Association observed in nonsmokers who drank more than two cups daily
A long-term study published online December 9, 2015, in the journal Neurology reports an association between midlife milk consumption and signs of Parkinson’s disease-related neuron loss in the brain. Researchers examined whether milk intake in midlife relates to neuron density in the substantia nigra, a brain region that degenerates in Parkinson’s disease, and whether residues of an organochlorine pesticide, heptachlor epoxide, might be involved.
“Previous studies have suggested links between dairy products and Parkinson’s disease,” said R. D. Abbott, PhD, of Shiga University of Medical Science, the study’s lead author. “This study focused specifically on milk and postmortem signs of neuron loss in the substantia nigra.”
The analysis used data from 449 Japanese-American men (average age 54 at baseline) who were part of the Honolulu-Asia Aging Study. Participants were followed for more than 30 years and examined after death through brain autopsy. Investigators measured neuron density in the substantia nigra and, in a subset of 116 brains, tested for residues of heptachlor epoxide, an organochlorine pesticide that was detected at unusually high levels in the milk supply in Hawaii in the early 1980s when it was used in pineapple agriculture.
The study found that nonsmokers who consumed more than 16 ounces of milk per day (roughly more than two cups) had substantially lower neuron density in the substantia nigra than those who drank less milk. Specifically, after excluding cases of diagnosed Parkinson’s disease and dementia with Lewy bodies, adjusted neuron density was about 41.5% lower in high milk consumers in most quadrants of the substantia nigra (95% confidence interval 22.7%–55.7%, p < 0.001). Among men who had ever smoked, the researchers found no association between milk intake and neuron density, consistent with prior observations that smoking is linked to a lower risk of developing Parkinson’s disease.
Heptachlor epoxide residues were more often detected in brains of men who reported the highest milk consumption: residues appeared in 90% of brains from men who drank the most milk compared with 63% of brains from those who reported no milk intake. Abbott emphasized that the study did not directly confirm heptachlor epoxide contamination in the actual milk consumed by participants. The findings show an association but do not prove causation between milk intake, pesticide residues, and neuron loss consistent with Parkinson’s disease pathology.
Honglei Chen, MD, PhD, of the National Institute of Environmental Health Sciences and author of an accompanying editorial, noted several possible explanations for the observed association, including chance. Chen also pointed out a key limitation: milk intake was recorded only once at the start of the study (1965–1968), and researchers assumed this single measure reasonably reflected long-term dietary habits.
Despite limitations, the study provides an important epidemiological contribution to understanding potential environmental and dietary factors associated with Parkinson’s disease, highlighting the need for further research into whether organochlorine pesticide contamination of milk contributes to substantia nigra neurodegeneration.
Funding: The research received support from the National Institute on Aging, the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, the Department of the Army, the Department of Veterans Affairs, and Kuakini Medical Center.
Source: Rachel Seroka, American Academy of Neurology press coverage. Image credit: public domain image. Original research: “Midlife milk consumption and substantia nigra neuron density at death,” published online December 9, 2015, by Robert D. Abbott et al. in Neurology.
Abstract
Midlife milk consumption and substantia nigra neuron density at death
Objective: To investigate whether midlife milk intake is associated with later-life loss of neurons in the substantia nigra and with brain residues of organochlorine pesticides in decedents from the Honolulu-Asia Aging Study.
Methods: Milk intake was assessed between 1965 and 1968 for 449 men aged 45–68 who later underwent postmortem brain examination (1992–2004). Neuron density (count/mm2) was measured in quadrants of transverse substantia nigra sections. In 116 brains, residues of heptachlor epoxide were also measured; this pesticide had been detected at high concentrations in Hawaii’s milk supply in the early 1980s.
Results: Among nonsmoking decedents, neuron density was lowest in those reporting high milk consumption (>16 oz/day). After excluding cases with Parkinson’s disease and dementia with Lewy bodies, adjusted neuron density in most quadrants was 41.5% lower for high milk intake compared with lower intake (95% CI 22.7%–55.7%, p < 0.001). Heptachlor epoxide residues appeared in 9 of 10 brains from the highest milk consumers versus 63.4% (26/41) of brains from non-milk drinkers (p = 0.017). No association between milk intake and neuron density was observed in men who had ever smoked.
Conclusions: Midlife milk intake was associated with substantia nigra neuron loss in decedent brains without clinical Parkinson’s disease. Further research is needed to determine whether organochlorine pesticide contamination of milk contributes to substantia nigra neurodegeneration and to clarify mechanisms linking dairy consumption and Parkinson’s disease risk.