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Poor diet quality (DQ) is associated with poor cognition and increased neurodegeneration, including Alzheimer’s disease (AD). We are interested in the role of DQ on cognitive functioning (by sex and increasing genetic risk for AD), in a sample of African American (AA) middle-aged adults. We analysed a sub-group of participants (about 55 % women; mean follow-up time of about 4·7 years) from the Healthy Aging in Neighborhoods of Diversity across the Life Span study with a genetic risk score for AD (hAlzScore). The Healthy Eating Index-2010, Dietary Approaches to Stop Hypertension and the mean adequacy ratio computed at baseline (2004–2009) and follow-up visits (2009–2013) were used to assess initial DQ and change over time. Linear mixed-effects regression models were utilised, adjusting for select covariates, selection bias and multiple testing. DQ change (ΔDQ) was associated with California Verbal Learning Test-List A – overall (0·15 (se 0·06), P = 0·008) and in women (0·21 (se 0·08), P = 0·006), at highest AD risk, indicating protective effects over time. Greater AD risk was longitudinally associated with poorer Clock Command Test scores in men. Poor DQ was positively and cross-sectionally associated with Trails B scores, but in women only. Better-quality diet was associated with a slower decline in verbal memory among AA women, with greater AD risk. Insufficient clinical evidence and/or mixed findings dictate that more studies are needed to investigate brain morphology and volume changes in relation to DQ in an at-risk population for AD, over time.
Serum uric acid (SUA), a causative agent for gout, is linked to dietary factors, perhaps differentially by race. Cross-sectional (SUAbase, i.e. baseline SUA) and longitudinal (SUArate; i.e. annual rate of change in SUA) associations of SUA with diet were evaluated across race and sex–race groups, in a large prospective cohort study of urban adults. Of 3720 African American (AA) and White urban adults participating in the Healthy Aging in Neighborhoods of Diversity across the Life Span study, longitudinal data (2004–2013, k=1·7 repeats, follow-up, 4·64 (sd 0·93) years) on n 2138 participants were used. The main outcome consisted of up to two repeated measures on SUA. Exposures included the dietary factors such as ‘added sugar’, ‘alcoholic beverages’, ‘red meat’, ‘total fish’, ‘legumes’, ‘total dairy product’, ‘caffeine’, ‘vitamin C’ and a composite measure termed ‘dietary urate index’. Mixed-effects linear regression models were conducted, stratifying by race and by race×sex. A positive association between legume intake and SUArate was restricted to AA, whereas alcohol intake was positively associated with SUAbase overall without racial differences. Added sugars were directly related to SUAbase among White men (P<0·05 for race×sex interaction), whereas dairy product intake was linked with slower SUArate among AA women, unlike among White women. Nevertheless, dairy product intake was associated with a lower SUAbase among Whites. Finally, the dietary urate index was positively associated with both SUAbase and SUArate, particularly among AA. In sum, race and sex interactions with dietary intakes of added sugars, dairy products and legumes were detected in determining SUA. Similar studies are needed to replicate these findings.
The role of dairy foods and related nutrients in cardiometabolic health aetiology is poorly understood. We investigated longitudinal associations between the metabolic syndrome (MetS) and its components with key dairy product exposures. We used prospective data from a bi-racial cohort of urban adults (30–64 years at baseline (n 1371)), the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS), in Baltimore City, MD (2004–2013). The average of two 24-h dietary recalls measured 4–10 d apart was computed at baseline (V1) and follow-up (V2) waves. Annual rates of change (Δ) in dairy foods and key nutrients were estimated. Incident obesity, central obesity and the MetS were determined. Among key findings, in the overall urban adult population, both cheese and yogurt (V1 and Δ) were associated with an increased risk of central obesity (hazard ratio (HR) 1·13; 95 % CI 1·05, 1·23 per oz equivalent of cheese (V1); HR 1·21; 95 % CI 1·01, 1·44 per fl oz equivalent of yogurt (V1)]. Baseline fluid milk intake (V1 in cup equivalents) was inversely related to the MetS (HR 0·86; 95 % CI 0·78, 0·94), specifically to dyslipidaemia–TAG (HR 0·89; 95 % CI 0·81, 0·99), although it was directly associated with dyslipidaemia–HDL-cholesterol (HR 1·10; 95 % CI 1·01, 1·21). Furthermore, ΔCa and ΔP were inversely related to dyslipidaemia–HDL and MetS incidence, respectively, whereas Δdairy product fat was positively associated with incident TAG–dyslipidaemia and HDL-cholesterol–dyslipidaemia and the MetS. A few of those associations were sex and race specific. In sum, various dairy product exposures had differential associations with metabolic disturbances. Future intervention studies should uncover how changes in dairy product components over time may affect metabolic disorders.
