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Journal ArticleDOI

Halk sağliği yönünden obezite

01 Mar 1998-Vol. 51, Iss: 03, pp 1

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Journal Article
TL;DR: A review of various epidemiological methods used to address the development of obesity as well as an updated summary of the existing evidence are provided.
Abstract: The epidemiological evidence that a high-fat diet promotes the development of obesity is considered suggestive but not definitive. The purpose of this paper is to provide a review of various epidemiological methods that have been used to address this issue as well as an updated summary of the existing evidence. Ecological studies describing dietary fat intake and obesity at the population level provide mixed results and are likely to be biased by both confounding and unknown data quality factors that differ systematically across the populations studied. Cross-sectional studies are generally in agreement that the concentration of fat in the diet is positively associated with relative weight. Prospective studies of diet in relation to subsequent weight change give inconsistent results. This may be due to behavioural factors such as dieting in response to weight gain; in addition, this type of study rarely takes into account the possible interaction between genetic predisposition and dietary fat in promoting weight gain. Finally, intervention studies in free-living subjects are considered, providing evidence of a consistent but short-lived period of active weight loss on low-fat diets. The experimental evidence on this relationship is more conclusive than the epidemiological evidence, although biological mechanisms remain controversial. Some areas for future epidemiological research involve: longitudinal studies of dietary fat intake as a predictor of growth in children; observational studies relating total dietary fat and specific types of fat to overall as well as regional adiposity; and randomized intervention studies of the effect of low-fat diets with particular emphasis on and familial predisposition to obesity and other possible modifying factors.

453 citations


Journal Article
TL;DR: The hypothesis that obesity is a significant risk factor for clinically relevant nosocomial infections in surgical patients in obese and normal weight surgical patients is supported.
Abstract: Obesity has long been considered a potential risk factor for poor outcome following surgical procedures. However, controversy exists regarding the clinical impact of this problem because of a paucity of data regarding the incidence and risk of nosocomial infections in obese surgical patients. This retrospective study was undertaken to compare the nosocomial infection rate in obese and normal weight surgical patients. All patients undergoing general, urologic, vascular, thoracic, or gynecologic surgical procedures between October 1 and December 31, 1991, were reviewed. Nosocomial infection data were obtained from the Department of Hospital Epidemiology. A total of 849 patients were evaluated, of which 536 (63%) were normal weight (BMI 31 kg/m2). Age, mortality, and American Society of Anesthesia (ASA) risk scores did not differ among the three groups. There were significant increases in the number and percent of nosocomial infections in the obese populations, with rates of 0.05 per cent in normal weight, compared to 2.8 per cent and 4.0 per cent in obese and severely obese groups (P < 0.01). Infections consisted of seven wound infections, five C. difficile infections, one pneumonia, and three bacteremias. No differences in distribution between groups were evident. Mortality was similar among the groups. These data support the hypothesis that obesity is a significant risk factor for clinically relevant nosocomial infections in surgical patients.

211 citations


Journal ArticleDOI
23 Sep 1989-BMJ
TL;DR: Changes in body weight have a great influence on arterial hypertension independent of the effect of attained weight, particularly in obese subjects.
Abstract: OBJECTIVE--To assess the relations among prevalence of arterial hypertension, history of weight change, and current body weight in the range from normal weight to severe obesity. DESIGN--Retrospective analysis of medical records of men registered with Danish military authorities from 1943 to 1977 and followed up four to 40 years later. SETTING--Draft board of Copenhagen and surrounding counties and the rest of Sjaelland and surrounding islands. SUBJECTS--964 Men who were severely obese (body mass index greater than or equal to kg/m2 at the first examination) and 1134 random controls. MAIN OUTCOME MEASURES--Blood pressure and weight. RESULTS--Hypertension was more prevalent in subjects with an unchanged body mass index as that index increased over the range studied. At any body mass index hypertension was more prevalent in subjects who had increased to this index and less common in those who had decreased to it than in those who had stayed the same weight since the first examination. Hypertension among controls was most common in those subjects who had become obese during adulthood. CONCLUSIONS--Changes in body weight have a great influence on arterial hypertension independent of the effect of attained weight, particularly in obese subjects.

125 citations


Journal ArticleDOI
01 Dec 1994-Stroke
TL;DR: It is concluded that elevated body mass is associated with an increased risk of thromboembolic stroke in nonsmoking men in older middle age who are free of commonly observed conditions related to cardiovascular disease.
Abstract: While evidence suggests that obesity has an independent relation to coronary artery disease, similar findings for stroke have not been established. The purpose of this study was to examine the relation between body mass index and the risk of thromboembolic stroke independently of other risk factors.Since 1965, the Honolulu Heart Program has followed a cohort of men in a prospective study of cardiovascular disease. This article examines the relationship between the baseline measurement of body mass index and the risk of thromboembolic stroke in 1163 nonsmoking men in older middle age (55 to 68 years). Men who had an elevated risk of stroke due to hypertension, diabetes, and other risk factors were excluded from the analysis.After 22 years of follow-up, the rate of stroke increased significantly with increasing levels of body mass (P < .01). In the bottom tertile of the body mass index, the rate of thromboembolic stroke was 28.7 per 1000 (11/383). In the middle tertile, the rate was increased by 40% to 40.7...

102 citations


Journal ArticleDOI
TL;DR: Abdominal obesity should be considered as a factor that exacerbates an individual's susceptibility to cardiovascular disease, and variations in several genes relevant to lipid and lipoprotein metabolism may alter the relation of abdominal obesity to dyslipoproteinemias.
Abstract: Obesity has a multifactorial origin. However, although environmental variables undoubtedly play a role in the development of obesity, it is now clear that genetic variation is also involved in the determination of an individual's susceptibility to body fat accumulation. In addition, it is also widely accepted that obesity is not a single homogeneous phenotype. It is also heterogeneous regarding its causes and metabolic complications. The regional distribution of body fat appears to be an important correlate of the metabolic complications that have been related to obesity. Due to their higher accumulation of abdominal fat, men are generally more at risk for the metabolic complications of obesity than women whereas some obese women, with large gluteal-femoral adipose depots may have a cosmetic problem which may not necessarily require medical intervention. Several studies have been conducted to understand the mechanisms by which abdominal obesity is related to diabetes, hypertension and cardiovascular disease. It appears that the increased risk of abdominal obesity is the result of complex hormonal and metabolic interactions. Studies in genetic epidemiology have shown that both total body fatness and the regional distribution of body fat have a significant genetic component. Standardized intervention studies using an identical twin design have shown that individuals that have the same genetic background tend to show similar changes in body fat and in plasma lipoprotein levels when exposed to standardized caloric excess or energy restriction. Finally, although abdominal obesity is a significant risk factor for cardiovascular disease, not every abdominal obese subject will experience metabolic complications, suggesting that some obese individuals may be more susceptible than others. Variation in several genes relevant to lipid and lipoprotein metabolism may alter the relation of abdominal obesity to dyslipoproteinemias. Abdominal obesity should therefore be considered as a factor that exacerbates an individual's susceptibility to cardiovascular disease.

64 citations