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Ratings of 830 jobs on 45 characteristics: factor and cluster analyses into age-enhanced, age-neutral and age-counteracted, and age-impaired categories.

The current study measured the critical elements of jobs and characterized the jobs' suitability for aging workers based on ratings of those elements. The sample consisted of 830 job titles collected by the Employment and Vocational Training Administration in Taiwan. For each job the ratings of 45 specific variables, falling into three major classes, were factor analyzed, using principal components analysis with varimax rotation. A nine-factor solution explained 50.1% of the variance. Using a nonhierarchical clustering procedure, 830 jobs were classified into three homogeneous clusters which were significantly different on nine factors except for Manual Dexterity. Mapping the ratings on the 9 factors and the characteristics of aging workers, the four job clusters were defined as Age-enhanced, Age-neutral, and Age-counteracted, and Age-impaired to describe the suitability for aging workers.

Age Factors↗

Total body bone mineral content in small-for-gestational -age, appropriate-for-gestational -age, large-for-gestational -age term infants and appropriate-for-gestational -age preterm infants.

BACKGROUND: Metabolic bone disease is a recognized complication in very low birth weight infants. Inadequate postnatal intake of calcium and phosphorus is probably important in the pathogenesis of bone disease in the newborn. A few studies have shown lower bone mineral content at birth in small for gestational age (SGA) than in appropriate for gestational age (AGA) infants. The present study was designed to compare total body bone mineral (TBBM) content in AGA, SGA, and large for gestational age (LGA) term infants. Also, it was designed to evaluate extrauterine changes in TBBM in preterm infants. METHODS: Ten SGA [mean +/- S.D. birth weight (B.W.) was 1.7 +/- 0.2 Kg, gestational age (G.A.), 39.0 +/- 0.8 weeks], ten AGA (B.W.; 3.3 +/- 0.4 Kg; G.A.: 39.3 +/- 1.4 weeks), ten LGA (B.W.: 4.4 +/- 0.3 Kg; G.A.: 40.4 +/- 0.9 weeks) term infants and ten AGA preterm infants (B.W.: 1.6 +/- 0.3 Kg; G.A.: 31.9 +/- 1.9 weeks) were enrolled in this study. TBBM content was measured using dual-photon-absorptiometry at 1 week postnatally in SGA, AGA, LGA term infants and in preterm infants at 1, 6, 12 weeks postnatally. Serum total calcium, phosphorus, magnesium, alkaline phosphatase activity (alk-p), parathyroid hormone (PTH), 25-hydroxyvitamin D (25-OHD) and urinary calcium, phosphorus, creatinine were measured at 1 week postnatally in all studied infants and 6, 12 weeks, postnatally in preterm infants. Preterm and SGA term infants received premature formula enriched with calcium, phosphorus and vitamin D. RESULTS: There was no significant difference (p > 0.05) in serum calcium, phosphorus, magnesium, alk-p, PTH, 25-OHD and urinary calcium, phosphorus, creatinine values among SGA, AGA and LGA term infants at one week of age. Also, there was no significant difference in serum biochemical values in preterm infants at 1, 6, 12 weeks postnatally. Significantly lower (p < 0.05) urinary phosphorus values were found in preterm than in term infants. TBBM content was lower (p < 0.05) in SGA term infants than in AGA and LGA term infants. Premature infants had lower (p < 0.01) TBBM values than term AGA infants; however, TBBM values increase with postnatal age in preterm infants. CONCLUSIONS: Biochemical or marked radiological evidence of metabolic bone disease did not develop in any of the studied preterm infants. It appears that feeding permature infants with formula enriched with phosphorus, calcium and vitamin D may provide sufficient mineral for bone mineralization.

Birth Weight↗

Diseases and aging: patterns of morbidity with age; relationship between aging and age-associated diseases.

