Ketogenic Diet in Autism and Core Symptoms

Ketogenic Diet Improves Core Symptoms of Autism in BTBR Mice.


AUTISM SPECTRUM DISORDERS SHARE THREE CORE SYMPTOMS: impaired sociability, repetitive behaviors and communication deficits. Incidence is rising, and current treatments are inadequate.

Seizures are a common comorbidity, and since the 1920’s a high-fat, low-carbohydrate ketogenic diet has been used to treat epilepsy. Evidence suggests the ketogenic diet and analogous metabolic approaches may benefit diverse neurological disorders.

Here we show that a ketogenic diet improves autistic behaviors in the BTBR mouse. Juvenile BTBR mice were fed standard or ketogenic diet for three weeks and tested for sociability, self-directed repetitive behavior, and communication.

In separate experiments, spontaneous intrahippocampal EEGs and tests of seizure susceptibility (6 Hz corneal stimulation, flurothyl, SKF83822, pentylenetetrazole) were compared between BTBR and control (C57Bl/6) mice.

Ketogenic diet-fed BTBR mice showed

increased sociability in a three-chamber test,

decreased self-directed repetitive behavior, and

improved social communication of a food preference.

Although seizures are a common comorbidity with autism, BTBR mice fed a standard diet exhibit neither spontaneous seizures nor abnormal EEG, and have increased seizure susceptibility in just one of four tests.

Thus, behavioral improvements are dissociable from any antiseizure effect.

Our results suggest that a ketogenic diet improves multiple autistic behaviors in the BTBR mouse model. Therefore, ketogenic diets or analogous metabolic strategies may offer novel opportunities to improve core behavioral symptoms of autism spectrum disorders.


Early life seizures and autism – Rapamycin might be preventive

We already know that there’s some kind of connection between epilepsy and autism: Children who have seizures as newborns not uncommonly develop autism, and studies indicate that about 40 percent of patients with autism also have epilepsy. New research at Boston Children’s Hospital finds a reason for the link, and suggests a way to break it — using an existing drug that’s already been given safely to children.

In the online journal PLoS ONE, Frances Jensen, MD, in the Department of Neurology and the F.M. Kirby Neurobiology Center at Boston Children’s, and lab members Delia Talos, PhD, Hongyu Sun, MD, PhD, and Xiangping Zhou, MD, PhD, showed in a rat model that early-life seizures not only lead to epilepsy later in life, but also produce autistic-like behaviors.

Drilling deeper, they showed that early seizures hyper-activate a group of signaling molecules collectively known as the mTOR pathway. This increased signaling – above and beyond the normal surge that happens early in life – disrupts the normal balance of connections (synapses) in the rats’ developing brains. The rats go on to develop epilepsy and altered social behavior, and Jensen believes something parallel happens in humans.

But here’s what’s exciting. They did other experiments where they gave the rats the drug rapamycin, which disables the mTOR pathway, before and after seizures. The mice did not show abnormal synapse or circuit development, and were less likely to have seizures later in life. Autistic-like symptoms appeared less often.

This entry was posted in Autism, co-morbid, Environment, epilepsy, Immune System, Inflammation, Mice, Neurology, Physiology, Treatment. Bookmark the permalink.

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