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Abstract

Background: Constipation is frequent in PD, although its onset in relation to clinical PD has not been well described. Demonstration that constipation can precede clinical PD could provide important clues to understanding disease progression and etiology. The purpose of this report is to examine the association between the frequency of bowel movements and the future risk of PD.
Methods: Information on the frequency of bowel movements was collected from 1971 to 1974 in 6790 men aged 51 to 75 years without PD in the Honolulu Heart Program. Follow-up for incident PD occurred over a 24-year period.
Results: Ninety-six men developed PD an average of 12 years into follow-up. Age-adjusted incidence declined consistently from 18.9/10,000 person-years in men with <1 bowel movement/day to 3.8/10,000 person-years in those with >2/day (p = 0.005). After adjustment for age, pack-years of cigarette smoking, coffee consumption, laxative use, jogging, and the intake of fruits, vegetables, and grains, men with <1 bowel movement/day had a 2.7-fold excess risk of PD versus men with 1/day (95% CI: 1.3, 5.5; p = 0.007). The risk of PD in men with <1 bowel movement/day increased to a 4.1-fold excess when compared with men with 2/day (95% CI: 1.7, 9.6; p = 0.001) and to a 4.5-fold excess versus men with >2/day (95% CI: 1.2, 16.9; p = 0.025).
Conclusions: Findings indicate that infrequent bowel movements are associated with an elevated risk of future PD. Further study is needed to determine whether constipation is part of early PD processes or is a marker of susceptibility or environmental factors that may cause PD.

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Letters to the Editor
6 November 2001
Reply to Dr. Lesser's letter
R D Abbott
H Petrovitch, L R White, G W Ross

While further explanation is needed, the long interval between reported constipation and the diagnosis of Parkinson's disease (PD) in our study may provide some insights into the pathogenesis of PD and related histologic changes beginning as early as age 25. [2] Dr. Lesser speculates that infrequent bowel movements might allow neurotoxins greater access to the central nervous system, and that cumulative exposure to certain neurotoxins at low levels over many years might explain the association we observed. While this is an important possibility, one argument against this is that rates of PD seem to be slightly lower in women, even though bowel movement frequency is greater in men. [3].

We favor the idea that some persons may be at increased risk for the development of PD by virtue of a life-long paucity of sympathetic and dopaminergic neural reserves, manifested by constipation as a constitutional gastrointestinal characteristic, and by a lowering of thresholds for the appearance of PD as neurons are lost from the substantia nigra, regardless of the cause of such losses.

We agree with the second observation of Dr. Lesser, as we also note in our paper [1], that there may be underlying environmental factors that can impact the risk of PD. Like many chronic diseases that appear in later life, it is likely that both constitutional and environmental factors contribute to an increased risk of disease. While this may be discouraging to persons hoping to prevent disease with a single intervention, the more realistic view is that strategy for prevention (such as avoiding exogenous neurotoxins) may ultimately be most important and most effective in persons whose risk begins at a high level because of a genetic or constitutional susceptibility.

References:

1. Abbott RD, Petrovitch H, White LR, et al. Frequency of bowel movements and the future risk of Parkinson's disease. Neurology 2001;57:456-462.

2. Gibb WRG, Lees AJ. The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson's disease. J Neurol Neurosurg Psychiatry 1988;51:745-752.

3. Everhart JE, Go VLW, Johannes RS, Fitzsimmons SC, Roth HP, White LR. A longitudinal survey of self-reported bowel habits in the United States. Dig Dis Sci 1989;34:1153-1162.

6 November 2001
Frequency of bowel movements and the future risk of Parkinson's disease
Gerson T Lesser

Abbott et al. [1] have collected unique longitudinal information relating a less frequent bowel habit to greater risk for future Parkinson's disease (PD). However, it is difficult to accept the conclusion that this manifestation of PD (constipation) predates the motor symptoms by so many years. Furthermore, since a particular individual's bowel habit tends to remain nearly constant through adult life, one must assume that the bowel habits of the great majority of those recorded in 1971-1974 had already been "in place" for many years, probably decades. The present findings support this assumption, as intra-individual bowel movements were significantly correlated 20+ years apart. [1] Using this assumption, one can extend the average 12-year interval (observed from 1971-74) from "onset" of constipation to the clinical diagnosis of PD by perhaps two decades and, more reasonably, estimate this interval to be some 25-35 years. From various sources of information, the latency period of presymptomatic PD neurodegeneration has been projected to be as long as 20 years, or as short as <5 years. [2] Even if one accepts and extends the longest of these estimates, an average interval of 25-35 years between an early manifestation of PD (constipation) and the appearance of clinical motor disease seems highly unlikely.

