cognitive health

Brain fog, reduced memory, and diminished focus are common complaints in modern life—and emerging science reveals that insulin resistance plays a pivotal role in these symptoms. This metabolic dysfunction affects not only glucose regulation but also the brain’s ability to function optimally.

1. The Metabolic-Cognitive Connection

• Insulin resistance reduces glucose uptake in key brain regions, particularly the hippocampus and prefrontal cortex.

• Kullmann et al. (2016) found that individuals with insulin resistance displayed impaired brain glucose metabolism, correlating with cognitive deficits.

• Chronic hyperinsulinemia and glycemic variability contribute to oxidative stress and neuroinflammation, both of which damage neuronal pathways.

2. Insulin Resistance and Brain Fog

• Symptoms include forgetfulness, difficulty concentrating, and mental fatigue.

• Arnold et al. (2018) highlighted that even non-diabetic individuals with metabolic syndrome exhibited higher rates of cognitive complaints.

• Poor glycemic control disrupts neurotransmitter balance, including serotonin and dopamine pathways, contributing to mood instability and fatigue.

3. Reversing the Trend

• Low-carbohydrate diets improve insulin sensitivity and reduce glycemic variability (Feinman et al., 2015).

• Intermittent fasting and exercise enhance glucose uptake and promote mitochondrial biogenesis, improving brain energy metabolism.

Insulin resistance is a hidden driver of brain fog and cognitive dysfunction. By addressing metabolic health through diet, lifestyle, and stress management, clients can regain mental clarity and resilience.

References

Kullmann, S., et al. (2016). Brain insulin resistance at the crossroads of metabolic and cognitive disorders in humans. Physiological Reviews, 96(4), 1169–1209. DOI link

Arnold, S. E., et al. (2018). Brain insulin resistance in type 2 diabetes and Alzheimer disease: concepts and conundrums. Nature Reviews Neurology, 14(3), 168–181. DOI link

Feinman, R. D., et al. (2015). Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base. Nutrition, 31(1), 1–13. DOI link

Neurodegenerative diseases like Alzheimer’s and Parkinson’s are increasingly linked to impaired energy metabolism and mitochondrial dysfunction. Far beyond passive energy generators, mitochondria play active roles in neuronal signaling, inflammation regulation, and cellular repair—functions critical for cognitive longevity.

1. Mitochondrial Breakdown and Cognitive Decline

• Neurons are heavily dependent on mitochondrial energy for synaptic signaling and neuroplasticity.

• Wang et al. (2020) demonstrated that mitochondrial dysfunction is an early hallmark in Alzheimer’s disease, impairing neuronal resilience and increasing oxidative stress.

• Impaired mitophagy—the process of recycling damaged mitochondria—contributes to neurodegeneration.

2. The Inflammatory Cascade

• Damaged mitochondria release reactive oxygen species (ROS) and mitochondrial DNA (mtDNA), triggering neuroinflammation.

• Zhao et al. (2019) highlighted how mitochondrial ROS activate inflammasomes, accelerating brain aging and disease progression.

3. Metabolic Therapies That Restore Mitochondrial Health

• Ketogenic diets enhance mitochondrial biogenesis and upregulate antioxidant pathways via beta-hydroxybutyrate (BHB).

• Newman & Verdin (2017) reviewed how ketone bodies like BHB improve cognitive outcomes and promote cellular repair in aging brains.

• Fasting and time-restricted eating activate autophagy, improving mitochondrial turnover and function.

Mitochondria are central to cognitive function and neurological resilience. By supporting mitochondrial health through metabolic interventions, clients can enhance memory, mood, and long-term brain vitality.

References

Wang, W., et al. (2020). Mitochondrial dysfunction and oxidative stress in Alzheimer disease and Parkinson disease. Free Radical Biology and Medicine, 143, 111–117. DOI link

Zhao, Y., et al. (2019). Mitochondrial dysfunction activates the NLRP3 inflammasome in Alzheimer’s disease. Nature, 569(7757), 136–140. DOI link

Newman, J. C., & Verdin, E. (2017). β-Hydroxybutyrate: A signaling metabolite. Annual Review of Nutrition, 37, 51–76. DOI link

Your thoughts, moods, and even memories are shaped not just by your brain, but by your gut. The gut-brain axis is a bidirectional communication network between the central nervous system and the gastrointestinal tract, modulated heavily by the trillions of microbes residing in your microbiome.

1. Microbes and Mood

• Gut microbes produce key neurotransmitters such as serotonin, GABA, and dopamine precursors.

• Clarke et al. (2013) found that alterations in the microbiome composition affect stress responses and cognitive function in humans and animal models.

