The study will explore whether early stage memory loss (SMC & MCI) and the comorbidity of Metabolic Syndrome are symptomatic of peripheral and cerebral cellular hypo-metabolism induced by chronic insulin resistance. We will attempt to show that consequential to systemic hyperinsulinemia, aberrant crosstalk between the mitochondria and nuclear genome results in the dysregulation of the regulatory kinases mediating metabolic state and intracellular/extracellular signaling: mTOR and AMPK. The suppression of AMPK signals with chronic overexpression of mTOR signaling will adapt rRNA synthesis away from nutrient availability and toward ATP consuming processes: the biosynthesis of cholesterol, triglycerides, glycogen with inhibition of fatty acid oxidation, histone acetylation with a down-regulation of NAD+ (nicotinamide adenine dinucleotide coenzyme) and SAHH (S-adenosylhomocysteine hydrolase) cofactors leading to global DNA hypo-methylation and local hyper-methylation, suppression of the SAM/SAH ratio, the inhibition of SIRT (sirtuin) expression and normalized whole blood histamine levels. These epigenetic shifts mediate global metabolic inflexibility by channeling fuel substrates toward cytosolic, substrate level phosphorylation (SLP) via over expression of the glycolytic enzymes including PDK (pyruvate dehydrogenase kinase) and away from mitochondrial oxidation mediated by the suppression of PDC (pyruvate dehydrogenase complex), the major regulatory gateway of metabolism between glycolysis and citric acid cycle. We will attempt to show that activation of the AMPK pathway via induced and controlled dietary ketosis will inhibit mTOR signaling away from the biosynthesis of energy and SLP toward the generation of ATP by increasing the cellular AMP/ATP ratio, thus regulating oxidative metabolic signals and attenuating global, cellular hypo-metabolism evidenced by marked reductions in lipid synthesis and LP-IR score (particle concentration and size), HgA1c (hemoglobin A1c), fasting insulin/HOMA-IR (homeostatic model assessment of insulin resistance), blood ketones, fasting triglycerides together with epigenetic regulation of DNA methylation status including normalized whole blood histamine levels and homocysteine regulation. Improvement in cerebral glucose metabolism and corresponding diagnosis of SMC/MCI will be assessed by the objective changes in the outcome measures of MoCA (Montreal Cognitive Assessment), MMSE (Mini-Mental State Exam) and BVMT-R (Brief Visuospatial Memory Test-Revised) administered at baseline and week 12.