Updated: Jun 8, 2021
Blended excerpts from Potential Within A Guide to Nutritional Empowerment
Authored by Franco Cavaleri ISBN 0-9731701-0-7
Original post: February 1, 2011
This article is composed of multiple excerpts to result in tone and content shifts and reference numbering that may be out of order.
Experts have claimed for some time that vanadyl sulfate (VS )can assist insulin in its physiological role, but only if a condition of insulin resistance or glucose intolerance previously exists. Research has revealed that insulin function isn’t raised above baseline levels and, as a result, an individual with normal insulin function isn’t affected negatively by the administration of vanadium in the orthomolecular doses I recommend. That is, hypoglycemia isn’t a common occurrence with VS administration.
Type II diabetes and insulin resistance often go undetected until they reach advanced states. Long before diagnosis, the secondary damage insulin resistance elicits will induce severe metabolic havoc. Avoiding early stages of insulin resistance and diabetes is critical to general disease prevention and anti-aging. Using VS supplementation as an occasional membrane reset, as we’ll see, is a great preventive strategy. VS has been shown to undo completely the damage in the cell membrane that results in insulin resistance and Type II diabetes. However, VS doesn’t compensate for poor insulin function by simply raising the body’s sensitivity to insulin the way metformin might. The metallo-mineral actually promotes reconstruction of the functional system that might have broken down.
A 2002 study from the Faculty of Pharmaceutical Sciences at the University of British Columbia indicates just how this pharmacology unfolds. The report demonstrates that vanadium stimulates the transcription and translocation of the glucose transporter GLUT4. Concentrations of GLUT4 on the cell membranes increases toward normal levels with supplementation of VS or Bis (maltolato) oxovanadium, an organic type of vanadium. The metallo-mineral actually fuels or activates gene activity to normalize cell sensitivity to insulin—another example of nutraceuticals reviving the genetic potential within.
Reincorporation of these transporters into the insulin-responsive cell membranes reestablishes normal insulin responsiveness. Its activity isn’t stimulatory but more like a reconstruction of the normal regulatory system. This also explains how the normalized activity stays in place after administration of the vanadium source is terminated. These studies clearly illustrate that a healthy metabolic state in the nondiabetic or insulin-normal individual isn’t affected by vanadium administration. Normal levels of GLUT4 can’t be further enhanced. In fact, research demonstrates that metabolic homeostasis or glucose control is maintained with lower plasma insulin levels after vanadium supplementation (5). That’s the ultimate goal of the anti-aging strategy!
By instilling insulin efficiency, VS can reduce the risk for the discussed secondary diseases associated with insulin resistance: cardiovascular disease, inflammatory afflictions, obesity, asthma, cognitive disorders, and more. Research commencing in 1984 at the University of British Columbia by Dr. John H. McNeill, et al, showed that oral VS could eliminate diabetes in rats, seemingly reversing the condition and “normalizing” insulin sensitivity. Multiple studies that followed this early report clearly confirmed these findings. Many human trials conducted in the mid-1990s confirmed the results found in rats, with human daily doses of vanadyl sulfate and/or sodium metavanadate ranging from 100 mg to 300 mg daily and, most important, with indications of no toxic effects (6, 7, 8, 9,10)!
The preceding references are documents generated at Harvard University, Albert Einstein College of Medicine, Temple University, and the University of British Columbia, a wide array of credible independent work. It’s as though VS resets the biological clock and, in a sense, it does. These studies also disclose that vanadium enhances glucose uptake by the heart.
Dr. Julian Whitaker wrote about the therapeutic potential of VS in his November 1994 newsletter. He advocated the use of VS in daily quantities of 150 mg, and his very statements conveyed that this was “without adverse effects other than some gastrointestinal disturbances” for some. He, too, referred to an early McNeill University of British Columbia study to support his claims for VS. I’ve worked closely with other medical and research professionals in the field of sports nutrition, anti-aging, and therapeutic and general preventive nutrition and have lectured nationwide on these topics. The positive feedback from individuals who have applied these strategies is heart-warming.
A few experts still insist, however, that VS can be toxic, but there are just as many who feel that the metallo-mineral is safe. One concern in a recent debate I was involved in pointed to studies performed on rats that ended in multiple deaths of the animals which, of course, is something to worry about. In fact, I was already using VS when the studies demonstrating it could be toxic became public. However, the results many people had experienced with VS were just too amazing to discount the supplement out of hand, so I dug deeper to find more evidence to support its safety.
Besides, those who were using VS on my recommendation, including myself, didn’t experience side effects, and I’d been taking it on and off for several years. However, in order to appreciate how safe vanadium is we must remember that, like other metals or
minerals, it exists in different forms. In addition, certain factors—such as oxidative status of the body—can contribute to toxicity of an otherwise nontoxic substance. In fact, many factors would be involved in the metabolism of this substance just as the case is with all of our common nutraceuticals. The right synergy is the key to its correct application.
