Maintaining stable blood sugar levels is essential for overall health. However, frequent sugar spikes—sudden increases in blood glucose—may have a far-reaching effect on the brain, potentially contributing to conditions like Alzheimer’s disease. Sometimes referred to as “type 3 diabetes,” Alzheimer’s has been linked to patterns of insulin resistance in the brain that mirror those observed in type 2 diabetes. In this article, we will explore what sugar spikes are, how they impact the brain, and why some experts have coined the term “type 3 diabetes” to describe Alzheimer’s disease. We’ll also discuss practical steps you can take to maintain balanced blood sugar and support cognitive function.

Introduction

Alzheimer’s disease is a progressive neurodegenerative disorder characterized by memory loss, cognitive impairment, and behavioral changes. In recent years, growing evidence has pointed to a possible link between persistent sugar spikes in the bloodstream and detrimental changes in brain chemistry (1,3). These spikes can lead to insulin resistance, inflammation, and oxidative stress—factors that may set the stage for Alzheimer’s pathology. Researchers have even used the term “type 3 diabetes” to describe Alzheimer’s, emphasizing how metabolic dysfunction in the brain mirrors systemic insulin resistance (3).

What Are Sugar Spikes?

A “sugar spike” occurs when blood glucose levels rise sharply after meals—usually meals high in refined carbohydrates or sugary foods, but even eating large portions of complex carbohydrates like brown rice will do it. While occasional mild surges in glucose are normal, repeated and severe spikes can be harmful over time. Rapid blood sugars spikes above 140 mg/dl for people without diabetes are damaging. Here’s why:

Excess Insulin Release: The pancreas produces more insulin to quickly lower elevated blood sugar. Over time, this can contribute to insulin resistance if the body’s cells stop responding effectively (1). It will also lead to eventual “exhaustion” of the pancreas and its ability to produce enough insulin.

Inflammatory Response: Frequent sugar spikes can trigger low-grade inflammation, which is thought to underlie many chronic diseases, including those affecting the brain (2,5).

Oxidative Stress: Rapid fluctuations in glucose increase free radicals, leading to oxidative stress that damages cells and tissues, including neurons (1,6).

Because the brain relies on a steady supply of glucose to function optimally, extreme fluctuations in blood sugar can set off a cascade of problems that impair brain health.

The Brain Under Siege: Mechanisms Behind “Type 3 Diabetes”

Impaired Insulin Signaling

Insulin is not just about controlling blood sugar in the body; it’s also vital for normal brain function. When insulin resistance develops in the brain, neurons struggle to take up glucose for energy (1,3). This energy deficit can lead to:

Reduced neuronal survival

Impaired synaptic plasticity (the ability of neurons to adapt and change)

Declines in memory and learning

Amyloid-β Accumulation

Another characteristic hallmark of Alzheimer’s is the build-up of amyloid-β (Aβ) plaques. Insulin-degrading enzyme (IDE) normally helps break down both insulin and amyloid-β. However, when insulin levels are chronically elevated (often due to repeated blood sugar spikes), this enzyme gets overwhelmed or becomes less effective at clearing amyloid-β (2,5). The result is an accumulation of these plaques that disrupt normal neuronal function. Recent clinical trials of anti-amyloid therapies have produced mixed results, leading to ongoing debates about the role of amyloid-β plaques in Alzheimer’s disease progression. Some FDA-approved medications targeting amyloid-β have shown limited clinical efficacy. The FDA’s approval of aducanumab in 2021 sparked significant debate due to inconsistent clinical trial results and concerns about its efficacy.  This controversy led to reduced prescriptions and eventual suspension of its sales by Biogen in 2024. However, newer drugs have demonstrated modest benefits in slowing cognitive decline. This has prompted a reevaluation of the amyloid cascade hypothesis and a shift towards viewing Alzheimer’s as a complex, multi-factorial disease requiring diverse therapeutic approaches. Cummings et al., 2021; Budd Haeberlein et al., 2022; Selkoe & Hardy, 2016

Tau Hyperphosphorylation

Tau proteins help stabilize microtubules in neurons. In Alzheimer’s disease, these proteins can become abnormally phosphorylated (hyperphosphorylated), leading to the formation of neurofibrillary tangles. Research suggests that insulin resistance exacerbates tau hyperphosphorylation, further impairing neuronal transport and contributing to cognitive decline (1,4).