Serum uric acid (SUA), a causative agent for gout among others, is affected by both genetic and dietary factors, perhaps differentially by sex. We evaluated cross-sectional (SUAbase) and longitudinal (SUArate) associations of SUA with a genetic risk score (GRS), diet and sex. We then tested the interactive effect of GRS, diet and sex on SUA. Longitudinal data on 766 African-American urban adults participating in the Healthy Aging in Neighborhood of Diversity across the Lifespan study were used. In all, three GRS for SUA were created from known SUA-associated SNP (GRSbase (n 12 SNP), GRSrate (n 3 SNP) and GRStotal (n 15 SNP)). Dietary factors included added sugar, total alcohol, red meat, total fish, legumes, dairy products, caffeine and vitamin C. Mixed-effects linear regression models were conducted. SUAbase was higher among men compared with that among women, and increased with GRStotal tertiles. SUArate was positively associated with legume intake in women (γ=+0·14; 95 % CI +0·06, +0·22, P=0·001) and inversely related to dairy product intake in both sexes combined (γ=−0·042; 95 % CI −0·075, −0·009), P=0·010). SUAbase was directly linked to alcohol consumption among women (γ=+0·154; 95 % CI +0·046, +0·262, P=0·005). GRSrate was linearly related to SUArate only among men. Legume consumption was also positively associated with SUArate within the GRStotal’s lowest tertile. Among women, a synergistic interaction was observed between GRSrate and red meat intake in association with SUArate. Among men, a synergistic interaction between low vitamin C and genetic risk was found. In sum, sex–diet, sex–gene and gene–diet interactions were detected in determining SUA. Further similar studies are needed to replicate our findings.
Poor diet quality contributes to morbidity, including poor brain health outcomes such as cognitive decline and dementia. African Americans and individuals living in poverty may be at greater risk for cognitive decrements from poor diet quality.
Baltimore, MD, USA.
Participants were 2090 African Americans and Whites (57 % female, mean age=47·9 years) who completed two 24 h dietary recalls. We examined cognitive performance and potential interactions of diet quality with race and poverty status using baseline data from the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study. Healthy Eating Index-2010 (HEI-2010) scores were calculated and interpreted using federal guidelines. A neurocognitive test battery was administered to evaluate cognitive function over several domains.
Linear regression analyses showed that lower HEI-2010 scores were associated with poorer verbal learning and memory (P<0·05) after adjustment for covariates. Diet quality within the sample was poor. Significant interactions of HEI-2010 and poverty status (all P<0·05) indicated that higher diet quality was associated with higher performance on tests of attention and cognitive flexibility, visuospatial ability and perceptual speed among those below the poverty line. No significant race interactions emerged. Higher diet quality was associated with better performance on two measures of verbal learning and memory, irrespective of race and poverty status.
Findings suggest that diet quality and cognitive function are likely related at the population level. Future research is needed to determine whether the association is clinically significant.
Analysing dietary data to capture how individuals typically consume foods is dependent on the coding variables used. Individual foods consumed simultaneously, like coffee with milk, are given codes to identify these combinations. Our literature review revealed a lack of discussion about using combination codes in analysis. The present study identified foods consumed at mealtimes and by race when combination codes were or were not utilized.
Duplicate analysis methods were performed on separate data sets. The original data set consisted of all foods reported; each food was coded as if it was consumed individually. The revised data set was derived from the original data set by first isolating coded foods consumed as individual items from those foods consumed simultaneously and assigning a code to designate a combination. Foods assigned a combination code, like pancakes with syrup, were aggregated and associated with a food group, defined by the major food component (i.e. pancakes), and then appended to the isolated coded foods.
