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Midlife milk consumption and substantia nigra neuron density at death.
Neurology 2016; 86(6):512-9Neur

Abstract

OBJECTIVE

To examine the relationship between midlife milk intake and Parkinson disease (PD) incidence through associations with substantia nigra (SN) neuron density and organochlorine pesticide exposure in decedent brains from the Honolulu-Asia Aging Study.

METHODS

Milk intake data were collected from 1965 to 1968 in 449 men aged 45-68 years with postmortem examinations from 1992 to 2004. Neuron density (count/mm(2)) was measured in quadrants from a transverse section of the SN. Additional measures included brain residues of heptachlor epoxide, an organochlorine pesticide found at excessively high levels in the milk supply in Hawaii in the early 1980s.

RESULTS

Neuron density was lowest in nonsmoking decedents who consumed high amounts of milk (>16 oz/d). After removing cases of PD and dementia with Lewy bodies, adjusted neuron density in all but the dorsomedial quadrant was 41.5% lower for milk intake >16 oz/d vs intake that was less (95% confidence interval 22.7%-55.7%, p < 0.001). Among those who drank the most milk, residues of heptachlor epoxide were found in 9 of 10 brains as compared to 63.4% (26/41) for those who consumed no milk (p = 0.017). For those who were ever smokers, an association between milk intake and neuron density was absent.

CONCLUSIONS

Milk intake is associated with SN neuron loss in decedent brains unaffected by PD. Whether contamination of milk with organochlorine pesticides has a role in SN neurodegeneration warrants further study.

Authors+Show Affiliations

From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco. rda3e@virginia.edu.From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco.From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco.From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco.From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco.From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco.From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco.From the Center for Epidemiologic Research in Asia (R.D.A.), Shiga University of Medical Science, Otsu, Japan; the Pacific Health Research and Education Institute (R.D.A., G.W.R., H.P., J.S.N., L.R.W.), Honolulu; the Department of Medicine (G.W.R.) and the John A. Hartford Foundation Center of Excellence in Geriatrics, Department of Geriatric Medicine (R.D.A., G.W.R., H.P., K.H.M.), John A. Burns School of Medicine, University of Hawaii, Honolulu; the Veterans Affairs Pacific Islands Health Care System (G.W.R., H.P., L.R.W.), Honolulu; Kuakini Medical Center (K.H.M.), Honolulu, HI; the National Institute on Aging (L.J.L.), Bethesda, MD; and the San Francisco Veterans Affairs Medical Center and the Department of Neurology (C.M.T.), University of California, San Francisco.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

26658906

Citation

Abbott, Robert D., et al. "Midlife Milk Consumption and Substantia Nigra Neuron Density at Death." Neurology, vol. 86, no. 6, 2016, pp. 512-9.
Abbott RD, Ross GW, Petrovitch H, et al. Midlife milk consumption and substantia nigra neuron density at death. Neurology. 2016;86(6):512-9.
Abbott, R. D., Ross, G. W., Petrovitch, H., Masaki, K. H., Launer, L. J., Nelson, J. S., ... Tanner, C. M. (2016). Midlife milk consumption and substantia nigra neuron density at death. Neurology, 86(6), pp. 512-9. doi:10.1212/WNL.0000000000002254.
Abbott RD, et al. Midlife Milk Consumption and Substantia Nigra Neuron Density at Death. Neurology. 2016 Feb 9;86(6):512-9. PubMed PMID: 26658906.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Midlife milk consumption and substantia nigra neuron density at death. AU - Abbott,Robert D, AU - Ross,G Webster, AU - Petrovitch,Helen, AU - Masaki,Kamal H, AU - Launer,Lenore J, AU - Nelson,James S, AU - White,Lon R, AU - Tanner,Caroline M, Y1 - 2015/12/09/ PY - 2015/05/14/received PY - 2015/09/09/accepted PY - 2015/12/15/entrez PY - 2015/12/15/pubmed PY - 2016/7/21/medline SP - 512 EP - 9 JF - Neurology JO - Neurology VL - 86 IS - 6 N2 - OBJECTIVE: To examine the relationship between midlife milk intake and Parkinson disease (PD) incidence through associations with substantia nigra (SN) neuron density and organochlorine pesticide exposure in decedent brains from the Honolulu-Asia Aging Study. METHODS: Milk intake data were collected from 1965 to 1968 in 449 men aged 45-68 years with postmortem examinations from 1992 to 2004. Neuron density (count/mm(2)) was measured in quadrants from a transverse section of the SN. Additional measures included brain residues of heptachlor epoxide, an organochlorine pesticide found at excessively high levels in the milk supply in Hawaii in the early 1980s. RESULTS: Neuron density was lowest in nonsmoking decedents who consumed high amounts of milk (>16 oz/d). After removing cases of PD and dementia with Lewy bodies, adjusted neuron density in all but the dorsomedial quadrant was 41.5% lower for milk intake >16 oz/d vs intake that was less (95% confidence interval 22.7%-55.7%, p < 0.001). Among those who drank the most milk, residues of heptachlor epoxide were found in 9 of 10 brains as compared to 63.4% (26/41) for those who consumed no milk (p = 0.017). For those who were ever smokers, an association between milk intake and neuron density was absent. CONCLUSIONS: Milk intake is associated with SN neuron loss in decedent brains unaffected by PD. Whether contamination of milk with organochlorine pesticides has a role in SN neurodegeneration warrants further study. SN - 1526-632X UR - https://www.unboundmedicine.com/medline/citation/26658906/full_citation L2 - http://www.neurology.org/cgi/pmidlookup?view=long&amp;pmid=26658906 DB - PRIME DP - Unbound Medicine ER -