Clark W. Heath
American Cancer Society
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Featured researches published by Clark W. Heath.
The New England Journal of Medicine | 1997
Michael J. Thun; Richard Peto; Alan D. Lopez; J H Monaco; S J Henley; Clark W. Heath; Richard Doll
BACKGROUNDnAlcohol consumption has both adverse and beneficial effects on survival. We examined the balance of these in a large prospective study of mortality among U.S. adults.nnnMETHODSnOf 490,000 men and women (mean age, 56 years; range, 30 to 104) who reported their alcohol and tobacco use in 1982, 46,000 died during nine years of follow-up. We compared cause-specific and rates of death from all causes across categories of base-line alcohol consumption, adjusting for other risk factors, and related drinking and smoking habits to the cumulative probability of dying between the ages of 35 and 69 years.nnnRESULTSnCauses of death associated with drinking were cirrhosis and alcoholism; cancers of the mouth, esophagus, pharynx, larynx, and liver combined; breast cancer in women; and injuries and other external causes in men. The mortality from breast cancer was 30 percent higher among women reporting at least one drink daily than among nondrinkers (relative risk, 1.3; 95 percent confidence interval, 1.1 to 1.6). The rates of death from all cardiovascular diseases were 30 to 40 percent lower among men (relative risk, 0.7; 95 percent confidence interval, 0.7 to 0.8) and women (relative risk, 0.6; 95 percent confidence interval, 0.6 to 0.7) reporting at least one drink daily than among nondrinkers, with little relation to the level of consumption. The overall death rates were lowest among men and women reporting about one drink daily. Mortality from all causes increased with heavier drinking, particularly among adults under age 60 with lower risk of cardiovascular disease. Alcohol consumption was associated with a small reduction in the overall risk of death in middle age (ages 35 to 69), whereas smoking approximately doubled this risk.nnnCONCLUSIONSnIn this middle-aged and elderly population, moderate alcohol consumption slightly reduced overall mortality. The benefit depended in part on age and background cardiovascular risk and was far smaller than the large increase in risk produced by tobacco.
The Lancet | 1992
Richard Peto; Alan D. Lopez; Jillian Boreham; Michael J. Thun; Clark W. Heath
Prolonged cigarette smoking causes even more deaths from other diseases than from lung cancer. In developed countries, the absolute age-sex-specific lung cancer rates can be used to indicate the approximate proportions due to tobacco of deaths not only from lung cancer itself but also, indirectly, from vascular disease and from various other categories of disease. Even in the absence of direct information on smoking histories, therefore, national mortality from tobacco can be estimated approximately just from the disease mortality statistics that are available from all major developed countries for about 1985 (and for 1975 and so, by extrapolation, for 1995). The relation between the absolute excess of lung cancer and the proportional excess of other diseases can only be approximate, and so as not to overestimate the effects of tobacco it has been taken to be only half that suggested by a recent large prospective study of smoking and death among one million Americans. Application of such methods indicates that, in developed countries alone, annual deaths from smoking number about 0.9 million in 1965, 1.3 million in 1975, 1.7 million in 1985, and 2.1 million in 1995 (and hence about 21 million in the decade 1990-99: 5-6 million European Community, 5-6 million USA, 5 million former USSR, 3 million Eastern and other Europe, and 2 million elsewhere, [ie, Australia, Canada, Japan, and New Zealand]). More than half these deaths will be at 35-69 years of age: during the 1990s tobacco will in developed countries cause about 30% of all deaths at 35-69 (making it the largest single cause of premature death) plus about 14% of all at older ages. Those killed at older ages are on average already almost 80 years old, however, and might have died soon anyway, but those killed by tobacco at 35-69 lose an average of about 23 years of life. At present just under 20% of all deaths in developed countries are attributed to tobacco, but this percentage is still rising, suggesting that on current smoking patterns just over 20% of those now living in developed countries will eventually be killed by tobacco (ie, about a quarter of a billion, out of a current total population of just under one and a quarter billion).
