My 16-year old was recently (and suddenly) diagnosed with type-1 diabetes after a spate of debilitating migraines (we looked back at labs from almost a year ago from emergency room visits and her urine levels of glucose and ketones were very high, and no-one alerted us). Now that her glucose is stable and “lower” (averaging 105-ish) all the migraines and other symptoms have disappeared. She’s also in excellent health aside from this (good eater, good endurance, strong, high cognition back now that blood sugar is down, etc). That’s the good news. Now it’s the rest of her life, and I’d like to help her prevent the rapid functional declines seen by people who mismanage their serum glucose levels and insulin levels.
I’ve done my best to explain what I know of the mechanisms that diabetes shortens your life — either much too low (sudden hypoglycemic) and you pass out, or chronically too high and the proteins in your body — blood vessels especially — get glycated and lose function. So she (being much smarter than I am, and far smarter than I was at her age) has agreed to use a low-carb diet to try to stabilize/even out her glucose levels (watched using a CGM) and it is working very well. And it’s clear that on her rare “cheat days”, the mismatching rates between glucose absorption and insulin action wreak havoc and high volatility with serum blood glucose levels. It’s a clear management win.
I’ve been also thinking about longer term for her: maybe she should think about taking a supplement to help reduce any potential damage from Advance Glycolization End-products? — either already damaged in the year she went undiagnosed, or for potential mismatches in the future (or just to be in optimal health for whatever else comes). I’ve been thinking carnosine could be useful in helping her “clean out” AGEs from her proteins. But this may also impact insulin production (of which she has none to speak of) and other pathways unknown.
Anything else we should be considering? At 16 Rapamycin seems a bit early. Carnosine seems to me like a good idea in the nearer term. Metformin might inhibit glucose uptake but not in a good way. Acarbose might do the same (not in a good way). There seems to be significant research on managing type-2 but a real lack on type-1. There’s a number of others but I’d love your thoughts.
No rush on this but thoughts are much appreciated. Thanks.
Here’s another candidate for the anti-diabetes damage stack:
Pyridoxamine is one of three natural forms of vitamin B6, now in vegetarian capsules, available to buy in Supersmart’s catalogue. Several studies have shown that it is effective at inhibiting the formation of Advanced Glycation End-products (AGEs) and that it helps delay or prevent the development of certain complications of diabetes.
What do studies indicate about Pyridoxamine?
In vitro and animal studies suggest that pyridoxamine:
- Inhibits the formation of AGEs and ALEs (Advanced Lipoxidation End-products) by preventing oxidative damage from Amidori products and thus combats the development of diabetes complications and hyperlipidaemia.
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Reduces oxidative stress by inhibiting reactive oxygen species.
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Restricts increases in chemical modifications to tissue protein as well as in the diseases associated with these modifications, such as diabetes and atherosclerosis.
- Inhibits the formation of AGEs/ALEs and hyperlipidaemia, as shown in non-diabetic models, and protects against renal and vascular diseases; a phase II study of 84 patients showed that pyridoxamine slows down the progress of renal insufficiency.
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Protects the diabetic retina from various pathological changes and should therefore be of benefit in treating diabetic retinopathy. It inhibits AGE formation in the lens by enhancing the activity of aldose reductase and reacting with precursors of AGEs.
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Inhibits the progress of renal disease, as shown in research on diabetic animals, and reduces hyperlipidaemia and oxidant-antioxidant imbalances.
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Restores function of the beta cellsresponsible for insulin production as shown in animals with experimentally-induced diabetes.
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Neutralizes the highly-reactive and toxic carbonyl compounds formed from the breakdown of glucose and lipids.
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It seems vitamin B6 deficiency in type-1 diabetic women is an issue:
Type 1 diabetes impairs vitamin B6 metabolism at an early stage of women’s adulthood
Authors: Priscilla G. Massé, Jaclyn Boudreau, Carole C. Tranchant, Rodney Ouellette, and Karen L. EricsonAUTHORS INFO & AFFILIATIONS
Publication: Applied Physiology, Nutrition, and Metabolism
30 January 2012
https://doi.org/10.1139/h11-146
Abstract
Vitamin B6 (pyridoxine) metabolism in diabetes has never been investigated except for a few reports on plasma pyridoxal 5′-phosphate (PLP). These studies indicated that this most active (coenzyme) vitamer can be reduced. The present clinical investigation aimed to measure all vitamers in blood and urine by high performance liquid chromatography as well as important related factors, in women during active reproductive years. Thirty-two insulin-treated type 1 diabetic (T1D) patients, without renal complication, and 27 well-matched healthy controls, aged 30 to 40 years old, were recruited using rigorous criteria. Both groups had normal hemoglobin and serum albumin levels. Plasma PLP and pyridoxal (PL) did not differ significantly in the T1D group but alkaline phosphatase (ALP) activity was greater (p < 0.01). This produced a shift in plasma PLP-PL profile, as evidenced by a lower plasma PLP/PL ratio (p < 0.05). Enhanced ALP activity meant more PLP being dephosphorylated to PL (the membrane transfer form), with more ending up in erythrocytes to be rephosphorylated in its active form, as suggested by the significant positive correlation (p < 0.001) between plasma PL and erythrocyte PLP. More PL into blood circulation also means more oxidation of this vitamer to 4′-pyridoxic acid in kidneys, as confirmed by the positive correlation between plasma PL and urinary 4′-pyridoxic acid (p < 0.001). The positive correlation (p < 0.001) between ALP activity and glycosylated hemoglobin indicated a direct effect of the disease. The T1D-induced alteration in vitamin B6 metabolism, consecutive to enhanced ALP activity, may put patients at greater risk of vitamin B6 deficiency and diabetic complications.
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