Are these nutrient deficiencies on your radar when working with your diabetic patients?

When we think about risk factors for insulin resistance, pre-diabetes, and type-2 diabetes, we typically think of factors like weight, sedentary lifestyle, dietary habits, hyperlipidemia, and family history of the disease. On the other hand, it’s very rare that we think about nutritional deficiencies as risk factors for these metabolic concerns. In this article, I’ll share nutritional deficiencies that may contribute to the development of diabetes, and I’ll also share nutritional deficiencies that your patients who have been diagnosed with diabetes are especially at risk for.


Which nutritional deficiencies may increase patients’ risk for insulin resistance and diabetes?

A cohort study evaluated 903 adults and found them to be normoglycemic via fasting plasma glucose and oral glucose tolerance testing. [1] These patients’ vitamin D levels were also checked. Follow-up continued for a total of thirty to thirty-two years. By the end of the study, 47 of the patients had become diabetic and 337 of them had been diagnosed with pre-diabetes. The study authors reported that lower vitamin D levels were associated with increased risk of being diagnosed with diabetes. The study authors further noted that further research was needed in order to determine whether or not high 25-hydroxyvitamin D levels would be preventative in the development of type-2 diabetes or whether or not high levels would protect against the transition from pre-diabetes to type-2 diabetes.


While we need more robust research conducted on humans to come to a definite conclusion, pre-clinical research may shed some light on exactly how low vitamin D levels could be associated with increased risk for type-2 diabetes. First of all, we know from pre-clinical research that 1,25-dihydroxyvitamin D stimulates the pancreatic β-cells, leading to them secreting insulin. [2] As such, low vitamin D levels are associated with decreased insulin release and, as a result, elevated blood sugar levels. Low vitamin D levels could also contribute to diabetes diagnoses because of vitamin D’s role in inflammation modulation; specifically, low vitamin D levels have been associated with an increase in inflammatory markers like C-reactive protein.


What nutritional deficiencies are diabetic patients particularly at risk for?

According to research, there are a few nutritional deficiencies that diabetic patients are especially at risk for. First of all, we’ve known for quite some time that diabetic patients are more likely to be deficient in magnesium than their non-diabetic counterparts. [3] This hypomagnesemia has been linked to both poorer blood sugar control in diabetics and insulin resistance in nondiabetic elderly patients.


Additionally, research suggests that diabetic patients may also be more likely to be deficient in zinc. [4-6] Zinc plays critical roles in insulin homeostasis. For example, zinc has insulin mimetic properties and the mineral also plays an important role in insulin receptor signal transduction, insulin storage, and insulin secretion.


Furthermore, diabetic patients who are taking metformin are at greater risk for vitamin B12 deficiency, for the simple fact that metformin can impair the absorption of vitamin B12. [7] Therefore, if patients are taking metformin but aren’t significantly increasing their dietary intake of B12 or increasing their B12 through another means (e.g. additional oral supplementation, intramuscular injections, intravenous infusions), they may be at risk for lower levels of the vitamin down the road.


[To learn how to incorporate IV nutritional therapy into your practice, click here.]


Summary

In conclusion, research suggests that several nutritional deficiencies may be associated with insulin resistance, pre-diabetes, and diabetes. Specifically, preliminary research suggests that low levels of vitamin D may be associated with greater likelihood of being diagnosed with diabetes. Additionally, once patients have been diagnosed with diabetes, they may be at greater risk for magnesium and/or zinc deficiency. If they are taking metformin, they may also be at greater risk for vitamin B12 deficiency as well. As providers, we can be proactive about our patients’ potential for increased risk of developing these nutritional deficiencies by making recommendations that will support optimal levels, making it less likely that our patients will experience the worse prognosis that oftentimes accompanies these nutritional deficiencies.



[1] Park, S. K., Garland, C. F., Gorham, E. D., BuDoff, L., & Barrett-Connor, E. (2018). Plasma 25-hydroxyvitamin D concentration and risk of type 2 diabetes and pre-diabetes: 12-year cohort study. PloS one, 13(4), e0193070. https://doi.org/10.1371/journal.pone.0193070


[2] Lips, P., Eekhoff, M., van Schoor, N., Oosterwerff, M., de Jongh, R., Krul-Poel, Y., & Simsek, S. (2017). Vitamin D and type 2 diabetes. The Journal of steroid biochemistry and molecular biology, 173, 280–285. https://doi.org/10.1016/j.jsbmb.2016.11.021


[3] Tosiello L. (1996). Hypomagnesemia and diabetes mellitus. A review of clinical implications. Archives of internal medicine, 156(11), 1143–1148.


[4] Schmidt, L. E., Arfken, C. L., & Heins, J. M. (1994). Evaluation of nutrient intake in subjects with non-insulin-dependent diabetes mellitus. Journal of the American Dietetic Association, 94(7), 773–774. https://doi.org/10.1016/0002-8223(94)91947-x


[5] Walker A. F. (2007). Potential micronutrient deficiency lacks recognition in diabetes. The British journal of general practice : the journal of the Royal College of General Practitioners, 57(534), 3–4.


[6] Myers, S. A. (2015). "Zinc Transporters and Zinc Signaling: New Insights into Their Role in Type 2 Diabetes", International Journal of Endocrinology, 2015 (167503), 1-7. https://doi.org/10.1155/2015/167503


[7] Adams, J. F., Clark, J. S., Ireland, J. T., Kesson, C. M., & Watson, W. S. (1983). Malabsorption of vitamin B12 and intrinsic factor secretion during biguanide therapy. Diabetologia, 24(1), 16–18. https://doi.org/10.1007/BF00275941