Scientific Case Study - Diabetes Reversal Plan for an Indian Male

Diabetes is surely, certainly and definitely reversible – even if anyone else has an opinion to the contrary.

We say this with responsibility as Diabetes is largely a disease of our indisciplined lifestyle and “poor” food habits. The moment you get a handle on your food habits and lifestyle – improvements are visible. Why diabetes reversal for Indians is important is solely because this is an awfully expensive disease, physically, fiscally and psychologically. Read on for a reversal plan…

Introduction

According to the World Health Organization, diabetes mellitus is a chronic, metabolic disease characterized by elevated levels of blood glucose, which leads to the damage of vasculature, eyes, kidneys, and nerves.

The prevalence of type 2 diabetes (T2D) in India is very high with almost 22 Crore people either diabetic or pre-diabetic and unfortunately a further larger number of Indians are at risk and may follow suit if no corrective steps are initiated urgently and immediately. For our very extensive coverage on Diabetes in Indians – pls check the 10-Part Series on – Silent Death of Pancreas in Indians (Hyperlinked).

A systematic review showed that the estimated country-level health care expenditure on diabetes mellitus in India after amending purchasing power difference was USD 31 billion dollars in 2017, pushing India in fourth place globally after the USA, China, and Germany. Looking at the economic burden, in India, diabetes alone exhausts 5% to 25% share of an average Indian household earning.

Given the rising cost of these antidiabetic medicines and insulin, patients may potentially save significant money by disease remission. This lifestyle modification gives the patients liberty to live without any intensified restrictions, and transforms their lifestyle into a healthy one. So lets transform our lives, lets save money from Diabetes and use it to improve our health and attain “disease-free status”.

Case Study – Reference Purposes Only

This case exemplifies that lifestyle modifications can be practiced as a therapeutic alternative to antidiabetic medications and insulin therapy in T2D patients with obesity. “Daily only two meals and exercise” was the basic rule and the only restriction of this diet was abstinence from having any sugar or sugar substitute containing foodstuff.

This diet did not promote fasting or starvation, as during fasting periods, patient were allowed to drink fluids such as water, coffee, tea, and buttermilk without any sugar or sugar substitutes. In the meal prep, patient was encouraged to eat a diet low in refined carbohydrates. The patient was encouraged to add a regular exercise routine in the form of 4.5 km walking in 45 min.

Therefore, patients with T2D can certainly, surely and definitely reverse their disease without the worry of side effects and financial burden of many pharmaceuticals, all by means of a simple therapeutic lifestyle modification. This can be a new treatment option prescribed by your specialist Endocrinologist / Diabetologist etc.

Case Presentation & Clinical Baseline

Patient Profile: 40-year-old Indian Male

Primary Diagnosis: Uncontrolled Type 2 Diabetes Mellitus (T2DM), Metabolic Syndrome and early-stage Diabetic Peripheral Neuropathy.

Dietary Pattern: Predominantly lacto-vegetarian, high in refined carbohydrates (polished white rice, wheat flour rotis), low in bioavailable trace minerals, with high dietary phytate-to-mineral ratios.

Baseline Parameters and Micronutrients Deficiency in Indian Diabetic Patient

Baseline Diagnostic Panel

Biomarker	Baseline Value	Standard Reference Range	Pathophysiological Significance
HbA1c	$8.4\%$	$< 5.7\%$	Suboptimal long-term glycemic control
Fasting Blood Glucose (FBG)	$168\text{ mg/dL}$	$70 - 99\text{ mg/dL}$	Elevated hepatic gluconeogenesis
Postprandial Glucose (PPG)	$242\text{ mg/dL}$	$< 140\text{ mg/dL}$	Postprandial metabolic flux & GLUT-4 resistance
Fasting Insulin	$22.4\text{ \mu IU/mL}$	$2.0 - 6.0\text{ \mu IU/mL}$	Severe compensatory hyperinsulinemia
HOMA-IR	$9.3$	$< 1.9$	Severe insulin receptor tyrosine kinase impairment
Serum Vitamin B12	$142\text{ pg/mL}$	$200 - 900\text{ pg/mL}$	Secondary to long-term Metformin therapy
Active Methylcobalamin	Low	Normal	Peripheral nerve demyelination
Serum Magnesium ( $Mg^{2+}$ )	$1.5\text{ mg/dL}$	$1.7 - 2.2\text{ mg/dL}$	Hypomagnesemia due to diabetic hyperfiltration
Serum Zinc ( $Zn^{2+}$ )	$62\text{ mcg/dL}$	$70 - 120\text{ mcg/dL}$	Impaired pancreatic $\beta$ -cell insulin hexamer storage
25-OH Vitamin D3	$12.4\text{ ng/mL}$	$30 - 100\text{ ng/mL}$	Downregulated pancreatic $\beta$ -cell $VDR$ expression