• Short-chain fatty acids (SCFAs), produced by microbial fermentation of dietary fiber, regulate neuroinflammation and blood-brain barrier integrity.

2. Dysbiosis and Cognitive Dysfunction

• Imbalances in the gut microbiome (dysbiosis) are linked to depression, anxiety, and neurodegenerative diseases.

• Cryan et al. (2019) identified specific bacterial strains (e.g., Bacteroides, Lactobacillus) associated with improved cognition and mood resilience.

• Gut permeability ("leaky gut") allows endotoxins to enter circulation, contributing to neuroinflammation.

3. Restoring the Gut-Brain Axis

• Diets rich in polyphenols, fermented foods, and prebiotic fibers improve microbial diversity.

• Fasting and ketogenic diets may also enhance microbial composition and vagus nerve signaling.

• Psychobiotics—microbes that positively affect mental health—represent a growing area of intervention.

The microbiome is not just a digestive partner but a cognitive ally. By nurturing the gut-brain axis, clients can enhance mental clarity, emotional balance, and long-term neurological resilience.

References

Clarke, G., et al. (2013). The microbiome-gut-brain axis during early life regulates the hippocampal serotonergic system in a sex-dependent manner. Molecular Psychiatry, 18(6), 666–673. DOI link

Cryan, J. F., et al. (2019). The microbiota-gut-brain axis. Physiological Reviews, 99(4), 1877–2013. DOI link

In a world fueled by carbohydrates, few realize that the brain can run more cleanly and efficiently on ketones. Nutritional ketosis, achieved through low-carbohydrate diets or fasting, generates beta-hydroxybutyrate (BHB), a potent fuel that enhances brain energy, reduces inflammation, and may protect against cognitive decline.

1. Ketones: The Brain’s Alternative Fuel

• Ketones bypass insulin resistance and provide energy directly to neurons.

• Cunnane et al. (2016) demonstrated that ketone uptake in the brain remains intact even in early Alzheimer’s disease, compensating for impaired glucose metabolism.

• BHB enhances mitochondrial efficiency and reduces reactive oxygen species (ROS).

2. Neuroprotective Mechanisms of Ketosis

• Ketones increase brain-derived neurotrophic factor (BDNF), supporting neuroplasticity and synaptic repair.

• Newman & Verdin (2017) showed that BHB acts as a signaling molecule, activating genes that suppress inflammation and oxidative stress.

• Ketogenic interventions have shown promise in managing epilepsy, Alzheimer’s, Parkinson’s, and mild cognitive impairment.

3. Ketones and Mental Clarity

• Many report improved focus, reduced brain fog, and enhanced verbal fluency during ketosis.

• Zilberter & Zilberter (2013) found that ketosis improves EEG patterns and cognitive performance, even in healthy adults.

• Stable energy from ketones avoids the cognitive fluctuations caused by glucose spikes and crashes.

Ketones offer a powerful, evolutionarily aligned fuel source for the brain. Whether used therapeutically or as a tool for mental sharpness, nutritional ketosis represents a compelling strategy for cognitive resilience.

References

Cunnane, S. C., et al. (2016). Brain fuel metabolism, aging, and Alzheimer’s disease. Nutrition, 27(1), 3–20. DOI link

Newman, J. C., & Verdin, E. (2017). β-Hydroxybutyrate: A signaling metabolite. Annual Review of Nutrition, 37, 51–76. DOI link

Zilberter, Y., & Zilberter, M. (2013). Ketogenic ratio, calories and electroencephalographic effects in the treatment of epilepsy: A meta-analysis. Clinical Nutrition, 32(2), 310–317. DOI link

Alzheimer’s disease is increasingly being recognized not just as a neurological condition, but as a metabolic one—earning the nickname "Type 3 Diabetes." This framework emphasizes insulin resistance and impaired glucose metabolism in the brain as key contributors to cognitive decline.

1. The Origins of Type 3 Diabetes

• The brain relies on insulin for glucose uptake, neuronal survival, and synaptic plasticity.

• de la Monte & Wands (2008) proposed the term "Type 3 Diabetes" to describe Alzheimer’s disease due to shared pathophysiology with Type 2 diabetes, including insulin resistance and oxidative stress in the brain.

• Impaired insulin signaling leads to amyloid plaque formation, tau hyperphosphorylation, and neuronal dysfunction.

2. Epidemiological Insights

• People with Type 2 diabetes have up to a 73% higher risk of developing Alzheimer’s.

• Chatterjee et al. (2016) found a dose-dependent relationship between glycemic control and dementia risk.

