Effects of Low-Carb Diet on the Brain

These listings are quoted from scientific and medical journals. At then end of each listing, you'll find an expanation in jargon-free English. Every effort was made to keep the explanations true to the original article. However, bear in mind that the explanations were not written by a medical professional, and may contain errors. In a few places, I added my own thoughts. I've tried to mark what's my opinion and what is fact. Let us know if you have any suggestions for improvements or corrections.

Sincerely, Joshua M. Yelon

Effects of unbalanced diets on cerebral glucose metabolism in the adult rat.

al-Mudallal AS, Levin BE, Lust WD, Harik SI. Department of Neurology, Case Western Reserve University School of Medicine, Cleveland, OH, USA.
Neurology 1995 Dec;45(12):2261-2265

We measured regional cerebral metabolic rates for glucose and selected cerebral metabolites in rats fed one of the following diets for 6 to 7 weeks: (1) regular laboratory chow; (2) high-fat, carbohydrate-free ketogenic diet deriving 10% of its caloric value from proteins and 90% from fat; and (3) high-carbohydrate diet deriving 10% of its caloric value from proteins, 78% from carbohydrates, and 12% from fat. In preliminary experiments, we found that moderate ketosis could not be achieved by diets deriving less than about 90% of their caloric value from fat. Rats maintained on the ketogenic diet had moderately elevated blood beta-hydroxybutyrate (O.4 mM) and acetoacetate (0.2 mM), and a five- to 10-fold increase in their cerebral beta-hydroxybutyrate level. Cerebral levels of glucose, glycogen, lactate, and citrate were similar in all groups. 2-Deoxyglucose studies showed that the ketogenic diet did not significantly alter regional brain glucose utilization. However, rats maintained on the high-carbohydrate diet had a marked decrease in their brain glucose utilization and increased cerebral concentrations of glucose 6-phosphate. These findings indicate that long-term moderate ketonemia does not significantly alter brain glucose phosphorylation. However, even marginal protein dietary deficiency, when coupled with a carbohydrate-rich diet, depresses cerebral glucose utilization to a degree often seen in metabolic encephalopathies. Our results support the clinical contention that protein dietary deficiency coupled with increased carbohydrate intake can lead to CNS dysfunction.

Comments: The brain's primary fuel is glucose. Some people worry that on a low-carb diet, there would be a shortage of glucose to fuel the brain. So they tested it on rats. They gave the rats a low-carb diet. Of course, the usual low-carb things happened: their blood glucose dropped, and their livers started manufacturing ketones (ketosis). After a while, they checked the rats' brains. First, they found that while the blood glucose was low, the brains contained the normal amounts. This means the body was making sure that the brain had enough glucose, and was not having a problem doing it. Second, they found that the ketones were going straight to the brain. Now, ketones are a fuel source. So, very likely, this means that the brain was using ketone as a substitute fuel, to keep from running down the glucose supply. Meanwhile, the group that ate the low-fat diet ended up with a protein deficiency. This deficiency made it difficult for their brains to use glucose. In short, the brains of the low-carb rats received adequate energy supplies, the brains of the low-fat dieters were damaged by energy shortages.