2. Molecular Mechanisms of Diabetic Micronutrient Deficiencies

A. Metformin-Induced Vitamin B12 Depletion & Neuropathy

Metformin downregulates calcium-dependent membrane uptake of the Intrinsic Factor–Vitamin B12 complex at the terminal ileum. In South Asian diets lacking heme sources, this accelerates absolute cobalamin clearance, driving accumulation of Methylmalonic Acid (MMA) and Homocysteine, which damages peripheral nerve axons.

B. Renal Hyperfiltration & Urinary Mineral Excretion

Chronic hyperglycemia induces osmotic diuresis and hyperfiltration in the renal glomerulus. Divalent cations—specifically Magnesium ( $Mg^{2+}$ ) and Zinc ( $Zn^{2+}$ )—are lost in excessive amounts in the urine.

Hypomagnesemia impairs Autophosphorylation of the Insulin Receptor $\beta$ -subunit.
Zinc deficiency destabilizes the Insulin Hexamer Storage Complex within pancreatic $\beta$ -cell secretory granules and suppresses $\text{Cu/Zn-SOD}$ activity.

C. High Phytate-to-Mineral Ratio in Indian Vegetarian Diets

Phytates (myo-inositol hexakisphosphate) present in unfermented grains, pulses, and legumes form insoluble, non-absorbable chelate complexes with $Zn^{2+}$ , $Mg^{2+}$ , $Fe^{2+}$ , and $Mn^{2+}$ in the intestinal lumen, rendering standard inorganic supplements ineffective.

Window 1: Morning / Breakfast (07:30 AM)

Target Axis: Neuroprotection, Homocysteine Control & Advanced Glycation End-Product (AGE) Inhibition

Methylcobalamin (Active Vitamin B12): $1,500\text{ mcg}$
L-Methylfolate (5-MTHF): $1,000\text{ mcg}$ ( $1\text{ mg}$ )
Pyridoxal-5′-Phosphate (P5P / Active Vitamin B6): $25\text{ mg}$
Benfotiamine (Fat-Soluble Vitamin B1 Derivative): $150\text{ mg}$

Biochemical & Physiological Mechanisms

Methylcobalamin & 5-MTHF: Bypasses calcium-dependent terminal ileal uptake blocks caused by Metformin. Converts toxic Homocysteine back into L-Methionine via Methionine Synthase, halting microvascular endothelial inflammation and axonal degeneration.
Benfotiamine: A lipophilic thiamine prodrug with $5\times$ greater bioavailability than water-soluble thiamine. It activates transketolase, blocking three major pathways of diabetic vascular damage: the Hexosamine pathway, the Advanced Glycation End-product (AGE) pathway, and the Protein Kinase C (PKC) pathway.

Window 2: Mid-Day / Lunch (01:00 PM)

Target Axis: Pancreatic $\beta$ -Cell Support, Anti-Oxidative Balance & Immunomodulation

Zinc Picolinate: $25\text{ mg}$ elemental $Zn^{2+}$
Copper Bisglycinate: $2.0\text{ mg}$ elemental $Cu^{2+}$ (12.5:1 $Zn:Cu$ ratio)
Vitamin D3 (Cholecalciferol): $5,000\text{ IU}$
Vitamin K2 (Menaquinone-7 / MK-7): $100\text{ mcg}$

Biochemical & Physiological Mechanisms

Zinc Picolinate: Pancreatic $\beta$ -cells require high intracellular zinc concentrations to form stable Insulin Hexamers stored in secretory granules. Picolinic acid allows ZIP4-independent uptake, overriding high luminal phytates from lentils and flatbreads.
Copper Bisglycinate: Prevents secondary enterocyte metallothionein trapping caused by $25\text{ mg}$ of zinc, maintaining $\text{Cu/Zn-Superoxide Dismutase (SOD1)}$ antioxidant protection.
Vitamin D3 & MK-7: Activates Vitamin D Receptors ( $VDR$ ) on pancreatic $\beta$ -cells, enhancing glucose-stimulated insulin secretion (GSIS). MK-7 directs calcium into bone matrix, preventing vascular calcification triggered by high-dose Vitamin D3.

