Socioeconomic status in one’s childhood predicts offspring cardiovascular risk

ObjectiveTo test whether effects of socioeconomic environments can persist across generations, we examined whether parents’ childhood socioeconomic status (SES) could predict blood pressure (BP) trajectories in their youth across a 12-month study period and C-reactive protein (CRP) levels at one year follow-up. Methods: BP was assessed in 88 healthy youth (M age = 13 ± 2.4) at three study visits, each 6 months apart. CRP was also assessed in youth at baseline and one year follow-up. Parents reported on current and their own childhood SES (education and crowding). Results: If parents’ childhood SES was lower, their children displayed increasing SBP and CRP over the 12-month period, or conversely, the higher parents’ childhood SES, the greater the decrease in SBP and CRP in their youth over time. These effects persisted even after controlling for current SES. A number of other factors, including child health behaviors, parent psychosocial characteristics, general family functioning, and parent physiology could not explain these effects. Conclusion: Our study suggests that the SES environment parents grow up in may influence physical health across generations, here, SBP and CRP in their children, and hence that intergenerational histories are important to consider in predicting cardiovascular health in youth.     

The prospective association of socioeconomic status with C-reactive protein levels in the CARDIA study

Better health is a well-documented benefit of having a higher socioeconomic status (SES). Inflammation may be one pathway through which SES influences health. Using 2658 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study, we examine whether two measures of SES assessed at baseline (mean age, 32±4years)-years of education and household income-predict change in C-reactive protein (CRP) concentrations over the course of 13years. We also examine whether four health-related behaviors-smoking, fruit and vegetable consumption, physical activity, and alcohol consumption-mediate the prospective association of SES with CRP. Both higher education and household income predicted smaller increases in CRP over the 13years of follow-up independent of age, sex, race, CARDIA center, body mass, medical diagnoses, medications, and hormone use (among women). Associations did not differ by race or sex. When examined in separate analyses, smoking and fruit and vegetable intake each accounted for a significant proportion of the respective effects of education and household income on CRP change, and physical activity a significant proportion of the effect of household income. These findings suggest that poor health behaviors among persons of lower socioeconomic status can have long-term effects on inflammation.     

Parental education is related to C-reactive protein among female middle aged community volunteers

Growing evidence suggests that socioeconomic attributes of both childhood and adulthood confer risk for cardiovascular morbidity and mortality. In this study, we examine the association of both parental and individual educational attainment with C-reactive protein (CRP), an inflammatory mediator relevant to cardiovascular pathophysiology, in a mid-life community sample. Subjects were 811 men and women (394 men/417 women; 87% European-American/13% African-American), 30–54 years of age. Plasma concentrations of CRP were determined from blood samples obtained at a single session following an overnight fast. Regression analyses adjusting for age and race showed both parental education and individual education to be associated inversely with CRP in women, but not men. The relationship of parental education with CRP in women persisted on multivariable adjustment for both lifestyle risk factors (smoking, alcohol consumption, sleep, exercise, body mass index) and individual SES. Independent of reported personal educational attainment, mid-life adult women whose parents achieved fewer years of educational attainment exhibit higher levels of circulating CRP than women with higher parental education. This association may help explain the increased risk of atherosclerotic cardiovascular morbidity and mortality conferred by low childhood socioeconomic status.     

Early life stress and inflammatory mechanisms of fatigue in the Coronary Artery Risk Development in Young Adults (CARDIA) study

Fatigue is highly prevalent and causes serious disruption in quality of life. Although cross-sectional studies suggest childhood adversity is associated with adulthood fatigue, longitudinal evidence of this relationship and its specific biological mechanisms have not been established. This longitudinal study examined the association between early life stress and adulthood fatigue and tested whether this association was mediated by low-grade systemic inflammation as indexed by circulating C-reactive protein (CRP) and interleukin-6 (IL-6). In the Coronary Artery Risk Development in Young Adults (CARDIA) study, a population-based longitudinal study conducted in 4 US cities, early life stress was retrospectively assessed in 2716 African-American and white adults using the Risky Families Questionnaire at Year 15 examination (2000-2001, ages 33-45 years). Fatigue as indexed by a loss of subjective vitality using the Vitality Subscale of the 12-item Short Form Health Survey was assessed at both Years 15 and 20. While CRP was measured at both Years 15 and 20, IL-6 was measured only at Year 20. Early life stress assessed at Year 15 was associated with adulthood fatigue at Year 20 after adjustment for sociodemographic characteristics, body-mass index, medication use, medical comorbidity, smoking, alcohol consumption, physical activity, current stress, pain, sleep disturbance as well as Year 15 fatigue (adjusted beta 0.047, P=0.007). However, neither CRP nor IL-6 was a significant mediator of this association. In summary, early life stress assessed in adulthood was associated with fatigue 5 years later, but this association was not mediated by low-grade systemic inflammation.     

