since I eat a lot of protein, ingesting some extra manganese seems like a good precaution to make sure that my cells are performing the Urea Cycle properly. That way, the extra ammonia from the protein will be turned into urea, which has many benefits.
 
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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."

"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."
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.
 

Waremu

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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.

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.
 
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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.
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.
 

RWilly

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Keep in mind that molybdenum supplementation or too much food with molybdenum can also cause a copper deficiency.
 

Markus

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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.
I've been able to normalize my molybdenum levels to mid-range on hair tissue mineral analysis over the last couple of years.
 

Amazoniac

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I'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."​
1607867182038.png
"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)."​
1607867194038.png
"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."​
1607867201868.png
"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)."​
1607867209457.png
"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."​
1607867215177.png
"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:


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 [152], 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 [153], 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 [151]."​

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.
 
Last edited:

Nighteyes

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I'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:


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 [152], 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 [153], 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 [151]."​


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.
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 thing
 

Amazoniac

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For some reason there's an error message when I try to reply to your post.

I'll try to consume more pyridoxine to keep prolactin level within the undesirable range.

They were able to recreate the syndrome by giving sulfite when methionine concentration was already normal (Fig. 4), so it's likely that sulfite excess (rather than other factors that the correction of molybdenum could target) was responsible for it.


- Molybdenum Nutriture in Humans
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:
https://www.toxinless.com/ray-peat-the-bean-syndrome.pdf
:wave:

- Rowan Atkinson to Mr. Bean: A Story of Weakness to Success - Case Study
 

Amazoniac

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- Trace Elements in Human and Animal Nutrition (0-12-709065-7)

"Molybdenum occurs in low concentrations, comparable with those of manganese, in all the tissues and fluids of the body. Species differences appear to be small (70) and there is very little accumulation in any particular organ with age (60, 110). Typical normal concentrations for the principal body organs for adult men, rats, and chicks are given in Table 15."

1618327154358.png

"Human dental enamel can be relatively rich in molybdenum. A mean concentration of 5.5 ± 0.71 (range 0.7-39) ug Mo/g dry weight has been reported (79)."

"The response of the tissues to changes in dietary Mo is greatly influenced by dietary inorganic sulfate levels. A reduction in Mo retention, and hence lower tissue Mo concentrations, was first demonstrated as a consequence of high-sulfate intakes by **** (28) in the sheep. A similar effect is apparent in cattle (22) and rats (85). High dietary intakes of tungstate also reduce the levels of Mo in the tissues of rats and chicks (25, 60). The magnitude of the sulfate effect on the retention of molybdenum in the tissues of the sheep is illustrated in Table 16. The amounts of Mo in all the tissues examined are smaller at high- than at low-sulfate intakes, both when dietary Mo levels are high and low. It is further apparent from the figures in Table 16 that more than half the total body Mo is present in the skeleton, with the next largest proportions in the skin, wool, and muscles, and only about 2% of the total in the liver."

1618327165335.png

"Adult sheep and cows retain Mo concentrations in their livers of 25-30 ppm, so long as they are ingesting large or moderately large amounts of the element. These high levels rapidly return to normal when administration of the extra Mo ceases. The extent of retention in the liver and human tissues and the rate at which the levels fall depend on the amount and proportion, relative to Mo, of the inorganic sulfate. The level of Mo in the liver therefore gives little indication of the animal's dietary Mo status and is of limited diagnostic value for this purpose, unless the dietary sulfur and protein status is also known."

"Studies of Mo metabolism are of limited value unless the sulfur status of the diet is controlled. Protein intakes can also be important since this can be a source of endogenous sulfate. The potent influence of sulfate on Mo excretion, retention, and the route of excretion of absorbed Mo is illustrated by the following results obtained by **** (28). Sheep fed a diet of oaten chaff (<0.1% sulfate) plus 10 mg Mo/day excreted 63% of this molybdenum in the total excreta during a period of 4 weeks, of which 3-4.6% appeared in the urine. When fed a diet of lucerne chaff (0.3% sulfate) plus 10 mg Mo/day the recovery in the total excreta was 96%, of which 50-54% appeared in the urine. Fractionation of the lucerne revealed that inorganic sulfate was the factor responsible for the marked effect on molybdenum excretion. The administration of a single oral dose of potassium sulfate to the sheep on the cereal hay (low-sulfate) diet induced a rapid rise in urinary Mo excretion (Fig. 4). Sodium sulfate produced the same effect without the diuresis that accompanies the use of potassium sulfate, whereas potassium chloride induced diuresis had no effect on Mo excretion. Similar results were later obtained by Scaife (98), who fed sheep a low- and a high-sulfate diet plus 50 mg Mo in each case. On the low-sulfate diet only 5% of the Mo appeared in the urine compared with 30-40% on the high-sulfate diet."