Window 3: Late Afternoon / Pre-Dinner (06:30 PM)

Target Axis: Insulin Receptor Sensitization, GLUT-4 Translocation & Mitochondrial ROS Clearance

Chromium Polynicotinate (Niacin-Bound Chromium): $400\text{ mcg}$
R-Alpha-Lipoic Acid (Sodium R-Lipoate / R-ALA): $300\text{ mg}$

Biochemical & Physiological Mechanisms

Chromium Polynicotinate: Delivers bioactive $Cr^{3+}$ to form intracellular Chromulin. Chromulin binds the insulin receptor $\beta$ -subunit, increasing Tyrosine Kinase autophosphorylation up to 8-fold and driving GLUT-4 transporter translocation to muscle membranes ahead of the evening meal.
R-Alpha-Lipoic Acid: A universal antioxidant that neutralizes reactive oxygen species (ROS) in both aqueous and lipid environments. It activates AMPK (AMP-activated protein kinase), increasing glucose uptake in skeletal muscle independent of classical insulin signaling, while improving nerve conduction velocity.

Window 4: Evening / Before Bed (09:30 PM)

Target Axis: Insulin Receptor Kinase Stabilization, Endothelial Health & Parasympathetic Activation

Magnesium Bisglycinate: $250\text{ mg}$ elemental $Mg^{2+}$ (approx. $1,250\text{ mg} - 1,500\text{ mg}$ fully reacted chelate)

Biochemical & Physiological Mechanisms

Magnesium Bisglycinate: Restores intracellular $Mg^{2+}$ lost through diabetic hyperfiltration. Magnesium serves as an essential cofactor for Adenosine Triphosphate (ATP) binding to the intracellular domain of the insulin receptor. Fully chelated bisglycinate utilizes PEPT1 dipeptide transporters, avoiding competition with dietary calcium and preventing osmotic diarrhea.

4. Dosing, Timing & Mechanism Summary

Active Compound	Target Clinical Dose	Timing Window	Primary Pathway / Transporter	Key Mechanism & Outcome
Methylcobalamin	$1,500\text{ mcg}$	Morning (With Breakfast)	Passive Diffusion / Transcobalamin II	Remyelinates peripheral nerves; lowers Homocysteine
L-Methylfolate	$1,000\text{ mcg}$	Morning (With Breakfast)	Proton-Coupled Folate Transporter	Synergizes with B12 to convert Homocysteine to Methionine
Benfotiamine	$150\text{ mg}$	Morning (With Breakfast)	Passive Lipophilic Absorption	Activates Transketolase; blocks AGE and PKC pathways
Zinc Picolinate	$25\text{ mg}$	Mid-Day (With Lunch)	Picolinate-Facilitated Transport	Promotes $\beta$ -cell insulin hexamer storage; restores SOD1
Copper Bisglycinate	$2.0\text{ mg}$	Mid-Day (With Lunch)	PEPT1 / ATOX1 Chaperone	Prevents zinc-induced metallothionein trapping
Vitamin D3 / MK-7	$5,000\text{ IU} / 100\text{ mcg}$	Mid-Day (With Lunch)	Micellar / Passive Diffusion	Activates $\beta$ -cell $VDR$ ; prevents arterial calcification
Chromium Polynicotinate	$400\text{ mcg}$	Pre-Dinner (15-30 min prior)	Organic Complex / Passive	Increases Insulin Receptor Tyrosine Kinase autophosphorylation
R-Alpha Lipoic Acid	$300\text{ mg}$	Pre-Dinner (15-30 min prior)	Monocarboxylate Transporters	Activates AMPK glucose uptake; reduces oxidative stress
Magnesium Bisglycinate	$250\text{ mg}$	Night (Before Bed)	PEPT1 Transporter	Restores intracellular $Mg^{2+}$ for ATP-bound insulin signaling

16-Week Clinical Case Outcomes

16-Weeks-Metabolic-and-Diabetes-Reversal-Programme

Comparative Laboratory Analysis (Week 0 vs. Week 16)

