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Improving fruit and vegetable intake attenuates the genetic association with long-term weight gain.

ABSTRACT: BACKGROUND:Whether changes in fruit and vegetable intake can modify the effect of genetic susceptibility to obesity on long-term changes in BMI and body weight are uncertain. OBJECTIVE:We analyzed the interactions of changes in total and specific fruit and vegetable intake with genetic susceptibility to obesity in relation to changes in BMI and body weight. METHODS:We calculated a genetic risk score on the basis of 77 BMI-associated loci to determine the genetic susceptibility to obesity, and examined the interactions of changes in total and specific fruit and vegetable intake with the genetic risk score on changes in BMI and body weight within five 4-y intervals over 20 y of follow-up in 8943 women from the Nurses' Health Study (NHS) and 5308 men from the Health Professionals Follow-Up Study (HPFS). RESULTS:In the combined cohorts, repeated 4-y BMI change per 10-risk allele increment was 0.09 kg/m2 among participants with the greatest decrease in total fruit and vegetable intake and -0.02 among those with the greatest increase in intake (P-interaction <0.001; corresponding weight change: 0.20 kg compared with -0.06 kg). The magnitude of decrease in BMI associated with increasing fruit and vegetable intake was more prominent among participants with high genetic risk than those with low risk. Reproducible interactions were observed for fruits and vegetables separately (both P-interaction <0.001). Based on similar nutritional content, the interaction effect was greatest for berries, citrus fruits, and green leafy vegetables, and the interaction pattern persisted regardless of the different fiber content or glycemic load of fruits and vegetables. CONCLUSIONS:Genetically associated increased BMI and body weight could be mitigated by increasing fruit and vegetable intake, and the beneficial effect of improving fruit and vegetable intake on weight management was more pronounced in individuals with greater genetic susceptibility to obesity.

SUBMITTER: Wang T

PROVIDER: S-EPMC6736184 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Improving fruit and vegetable intake attenuates the genetic association with long-term weight gain.

Wang Tiange T Heianza Yoriko Y Sun Dianjianyi D Zheng Yan Y Huang Tao T Ma Wenjie W Rimm Eric B EB Manson JoAnn E JE Hu Frank B FB Willett Walter C WC Qi Lu L

The American journal of clinical nutrition 20190901 3

<h4>Background</h4>Whether changes in fruit and vegetable intake can modify the effect of genetic susceptibility to obesity on long-term changes in BMI and body weight are uncertain.<h4>Objective</h4>We analyzed the interactions of changes in total and specific fruit and vegetable intake with genetic susceptibility to obesity in relation to changes in BMI and body weight.<h4>Methods</h4>We calculated a genetic risk score on the basis of 77 BMI-associated loci to determine the genetic susceptibil ...[more]

PMID: 31301130

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Project description:BackgroundConsumption of added sugars has been considered a worldwide public health concern by its association with metabolic syndrome and its comorbidities. Meanwhile, current studies have suggested high-protein diets to promote weight loss and improved metabolic outcomes. Thus, this study aimed to investigate the effects of long-term high-protein diet (HPD, 34.3% protein) intake on high-sucrose-fed rats.MethodsWeaned male Wistar rats were randomized into two groups: rats fed a standard chow (CT/CT, 10% sucrose) or rats fed a high-sucrose diet (HSD, 25% sucrose) for a 20-week observational period. Subsequently, HS/HS animals were randomized into 3 new groups: rats maintained on HSD diet (HS/HS); rats submitted to HSD replacement by standard chow (HS/CT); and those with HSD replaced by HPD (HS/HP). All groups were followed up for 12 weeks during which we investigated the effects of HPD on body weight, energy intake, obesity development, glicemic/lipid profile, glucose tolerance, insulin resistance, tissue weight (adipose tissue, liver and skeletal muscles), lipolytic activity, liver lipoperoxidation and histology, as well as serum markers of hepatic function.ResultsPost-weaning exposure to HSD led to metabolic syndrome phenotype at adulthood, herein characterized by central obesity, glucose intolerance, dyslipidaemia and insulin resistance. Only HPD feeding was able to revert weight gain and adipose tissue accumulation, as well as restore adipose tissue lipolytic response to sympathetic stimulus. On the other hand, either HPD or withdrawal from HSD promoted very similar metabolic outcomes upon 12-week nutritional intervention. HS/HP and HS/CT rats showed reduced fasting serum levels of glucose, triacylglycerol and total cholesterol, which were correlated with the improvement of peripheral insulin sensitivity, as inferred from kITT and TyG Index values. Both nutritional interventions restored liver morphofunctional patterns, but only HPD restored lipid peroxidation.ConclusionsOur data showed that 12-week intake of an isocaloric moderately high-protein diet consistently restored high-sucrose-induced central adiposity and obesity in addition to the attenuation of other important metabolic outcomes, such as improvement of glucolipid homeostasis associated to increased insulin sensitivity and reversal of hepatic steatosis. On the other hand, simple withdrawal from high-sucrose consumption also promoted the abovementioned metabolic outcomes with no impact on body weight.