However, a more plausible hypothesis can be advanced to explain the important observations of Abbott et al. [1] It has always been considered that some environmental offender, alone or in various combinations, and perhaps only in susceptible individuals, may damage nigral cells; among those more recently advanced have been manganese or other heavy metals, combinations of metals, herbicides and organochlorine insecticides, [3] and various isoquinoline derivatives structurally related to MPTP. [4] Although enteral absorption and handling of various substances is exceedingly complex, [5] it seems logical that, over years, ingested substances with limited absorption would enter the bloodstream to a greater extent in those with slower intestinal transit. With such an hypothesis, the longer the existence of an infrequent bowel habit the more likely would a susceptible individual absorb sufficient "toxin" to effect the major neruodegeneration leading to full-blown PD.

Another observation of the present authors lends some support to underlying environmental factors in development of PD. [1] It appears that, in their Asian homelands, Orientals have lower prevalence of PD than European or U.S. Caucasians. However, the present report found the prevalence of PD in this cohort of Japanese ancestry living in the U.S. to be approximately the same as that of European or U.S. Caucasians.

References:

1. Abbott RD, Petrovitch H, White LR, et al. Frequency of bowel movements and the future risk of Parkinson's disease. Neurology 2001;57:456-462.

2. Veldman BAJ, Wijn AM, Knoers N, Praamstra P, Horstink MWIM. Genetic and environmental risk factors in Parkinson's disease. Clin Neurol Neurosurg 1998;100:15-26.

3. Corrigan FM, Wienburg CL, Shore RF, Daniel SE, Mann D. Organochlorine insecticides in substantia nigra in Parkinson's disease. J Toxicol Env Health Part A 2000;59:229-234.

4. McNaught KS, Carrupt PA, Altomare C, et al. Isoquinoline derivatives as endogenous neurotoxins in the aetiology of Parkinson's disease. Biochem Pharmacol 1998;56:921-933.

5. Diamond GL, Goodrum PE, Felter SP, Ruoff WL. Gastrointestinal absorption of metals. Drug & Chemical Toxicology 1998;21:223-251.

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Published In

Neurology®
Volume 57Number 3August 14, 2001
Pages: 456-462
PubMed: 11502913

Publication History

Received: January 19, 2001
Accepted: February 7, 2001
Published online: August 14, 2001
Published in print: August 14, 2001

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Affiliations & Disclosures

R. D. Abbott, PhD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
H. Petrovitch, MD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
L. R. White, MD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
K. H. Masaki, MD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
C. M. Tanner, MD, PhD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
J. D. Curb, MD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
A. Grandinetti, PhD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
P. L. Blanchette, MD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
J. S. Popper, MD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.
G. W. Ross, MD
From the Division of Biostatistics and Epidemiology (Dr. Abbott), University of Virginia School of Medicine, Charlottesville; Pacific Health Research Institute (Drs. Abbott, Petrovitch, White, Masaki, Curb, and Ross), Honolulu; Kuakini Medical Center and the Honolulu–Asia Aging Study (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, Popper, and Ross), Honolulu; Department of Medicine (Drs. Abbott, Petrovitch, White, Masaki, Curb, Blanchette, and Ross) and the Pacific Biomedical Research Center (Dr. Grandinetti), University of Hawaii John A. Burns School of Medicine, Honolulu; Parkinson’s Institute (Drs. Tanner and Ross), Sunnyvale, CA; and the Department of Veterans Affairs (Drs. Petrovitch, White, and Ross), Honolulu, HI.

Notes

Address correspondence and reprint requests to Dr. Robert D. Abbott, Pacific Health Research Institute, 846 South Hotel Street, Suite 303, Honolulu, HI 96813-2512; e-mail: [email protected]

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