You can prevent and reverse gestational diabetes, and lower your child’s risk of autism
• Xanthurenic acid (XA)—a tryptophan metabolite—is high in serum in gestational diabetes
• Xanthurenic acid binds insulin, impeding it’s action
• Vitamin B6 lowers xanthurenic acid levels to normal
• In two 1970s research studies, 86% and 100% of women with gestational diabetes normalized their blood sugar in two weeks by taking vitamin B6
• Gestational diabetes increases autism risk for the unborn child; vitamin B6 eliminates that extra risk
No, not kidding! If you’re a pregnant woman who never had any sort of diabetes before you became pregnant, and developed high blood sugar only after becoming pregnant (gestational diabetes), you can safely eliminate it all by yourself within two to three weeks. You might have the remedy at home already! If not, a trip to your favorite natural food store, compounding pharmacy, or maybe even an online order from the Tahoma Clinic Dispensary or other online source will equip you to eliminate gestational diabetes almost every time.
Of course, if you’re a man, you’ll never have this problem. However, your wife, sister, or daughter might, so keep this information in mind in case it’s ever needed.
One of many reasons gestational diabetes should be eliminated as rapidly as possible was discovered recently, and published in the Journal of the American Medical Association just last year. What is this reason? Autism!
Here’s what the researchers wrote: “Exposure to maternal gestational diabetes mellitus diagnosed by 26 weeks’ gestation was associated with increased risk of autism spectrum disorder in offspring.”[i] Yes, that’s extra risk for the child of developing autism!
But even though blood and urine sugar is higher than normal in those with gestational diabetes, gestational diabetes is not type 2 or even type 1 diabetes mellitus! To make this point clear to everyone, gestational diabetes should be renamed “diabetes mellitus xanthurenica” to clearly identify its cause: excess serum xanthurenic acid. When this renaming occurs, even conventional medicine might quit treating gestational diabetes with a “diabetic diet” and insulin and might instead actually treat the cause!
Here’s what WebMD says is the cause of gestational diabetes:
During pregnancy, the placenta…releases hormones that help your baby grow. Some of these make it harder for your body to make or use insulin. This is called insulin resistance….To keep your blood sugar levels steady, your pancreas has to make…as much as three times more [insulin] than usual. If it can’t make enough extra insulin, your blood sugar will rise and you’ll get gestational diabetes.[ii]
And here’s what the American Diabetes Association tells women:
Treatment for gestational diabetes always includes special meal plans and scheduled physical activity. It may also include daily blood glucose testing and insulin injections.[iii]
Let’s send a note to WebMD and the ADA: “Read the medical research!” What actually causes gestational diabetes was well researched between the 1940s and 1975, when a report[iv]summarized the earlier research and then explained that gestational diabetes is caused by excessive amounts of xanthurenic acid, usually present in blood in very low levels. All this xanthurenic acid combines with insulin molecules and blocks its activity. The “xanthurenic acid-insulin complex” can’t activate insulin receptors nearly as well as insulin alone does, and blood sugar rises.
Back to the causes of diabetes mellitus type 2 and type 1. In type 2, the cause is overproduction of insulin in response to carbohydrates (and dairy, but an explanation for that at another time). As the March issue of Green Medicine explains, overproduced, chronically high insulin causes insulin resistance, which in turn leads to even more insulin secretion to overcome that resistance, which leads to even more insulin secretion.
This back-and-forth upward-trending interplay (more insulin, more resistance, even more insulin, even more resistance, and so on) goes on and on (unless “carbs”—and dairy—are significantly restricted) until the insulin resistance is so strong it can’t be completely overcome, no matter how much insulin there may be. Blood sugar then goes too high—and it’s diagnosed as type 2 diabetes. This known cause of type 2 diabetes is very different than the cause of diabetes mellitus xanthurenica!
The cause of type 1 diabetes is much simpler. For a variety of reasons, the insulin-producing cells (“islet cells”) become weak and die. When that happens, insulin levels go lower and lower, until there’s very little insulin, or even none—and that’s type 1 diabetes. Again, a very different cause from diabetes mellitus xanthurenica.
