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Why Alzheimer's is Type 3 Diabetes

Is Alzheimer's "Type 3 Diabetes"? Explore the link between insulin resistance & cognitive decline. Learn about alternative theories & potential solutions.

9 min read
Jason Tran
JT
Published by Jason Tran
Sun Mar 23 2025
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Imagine a world where your memories, the very essence of who you are, begin to fade. This is the stark reality for millions affected by Alzheimer’s disease, a condition that’s rapidly becoming a leading cause of death worldwide 1.

But what if the key to understanding, and potentially even preventing, this devastating illness lies not in complex protein tangles, but in something far more familiar: insulin resistance? While we’ve long associated Alzheimer’s with plaques in the brain, a controversial theory is gaining momentum, suggesting that this cognitive decline is fundamentally linked to how our brains process energy.

Could Alzheimer’s, in essence, be “Type 3 Diabetes,”2 a metabolic disorder affecting the most vital organ of all?

Debunking the Plaque Theory of Alzheimer’s

The Dominance of Plaque Theory

For decades, the prevailing wisdom in Alzheimer’s research has centered around plaques – abnormal clusters of protein fragments that accumulate in the brain. The traditional understanding has been that these plaques are the primary culprits, physically disrupting neuronal communication and ultimately leading to the cognitive decline characteristic of Alzheimer’s disease. This “plaque theory” has dominated research efforts and guided the development of countless potential treatments.

Crumbling Foundations and Failed Treatments

However, the foundation of this theory is beginning to crumble. Despite billions of dollars invested in research and drug development targeting plaque reduction, a disturbing trend has emerged: drugs that successfully reduce or even eliminate plaques in the brain have consistently failed to improve cognition or slow the progression of Alzheimer’s 3.

If plaques were truly the root cause, wouldn’t removing them lead to tangible improvements in brain function? The lack of clinical success has cast a long shadow of doubt on the validity of the plaque theory.

Plaques in Healthy Brains

Adding further complexity, researchers have discovered that plaques aren’t exclusive to the brains of individuals with Alzheimer’s. Autopsy studies have revealed that many people who died with perfectly healthy cognitive function had significant plaque accumulation in their brains 4. This begs the question: if plaques are the direct cause of Alzheimer’s, why do so many individuals with plaques escape the disease entirely?

The Fabrication Scandal

Perhaps the most damning blow to the plaque theory came with the exposure of a “Fabrication Scandal.” The very first published papers that implicated plaques as a causal factor in Alzheimer’s disease were found to be based on fabricated data 5.

The scientists who published those reports were found to have engaged in scientific misconduct, effectively building the foundation of an entire field of research on fraudulent findings. Despite this controversy, they refused to retract the paper and continued to let years of research be wasted in the field.

A Shift in Focus

The implications are profound. Billions of dollars have been spent on research and drug development predicated on a theory that is not only failing to deliver results but is also potentially based on flawed and even fabricated data.

As the scientific community grapples with these revelations, a new perspective on Alzheimer’s is emerging, one that shifts the focus from protein plaques to the brain’s metabolic health and its ability to utilize energy.

Alzheimer’s and Insulin Resistance: A New Perspective

The Rise of the Insulin Resistance Theory

As the plaque theory of Alzheimer’s faces increasing scrutiny, a compelling alternative is gaining traction: the idea that Alzheimer’s disease is fundamentally linked to insulin resistance in the brain. This emerging theory proposes that the root of the problem isn’t necessarily the presence of plaques, but rather the brain’s impaired ability to utilize its preferred fuel source: ketones, or even its secondary fuel source – glucose.

Understanding “Type 3 Diabetes”

This has led some researchers to even propose the term “Type 3 Diabetes” to describe Alzheimer’s. However, it’s important to clarify that this isn’t necessarily a new form of diabetes in the traditional sense.

Instead, the term is used to highlight the striking parallels between Alzheimer’s and diabetes, specifically focusing on the concept of insulin resistance within the brain itself. In essence, “Type 3 Diabetes” emphasizes the metabolic dysfunction at the heart of the disease, suggesting that Alzheimer’s might be driven by impaired fuel metabolism in brain cells.

The Brain’s Energy Needs

To understand this connection, it’s crucial to appreciate the brain’s unique energy demands. The brain is an incredibly active and “hungry” organ, possessing a remarkably high metabolic rate 6. This means it requires a constant and substantial supply of energy to function optimally, powering everything from memory formation to basic cognitive processing.

Fuel Sources and Insulin’s Role

The brain can utilize two primary fuel sources – ketones and glucose – but it preferentially uses ketones. However, glucose is still important.

Glucose cannot simply diffuse into brain cells. In certain critical areas of the brain, glucose uptake is regulated by insulin. Much like how insulin acts as a “key” to unlock muscle cells and allow glucose to enter, insulin also plays a crucial role in opening the doors for glucose to enter specific brain regions.

The Energetic Gap in the Alzheimer’s Brain

Impaired Glucose Uptake

When insulin resistance develops in the brain, the critical process of glucose uptake is impaired. Even if blood glucose levels are high, the brain cells in affected regions struggle to absorb this essential fuel. This creates a situation where the brain’s primary energy source is effectively locked out.

