Most men are critically low in this essential mineral — and here’s what it’s doing to our health…
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Why men need more vanadium
Upon reading the lists of ingredients found in antidiabetic supplements, you will note that most of them contain vanadium.
Now why is this? Vanadium is not officially recognized as being an essential mineral.
Nor is there a single human enzyme reported to contain it.
Despite this fact, reports of vanadium deficiency in animals have been surfacing for decades.
For instance, vanadium‑deficient goats have higher death rates (25% vs 5%), bone deformities, increased thyroid weights, and higher spontaneous abortion rates that vanadium‑replete controls.
Vanadium deficiency symptoms have also been induced in chickens and in rats.
“No other trace metal has so long had so many supposed biological activities without having been proved to be essential.” (Schroeder, 1963)
For this reason, the ability of vanadium to lower elevated blood glucose has been difficult to explain.
This is a consistent effect, by the way. It was first reported over a century ago (Lyonnet, 1899).
Most researchers in the diabetes field take the position that vanadium works to inhibit the enzyme protein tyrosine phosphatase‑1B (PTP1B).
PTP1B is a negative regulator of the insulin signaling pathway.
Vanadium is viewed by these researchers simply as a pharmacological agent…
They don’t think of it as essential in any way.
If this view is correct, then vanadium would be no better than berberine as an antidiabetic…
And berberine is a safer and more potent PTP1B inhibitor than vanadium.
Yet there’s evidence that this view of how things work isn’t actually correct.
It’s possible that vanadium works instead to increase thyroid hormone production.
There are several lines of evidence to support this contention, all reported in experimental studies:
These researchers noted how haloperoxidases – enzymes that require vanadium – in bacteria are similar in function to thyroid peroxidase.
So they decided to focus on this interaction specifically.
They fed six groups of Wistar-Kyoto (WKY) rats three different doses of potassium iodide, two of vanadium, and all of them standard rat chow.
For eight weeks, they administered the supplements…
And then they killed the rodents and determined their thyroid parameters.
➣ In the two groups receiving no supplemental iodide, vanadium caused a twofold increase in thyroid peroxidase activity over controls.
In addition, plasma T4 and T3 concentrations also increased (but this is an expected consequence of enhancing this enzyme).
➣ They noted a similar result when comparing the two low‑iodide groups of rats.
The rats also given vanadium demonstrated a 20.6% increase in thyroid peroxidase activity, a 9% increase in plasma T4, and a 13% increase in plasma T3.
➣ And in the two groups receiving very high amounts of iodide, vanadium apparently accelerated the Wolff-Chaikoff effect (iodine-induced hypothyroidism).
Nonetheless, thyroid weights were reduced by vanadium in all three groups, an observation that would indicate thyroid sufficiency.
The thyroid naturally swells during hypothyroidism to capture more circulating iodide, with visible goiter being the extreme example.
“The findings suggest that vanadium may have a physiological role affecting iodine metabolism and thyroid function.”
This was not the only study showing this effect.
Nor is it particular to WKY rats, which are bred to have a bunch of metabolic problems.
Increased output of thyroid hormone has been demonstrated in pigeons (1987), diabetes‑prone Worcester rats (1996), and cattle (2009).
In a vanadium study using Worcester rats (both the normal and diabetes‑prone subtypes), researchers noted a similar effect…
But these rats ended up with even greater changes in thyroid hormones.
Under a diet with no supplemental iodide, vanadium increased plasma T3 by 33% in normal rats and 28% in the diabetes‑prone rats.
They saw much less change in the rats given supplemental iodide, further confirming the Uthus study (above) in this respect.
The bimodal effects notwithstanding, vanadium always enhances thyroid output in animals consuming natural iodide intakes.
The dose response of vanadium is best demonstrated in a study published this year.
In this case, the researchers used three different levels of vanadium and no supplemental iodide:
The researchers assigned 18 Hariana heifers to three groups.
They fed each group a diet consisting of either: 0.00, 2.50, or 5.00 parts per million of vanadium.
This was a long trial (90 days).
After that, they determined the cows’ serum parameters.
Just as in the studies of rats and pigeons, these researchers noted an increase in plasma thyroid hormone.
This effect was dose‑dependent.
And that places vanadium on the small list of minerals shown to positively influence thyroid in micro-molar concentrations.
Selenium and iodide are the other two.
Plasma thyroxine (T4) progressively increased proportionally to the vanadium dose – from baseline up to 120% and 126% of controls.
The results also showed corresponding increases in triiodothyronine (T3), the active form, and large increases in IGF‑1 (insulin-like growth factor 1).
“Supplementation of vanadium in present study resulted in dose‑dependent linear increase in plasma IGF‑1 and T4 concentration.”
This latter finding could have relevance to vanadium’s antidiabetic effects, as IGF‑1 acts similar to insulin in inducing glucose uptake in cells.
It’s worth noting that thyroid hormone has also been demonstrated to increase IGF‑1 levels.
Thyroid hormone also does other things that lower blood glucose, such as increasing the expression of GLUT4 in adipocytes and muscle cells.
(GLUT4 = insulin-regulated glucose transporter)
So ultimately, all confirmed biological effects of low‑dose vanadium supplementation can be recapitulated by thyroid hormone.
Here’s another example:
Feeding vanadium at only 25 ppm to chicks has been shown to “uncouple” their mitochondria.
This would have been impossible to explain decades ago.
But today it’s known that vanadium increases plasma T3 which transcribes for uncoupling protein‑3.
