TL;DR: The ketogenic diet forces the body to burn fat and produce ketone bodies — primarily beta-hydroxybutyrate (BHB) and acetoacetate — which the brain can use as an efficient alternative to glucose. This metabolic shift has a century of evidence behind it in epilepsy, where it reliably reduces seizure frequency in drug-resistant cases. More recent research shows promising but still moderate evidence that ketones can improve cognitive function in people with Alzheimer’s disease and mild cognitive impairment, likely by bypassing impaired glucose metabolism in the aging brain. For healthy adults seeking sharper thinking, however, the evidence is thin and largely anecdotal. Ketones are genuinely neuroprotective in certain contexts, but the full ketogenic diet is a demanding intervention with real trade-offs — gut microbiome disruption, adaptation side effects, nutrient gaps, and sustainability challenges — that may not be justified unless you belong to a population with clear evidence of benefit. MCT oil supplementation offers a less restrictive way to raise ketone levels modestly, and may be a more practical option for most people.
Introduction
The ketogenic diet was not invented in a Silicon Valley biohacking lab. It was developed in the 1920s at the Mayo Clinic as a treatment for epilepsy in children who did not respond to the limited anticonvulsant medications available at the time. Dr. Russell Wilder proposed in 1921 that a diet mimicking the metabolic effects of fasting — high in fat, very low in carbohydrates, and moderate in protein — could reproduce the anticonvulsant effects of starvation without the obvious problem of starving the patient indefinitely.
The diet worked. For decades, it was a mainstay of epilepsy treatment, particularly in pediatric neurology. It fell out of fashion as more effective anticonvulsant drugs became available in the mid-twentieth century, only to be revived in the 1990s when the Charlie Foundation brought public attention to its efficacy for drug-resistant seizures. Today, the ketogenic diet is experiencing an entirely different kind of revival — as a proposed cognitive enhancer, neuroprotective strategy, and intervention for neurodegenerative disease.
The central question this article addresses is not whether ketones are good for the brain. They clearly can be, in certain contexts. The question is who actually benefits from a ketogenic diet for cognitive purposes, and whether the demanding nature of the diet is justified by the evidence for different populations.
How Ketones Fuel the Brain
The brain is the most energy-demanding organ in the body. Despite representing only about 2 percent of body mass, it consumes roughly 20 percent of the body’s total energy expenditure. Under normal dietary conditions, glucose is the brain’s primary fuel — the organ burns approximately 120 grams of glucose per day.
But glucose is not the brain’s only option. When carbohydrate intake drops below approximately 20 to 50 grams per day and liver glycogen stores are depleted, the body enters a metabolic state called ketosis. The liver begins converting fatty acids into three ketone bodies: beta-hydroxybutyrate (BHB), acetoacetate, and acetone. BHB and acetoacetate are the metabolically significant ones — they cross the blood-brain barrier via monocarboxylate transporters and are taken up by neurons and glial cells as fuel.
The brain cannot burn fatty acids directly because they cannot efficiently cross the blood-brain barrier. Ketone bodies solve this problem — they are water-soluble, lipid-derived fuel molecules that give the brain access to the body’s fat stores during carbohydrate scarcity. During sustained ketosis, ketones can supply up to 60 to 70 percent of the brain’s energy needs, with glucose (produced through gluconeogenesis from amino acids and glycerol) covering the remainder.
Why Ketone Metabolism Matters
Ketone metabolism is not simply a backup system. It has several properties that may confer advantages in specific neurological contexts.
Greater mitochondrial efficiency. Ketones are metabolized through a slightly different pathway than glucose, and the process generates fewer reactive oxygen species (ROS) per unit of ATP produced. This means less oxidative stress on neurons during energy production. Veech and colleagues demonstrated in a series of studies published in the Annals of the New York Academy of Sciences (2004) that ketone body metabolism increased the hydraulic efficiency of the inner mitochondrial membrane, improving the free energy available from ATP hydrolysis by roughly 25 percent compared to glucose.