Do environments in infancy moderate the association between stress and inflammation in adulthood? Initial evidence from a birth cohort in the Philippines

Chronic inflammation is a potentially important pathway through which psychosocial stressors increase risk for cardiovascular disease. However, prior research on stress and inflammation has been conducted almost exclusively in high income, industrialized populations with low levels of infectious disease. In this study we test the hypothesis that psychosocial stressors are associated with elevated concentrations of C-reactive protein (CRP) among young adults in the Philippines (n = 1622), who have grown up in an ecological and epidemiological setting that differs substantially from that of the US. In addition, we apply a developmental, ecological perspective to consider whether microbial and nutritional environments in infancy alter patterns of association between stressors and CRP. Data come from the Cebu Longitudinal Health and Nutrition Survey, a prospective cohort study that began collecting data in 1983–1984 when participants were in utero. A series of regression models indicate trends toward significant interactions between perceived stress and environmental factors in infancy, including exposure to animal feces, season of birth, and birth weight. Parental absence in childhood was a significant predictor of CRP in adulthood in interaction with exposure to animal feces in infancy. Positive associations between stressors and CRP were only evident for individuals with lower levels of microbial exposure in infancy, or lower birth weight. These results suggest that early environments influence the development of inflammatory phenotypes in ways that moderate sensitivity to psychosocial stressors in adulthood, and they underscore the value of a comparative, developmental approach to research on social environments, inflammation, and disease.     

Childhood socioeconomic status,telomere length,and susceptibility to upper respiratory infection

Low socioeconomic status (SES) during childhood and adolescence has been found to predict greater susceptibility to common cold viruses in adults. Here, we test whether low childhood SES is associated with shorter leukocyte telomere length in adulthood, and whether telomere length mediates the association between childhood SES and susceptibility to acute upper respiratory disease in adulthood.At baseline, 196 healthy volunteers reported whether they currently owned their home and, for each year of their childhood, whether their parents owned the family home. Volunteers also had blood drawn for assessment of specific antibody to the challenge virus, and for CD8⁺CD28⁻ T-lymphocyte telomere length (in a subset, n = 135). They were subsequently quarantined in a hotel, exposed to a virus (rhinovirus [RV] 39) that causes a common cold and followed for infection and illness (clinical cold) over five post-exposure days.Lower childhood SES as measured by fewer years of parental home ownership was associated with shorter adult CD8⁺CD28⁻ telomere length and with an increased probability of developing infection and clinical illness when exposed to a common cold virus in adulthood. These associations were independent of adult SES, age, sex, race, body mass, neuroticism, and childhood family characteristics. Associations with infections and colds were also independent of pre-challenge viral-specific antibody and season. Further analyses do not support mediating roles for smoking, alcohol consumption or physical activity but suggest that CD8⁺CD28⁻ cell telomere length may act as a partial mediator of the associations between childhood SES and infection and childhood SES and colds.     

Socioeconomic status,C-reactive protein,immune factors,and responses to acute mental stress

Low socioeconomic status (SES) is associated with increased risk of coronary heart disease and immune-related disorders. We hypothesised that SES would be inversely associated with the acute phase reactant C-reactive protein (CRP) and with circulating lymphocyte levels, and that lymphocyte responses to acute psychological stress would also vary with SES. CRP was obtained from 226, and lymphocyte counts from 127 healthy volunteers from the Whitehall II cohort, and SES was defined primarily by grade of employment. CRP concentration was greater in lower compared with higher SES participants (1.18+/-0.75 vs. 0.75+/-0.8 mg/l,p=.002) independently of sex, age, body mass, waist/hip ratio, smoking, alcohol, and season of the year. Similar differences were evident when SES was defined by income and educational attainment. Higher SES was also associated with lower total lymphocyte (p=.023), T-lymphocyte (p=.024) and natural killer (NK) cell counts (p=.006). Total, T- and B-lymphocyte, and NK cell counts increased with stress, but immune stress reactivity did not vary with SES. Post-stress recovery was delayed in women compared with men. The results suggest that moderate inflammation and immune activation may be processes through which lower SES increases disease risk.     