Patterns of morbidity with age can be schematically represented in three situations: 1) as a progressive illness, such as Alzheimer's disease, leading to a relatively rapid functional decline. 2) as a catastrophic event, such as a stroke or hip fracture, leading to a decline in function with improvement after rehabilitation. 3) as normal aging with gradual progressive functional decline. Results from the New Mexico Aging Process Study provide some unique insights about the consequences of the effects of aging on the nutritional status of healthy elderly people. Between 1979 and 1989, anthropometric and biochemical markers as well as dietary intakes remained relatively constant in this healthy elderly population. Thus, the aging process alone may have little or no important consequences on the nutritional status of healthy elderly individuals. However, the adaptation of pancreatic and intestinal function to undernutrition and refeeding can be perturbed in these individuals.

Accidental Falls↗

Advanced glycation end products (AGEs) co-localize with AGE receptors in the retinal vasculature of diabetic and of AGE-infused rats.

Advanced glycation end products (AGEs), formed from the nonenzymatic glycation of proteins and lipids with reducing sugars, have been implicated in many diabetic complications; however, their role in diabetic retinopathy remains largely unknown. Recent studies suggest that the cellular actions of AGEs may be mediated by AGE-specific receptors (AGE-R). We have examined the immunolocalization of AGEs and AGE-R components R1 and R2 in the retinal vasculature at 2, 4, and 8 months after STZ-induced diabetes as well as in nondiabetic rats infused with AGE bovine serum albumin for 2 weeks. Using polyclonal or monoclonal anti-AGE antibodies and polyclonal antibodies to recombinant AGE-R1 and AGE-R2, immunoreactivity (IR) was examined in the complete retinal vascular tree after isolation by trypsin digestion. After 2, 4, and 8 months of diabetes, there was a gradual increase in AGE IR in basement membrane. At 8 months, pericytes, smooth muscle cells, and endothelial cells of the retinal vessels showed dense intracellular AGE IR. AGE epitopes stained most intensely within pericytes and smooth muscle cells but less in basement membrane of AGE-infused rats compared with the diabetic group. Retinas from normal or bovine-serum-albumin-infused rats were largely negative for AGE IR. AGE-R1 and -R2 co-localized strongly with AGEs of vascular endothelial cells, pericytes, and smooth muscle cells of either normal, diabetic, or AGE-infused rat retinas, and this distribution did not vary with each condition. The data indicate that AGEs accumulate as a function of diabetes duration first within the basement membrane and then intracellularly, co-localizing with cellular AGE-Rs. Significant AGE deposits appear within the pericytes after long-term diabetes or acute challenge with AGE infusion conditions associated with pericyte damage. Co-localization of AGEs and AGE-Rs in retinal cells points to possible interactions of pathogenic significance.

Animals↗

Comparison of visually estimated age with physiologically predicted age as indicators of rates of aging.

The commonly held view that people age at different rates derives largely from visual estimates of age. Although most people "look their age' everyone can cite examples of individuals in middle and late adulthood who appear to be aging very slowly or very rapidly. Efforts to quantify aging rates scientifically require measurement of a large number of physiological parameters in a large population sample. This paper compares visual estimates of age with physiologically predicted measures to determine their value as indicators of the rate of aging. This study used data from 1086 male participants in the Baltimore Longitudinal Study of the Gerontology Research Center, NIA. These men have provided comprehensive biomedical and psychosocial data at one and one-half years intervals for as long as 20 years. The visual estimate of age was made by the examining physician at the first study visit of each participant, without knowledge of the man's actual age. The error of this estimate was determined by subtracting actual age from estimated age. Correlation analysis of error in estimated age with an objective assessment of biological age based on physiological variables indicated a significant association between the two approaches. When men who have died since their study participation were compared with survivors, the former were found to have been significantly 'older for their age' than the latter using both visual and physiological estimate approaches. To determine whether certain lifestyle traits were associated with variation in these two indicators, multiple regression analyses were performed. These showed that men who smoked, who were fatter, or who were in poor health were predicted as older than their chronological age peers using both approaches. Results of this study suggest that the easily determined visual estimate of age may be a useful indicator of aging rate within a population.

Adolescent↗

The relationships between dental age, chronological age and bone age in Turkish adolescents with constitutional delay of growth.

