This article is really complicated with lots of tabs to open so you can review the results of the research, so I'm just providing the abstract and the conclusions, however, from my limited knowledge of nutrition and chemistry, I'd say it's worth a try.
Advances in Nutrition, Volume 11, Issue 6, November 2020, Pages 1583–1602, https://doi.org/10.1093/advances/nmaa073
Published: 29 June 2020
ABSTRACT
Alzheimer disease (AD) is a global health concern with the majority of pharmacotherapy choices consisting of symptomatic treatment. Recently, ketogenic therapies have been tested in randomized controlled trials (RCTs), focusing on delaying disease progression and ameliorating cognitive function. The present systematic review aimed to aggregate the results of trials examining the effects of ketogenic therapy on patients with AD/mild cognitive impairment (MCI). A systematic search was conducted on PubMed, CENTRAL, clinicaltrials.gov, and gray literature for RCTs performed on adults, published in English until 1 April, 2019, assessing the effects of ketogenic therapy on MCI and/or AD compared against placebo, usual diet, or meals lacking ketogenic agents. Two researchers independently extracted data and assessed risk of bias with the Cochrane tool. A total of 10 RCTs were identified, fulfilling the inclusion criteria. Interventions were heterogeneous, acute or long term (45–180 d), including adherence to a ketogenic diet, intake of ready-to-consume drinks, medium-chain triglyceride (MCT) powder for drinks preparation, yoghurt enriched with MCTs, MCT capsules, and ketogenic formulas/meals. The use of ketoneurotherapeutics proved effective in improving general cognition using the Alzheimer's Disease Assessment Scale-Cognitive, in interventions of either duration. In addition, long-term ketogenic therapy improved episodic and secondary memory. Psychological health, executive ability, and attention were not improved. Increases in blood ketone concentrations were unanimous and correlated to the neurocognitive battery based on various tests. Cerebral ketone uptake and utilization were improved, as indicated by the global brain cerebral metabolic rate for ketones and [11C] acetoacetate. Ketone concentrations and cognitive performance differed between APOE ε4(+) and APOE ε4(−) participants, indicating a delayed response among the former and an improved response among the latter. Although research on the subject is still in the early stages and highly heterogeneous in terms of study design, interventions, and outcome measures, ketogenic therapy appears promising in improving both acute and long-term cognition among patients with AD/MCI.
Alzheimer disease (AD) is a global health concern with the majority of pharmacotherapy choices consisting of symptomatic treatment. Recently, ketogenic therapies have been tested in randomized controlled trials (RCTs), focusing on delaying disease progression and ameliorating cognitive function. The present systematic review aimed to aggregate the results of trials examining the effects of ketogenic therapy on patients with AD/mild cognitive impairment (MCI). A systematic search was conducted on PubMed, CENTRAL, clinicaltrials.gov, and gray literature for RCTs performed on adults, published in English until 1 April, 2019, assessing the effects of ketogenic therapy on MCI and/or AD compared against placebo, usual diet, or meals lacking ketogenic agents. Two researchers independently extracted data and assessed risk of bias with the Cochrane tool. A total of 10 RCTs were identified, fulfilling the inclusion criteria. Interventions were heterogeneous, acute or long term (45–180 d), including adherence to a ketogenic diet, intake of ready-to-consume drinks, medium-chain triglyceride (MCT) powder for drinks preparation, yoghurt enriched with MCTs, MCT capsules, and ketogenic formulas/meals. The use of ketoneurotherapeutics proved effective in improving general cognition using the Alzheimer's Disease Assessment Scale-Cognitive, in interventions of either duration. In addition, long-term ketogenic therapy improved episodic and secondary memory. Psychological health, executive ability, and attention were not improved. Increases in blood ketone concentrations were unanimous and correlated to the neurocognitive battery based on various tests. Cerebral ketone uptake and utilization were improved, as indicated by the global brain cerebral metabolic rate for ketones and [11C] acetoacetate. Ketone concentrations and cognitive performance differed between APOE ε4(+) and APOE ε4(−) participants, indicating a delayed response among the former and an improved response among the latter. Although research on the subject is still in the early stages and highly heterogeneous in terms of study design, interventions, and outcome measures, ketogenic therapy appears promising in improving both acute and long-term cognition among patients with AD/MCI.