Reduced oxidative stress. BHB has direct antioxidant properties beyond the metabolic efficiency gains. Shimazu and colleagues (2013), in work published in Science, demonstrated that BHB acts as an endogenous inhibitor of class I histone deacetylases (HDACs), which upregulates the expression of genes involved in oxidative stress resistance — including FOXO3a, catalase, and mitochondrial superoxide dismutase (MnSOD). This epigenetic signaling role means BHB is not merely a fuel molecule but also a regulatory molecule that can influence gene expression in neurons.
GABA/glutamate balance. Ketone metabolism alters the ratio of the inhibitory neurotransmitter GABA to the excitatory neurotransmitter glutamate in the brain. Yudkoff and colleagues (2005), in research published in Epilepsy Research, showed that ketone body metabolism shifts amino acid handling in a way that favors GABA synthesis and reduces glutamate accumulation. This is likely a key mechanism behind the anticonvulsant effect of the ketogenic diet — seizures are fundamentally a problem of excessive neuronal excitation — and it may also be relevant to other conditions involving excitotoxicity, including neurodegenerative disease.
Preserved uptake in the aging brain. One of the most significant findings in this field comes from the work of Stephen Cunnane and colleagues at the University of Sherbrooke. Using PET imaging with both fluorodeoxyglucose (FDG, for glucose) and carbon-11-acetoacetate (for ketones), they demonstrated that while the aging brain — and particularly the Alzheimer’s brain — shows progressively impaired glucose uptake, ketone uptake remains largely intact. Their 2016 study published in Alzheimer’s and Dementia showed that brain ketone metabolism was not significantly different between healthy elderly controls and patients with mild Alzheimer’s disease, even though glucose hypometabolism was clearly evident in the Alzheimer’s group. This finding is the foundation of the “energy rescue” hypothesis: that supplying the brain with ketones may compensate for a glucose utilization deficit that worsens with age and disease.
Evidence by Population
The evidence for cognitive benefits of the ketogenic diet varies dramatically depending on who is being studied. Lumping all populations together is one of the most common errors in discussions of keto and the brain.
Epilepsy: Strong Evidence
The ketogenic diet’s efficacy in epilepsy is not debated — it is established clinical practice supported by over a century of clinical use and multiple randomized controlled trials.
Neal and colleagues (2008), in a landmark study published in The Lancet Neurology, conducted the first randomized controlled trial of the ketogenic diet for childhood epilepsy. They randomized 145 children aged 2 to 16 years with drug-resistant epilepsy to either a ketogenic diet or a control condition (no dietary change). After three months, 38 percent of children in the ketogenic diet group had greater than 50 percent seizure reduction, compared to only 6 percent in the control group. Seven percent of the ketogenic diet group achieved greater than 90 percent seizure reduction.
A Cochrane systematic review by Martin-McGill and colleagues (2020) confirmed these findings across multiple trials, concluding that the ketogenic diet is an effective treatment for drug-resistant epilepsy, with approximately 50 to 60 percent of patients achieving meaningful seizure reduction. The modified Atkins diet and low-glycemic-index treatment — less restrictive variants that still produce some degree of ketosis — also showed efficacy, though generally with somewhat smaller effect sizes.
The cognitive dimension of epilepsy treatment is important but often overlooked. Uncontrolled seizures themselves damage the brain and impair cognitive function. Frequent seizure activity, and particularly the subclinical epileptiform discharges that can occur between overt seizures, disrupts learning, memory consolidation, and attention. By reducing seizure burden, the ketogenic diet can indirectly improve cognitive function in epilepsy patients — sometimes dramatically. Parents and clinicians frequently report improvements in alertness, engagement, and developmental progress that go beyond simple seizure counts.
Alzheimer’s Disease and Mild Cognitive Impairment: Moderate Evidence
The application of ketogenic interventions to Alzheimer’s disease is grounded in the glucose hypometabolism observation described above. If the Alzheimer’s brain is struggling to use glucose but can still use ketones, then providing ketones — either through diet or supplements — might address a genuine energy deficit.