The aim of this study was to investigate the relationships between dental age and bone age in Turkish adolescents with constitutional delay of growth and compare them with a group of normal, healthy adolescents. Left hand and wrist radiographs and dental panaromic radiographs of 33 adolescents (25 boys and 8 girls) aged between 10 and 16 years with constitutionally delayed growth were assessed. The control group comprised 41 healthy adolescents (24 boys, 17 girls) aged between 10 and 16 years. Bone age was determined according to Greulich and Pyle; dental age was assessed using the Demirjian method. In the control group, no statistical difference was found between chronological, bone and dental ages. In the group of adolescents with constitutional growth delay, there was no significant difference between chronological age and dental age, but the differences between dental age and bone age and between chronological age and bone age were found to be statistically significant. It was found that Demirjian's dental age assessment is a valid method for scoring dental age in Turkish adolescents. Adolescents with constitutional delay of growth had dental maturation appropriate for chronological age, but not for bone age.

Adolescent↗

Spatial learning impairment in aged rats: comparing between aged basal forebrain lesioned and normal aged rats.

Normal aged rats (26 months) displayed significant impairments in learning the Morris water maze task as compared with young adult rats (3 months). The learning deficits of aged basal forebrain (BF)-lesioned rats (26 months; ethylcholine aziridinium ion was injected into the bilateral basal forebrain at 3 months age) were more severe than those of normal aged rats. Choline acetyltransferase (ChAT) in the frontal cortex of aged BF-lesioned rats activity was significantly reduced, but not in normal aged rats which level was almost the same as that in young adult rats. Histological examination showed that cholinergic fibers (acetylcholinesterase staining) in the frontal cortex reduced in aged BF-lesioned rats, but not in normal aged rats. The number of binding sites (Bmax) for [3H]vesamicol, a ligand for the vesicular acetylcholine transporter, in the frontal cortex of normal aged rats was significantly less than that in young adult rats, while the Bmax of aged BF-lesioned rats was higher than that of normal aged rats. The levels of monoamines and their metabolites in the frontal cortex and striatum but not hippocampus of aged BF-lesioned rats were markedly reduced as compared with those of normal aged and young adult rats. These results taken together indicate that normal aged and aged BF-lesioned rats exhibit learning deficits and that the differences of the severity of spatial learning deficits between normal aged and aged BF-lesioned rats may be due to, at least in part, the different properties of cathecolaminergic, serotonergic and cholinergic dysfunctions in the discrete brain sites.

Acetylcholinesterase↗

Toxicity of the AGEs generated from the Maillard reaction: on the relationship of food-AGEs and biological-AGEs.

Advanced glycation end products (AGEs) are generated in the late stages of Maillard reaction in foods and biological systems. These products are mostly formed by the reactions of reducing sugar or degradation products of carbohydrates, lipids, and ascorbic acid. AGEs exist in high concentration in foods, but in relatively low concentrations in most of the biological systems. Recently, some AGEs have been reported to be toxic, and were proposed to be causative factors for various kinds of diseases, especially diabetes and kidney disorder, through the association with receptor of AGE (RAGE). It has also been reported that food-derived AGEs (food-AGEs) may not be a causative factor for pro-oxidation. However, the relationship of food-AGEs and biological-derived AGEs (biological-AGEs) is not clear. In this review, the following issues are discussed: the formation of AGEs in foods and biological systems; identification of the main AGEs in foods and biological systems; absorption of food-AGEs; the effects of AGEs in vivo; relationship between food-AGEs and biological-AGEs; possible defense mechanism against AGEs in vivo and finally, the problems to be solved concerning the toxicity of AGEs.

Absorption↗

Age is not necessarily aging: another step towards understanding the "clocks" that time aging.

