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R K Ross

Publications and source records attributed to R K Ross.

At least 55 records · Page 3Linked to original sources
PubMed1999

Serum concentrations of carotenoids, alpha-tocopherol, fatty acids, and lipid peroxides among Japanese in Japan, and Japanese and Caucasians in the US.

Serum concentrations of carotenoids, alpha-tocopherol, fatty acids, and thiobarbituric acid-reactive substances (TBARS) were measured in 217 Japanese residents of Japan, and in 99 Japanese and 100 Caucasian residents of the US, aged from 50 y to 74 y. In females, serum values of carotenoids such as beta-carotene (BC) and zeaxanthin & lutein (ZL) were highest among Japanese in Japan, followed by Japanese in the US and Caucasians in the US. In males, these values, except for serum BC values, were also highest among Japanese in Japan. Moreover, serum values of n-3 polyunsaturated fatty acids (n-3PUFAs) such as eicosapentaenoic acid and docosahexaenoic acid were significantly higher among Japanese in Japan than among Japanese and Caucasians in the US in both sexes. In contrast, serum values of n-6 polyunsaturated fatty acids such as linoleic acid and arachidonic acid were lowest among Japanese in Japan. For women, serum levels of n-9 unsaturated fatty acids were lowest among Japanese living in Japan. Serum TBARS values were highest among Japanese in Japan, followed by Japanese in the US and Caucasians in the US. A significant positive correlation was observed between serum values of TBARS and n-3 PUFAs among Japanese both in Japan and in the US. Serum TBARS values showed a significant inverse relationship with the serum values of BC and ZL among Japanese in Japan and with those of BC among Japanese in the US. These relationships were not always observed among Caucasians in the US. The results of this study suggest that the high TBARS values among Japanese in Japan may depend in part on lipid peroxidation induced in vitro by n-3PUFAs, while high reduction of lipid peroxidation could be expected among Japanese in Japan with high antioxidants such as BC and ZL. In conclusion, serum levels of nonprovitamin A carotenoids such as ZL may be a useful intake marker of vegetables. Dietary intakes of dark green vegetables and fish rich in n-3PUFAs might be more important in the prevention of some sites of cancer and of ischemic heart disease.

Aged↗
PubMed1999

Alcohol consumption and breast cancer oestrogen and progesterone receptor status.

We examined the role of alcohol on the risk of breast cancer by the joint oestrogen receptor (ER) and progesterone receptor (PR) status of the tumour using data from two case-control studies conducted in Los Angeles County, USA. Eligible premenopausal patients were 733 women aged < or =40 years and first diagnosed from 1 July 1983 to 1 January 1989. Eligible postmenopausal patients were 1169 women aged 55-64 years and first diagnosed from 1 March 1987 to 31 December 89. Patients were identified by the University of Southern California Cancer Surveillance Program. Neighbourhood controls were individually matched to patients by parity (premenopausal patients) and birth date (+/-3 years). ER and PR status were obtained from medical records for 424 premenopausal and 760 postmenopausal patients. The analyses included 714 premenopausal and 1091 postmenopausal control subjects. Alcohol use was generally not associated with premenopausal risk of breast cancer, regardless of hormone-receptor status. Among the postmenopausal women, those who consumed, on average, > or =27 g of alcohol/d experienced an odds ratio (OR) of 1.76 [95% confidence interval (CI) 1.14-2.71] for ER-positive/PR-positive breast cancer relative to women who reported no alcohol consumption. Alcohol use was less clearly associated with risk of other receptor types among postmenopausal women. These data suggest that alcohol may preferentially increase risk of ER-positive/PR-positive breast cancer in postmenopausal women.

Adult↗
PubMed1999

Diet, body size and menarche in a multiethnic cohort.

A multiethnic cohort of 1378 Southern California school girls aged 8-13 years was followed for 4 years to evaluate factors predicting age at menarche, a risk factor for breast cancer. Height and weight were measured and dietary intake was assessed using a semi-quantitative food frequency questionnaire. Of 939 girls providing data on menarcheal status, 767 were premenarcheal at the start of the study; 679 girls provided acceptable dietary data and were included in the analyses. Cox proportional hazards models were used to assess the relationship between diet, body size, ethnicity and age at menarche. Hispanic, Asian/Pacific Island and African-American girls were more likely to experience early menarche than non-Hispanic white girls. Tall (> 148.6 cm) versus short (< 135.9 cm) girls experienced earlier menarche (relative hazard (RH) = 2.9, 95% confidence interval (CI) 2.1-4.1) as did those with high Quetelet's index (QI, kg m(-2)) (> 20.7) versus low QI (< 16.1) (RH = 2.2, 95% CI 1.7-2.9). Of all the dietary variables analysed, only energy intake was related to age at menarche. High versus low energy intake (> 12,013 kJ vs < 7004 kJ) was associated with a delay in menarche (RH = 0.7, 95% CI 0.5-0.9); this finding was limited to a subset of heavy Hispanic girls who appeared to underreport their dietary intake.