Henderson and colleagues (2009), in a study published in Nutrition and Metabolism, conducted one of the earliest randomized controlled trials of a ketogenic agent (AC-1202, a medium-chain triglyceride formulation) in mild to moderate Alzheimer’s disease. In this 90-day, double-blind, placebo-controlled study of 152 patients, subjects receiving the MCT-based intervention showed significant improvement on the Alzheimer’s Disease Assessment Scale-Cognitive subscale (ADAS-Cog) — but only in the subset of patients who did not carry the APOE4 allele. APOE4 carriers showed no significant benefit. This genotype-dependent response has been a recurring theme in the literature and may relate to differences in how APOE4 carriers metabolize ketones or transport fatty acids across the blood-brain barrier.
Krikorian and colleagues (2012), in a small but well-designed study published in Neurobiology of Aging, randomized 23 older adults with mild cognitive impairment (MCI) to either a very low-carbohydrate diet (5 to 10 percent of calories from carbohydrates) or a high-carbohydrate diet (50 percent of calories from carbohydrates) for six weeks. The low-carbohydrate group showed improved verbal memory performance, and the degree of improvement correlated with the level of urinary ketone bodies — a dose-response relationship that strengthens the case for a causal connection.
Fortier and colleagues (2021), in the BENEFIC trial published in Alzheimer’s Research and Therapy, tested six months of MCT oil supplementation (30 grams per day) versus placebo in 122 patients with MCI. The MCT group showed significant improvement in several cognitive domains, including episodic memory and language, and the improvements correlated with increases in brain ketone uptake as measured by PET imaging. This study is particularly valuable because it used objective neuroimaging to confirm that the intervention was actually changing brain metabolism, not just relying on serum ketone levels as a proxy.
A systematic review by Grammatikopoulou and colleagues (2020), published in Advances in Nutrition, assessed the aggregate evidence for ketogenic interventions in Alzheimer’s disease and MCI and concluded that the evidence was “promising but preliminary.” The authors noted that most studies were small, short-term, and used heterogeneous protocols, making definitive conclusions difficult. They called for larger, longer randomized controlled trials.
The evidence in this population is graded as moderate — there are clear mechanistic reasons to expect benefit, and the clinical data is moving in the right direction, but the studies remain too few, too small, and too short to be definitive. The APOE4 genotype interaction adds complexity that has not been resolved.
Healthy Adults: Limited Evidence
This is where the gap between popular enthusiasm and scientific evidence is widest. The claim that a ketogenic diet sharpens cognition in healthy, cognitively intact adults is not well supported by controlled studies.
A handful of studies have examined cognitive performance in healthy adults following ketogenic diets. Brinkworth and colleagues (2009), in a study published in the American Journal of Clinical Nutrition, compared cognitive function in 93 overweight or obese adults randomized to either a very low-carbohydrate ketogenic diet or a low-fat diet for one year. Both groups showed comparable improvements in working memory and processing speed, with no significant differences between diets. The improvements in both groups were attributed to weight loss itself rather than to macronutrient composition.
Murray and colleagues (2016), in a study published in Frontiers in Physiology, showed that exogenous ketone supplementation improved cognitive performance during hypoglycemia — a finding relevant to specific clinical scenarios but not to the everyday experience of healthy, well-fed adults.
Some short-term studies and many anecdotal reports describe improved mental clarity and focus during ketosis. However, these reports are confounded by multiple factors: the placebo effect of adopting any new health regimen, the elimination of ultra-processed foods and refined sugars (which would be expected to improve cognition regardless of ketosis), improved blood sugar stability, and the potential mood-elevating effects of BHB itself. It is very difficult to disentangle “benefits of ketosis” from “benefits of removing junk food” when someone simultaneously does both.
There is also a well-documented adaptation period — colloquially known as “keto flu” — during the first one to two weeks of carbohydrate restriction, during which many people report worsened cognitive function, brain fog, irritability, and difficulty concentrating. This temporary impairment is likely due to the brain adapting to ketone utilization and to fluid and electrolyte shifts that accompany the initial phase of ketosis. It complicates short-term studies of cognitive performance on ketogenic diets and may explain some negative findings.
MCT Oil: A Shortcut to Ketones
Medium-chain triglycerides (MCTs) are fats with carbon chain lengths of 6 to 12 carbons — primarily caprylic acid (C8) and capric acid (C10). Unlike long-chain fats, MCTs are rapidly absorbed, transported directly to the liver via the portal vein, and converted to ketone bodies regardless of overall dietary carbohydrate intake. This makes MCT oil a way to raise brain ketone levels without the full carbohydrate restriction of a ketogenic diet.