Hofer and Sliwinski raise a critical concern regarding a popular practice in aging research of inferring associations among aging changes of different processes from correlations based on cross-sectional age differences. It is shown analytically that cross-sectional information drawn from age-heterogeneous samples is not suitable for answering questions about the interdependence between aging changes. While in general we agree with the problem pointed out by Hofer and Sliwinski, the two aims of this commentary are: (1) to highlight links between the specific concern and two long-standing issues confronting life-span researchers and (2) to introduce alternative approaches that are currently underutilized in gerontological research. We elaborate general issues with respect to challenges in inferring aging changes from age differences and using age as a proxy for aging. We show that several other sources of variance independent of rates of change, such as cohort- and mortality-related selection effects, are confounded in age-heterogeneous designs. We suggest general considerations for developing more explicit theories of cognitive aging in the future. Alternative research methods and paradigms for studying the causes and mechanisms of the aging mind at different time scales and levels are also highlighted. The role of chronological age in aging research is rather "superficial". To understand the underlying processes and mechanisms of cognitive aging, classical process-oriented, rather than solely age-oriented, theoretical conceptions need to be reconsidered and reified with new methodological and empirical advances. Concerted gerontological research endeavors utilizing recent progresses made in statistical analyses of dynamic processes and in cognitive and computational neurosciences that may lead to fruitful breakthroughs.

Aged↗

[Capacity of weight-for-age and length-for-age to predict stunting at 3 years of age].

OBJECTIVE: To compare the capacity of two cut-off points of weight-for-age and length-for-age (-1 and -2 standard deviations) at different ages in the interval between birth and 30 months to predict stunting in three year old children. MATERIAL AND METHODS: Data from a longitudinal study in Guatemala were used to evaluate the hypothesis that the capacity of cut-off values of weight-for-age and length-for-age to predict stunting at three years of age varies according to age. RESULTS: Length-for-age at -1 standard deviation (SD) of the WHO/NCHS mean reference values is a satisfactory prognostic indicator of stunting at three years of age during the first semester of life, while the same index at -2 SD is adequate after 9 months of age. Weight-for-age at -1 SD is a suitable indicator only at 9 months and at -2 SD the indicator is satisfactory between 15 and 24 months of age. CONCLUSION: The capacity to predict stunting at three years of age, for weight-for-age and length-for-age cut-off values varies according to age.

Age Factors↗

Age distribution of breast cancer in Lebanon: increased percentages and age adjusted incidence rates of younger-aged groups at presentation.

BACKGROUND: Breast cancer is the most common cancer in Lebanese women. Lebanon has no national cancer registry and the American University of Beirut Medical Center (AUBMC) is one of the largest hospitals in Lebanon and has a fully operational cancer registry. Earlier studies showed that it sees about one third of all cancer cases in Lebanon. METHODS: All female breast cancer patients recorded at AUBMC between 1983 and 2000 were evaluated. We used the sex-specific age distribution of 1995 Lebanese Population and Housing Survey to estimate the age-specific incidence of breast cancer in Lebanon. The results were calculated as number and proportion of cases, 10-year age-specific incidence rates, crude rates and age standardized rates (ASR) per 100,000 population. The ASR per 100,000 population was estimated by the direct method with the use of the World Standard Population. RESULTS: Between 1983 and 2000, there were a total of 16421 cancers of which 8007 were in women. There were 2673 female breast cancers, averaging 148 cases per year (Range:94-202). Almost half of cases (49.1%) were in women below the age of fifty. The mean age was:49.8 years +/- 13.9 years. Ten-year age groups distribution showed that 4.7% were below 30 years of age, 16.1% were 30-39 years, 28.3% were 40-49 years, 26.3% were 50-59 years, 16.9 % were 60-69 years, 6.1% were 70-79 years and 1.6% were 80 years of age or older. Twenty-two patients (0.9 %) had their age missing in the records. Overall ASR was 30.6, for a crude rate of 27.7. Age adjusted incidence rate had its peak in women aged 50-59, followed by women 40-49 then 60-69 with values of 96.3, 79.9 and 77.4 per 100,000 respectively. We also noted 19 male breast cancer cases corresponding to 0.7% of the 2692 combined total. CONCLUSIONS: The percentage of women with breast cancer in Lebanon seen at AUBMC in pre-menopausal and younger-aged groups is higher than those reported from western countries. Our results emphasize the need to search for possible environmental, lifestyle and/or genetic risk factors in Lebanon. Our study also shows the importance of implementing early detection and screening programs which, along with high quality mammography and medical care, can have a positive impact on survival, especially in younger-aged women.