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"Inorganic sulfate increases urinary Mo excretion in the marsupial Setonix brachyurus without significantly increasing urine volume (9) and alleviates Mo toxicity in all species studied. Whether the effect of sulfate on toxicity is mediated entirely through an influence on the pattern of Mo excretion is doubtful. In rats (85) and cattle (22), as in sheep, sulfate reduces Mo retention in the tissues, presumably through increased urinary excretion. No such reduction in tissue Mo retention by sulfate occurs in the chick, despite a marked beneficial effect on the manifestations of Mo toxicity (25)."

"In the sheep sulfate limits Mo retention both by reducing intestinal absorption and by increasing urinary excretion, the extent of each depending on the previous history of the animal with respect to Mo and sulfate intakes (29, 98). The increased urinary excretion is not a passive result of the greater urinary volume that occurs on high-sulfate diets (28). Several diuretics increase urine volume without increasing Mo excretion (20). The sulfate effect is highly specific and in sheep is not shared by such anions as tungstate, selenate, silicate, permanganate, phosphate, malonate, and citrate (29, 98). The capacity of sulfate to alleviate Mo toxicity in the rat is also not shared by citrate, tartrate, acetate, bromide, chloride, or nitrate (115). However, sulfate of endogenous origin can be just as effective as dietary inorganic sulfate. This is indicated by the effects of high protein diets, by the catabolic breakdown of body tissue, and by the administration of thiosulfate and methionine to sheep (29, 98). The protective action of methionine, cystine, and thiosulfate administration to rats fed high-Mo diets (48, 116) may also result from the production of endogenous sulfate."

"The influence of sulfate on Mo absorption and excretion is explained by **** (29) on the hypothesis that inorganic sulfate interferes with, and if its concentration is high enough, prevents the transport of Mo across membranes. Such an effect would increase Mo excretion through the rise in the sulfate concentration in the ultrafiltrate of the kidney glomerulus which follows high-sulfate intakes, impeding or blocking Mo reabsorption through the kidney tubule. The mechanism of this postulated interference with membrane transport is still unknown."

"In the early experiments with rats fed low-Mo diets intestinal xanthine oxidase levels were reduced below normal, but neither the growth nor the purine metabolism of the depleted animals was affected (93, 94). Similar low-Mo diets were equally well tolerated by chicks but when tungstate, a Mo antagonist, was added to give W:Mo ratios of 1000:1 and 2000:1, the birds exhibited reduced growth and tissue molybdenum and xanthine oxidase levels, and their capacity to oxidize xanthine to uric acid was lowered (60). All these effects were prevented by additional dietary molybdenum. These findings were confirmed by Leach and Norris (77) both with chicks fed a purified casein diet containing 0.5-0.8 ppm Mo plus added tungsten and with highly depleted chicks from hens fed a special low-mineral diet. Subsequently Richert and co-workers (95) showed that Mo depletion influences uric acid formation in the rat. The uric acid and allantoin normally excreted by this species were not formed in the absence of xanthine oxidase in the liver."

"The Mo content of foods varies greatly within and among the different classes of foodstuffs comprising human dietaries, particularly in relation to the soil type from which they are derived. In fact, Warren and co-workers (119), in a study of the trace mineral content of vegetables from different locations in British Columbia, reported that some vegetables had 500 times more molybdenum than others."

"Schroeder and co-workers (99) suggest that the probable Mo intake from standard good diets might average 350 ug/day for adults. This estimate appears high when compared with the 128 ± 34 ug Mo/day reported for adult diets in England (55) and the 48-96 ug Mo/day obtained for four young adult women in New Zealand (96). The Mo intakes of individuals in some areas of Armenia (Soviet Union) have been reported to be as high as 10-15 mg/day compared with 1-2 mg/day in nearby areas, where the population had a low incidence of gout (73). At Mo intakes up to 1.5 mg/day, which can occur in some areas in individuals with sorghum grain as a staple dietary item, uric acid metabolism is not affected but Cu excretion is greatly increased (27)[.]"