Adolescent↗
PubMed1999

Lifetime exercise activity and breast cancer risk among post-menopausal women.

Lifetime exercise activity has been linked to breast cancer risk among young women. However, no study has specifically evaluated whether lifetime exercise activity is related to the breast cancer risk of post-menopausal women. We conducted a population-based case-control study of post-menopausal white women (1123 newly diagnosed cases and 904 healthy controls) aged 55-64 who lived in Los Angeles County, California, USA to evaluate this relationship. Although neither exercise activity from menarche to age 40 years, nor exercise after age 40 separately predicted breast cancer risk, risk was lower among women who had exercised each week for at least 17.6 MET-hours (metabolic equivalent of energy expenditure multiplied by hours of activity) since menarche than among inactive women (odds ratio (OR) = 0.55; 95% confidence interval (CI) 0.37-0.83). Exercise activity was not protective for women who gained considerable (> 17%) weight during adulthood. However, among women with more stable weight, breast cancer risk was substantially reduced for those who consistently exercised at high levels throughout their lifetime (OR = 0.42; 95% CI 0.24-0.75), those who exercised more than 4 h per week for at least 12 years (OR = 0.59; 95% CI 0.40-0.88), and those who exercised vigorously (24.5 MET-hours per week) during the most recent 10 years (OR = 0.52; 95% CI 0.32-0.85). Strenuous exercise appears to reduce breast cancer risk among post-menopausal women who do not gain sizable amounts of weight during adulthood.

Adult↗
PubMed1999

Regular use of analgesics is a risk factor for renal cell carcinoma.

Phenacetin-based analgesics have been linked to the development of renal pelvis cancer and renal cell carcinoma (RCC). The relationship between non-phenacetin types of analgesics and kidney cancer is less clear, although laboratory evidence suggests that these drugs possess carcinogenic potential. A population-based case-control study involving 1204 non-Asian RCC patients aged 25-74 and an equal number of sex-, age- and race-matched neighbourhood controls was conducted in Los Angeles, California, to investigate the relationship between sustained use of analgesics and risk of RCC according to major formulation categories. Detailed information on medical and medication histories, and other lifestyle factors was collected through in-person interviews. Regular use of analgesics was a significant risk factor for RCC in both men and women (odds ratio (OR) = 1.6, 95% confidence interval (CI) = 1.4-1.9 for both sexes combined). Risks were elevated across all four major classes of analgesics (aspirin, non-steroidal anti-inflammatory agents other than aspirin, acetaminophen and phenacetin). Within each class of analgesics, there was statistically significant increasing risk with increasing level of exposure. Although there was some minor variability by major class of formulation, in general individuals in the highest exposure categories exhibited approximately 2.5-fold increase in risk relative to non- or irregular users of analgesics. Subjects who took one regular-strength (i.e. 325 mg) aspirin a day or less for cardiovascular disease prevention were not at an increased risk of RCC (OR = 0.9, 95% CI = 0.6-1.4).

Acetaminophen↗
PubMed1999

Androgen metabolism and prostate cancer: establishing a model of genetic susceptibility.

The prostate is an androgen-regulated organ, which has led to longstanding interest in the role of androgens in prostate carcinogenesis. Although evidence of a hormonal etiology for prostate cancer is strong, it is almost entirely circumstantial. Much of the problem in proving a causal relationship relates to the continued difficulties in reliably measuring human tissue-specific exposure to endogenous steroid hormones. The international and racial-ethnic variations in prostate cancer incidence, combined with the effects of migration on risk patterns, have suggested that genetic factors play a central role in determining prostate cancer risk. We are developing a polygenic model of prostate carcinogenesis, focused around a series of genes involved in androgen biosynthesis, transport and metabolism. We have begun to develop this model by utilizing sequence variants to study how polymorphic markers in two genes (SRD5A2 and AR) are related to prostate cancer risk within and between racial-ethnic groups. We are now collaborating with the Whitehead Institute/MIT, Center for Genome Research, to screen for single nucleotide polymorphisms in additional genes relevant to the androgen pathway and prostate cell growth. The model when fully developed can potentially provide a basis for targeting populations for screening interventions and for implementing primary preventive strategies.