Adult↗

Survival of fetal hippocampal CA3 cell grafts in the middle-aged and aged hippocampus: effect of host age and deafferentation.

The potential application of neural transplantation to many neurodegenerative disorders at early stages of disease progression would involve middle-aged and aged persons. Hence, it is important to examine critically the extent of graft cell survival in both intact and partially deafferented middle-aged and aged brain. We investigated the degree of survival of 5'-bromodeoxyuridine (BrdU)-labeled fetal hippocampal CA3 cells after grafting into both intact hippocampus and partially deafferented hippocampus (i.e., hippocampus contralateral to intracerebroventricular administration of kainic acid) of middle-aged and aged Fischer 344 rats. Absolute cell survival within these grafts was rigorously analyzed using BrdU immunostaining of serial sections and the optical fractionator cell counting method. In the intact hippocampus, graft cell survival was 23% of injected cells for middle-aged rats and 18% for aged rats, which is consistent with the survival of fetal hippocampal cells in the intact young adult hippocampus reported earlier (Shetty and Turner [1995] Neuroscience 67:561-582). A partial deafferentation at the time of grafting significantly enhanced the degree of graft cell survival to 35% of injected cells in the middle-aged hippocampus and 27% in the aged hippocampus. However, the overall graft cell survival after deafferentation was significantly (30%) greater in the middle-aged hippocampus compared with the aged hippocampus. These results reveal that 1) the degree of survival of fetal neural cells in the intact mature brain remains constant with aging and 2) a partial deafferentation of the mature host brain at the time of grafting enhances survival of grafted fetal cells, regardless of the host age. However, the overall extent of graft cell survival after deafferentation depends on the age of the mature brain at the time of deafferentation.

Age Factors↗

The Age-Related Eye Disease Study system for classifying age-related macular degeneration from stereoscopic color fundus photographs: the Age-Related Eye Disease Study Report Number 6.

PURPOSE: To describe the system for grading age-related macular degeneration from fundus photographs in the Age-Related Eye Disease Study. This is a prospective multicenter cohort study of the course of age-related macular degeneration and a placebo-controlled clinical trial of the effect of high-dose vitamin and mineral supplements on development of advanced age-related macular degeneration. METHODS: Standardized stereoscopic 30-degree color fundus photographs are taken at 11 clinical centers and evaluated by graders at a reading center for quality and age-related macular degeneration abnormalities. Macular subfields are defined by a grid, and presence and severity of various age-related macular degeneration abnormalities are graded using standard/example photographs and measuring circles. Advanced age-related macular degeneration abnormalities (presence/absence) include retinal pigment epithelial detachment, serous (or hemorrhagic) sensory retinal detachment, hard exudates, subretinal/subretinal pigment epithelial hemorrhage, subretinal fibrous tissue, and photocoagulation scars. Other abnormalities (multistep scales) include retinal pigment epithelial abnormalities (geographic atrophy, depigmentation, and increased pigment), and drusen (size, type [hard versus soft distinct or indistinct], and total area). Contemporaneous variability is tested by having different graders evaluate samples of photographs, and temporal variability by annual regrading of a dedicated subset. RESULTS: In a cumulative sample of 1230 eyes for contemporaneous reproducibility, agreement on advanced age-related macular degeneration was 96% (kappa = 0.88) and for four-step age-related macular degeneration level was 83% (kappa = 0.77). Agreement was moderate for pigment epithelial detachment (kappa = 0.54) and substantial for serous sensory retinal detachment, hard exudates, subretinal/subretinal pigment epithelial hemorrhage, subretinal fibrous tissue, and central geographic atrophy (kappa = 0.73-0.82). For pigment abnormalities, agreement was substantial for geographic atrophy (kappa = 0.63; kappa(weighted) = 0.71, 0.75 weight for one-step disagreements), and moderate for depigmentation (kappa = 0.41, kappa(weighted) = 0.51) and increased pigment (kappa = 0.54, kappa(weighted) = 0.71). For drusen, agreement was moderate to substantial for presence/maximum size (kappa = 0.50, kappa(weighted) = 0.68), type (kappa = 0.61, kappa(weighted) = 0.69), and area (kappa = 0.56, kappa(weighted) = 0.77). Six annual regrades of 119 eyes showed little temporal drift in grading of various age-related macular degeneration abnormalities, except for drusen type. CONCLUSIONS: The Age-Related Eye Disease Study has demonstrated satisfactory reliability for detecting onset of advanced age-related macular degeneration in a cohort, and moderate to substantial agreement on various abnormalities across the age-related macular degeneration spectrum. The Age-Related Eye Disease Study system for classification of age-related macular degeneration is suitable for longitudinal multicenter studies.

