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Does coffee protect against the development of Parkinson disease (PD)?
BACKGROUND: The suffering of patients with PD is substantial, and understanding risk factors for its development could make prevention or amelioration of its course possible. This prospective cohort study evaluated the effect of coffee and caffeine on the development of PD.
POPULATION STUDIED: A total of 8004 Japanese American men aged between 45 and 68 years were enrolled in the Honolulu Heart Program between 1965 and 1968. The subjects were identified through World War II selective services files; the median age was 53 years at enrollment. Women, other races, and younger men were not represented in this study, so family physicians should be cautious about generalizing the results to those patients.
STUDY DESIGN AND VALIDITY: This prospective cohort study was initiated more than 30 years ago. Caffeine and coffee intake was assessed at enrollment by 24-hour dietary recall, and 6 years later by food frequency questionnaire. Incident cases of PD were identified by review of hospitalization records, death certificates, and local neurologists’ records using well-established published case definitions and after 1991 direct examination of the entire cohort by a study neurologist. Proportional hazards modeling was used to adjust for age and cigarette smoking and to assess potential confounding by alcohol intake, dietary fat, physical activity, cholesterol, hypertension, and diabetes. This study was well done. Its strengths include its prospective design, rigorous assessment of dietary intake, excellent follow-up, careful case ascertainment, and assessment for a variety of confounding variables. Minor weaknesses include the lack of reviewers blind to exposure and the possibility of other confounding variables, such as medical treatments or dietary trace elements.
OUTCOMES MEASURED: The primary outcome was the relative risk of PD for different levels of coffee and caffeine consumption. The authors did not measure the clinical outcomes of PD, such as functional status or quality of life, which might be valuable for primary care physicians who are considering advising substantial lifestyle change to prevent PD.
RESULTS: A total of 8004 subjects (99.9% of the original cohort) were followed for an average of 27 years; 102 cases of PD were identified. The adjusted relative risk of developing PD was 5.1 (95% confidence interval, 1.8-14.4; number needed to treat=125) for noncoffee drinkers compared with those who drank 28 ounces or more of coffee per day. A dose-response relationship was observed; higher amounts of daily coffee intake were associated with lower relative risks of PD. This relationship was also seen with caffeine and caffeine derived from noncoffee sources. Other nutrients found in coffee (ie, niacin) or used in coffee (ie, milk or sugar) were analyzed and found to have no impact on the relationship observed between coffee and PD.
This well-designed prospective study provides good evidence that an inverse relationship exists between coffee intake and the development of PD and suggests that caffeine may be an important mediator of this effect. However, a single study does not prove that coffee is protective. The mechanism by which coffee may protect against PD is not understood, and confounding variables not measured in this study could be responsible for the results obtained. Consistent findings with multiple well-designed studies in a variety of populations are needed before a causal relationship can be established.
Should family physicians advise patients to drink coffee? The prevalence of PD in family practice is significant but still relatively small. The increased rate of PD for patients with more usual amounts of coffee each day (4-28 oz/day) is modest. There may also be health risks of drinking large amounts of coffee per day, although few have been identified in the literature. Clinicians should not counsel patients to drink coffee to protect against PD until more data become available.
BACKGROUND: The suffering of patients with PD is substantial, and understanding risk factors for its development could make prevention or amelioration of its course possible. This prospective cohort study evaluated the effect of coffee and caffeine on the development of PD.
POPULATION STUDIED: A total of 8004 Japanese American men aged between 45 and 68 years were enrolled in the Honolulu Heart Program between 1965 and 1968. The subjects were identified through World War II selective services files; the median age was 53 years at enrollment. Women, other races, and younger men were not represented in this study, so family physicians should be cautious about generalizing the results to those patients.
STUDY DESIGN AND VALIDITY: This prospective cohort study was initiated more than 30 years ago. Caffeine and coffee intake was assessed at enrollment by 24-hour dietary recall, and 6 years later by food frequency questionnaire. Incident cases of PD were identified by review of hospitalization records, death certificates, and local neurologists’ records using well-established published case definitions and after 1991 direct examination of the entire cohort by a study neurologist. Proportional hazards modeling was used to adjust for age and cigarette smoking and to assess potential confounding by alcohol intake, dietary fat, physical activity, cholesterol, hypertension, and diabetes. This study was well done. Its strengths include its prospective design, rigorous assessment of dietary intake, excellent follow-up, careful case ascertainment, and assessment for a variety of confounding variables. Minor weaknesses include the lack of reviewers blind to exposure and the possibility of other confounding variables, such as medical treatments or dietary trace elements.
