Alzheimer's and insulin - Identify the hidden connection

Wednesday, July 20, 2011 by: Arthur Gazaryants, L.Ac.
Tags: Alzheimer's, insulin, health news

(NewsTarget) Several recent studies (1, 2, 3, 4, 5, 6) are demonstrating a number of common factors in the cause and progression of Alzheimer's disease (AD) and diabetes mellitus. These include impaired glucose utilization due to insulin resistance, a decrease in growth factors such as IGF-1 and IGF-2, lowered energy production and increased oxidative stress - all hallmark symptoms of both conditions.

What is Alzheimer's Disease?
AD is a chronic, neuro-degenerative, inflammatory condition of the brain associated with neuronal loss, beta-amyloid plaque deposits, increased activity of catabolic genes and pathways, decreased energy production, mitochondrial activity, and free radical stress. It affects the areas of the brain responsible for learning and memory, but it is not limited to those areas. Profound memory loss and progressive dementia are characteristic symptoms and signs of AD.

What is Diabetes?
Diabetes is a condition in which the body cannot regulate its own blood sugar because pancreatic insulin production decreases and ultimately stops. Blood sugar rises as cells are "starved" for energy. Diabetes and pre-diabetes are both characterized by a phenomenon called insulin resistance, in which a greater burden is placed on the pancreas to make more insulin. Insulin levels then creep higher with each meal.

As those insulin levels rise, the body further decreases the number of insulin receptors, so progressively less glucose is able to enter target sites. If this condition is poorly managed or goes untreated, the pancreas eventually exhausts itself, which is when diabetics become insulin-dependent. Insulin (an anabolic hormone) is responsible for healthy energy metabolism, mitochondrial function and the clearing of free radicals. The inevitable decline of insulation production leads to oxidative stress, impaired metabolism, chronic disease, inflammation and, ultimately, cell death.

Energy Production and the Brain
The brain is a highly metabolic organ. Even though it constitutes only two percent of total body weight, it consumes about 20 percent of total energy. Its high-energy requirements create reliance on healthy brain mitochondrial function. Any decline in mitochondrial energy production can have a severe impact on brain health and the development of neuro-degenerative diseases, including cognitive decline, an early symptom of AD (6, 7) .

Insulin and the Brain
Unlike muscle and other non-neurological tissue, the brain doesn't store any meaningful levels of glucose, so it relies on its own production of insulin and IGF-1 and IGF-2 for a constant supply of glucose (5). When these and other related growth factors decline - which also happens in diabetes - it leads to progressive brain degeneration due to impaired energy metabolism, mitochondrial function oxidative stress, neuro-inflammation, DNA damage and cell death. All early signs of AD.

Cortisol and the Brain
Cortisol is a stress hormone, produced in response to low glucose/energy in brain cells as well as inflammatory and oxidative stress. In diabetes, glucose has trouble reaching brain cells; therefore, significant amounts of inflammatory stress and cortisol are produced. Unfortunately, chronic cortisol overproduction has a neuro-degenerative effect on the brain, the hippocampus in particular (8, 9, 10). This area is responsible for memory and learning, and it is affected greatly in AD (9). The hippocampus is significantly smaller in diabetics than in non-diabetics.

The explosion of recent studies showing significant overlap between AD and diabetes has resulted in a new term: "Type 3 Diabetes Mellitus" or T3DM. It is not the same as type 1 or type 2 diabetes, but a brand new type of diabetes that involves the brain.

Over the years, we have learned how to treat diabetes: alternative medicine being especially effective in both prevention and treatment. Given the many similarities between the two diseases, we could now be on the threshold of adequately treating AD.

References:
1. Intranasal insulin improves cognition and modulates beta-amyloid in early AD. Neurol. 2008 Feb 5;70(6):440-8. Epub 2007 Oct 17.
2. Preserved cognition in patients with early Alzheimer disease and amnestic mild cognitive impairment during treatment with rosiglitazone: a preliminary study. Am J Geriatr Psychiatry. 2005 Nov;13(11):950-8.
3. Alzheimer's Disease Is Type 3 Diabetes - Evidence Reviewed. J Diabetes Sci Tech Volume 2, Issue 6, November 2008.
4. Review of insulin and insulin-like growth factor expression, signaling, and malfunction in the central nervous system: Relevance to Alzheimer's disease. J Alzheimer's Disease 7 (2005) 45-61.
5. Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer's disease - is this type 3 diabetes? J Alzheimer's Disease 7 (2005) 63-80.
6. Brain mitochondrial dysfunction as a link between Alzheimer's disease and diabetes. J Neurol Sci. 2007;257(1-2):206-14.
7. Possible implications of Insulin Resistance and Glucose metabolism in Alzheimer`s disease pathogenesis. J Cell Mol Med. 2011 Mar 24. doi: 10.1111/j.1582-4934.2011.01318.
8. Relationships between cortisol, DHEA sulphate and insulin-like growth factor-I system in dementia. J End Invest. 2001 Mar;24(3):139-46.
9. Therapeutic implications of HPA axis abnormalities in Alzheimer`s disease: review and update. Psychopharm Bull. 2003 Spring;37(2):120-34.
10. Cortisol, learning, memory, and attention in relation to smaller hippocampal volume in police officers with PTSD. Bio Psyc Volume 59, Issue 2, 15 Jan 2006: 171-177

About the author

Arthur Gazaryants, L.Ac.,
Licensed Acupuncturist and Herbalist
website: www.Artupuncture.com