Inflammation in obese children and adolescents: Association with psychosocial stress variables and effects of a lifestyle intervention

Obesity in childhood and adolescence is a complex health issue that has detrimental effects on the physical and psychological health of the youngster, both in the short and long term. A characteristic of obesity is the associated chronic low-grade inflammation which can result in insulin resistance. Previous research suggested that biomarkers referring to such increased inflammation may help in understanding resistance to weight loss. Whether and how psychosocial factors are related with inflammation remains to be proven. The current study consisted of 594 children and adolescents (7–19 years), of whom 480 had follow-up data, who enrolled for a ten-month inpatient multidisciplinary obesity treatment consisting of healthy food routines, physical activities and psychological treatment. The purpose of the study was to explore (1) the relationship between inflammation and psychosocial stress variables (i.e., depressive symptoms, eating behavior, concerns about eating/shape/weight, insecure parent-child attachment) (correlational and multiple regression analysis), (2) whether a lifestyle intervention for obese youngsters results in decreased C-reactive protein (CRP) values (paired t-test) and (3) which psychosocial variables influence this CRP change as indication of treatment success (multiple regression analysis with change in BMI as control variable). Results showed that the psychosocial stress variables emotional eating, external eating and attachment anxiety are related to higher CRP values. Our data further suggested that a lifestyle intervention decreases the CRP values. This significant reduction in blood inflammatory marker was besides being influenced by weight loss also dependent on psychosocial variables, more specific on self-reported attachment avoidance, as this latter was related to less CRP decrease.     

Childhood socioeconomic status and inflammation: A systematic review and meta-analysis

Recent research suggests that risk for chronic diseases of aging including cardiovascular disease, diabetes, and even cancer can be programmed early in the lifespan as a result of exposure to chronic stressors like low socioeconomic status (SES) that are hypothesized to promote a pro-inflammatory response in immune cells that results in chronic, systemic inflammation. The present paper conducted a meta-analysis to establish whether exposure to low (versus higher) SES in childhood and adolescence is associated with higher levels of inflammation (as measured by C-reactive protein, IL-6, and fibrinogen) concurrently and in adulthood. We conducted meta-analyses with both unadjusted bivariate associations between SES and inflammation and with adjusted associations that controlled for a range of covariates including demographic factors, body mass index, smoking, physical activity and current SES. A systematic review of Pubmed and PsycINFO identified a total 35 studies (26 with unadjusted and 31 adjusted effect sizes) to be included in the meta-analysis. Random-effects meta-analysis showed that individuals who were exposed to low SES in childhood and adolescence had significantly higher levels of inflammatory markers (r = −0.07, p < .001, 95% CI = −0.09, −0.05). This association remained significant in adjusted analyses (r = −0.06, p < .001, 95% CI = −0.09, −0.03). However, the relationship between childhood SES and inflammation was non-significant in a meta-analysis with longitudinal studies that all controlled for adulthood SES (r = −0.03, p = .356, 95% CI = −0.08, 0.03). Future longitudinal research should utilize measurement of inflammatory markers at multiple time points to further examine the complex relationships between SES and health both in childhood and adulthood.     

Early childhood risk exposures and inflammation in early adolescence

There is now reliable evidence that early psychosocial stress exposures are associated with behavioral health in children; the degree to which these same kinds of stress exposures predict physical health outcomes is not yet clear. We investigated the links between economic adversity, family and caregiving stress in early childhood and several markers of immune function in early adolescence. The sample is derived from the Family Life Project, a prospective longitudinal study of at-risk families. Socio-demographic and psychosocial risks have been assessed at regular intervals since the children were first assessed at 2 months of age. When the children were early adolescents, we conducted an in-depth health assessment of a subsample of families; blood samples were collected from venipuncture for interleukin(IL)-6, Tumor Necrosis Factor (TNF)-alpha, and C-reactive protein (CRP), as well as glucocorticoid resistance. Results indicated limited but reliable evidence of an association between early risk exposure and inflammation in adolescence. Specifically, caregiver depressive symptoms in early childhood predicted elevated CRP almost a decade later, and the prediction was significant after accounting for multiple covariates such as socio-economic adversity, health behaviors and body mass index. Our findings provide strong but limited evidence that early stress exposures may be associated with inflammation, suggesting one mechanism linking early stress exposure to compromised behavioral and somatic health.     

Childhood family structure and personality disorders in adulthood.