Androgens↗
PubMed1999

Urinary excretion of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in White, African-American, and Asian-American men in Los Angeles County.

Meats, such as beef, pork, poultry, and fish, cooked at high temperatures produce heterocyclic aromatic amines, which have been implicated indirectly as etiological agents involved in colorectal and other cancers in humans. This study examined the urinary excretion of a mutagenic/carcinogenic heterocyclic aromatic amine, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), among 45 African-American, 42 Asian-American (Chinese or Japanese), and 42 non-Hispanic white male residents of Los Angeles who consumed an unrestricted diet. Total PhIP (free and conjugated) was isolated from overnight urine collections, purified by immunoaffinity chromatography, and then quantified by high-pressure liquid chromatography combined with electrospray ionization mass spectrometry. Geometric mean levels of PhIP in Asian-Americans and African-Americans were approximately 2.8-fold higher than in whites. The urinary excretion levels of PhIP were not associated with intake frequencies of any cooked meat based on a self-administered dietary questionnaire, in contrast to our earlier finding (Ji et al., Cancer Epidemiol. Biomark. Prev., 3: 407-411, 1994) of a positive and statistically significant association between bacon intake and the urinary level of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) among this same group of study subjects. Although there is a statistically significant association between urinary levels of PhIP and MeIQx (2-sided P = 0.001), 10 subjects (8%) displayed extreme discordance between urinary PhIP and MeIQx levels. Several factors, including variable contents of heterocyclic aromatic amines in food, enzymic and interindividual metabolic differences, and analytical methodology determine the degree of concordance between the urinary excretion levels of PhIP and MeIQx. Accordingly, urinary excretion levels of a single heterocyclic aromatic amine can only serve as an approximate measure of another in estimating exposure to these compounds in humans consuming unrestricted diets.

Adult↗
PubMed1999

Helicobacter pylori infection and risk of gastric cancer in Shanghai, China: updated results based upon a locally developed and validated assay and further follow-up of the cohort.

Infection with Helicobacter pylori has been associated with an increased risk of gastric cancer in low-risk populations. However, our previous results (P. M. Webb et al., Int. J. Cancer, 67: 603-607, 1996) from an ongoing prospective study in Shanghai, China, a relatively high-risk population, failed to show an association between H. pylori infection and the subsequent risk of gastric cancer. That previous study had a relatively short time period of follow-up and the enzyme-linked immunosorbent assay (ELISA) used was based on strains found in Southern England and without validation among the Chinese. Either one of these two factors could have had an impact on the validity of those earlier observations. An ELISA developed and validated among Shanghai residents was used in the present study to reexamine specific antibodies to H. pylori in 188 gastric cancer patients and 548 control subjects. All of the cases of gastric cancer were identified during the first 12 years of follow-up of a cohort of 18,244 men, ages 45-64 years in Shanghai, from whom blood samples were collected at enrollment during 1986-1989. For each cancer case, three cancer-free control subjects were randomly selected from the cohort and matched to the index cases by age (within 2 years), month and year of sample collection, and neighborhood of residence. The Shanghai-based ELISA detected a higher prevalence of serum antibodies to H. pylori than the English-based assay in both gastric cancer cases (86 versus 53%) and control subjects (85 versus 56%). Virtually all of the subjects (98%) who were H. pylori-seropositive by the English-based assay tested positive by the Shanghai-based assay. On the other hand, 73% of gastric cancer cases and 68% of control subjects who were seronegative according to the English-based assay tested positive by the Shanghai-based assay. Using this alternative assay, combined with increased follow-up, our latest data contradict our earlier findings and show a statistically significant association between H. pylori seropositivity and gastric cancer risk (odds ratio, 1.84; 95% confidence interval, 1.08-3.11). We noted an increasing rate of seropositivity among cases as the time interval between cohort enrollment and cancer diagnosis increased. Among subjects followed for 5 or more years after enrollment, the odds ratio for gastric cancer related to H. pylori seropositivity was 3.74 (95% confidence interval, 1.51-9.30).

Antibodies, Bacterial↗
PubMed1999

Increased risk of renal cell carcinoma subsequent to hysterectomy.

