World Alzheimer’s Day – Is Alzheimers Type 3 Diabetes?

World Alzheimer’s Day – Is Alzheimers Type 3 Diabetes?

Is Alzheimers Type 3 Diabetes?

by Jonathan Mallory

 

Staring endlessly at a blank screen, waiting restlessly for the words that once flowed so smoothly. Straining with great effort to communicate clearly, wading through an ever-hardening pool of concrete which seems impossible to drain from the mind. Within the slowly shrinking space which is now only a remnant of what once was, those stricken with dementia fight feelings of loneliness, misunderstanding, and frustration.

A form of dementia, Alzheimer’s disease is a gradual loss of memory typically observed amongst elderly individuals. Implications of the disease and related symptoms are of growing concern in South Africa. With an estimated 186,000 people living with dementia in 2016, this number is expected to increase by over 50% within the next 15 years. A projection of great consequence, this statistic is overshadowed by the commonly-held, damaging belief that dementia is merely a sign of aging for which there is no cure.

These misconceptions prevent elderly individuals from receiving the appropriate medical advice they so desperately need. Initiatives such as World Alzheimer’s Day seek to shed light on the debilitating nature of dementia and its association with Alzheimer’s. On this day of increased awareness and understanding, The Noakes Foundation promotes scientifically grounded advice which negates prevalent misconceptions surrounding the neurodegenerative disease. Although complex and in some cases difficult to process, the proposed pathologies of Alzheimer’s provide insight into potential treatments and lead to a greater understanding of related symptoms.

Those diagnosed with Alzheimer’s disease experience a slow decline in brain activity. Tissues and nerve cells essential for the retention of short-term memories slowly degrade in the presence of substances which indicate disease onset.

One such substance is a protein known as β-amyloid. This protein surrounds brain cells and is thought to increase their susceptibility to damage from various sources. Many scientists in search of a cure for Alzheimer’s disease look to target this molecule. Another commonly observed marker of the disease is the decreased use of glucose as a source of fuel in the brain as tissues become increasingly insulin resistant. Although seemingly unrelated, both the prevalence of β-amyloid protein and decreased glucose metabolism in the brain have a mutual source.

Diets high in carbohydrate lead to an increase in blood glucose levels. The hormone, insulin, signals for the uptake of glucose from the blood by various bodily tissues. Those resistant to insulin secrete an excess amount of the hormone in order to stabilize glucose fluctuations. As the body becomes increasingly impervious to the effects of insulin, the amount of glucose in the blood remains elevated for longer periods of time. This is detrimental to the function of certain proteins which are commonly found in the blood stream.

The brain needs cholesterol to protect essential neurons from being damaged by harmful molecules produced during glucose metabolism. Apo E lipoproteins are responsible for carrying cholesterol to the brain and are highly sensitive to excess sugars in the blood.

Sugar molecules such as glucose and fructose attach themselves to the lipoprotein, preventing the transportation of cholesterol to the blood-brain barrier. Astrocytes, cells located in outer brain tissues, are control points responsible for the protection of neurons. They recognize the damaged Apo E lipoproteins and respond by producing β-amyloid protein. In the absence of cholesterol, β-amyloid has been shown to function as a secondary protective measure for neurons.

The emergency response molecule is less effective than cholesterol in shielding neurons, and still results in some damage to essential brain cells. Most of these damage-inducing molecules are by-products of glucose metabolism. One literature review detailing the effects of a high carbohydrate diet on the development of Alzheimer’s disease suggests that β-amyloid protein intentionally halts glucose metabolism through the inhibition of insulin receptors. The insulin resistant inducing protein protects neurons by inhibiting the production of harmful molecules. Without glucose metabolism, the brain must derive its energy from an alternate source.

Studies have shown that a high fat, low carb diet provides the brain with a fuel source known as ketone bodies to be used during the impairment of glucose metabolism. Following the consumption of fats, a metabolic process is initiated in which free fatty acids are produced. The free fatty acids are converted to ketone bodies which are free to circulate in the blood stream. Once they have crossed over into the brain, the ketone bodies can be utilized as a secondary source of fuel. Diets high in carbs and low in fats may further Alzheimer’s disease by depriving the brain of much-needed energy. Not only does the consumption of carbs prevent the transport of protective cholesterol to the neurons, but it also provides an unusable source of fuel to the insulin resistant brain tissues. Damaged neurons lacking in energy are eventually disposed of as the brain no longer has a use for them. The neurodegeneration that follows results in a loss of memory and further development of Alzheimer’s disease.

These theories and concepts are supported by past studies. Multiple short-term dietary interventions have provided support for improved insulin sensitivity and memory of individuals in the early stages of Alzheimer’s disease. Participants in these studies experienced improvements in markers of the condition such as inflammation, oxidation, and apoptosis. Further experimentation involving larger sample sizes is required to gain a fuller understanding of how low carb, high fat diets affect those with Alzheimer’s disease.

Many elderly South Africans suffering from dementia are victims of a legitimate neurodegenerative disease. Although researchers struggle to find a cure for this condition, preventative measures exist which can potentially slow its development. Consider a low carbohydrate, high fat diet as the next step for you or your loved one suffering from Alzheimer’s disease.

 

 

References

1. Prince, Prof Martin. World Alzheimer Report 2016: Improving healthcare for people living with dementia. Alzheimer’s Disease International. Sept., 2016
2. Alzheimer’s Association. Alzheimer’s Disease. Alz. 2017  
3. Craft, Suzanne. Insulin resistance syndrome and Alzheimer’s disease: Age- and obesity-related effects on memory, amyloid, and inflammation. Dec., 2005, 26(1): 65-69
4. J. Hardy, D.J. Selkoe. The amyloid hypothesis of Alzheimer’s disease: progress and problems on the road to therapeutics. Science, 297 (2002), pp. 353-356
5. Krikorian, Robert et al. Enhanced cerebral bioenergetics with dietary ketosis in Mild Cognitive Impairment. Nutrition and Aging. 2014, 223-232
6. Seneff, Stephanie. Nutrition and Alzheimer’s disease: The detrimental role of high carbohydrate diet. Science Direct. European Journal of Internal Medicine. April 2011, 22(2): 134-140
7. Lying-Tunell U. Lindblad BS, Malmlund HO, Persson B. Cerebral blood flow and metabolic rate of exygen, glucose, lactate, pyruvate, ketone bodies and amino acids. Acta Neurol Scan. 1981;63:337-50.
8. Krikorian, Robert et al. Dietary ketosis enhances memory in mild cognitive impairment. NCBI. Neurobiol Aging. Feb., 2012, 33(2): 425.e19-425.e27
9. ST, Henderson. High carbohydrate diets and Alzheimer’s disease. NCBI. Med Hypotheses.  2004, 62(5): 689-700

 

Jonathan is a senior Biochem major at Clemson University and his focus is in public health – he has just completed his internship at The Noakes Foundation where he facilitated a pilot study the Foundation ran.