Conclusions
Currently, there are no approved drugs to delay or halt the progress of cognitive decline in AD (124). Although faith in the therapeutic effects of the KD was initially attributed to Hippocrates (136), research on ketoneurotherapeutics for AD appears young. The results underline that, collectively, the efficacy of ketogenic therapy in MCI/AD appears promising, indicating that it is more than a symptomatic remedy (137). Nevertheless, research is still scattered and heterogeneous in terms of study design, intervention, participants, and outcomes of interest. Predefining a set of important outcomes for relevant RCTs would add weight to the evidence and aid toward the development of recommendations advocating for the usefulness of ketogenic therapy in AD. Thus, apart from reviewing the available RCTs assessing the efficacy of ketoneurotherapeutics on AD, the present study can also serve as a primer for the design of future clinical trials, to support public health translation and promote the KD as an evidence-based AD prescription remedy.
Currently, there are no approved drugs to delay or halt the progress of cognitive decline in AD (124). Although faith in the therapeutic effects of the KD was initially attributed to Hippocrates (136), research on ketoneurotherapeutics for AD appears young. The results underline that, collectively, the efficacy of ketogenic therapy in MCI/AD appears promising, indicating that it is more than a symptomatic remedy (137). Nevertheless, research is still scattered and heterogeneous in terms of study design, intervention, participants, and outcomes of interest. Predefining a set of important outcomes for relevant RCTs would add weight to the evidence and aid toward the development of recommendations advocating for the usefulness of ketogenic therapy in AD. Thus, apart from reviewing the available RCTs assessing the efficacy of ketoneurotherapeutics on AD, the present study can also serve as a primer for the design of future clinical trials, to support public health translation and promote the KD as an evidence-based AD prescription remedy.
A second review: probably a lot of duplication.
Ketogenic Diet for the Treatment and
Prevention of Dementia: A Review.
Journal of Geriatric Psychiatry
and Neurology
2021, Vol. 34(1) 3-10 (excerpt)
The ketogenic diet is a high-fat and low carbohydrate-based diet. It is thought to simulate the metabolic effects of starvation by forcing the body away from its traditional fuel source, glucose, to primarily use fats. Fats are converted by the body to various ketone bodies (eg, acetoacetate, b-hydroxybutyrate, and acetone) used by the cells for fuel. This diet was originally described in the 1920s after the observation of the beneficial effects of starvation on seizure frequency in children with epilepsy.18 The keys to a ketogenic diet are to limit total caloric intake and, more importantly, carbohydrate intake. In this diet, total daily carbohydrate intake is typically limited to 10 to 50 grams or 5% to 10% of total caloric intake.19,21,22 It is important to note that a ketogenic diet differs from other low-carbohydrate diets. The level of carbohydrates in a ketogenic diet is drastically lower than that of most traditional “low-carbohydrate” diets used for weight loss. One form of the various ketogenic diet protocols uses large amounts of medium-chain triglycerides (MCT) as part of the diet to help enhance ketone production.23 Shorter than traditional triglyceride chains, MCTs are transported more directly to the liver and enter without the assistance of carnitine, a metabolic compound responsible for the transport of fatty acid chains that are broken down for energy. The MCTs are more rapidly broken down into ketones and energy. Regardless of specific carbohydrate consumption levels, the essential goal of the ketogenic diet is the production of ketone bodies. The degree of ketone body production will vary by individual and diet factors. Some people using this diet will even test themselves for ketones using either blood or urine to ensure the adequacy of their regimen.
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