Healthy Aging in Neighborhoods of Diversity across the Life Span study.
African-American and White adults with two dietary recalls (n 2177).
Differences existed in lists of foods most frequently consumed by mealtime and race when comparing results based on original and revised data sets. African Americans reported consumption of sausage/luncheon meat and poultry, while ready-to-eat cereals and cakes/doughnuts/pastries were reported by Whites on recalls.
Use of combination codes provided more accurate representation of how foods were consumed by populations. This information is beneficial when creating interventions and exploring diet–health relationships.
Gene polymorphisms provide a means to obtain unconfounded associations between carotenoids and various health outcomes. In the present study, we tested whether gene polymorphisms and gene scores linked to low serum carotenoid status are related to metabolic disturbance and depressive symptoms in African-American adults residing in Baltimore city, MD, using cross-sectional data from the Healthy Aging in Neighborhoods of Diversity across the Life Span study (age range 30–64 years, n 873–994). We examined twenty-four SNP of various gene loci that were previously shown to be associated with low serum carotenoid status (SNPlcar). Gene risk scores were created: five low specific-carotenoid risk scores (LSCRS: α-carotene, β-carotene, lutein+zeaxanthin, β-cryptoxanthin and lycopene) and one low total-carotenoid risk score (LTCRS: total carotenoids). SNPlcar, LSCRS and LTCRS were entered as predictors for a number of health outcomes. These included obesity, National Cholesterol Education Program Adult Treatment Panel III metabolic syndrome and its components, elevated homeostatic model assessment of insulin resistance, C-reactive protein, hyperuricaemia and elevated depressive symptoms (EDS, Center for Epidemiologic Studies-Depression score ≥ 16). Among the key findings, SNPlcar were not associated with the main outcomes after correction for multiple testing. However, an inverse association was found between the LTCRS and HDL-cholesterol (HDL-C) dyslipidaemia. Specifically, the α-carotene and β-cryptoxanthin LSCRS were associated with a lower odds of HDL-C dyslipidaemia. However, the β-cryptoxanthin LSCRS was linked to a higher odds of EDS, with a linear dose–response relationship. In summary, gene risk scores linked to low serum carotenoids had mixed effects on HDL-C dyslipidaemia and EDS. Further studies using larger African-American population samples are needed.
We examined longitudinal associations of vitamin D receptor (VDR) and megalin (LRP2; LDL receptor-related protein-2) gene polymorphisms with central adiposity. We used data from the Baltimore Longitudinal Study of Aging (BLSA), an ongoing prospective open cohort study. Study participants consisted of non-Hispanic white adults residing in Baltimore city, with one or more visits at age ≥50 years, and complete data (n 609–617). Repeated assessments on waist circumference (WC) and waist:hip ratio (WHR) were available. Multiple linear mixed models were used to estimate mid-follow-up age central adiposity level and annual rate of change with cut-points set at the sex-specific 80th percentile. The four binary outcomes were: ‘elevated central adiposity’ (ECA-WC and ECA-WHR) and ‘significant increase in central adiposity’ (SICA-WC and SICA-WHR). SNP for VDR (four SNP: (1) rs11568820 (CdX-2:T/C); (2) rs1544410 (BsmI:G/A); (3) rs7975232 (ApaI:A/C); (4) rs731236 (TaqI:G/A)) and Megalin (three SNP: (1) rs3755166:G/A; (2) rs2075252:C/T; (3) rs4668123:C/T) genes were selected. SNP latent classes (SNPLC) and SNP haplotypes (SNPHAP) were created. Multiple logistic regression analyses indicated that, in men, higher ECA-WHR odds were associated with SNPLC Megalin2:rs3755166[–]/rs2075252[TT]/rs4668123[T–] (v. Megalin1:rs3755166[–]/rs2075252[CC]/rs4668123[–]) (OR 2·87; 95 % CI 1·15, 7·12; P = 0·023) and that SNPLC Megalin3:rs3755166[–]/rs2075252[CT]/rs4668123[–] (v. Megalin1) was linked to lower SICA-WC odds (OR 0·48; 95 % CI 0·26, 0·88; P = 0·019) (P > 0·05 for sex × SNPLC). In women, VDR3 SNPHAP (GAA:bAT) was related to lower odds of ECA-WC (OR 0·37; 95 % CI 0·16, 0·87; P = 0·023) (P < 0·05 for sex × SNPHAP), VDR1 SNPHAP (GCA:baT) was associated with greater odds and VDR3 SNPHAP (GAA:bAT) with lower odds of SICA-WC (P > 0·05 for sex × SNPHAP). Vitamin D-related gene polymorphisms were associated with central adiposity status and change. Future mechanistic studies are needed to confirm those polymorphisms' biological significance to central adiposity.
