Ronald Grisanti D.C., D.A.B.C.O., D.A.C.B.N., M.S., CFMP

A recent patient was concerned that despite watching her diet and taking her diabetes medication her hemoglobin A1C (HbA1c) keeps going up.

Remember, HbA1c is a lab test that shows the average level of blood sugar (glucose) over the previous 3 months. It shows how well you are controlling your diabetes. 

An elevated HbA1c greater than 5.7% indicates that the diabetes is not well regulated and is in fact accelerating aging, increasing your chances of getting painful neuropathies, kidney failure needing dialysis, cataracts, amputations, and retinopathy blindness.

What could possibly be missed by her primary doctor?

One major cause of the unregulated glycosylated hemoglobin is an unrecognized B6 deficiency.

An excellent “functional” test to check for a pyridoxine (B-6) deficiency is the xanthurenate organic acid test. An elevated xanthurenate test is a sensitive marker for a B-6 deficiency.

This is an Organic Acid Test from Genova

This is an Organic Acid Test from Genova

But wait.. there is more to the story.

You can take B-6 and it may not work.


Because of a zinc deficiency.

When hidden zinc deficiency is present, the body cannot convert B6 to its active form, pyridoxal-5-phosphate or P5P. P5P, essential in normalizing the glycosylated hemoglobin and its deficiency, is an indicator that improperly metabolized sugars are accelerating aging, cataracts, kidney failure, heart disease, nerve damage and more.

This is the intracellular nutrient test from Doctor's Data

This is the intracellular nutrient test from Doctor’s Data

But there is more to the story.

Elevated stored phthalates (plastics) in the body interfere with zinc metabolism.

This is a Phthalate Test from Genova

This is a Phthalate Test from Genova

This is the power of functional medicine. Seeking to find the cause of the cause of the cause.

HbA1c —> B-6 deficiency —> Zinc deficiency —> Stored Phthalates

I have never yet met a diabetologist who even orders the above much less knows how to interpret it.

To ignore fixing the chemistry in an overtly metabolic disease is outright wrong.

Unfortunately, what I have seen from reading thousands of medical records is the fact that most doctors merely resort to the one size fits all approach and medicate the disease. Rarely if ever have I read where a doctor investigated why the HA1C was elevated.

This results in a tragic waste of life as well as incurring an enormous and unnecessary expense and suffering.

You may be interested to know that because of the phthalate load, many folks (even without diabetes) unnecessarily get multiple diseases. These can range from Nonalcoholic steatohepatitis or NASH (a common, often “silent” liver disease), heart disease or cancers to Parkinson’s disease, arthritis, or Alzheimer’s.

Clearly they all lead to accelerated aging because of the shared causes.

For a doctor to check your glycosylated hemoglobin A1C every 3 months yet never know your zinc and B6 levels (among many others) is plain wrong in this sophisticated era.

Your life depends on the decisions you make. This information has a huge bearing on whether your diabetes blinds you in future years.


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Jain SK, et al, Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation and (Na+ + K+)-ATPase activity reduction in high glucose-treated human erythrocytes, Free Rad Biol Med 30:232-37, 2001

Onarato JM, et al, Pyridoxamine, an inhibitor of glycation reactions, also inhibits lipid peroxidation reactions, J Biol Chem, 275:21177-84, 2000

Metz TO, et al, Pyridoxamine traps intermediates in lipid peroxidation reactions in vivo: evidence on the role of lipids and chemical modification of protein and development of diabetic complications, J Biol Chem 278:42012-19, 2003

Booth AA, et al, Thiamine pyrophosphate and pyridoxamine inhibit the formation of antigenic advanced glycation endproducts: comparison with aminoguanidine, Biochem Biophys Res Commun, 220:113-19, 1996

Stitt A, et al, The AGE inhibitor pyridoxine and inhibits development of retinopathy in experimental diabetes, Diabetes 51:2826-32, 2000

Laines-Cessac P, et al, Mechanisms of the inhibition of human erythrocyte pyridoxal kinase by drugs, Biochem Pharmacol 54:863-70, 1997