In etiological studies of renal cell carcinoma, the associations between exogenous hormones, reproductive factors, or gynecological operations have not been well examined. Our aim was to evaluate gender-specific risk factors for renal cell carcinoma using data from a population-based case-control study conducted in Los Angeles, California and to elucidate possible underlying mechanisms. A population-based case-control study involving 422 female renal cell carcinoma patients, ages 25-74 years, and an equal number of sex-, age-, and race-matched neighborhood controls was conducted in Los Angeles, California. Detailed information regarding reproductive history, hysterectomy, use of exogenous estrogens, and other medical and lifestyle factors was collected through in-person interviews. Compared to women with an intact uterus, those who had undergone hysterectomy were at an increased risk for renal cell carcinoma (odds ratio, 1.8; 95% confidence interval, 1.3-2.5). Parity and use of estrogen replacement therapy were no longer risk factors for renal cell carcinoma when hysterectomy was adjusted for in the analysis. No association between renal cell carcinoma and use of oral contraceptives was found. Limited epidemiological data do not support an endocrine explanation for the observed hysterectomy-renal cell cancer association. We conjecture that unintentional injury to the ureter during the surgical procedure, which results in renal cell damage and consequent renal cell proliferation, may be a cause of the increased cancer risk in hysterectomized women.

Adult↗
PubMed1998

Androgen metabolism and prostate cancer: establishing a model of genetic susceptibility.

The prostate is an androgen-regulated organ, which has led to long-standing interest in the role of androgens in prostate carcinogenesis. Although evidence of a hormonal etiology for prostate cancer is strong, it is almost entirely circumstantial. Much of the problem in proving a causal relationship relates to the continued difficulties in reliably measuring human tissue-specific exposure to endogenous steroid hormones. The international and racial-ethnic variations in prostate cancer incidence, combined with the effects of migration on risk patterns, have suggested that whereas environmental factors are likely to be important, genetic factors might also play a central role in determining prostate cancer risk. We are developing a polygenic model of prostate carcinogenesis focused around a series of genes involved in androgen biosynthesis and androgen activation, transport, and metabolism in the prostate. In this developing model, we have initially targeted four genes based on three main criteria: (a) all encode products that play important roles in inducing androgen stimulation in the prostate; (b) all are polymorphic; and (c) all show substantial allelic variation in the polymorphic marker among the racial-ethnic groups of greatest interest in terms of prostate cancer risk. In addition to studying how the polymorphic markers of interest are related to prostate cancer development within and between racial-ethnic groups, we are concurrently evaluating whether genotypic variations correlate in the anticipated direction with biochemical parameters in vitro and in vivo. We summarize the development of this model and the state of knowledge related to each of the genes comprising the current model. We discuss the extent to which the current model can explain demographic variation in prostate cancer risk as well as the potential for future expansion of the model to incorporate environmental risk factors as well as additional genes. The model, when fully developed, can potentially provide a basis for targeting populations for screening interventions and/or preventive strategies aimed at the multigene products or at the genes themselves.

3-Hydroxysteroid Dehydrogenases↗
PubMed1998

Cruciferous vegetables in relation to renal cell carcinoma.

Little is known about the possible role of diet in the development of renal cell carcinoma (RCC). A population-based case-control study was conducted in non-Asians of Los Angeles; it included 1,204 RCC patients and an equal number of neighborhood controls matched to the index cases by sex, date of birth (within 5 years) and ethnicity. Information on intake frequencies of food groups rich in vitamins A and C, various carotenoids and nitrosamines or their precursors was collected through in-person, structured interviews. After adjustment for non-dietary risk factors including level of education, obesity, history of hypertension, cigarette smoking and regular use of analgesics and amphetamines, there were strong inverse associations between cruciferous and dark green vegetable intakes and RCC risk (both p values for linear trend < 0.001). In terms of nutrients, there were significant inverse associations of RCC risk with consumption of a variety of carotenoids including alpha-carotene (p < 0.001), beta-carotene (p = 0.004), beta-cryptoxanthin (p = 0.01) and lutein (p = 0.005). However, after adjustment for these nutrients, we still observed a significant residual effect of cruciferous vegetables, suggesting that other substances present in these vegetables may be responsible, at least partially, for the observed reduction in risk of RCC. Dietary nitrosamines and their precursors were not related to RCC risk.

Adult↗
PubMed1998

Association of prostate cancer with vitamin D receptor haplotypes in African-Americans.