Project description:BackgroundA growing amount of data suggests that n-3 (ω-3) polyunsaturated fatty acid (PUFA) intake may modify the genetic association with weight change.ObjectivesWe aimed to prospectively test interactions of habitual consumption of n-3 PUFAs or fish, the major food source, with overall genetic susceptibility on long-term weight change.DesignGene-diet interactions were examined in 11,330 women from the Nurses' Health Study (NHS), 6773 men from the Health Professionals Follow-Up Study (HPFS), and 6254 women from the Women's Health Initiative (WHI).ResultsIn the NHS and HPFS cohorts, food-sourced long-chain n-3 PUFA intake showed directionally consistent interactions with genetic risk score on long-term changes in BMI (P-interaction = 0.01 in the HPFS, 0.15 in the NHS, and 0.01 in both cohorts combined). Such interactions were successfully replicated in the WHI, an independent cohort (P-interaction = 0.02 in the WHI and 0.01 in the combined 3 cohorts). The genetic associations with changes in BMI (in kg/m2) consistently decreased (0.15, 0.10, 0.07, and -0.14 per 10 BMI-increasing alleles) across the quartiles of long-chain n-3 PUFAs in the combined cohorts. In addition, high fish intake also attenuated the genetic associations with long-term changes in BMI in the HPFS (P-interaction = 0.01), NHS (P-interaction = 0.03), WHI (P-interaction = 0.10), and the combined cohorts (P-interaction = 0.01); and the differences in BMI changes per 10 BMI-increasing alleles were 0.16, 0.06, -0.08, and -0.18, respectively, across the categories (≤1, 1∼4, 4∼6, and ≥7 servings/wk) of total fish intake. Similar interactions on body weight were observed for fish intake (P-interaction = 0.003) and long-chain n-3 PUFA intake (P-interaction = 0.12).ConclusionOur study provides replicable evidence to show that high intakes of fish and long-chain n-3 PUFAs are associated with an attenuation of the genetic association with long-term weight gain based on results from 3 prospective cohorts of Caucasians.

Project description:BackgroundSeveral prospective Western studies have reported an inverse association of vegetable and fruit intake with dementia risk. However, there is limited epidemiologic evidence in Asians. This study investigated the association of intakes of vegetables, fruits, and their nutrients on the risk of incident dementia and its subtypes in a Japanese community.MethodsA total of 1071 participants (452 men and 619 women) aged ≥60 years without dementia at baseline were prospectively followed up for 24 years. Intakes of vegetables, fruits, and nutrients were evaluated using a 70-item semiquantitative food frequency questionnaire at baseline and were categorized into quartiles separately by gender. The outcome measure was the development of dementia and its subtypes-namely, Alzheimer's disease (AD) and vascular dementia (VaD). The risk estimates of incident dementia were computed using a Cox proportional hazards model.ResultsDuring the long-term follow-up period, 464 subjects developed dementia, of whom 286 had AD and 144 had VaD. Higher vegetable intake was associated gradually with lower risk of developing dementia and AD (both P-trend < 0.05), but not VaD, after adjusting for confounders. Subjects allocated the highest quartile of vegetable intake had 27 and 31% lower risk of dementia and AD, respectively, than those with the lowest quartile. The risk of dementia decreased significantly with higher intakes of vitamin A, riboflavin, vitamin C, magnesium, calcium, and potassium (all P-trend < 0.05). Subjects with higher total dietary fiber intake tended to be at decreased risk for total dementia (P-trend = 0.07). Meanwhile, there were no significant associations between fruit intake and the risk of dementia and its subtypes.ConclusionHigher intakes of vegetables and their constituent nutrients were associated with a lower risk of dementia in Japanese older adults. A diet rich in vegetables may be beneficial in reducing the dementia risk in Asians.

