It’s a fishy situation: On the one hand, multiple scientific studies have found that eating seafood helps protect against dementia. On the other hand (or fin), seafood also is a source of the element mercury, which has been thought to cause damage to cells in the brain, contributing to cognitive impairment.
Now a study lead by researchers from Rush University Medical Center has provided the first report on the relationship of brain concentrations of mercury to brain neuropathology and diseases associated with dementia. Study results were published in the Feb. 2 issue of the Journal of the American Medical Association.
Even though mercury levels in the brain increased with seafood consumption, the researchers found that the increase in mercury levels were not associated with increased brain neuropathologies (i.e., harm to the brain). Rather, they found that seafood consumption was associated with less Alzheimer’s disease neuropathology despite the increased mercury levels. Further, the protective association of seafood was only observed among individuals with a common genotype (APOE-e4) that increases the risk of developing Alzheimer’s disease. The APOE is a gene involved in cholesterol transport to neurons.
The same research study also found no correlation between consumption of fish oil supplements and brain neuropathologies. However, no firm conclusions can be derived because of the low frequency of fish oil supplement use in this study population. “Seafood consumption is promoted for its many health benefits even though it’s contaminated by mercury,” says Martha Clare Morris, ScD, a Rush nutritional epidemiologist who led the study. “Since mercury is a known neurotoxin, we wanted to determine whether seafood consumption is correlated with increased brain mercury levels in older adults, and also whether seafood consumption or brain mercury levels are correlated with brain neuropathologies.”
The researchers found that seafood consumption was significantly correlated with less Alzheimer disease pathology, including lower density of amyloid plaques in the brain and less severe and widespread tangles within the neurons. Whereas plaques and tangles are the defining features of Alzheimer’s dementia (characterized clinically by memory loss and decline in other thinking abilities), data suggest that some degree of plaques and tangles accumulate in the brains of most adults, even those without dementia.
The study findings were derived from 286 postmortem brain autopsies performed on a cohort of individuals initially free of dementia that the researchers followed for an average of 4.5 years until their death. Tissue concentrations of mercury and selenium were measured using instrumental neutron activation analyses. The comparatively large number of brains analyzed decreases the likelihood that the findings are due to chance.
The participants’ seafood intake was measured by multiple food frequency questionnaires completed in the years before their death. The level of seafood intake in the study population was moderate, and therefore the findings cannot be generalized to populations with higher seafood consumption or to populations with high mercury exposure.
It is likely that the types of fish consumed by the study participants reflect the top 10 consumed species in the U.S., which have low to moderate levels of mercury. Nevertheless, the levels of mercury in the study population were comparable to levels previously reported for cortical brain regions.
The National Institute of Aging and the National Institute of Environmental Health Sciences funded the study.
The study done by Rush University Medical Center.