Reliance on Ketones and Its Challenges

In response to this glucose deprivation, the brain is forced to rely more heavily on ketones as an alternative fuel source. Ketones, produced during periods of fasting or when following a ketogenic diet, can bypass the insulin-dependent pathway and provide energy to brain cells.

However, a major challenge arises for individuals who are also insulin resistant. Often, people with insulin resistance are in a state where their bodies are not efficiently producing ketones.

Constant consumption of carbohydrates and elevated insulin levels can suppress ketone production, leaving the brain without a sufficient supply of either glucose or ketones.

The Brain’s Energy Deficit

This creates an “energetic gap” within the brain. The brain’s metabolic demands remain high, but its access to readily available fuel is severely limited.

As a result, brain cells are forced to operate at a reduced capacity. This energy deficit manifests as a decline in cognitive function, impacting memory, learning, and overall mental acuity – the hallmarks of Alzheimer’s disease.

The Prevalence of Insulin Resistance in Alzheimer’s Patients

Varied Findings in Research

The compelling link between insulin resistance and Alzheimer’s is compelling, but what does the research actually show about how many Alzheimer’s patients are also insulin resistant? Studies examining this connection have yielded varied findings, with estimates ranging from approximately 40% to as high as 80% of individuals with Alzheimer’s exhibiting signs of insulin resistance 7.

Complexity of Measurement

These seemingly disparate numbers highlight a crucial point: measuring insulin resistance is complex, and the different methodologies used in these studies can significantly influence the results. For instance, some studies may rely on fasting glucose levels as a proxy for insulin resistance, while others may use more sophisticated measures like the Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) or glucose tolerance tests.

The sensitivity and specificity of these different methods can vary, potentially contributing to the observed range in prevalence estimates.

Dr. de la Monte’s Contribution

Notably, Dr. Suzanne de la Monte at Brown University has been a leading voice in advocating for the “Type 3 Diabetes2 concept, emphasizing the profound metabolic dysfunction that often underlies Alzheimer’s disease. Her research has consistently drawn attention to the high prevalence of insulin resistance in Alzheimer’s patients, reinforcing the idea that impaired glucose metabolism is a critical factor in the development and progression of the disease.

The Need for Standardized Measurement

Even with the variability in prevalence estimates, the evidence strongly suggests that a significant proportion of individuals with Alzheimer’s also exhibit insulin resistance. This underscores the importance of considering metabolic factors when assessing risk and developing potential interventions for this devastating condition.

Further research is needed to refine our understanding of the interplay between insulin resistance, brain energy metabolism, and the pathogenesis of Alzheimer’s disease. Standardizing the way that insulin resistance is measured will undoubtedly help in future studies as well.

Conclusion

A Paradigm Shift in Understanding

The journey through the complexities of Alzheimer’s disease reveals a paradigm shift in our understanding. While the traditional focus on plaques has dominated research for years, the emerging evidence points to a critical link between Alzheimer’s and insulin resistance.

This “Type 3 Diabetes” perspective suggests that impaired brain energy metabolism, specifically the brain’s difficulty utilizing glucose due to insulin resistance, may be a driving force behind cognitive decline. As the plaque theory crumbles and this metabolic viewpoint grows, we need to remember fabricated data can drastically skew our knowledge.

Supporting Evidence and Future Directions

The findings are supported by the presence of brain glucose hypometabolism in Alzheimer’s patients, as well as the connection to other neurological disorders with similar metabolic profiles. Although studies vary, many of them show as high as 80% of Alzheimer’s patients are also insulin resistance. As always, standardization of measurement is key for future research.

While more research is undoubtedly needed, addressing insulin resistance through lifestyle interventions and targeted therapies holds promise for improving brain health and potentially mitigating the devastating effects of Alzheimer’s. Explore other related posts on our site to delve deeper into the fascinating world of metabolic health and neurological well-being.

Footnotes

  1. Nichols, E., Steinmetz, J.D., Vollset, S.E. et al. Global burden of Alzheimer’s disease and other dementias, 1990–2016. Lancet Neurol. 18, 87–104 (2019).

  2. De la Monte, Suzanne M., and Jack R. Wands. “Alzheimer’s disease is type 3 diabetes—evidence reviewed.” Journal of diabetes science and technology 2.6 (2008): 1101-1113. 2

  3. Doody, R.S.; Thomas, R.G.; Farlow, M.; Tariot, P.; Graham, S.; Pfeiffer, E.; John, S.; Santiago, J.; Hey, J.; Mohs, R.; et al. Phase 3 Trials of Solanezumab for Mild-to-Moderate Alzheimer’s Disease. N. Engl. J. Med. 2014, 370, 311–321.

  4. Price JL, McKeel DW Jr, Buckles VD, Morris JC. Neuropathology of nondemented elderly subjects. Ann Neurol. 2009 Nov;66(5):591-604.

  5. সার্ভার, সুদীপ্ত; ঠাকুর, অঞ্জন; রেডী, পি হেমচন্দ্র. Amyloid cascade hypothesis in Alzheimer’s disease. Journal of Neurochemistry 2024, 169, 71-96.

  6. Raichle ME, Mintun MA. Brain work and brain imaging. Annu Rev Neurosci. 2006;29:449-76.

  7. de la Monte SM. Insulin resistance and neurodegeneration: progress towards the development of new therapeutics for Alzheimer’s disease. Drugs. 2017 Jul;77(1):47-65.

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