In previous studies, allelic variation in the 3' end of the vitamin D receptor gene was associated with increased risk of prostate cancer in white men. Several polymorphisms, including a BsmI restriction site and a poly(A) microsatellite, can be used interchangeably to mark the unidentified locus in whites. In African-Americans, however, these markers are not interchangeable, due to weaker linkage disequilibrium in this genomic region in this population. Here, we genotyped both the BsmI and poly(A) markers for 151 African-American prostate cancer cases (102 localized and 49 advanced) and 174 African-American male controls from a large epidemiological cohort. A direct haplotyping procedure was devised to determine BsmI/poly(A) haplotypes for double heterozygotes so that haplotypes could be used as allelic markers in standard logistic regression analyses. Using BsmI alone, b alleles were associated with a 2-fold decrease in risk of advanced prostate cancer. The association was, however, confined to haplotypes carrying a long (L) allele of the poly(A) microsatellite. BL and bL haplotypes were associated with increased and decreased risk, respectively, whereas neither BS nor bS haplotypes were associated with prostate cancer risk. An allelic variant that confers increased risk of advanced prostate cancer appears to be associated with the BsmI/poly(A) BL haplotype in African-Americans.

Aged↗
PubMed1998

Use of oral contraceptives and risk of breast cancer in young women.

Many studies have shown that oral contraceptive (OC) use increases a young woman's risk of breast cancer, although some studies suggest that the risk may be limited to recent use. The objective of this study was to determine what particular aspects of OC use could be important for breast cancer development at an early age in the cohort of women who had the opportunity to use OCs all of their reproductive life. The cases were first diagnosed with breast cancer at age 40 or younger between 1983 and 1988, and identified by the Los Angeles County Cancer Surveillance Program. Control subjects were individually matched to participating cases on birth date (within 36 months), race (white), parity (nulliparous versus parous), and neighborhood of residence. Detailed OC histories were obtained during in-person interviews with subjects. In general the risk estimates were small, and not statistically significant. Compared to no use, having used OCs for 12 years or more was associated with a modest non-significant elevated breast cancer risk with an odds ratio (OR) of 1.4 (95% confidence interval (CI) = 0.8-2.4). Long-term (12 years or more) users of high-dose estrogen pills had a non-significant 60% higher breast cancer risk than never users (CI = 0.9-3.2). Early use was associated with slightly higher ORs among young women (age < or =35), and among parous women. Recent use was associated with somewhat higher ORs among parous women and women above age 36. Analyses by stage, body weight, and family history yielded similar results. This study is consistent with a modest effect of early OC use on breast cancer risk in young women.

Adult↗
PubMed1998

Hypertension, obesity and their medications in relation to renal cell carcinoma.

A population-based, case-control study was conducted in Los Angeles County, California, to investigate the inter-relationships of obesity, hypertension and medications in relation to renal cell carcinoma (RCC) risk. A total of 1204 RCC patients and an equal number of neighbourhood controls were included. Obesity was a strong risk factor for RCC. A fourfold increase in risk was observed for those with usual body mass index (kg m(-2)) of > or = 30 vs < 22. A history of hypertension was another strong, independent risk factor for RCC [odds ratio (OR) = 2.2; 95% confidence interval (CI) = 1.8, 2.6]. There was little evidence that use of diuretics was directly related to RCC development. Use of diuretics for reasons other than hypertension (primarily for weight control) was unrelated to risk among self-reported normotensive subjects (OR = 1.2; 95% CI = 0.7, 2.2). Among hypertensive subjects, heavy users of diuretics experienced similar risk as light users (OR = 0.9 among subjects with lifetime dose of > or = 137 g compared with those with lifetime dose of < 43 g). Similarly, normotensive subjects who took non-diuretic antihypertensives regularly showed no increased risk for RCC (OR = 1.1; 95% CI = 0.6-1.8), and intake among hypertensive subjects did not further increase their risk. Regular use of amphetamine-containing diet pills was associated with a twofold increase in RCC risk (95% CI = 1.4-2.8) and the risk increased with increasing dose of amphetamines. However, the fraction of cases possibly related to this exposure is small (population-attributable risk = 5%).

Adult↗
PubMed1998

The effect of finasteride on the prostate gland in men with elevated serum prostate-specific antigen levels.