Cohort Studies↗

Antioxidant vitamin and mineral supplements for age-related macular degeneration.

BACKGROUND: It has been proposed that antioxidants may prevent cellular damage in the retina by reacting with free radicals produced in the process of light absorption. OBJECTIVES: The objective of this review is to assess the effects of antioxidant vitamin and/or mineral supplementation on the progression of age-related macular degeneration. SEARCH STRATEGY: The Cochrane Eyes and Vision Group specialised registered, the Cochrane Controlled Trials Register - Central, MEDLINE, the Science Citation Index, and the reference lists of relevant articles were searched. Investigators of included studies were contacted. The most recent searches were performed in December 1999. SELECTION CRITERIA: All randomised trials comparing an antioxidant vitamin and/or mineral supplement (alone or in combination) to control in people with age-related macular degeneration were included. DATA COLLECTION AND ANALYSIS: The reviewer extracted data and assessed trial quality. Due to the small number of trials identified, and variable methods of collecting and presenting outcome data, no statistical summary measure was calculated. MAIN RESULTS: Four published, two unpublished and two ongoing trials were identified. Published trials to date have been small and results inconsistent. Adverse effects and quality of life for people with age-related macular degeneration have not been addressed. REVIEWER'S CONCLUSIONS: The question as to whether people with age-related macular degeneration should take antioxidant vitamin or mineral supplements to prevent progression of the disease has not been answered by research to date. The results of ongoing trials are awaited.

Antioxidants↗

The relationship between bone age, chronological age and dental age in children with isolated growth hormone deficiency.

AIM: To relate dental age and bone age to chronological age in a group of children with isolated growth hormone deficiency (GHD). DESIGN: A group of 25 children between the ages of 6 and 18 years, diagnosed as having GHD were studied. Of these, 16 were male and nine were female, undergoing replacement therapy with growth hormone (GH) over 2.5 years. Dental age (DA) was estimated from orthopantograms (Haavicko Methods) and compared to bone age (BA) by Greulich and Pyle Standards, and chronological age (CA). RESULTS: CA versus BA--there was a statistically significant difference of 1.52 years between the average chronological age and bone age (t = 5.61, P < 0.001). CA versus DA--there was a statistically significant difference of 0.92 years between the average chronological age and dental age (t = 3.93, P < 0.001). BA versus DA--statistically nonsignificant differences were found between the average bone age and dental age (t = -0.60, P = 0.10). CONCLUSION: After 2.5 years of therapy with growth hormone both DA and BA showed a significant delay compared to CA. Despite the fact that some catch-up occurs in speed of growth there is no evidence from the children in our study that might support the occurrence of a similar speed-up in dental age.

Adolescent↗

Cognitive and neurologic development of the premature, small for gestational age infant through age 6: comparison by birth weight and gestational age.

OBJECTIVE: To compare the neurologic and cognitive outcomes of 129 premature small for gestational age (SGA) infants with 300 premature appropriate for gestational age (AGA) infants through 6 years of age. DESIGN: Infants born at < or = 37 weeks gestational age and < or = 2500 g with birth weight 2 standard deviations or more below the mean birth weight for gestational age were categorized as SGA. Cognitive and neurologic outcomes of SGA and AGA prematures at 1, 2, 3, and 5 and/or 6 years of age were compared when the infants were stratified by gestational age in 2-week intervals or by birth weight in 500-g intervals. The association between SGA/AGA and neurologic status on cognitive outcomes at each age was also examined. RESULTS: SGA infants had significantly poorer cognitive scores at each age when compared with AGA infants of similar gestational ages. Normal neurologic status was more likely at all assessments for the AGA than for SGA infants of comparable gestational age. There were no differences between SGA and AGA children in cognitive or neurologic outcomes at any age when grouped by birth weight. Cognitive impairment was closely associated with neurologic abnormality in both SGA and AGA groups. There was, nevertheless, a significant effect of SGA on cognitive outcome independent of neurologic status at all ages except 3 years. CONCLUSIONS: Irrespective of degree of prematurity, SGA infants are at greater risk for neurodevelopmental impairment than are equally premature AGA infants. The cognitive impairment can be largely, but not entirely, attributed to a higher incidence of neurologic abnormalities in the SGA infants at each gestational age.