BACKGROUND: The association between childhood family structure and sociodemographic characteristics and personality disorders (PDs) in a general population sample was studied. METHODS: This study is a substudy of the prospective Northern Finland 1966 Birth Cohort Project with 1588 young adult subjects. The case-finding methods according to the DSM-III-R criteria for PDs were: (1) Structured Clinical Interview for DSM-III-R (SCID) for 321 cases who participated in a 2-phase field study, (2) Finnish Hospital Discharge Register data, and (3) analysis of the patient records in public outpatient care in 1982-1997. Statistical analyses were performed on the association between PDs and family background factors. RESULTS: Altogether 110 (7.0%) of the subjects had at least one probable or definite PD. After adjusting for confounders (gender, parental social class and parental psychiatric disorder) the results indicated that single-parent family type in childhood was associated with cluster B PDs in adulthood. Being an only child in childhood was associated with cluster A PDs. No special childhood risk factors were found for cluster C PDs. CONCLUSIONS: Results suggest that single-parent family type at birth and being an only child in the 1960s are associated with PD in adulthood. Further studies are needed to explore the psychosocial aspects of family environment which may nowadays promote vulnerability to PDs in adulthood.     

Prospective associations,longitudinal patterns of childhood socioeconomic status,and white matter organization in adulthood

The association between childhood socioeconomic status (SES) and brain development is an emerging area of research. The primary focus to date has been on SES and variations in gray matter structure with much less known about the relation between childhood SES and white matter structure. Using a longitudinal study of SES, with measures of income‐to‐needs ratio (INR) at age 9, 13, 17, and 24, we examined the prospective relationship between childhood SES (age 9 INR) and white matter organization in adulthood using diffusion tensor imaging. We also examined how changes in INR from childhood through young adulthood are associated with white matter organization in adult using a latent growth mixture model. Using tract‐based spatial statistics (TBSS) we found that there is a significant prospective positive association between childhood INR and white matter organization in the bilateral uncinate fasciculus, bilateral cingulum bundle, bilateral superior longitudinal fasciculus, and corpus callosum (p < .05, FWE corrected). The probability that an individual was in the high‐increasing INR profile across development compared with the low‐increasing INR profile was positively associated with white matter organization in the bilateral uncinate fasciculus, left cingulum, and bilateral superior longitudinal fasciculus. The results of the current study have potential implications for interventions given that early childhood poverty may have long‐lasting associations with white matter structure. Furthermore, trajectories of socioeconomic status during childhood are important—with individuals that belong to the latent profile that had high increases in INR having greater regional white matter organization in adulthood.     

Early childhood socioeconomic status is associated with circulating interleukin-6 among mid-life adults

It is proposed that socioeconomic conditions in early childhood effect immune programming, with poorer conditions resulting in adult phenotypes that are prone to inflammation. Recent evidence supports this possibility, showing an inverse association of childhood SES with adult markers of systemic inflammation. In this study, we further investigate this association, extending prior studies to include an examination of multiple indices of SES across distinct periods of childhood. Subjects were 112 men and women, 40–60 years of age (88.6% Caucasian). Childhood SES was indexed by a composite of three indicators of parental wealth (parental home and vehicle ownership, and number of bedrooms per child in the family home) averaged across 2 year periods of childhood between 1 and 18 years old. Higher adult serum concentrations of interleukin (IL)-6 were associated with lower SES in early childhood (years 1–2) (β = −.05, p < .05), associations that were independent of adult age, personal income, educational attainment, gender, race, body mass index, and physical activity. These associations support recent suggestions that the early environment may program immune phenotypes that contribute to disease risk.     

Socioeconomic status variables predict cardiovascular disease risk factors and prospective mortality risk among women with chest pain. The WISE Study

This study examined the relationship between socioeconomic status (SES), coronary artery disease (CAD) risk factors, and all-cause mortality in a cohort of women with chest pain. A total of 743 women (mean age = 59.6 years) with chest pain who were referred for coronary angiography completed a diagnostic protocol including CAD risk factor assessment, ischemic testing, psychosocial testing, and queries of SES. Patients were followed for about 2 years to track subsequent all-cause mortality. Results indicated that low SES was associated with CAD risk factors, including higher BMI and waist-hip ratios, cigarette smoking, lower reported activity levels, and a greater probability of hypertension. Low income also predicted all-cause mortality (RR = 2.7, 95% CI 1.4, 5.2), including after adjusting for proposed psychosocial and behavioral variables (RR = 5.9, 95% CI 1.2-29.7). Future research will require a thorough a priori focus on potential mechanisms to better understand SES effects on health.     