Coconut oil, which contains approximately 60 percent MCTs, was the basis for early popular interest in ketone-based Alzheimer’s interventions, driven largely by anecdotal reports from caregivers. However, coconut oil is not an efficient source of the most ketogenic MCTs — it is high in lauric acid (C12), which behaves more like a long-chain fat metabolically. Purified MCT oil, and particularly C8-dominant formulations, produces significantly higher ketone levels per gram consumed.
The BENEFIC trial by Fortier and colleagues (2021) used 30 grams per day of MCT oil and achieved meaningful increases in brain ketone uptake and cognitive improvements in MCI patients. This dosing produced serum BHB levels in the range of 0.3 to 0.5 mmol/L — modest compared to nutritional ketosis (typically 0.5 to 3.0 mmol/L) but apparently sufficient to make a measurable difference in a brain with compromised glucose metabolism.
MCT oil is not without side effects. Gastrointestinal distress — cramping, diarrhea, nausea — is common at higher doses, particularly when introduced abruptly. Gradual dose escalation over one to two weeks (starting at 5 grams per day and increasing to 15 to 30 grams) substantially improves tolerability.
For individuals interested in the cognitive effects of ketones but unwilling or unable to sustain a full ketogenic diet, MCT oil supplementation represents a more practical and less disruptive option — particularly for older adults at risk for cognitive decline.
Long-Term Sustainability and Risks
The ketogenic diet is one of the most restrictive mainstream dietary patterns. It typically limits carbohydrate intake to 20 to 50 grams per day — roughly the amount in a single apple or a cup of cooked rice. This means eliminating or drastically reducing not only obvious sources like bread, pasta, and sugar, but also most fruits, many vegetables (particularly starchy ones), legumes, and whole grains.
Adherence
Long-term adherence to ketogenic diets is poor in most studies. Batch and colleagues (2020), in a systematic review published in Nutrients, noted that dropout rates in ketogenic diet trials are consistently high, often exceeding 40 percent in studies lasting six months or more. For a dietary intervention that may need to be sustained over years to deliver meaningful cognitive protection, this is a significant practical limitation.
Nutrient Gaps
Strict ketogenic diets restrict or eliminate several food groups that are important sources of fiber, vitamins, minerals, and phytochemicals. Fiber intake is typically very low, which has implications for gut health and the microbiome (discussed below). Potassium, magnesium, folate, and vitamin C intake may be compromised unless careful attention is paid to food selection. Well-formulated ketogenic diets that emphasize non-starchy vegetables, nuts, seeds, and organ meats can mitigate many of these gaps, but many people following popular versions of the diet do not achieve this level of dietary sophistication.
Gut Microbiome Impact
The gut microbiome has emerged as a significant player in brain health through the gut-brain axis. Ketogenic diets substantially alter the composition of the gut microbiota. Ang and colleagues (2020), in research published in Cell, demonstrated that ketogenic diets in humans reduced populations of Bifidobacteria and Actinobacteria — generally considered beneficial taxa — and decreased levels of pro-inflammatory Th17 immune cells in the gut. The reduction in Th17 cells may be beneficial in autoimmune or neuroinflammatory conditions, but the reduction in Bifidobacteria and overall microbial diversity raises concerns about long-term gut health.
Olson and colleagues (2018), in a study published in Cell, showed that the gut microbiome is actually required for the anti-seizure effects of the ketogenic diet in a mouse model of epilepsy — germ-free mice did not benefit from the diet, and the specific gut microbial changes induced by ketosis were necessary for its anticonvulsant activity. This suggests a complex and not fully understood relationship between ketosis, the microbiome, and brain function.
The long-term consequences of a ketogenic-diet-altered microbiome for brain health are unknown. Given the growing evidence that microbial diversity and short-chain fatty acid production (which depends on dietary fiber) are important for neurological health — a relationship explored in detail in our guide to the gut-brain axis — this is a genuine concern that should temper enthusiasm for indefinite ketogenic dieting.