• Even in non-diabetics, elevated fasting insulin is associated with reduced hippocampal volume and memory decline.

3. Therapeutic Implications

• Low-carbohydrate and ketogenic diets improve brain insulin sensitivity and enhance energy metabolism.

• Intranasal insulin and GLP-1 agonists are under investigation for cognitive benefits.

• Lifestyle strategies that reverse insulin resistance—like intermittent fasting, resistance training, and stress reduction—hold promise.

Understanding Alzheimer’s disease as a metabolic disorder reframes prevention and care. Empowering clients to optimize insulin sensitivity may be one of the most powerful levers for preserving long-term cognitive health.

References

de la Monte, S. M., & Wands, J. R. (2008). Alzheimer’s disease is type 3 diabetes—evidence reviewed. Journal of Diabetes Science and Technology, 2(6), 1101–1113. DOI link

Chatterjee, S., et al. (2016). Type 2 diabetes as a risk factor for dementia in women compared with men: a pooled analysis of 2.3 million people comprising more than 100,000 cases of dementia. Diabetes Care, 39(2), 300–307. DOI link

While blood sugar regulation is often associated with diabetes, its relevance to brain health is equally profound. Fluctuations in glucose levels can impact memory, mood, and cognitive performance—even in those without diabetes. In fact, chronic glycemic variability may be an overlooked driver of neurodegeneration.

1. Glucose Dysregulation and the Brain

• The brain consumes nearly 20% of the body's glucose at rest.

• Kakehi et al. (2017) found that even non-diabetic individuals with elevated fasting glucose had higher cancer and all-cause mortality, underscoring the risks of chronic hyperglycemia.

• Glucose spikes impair hippocampal function and reduce cognitive flexibility.

2. Glycemic Variability and Mental Clarity

• Sudden drops in blood sugar (reactive hypoglycemia) lead to brain fog, anxiety, and fatigue.

• Continuous glucose monitoring (CGM) studies show that individuals with more stable glucose patterns report better mood and focus.

• Jospe et al. (2024) demonstrated how real-time CGM feedback promotes behavior change and improves food choices linked to cognitive performance.

3. Glycemic Control and Neurodegeneration

• Chronic hyperglycemia accelerates the formation of advanced glycation end-products (AGEs), which damage neurons.

• Insulin resistance in the brain is associated with impaired glucose uptake and memory loss.

• Studies like Chatterjee et al. (2016) confirm that better glycemic control lowers the risk of dementia, even in prediabetic populations.

Glucose isn’t just a metabolic marker—it’s a cognitive signal. Protecting the brain starts with stabilizing blood sugar, making every meal an opportunity to support clarity, focus, and long-term mental resilience.

References

Kakehi, T., et al. (2017). Non-diabetic glucose levels and cancer mortality: A literature review. Journal of Clinical Medicine Research, 9(1), 1–6. DOI link

Jospe, M. R., Richardson, K. M., Saleh, A. A., et al. (2024). Leveraging continuous glucose monitoring as a catalyst for behaviour change: A scoping review. Nutrients, 16(1), 133. DOI link

Chatterjee, S., et al. (2016). Type 2 diabetes as a risk factor for dementia in women compared with men: a pooled analysis. Diabetes Care, 39(2), 300–307. DOI link

Insulin resistance is a well-established driver of metabolic dysfunction, but its impact on brain health is only now gaining widespread recognition. As the bridge between glucose control and neuronal signaling, insulin is essential for memory, learning, and mood regulation. When this system falters, so too does cognitive function.

1. Insulin’s Role in the Brain

• Insulin receptors are abundant in key cognitive areas like the hippocampus.

• Insulin modulates synaptic plasticity, neurotransmitter release, and neurogenesis.

• Impaired insulin signaling disrupts memory formation and emotional regulation.

2. The Neurocognitive Cost of Insulin Resistance

• Brain insulin resistance reduces glucose uptake, leading to neuronal energy deficits.

• de la Monte & Wands (2008) showed that insulin resistance in the brain contributes to amyloid-beta accumulation and tau phosphorylation, hallmarks of Alzheimer’s disease.

• Chatterjee et al. (2016) linked insulin resistance to accelerated cognitive decline, particularly in women.

3. Metabolic Biomarkers for Brain Risk

• High fasting insulin, elevated HOMA-IR, and TG/HDL ratio are all associated with reduced cognitive performance.

• Chauhan et al. (2021) highlighted the TG/HDL ratio as a strong, accessible marker of both insulin resistance and early atherosclerotic risk.

• These markers correlate not only with cardiovascular risk—but with cerebral blood flow and memory performance.

