Type 3 Diabetes
What is Type 3 Diabetes?
The term “type 3 diabetes” is becoming increasingly used when discussing Alzheimer’s disease (AD), due to research connecting insulin resistance and cognitive decline.[1] As the most common form of dementia, Alzheimer’s disease is linked to the buildup of abnormal plaques and tangled proteins in the brain. These disrupt communication between neurons, impairing their function and eventually leading to the loss of brain cells. Presenting as impaired memory, cognitive decline, and behavioural changes, AD is primarily observed in older adults, with the disease incidence doubling every 5 years after age 65.[2]
In addition to contributing to an increased risk of cardiovascular diseases, retinopathy, neuropathy, kidney disease, liver damage, and infections, diabetes also increases the risk of developing AD.[3], [4] The impaired glucose metabolism seen with diabetes can disrupt highly sensitive neuronal function. Peripheral insulin resistance, which is when the body’s muscles, fat, and liver stop responding properly to insulin, also reduce insulin signalling in the central nervous system. This disruption in the brain’s metabolism is seen by a decrease in energy-producing ATP molecules in the brain, with ATP production continuing to decline as the intensity of AD increases.[5] Insulin resistance can also contribute to neuroinflammation and oxidative stress, in addition to impairing the processing and clearance of abnormal amyloid‑β proteins, key pathophysiological components of AD.[6], [7]

Risk factors for developing AD include smoking, high blood pressure, physical inactivity, obesity, poor diet, excessive alcohol intake, depression, low levels of cognitive engagement, and traumatic brain injury.[8] Genetics and gender also play a role in the development of the disease. Women are at a greater risk than men, partly because they typically live longer, experience changing estrogen levels, and are more likely to develop age-related frailty—a condition marked by reduced strength and resilience that increases vulnerability to health problems. Many genes have also been associated with the development of AD;[9] however, it has been estimated that one third of AD worldwide is related to modifiable risk factors, such as previously mentioned physical inactivity, obesity, hypertension, and diabetes.[10]
Lifestyle Factors
MIND Diet
The MIND diet encompasses components of both the Dietary Approaches to Stop Hypertension (DASH) diet and the Mediterranean diet, in that both include low sodium, plant-based foods, whole grains, regular olive oil consumption, and limited animal and high saturated–fat foods, with the addition of an abundance of green leafy vegetables and berries.[11] Observational studies of over 900 healthy older adults adhering to a MIND style diet found a reduced risk of AD and a slower rate of cognitive decline.[12], [13] A diet rich in whole foods (including fruits and vegetables, whole grains, nuts, and legumes), and low in refined carbohydrates (such as white bread, pasta, and baked goods), like the MIND diet, is also consistently associated with a lower risk of diabetes.[14]
Green leafy vegetables, a key component of this eating paradigm, may also help slow cognitive decline. They are rich in vitamins, minerals, and flavonoids—including folate, lutein, nitrate, phylloquinone, alpha-tocopherol, and kaempferol—nutrients whose intakes have each been found to be significantly associated with reduced rates of cognitive decline.[15] Higher fish intake may also be protective against AD development.[16] DHA, an omega‑3 fatty acid found in fish, is a key membrane phospholipid in the brain. A higher intake of fatty fish, consumed more than once per week, has been correlated with a reduced risk of AD in comparison to those who do not incorporate fish into their diet.[17]

Exercise
Physical exercise may also be a component of a holistic approach to managing AD. Older adults who incorporate physical activity into their lifestyle are more likely to maintain cognition through exercise’s positive impact on cerebral blood flow, inflammation, and amyloid‑β turnover.[18] Multimodal exercise—encompassing strength, flexibility, aerobic, cognition, and agility/coordination-type activity—has been found to have positive effects on cognitive, functional, and behavioural outcomes amongst those with mild to moderate Alzheimer’s.[19] The cognitive benefits include improvements in sustained attention, visual memory, and frontal cognition.[20]