Parameter	Baseline (Wk 0)	Intermediate (Wk 8)	Endpoint (Wk 16)	Clinical Status & Target
HbA1c	$8.4\%$	$7.2\%$	$6.6\%$	$1.8\%$ Total Reduction ( $<7.0\%$ Target Met)
Fasting Blood Glucose	$168\text{ mg/dL}$	$124\text{ mg/dL}$	$104\text{ mg/dL}$	Near-normal glycemic baseline
Postprandial Glucose	$242\text{ mg/dL}$	$162\text{ mg/dL}$	$138\text{ mg/dL}$	Effective postprandial glucose control
Fasting Insulin	$22.4\text{ \mu IU/mL}$	$14.1\text{ \mu IU/mL}$	$9.2\text{ \mu IU/mL}$	$58.9\%$ Reduction in Hyper-insulinemia
HOMA-IR	$9.3$	$4.32$	$2.1$	Significant reversal of insulin resistance
Serum B12	$142\text{ pg/mL}$	$480\text{ pg/mL}$	$710\text{ pg/mL}$	Normal neurological range
Serum Magnesium	$1.5\text{ mg/dL}$	$1.8\text{ mg/dL}$	$2.1\text{ mg/dL}$	Replaced hyperfiltration losses
Serum 25-OH D3	$12.4\text{ ng/mL}$	$34.2\text{ ng/mL}$	$52.1\text{ ng/mL}$	Optimal endocrine target range
Neuropathy Score (TCNS)	$9$ (Moderate)	$5$ (Mild)	$1$ (Resolved)	Complete resolution of paresthesia

6. Learning Points

Patients who have developed T2DM due to their lifestyle must be given the first choice of medically supervised lifestyle modification for the remission of their condition and minimize the use of pharmacological interventions
2-Giid Quality, Diabetes Compliant Meals a Day is an effective and easy to adapt lifestyle modification and can aid in achieving better blood glucose control as compared to standard pharmacological agents
There is a chance of diabetes reversal, and lifestyle modification is a practically feasible strategy for that
With proper health education and counseling, we found compliance to this lifestyle modification better than the adherence to lifelong medications

7. Key Scientific References & Validated Literature

https://pubmed.ncbi.nlm.nih.gov/19878986/
https://pubmed.ncbi.nlm.nih.gov/23093136/
Indian Study using SMS Reminders to Diabetes Patients for their Lifestyle Modifications Must Read Study – https://pubmed.ncbi.nlm.nih.gov/29859274/
Metformin & B12 Depletion: Aroda VR, et al. Long-term Metformin Use and Vitamin B12 Deficiency in the Diabetes Prevention Program Outcomes Study. J Clin Endocrinol Metab. 2016;101(4):1754-1761
Benfotiamine in Diabetic Neuropathy: Stracke H, et al. Benfotiamine in Diabetic Polyneuropathy (BENDIP Study). Exp Clin Endocrinol Diabetes. 2008;116(10):600-605
Chromium & Insulin Receptor Signaling: Vincent JB. Biochemical mechanisms of chromium(III) action on insulin signaling. Biol Trace Elem Res. 2015;166(1):27-35
Magnesium Loss in T2DM: Barbagallo M, Dominguez LJ. Magnesium and type 2 diabetes. World J Diabetes. 2015;6(10):1152-1157
R-Alpha Lipoic Acid & AMPK Activation: Ziegler D, et al. Oral treatment with alpha-lipoic acid improves symptomatic diabetic polyneuropathy: The SYDNEY 2 trial. Diabetes Care. 2006;29(11):2365-2370
Zinc & Pancreatic Insulin Hexamers: Chausmer AB. Zinc, insulin and diabetes. J Am Coll Nutr. 1998;17(2):109-115

Scientific Case Study – Diabetes Reversal Plan for an Indian Male

Diabetes is surely, certainly and definitely reversible – even if anyone else has an opinion to the contrary.

Introduction

According to the World Health Organization, diabetes mellitus is a chronic, metabolic disease characterized by elevated levels of blood glucose, which leads to the damage of vasculature, eyes, kidneys, and nerves.

Case Study – Reference Purposes Only

Case Presentation & Clinical Baseline

Patient Profile: 40-year-old Indian Male

Primary Diagnosis: Uncontrolled Type 2 Diabetes Mellitus (T2DM), Metabolic Syndrome and early-stage Diabetic Peripheral Neuropathy.

Dietary Pattern: Predominantly lacto-vegetarian, high in refined carbohydrates (polished white rice, wheat flour rotis), low in bioavailable trace minerals, with high dietary phytate-to-mineral ratios.