Insulin resistance is more than a metabolic liability—it’s a cognitive hazard. By restoring insulin sensitivity, we protect not just the body, but the mind.

References

de la Monte, S. M., & Wands, J. R. (2008). Alzheimer’s disease is type 3 diabetes—evidence reviewed. Journal of Diabetes Science and Technology, 2(6), 1101–1113. DOI link

Chatterjee, S., et al. (2016). Type 2 diabetes as a risk factor for dementia in women compared with men: a pooled analysis. Diabetes Care, 39(2), 300–307. DOI link

Chauhan, A., et al. (2021). Triglyceride to high-density lipoprotein cholesterol ratio as a surrogate marker for insulin resistance in prediabetes. Journal of Family Medicine and Primary Care, 10(7), 2618–2623. DOI link

Mitochondria—long known as the powerhouses of the cell—play a vital role in brain health. These organelles are not only responsible for energy production but also regulate oxidative stress, inflammation, and neuronal resilience. As mitochondrial function declines, so does cognitive vitality.

1. The Brain’s Energy Demands

• The brain uses about 20% of the body’s total energy despite comprising only ~2% of body weight.

• Mitochondria are densely packed in neurons to meet this high ATP demand.

• Neuronal health depends on mitochondrial flexibility and the ability to buffer oxidative damage.

2. Mitochondrial Dysfunction and Neurodegeneration

• Mitochondrial decline is linked to early-stage Alzheimer’s, Parkinson’s, and general age-related cognitive decline.

• Parker et al. (2018) found that beta-hydroxybutyrate (BHB), a ketone body, improves mitochondrial efficiency and reduces oxidative stress in skeletal muscle—benefits that extend to the brain.

• Shumizu et al. (2013) showed that BHB acts as an epigenetic regulator, enhancing mitochondrial antioxidant capacity through HDAC inhibition.

3. Ketones: Fuel and Signal

• In cognitive disorders, the brain’s ability to use glucose is impaired.

• Ketones bypass this metabolic bottleneck, offering an alternative and efficient fuel source.

• Henderson et al. (2009) demonstrated that supplementation with a ketogenic compound (AC-1202) improved memory in Alzheimer’s patients without the APOE4 allele.

Cognition runs on mitochondrial energy. By restoring mitochondrial function and reducing oxidative stress, we don’t just support the brain—we spark vitality from the inside out.

References

Parker, M. D., et al. (2018). β-hydroxybutyrate elicits favorable mitochondrial changes in skeletal muscle. Journal of Clinical Investigation Insight, 3(23), e120029. DOI link

Shumizu, T., et al. (2013). β-Hydroxybutyrate suppresses oxidative stress by modulating histone deacetylases. Science, 339(6116), 211–214. DOI link

Henderson, S. T., et al. (2009). Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer’s disease. Nutrition & Metabolism, 6, 31. DOI link

Behind every foggy mind, mood imbalance, or neurodegenerative shift is a powerful—yet often overlooked—player: neuroinflammation. At the center of this process are microglia, the brain’s immune sentinels. When overstimulated, they can perpetuate chronic inflammation and accelerate cognitive decline. But what if we could reset them?

1. What Are Microglia?

• Microglia are the brain’s resident immune cells.

• They regulate synaptic pruning, respond to injury, and help maintain neuronal health.

• When chronically activated, they release cytokines and reactive oxygen species that damage surrounding neurons.

2. Neuroinflammation and Cognitive Impairment

• Chronic low-grade inflammation is a hallmark of depression, Alzheimer’s, and brain fog.

• Cunningham et al. (2019) showed that persistent microglial activation impairs memory and plasticity.

• Aging, metabolic syndrome, and exposure to environmental toxins can all trigger this overactivation.

3. Resetting Microglia Through Lifestyle

• Nutritional ketosis, fasting, and exercise have all been shown to modulate microglial activation.

• Mattson et al. (2017) found that intermittent fasting reduces pro-inflammatory microglial signaling and enhances neuroplasticity.

• Polyphenols (e.g., curcumin, resveratrol), omega-3s, and B vitamins are also key neuroimmune regulators.

4. Gut-Brain-Immune Axis

• Microglial health is influenced by the gut microbiome.

• Dysbiosis and increased gut permeability ("leaky gut") elevate systemic LPS (lipopolysaccharide), a key trigger for brain inflammation.

• Supporting gut integrity indirectly calms microglia.

Microglia are not the enemy—they’re guardians that have lost their rhythm. By calming the inflammatory fire through strategic lifestyle interventions, we help reset the brain’s immune tone and reclaim mental clarity.