Evidence for skin-deep resilience using a co-twin control design: Effects on low-grade inflammation in a longitudinal study of youth

This study tested the skin-deep resilience hypothesis – that low socioeconomic status (SES) youth who are working hard to succeed in life experience good psychological and educational outcomes but at a cost to their physical health – in a sample of monozygotic (MZ) twins. The National Longitudinal Study of Adolescent Health (Add Health) contained a sample of 226 MZ twin pairs at Wave 1 (M age = 16 years), of whom 141 pairs completed the Wave 4 assessment 13 years later (M age = 29 years). Family SES was measured at Wave 1 via income, education, and occupation. Conscientiousness was measured at Wave 4 as an indicator of those who were working hard to succeed in life. Outcomes measured at Wave 4 included low-grade inflammation (C-reactive protein, CRP), mental health (depression, problematic alcohol use), and academic success (educational attainment). A co-twin control design was utilized which directly compared within-twin differences in the association between conscientiousness and life outcomes. Main effects of between-twin conscientiousness were found such that higher levels of conscientiousness were associated with higher educational attainment, fewer symptoms of depression, and less problematic alcohol use, across all SES groups. An interaction between family SES and within-twin difference in conscientiousness was found for CRP, such that, among twins growing up in lower SES households, the twin with higher levels of conscientiousness had higher levels of CRP. These patterns provide support for the phenomenon of skin-deep resilience using a twin methodology that reduces the possibility of confounding by shared genetic and environmental factors.     

Toward a comprehensive developmental model for major depression in women

OBJECTIVE: Major depression is a multifactorial disorder with many etiologic variables that are interrelated through developmental pathways. The authors used structural equation modeling to generate a developmental model for the etiology of major depression in women. METHOD: Data from 1,942 adult female twins, interviewed up to four times over a 9-year period, were used to construct a developmental model to predict depressive episodes in the year before the most recent interview. Eighteen risk factors in five developmental tiers were considered: 1) childhood (genetic risk, disturbed family environment, childhood sexual abuse, and childhood parental loss), 2) early adolescence (neuroticism, self-esteem, and early-onset anxiety and conduct disorder), 3) late adolescence (educational attainment, lifetime traumas, social support, and substance misuse), 4) adulthood (history of divorce and past history of major depression), and 5) the last year (marital problems, difficulties, and stressful life events). RESULTS: The best fitting model included six correlations and 64 paths, provided an excellent fit to the data, and explained 52% of the variance in liability to episodes of major depression. The findings suggest that the development of risk for major depression in women results from three broad pathways reflecting internalizing symptoms, externalizing symptoms, and psychosocial adversity. CONCLUSIONS: Major depression is an etiologically complex disorder, the full understanding of which will require consideration of a broad array of risk factors from multiple domains. These results, while plausible, should be treated with caution because of problems with causal inference, retrospective recall bias, and the limitations of a purely additive statistical model.     

C-reactive protein,Epstein-Barr virus,and cortisol trajectories in refugee and non-refugee youth: Links with stress,mental health,and cognitive function during a randomized controlled trial

Experiencing childhood adversity has been associated with significant changes in inflammation, cell-mediated immunocompetence, and cortisol secretion. Relatively few studies have examined, longitudinally, alterations to inflammatory processes during adolescence, especially outside Western contexts; none have evaluated biomarker trajectories for at-risk youth in response to a structured behavioral intervention. We conducted a randomized controlled trial evaluating the efficacy of a humanitarian intervention targeting stress-alleviation, with 12–18 year-old Syrian refugees (n = 446) and Jordanian non-refugees (n = 371) living side-by-side in war-affected communities in Jordan. We measured C-reactive protein (CRP), Epstein-Barr virus antibodies (EBV), and hair cortisol concentration (HCC) at three timepoints (pre/post intervention and 11 month follow-up), and assessed three main outcomes (psychosocial stress, mental health, and cognitive function). Using growth mixture models, regressions, and growth curve models, we identified three distinct trajectories for CRP, two for EBV, and three for HCC, and examined their associations with age, gender, BMI, poverty, and trauma. We found associations with BMI for CRP, refugee status for EBV, and BMI and gender with HCC trajectory. In terms of health outcomes, we found associations between rising CRP levels and perceived stress (B = −2.92, p = .007), and between HCC hypersecretion and insecurity (B = 7.21, p = .017). In terms of responses to the intervention, we observed no differential impacts by CRP or EBV trajectories, unlike HCC. These results suggest that commonly-assayed biomarkers do not associate with health outcomes and respond to targeted interventions in straightforward ways. Our study is the first to examine multiple biomarker trajectories in war-affected adolescents, in order to better evaluate the extent, timing, and malleability of the biological signatures of poverty, conflict, and forced displacement.     