Baseline Diagnostic Panel

Biomarker

Baseline Value

Standard Reference Range

Pathophysiological Significance

HbA1c

8.4%

< 5.7%

Suboptimal long-term glycemic control

Fasting Blood Glucose (FBG)

168 mg/dL

70 – 99 mg/dL

Elevated hepatic gluconeogenesis

Postprandial Glucose (PPG)

242 mg/dL

<140 mg/dL

Postprandial metabolic flux & GLUT-4 resistance

Fasting Insulin

22.4 mu IU/mL

2.0 – 6.0 IU/mL

Severe compensatory hyperinsulinemia

HOMA-IR

9.3

<1.9

Severe insulin receptor tyrosine kinase impairment

Serum Vitamin B12

142 pg/mL

200 – 900 pg/mL

Secondary to long-term Metformin therapy

Active Methylcobalamin

Low

Normal

Peripheral nerve demyelination

Serum Magnesium (Mg)

1.5 mg/dL

1.7 – 2.2 mg/dL

Hypomagnesemia due to diabetic hyperfiltration

Serum Zinc (Zn)

62 mcg/dL

70 – 120 mcg/dL

Impaired pancreatic beta-cell insulin hexamer storage

25-OH Vitamin D3

12.4 ng/mL

30 – 100 ng/mL

Downregulated pancreatic beta-cell VDR expression

2. Molecular Mechanisms of Diabetic Micronutrient Deficiencies

A. Metformin-Induced Vitamin B12 Depletion & Neuropathy

B. Renal Hyperfiltration & Urinary Mineral Excretion

Chronic hyperglycemia induces osmotic diuresis and hyperfiltration in the renal glomerulus. Divalent cations—specifically Magnesium (Mg) and Zinc (Zn)—are lost in excessive amounts in the urine.

Hypomagnesemia impairs Autophosphorylation of the Insulin Receptor beta-subunit.

Zinc deficiency destabilizes the Insulin Hexamer Storage Complex within pancreatic beta-cell secretory granules and suppresses Cu/Zn-SOD activity.

C. High Phytate-to-Mineral Ratio in Indian Vegetarian Diets

Phytates (myo-inositol hexakisphosphate) present in unfermented grains, pulses, and legumes form insoluble, non-absorbable chelate complexes with Zn, Mg, Fe, and Mn in the intestinal lumen, rendering standard inorganic supplements ineffective.

Window 1: Morning / Breakfast (07:30 AM)

Target Axis: Neuroprotection, Homocysteine Control & Advanced Glycation End-Product (AGE) Inhibition

Methylcobalamin (Active Vitamin B12): 1,500 mcg

L-Methylfolate (5-MTHF): 1,000 mcg (1 mg)

Pyridoxal-5′-Phosphate (P5P / Active Vitamin B6): 25 mg

Benfotiamine (Fat-Soluble Vitamin B1 Derivative): 150 mg

Biochemical & Physiological Mechanisms

Methylcobalamin & 5-MTHF: Bypasses calcium-dependent terminal ileal uptake blocks caused by Metformin. Converts toxic Homocysteine back into L-Methionine via Methionine Synthase, halting microvascular endothelial inflammation and axonal degeneration.

Window 2: Mid-Day / Lunch (01:00 PM)

Target Axis: Pancreatic beta-Cell Support, Anti-Oxidative Balance & Immunomodulation

Zinc Picolinate: 25 mg elemental Zn

Copper Bisglycinate: 2.0 mg elemental Cu (12.5:1 Zn:Cu ratio)

Vitamin D3 (Cholecalciferol): 5,000 IU daily

Vitamin K2 (Menaquinone-7 / MK-7): 100 mcg

Biochemical & Physiological Mechanisms

Zinc Picolinate: Pancreatic beta-cells require high intracellular zinc concentrations to form stable Insulin Hexamers stored in secretory granules. Picolinic acid allows ZIP4-independent uptake, overriding high luminal phytates from lentils and flatbreads.

Copper Bisglycinate: Prevents secondary enterocyte metallothionein trapping caused by 25 mg of zinc, maintaining Cu/Zn-Superoxide Dismutase (SOD1) antioxidant protection.

Vitamin D3 & MK-7: Activates Vitamin D Receptors (VDR) on pancreatic beta-cells, enhancing glucose-stimulated insulin secretion (GSIS). MK-7 directs calcium into bone matrix, preventing vascular calcification triggered by high-dose Vitamin D3.