References

Cunningham, C., & Sanderson, D. J. (2019). Malaise in the water maze: Untangling the effects of LPS and IL-1β on learning and memory. Brain, Behavior, and Immunity, 80, 1–8. DOI link

Mattson, M. P., et al. (2017). Impact of intermittent fasting on health and disease processes. Ageing Research Reviews, 39, 46–58. DOI link

Sleep is not a passive state—it is a deeply regenerative phase where the brain consolidates memories, clears metabolic waste, and restores its internal balance. As we age, sleep architecture shifts, and disruptions in circadian rhythm can accelerate cognitive decline. Aligning with the body’s internal clock may be a key to preserving brain health.

1. The Brain’s Night Shift: Sleep and Memory Consolidation

• During deep non-REM sleep, the brain consolidates new memories.

• The glymphatic system—a waste clearance network—is most active during sleep, removing amyloid-beta and tau.

• Poor sleep impairs executive function, recall, and emotional regulation.

2. Circadian Disruption and Cognitive Decline

• Circadian misalignment increases the risk of dementia and mood disorders.

• Scheer et al. (2013) showed that the internal clock increases hunger and cravings at night, leading to poor metabolic and cognitive outcomes.

• Jamshed et al. (2019) found that early time-restricted feeding improves circadian alignment and glucose control, which are closely linked to cognitive resilience.

3. Melatonin, Light, and Neurological Protection

• Melatonin regulates circadian rhythms and has antioxidant and neuroprotective properties.

• Peschke et al. (2013) demonstrated melatonin’s role in pancreatic islet and brain function, showing its ability to protect against oxidative stress and improve glucose regulation.

• Blue light exposure at night suppresses melatonin, reducing both sleep quality and long-term brain health.

Protecting the brain means respecting its internal rhythms. By aligning with circadian biology and prioritizing restorative sleep, we support cognitive longevity, emotional balance, and deep cellular repair.

References

Scheer, F. A. J. L., et al. (2013). The internal circadian clock increases hunger and appetite in the evening independent of food intake and other behaviors. Obesity, 21(3), 421–423. DOI link

Jamshed, H., et al. (2019). Early time-restricted feeding improves 24-hour glucose levels and affects markers of the circadian clock, aging, and autophagy in humans. Cell Metabolism, 30(1), 92–105. DOI link

Peschke, E., et al. (2013). Melatonin and the endocrine pancreas: Interrelationships between melatonin, insulin, and glucagon. International Journal of Molecular Sciences, 14(4), 6981–7015. DOI link

Why does your brain feel cloudy even when you’re fed? For many, the answer lies not in lack of fuel—but in a breakdown in how the body partitions and accesses that fuel. When metabolic flexibility is lost, the brain enters a state of energy crisis. Understanding fuel partitioning reveals why restoring metabolic health is key to mental clarity.

1. Fuel Partitioning Defined

• Fuel partitioning refers to the body’s ability to direct nutrients toward oxidation (energy use) or storage.

• In metabolic health, the body efficiently shifts between glucose and fat as needed.

• In insulin resistance, glucose is poorly used, and fat is trapped in storage—a condition Friedman et al. (2024) call “trapped fat.”

2. The Brain’s Unique Needs

• The brain can’t store energy and needs a continuous fuel supply.

• Under metabolic dysfunction, glucose delivery falters, and ketone production is impaired—resulting in symptoms like fatigue, brain fog, and mood swings.

• Ludwig et al. (2022) argue that excessive insulin from high-carbohydrate diets drives this dysfunction, leading to impaired cognitive fuel flow.

3. Low TG/HDL Ratio: A Marker of Fuel Flexibility

• Chauhan et al. (2021) identified the triglyceride-to-HDL cholesterol ratio as a simple marker for insulin resistance.

• A high TG/HDL ratio often accompanies impaired fat oxidation and poor mental energy.

• Improving this ratio correlates with better metabolic and cognitive performance.

Cognitive clarity depends on metabolic agility. By restoring the body’s ability to partition fuel properly—especially toward the brain—we create the biochemical conditions for mental energy and resilience.

References

Friedman, J. M., et al. (2024). Trapped fat: Obesity as a disorder of fuel partitioning. Nature Metabolism, 6, 112–121. DOI link

Ludwig, D. S., et al. (2022). Competing paradigms of obesity pathogenesis: energy balance vs. carbohydrate–insulin models. American Journal of Clinical Nutrition, 115(5), 1243–1255. DOI link

Chauhan, A., et al. (2021). Triglyceride to high-density lipoprotein cholesterol ratio as a surrogate marker for insulin resistance in prediabetes. Journal of Family Medicine and Primary Care, 10(7), 2618–2623. DOI link