CA: A Cancer Journal for Clinicians | 1998
Sheryl L. Parker; Kourtney Johnston Davis; Phyllis A. Wingo; Lynn A. G. Ries; Clark W. Heath
Key findings on cancer incidence and mortality are presented for five racial and ethnic groups in the United States--African Americans, American Indians, Asians and Pacific Islanders, Hispanics, and whites. Information on the prevalence of cancer risk factors and screening examinations among these racial and ethnic groups is also included.
Cancer Causes & Control | 1996
Dawn Willis; Eugenia E. Calle; Heidi L. Miracle-McMahill; Clark W. Heath
This study examines the relationship between fatal breast cancer and use of estrogen replacement therapy (ERT) among women in a large prospective study in the United States. After nine years of follow-up, 1,469 breast cancer deaths were observedin a cohort of 422,373 postmenopausal women who were cancer free at study entry and who supplied information on estrogen use. Results from Cox proportional hazards modeling, adjusted for 11 other potential risk factors, showed that ever-use of ERT was associated with a significantly decreased risk of fatal breast cancer (rate ratio [RR]=0.84,95 percent confidence interval [CI]=0.75–0.94). There was a moderate trend (P=0.07) of decreasing risk with younger age at first use of ERT. This decreased risk was most pronounced in women who experienced natural menopause before the age of 40 years (RR=0.59, CI=0.40–0.87). There was no discernible trend of increasing risk with duration of use in estrogen users at baseline or former users, nor was there any trend in years since last use in former users. The relationship between ERT and breast cancer mortality differed by age at menarche and by a self-reported history of breast cysts. No increased risk of fatal breast cancer with ERT was observed with estrogen use status (baseline/former), age at first use, duration of use, or years since last use. These findings suggest that ever-use of ERT is associated with a 16 percent decreased risk of fatal breast cancer.
Social Science & Medicine | 1998
Henry S. Kahn; Lilith M. Tatham; Elsie R. Pamuk; Clark W. Heath
Geographic regions characterized by income inequality are associated with adverse mortality statistics, but the pathophysiologic mechanisms that mediate this ecologic relationship have not been elucidated. This study used a United States mail survey of 34158 male and 42741 female healthy-adult volunteers to test the association between residence in geographic regions with relative income inequality and the likelihood of weight gain at the waist. Respondents came from 21 states that were characterized by the household income inequality (HII) index, a measure reflecting the proportion of total income received by the more well off 50% of households in the state. The main outcome measure was self-reported weight gain mainly at the waist as opposed to weight gain at other anatomic sites. After controlling for age, other individual-level factors, and each states median household income, mens likelihood of weight gain at the waist was positively associated (p = 0.0008) with the HII index. Men from states with a high HII (households above the median receive 81.6% to 82.6% of the income) described weight gain at the waist more often than men from states with a low HII (households above the median receive 77.0% to 78.5% of the income) (odds ratio = 1.12, 95% confidence interval 1.03 to 1.22). Womens results showed a non-significant trend in the same direction. An association between ecologically defined socio-environmental stress and abdominal obesity may help to clarify the pathophysiologic pathways leading to several major chronic diseases.
Cancer | 1997
Bruce A. Ruggeri; Lingyi Huang; David Berger; Hong Chang; Andres J. P. Klein-Szanto; Tamra L. Goodrow; Moira Wood; Takeshi Obara; Clark W. Heath; Henry T. Lynch
The molecular pathology underlying the development and progression of ductal pancreatic adenocarcinoma is poorly understood relative to that of other major cancers in industrialized societies. The frequency, nature, and distribution of p53 abnormalities, their temporal relationship to the metastatic and clinicopathologic phenotypes of sporadic and familial pancreatic cancer, and their consequent effects on the genetics and expression of critical wild‐type p53‐regulated genes (mdm‐2 and p21/WAF‐1) warrant examination in pancreatic adenocarcinoma. This molecular and immunochemical study of the p53, mdm‐2, and p21/WAF‐1 genes and gene products examined the largest series of nonneoplastic, neoplastic, and metastatic ductal pancreatic lesions reported to date in relation to clinicopathologic profile.