Birth Weight↗

Does weight loss from middle age to old age explain the inverse weight mortality relation in old age?

The authors examined body mass index at middle age, body mass index in old age, and weight change between age 50 years and old age in relation to mortality in old age. The study population from the Established Populations for Epidemiologic Studies of the Elderly consisted of 6,387 whites age 70 years or older who experienced 2,650 deaths during the period 1982-1987. Mortality risk was highest for persons in the heaviest quintile of body mass index at age 50 (men, relative risk (RR) = 1.33, 95% confidence interval (CI) 1.13-1.57; women, RR = 1.31, 95% CI 1.12-1.53) compared with persons in the middle quintile. This pattern was reversed for body mass index in old age, with persons in the lowest quintile having the highest mortality risk (men, RR = 1.40, 95% CI 1.19-1.65; women, RR = 1.38, 95% CI 1.17-1.63) relative to persons in the middle quintile. This reversal was explained, in part, by weight change. Compared with persons with stable weight, those who lost 10 percent or more of body weight between age 50 and old age had the highest risk of mortality (men, RR = 1.69, 95% CI 1.45-1.97; women, RR = 1.62, 95% CI 1.38-1.90). Exclusion of participants who lost 10 percent or more of their weight and adjustment for health status eliminated the higher risk of death associated with low weight. The inverse association of weight and mortality in old age appears to reflect illness-related weight loss from heavier weight in middle-age. Weight history may be critical to understanding weight and mortality relations in old age.

Aged↗

Weight change between age 50 years and old age is associated with risk of hip fracture in white women aged 67 years and older.

BACKGROUND: Although changes in body weight with aging are common, little is known about the effects of weight change on health in old age. OBJECTIVES: To study the effects of weight loss and weight gain from age 50 years to old age on the risk of hip fracture among postmenopausal white women aged 67 years and older and to determine if the level of weight at age 50 years modifies this risk. METHODS: The association between weight change and the risk of hip fracture was studied in 3683 community-dwelling white women aged 67 years and older from three sites of the Established Populations for Epidemiologic Studies of the Elderly. RESULTS: Extreme weight loss (10% or more) beginning at age 50 years was associated in a proportional hazards model with increased risk of hip fracture (relative risk [RR], 2.9; 95% confidence interval [CI], 2.0-4.1). This risk was greatest among women in the lowest (RR, 2.3; CI, 1.1-4.8) and middle (RR, 2.8; CI, 1.5-5.3) tertiles of body mass index at age 50 years. Among the thinnest women, even more modest weight loss (5% to < 10%) was associated with increased risk of hip fracture (RR, 2.3; CI, 1.0-5.2). Weight gain of 10% or more beginning at age 50 years provided borderline protection against the risk of hip fracture (RR, 0.7; CI, 0.4-1.0). The RRs for weight gain of 10% or more were protective only among women in the middle and high tertiles of body mass index at age 50 years and were not significant (middle tertile RR, 0.8; CI, 0.3-1.8; high tertile RR, 0.6; CI, 0.2-1.9). CONCLUSIONS: Weight history is an important determinant of the risk of hip fracture. Weight loss beginning at age 50 years increases the risk of hip fracture in older white women, especially among those who are thin at age 50 years; weight gain of 10% or more decreases the risk of hip fracture. Physicians should include weight history in their assessment of postmenopausal older women for risk of hip fracture.

Age Factors↗