We examined the relationship of elevated depressive symptoms with antioxidant status. Cross-sectional data from the National Health and Nutrition Examination Surveys 2005–6 on US adults aged 20–85 years were analysed. Depressive symptoms were measured using the Patient Health Questionnaire with a score cut-off point of 10 to define ‘elevated depressive symptoms’. Serum antioxidant status was measured by serum levels of carotenoids, retinol (free and retinyl esters), vitamin C and vitamin E. The main analyses consisted of multiple logistic and zero-inflated Poisson regression models, taking into account sampling design complexity. The final sample consisted of 1798 US adults with complete data. A higher total serum carotenoid level was associated with a lower likelihood of elevated depressive symptoms with a reduction in the odds by 37 % overall with each sd increase in exposure, and by 34 % among women (P< 0·05). A dose–response relationship was observed when total serum carotenoids were expressed as quartiles (Q4 (1·62–10·1 μmol/l)v. Q1(0·06–0·86 μmol/l): OR 0·41; 95 % CI 0·23, 0·76, P< 0·001; P for trend = 0·035), though no significant associations were found with the other antioxidant levels. Among carotenoids, β-carotene (men and women combined) and lutein+zeaxanthins (women only, after control for dietary lutein+zeaxanthin intake and supplement use) had an independent inverse association with elevated depressive symptoms among US adults. None of the other serum antioxidants had a significant association with depressive symptoms, independently of total carotenoids and other covariates. In conclusion, total carotenoids (mainly β-carotene and lutein+zeaxanthins) in serum were associated with reduced levels of depressive symptoms among community-dwelling US adults.
The present study examined the association of serum ferritin with CHD risk using the Framingham Heart Study's 10-year risk algorithm.
Ordinal logistic regression modelling was used to interpret risk. Proportional odds modelling assessed four divisions of ranked CHD risk (4, high; 3, increased; 2, slight; 1, minimal), separately by sex.
Baltimore, MD, USA.
African-American and white participants (n 1823) from baseline of the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) study, aged 30–64 years.
For men, there was a 0·5 % increase in risk for every 10-unit rise in serum ferritin (pmol/l). Other significant predictors included increased BMI, white race, unemployment and C-reactive protein ≥9·5 mg/l. For women, there was a 5·1 % increase in risk per 10-unit rise in serum ferritin (pmol/l). Other significant predictors included increased BMI, lower education, unemployment and C-reactive protein ≥9·5 mg/l.
Serum ferritin is a significant predictor of 10-year hard CHD risk for HANDLS study participants, a low-income, urban population. Serum ferritin, independent of elevated C-reactive protein, was associated with increased 10-year CHD risk for HANDLS participants. To our knowledge, these data provide the first evidence of the role of serum ferritin as a risk factor for hard CHD in African-American and white postmenopausal women in the USA. Future research on cardiovascular events from this prospective study may confirm the association.
To study the association between the availability of healthy foods and BMI by neighbourhood race and socio-economic status (SES).
Trained staff collected demographic information, height, weight and 24 h dietary recalls between 2004 and 2008. Healthy food availability was determined in thirty-four census tracts of varying racial and SES composition using the Nutrition Environment Measures Survey–Stores in 2007. Multilevel linear regression was used to estimate associations between healthy food availability and BMI.
Baltimore City, Maryland, USA.
Adults aged 30–64 years (n 2616) who participated in the Healthy Aging in Neighborhoods of Diversity across the Life Span study.
