Neurological - Alzheimer’s


The Problem
Alzheimer’s disease is often referred to as “type 3 diabetes”  because of its strong association with insulin resistance (1,2).  Any insulin resistance in the brain decreases the ability of the brain to generate sufficient cellular energy from glucose to maintain cellular activity.  As a result, the cell’s ability to remove the aggregated proteins associated with Alzheimer’s disease is compromised (3).  These aggregated proteins promote neuroinflammation by increasing oxidative stress. This leads to the death of the nerve cell.  When enough nerve cells are destroyed, cognitive memory is lost.

The Traditional Medical Approach
There is no approved drug for treating Alzheimer’s.  Thus, your best prevention is the reduction of insulin resistance.

The Metabolic Engineering™ Approach
The molecular mechanism that links insulin resistance and oxidative stress to Alzheimer’s may be decreased AMPK activity (4). 

The goal of Metabolic Engineering™ is to reduce insulin resistance by increasing AMPK activity.  Using the Zone diet component of Metabolic Engineering™ to restrict calories without hunger or fatigue is the most powerful dietary approach for lowering insulin resistance because of its direct impact on increasing AMPK activity.  The omega-3 fatty acid dietary component of Metabolic Engineering™ reduces neuroinflammation and promotes resolution.  The polyphenol dietary component of Metabolic Engineering™ reduces oxidative stress.  Equally important is that the omega-3 fatty acid and polyphenol components of Metabolic Engineering™ are also indirect activators of AMPK activity.   Thus, combining all three dietary interventions in Metabolic Engineering™ provides the optimal approach to maximizing AMPK activity to reduce insulin resistance.

Since the development of insulin resistance precedes the development of Alzheimer’s by more than a decade, using Metabolic Engineering™ to reduce insulin resistance becomes your best dietary therapy to reduce the likelihood of developing cognitive dysfunction later in life.

1. Kandimalla R, Thirumala V, Reddy PH. Is Alzheimer’s disease a type 3 diabetes? A critical appraisal.  Biochim Biophys Acta Mol Basis Dis. 2017; 1863:1078-1089. doi: 10.1016/j.bbadis.2016.08.018.

2. Michailidis M, Moraitou D, Tata DA, Kalinderi K, Papamitsou T, Papaliagkas V. Alzheimer’s disease as type 3 diabetes: Common pathophysiological mechanisms between Alzheimer’s disease and type 2 diabetes

3. Dewanjee S, Chakraborty P, Bhattacharya H, Chacko L, Singh B, Chaudhary A, Javvaji K, Pradhan SR, Vallamkondu J, Dey A, Kalra RS, Jha NK, Jha SK, Reddy PH, Kandimalla R. Altered glucose metabolism in Alzheimer’s disease:  Role of mitochondrial dysfunction and oxidative stress. Free Radic Biol Med. 2022; 193(Pt 1):134-157. doi: 10.1016/j.freeradbiomed.2022.09.032.

4. Yang L, Jiang Y, Shi L, Zhong D, Li Y, Li J, Jin R. AMPK: Potential therapeutic target for Alzheimer’s disease. Curr Protein Pept Sci. 2020; 21:66-77.doi: 10.2174/1389203720666190819142746.