Continuous electronic fetal monitoring during prolonged labor may be a risk factor for having a child diagnosed with autism spectrum disorder.

In just 50 years the prevalence of autism spectrum disorder has vaulted from extremely rare to common in every community. During this time, a large body of scientific literature has been amassed regarding what environmental, genetic, maternal, or obstetric factors may be at work. The hypothesis presented here identifies two developments in today's childbirth experience that, in combination, may provide the key: 1) a significant increase in the mean duration of labor and 2) the adoption of continuous electronic fetal monitoring utilizing Doppler ultrasound as the standard of care even in low-risk pregnancies. Together, these two factors have created an unprecedented fetal environment that has the potential to affect neuronal migration and cause non-inherited genetic disruptions. This paper will briefly describe the nature and history of contributing factors, why there may be a link between evolving maternal characteristics, obstetric trends and the increase in autism, as well as the means by which the hypothesis can be tested.

Low-dose X-ray imaging may increase the risk of neurodegenerative diseases.

The hypothesis presented here explores the possibility that X-ray imaging commonly used in dental practices may be a shared risk factor for sporadic dementias and motor-neuron diseases. As the evidence will suggest, the brain is ill-equipped to manage the intrusion of low-dose ionizing radiation (IR) beyond that which is naturally occurring. When the brain's antioxidant defenses are overwhelmed by IR, it produces an abundance of reactive oxygen species (ROS) that can lead to oxidative stress, mitochondrial dysfunction, loss of synaptic plasticity, altered neuronal structure and microvascular impairment that have been identified as early signs of neurodegeneration in Alzheimer's disease, Parkinson's, amyotrophic lateral sclerosis, vascular dementia and other diseases that progressively damage the brain and central nervous system. Although genes play a role in all outcomes, the focus here will be on the non-genetic processes at work. Common assumptions regarding the risks of low-dose IR will be addressed, such as: 1) comparing rapid, repeated bursts of man-made IR sent exclusively into the head to equivalent amounts of head-to-toe background IR over longer periods of time; 2) whether epidemiological studies that dismiss concerns regarding low-dose IR due to lack of evidence it causes cancer, heritable mutations or shortened life spans also apply to neurodegeneration; and 3) why even radiation-resistant neurons can be severely impacted by IR exposure, due to IR-induced injury to the processes they need to function. Also considered will be the difficulty of distinguishing the effects of dental X-ray exposure from similarly low amounts of background IR and where to find the evidence that they may, in fact, be responsible for neurodegeneration. Finally, the long-standing belief that whatever risks are inherent in dental radiography must be undertaken for the sake of oral health is challenged on two counts: 1) while dentists continue to drape their patients in lead-lined aprons, the most effective IR safety precautions are often ignored; and 2) there is an alternative dental imaging technology that does not use IR. While the thrust of this article will be on dental radiation and will touch on how age, gender, X-ray equipment and protocols may increase risk, chiropractic radiographs also will be considered because they focus exclusively on the central nervous system. If X-ray imaging is found to be associated with neurodegeneration, the risk-versus-benefit must be reevaluated, every means of reducing exposure implemented and imaging protocols revised.

Dental X-ray exposure and Alzheimer's disease: a hypothetical etiological association.

Despite the fact that Alzheimer's disease was identified more than 100 years ago, its cause remains elusive. Although the chance of developing Alzheimer's disease increases with age, it is not a natural consequence of aging. This article proposes that dental X-rays can damage microglia telomeres - the structures at the end of chromosomes that determine how many times cells divide before they die - causing them to age prematurely. Degenerated microglia lose their neuroprotective properties, resulting in the formation of neurofibrillary tau tangles and consequently, the neuronal death that causes Alzheimer's dementia. The hypothesis that Alzheimer's is caused specifically by microglia telomere damage would explain the delay of one decade or longer between the presence of Alzheimer's brain pathology and symptoms; telomere damage would not cause any change in microglial function, it would just reset the countdown clock so that senescence and apoptosis occurred earlier than they would have without the environmental insult. Once microglia telomere damage causes premature aging and death, the adjacent neurons are deprived of the physical support, maintenance and nourishment they require to survive. This sequence of events would explain why therapies and vaccines that eliminate amyloid plaques have been unsuccessful in stopping dementia. Regardless of whether clearing plaques is beneficial or harmful - which remains a subject of debate - it does not address the failing microglia population. If microglia telomere damage is causing Alzheimer's disease, self-donated bone marrow or dental pulp stem cell transplants could give rise to new microglia populations that would maintain neuronal health while the original resident microglia population died.