History of Unemployment Predicts Future Elevations in C-Reactive Protein among Male Participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study

Background   Unemployment is associated with risk of future morbidity and premature mortality. Purpose   To examine whether unemployment history predicts future C-reactive protein (CRP) levels in male participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Methods   Unemployment, body mass index (BMI), and health behaviors were measured at 7, 10, and 15 years post-recruitment. CRP was measured at Years 7 and 15. Results   Having a history of unemployment at Year 10 was associated with higher CRP at Year 15, independent of age, race, BMI, Year 7 CRP, Year 15 unemployment, and average income across Years 10–15. Poor health practices and depressive symptoms explained 22% of the association, but Year 10 unemployment history remained a significant predictor. Findings did not differ across age, race, education, or income. Conclusions   Discrete episodes of unemployment may have long-term implications for future CRP levels.     

Pathways to inflammation in adolescence through early adversity,childhood depressive symptoms,and body mass index: A prospective longitudinal study of Chilean infants

Early adversity, depression, and obesity are associated with increases in low-grade inflammation. However, there are few prospective and longitudinal studies to elucidate how these associations unfold in children. The present study used latent growth curve models to examine pathways between family adversity in infancy, depressive symptoms in childhood, body mass index (BMI) in childhood, and inflammation in adolescence (age = 16–18). The study is an adolescent follow-up of infants from working-class communities around Santiago, Chile, who participated in a preventive trial of iron supplementation at 6 months of age. Anthropometrics, stressful life events, maternal depression, socioeconomic status, and developmental assessments were measured at 12 months, 5 years, 10 years, and adolescence. In adolescence, participants provided blood samples for high-sensitivity C-reactive protein (hsCRP) assessment. Greater exposure to early adversity in the form of interpersonal conflict stress in infancy indirectly associated with increased hsCRP through its association to increased intercept and slope of childhood BMI. Depressive symptoms at any time were not directly or indirectly associated with increased hsCRP. These findings contribute to our understanding of how early family adversity and its associations with obesity and depressive symptoms across childhood are linked to low-grade, chronic inflammation in adolescence. The model identified as best capturing the data supported the pivotal role of childhood BMI in explaining how early-life adversity is associated with inflammation in adolescence.     

老年2型糖尿病患者的炎症因子水平与认知功能障碍的关系

目的探讨老年2型糖尿病患者的C反应蛋白、IL-1β等炎症因子水平与认知功能障碍的关系。方法60岁以上的住院患者120例,其中2型糖尿病组80例,非糖尿病对照组40例,对所有患者应用简易智能精神检查量表（MMSE）进行评分;测量身高、体重、腰围、臀围,计算体重指数（BMI）及腰臀比（WHR）;运用ELISA法检测白细胞介素-1β（IL-1β）水平、免疫扩散法检测C反应蛋白（CRP）水平、高压液相色谱法测定糖化血红蛋白（HbA1c）水平、葡萄糖氧化酶法测定空腹血糖（FBG）水平、放射免疫法测定空腹胰岛素（FINS）水平,并计算胰岛素抵抗指数（HOMA—IR）[HOMA—IR=FBG＊FINS／22．5];比较各组间BMI、WHR、HbA1C、HOMA—IR、CRP、IL-1β、肝肾功能、血压、血脂等指标及与MMSE评分之间的关系。结果（1）老年2型糖尿病组与老年非糖尿病组在年龄、性别、文化程度、家庭收入、是否吸烟、血压、血脂及肝肾功能等方面比较无明显差异（P〉0．05）;（2）与非糖尿病组相比,老年2型糖尿病组的BMI、WHR、HbA1c、HO—MA—IR、CRP及IL-1β显著升高（P〈0．05）,而MMSE评分明显低于非糖尿病组（P〈0．01）;老年2型糖尿病组MMSE评分与WHR、HbA1C、HOMA-IR、CRP和IL-1β呈负相关。结论腹型肥胖、慢性高血糖、胰岛素抵抗及炎症反应可能是老年2型糖尿病患者认知功能障碍的相关因素。