“Type 3 Diabetes”: How Addressing Brain Insulin Resistance Can Help with Alzheimer’s Disease

Alzheimer’s disease has long been viewed as a disease of memory loss and aging — but new research tells a different story. Behind the plaques and tangles, a deeper dysfunction is emerging: insulin resistance in the brain.

This has led scientists to nickname Alzheimer’s “Type 3 Diabetes” — a condition where the brain becomes resistant to insulin, disrupting its ability to use glucose for energy.

The result? Neuronal starvation, inflammation, oxidative stress, and ultimately, cognitive decline.

In this article, we’ll explore the powerful link between diabetes and Alzheimer’s, why brain insulin resistance may be a root cause, and how addressing it through lifestyle, nutrition, and functional medicine may help protect and preserve brain function.

The Diabetes-Alzheimer’s Connection: What the Research Shows

People with type 2 diabetes are up to twice as likely to develop Alzheimer’s disease.
Insulin resistance increases the risk of vascular dementia, cognitive decline, and mild cognitive impairment (MCI).
Brain scans show that Alzheimer’s patients often have impaired glucose uptake in areas of the brain responsible for memory and decision-making — even before symptoms start.

This dysfunction in brain energy metabolism is so significant that Alzheimer’s is increasingly being reclassified as a metabolic disease of the brain — or Type 3 Diabetes.

What Is Brain Insulin Resistance?

Insulin is known for its role in controlling blood sugar, but it also plays vital roles in the brain:

Regulates glucose uptake by neurons
Supports memory, learning, and synaptic plasticity
Reduces inflammation and oxidative damage
Promotes the clearance of beta-amyloid plaques

When the brain becomes resistant to insulin:

Neurons can’t get the fuel (glucose) they need
Inflammatory and oxidative pathways are activated
Beta-amyloid clearance is reduced, accelerating plaque buildup

This combination of energy starvation and toxic accumulation damages brain cells and drives neurodegeneration.

Signs of Brain Insulin Resistance

You don’t need full-blown type 2 diabetes to experience insulin resistance in the brain. In fact, many people with Alzheimer’s symptoms have:

Normal blood glucose levels
Mild insulin resistance or metabolic dysfunction
A high-carb or ultra-processed diet history
A sedentary lifestyle

Early signs of brain insulin resistance may include:

Memory lapses
Brain fog
Fatigue after meals
Sugar cravings
Mood swings
Poor focus or word-finding difficulty

These are not just signs of aging — they may be early metabolic warnings from your brain.

How Insulin Resistance Drives Alzheimer’s Disease

1. Disrupted Brain Energy Metabolism

Neurons rely on glucose for energy. Without insulin signaling, they can't use it efficiently — resulting in cellular energy deficits.

2. Beta-Amyloid Accumulation

Insulin-degrading enzyme (IDE) helps clear both insulin and beta-amyloid. High insulin levels in the brain can overwhelm IDE, allowing beta-amyloid to build up into plaques.

3. Neuroinflammation

Insulin resistance increases cytokines and oxidative stress, damaging brain tissue and impairing communication between neurons.

4. Tau Tangle Formation

Insulin signaling helps regulate tau protein. When it’s disrupted, tau becomes hyperphosphorylated, forming tangles that kill neurons.

Together, these changes create a neurotoxic environment where the brain can no longer function or repair itself effectively.

Can Addressing Brain Insulin Resistance Help with Alzheimer’s?

Emerging evidence suggests yes — improving metabolic health may slow progression, improve symptoms, or even prevent Alzheimer’s in at-risk individuals.

Interventions that improve brain insulin sensitivity:

Low-glycemic, anti-inflammatory diets (e.g., Mediterranean, ketogenic, or MIND diet)
Exercise, which improves both insulin sensitivity and brain-derived neurotrophic factor (BDNF)
Intermittent fasting, which enhances mitochondrial function and reduces inflammation
Targeted supplements (like berberine, alpha-lipoic acid, PQQ, magnesium threonate, and DHA)
Intranasal insulin therapy (being studied for its ability to bypass the blood-brain barrier)

These interventions aim to restore fuel supply to the brain, reduce neuroinflammation, and improve cognitive resilience.

Functional Medicine Approach to "Type 3 Diabetes" and Cognitive Decline

At Sheen Vein and Cosmetics, we view Alzheimer’s not as an inevitable part of aging — but as a metabolically-driven, preventable condition that can be slowed with the right tools.

Our functional medicine approach includes:

1. Advanced Metabolic Testing

Fasting insulin, HOMA-IR
Glucose tolerance testing
Inflammatory markers (CRP, IL-6, TNF-α)
ApoE genetic testing (to assess Alzheimer’s risk)

2. Gut-Brain Axis Support

Identify dysbiosis and leaky gut, which contribute to brain inflammation
Use probiotics, prebiotics, and gut-healing nutrients

3. Mitochondrial and Cognitive Support

NAD+, CoQ10, PQQ, and Lion’s Mane mushroom
Magnesium L-threonate for brain bioavailability
Red light therapy and PEMF to boost cellular energy in the brain

4. Personalized Lifestyle Plan

Nutrition, exercise, fasting, and sleep optimization
Stress management tools to reduce cortisol and inflammation

Our goal is to restore brain insulin sensitivity, protect neurons, and enhance neuroplasticity — helping you or your loved one stay mentally sharp and independent longer.

It's Never Too Early to Act

Whether you’re noticing early memory changes or simply want to prevent Alzheimer’s, now is the time to focus on brain metabolism.

Alzheimer’s may take decades to develop, but the early damage is often silent. By addressing insulin resistance now — even if only mild — you can dramatically lower your future risk.

Call to Action:
Is your brain showing signs of insulin resistance? Take control now. Contact Sheen Vein and Cosmetics to schedule a functional medicine consultation and learn how we can help protect and restore your cognitive health by addressing the metabolic root causes of Alzheimer’s disease.

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