Cardiovascular Considerations
Ketogenic diets are typically high in saturated fat, and they reliably increase LDL cholesterol in a subset of individuals — sometimes dramatically. Whether this increase in LDL translates to increased cardiovascular risk in the context of a ketogenic diet is debated and likely depends on individual genetics, the type of fats consumed, and the overall metabolic context. However, cardiovascular health is itself a major determinant of brain health — vascular dementia is the second most common cause of dementia, and cerebrovascular disease contributes to most cases of Alzheimer’s as well. Any dietary pattern that worsens cardiovascular risk factors in a given individual is indirectly threatening brain health, regardless of any direct ketone-related benefits.
Who Clearly Benefits
Based on the current evidence, the populations with the strongest case for a ketogenic dietary intervention are:
People with drug-resistant epilepsy. The evidence here is unambiguous. If anticonvulsant medications are not adequately controlling seizures, the ketogenic diet or a modified variant (modified Atkins diet, low-glycemic-index treatment) should be seriously considered under medical supervision. The cognitive benefits in this group come both directly from ketone metabolism and indirectly from seizure reduction.
People with mild cognitive impairment or early Alzheimer’s disease. The evidence is moderate but the mechanistic rationale is strong. For individuals already experiencing cognitive decline — particularly those without the APOE4 allele — a trial of either a ketogenic diet or MCT oil supplementation is reasonable, ideally in coordination with a physician. The BENEFIC trial and related studies suggest that even modest ketone elevation through MCT supplementation can be beneficial.
People with type 2 diabetes or significant insulin resistance. Although the evidence specifically for cognitive outcomes in this group is limited, the ketogenic diet’s well-documented ability to improve glycemic control and insulin sensitivity is indirectly brain-protective. Chronic hyperglycemia and insulin resistance are established risk factors for cognitive decline and Alzheimer’s disease. However, the Mediterranean diet achieves many of the same metabolic improvements with a broader food base and stronger direct evidence for cognitive outcomes.
Who Probably Does Not Need It
Cognitively healthy younger adults. If you are under 50, cognitively intact, and metabolically healthy, there is no meaningful evidence that a ketogenic diet will make you smarter, more focused, or more productive. The “mental clarity” reported by many keto dieters may be real but is likely attributable to improved blood sugar stability, elimination of ultra-processed foods, and expectation effects — none of which require ketosis. A well-constructed Mediterranean or MIND diet achieves most of these benefits with far less restriction.
People who exercise intensely. High-intensity and glycolytic exercise performance is consistently impaired on ketogenic diets. If your cognitive health strategy includes vigorous exercise — and it should, given that exercise is among the best-supported interventions for brain health — a ketogenic diet may work against that goal. Endurance performance can be maintained or even enhanced in fat-adapted athletes, but this adaptation takes weeks to months.
People who would find the diet stressful or socially isolating. Chronic psychological stress and social isolation are risk factors for cognitive decline. If maintaining a ketogenic diet causes significant stress, anxiety about food choices, social friction, or disordered eating patterns, those harms may outweigh any theoretical ketone-related benefits.
Practical Takeaway
Ketones are a legitimate alternative brain fuel with documented neuroprotective properties — reduced oxidative stress, improved mitochondrial efficiency, and favorable effects on neurotransmitter balance. The biology is real, not hype.
The strength of evidence varies enormously by population. Epilepsy: strong. Alzheimer’s and MCI: moderate and growing. Healthy adults: limited and largely anecdotal.
The aging brain’s ability to use ketones remains intact even when glucose uptake declines. This is the most important finding driving interest in ketogenic interventions for neurodegeneration, and it is well-supported by PET imaging studies.
MCT oil supplementation (15 to 30 grams per day) is a practical alternative to a full ketogenic diet for raising brain ketone levels. It is easier to sustain, better tolerated with gradual introduction, and has direct trial evidence in MCI populations.
The ketogenic diet has real trade-offs — gut microbiome disruption, nutrient gaps, poor long-term adherence, potential cardiovascular concerns, and a difficult adaptation period. These must be weighed against potential benefits.
