A new study has found that higher than normal levels of a thyroid gland hormone, called thyroxine, could put a person at greater risk of developing dementia. This result was published in the journal Neurology by researchers involved in what is known as the Rotterdam Study.
The Rotterdam Study is a population-based cohort study which began in 1990 and recruited close to 10,000 men and women from the Netherlands who were aged 55 years and over. The aim of the study was to investigate factors that determine the occurrence of cardiovascular, neurological, ophthalmological, endocrinological, and psychiatric diseases in elderly people. Participants would fill out medical questionnaires and attend a medical facility for a regular check-ups and tests.
In this study’s analysis, the researchers wanted to look at two specific hormones produced by the thyroid gland – the thyroid-stimulating hormone (TSH) produced by the thyroid gland and free thyroxine, which is actually produced based on levels of TSH and helps control the body’s metabolism. Over the course of the analysis period, 601 participants developed dementia. The researchers noted that dementia risk was higher in individuals with higher levels of free thyroxine. The researcher’s hypothesised that a malfunctioning thyroid gland may impact dementia risk through nonvascular pathways.
This hypothesis does link with previous research which has noted that when the thyroid gland doesn’t function properly, it can release too much or too little of these hormones, making the metabolism run either too fast or too slow. In this study, it seems that dementia risk may be linked to an overproduction of thyroxine, but the ‘why’ remains unknown.
An alternate hypothesis proposed by researchers suggests the possibility that excess free thyroxine may alter gene expression in critical neural pathways or that neurotoxicity secondary to oxidative stress may lead to premature neuronal death.
What the researchers can be certain on however is that further research is needed to better understand the pathways in which thyroid function affects dementia risk, and whether treating this problem can reduce your risk of dementia.