Incorporating exercise may not only benefit those diagnosed with dementia, but also presymptomatic adults.[21] The positive impacts of exercise on blood-sugar control are also abundant, including improving insulin sensitivity, lowering blood glucose, and maintaining a healthy body weight.[22]
Other lifestyle habits beside physical activities, including smoking cessation and limiting alcohol consumption, can also be beneficial for reducing diabetes and AD risk.[23]

Supplementation
Although no vitamin or supplement have been proven to prevent Alzheimer’s disease, multivitamin supplementation amongst older adults has been shown to improve memory, as exhibited by improved immediate and longer-term memory recall, in comparison to adults taking placebo.[24], [25]
Vitamin deficiencies may also increase the risk of AD. Vitamin D plays an important role in neurotransmission, neuroprotection, and neuroplasticity, and deficiency is significantly associated with an increased risk of both AD and other forms of dementia.[26] A vitamin D deficiency can also increase the risk of insulin resistance and, amongst diabetics, correcting a vitamin D deficiency helps improve blood sugar parameters.[27]
Vitamin B₁₂ status is also an important consideration. Vitamin B₁₂ deficiency is a reversible cause of dementia, and significant improvements in cognition can be seen following B₁₂ supplementation.[28]
Supplements targeted more specifically towards blood-sugar regulation may include berberine, a phytochemical with blood sugar–lowering effects which can also improve insulin resistance.[29]
The Bottom Line
Alzheimer’s disease, sometimes called “type 3 diabetes,” is closely linked to how well your body manages insulin and blood sugar. Maintaining a healthy diet, staying active, incorporating the right supplements, and supporting balanced blood sugar, along with the guidance from your health-care practitioner, can all help lower the risk of developing Alzheimer’s disease, now increasingly referred to as “type 3 diabetes.”

Dr. Jill Northrup, ND
A Toronto-based naturopathic doctor with a passion for health and natural medicines, she values an evidence-based treatment approach and emphasizes patient education and preventative medicine in her practice.
aspire-health.ca
References
[1] Meng, X., H. Zhang, Z. Zhao, S. Li, X. Zhang, R. Guo, H. Liu, et al. “Type 3 diabetes and metabolic reprogramming of brain neurons: Causes and therapeutic strategies.” Molecular Medicine 31, no. 1 (2025): 61.
[2] Kumar, A., J. Sidhu, F. Lui, and J.W. Tsao. “Alzheimer disease.” In: StatPearls [Internet]. Treasure Island: StatPearls Publishing; 2024.
[3] Meng et al, op. cit.
[4] Farmaki, P., C. Damaskos, N. Garmpis, A. Garmpi, S. Savvanis, and E. Diamantis. “Complications of the type 2 diabetes mellitus.” Current Cardiology Reviews 16, no. 4 (2020): 249–251.
[5] Meng et al, op. cit.
[6] Meng et al, op. cit.
[7] Nguyen, T.T., Q.T.H. Ta, T.K.O. Nguyen, T.T.D. Nguyen, and V. Van Giau. “Type 3 diabetes and its role implications in Alzheimer’s disease.” International Journal of Molecular Sciences 21, no. 9 (2020): 3165.
[8] Alzheimer Society. Risk factors. Toronto: Alzheimer Society, 2023, available from https://alzheimer.ca/sites/default/files/documents/Risk-factors_Alzheimer-Society-Canada.pdf.
[9] Ibid.
[10] Norton, S., F.E. Matthews, D.E. Barnes, K. Yaffe, and C. Brayne. “Potential for primary prevention of Alzheimer's disease: An analysis of population-based data.” The Lancet. Neurology 13, no. 8 (2014): 788–794.
[11] Morris, M.C., C.C. Tangney, Y. Wang, F.M. Sacks, D.A. Bennett, and N.T. Aggarwal. “MIND diet associated with reduced incidence of Alzheimer’s disease.” Alzheimer's & Dementia 11, no. 9 (2015): 1007–1014.
[12] Ibid.
[13] Morris, M.C., C.C. Tangney, T. Wang, F.M. Sacks, L.L. Barnes, D.A. Bennett, and N.T. Aggarwal. “MIND diet slows cognitive decline with aging.” Alzheimer's & Dementia 11, no. 9 (2015): 1015–1022.
