Study finds ketogenic diet improves memory in adults with cognitive impairment

ketogenic

Recent findings suggest that a very low-carbohydrate diet may boost memory in older adults with mild cognitive impairment.

Under fairly extreme low-carb conditions, the body starts to use compounds called ketones, made from the metabolism of fat or protein, as a source of fuel. This state, ketosis, occurs naturally and is quite different from ketoacidosis which is a serious problem caused by severe metabolic disturbances.


A new study tested a ketogenic diet in people with mild cognitive impairment, sometimes a precursor to dementia. For six weeks, half of the 23 participants ate a ketogenic diet, with five to 10 percent of calories coming from carbohydrates, while the others ate a high-carbohydrate diet, 50 percent of calories from carbohydrates.


Those on the ketogenic diet showed significant improvements in verbal memory compared to the other group. The higher their ketone levels, measured in urine, the better their verbal memory.


Robert Krikorian, Ph.D., of the University of Cincinnati, Ohio, and colleagues believe that ketones provide ready fuel for the brain, and may enhance cognitive function.


They report in the journal that the ketosis group also saw significant benefits in terms of weight loss and waist circumference reduction, as well as reductions in fasting blood glucose and insulin levels.


"These findings indicate that very low carbohydrate consumption, even in the short term, can improve memory function in older adults with increased risk for Alzheimer's disease," they write.


"To our knowledge, these data demonstrate for the first time that carbohydrate restriction can produce memory enhancement in this at-risk population."


The experts point out that this effect may be partly due to a correction of hyperinsulinemia, or excess insulin in the blood, but that "other mechanisms associated with ketosis such as reduced inflammation and enhanced energy metabolism also may have contributed to improved neurocognitive function."


Finding new approaches to tackling mild cognitive impairment is crucial, they add, as there are currently 5.3 million cases of Alzheimer's disease in the United States. This figure is estimated to rise to 16 million by the year 2050, and there is no cure.


"Accordingly, prevention and mitigation of risk will be essential to reduce the impact of this ominous public health problem," said Krikorian and colleagues.


They explain that interventions begun in individuals with pre-dementia conditions such as mild cognitive impairment might halt progression of cognitive decline. It's also the case that rates of obesity and diabetes are reaching epidemic proportions.


"The co-occurrence of dementia and metabolic disease reflects the fact that metabolic disturbance is a fundamental factor contributing to neurodegeneration," said the authors.


Type II diabetes is known to increase the risk of dementia. Some studies suggest that 39 percent of Alzheimer's cases are due solely to excess insulin, which occurs in response to insulin resistance.


Overall, excess insulin in the blood can accelerate neurodegenerative processes via dysregulation of insulin receptors and pro-inflammatory molecules. Proper regulation of these pro-inflammatory molecules is essential to memory function, and to avoid the buildup of beta amyloid plaques in the brain.


"Dietary approaches to dementia prevention represent interesting and underutilized interventions," the team says.


Previous work indicates that a higher intake of fruits and vegetables may lower the risk of cognitive decline and dementia. This effect could be due in part to regulation of inflammation, as with the insulin-lowering ketosis diet.


They point out that the ketogenic diet has been used to suppress epileptic seizures since the 1920s, though it fell out of favor when pharmacological therapies were developed.


"There are indications that ketone metabolism may be beneficial in other clinical conditions," the team said, because it protects against neuronal damage and slows neurodegeneration, compared with glucose metabolism.


"As compared with glucose metabolism, central ketone metabolism generates lower levels of oxidative stress, which has also been identified as a fundamental factor contributing to neurodegeneration," they add.


The authors call for further investigation of this type of diet to measure its "preventive potential and mechanisms of action in the context of early neurodegeneration."


Discovering the mechanisms of neural action of the diet, including metabolic and neuroprotective factors in conjunction with neurocognitive effects, "will be of particular interest and should have implications for understanding the etiology of neurodegeneration," they write.


Finally, it is important to know whether the benefits of the diet persist once an individual returns to their normal diet.




"Should this approach prove to to have benefit beyond the period of intervention, it might be applied briefly and intermittently as a prophylactic strategy, an approach that would mitigate many concerns about chronic, severe carbohydrate restriction," they concluded.
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