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While the alleged link between vaccines — particularly the measles, mumps, and rubella (MMR) vaccine — and autism has been thoroughly discredited in more than 20 well-conducted studies of vaccine side effects , fears about the side effects of vaccination nevertheless remain a major factor influencing the healthcare decisions some parents make. This has led to an increasing percentage of unvaccinated children in the U.S. in recent years, which in turn has ramifications for public health.
A recent study published in the Journal of the American Medical Association, however, sheds new light on physiological roots — though not causes — of autism , and in so doing rules out the potential for any link between vaccination and development of the disease. In the study, researchers examined the size and number of neurons in the prefrontal cortex of young deceased males with autism, and compared the data to that obtained from young deceased non-autistic males.
With data adjusted for age, compared to the control brains (brains of children without autism), brains of autistic children had 67% more neurons in a region called the prefrontal cortex, which is associated with cognitive development, communication, and social and emotional function. The brains of the autistic children were also significantly heavier (by an average of 17.6%) than those of the non-autistic children, despite the fact that brain weight didn’t vary significantly among non-autistic children (average variation of 0.2%).
While this was a preliminary study involving only 13 children, the data nevertheless reveal significant differences between the brains of autistic and non-autistic children. Total neuron number and brain weight aside, there was another difference between the autistic and non-autistic brains: those of non-autistic children showed better correlation between neuron number and brain weight. That is to say, while both neuron number and brain weight were greater in autistic children than in non-autistic children, the increased weight of the brain was less than expected based upon the greatly increased number of neurons. This suggests a neural pathology, rather than simply a “larger than normal” brain.
Cortical neurons, such as those in the prefrontal cortex, proliferate between about 10 and 20 weeks of gestation — that is to say, prenatally — and no longer proliferate once a baby has been born. As such, the study authors point out, the tremendously increased neuron count suggests that autism has its roots in prenatal development, as opposed to being caused by exposure to some causative agent (including vaccinations) during infancy or toddlerhood.
The study did not attempt to determine the ultimate cause of autism, nor did the authors speculate as to whether the neural pathology was due to over-proliferation of neurons prenatally, failure of normal apoptosis, or both.
It’s not unreasonable to hypothesize, however, that — particularly as the brain changes associated with autism appear to happen prenatally — a combination of factors could be involved. Animal studies show that gene dysregulation can result in neuronal overabundance , and the emerging field of epigenetics has demonstrated the potential of environmental factors to turn genes off and on.
Autism researchers still have much to learn about the mechanisms by which children become susceptible to and develop autism — and more importantly, about what might be done to prevent it. Still, by revealing that autism is, in all likelihood, determined prenatally, medical researchers can help parents to focus their concerns and make more accurate risk-to-benefit judgements regarding early childhood health decisions, such as vaccination schedules. As the number of vaccinations has risen over the years, parents and physicians often discuss alternative vaccination schedules.
- Poland GA. MMR Vaccine and Autism: Vaccine Nihilism and Postmodern Science. Mayo Clin Proc. 2011 Sep;86(9):869-71.
- Courchesne et al. Neuron number and size in prefrontal cortex of children with autism. JAMA. 2011 Nov 9;306(18):2001-10.
- Chenn and Walsh. Regulation of cerebral cortical size by control of cell cycle exit in neural precursors. Science. 2002 Jul 19;297(5580):365-9.