"Miltmore and Mason (88) claim that the critical Cu:Mo ratio in animal feeds is 2.0 and that feeds or pastures with lower ratios would be expected to result in conditioned Cu deficiency. In a study of fodders and grains grown in British Columbia these workers found an extremely wide Cu:Mo ratio, ranging from 0.1 to 52.7 in individual samples. The results of a study of English pastures also indicate the importance of the Cu:Mo ratio to the incidence of hypocuprosis in sheep, but they point to a higher critical ratio than 2.0, perhaps closer to 4.0 (3)."

"Recent evidence obtained by Suttle (105) indicates that Mo can interfere with Cu metabolism at dietary levels below the 5 ppm or more that occur in teart and peat [?] scours pastures, or the high-Mo levels that have usually been employed in experiments with laboratory species. Groups of hypocupremic ewes were repleted with a semipurified diet containing 8 mg Cu/kg and one of four dietary levels of Mo: 0.5, 2.5, 4.5, and 8.5 mg/kg. Using rate of recovery in plasma Cu as a measure of the efficiency of Cu utilization, the successive increments in dietary Mo were found to decrease that efficiency by 40, 80, and 40%, respectively (see Table 17)."

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"Balance studies in man provide further evidence that relatively low levels of dietary Mo can affect Cu metabolism. Deosthale and Gopalan (27) observed significant increases in urinary Cu excretion from 24 ug/day at a Mo intake of 160 ug/day to 42 and 77 ug/day at Mo intakes of 540 and 1540 ug/day, respectively. There was no effect on fecal Cu excretion but the high serum Cu levels suggest that the Mo induced increased tissue Cu mobilization. In this study the higher dietary Mo levels were obtained from the Mo present naturally in high-Mo samples of sorghum grain. This raises the possibility of a Mo-induced Cu deficiency arising in populations where such grains comprise the staple diet."

"It is important to appreciate that Mo and sulfate can either increase or decrease the Cu status of an animal, depending on their intakes relative to that of copper. Thus, as shown in Chapter 3, chronic Cu poisoning can occur in sheep with moderate Cu intakes and very low levels of Mo and sulfate. Conversely, depletion of the animal's copper reserves, to the extent of clinical signs of Cu deficiency, can arise on normal Cu and high Mo and sulfate intakes (125). Furthermore, sulfate can either aggravate or ameliorate the toxic effects of Mo, depending on the Cu status of the animal. Gray and Daniel (49) showed that when the Cu stores of rats were low and a Cu-deficient diet was fed, small amounts of Mo produced toxic symptoms that were intensified by the simultaneous addition of sulfate. By contrast, when the Cu stores and dietary Cu were adequate, larger amounts of Mo were required to produce molybdenosis, and sulfate completely prevented the harmful effects of Mo. Furthermore, several studies with pigs have failed to show significant reductions in tissue Cu levels from high dietary intakes of Mo and sulfate (24, 72), even at levels of 1500 ppm Mo, which substantially depressed growth and reduced plasma clearance of injected 64Cu (103)."

"The Cu-Mo-S interaction can be modified by other dietary factors. **** (29) showed that Mn intakes can block or antagonize the limiting effect of Mo on Cu retention in the sheep, even in the presence of adequate sulfate, and that when sheep are on a high-protein diet, Mo and Mn together exert a severely limiting effect on Cu retention."

"Mills (87) contends that molybdate and sulfate restrict Cu utilization in sheep by depressing Cu solubility in the digestive tract through the precipitation of insoluble cupric sulfide. Higher sulfide levels were observed in the rumen of sheep fed Mo plus sulfate than in those fed sulfate alone, and the level of soluble copper in this site was inversely related to the sulfide level. Spais et al. (102) have also suggested that the sulfide formed in the rumen from high sulfate intakes acts by binding feed copper to insoluble copper sulfide. Gawthorne and Nader (45) have shown that sulfide concentrations can increase in the rumen when molybdate is infused, despite Mo inhibition of sulfide production, because of a second action of molybdate inhibiting the rate of apparent absorption of sulfide from the rumen. It is further apparent from the recent work of Huisingh et al. (66) that the effect of Mo on sulfide production by ruminal microorganisms in sheep depends on the source of the sulfur. Dietary Mo significantly inhibited the production of sulfide from sulfate but noticeably enhanced the production of sulfide from methionine."