Project description:ObjectiveTo investigate whether improving adherence to healthy dietary patterns interacts with the genetic predisposition to obesity in relation to long term changes in body mass index and body weight.DesignProspective cohort study.SettingHealth professionals in the United States.Participants8828 women from the Nurses' Health Study and 5218 men from the Health Professionals Follow-up Study.ExposureGenetic predisposition score was calculated on the basis of 77 variants associated with body mass index. Dietary patterns were assessed by the Alternate Healthy Eating Index 2010 (AHEI-2010), Dietary Approach to Stop Hypertension (DASH), and Alternate Mediterranean Diet (AMED).Main outcome measuresFive repeated measurements of four year changes in body mass index and body weight over follow-up (1986 to 2006).ResultsDuring a 20 year follow-up, genetic association with change in body mass index was significantly attenuated with increasing adherence to the AHEI-2010 in the Nurses' Health Study (P=0.001 for interaction) and Health Professionals Follow-up Study (P=0.005 for interaction). In the combined cohorts, four year changes in body mass index per 10 risk allele increment were 0.07 (SE 0.02) among participants with decreased AHEI-2010 score and -0.01 (0.02) among those with increased AHEI-2010 score, corresponding to 0.16 (0.05) kg versus -0.02 (0.05) kg weight change every four years (P<0.001 for interaction). Viewed differently, changes in body mass index per 1 SD increment of AHEI-2010 score were -0.12 (0.01), -0.14 (0.01), and -0.18 (0.01) (weight change: -0.35 (0.03), -0.36 (0.04), and -0.50 (0.04) kg) among participants with low, intermediate, and high genetic risk, respectively. Similar interaction was also found for DASH but not for AMED.ConclusionsThese data indicate that improving adherence to healthy dietary patterns could attenuate the genetic association with weight gain. Moreover, the beneficial effect of improved diet quality on weight management was particularly pronounced in people at high genetic risk for obesity.

Project description:BackgroundPhthalates are endocrine disrupting chemicals that may influence weight status; however, few studies have considered weight gain during pregnancy and subsequent long-term weight changes in women.ObjectiveTo determine associations of prenatal phthalate exposure with maternal weight during pregnancy and through up to seven years post-delivery.MethodsWe analyzed 15 urinary phthalate biomarker concentrations during the 2nd and 3rd trimesters among 874 pregnant women enrolled in the Programming Research in Obesity, Growth Environment and Social Stress Study in Mexico City. We examined three time-specific maternal weight outcomes: gestational weight gain (between 2nd and 3rd trimesters), short-term weight (between 3rd trimester and 12 months post-delivery), and long-term weight (between 18 months and 6-7 years post-delivery). We used Bayesian Kernel Machine Regression (BKMR) to estimate associations for the total phthalate mixture, as well as multivariable linear mixed models for individual phthalate biomarkers.ResultsAs a mixture, 2nd trimester urinary phthalate biomarker concentrations were associated with somewhat lower gestational weight gain between the 2nd and 3rd trimesters (interquartile range, IQR, difference: -0.07 standard deviations, SD; 95% credible interval, CrI: -0.20, 0.06); multivariable regression and BKMR models indicated that this inverse association was primarily driven by mono-2-ethyl-5-carboxypentyl terephthalate (MECPTP). Prenatal (2nd and 3rd trimesters) urinary phthalate mixture concentrations were positively associated with maternal weight change through 12 months postpartum (IQR difference: 0.11 SD; 95% CrI: 0.00, 0.23); these associations persisted from 18 months to 6-7 years follow-up (IQR difference: 0.07 SD; 95% CrI: 0.04, 0.10). Postpartum weight changes were associated with mono-3-carboxypropyl phthalate (MCPP) and MECPTP.ConclusionsPrenatal phthalate exposure was inversely associated with gestational weight gain and positively associated with long-term changes in maternal weight. Further investigation is required to understand how phthalates may influence body composition and whether they contribute to the development of obesity and other cardiometabolic diseases in women.

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Improving fruit and vegetable intake attenuates the genetic association with long-term weight gain.

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Improving fruit and vegetable intake attenuates the genetic association with long-term weight gain.

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