APOE4 carriers may respond differently to ketogenic interventions. The limited available data suggests reduced benefit in this genotype, though the evidence is preliminary. APOE4 carriers considering keto for cognitive purposes should discuss genetic testing results with their physician.
If you are cognitively healthy and not managing a specific condition, a Mediterranean or MIND diet with optional MCT oil is likely a better strategy than a full ketogenic diet. It provides broader nutritional coverage, stronger overall evidence for cognitive outcomes, and far greater long-term sustainability.
Frequently Asked Questions
How long does keto adaptation take, and will I experience brain fog?
Most people experience some degree of cognitive impairment during the first one to two weeks of a ketogenic diet — the so-called “keto flu.” Symptoms include brain fog, difficulty concentrating, irritability, headache, and fatigue. These are primarily caused by fluid and electrolyte shifts (sodium, potassium, and magnesium losses increase dramatically in early ketosis), glycogen depletion, and the brain’s incomplete adaptation to ketone utilization. Full neurological adaptation — the upregulation of monocarboxylate transporters and ketone-metabolizing enzymes in the brain — takes approximately three to four weeks. Adequate electrolyte supplementation (particularly sodium and magnesium) during the transition period substantially reduces these symptoms.
Is exogenous ketone supplementation as effective as the ketogenic diet?
Exogenous ketones — typically ketone esters or ketone salts — raise blood BHB levels rapidly without dietary carbohydrate restriction. They are being actively studied as a more practical way to deliver ketones to the brain. Myette-Cote and colleagues (2019), in research published in the Journal of Physiology, showed that a ketone monoester beverage rapidly increased blood BHB and improved cognitive performance during experimentally induced hypoglycemia. However, exogenous ketones produce transient elevations lasting a few hours, whereas nutritional ketosis provides sustained ketone availability. Whether intermittent ketone elevation from supplements produces the same long-term neuroprotective effects as sustained dietary ketosis is unknown. The cost of ketone ester supplements is also currently prohibitive for daily use.
Can I do a “cyclical” ketogenic diet for brain benefits?
Cyclical ketogenic diets — alternating periods of strict keto with periods of higher carbohydrate intake — are popular among athletes and in biohacking communities. There is no direct research on cyclical keto and cognitive outcomes. In theory, cycling in and out of ketosis could provide intermittent ketone exposure while mitigating some of the sustainability and nutrient gap concerns of continuous ketosis. However, each transition back into ketosis involves a re-adaptation period, and the frequent carbohydrate refeeding may prevent the deeper metabolic adaptations that occur with sustained ketosis. This approach is speculative and untested for cognitive purposes.
Does the ketogenic diet affect mood and mental health?
There is emerging evidence that ketogenic diets may benefit certain psychiatric conditions. Pilot studies and case series have reported improvements in bipolar disorder, depression, and schizophrenia on ketogenic diets, though the evidence base is still very early. The mechanisms may involve GABA/glutamate balance, reduced neuroinflammation, and improved mitochondrial function — pathways that overlap with the cognitive mechanisms discussed above. However, some individuals report increased anxiety or mood instability on ketogenic diets, and the restrictive nature of the diet can exacerbate disordered eating patterns. Anyone with a psychiatric condition should undertake dietary changes with clinical supervision.
Is a ketogenic diet safe during pregnancy or for children?
A ketogenic diet should not be undertaken during pregnancy without medical supervision. Ketosis during pregnancy has not been well studied, and there are theoretical concerns about the effects of sustained ketosis on fetal brain development. For children, the ketogenic diet is an established medical intervention for epilepsy but should only be implemented under the guidance of a specialized medical team — typically a neurologist and a dietitian experienced in therapeutic ketogenic diets. It is not appropriate as a general dietary approach for children.
Sources
Wilder, R. M. (1921). The effects of ketonemia on the course of epilepsy. Mayo Clinic Proceedings, 2, 307–308.
Neal, E. G., Chaffe, H., Schwartz, R. H., Lawson, M. S., Edwards, N., Fitzsimmons, G., … & Cross, J. H. (2008). The ketogenic diet for the treatment of childhood epilepsy: a randomised controlled trial. The Lancet Neurology, 7(6), 500–506.