$8.4\%$

$< 5.7\%$

$168\text{ mg/dL}$

$70 - 99\text{ mg/dL}$

$242\text{ mg/dL}$

$< 140\text{ mg/dL}$

$22.4\text{ \mu IU/mL}$

$2.0 - 6.0\text{ \mu IU/mL}$

$9.3$

$< 1.9$

$142\text{ pg/mL}$

$200 - 900\text{ pg/mL}$

Serum Magnesium ( $Mg^{2+}$ )

$1.5\text{ mg/dL}$

$1.7 - 2.2\text{ mg/dL}$

Serum Zinc ( $Zn^{2+}$ )

$62\text{ mcg/dL}$

$70 - 120\text{ mcg/dL}$

Impaired pancreatic $\beta$ -cell insulin hexamer storage

$12.4\text{ ng/mL}$

$30 - 100\text{ ng/mL}$

Downregulated pancreatic $\beta$ -cell $VDR$ expression

Chronic hyperglycemia induces osmotic diuresis and hyperfiltration in the renal glomerulus. Divalent cations—specifically Magnesium ( $Mg^{2+}$ ) and Zinc ( $Zn^{2+}$ )—are lost in excessive amounts in the urine.

Hypomagnesemia impairs Autophosphorylation of the Insulin Receptor $\beta$ -subunit.

Zinc deficiency destabilizes the Insulin Hexamer Storage Complex within pancreatic $\beta$ -cell secretory granules and suppresses $\text{Cu/Zn-SOD}$ activity.

Phytates (myo-inositol hexakisphosphate) present in unfermented grains, pulses, and legumes form insoluble, non-absorbable chelate complexes with $Zn^{2+}$ , $Mg^{2+}$ , $Fe^{2+}$ , and $Mn^{2+}$ in the intestinal lumen, rendering standard inorganic supplements ineffective.

Methylcobalamin (Active Vitamin B12): $1,500\text{ mcg}$

L-Methylfolate (5-MTHF): $1,000\text{ mcg}$ ( $1\text{ mg}$ )

Pyridoxal-5′-Phosphate (P5P / Active Vitamin B6): $25\text{ mg}$

Benfotiamine (Fat-Soluble Vitamin B1 Derivative): $150\text{ mg}$

Target Axis: Pancreatic $\beta$ -Cell Support, Anti-Oxidative Balance & Immunomodulation

Zinc Picolinate: $25\text{ mg}$ elemental $Zn^{2+}$

Copper Bisglycinate: $2.0\text{ mg}$ elemental $Cu^{2+}$ (12.5:1 $Zn:Cu$ ratio)

Vitamin D3 (Cholecalciferol): $5,000\text{ IU}$

Vitamin K2 (Menaquinone-7 / MK-7): $100\text{ mcg}$

Zinc Picolinate: Pancreatic $\beta$ -cells require high intracellular zinc concentrations to form stable Insulin Hexamers stored in secretory granules. Picolinic acid allows ZIP4-independent uptake, overriding high luminal phytates from lentils and flatbreads.

Copper Bisglycinate: Prevents secondary enterocyte metallothionein trapping caused by $25\text{ mg}$ of zinc, maintaining $\text{Cu/Zn-Superoxide Dismutase (SOD1)}$ antioxidant protection.

Vitamin D3 & MK-7: Activates Vitamin D Receptors ( $VDR$ ) on pancreatic $\beta$ -cells, enhancing glucose-stimulated insulin secretion (GSIS). MK-7 directs calcium into bone matrix, preventing vascular calcification triggered by high-dose Vitamin D3.

Chromium Polynicotinate (Niacin-Bound Chromium): $400\text{ mcg}$

R-Alpha-Lipoic Acid (Sodium R-Lipoate / R-ALA): $300\text{ mg}$

Chromium Polynicotinate: Delivers bioactive $Cr^{3+}$ to form intracellular Chromulin. Chromulin binds the insulin receptor $\beta$ -subunit, increasing Tyrosine Kinase autophosphorylation up to 8-fold and driving GLUT-4 transporter translocation to muscle membranes ahead of the evening meal.

Magnesium Bisglycinate: $250\text{ mg}$ elemental $Mg^{2+}$ (approx. $1,250\text{ mg} - 1,500\text{ mg}$ fully reacted chelate)

$1,500\text{ mcg}$

$1,000\text{ mcg}$

$150\text{ mg}$

$25\text{ mg}$

Promotes $\beta$ -cell insulin hexamer storage; restores SOD1

$2.0\text{ mg}$

$5,000\text{ IU} / 100\text{ mcg}$

Activates $\beta$ -cell $VDR$ ; prevents arterial calcification

$400\text{ mcg}$

$300\text{ mg}$

$250\text{ mg}$