But doesn’t everyone’s body chemistry make xanthurenic acid? (It’s a metabolite of tryptophan.) Indeed, 100% of us have this body chemistry. So why don’t we all have gestational diabetes even if we’re not pregnant or even women? The reason is that levels of xanthurenic acid are relatively low in most of us (unless we’re deficient in a certain B vitamin to be named later), so not very much of the “xanthurenic acid-insulin complex” is formed.
What’s different during pregnancy? Among other things, it’s a combination of “genetic” causes together with those really-high-estrogen levels that women’s bodies make when pregnant—way, way more than when not pregnant. But why does all that extra estrogen cause only a minority of women’s bodies to make lots more xanthurenic acid and develop gestational diabetes, when most women’s bodies don’t do that?
That’s the “genetic” part: women who develop gestational diabetes have “weakness” in the enzymes that metabolize tryptophan into serotonin and melatonin, but no weakness in the enzymes that metabolize tryptophan into xanthurenic acid. Without the pregnancy levels of estrogen “putting pressure” on these weak enzymes, they can perform as they do in most women—metabolizing much less of their tryptophan into xanthurenic acid, and much more of it into many other molecules we’ve all heard about, including serotonin and melatonin.
With the high levels of estrogen during pregnancy, the weak enzymes falter and metabolize much more tryptophan than usual into xanthurenic acid and much less into melatonin, serotonin, and related molecules. If there’s much more xanthurenic acid, there’s much more “insulin-xanthurenic acid complex” formed, and greater impairment of insulin activity. With enough insulin impaired, diabetes—“gestational”—is the result.
But a woman can’t stop being pregnant (for many months, anyway), and she definitely can’t change her genetics, so she can’t really rid herself of gestational diabetes, returning to normal blood sugar levels (while reducing her baby’s risk of autism, too) within two to three weeks. Or can she?
Yes, she can! To understand how, here is a refresher on what many of us learned—or should have learned—in high school and college chemistry about how enzymes change one molecule into another.
The key is that enzymes never work alone. They’re always aided by co-factors that are almost always “essential” (necessary to life) vitamins and minerals! Without those co-factors, the enzymes can’t function, and ultimately we die. That’s why they’re defined as “essential” nutrients!
“Weak” enzyme function can frequently be strengthened by adding in more co-factors! A key co-factor for the enzymes that metabolize tryptophan into serotonin and melatonin is vitamin B6. Here are the results that women with gestational diabetes achieved by taking extra vitamin B6 to strengthen their genetically “weak” enzymes.
In 1975, fourteen pregnant women were diagnosed with gestational diabetes by the standard glucose tolerance test. All the women took 100 milligrams of vitamin B6 (as pyridoxine) daily for two weeks. Repeat testing found that twelve of the fourteen (86%) no longer had the problem![v]
In 1977, different researchers reported almost identical results in the same length of time for thirteen women.[vi] All took 100 milligrams daily of vitamin B6 (as pyridoxine). Glucose tolerance tests were done before and after. All fourteen women (100%) had “statistically significant” improvements in their glucose tolerance tests. The researchers wrote: “Low vitamin B6 levels appear to alter metabolic pathways which result in a lowering of the biologic activity of endogenous insulin.” In English: vitamin B6 strengthened specific weak enzymes so that less xanthurenic acid was available to be “complexed” with insulin, blocking its activity. Better blood sugar control was regained.
The 1975 and 1977 research was actually done more than two decades after several groups of researchers[vii],[viii],[ix],[x] had confirmed in the early 1950s that vitamin B6 returned levels of xanthurenic acid to normal. For the technically inclined, all the 1950s research and much more was reviewed in a 1960 publication titled, “The Effect of Vitamin Supplementation on the Urinary Excretion of Tryptophan Metabolites by Pregnant Women”[xi]—which confirmed that pyridoxine lowered xanthurenic acid!
And one last fact: textbooks of laboratory medicine in the 1940s told us that higher-than-usual xanthurenic acid in urine is diagnostic for vitamin B6 deficiency! It’s 2016, yet despite all this forty- to seventy-year-old basic science and clinical research demonstrating the cause and cure of gestational diabetes, it’s still not being applied!