Among individuals living in predominantly white neighbourhoods, high availability of healthy foods was associated with significantly higher BMI compared with individuals living in neighbourhoods with low availability of healthy food after adjustment for demographic variables (β = 3·22, P = 0·001). Associations were attenuated but remained significant after controlling for dietary quality (β = 2·81, P = 0·012).
Contrary to expectations, there was a positive association between the availability of healthy food and higher BMI among individuals living in predominantly white neighbourhoods. This result could be due to individuals in neighbourhoods with low healthy food availability travelling outside their neighbourhood to obtain healthy food.
To assess the predictive values of various adiposity indices for metabolic syndrome (MetS) among adults using baseline data from the Healthy Aging in Neighborhoods of Diversity across the Life Span (HANDLS) cohort.
In a cross-sectional study, BMI, waist circumference (WC), body composition by dual-energy X-ray absorptiometry (DEXA) and metabolic risk factors such as TAG, HDL cholesterol, blood pressure, fasting glucose and insulin, uric acid and C-reactive protein were measured. Receiver-operating characteristic (ROC) curves and logistic regression analyses were conducted.
White and African-American US adults (n 1981), aged 30–64 years.
In predicting risk of MetS using obesity-independent National Cholesterol Education Program Adult Treatment Panel III criteria, percentage total body fat mass (TtFM) assessed using DEXA measuring overall adiposity had no added value over WC. This was true among both men (area under the ROC curve (AUC) = 0·680 v. 0·733 for TtFM and WC, respectively; P < 0·05) and women (AUC = 0·581 v. 0·686). Percentage rib fat mass (RbFM) was superior to TtFM only in women for MetS (AUC = 0·701 and 0·581 for RbFM and TtFM, respectively; P < 0·05), particularly among African-American women. Elevated percentage leg fat mass (LgFM) was protective against MetS among African-American men. Among white men, BMI was inferior to WC in predicting MetS. Optimal WC cut-off points varied across ethnic–sex groups and differed from those recommended by the National Institutes of Health/North American Association for the Study of Obesity.
The study provides evidence that WC is among the most powerful tools to predict MetS, and that optimal cut-off points for various indices including WC may differ by sex and race.
Previous research has shown that reading ability is a stronger predictor of cognitive functioning than years of education, particularly for African Americans. The current study was designed to determine whether the relative influence of literacy and education on cognitive abilities varies as a function of race or socioeconomic status (SES). We examined the unique influence of education and reading scores on a range of cognitive tests in low- and higher-SES African Americans and Whites. Literacy significantly predicted scores on all but one cognitive measure in both African American groups and low-SES Whites, while education was not significantly associated with any cognitive measure. In contrast, both education and reading scores predicted performance on many cognitive measures in higher-SES Whites. These findings provide further evidence that reading ability better predicts cognitive functioning than years of education and suggest that disadvantages associated with racial minority status and low SES affect the relative influence of literacy and years of education on cognition. (JINS, 2009, 15, 580–589.)
In the Baltimore Longitudinal Study of Aging (BLSA), we examined the temporal unfolding of declining performance on tests of episodic memory (Free Recall on the Free and Cued Selective Reminding Test), executive function (Category Fluency, Letter Fluency, and Trails), and Verbal Intelligence (Nelson, 1982; American Version of the Nelson Adult Reading Test [AMNART]) before the diagnosis of dementia in 92 subjects with incident Alzheimer's disease (AD) followed for up to 15 years before diagnosis. To examine the preclinical onset of cognitive decline, we aligned subjects at the time of initial AD diagnosis and examined the cognitive course preceding diagnosis. We found that declines in performance on tests of episodic memory accelerated 7 years before diagnosis. Declining performance on tests of executive function accelerated 2–3 years before diagnosis, and verbal intelligence declined in close proximity to diagnosis. This cognitive profile is compatible with pathologic data suggesting that structures which mediate memory are affected earlier than frontal structures during the preclinical onset of AD. It also supports the view that VIQ as estimated by the AMNART does not decline during the preclinical onset of AD. (JINS, 2008, 14, 266–278.)Supported in part by grants AG017854, AG08325, AG03949, and AG16573 from the National Institutes of Health, and by the National Institute on Aging Intramural Research Program of the National Institutes of Health.
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