The new work suggests long-ago lead exposure can make an aging person's brain work as if it's five years older than it really is. If that's verified by more research, it means that sharp cuts in environmental lead levels more than 20 years ago didn't stop its widespread effects.
"We're trying to offer a caution that a portion of what has been called normal aging might in fact be due to ubiquitous environmental exposures like lead," says Dr. Brian Schwartz of Johns Hopkins University.
A longitudinal study found that those with higher bone lead levels seemed to age more rapidly.
Hu and his colleagues took a slightly different approach in a 2004 study of 466 men with an average age of 67. Those men took a mental-ability test twice, about four years apart on average. Those with the highest bone lead levels showed more decline between exams than those with smaller levels, with the effect of the lead equal to about five years of aging.
Nobody is claiming that lead is the sole cause of age-related mental decline, but it appears to be one of several factors involved, Hu stressed.
In a study of almost 1,000 persons 50–70 years of age randomly selected from the general population in the Baltimore Memory Study (BMS), a cross-sectional analysis showed that relatively low current blood lead levels were not associated with cognitive domain scores. However, moderate tibia lead levels (mean ~ 19 µg/g) were significantly associated with worse performance in all seven cognitive domains (Shih et al. 2006). Thus, in the environmental studies of older adults, the most consistent findings across studies are associations between bone lead levels and cognitive function. The associations in the BMS were cross-sectional, whereas the predominant associations in the NAS were with change in cognitive function over time, although a significant cross-sectional association with MMSE score was also observed in this sample. Taken together, these data suggest that at environmental exposure levels, the effects of cumulative exposure are more pronounced than recent effects of current exposure. The absence of associations in the Stokes et al. (1998) study could be because of the younger age of studied subjects, the very low current blood and tibia lead levels, or the inadequacy of tibia lead in the third decade of life to estimate early life dose (Hoppin et al. 2000).
So what to do about your accumulated bone lead? One possible long term response might be thiamine (or thiamin - vitamin B1) supplementation. Thamine enhances lead excretion in rodents and also in sheep and other animals.
|Share |||Randall Parker, 2008 January 29 08:50 PM Aging Diet Brain Studies|