[14] Ardisson Korat, A.V., W.C. Willett, and F.B. Hu. “Diet, lifestyle, and genetic risk factors for type 2 diabetes: A review from the Nurses’ Health Study, Nurses’ Health Study 2, and Health Professionals’ Follow‑up Study.” Current nutrition reports 3 (2014): 345–354.
[15] Morris, M.C., Y. Wang, L.L. Barnes, D.A. Bennett, B. Dawson‑Hughes, and S.L. Booth. “Nutrients and bioactives in green leafy vegetables and cognitive decline: Prospective study.” Neurology 90, no. 3 (2018): e214–e222.
[16] Morris, M.C., D.A. Evans, J.L. Bienias, C.C. Tangney, D.A. Bennett, R.S. Wilson, N. Aggarwal, and J. Schneider. “Consumption of fish and n‑3 fatty acids and risk of incident Alzheimer disease.” Archives of Neurology 60, no. 7 (2003): 940–946.
[17] Ibid.
[18] De la Rosa, A., G. Olaso‑Gonzalez, C. Arc‑Chagnaud, F. Millan, A. Salvador‑Pascual, C. García‑Lucerga, C. Blasco‑Lafarga, et al. “Physical exercise in the prevention and treatment of Alzheimer's disease.” Journal of Sport and Health Science 9, no. 5 (2020): 394–404.
[19] Hernandez, S.S., P.F. Sandreschi, F.C. da Silva, B.A. Arancibia, R. da Silva, P.J. Gutierres, and A. Andrade. “What are the benefits of exercise for Alzheimer’s disease? A systematic review of the past 10 years.” Journal of Aging and Physical Activity 23, no. 4 (2015): 659–668.
[20] Ibid.
[21] De la Rosa et al, op. cit.
[22] American Diabetes Association; Bantle, J.P., J. Wylie-Rosett, A.L. Albright, C.M. Apovian, N.G. Clark, M.J. Franz, B.J. Hoogwerf, et al. “Nutrition recommendations and interventions for diabetes: A position statement of the American Diabetes Association.” Diabetes Care 31, Suppl. 1 (2008): S61–S78.
[23] Alzheimer’s Society, op. cit.
[24] National Institute on Aging. What do we know about diet and prevention of Alzheimer’s disease? 2023‑11‑20, available from https://www.nia.nih.gov/health/alzheimers-and-dementia/what-do-we-know-about-diet-and-prevention-alzheimers-disease.
[25] Yeung, L.K., D.M. Alschuler, M. Wall, H. Luttmann‑Gibson, T. Copeland, C. Hale, R.P. Sloane, H.D. Sesso, J.E.Manson, and A.M. Brickman. “Multivitamin supplementation improves memory in older adults: A randomized clinical trial.” The American Journal of Clinical Nutrition 118, no. 1 (2023): 273–282.
[26] Chai, B., F. Gao, R. Wu, T. Dong, C. Gu, Q. Lin, and Y. Zhang. (2019). “Vitamin D deficiency as a risk factor for dementia and Alzheimer’s disease: An updated meta-analysis.” BMC Neurology 19, no. 1 (2019): 284.
[27] Lei, X., Q. Zhou, Y. Wang, S. Fu, Z. Li, and Q. Chen. “Serum and supplemental vitamin D levels and insulin resistance in T2DM populations: A meta-analysis and systematic review.” Scientific Reports 13, no. 1 (2023): 12343.
[28] Sashindran, V.K., V. Aggarwal, and A. Khera. “Prevalence of vitamin B12 deficiency in elderly population (> 60 years) presenting with dementia to outpatient department.” Medical Journal, Armed Forces India 78, no. 1 (2022): 94–98.
[29] Ye, Y., X. Liu, N. Wu, Y. Han, J. Wang, Y. Yu, and Q. Chen. “Efficacy and safety of berberine alone for several metabolic disorders: A systematic review and meta-analysis of randomized clinical trials.” Frontiers in Pharmacology 12 (2021): 653887.