Studies have shown that vanadium as vanadate can compete with phosphate transport at the specialized carrier proteins in cell membranes responsible for the movement of phosphates into the cells. One particular study revealed that when taken in high doses—in excess of 10 mg orally daily—vanadate can inhibit amino-acid transport across the intestinal mucosa (11). The result can be severe immune depression, lean-mass catabolism, and even death in extreme cases. However, subsequent studies indicate that vanadium doesn’t affect amino-acid transport (12). This contradictory evidence was quite frustrating for me. There are so many positive health benefits for vanadium administration, including the ability to reduce elevated serum-free fatty acids (13). My intense research eventually paid off.
Interestingly studies also show that in minute doses, vanadate stimulates the same phosphate-transport protein system instead of inhibiting it, in turn promoting alanine (an important amino acid) dispersal and increasing cAMP production intracellularly. As described earlier, this incremental cAMP helps prime cells much as the cell-rejuvenating herb coleus forskohlii does. The VS doses we’re talking about for therapy for insulin resistance or diabetes, though, far exceed 10 mg daily, but the important fact is that I’m not advocating supplementation of vanadate, the form the studies show to be toxic. The source of vanadium to use is the reduced form, vanadyl sulfate (VS).
Vanadium is reduced by glutathione into the VS state in the gastrointestinal lumen before absorption (14). This reduction also takes place via glutathione mediation in the plasma and other body fluids as well as within cells.
Why is all of this biochemistry relevant to vanadium’s safety? If vanadium does interfere with amino-acid absorption, it’s the vanadate form we should be concerned about. Studies demonstrate that surrounding cellular conditions predispose the cell to the potential toxicity of the metal. The factor promoting toxicity is oxidative stress—free radicals. The VS form has been shown not to compete with the phosphate-transport proteins or amino-acid dispersal, but when oxidized to its vanadate form by free radicals, it can be toxic. VS isn’t catabolic as many previous studies have concluded.
The trick to supplementing VS safely and more effectively for insulin control is to use it concurrently with glutathione boosters such as NAC and alpha lipoic acid—500 mg of the former and 300 to 400 mg daily of the latter in divided doses. This extra cellular augmentation of glutathione will support the reduced, less-invasive state of VS in the body while the enhanced glutathione and alpha lipoic acid levels will bolster the previously outlined cell membrane’s GTF complex for better insulin function. It might be a good idea to supplement VS concurrently with glutathione itself to help maintain the reduced state of the former in the gut. In our cells VS exists as a complex of protein or peptides such as the glutathione-vanadium type.
This strategy has worked wonders for me and for those who have applied it. My 225-pound, massively muscled physique during my competitive bodybuilding years was definitely not a picture of an individual facing protein or amino-acid deficiency. Besides, even if VS did present some level of toxicity, it might not be the sort insulin resistance or diabetes blasts the body with. Second, since VS only has to be employed in short bursts, if there are any toxic effects, they can be eliminated with proper strategy. To discuss my own findings and results, I spoke directly with Dr. John McNeill at his University of British Columbia office, and he enlightened me about several facts. His research on VS began back in 1984. It was his work that prompted me to begin using VS in 1988. He disclosed that the animal deaths my colleagues justifiably heeded were finally attributed to a lack of water consumption, which for diabetic subjects imposes grave danger. McNeill said that VS saturation of the drinking water seemed to cause the animals to refrain from drinking. Eventually the researchers overcame the problem and the studies progressed with success.
Not drinking water might also account for the catabolic effects on lean mass that some scientists attribute to VS administration. Dehydration could cause measures that infer lean-muscle catabolism. Dr. McNeill claims that VS affects amino-acid transport nominally, if at all, and catabolism caused by amino-acid-starved tissue isn’t likely, which confirms my findings. Until recently the method in which VS induces insulin efficiency wasn’t known. Today we understand that VS actually enters the cell to facilitate the incorporation of more glucose-transport sites at the membrane surface by modifying gene activity—kick-starting the healthy potential in all of us.
In addition to this remarkable finding, even more recently, resistin has been shown to be inhibited by VS. Resistin is a newly discovered hormone that adipocytes, or fat cells, produce. If you carry more body fat, you tend to produce a greater amount of resistin, which is somehow involved in cytokine production and insulin function. Both cytokines and insulin are involved in and significantly influence inflammatory and immune-system activity. At first the conclusions from these groundbreaking studies were that resistin interfered with insulin to induce insulin resistance, but apparently that’s only partially true. It’s now known that resistin does somehow interact with insulin, but the precise activity hasn’t been determined.
Resistin also facilitates tumor necrosis factor (TNF) production, which is implicated in inflammatory conditions such as arthritis and other common diseases (15). Carry more body fat and you carry a higher risk for disease. VS blocks resistin activity to prevent this disease-promoting factor. It also decreases the risk of hypercholesterolemia, hypertension, and atherosclerosis (16, 17). Based on the newly found resistin hormone chemistry, VS administration should also have a positive influence on chronic inflammatory conditions. However, I must stress that the anti-inflammatory activity is anecdotal and even theoretical at this point.
see Vanadyl Sulfate (VS) referencing on the Nutraceutical-Pharmaceutical Interactions database