OUTCOMES MEASURED: The primary outcome was the relative risk of PD for different levels of coffee and caffeine consumption. The authors did not measure the clinical outcomes of PD, such as functional status or quality of life, which might be valuable for primary care physicians who are considering advising substantial lifestyle change to prevent PD.
RESULTS: A total of 8004 subjects (99.9% of the original cohort) were followed for an average of 27 years; 102 cases of PD were identified. The adjusted relative risk of developing PD was 5.1 (95% confidence interval, 1.8-14.4; number needed to treat=125) for noncoffee drinkers compared with those who drank 28 ounces or more of coffee per day. A dose-response relationship was observed; higher amounts of daily coffee intake were associated with lower relative risks of PD. This relationship was also seen with caffeine and caffeine derived from noncoffee sources. Other nutrients found in coffee (ie, niacin) or used in coffee (ie, milk or sugar) were analyzed and found to have no impact on the relationship observed between coffee and PD.
This well-designed prospective study provides good evidence that an inverse relationship exists between coffee intake and the development of PD and suggests that caffeine may be an important mediator of this effect. However, a single study does not prove that coffee is protective. The mechanism by which coffee may protect against PD is not understood, and confounding variables not measured in this study could be responsible for the results obtained. Consistent findings with multiple well-designed studies in a variety of populations are needed before a causal relationship can be established.
Should family physicians advise patients to drink coffee? The prevalence of PD in family practice is significant but still relatively small. The increased rate of PD for patients with more usual amounts of coffee each day (4-28 oz/day) is modest. There may also be health risks of drinking large amounts of coffee per day, although few have been identified in the literature. Clinicians should not counsel patients to drink coffee to protect against PD until more data become available.
BACKGROUND: The suffering of patients with PD is substantial, and understanding risk factors for its development could make prevention or amelioration of its course possible. This prospective cohort study evaluated the effect of coffee and caffeine on the development of PD.
POPULATION STUDIED: A total of 8004 Japanese American men aged between 45 and 68 years were enrolled in the Honolulu Heart Program between 1965 and 1968. The subjects were identified through World War II selective services files; the median age was 53 years at enrollment. Women, other races, and younger men were not represented in this study, so family physicians should be cautious about generalizing the results to those patients.
STUDY DESIGN AND VALIDITY: This prospective cohort study was initiated more than 30 years ago. Caffeine and coffee intake was assessed at enrollment by 24-hour dietary recall, and 6 years later by food frequency questionnaire. Incident cases of PD were identified by review of hospitalization records, death certificates, and local neurologists’ records using well-established published case definitions and after 1991 direct examination of the entire cohort by a study neurologist. Proportional hazards modeling was used to adjust for age and cigarette smoking and to assess potential confounding by alcohol intake, dietary fat, physical activity, cholesterol, hypertension, and diabetes. This study was well done. Its strengths include its prospective design, rigorous assessment of dietary intake, excellent follow-up, careful case ascertainment, and assessment for a variety of confounding variables. Minor weaknesses include the lack of reviewers blind to exposure and the possibility of other confounding variables, such as medical treatments or dietary trace elements.
OUTCOMES MEASURED: The primary outcome was the relative risk of PD for different levels of coffee and caffeine consumption. The authors did not measure the clinical outcomes of PD, such as functional status or quality of life, which might be valuable for primary care physicians who are considering advising substantial lifestyle change to prevent PD.
RESULTS: A total of 8004 subjects (99.9% of the original cohort) were followed for an average of 27 years; 102 cases of PD were identified. The adjusted relative risk of developing PD was 5.1 (95% confidence interval, 1.8-14.4; number needed to treat=125) for noncoffee drinkers compared with those who drank 28 ounces or more of coffee per day. A dose-response relationship was observed; higher amounts of daily coffee intake were associated with lower relative risks of PD. This relationship was also seen with caffeine and caffeine derived from noncoffee sources. Other nutrients found in coffee (ie, niacin) or used in coffee (ie, milk or sugar) were analyzed and found to have no impact on the relationship observed between coffee and PD.
This well-designed prospective study provides good evidence that an inverse relationship exists between coffee intake and the development of PD and suggests that caffeine may be an important mediator of this effect. However, a single study does not prove that coffee is protective. The mechanism by which coffee may protect against PD is not understood, and confounding variables not measured in this study could be responsible for the results obtained. Consistent findings with multiple well-designed studies in a variety of populations are needed before a causal relationship can be established.
Should family physicians advise patients to drink coffee? The prevalence of PD in family practice is significant but still relatively small. The increased rate of PD for patients with more usual amounts of coffee each day (4-28 oz/day) is modest. There may also be health risks of drinking large amounts of coffee per day, although few have been identified in the literature. Clinicians should not counsel patients to drink coffee to protect against PD until more data become available.