But you—yes, you, if you want to prevent gestational diabetes or cure yourself of it—can apply this extensive science. You can safely prevent or cure gestational diabetes yourself, and at the same time reduce your child’s risk of autism!
To eliminate gestational diabetes, use pyridoxal phosphate, not pyridoxine
Don’t use the “pyridoxine” form of vitamin B6. That’s actually the “inactive” form of vitamin B6,which actually does not activate the receptors for this vitamin. Most—but not all—humans can “activate” pyridoxine, but we have no way (without testing) to know if you are in the pyridoxine-activating group or not. (It’s quite possible that the 14% whose gestational diabetes didn’t disappear in the 1975 research summarized above were “poor activators” of pyridoxine.)
To make sure the pyridoxine actually does its job, it’s best to use the “active” form, pyridoxal-5-phosphate (usually shortened to P5P), fortunately available nearly everywhere supplements are sold, usually in a 50 milligram size. Don’t stop using your “pregnancy multivitamin/ mineral supplement” as it contains the rest of the B-complex vitamins which “back up” the pyridoxal-5-phosphate.
Check with your “natural medicine” doctor…
1. If you have any doubts at all about doing this!
2. Towards the anticipated delivery date. Vitamin B6 in both forms can inhibit the production of prolactin,[xii] the hormone necessary for normal lactation and nursing. Work with a physician skilled and knowledgeable in natural and nutritional medicine to help you determine (possibly while checking your own blood sugar) a P5P “tapering schedule” so you can nurse your child normally. This physician will also be able to tell you about botanicals used for centuries by to improve lactation should they be needed.
A special thank you to author Adelle Davis, whose description of the research findings in reference #4 has helped me to help women reverse gestational diabetes for more than thirty years!
Published in: Aug 5, 2016 | www.GreenMedicineNewsletter.com
References
[i] Xiang A, et al. “Association of Maternal Diabetes with Autism in Offspring.” JAMA 2015;313(14):1425-1434.
[ii] http://www.webmd.com/diabetes/gestational-diabetes-guide/what-causes-gestational diabetes
[iii] http://www.diabetes.org/diabetes-basics/gestational/how-to-treat-gestational.html
[iv] Kotake Y, Ueda T, et al. “The Physiological Significance of the Xanthurenic Acid-InsulinComplex.” J Biochem 1975;77:685-687.
[v] Bennink HJ, Schreurs WH. “Improvement of oral glucose tolerance in gestational diabetes by pyridoxine.” Br Med J. 1975 Jul 5;3(5974):13-5.
[vi] Spellacy WN, Buhi WC, and Birk SA. “Vitamin B6 treatment of gestational diabetes mellitus: Studies of blood glucose and plasma insulin.” Am J Ob Gyn 1977;127(6):599-602.
[vii] Sprince H, Lowy, RS, et al. Studies on the urinary excretion of ‘”xanthurenic acid’” during normal and abnormal pregnancy: A survey of the excretion of ‘”xanthurenic acid” ’ in normal nonpregnant, normal pregnant, pre-eclamptic, and eclamptic women.” Am J Obstet Gyn. 1951;62:84.
[viii] Vandelli, I. “The use of vitamin B. (pyridoxine) for suppressing the elimination of xanthurenic acid in pregnant and non-pregnant women following the oral intake of a measured quantity of tryptophan.” Acta vitamin. (Milano) 1951;5:55.
[ix] Wachstein M, Gudaitis A. “Disturbance of vitamin B6 metabolism in pregnancy. II. The influence of various amounts of pyridoxine hydrochloride upon the abnormal tryptophane load test in pregnant women.” J Lab Clin Med 1953;42:98.
[x] Wachstein M., Lobel S. “Abnormal tryptophan metabolites in human pregnancy and their relation to deranged vitamin B, metabolism.” Proc Soc Exp Biol (N.Y.) 1954;86:624.
[xi] Brown RR, Thornton MJ, Price JM. “The Effect of Vitamin Supplementation on the Urinary Excretion of Tryptophan Metabolites by Pregnant Women.” J Clin Invest 1961.
[xii] Ren S-G, Melmed S. Pyridoxal Phosphate Inhibits Pituitary Cell Proliferation And Hormone Secretion. Endocrinology 2006;147(8):3936-3942