"A metabolic interference of Cu by Mo is not confined to the gastrointestinal tract. Accumulation of sulfide in the tissues as a consequence of the depressed sulfide oxidase activity is known to occur in the molybdenotic rat (114, 123). This represents a possible further factor in the effect of Mo on Cu utilization. Such tissue sulfide accumulation could lead to a precipitation of insoluble unavailable cupric sulfide (53, 101, 102). Sulfide oxidase activity appears to be dependent on the in vivo supply of copper (101), so that high dietary Cu levels will help to maintain sulfide oxidase activity while the inhibiting effect of Mo on this enzyme is taking place. In this way an endogenous supply of sulfate will emerge which in turn will prevent Mo accumulation in the tissues. The protective action of copper against Mo toxicity could be explained to some degree by such a mechanism, the effectiveness of which will clearly depend on the intake of Cu relative to that of Mo."​
 

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- Molybdenum Intake Influences Molybdenum Kinetics in Men

"The objectives of this study were to determine physiologic adaptations that occur when humans are exposed to a wide range of molybdenum intake levels and to identify the pathways that are influenced by dietary intake. Four males consumed each of 5 daily molybdenum intakes of 22, 72, 121, 467, and 1490 ug/d (0.23, 0.75, 1.3, 4.9, and 15.5 mmol/d) for 24 d each. During each treatment period, oral and intravenous doses of 100Mo and 97Mo were administered. Serial plasma, urine, and fecal samples were analyzed for labeled and unlabeled molybdenum. Compartmental modeling was used to determine rates of distribution and elimination at each dietary intake level."

"Three pathways were sensitive to daily molybdenum intake: absorption efficiency, tissue uptake, and urinary output. The same pathways were sensitive to intake in the previous kinetic study when subjects consumed a low molybdenum diet of 22 ug/d for 102 d followed by molybdenum repletion with 467 ug/d (11). The subjects in this study were healthy young men and the responses may be different in other age groups or in women."

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"Urinary output appears to be the key pathway for regulating the body's exposure to molybdenum. Transitioning from 22 ug/d to 72 ug/d resulted in a tripling of the fraction of plasma molybdenum excreted into urine. Further transitioning from 121 ug/d to 467 ug/d resulted in an additional doubling of fractional transfer of plasma molybdenum into urine. Fractional transfer of molybdenum from plasma into urine did not increase further at highest level, which may suggest that the capacity for urinary excretion was exceeded. The high intake combined with the lack of increase in fractional excretion led to a substantial retention in molybdenum at the highest intake level."

"Fractional uptake of molybdenum from plasma into tissues was constant for intakes below 467 ug/d but decreased by ~72% when daily molybdenum intake increased to 1490 ug. The decrease at the highest level could suggest the capacity of the tissues to store molybdenum was exceeded."

"Absorption of molybdenum from the intestine increased at higher molybdenum intakes, which led to a decreased fractional transfer of molybdenum from the GIT into feces. Absorption efficiency was 90% for the lower intake levels and 94% for the higher intake levels. Increased absorption with increased intake may be due to saturation of binding of molybdenum to other food components as luminal Mo content increases."

"Comparison of parameter values for the first phase of this study and the depletion phase of the previous study (11) provides insight into the effect of adaptation on molybdenum kinetics. In the depletion study, tissue deposition of molybdenum occurred more rapidly than in this study. In addition, transfer of molybdenum into the GIT via bile occurred more slowly in the previous study. Differences may be explained by the different lengths of treatment periods between the 2 studies (24 d for this study vs. 102 d for the previous study). It is likely that the subjects undergoing the shorter treatment period did not fully adapt to the intake level. The adaptation would result in conservation of tissue molybdenum during low intake."

"The bioavailability of food-bound molybdenum was found to be lower than that for purified molybdenum. On average, the bioavailability of the food-bound molybdenum was 83%, as determined from fitting data for molybdenum in the supplement form vs. the food-bound form." "Our previous kinetic analysis (11) found the bioavailability of food-bound molybdenum to be 76%, in good accord with these findings. Another study also showed that the food matrix can alter molybdenum bioavailability (20). In that study, foods were intrinsically labeled with molybdenum, and although the kale matrix did not inhibit the absorption of molybdenum, the soy matrix reduced molybdenum bioavailability by 37% compared with the purified dose."


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