Oxidative Stress and Inflammation

Repeated spikes in blood sugar can lead to chronic oxidative stress and inflammation, especially in a brain already vulnerable to metabolic disturbances (1,6). Over time, these factors damage neurons and blood vessels, accelerating the neurodegenerative process. Chronic inflammation is especially detrimental to brain cells, as it disrupts synaptic communication and promotes cellular death.

The term “type 3 diabetes” was coined to underscore the surprising similarities between Alzheimer’s disease and classic forms of diabetes:

Brain-Specific Insulin Resistance: Much like the insulin resistance seen in type 2 diabetes, but localized primarily in the brain (3).

Similar Pathological Processes: Both conditions feature impaired insulin signaling and chronic inflammation (4).

Deficiency and Resistance: The brain may exhibit both insulin deficiency and resistance, reflecting the systemic issues seen in type 1 and type 2 diabetes, but with a distinct, localized impact (2). Insulin deficiency in the brain is a crucial aspect of this “type 3 diabetes” concept. It refers to a state where the brain has insufficient insulin to function optimally, which can occur due to reduced local production or inadequate supply from the bloodstream. This deficiency can lead to impaired cognitive function, altered brain metabolism, and accelerated neurodegeneration. The insulin deficiency in Alzheimer’s disease is unique because it coexists with insulin resistance. This dual problem creates a vicious cycle where the brain’s inability to use insulin effectively may trigger increased production, potentially leading to eventual deficiency as the system becomes overwhelmed.

While this terminology Type 3 Diabetes is still debated, it has generated useful dialogue about the importance of metabolic health for cognitive longevity.

Cognitive Decline

Inefficient insulin signaling in the brain compromises glucose uptake and utilization. Neurons starved of their primary fuel source become less effective at communication, leading to cognitive decline and memory problems (1,7). Over time, these deficits become more pronounced, aligning with the onset of Alzheimer’s symptoms.Accelerated Neurodegeneration

The combination of amyloid-β plaques, hyperphosphorylated tau proteins, and chronic inflammation sets the stage for widespread neuronal loss (1,4). This degenerative process can advance slowly and subtly until noticeable symptoms—like significant memory lapses—surface.

Altered Brain Metabolism

When insulin resistance is high, the brain can’t efficiently access glucose. This metabolic inefficiency exacerbates energy deficits, further impairing neuronal function (6,7). Some researchers are exploring whether alternative fuels, like ketones, could help bypass this glucose deficit, although more studies are needed.

Vascular Complications

Chronic high blood sugar can damage blood vessels and reduce blood flow to the brain, compounding the problem of inadequate glucose delivery. Over time, compromised blood flow can worsen cognitive decline by depriving neurons of oxygen and nutrients critical for survival.

While sugar spikes are a critical piece of the puzzle, other factors also contribute to the risk of Alzheimer’s:

Genetics: Certain genes (like APOE-e4) increase susceptibility to Alzheimer’s.

Lifestyle Factors: Poor diet, lack of exercise, and chronic stress exacerbate insulin resistance and inflammation.

Age: Advancing age remains the strongest risk factor for Alzheimer’s.

Nonetheless, the growing body of research linking insulin resistance to cognitive decline underscores the importance of maintaining good metabolic health for optimal brain function (9).

Balanced Meals: Combine proteins, healthy fats, and complex carbohydrates in every meal to slow glucose absorption.

Portion Control: Overeating can trigger larger sugar spikes; aim for moderate, well-timed meals.

Fiber Intake: High-fiber foods (vegetables, whole grains, legumes) help stabilize blood sugar. Fiber also happens to be the most anti-inflammatory substance we can consume. This anti-inflammatory effect is mediated through good intestinal bacteria that feed on fiber and send messages to our immune system to decrease inflammation throughout our body.