Cancer | 1999
David H. Berger; Hong Chang; Moira Wood; Lingyi Huang; Clark W. Heath; Theresa Lehman; Bruce A. Ruggeri
Cigarette smoking is among the few unequivocal risk factors for the development of pancreatic ductal adenocarcinoma (PDAC). Activating mutations in codon 12 of the K‐ras protooncogene is a frequent and early molecular event in the pathogenesis of PDAC and a variety of nonmalignant ductal pancreatic lesions. The molecular epidemiologic relation between heavy cigarette smoking and mutational activation of K‐ras in PDAC has been examined to a limited extent. The authors have examined the mutational status of K‐ras in nonneoplastic pancreata in relation to cigarette smoking status.
Cancer Causes & Control | 1998
Carmen Rodriguez; Lilith M. Tatham; Eugenia E. Calle; Michael J. Thun; Eric J. Jacobs; Clark W. Heath
Objectives: It is difficult to separate the possible role of fertility drugs from underlying infertility as risk factors for ovarian cancer. The present study examined the relationship between self-reported infertility and death from ovarian cancer among married women unlikely to have been exposured to fertility drugs.Methods: Women were selected for study from the 676,526 female participants in Cancer Prevention Study II (CPS-II). After twelve years of follow-up, 797 deaths from ovarian cancer were observed among women with no prior history of cancer or hysterectomy and 40 years of age or older in 1967 when ovulatory stimulants were approved in the United States. Cox proportional hazards modeling was used to compute rate ratios (RRs) and to adjust for other potential risk factors.Results: Overall, self-reported infertility was not significantly associated with ovarian cancer mortality (adjusted rate ratio (RR)u2009=u20091.1, 95 percent confidence interval (CI)u2009=u20090.9-1.3). Ovarian cancer death rates among nulligravid women with self-reported infertility, however, were 40 percent higher than for nulligravid women who never tried to become pregnant (RRu2009=u20091.4, 95 percent CIu2009=u20090.9-2.4). Multigravid women who reported infertility problems were not at increased risk.Conclusions: These results suggest that infertility itself, without concomitant exposure to fertility drugs, may increase risk of fatal ovarian cancer among nulligravid women.
International Journal of Obesity | 1997
Henry S. Kahn; Lilith M. Tatham; Clark W. Heath
OBJECTIVE: To identify contrasts between the risk factors associated with abdominal weight gain and those associated with peripheral weight gain. DESIGN: Prospective mail survey. SUBJECTS: 44u2005080 white, non-Hispanic, healthy women who were questioned in 1982 (baseline age 40–54u2005y) and 1992 about weight, diet, alcohol use, smoking, 10 physical activities and other variables. MEASUREMENTS: Self reports in 1992 identified 4261 women who gained weight in the abdomen and 7440 women who gained in the periphery (sites other than the abdomen). Using identical logistic models adjusted for age, baseline body mass index (BMI) and numerous covariates, the abdominal-gain group and the peripheral-gain group were separately compared with 10u2005888 women who did not gain weight. RESULTS: The likelihood of abdominal gain exceeded that of peripheral gain (by comparison of estimated odds ratios, abdominal vs peripheral) for high meat eaters (1.50 vs 1.15), frequent users of liquor (1.09 vs 0.54), moderate cigarette smokers (0.86 vs 0.59), heavy cigarette smokers (0.96 vs 0.36), cigarette quitters (2.13 vs 1.63), women with high parity (1.52 vs 1.15) and those who reported major weight gain since age 18u2005y (1.22 vs 0.65). Abdominal gain was less likely than peripheral gain for high vegetable eaters (0.71 vs 0.91), women who exercised ≥4u2005h/wk [(especially aerobics/calisthenics (0.28 vs 0.91) or walking (0.84 vs 1.06)], women who completed menopause (0.74 vs 0.98) and consistent users of estrogen replacement therapy (0.93 vs 1.22). CONCLUSION: A behavior or characteristic may be associated differently with the risks of abdominal and peripheral weight gain. This insight could strengthen recommendations for preventing major chronic diseases.
CA: A Cancer Journal for Clinicians | 1996
Clark W. Heath
The idea that exposure to power-frequency electric and magnetic fields might contribute to cancer causation has been under investigation for nearly two decades. A number of epidemiologic studies have been undertaken, but findings have been weak, inconsistent, and inconclusive. This article provides an updated survey of epidemiologic information and considers those data in relation to the many scientific uncertainties that still persist.