It seems like uncoupling the mitochondria from ATP synthesis should spare glucose and not burn it…
But this process actually increases oxygen uptake and heat production by linking metabolism with GTP synthesis instead.
So, okay, PTP1B inhibitors work to lower glucose via insulin.
But the fact that this doesn’t “uncouple” mitochondria such as thyroid hormone argues against vanadium working through this enzyme (PTP1B).
“Thyroid status, but not insulin status, affects expression of avian uncoupling protein mRNA in chickens.”
There are many other reasons to suppose that PTP1B is not vanadium’s target in vivo (in living cells) as is commonly supposed.
Although vanadium does potently inhibit this enzyme in vitro (on lab slides), it can only do so in the form of vanadate.
Isolated PTB1B is completely unaffected by similar concentrations of vanadyl ion, the main circulating form of vanadium.
Even when using vanadate, the most potent vanadium species, impossibly high concentrations are needed to enhance glucose uptake in intact cells with plasma membranes.
“…lower concentrations of sodium orthovanadate…were completely ineffective in either directly activating glucose transport or further enhancing the effects of maximal insulin in isolated adipocytes.”
The highest human doses of vanadyl sulfate result in plasma vanadium concentrations of merely 1.44 μM after three weeks.
And most of that is bound to transferrin.
(Transferrin is the main protein in the blood that binds to iron and transports it throughout the body.)
So the even smaller amount of free vanadate probably can’t be expected to affect PTP1B.
Vanadate also inhibits Na+/K+‑ATPase at lower concentrations than PTP1B.
| A little note here: Na⁺/K⁺-ATPase is sodium-potassium adenosine triphosphatase. It’s also known as the sodium-potassium pump, an enzyme in the plasma membrane of all animal cells. It performs several functions in cell physiology. |
And, since supplementation doesn’t affect salt metabolism, you’d think vanadyl ions are the main form.
And here is something completely unexplainable under the PTP1B paradigm…
The effects of vanadium persist long after the plasma concentrations become undetectable.
This effect is well documented in rats – and also occurs in humans:
This study used six diabetic patients given 100 mg of vanadyl sulfate per day.
The subjects served as their own controls:
They got placebo for two weeks, vanadium sulfate for three weeks, and then placebo again for another two weeks.
The researchers determined plasma glucose parameters at the end of each study period.
They also performed a euglycemic clamp study.
Upon vanadyl sulfate treatment, fasting plasma glucose declined from 210 to 181 mg/dL.
Plasma insulin remained constant. But growth hormone more than tripled (0.7 vs 2.3 ng/mL).
Triiodothyronine (T3) is well known for doing this, needing only a 10-nanomolar concentration to increase growth hormone mRNA by two and a half times.
“After 3 weeks on vanadyl sulfate, fasting plasma glucose declined significantly.”
In the euglycemic clamp test, the researchers held both plasma glucose and plasma insulin constant while they infused glucose into the subjects:
They discovered that after vanadyl sulfate treatment, more glucose could be infused while maintaining constant plasma levels.
This difference between the pre‑ and post‑supplementation infusion rates shows its effect on cellular glucose uptake.
In this study it certainly had this effect.
The average glucose uptake increased significantly in subjects after three weeks of vanadyl sulfate.
Not only that, the effect persisted for two weeks after vanadyl sulfate was withdrawn:
During that time, plasma vanadium concentrations went down from 1.44 to 0.19 μM.
This effectively negates the possibility that vanadium works by inhibiting PTP1B, even after assuming all vanadyl ions are transformed into vanadate.
The study’s author came to the same conclusion.
These effects are more compatible with vanadium being an enzymatic cofactor of some kind.
Molybdenum is another mineral found in ultra‑trace concentrations in food.
In spite of its low natural occurrence, molybdenum is a necessary cofactor for three important enzymes: sulfite oxidase, xanthine oxidase, and aldehyde oxidase.
“Effects from vanadium occur in the nanomolar to millimolar range. Requirements for animal growth are low – about 50 to 500 ppb.”
Vanadium could logically be suspected to be a cofactor for at least one enzyme, perhaps two…
And evidence points towards this being involved in thyroid metabolism somehow.
After all, a vanadium‑containing iodoperoxidase isolated from Zobellia galactanivorans (a bacteria from algae) has been shown to iodinate thymol blue (Fournier, 2014).
Thymol blue (a crystalline powder used as a pH indicator) is structurally similar to thyronine, the direct precursor for thyroid hormone…
And that makes these two enzymes similar in function.
Although thyroid peroxidase-1 has never been reported to contain a vanadium cofactor, thyroid peroxidase-2 is also expressed in the thyroid and presumed inactive.
The existence of this normally inactive enzyme has remained a mystery ever since its discovery.
Non-functioning enzymes are rarely expressed.
“An alternatively spliced form of thyroid peroxidase (TPO-2) was discovered… It is missing 57 amino acids near the middle of the sequence…”
This presumed inactivity is due to a deletion in the heme‑binding domain.
Yet its activity has never been tested in the presence of vanadium.
Could vanadium be the missing cofactor for thyroid peroxidase-2?
If that is true, it would explain why the scientists in the first study (above) noted a twofold increase in thyroid peroxidase activity with vanadium…
And that despite the fact that thyroid peroxidase-1 does not use this element.
“Finally, we found a remarkable persistence of the effects of vanadyl sulfate after discontinuation of the agent for 2 weeks. These findings are consistent with studies that have documented the beneficial effects of vanadyl treatment for up to 13 weeks after withdrawal of treatment in diabetic rats.”
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