Martin-McGill, K. J., Bresnahan, R., Levy, R. G., & Cooper, P. N. (2020). Ketogenic diets for drug-resistant epilepsy. Cochrane Database of Systematic Reviews, (6).
Veech, R. L. (2004). The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions. Annals of the New York Academy of Sciences, 1033, 137–150.
Shimazu, T., Hirschey, M. D., Newman, J., He, W., Shirakawa, K., Le Moan, N., … & Verdin, E. (2013). Suppression of oxidative stress by beta-hydroxybutyrate, an endogenous histone deacetylase inhibitor. Science, 339(6116), 211–214.
Yudkoff, M., Daikhin, Y., Nissim, I., Lazarow, A., & Nissim, I. (2005). Ketogenic diet, amino acid metabolism, and seizure control. Epilepsy Research, 68(2), 153–158.
Cunnane, S. C., Courchesne-Loyer, A., Vandenberghe, C., St-Pierre, V., Fortier, M., Hennebelle, M., … & Bherer, L. (2016). Can ketones help rescue brain fuel supply in later life? Implications for cognitive health during aging and the treatment of Alzheimer’s disease. Alzheimer’s and Dementia, 12(4), 459–472.
Henderson, S. T., Vogel, J. L., Barr, L. J., Garvin, F., Jones, J. J., & Costantini, L. C. (2009). Study of the ketogenic agent AC-1202 in mild to moderate Alzheimer’s disease: a randomized, double-blind, placebo-controlled, multicenter trial. Nutrition and Metabolism, 6(1), 31.
Krikorian, R., Shidler, M. D., Dangelo, K., Couch, S. C., Benoit, S. C., & Clegg, D. J. (2012). Dietary ketosis enhances memory in mild cognitive impairment. Neurobiology of Aging, 33(2), 425.e19–425.e27.
Fortier, M., Castellano, C. A., St-Pierre, V., Myette-Cote, E., Langlois, F., Roy, M., … & Cunnane, S. C. (2021). A ketogenic drink improves cognition in mild cognitive impairment: results of a 6-month RCT. Alzheimer’s Research and Therapy, 13(1), 96.
Grammatikopoulou, M. G., Goulis, D. G., Gkiouras, K., Theodoridis, X., Gkouskou, K. K., Evangeliou, A., … & Bogdanos, D. P. (2020). To keto or not to keto? A systematic review of randomized controlled trials assessing the effects of ketogenic therapy on Alzheimer disease. Advances in Nutrition, 11(6), 1583–1602.
Brinkworth, G. D., Buckley, J. D., Noakes, M., Clifton, P. M., & Wilson, C. J. (2009). Long-term effects of a very low-carbohydrate diet and a low-fat diet on mood and cognitive function. American Journal of Clinical Nutrition, 169(17), 1873–1880.
Ang, Q. Y., Alexander, M., Newman, J. C., Tian, Y., Cai, J., Upadhyay, V., … & Turnbaugh, P. J. (2020). Ketogenic diets alter the gut microbiome resulting in decreased intestinal Th17 cells. Cell, 181(6), 1263–1275.
Olson, C. A., Vuong, H. E., Yano, J. M., Liang, Q. Y., Nusbaum, D. J., & Hsiao, E. Y. (2018). The gut microbiota mediates the anti-seizure effects of the ketogenic diet. Cell, 173(7), 1728–1741.
Cunnane, S. C., Trushina, E., Morland, C., Prigione, A., Casadesus, G., Andrews, Z. B., … & Bhatt, D. L. (2020). Brain energy rescue: an emerging therapeutic concept for neurodegenerative disorders of ageing. Nature Reviews Drug Discovery, 19(9), 609–633.
Murray, A. J., Knight, N. S., Cole, M. A., Cochlin, L. E., Carter, E., Tchabanenko, K., … & Clarke, K. (2016). Novel ketone diet enhances physical and cognitive performance. Frontiers in Physiology, 7, 196.
Batch, J. T., Lamsal, S. P., Adkins, M., Sultan, S., & Ramirez, M. N. (2020). Advantages and disadvantages of the ketogenic diet: a review article. Nutrients, 12(3), 637.