Excessive insulin decreases vitamin D in 4 ways – problems for diabetic COVID-19

Created December 2020

Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management

BMJ Open Heart 2020;7:e001356. doi: 10.1136/openhrt-2020-001356

Isabella D Cooper 1, Catherine A P Crofts 2, James J DiNicolantonio 3, Aseem Malhotra 4, Bradley Elliott1, Yvoni Kyriakidou1 and Kenneth H Brookler 5

Vitamin D Life had wondered for 8 years why Diabetes seemed to consume Vitamin D.It appears that Insulin decreases the amount of vitamin D which gets to the bloodOverview Diabetes and vitamin D contains the following{include}Items in both categories Diabetes and Virus are listed here: {category}Items in both categories Gut and Probiotics are listed here: {category}See also Vitamin D Life* Gut-Friendly Vitamin D * many forms of vitamin D apparently are gut-friendly, even without good bacteria* How Vitamin D prevents Insulin Resistance – Sept 2020* Saudi study defines normal Vitamin D level to be 50 to 70 ng (diabetes, etc.) - June 2020* How Vitamin D both prevents and treats insulin resistance (Diabetes) – April 2019* Most Diabetics helped by Vitamin D (90 percent are deficient) – Nov 2019* Low Magnesium associated with diabetes, etc. – meta-analysis 2016* Low Level Laser Therapy greatly increased Vitamin D and Magnesium (for diabetics with nephropathy) – March 2019* Perhaps the LLLT decreased insulin, which resulted in more Mg and Vitamin D* How Vitamin D prevents Hyperglycemia – Sept 2020

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Risk factors for COVID-19 patients with poorer outcomes include pre-existing conditions: obesity, type 2 diabetes mellitus, cardiovascular disease (CVD), heart failure, hypertension, low oxygen saturation capacity, cancer, elevated: ferritin, C reactive protein (CRP) and D-dimer. A common denominator, hyperinsulinaemia, provides a plausible mechanism of action, underlying CVD, hypertension and strokes, all conditions typified with thrombi. The underlying science provides a theoretical management algorithm for the frontline practitioners.

Vitamin D activation requires magnesium.

Hyperinsulinaemia promotes:

  • magnesium depletion via increased renal excretion,

  • reduced intracellular levels,

  • lowers vitamin D status via sequestration into adipocytes and

  • hydroxylation activation inhibition.

Hyperinsulinaemia mediates thrombi development via:

  • fibrinolysis inhibition,

  • anticoagulation production dysregulation,

  • increasing reactive oxygen species,

  • decreased antioxidant capacity via nicotinamide adenine dinucleotide depletion,

  • haem oxidation and catabolism,

  • producing carbon monoxide,

  • increasing deep vein thrombosis risk and pulmonary emboli.

Increased haem-synthesis demand upregulates carbon dioxide production, decreasing oxygen saturation capacity. Hyperinsulinaemia decreases cholesterol sulfurylation to cholesterol sulfate, as low vitamin D regulation due to magnesium depletion and/or vitamin D sequestration and/or diminished activation capacity decreases sulfotransferase enzyme SULT2B1b activity, consequently decreasing plasma membrane negative charge between red blood cells, platelets and endothelial cells, thus increasing agglutination and thrombosis.

Patients with COVID-19 admitted with hyperglycaemia and/or hyperinsulinaemia should be placed on a restricted refined carbohydrate diet, with limited use of intravenous dextrose solutions. Degree/level of restriction is determined by serial testing of blood glucose, insulin and ketones. Supplemental magnesium, vitamin D and zinc should be administered . By implementing refined carbohydrate restriction, three primary risk factors, hyperinsulinaemia, hyperglycaemia and hypertension, that increase inflammation, coagulation and thrombosis risk are rapidly managed.

Tags: Diabetes Magnesium Virus