Prostate cancer is a disease associated with androgens. It has been hypothesized that reducing the conversion of testosterone (T) to dihydrotestosterone (DHT) in the prostate by the use of the drug finasteride, a 5alpha-reductase inhibitor, will reduce the incidence of prostate cancer. We investigated the chemopreventive potential of finasteride by evaluating its effect on the prostate gland of men with elevated serum prostate-specific antigen (PSA). Fifty-two men with elevated PSA and prostate sextant biopsies negative for cancer were randomized to receive finasteride 5 mg day(-1) (27 patients) or no medication (25 patients) for 12 months and were rebiopsied at 12 months. The biopsies were evaluated for the presence of cancer, the proportion of glandular and hyperplastic tissue, and the presence of high-grade prostatic intraepithelial neoplasia (PIN). Epithelial proliferation was assessed in the prestudy and 12-month biopsies by immunohistochemistry using antibody to proliferating cell nuclear antigen (PCNA). Serum blood samples were drawn at baseline and after 1, 3, 6 and 12 months of study. In the control group, serum levels of PSA and T were unchanged throughout the 12 months. In the finasteride group, PSA decreased 48% (P < 0.001), DHT decreased 67% (P < 0.001) and T increased 21% (P < 0.001). Histological evaluation of prestudy and 12-month biopsy specimens revealed that the finasteride group had a 30% reduction in the percentage of hyperplastic epithelial tissue (P = 0.002), although this decrease was not statistically significantly different between the finasteride and control groups (P = 0.11). In patients with PIN on prestudy biopsy, no change occurred in the PIN lesions with finasteride treatment. Finasteride also had no effect on the proliferation index of prostatic epithelial cells. Of the 27 patients treated with finasteride, eight (30%) had adenocarcinoma of the prostate detected on the 12-month biopsy, compared with one (4%) of the control patients (P = 0.025). In the treatment group, six cancers occurred in the eight patients with PIN on the prestudy biopsy; in the observation group no cancers were detected in the five patients with PIN on the prestudy biopsy (P = 0.021). Two cancers occurred in the 19 men in the treatment group with no evidence of PIN on the prestudy biopsy, compared with one cancer in the 20 men in the observation group with no evidence of PIN on the prestudy biopsy (P = 0.60). This study, using a novel model for evaluating short-term efficacy of chemopreventive or therapeutic agents in men at high risk of prostate cancer, provides little evidence that finasteride is an effective chemopreventive agent for prostate cancer in men with elevated PSA.

Adenocarcinoma↗
PubMed1998

Body weight and mortality: a prospective evaluation in a cohort of middle-aged men in Shanghai, China.

BACKGROUND: The relationship between relative body weight and mortality has been well studied in Western populations and remains controversial. Little is known about the weight-mortality association in less well fed people in developing countries. METHODS: A cohort of 18,244 Chinese men aged 45-64 years in Shanghai, China enrolled in a prospective study of diet and cancer during January 1986 through September 1989. At recruitment, height and usual body weight were collected through interview. An active, annual follow-up of the cohort was conducted for cancer and death. Proportional hazards regression method was used to examine the relation between body mass index (BMI, weight in kg/height in m2) and overall and cause-specific mortality. RESULTS: By 28 February 1995, 1198 deaths (498 from cancer, 422 from cardio- and cerebrovascular disease, and 278 from other causes) had been identified. We found a U-shaped relation between BMI and total mortality among lifelong non-smokers. Compared with non-smokers with BMI 21.0-<23.5, the relative risk (RR) for all cause mortality was 1.73 (95% confidence interval [CI]: 1.23-2.42) for men with BMI <18.5 and 1.48 (95% CI: 1.07-2.03) for men with BMI > or =26 after adjustment for age, level of education, and alcohol drinking. The elevated risk of death in men with BMI > or =26 was largely due to fatal cardio- and cerebro-vascular diseases. There was a nearly twofold excess risk of death from cardio- and cerebrovascular diseases among lifelong non-smokers with BMI > or =26 compared with non-smokers with BMI 21-<23.5 (95% CI: 1.17-3.22). On the other hand, the increased overall mortality risk in men with BMI <18.5 was primarily due to causes of an infectious origin. Exclusion of the first 4 years of follow-up data did not materially alter the BMI-mortality associations. CONCLUSION: Underweight and overweight both are associated with an increased risk of death in middle-aged Chinese men who never smoked cigarettes. The increased total mortality in overweight men is largely due to cardio- and cerebro-vascular diseases while the elevated risk of death in underweight men is attributed primarily to causes of an infectious nature.

Aged↗