Physical Activity: Regular exercise enhances insulin sensitivity, reducing the magnitude of sugar spikes by increasing the uptake of blood sugar into the muscles. It is best to engage in moderate physical activity within 30 minutes of meals for the strongest effect on controlling blood sugar spikes.

Stress Management: Chronic stress hormones can contribute to insulin resistance. Techniques like meditation or yoga can help.

Stay Hydrated: Adequate water intake helps regulate blood sugar and metabolic processes.

Monitor Blood Glucose: If you have prediabetes or diabetes, regularly checking your levels can alert you to significant spikes. Continuous glucose monitors are one of the best ways to track blood glucose levels throughout the day and some are now available even without prescription.

Medications

Some diabetes drugs that enhance insulin sensitivity—like metformin—are being evaluated for their potential to slow Alzheimer’s progression. Early studies suggest these medications might help the brain better manage glucose and reduce the oxidative stress associated with sugar spikes. While more large-scale clinical trials are needed, this line of research offers hope that improving metabolic balance could delay or mitigate cognitive decline.

Brain Imaging

Advanced imaging techniques, such as functional MRI and PET scans, may soon help detect subtle signs of insulin resistance in the brain before severe symptoms emerge. By spotting these early indications of metabolic dysfunction, doctors could implement interventions—like dietary changes or insulin-sensitizing treatments—earlier, potentially preventing or slowing the onset of Alzheimer’s.

 Nutritional Interventions

Specific eating patterns, including the Mediterranean and low-glycemic diets, are under investigation for their ability to reduce sugar spikes and support healthy cognitive function. These diets emphasize whole, nutrient-dense foods that help stabilize blood glucose and curb inflammation. Researchers are also examining whether targeted nutrient supplementation—such as omega-3 fatty acids or antioxidants—could further bolster brain health in conjunction with dietary changes.

As science unravels the connection between insulin resistance and neurodegeneration, we may find increasingly precise strategies to protect the brain from the effects of chronic high blood sugar.

The relationship between sugar spikes and Alzheimer’s disease, sometimes labeled as “type 3 diabetes,” sheds light on the deep interplay between metabolic and cognitive health. While this term is not universally accepted, the growing evidence highlights how insulin resistance and fluctuating blood glucose can damage the brain, accelerating processes associated with Alzheimer’s. By taking proactive steps—maintaining balanced meals, exercising regularly, and managing stress—you can help stabilize blood sugar levels and potentially safeguard long-term brain function.

References

De la Monte, S. M., & Wands, J. R. (2008). Alzheimer’s disease is type 3 diabetes—evidence reviewed. Journal of Diabetes Science and Technology, 2(6), 1101-1113.

Ferreira, L. S., Fernandes, C. S., Vieira, M. N., & De Felice, F. G. (2018). Insulin resistance in Alzheimer’s disease. Frontiers in Neuroscience, 12, 830.

Kandimalla, R., Thirumala, V., & Reddy, P. H. (2017). Is Alzheimer’s disease a type 3 diabetes? A critical appraisal. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 1863(5), 1078-1089.

Leszek, J., Trypka, E., Tarasov, V. V., Ashraf, G. M., & Aliev, G. (2017). Type 3 diabetes mellitus: A novel implication of Alzheimer’s disease. Current Topics in Medicinal Chemistry, 17(12), 1331-1335.

Neth, B. J., & Craft, S. (2017). Insulin resistance and Alzheimer’s disease: Bioenergetic linkages. Frontiers in Aging Neuroscience, 9, 345.

Steen, E., Terry, B. M., Rivera, E. J., Cannon, J. L., Neely, T. R., Tavares, R., … & de la Monte, S. M. (2005). Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease–is this type 3 diabetes? Journal of Alzheimer’s Disease, 7(1), 63-80.

Talbot, K., Wang, H. Y., Kazi, H., Han, L. Y., Bakshi, K. P., Stucky, A., … & Arnold, S. E. (2012). Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. Journal of Clinical Investigation, 122(4), 1316-1338.