AlPater Posted February 21, 2018 Author Report Share Posted February 21, 2018 Cognitive response to fish oil, blueberry, and combined supplementation in older adults with subjective cognitive impairment. McNamara RK, Kalt W, Shidler MD, McDonald J, Summer SS, Stein AL, Stover AN, Krikorian R. Neurobiol Aging. 2018 Apr;64:147-156. doi: 10.1016/j.neurobiolaging.2017.12.003. Epub 2017 Dec 12. PMID: 29458842 Abstract Given evidence that eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and anthocyanin-rich blueberries provide neurocognitive benefit, we investigated long-term supplementation in older adults with cognitive complaints. In a 24-week randomized, double-blind, placebo-controlled trial, elderly men and women received daily fish oil (FO) or blueberry (BB) or both. Diet records confirmed that participants reduced background consumption of EPA, DHA, and anthocyanins as prescribed. Erythrocyte EPA + DHA composition increased in the FO groups (p = 0.0001). Total urinary anthocyanins did not differ between the groups after supplementation but glycoside and native (food) forms increased only in the BB-supplemented groups. The FO (p = 0.03) and BB (p = 0.05) groups reported fewer cognitive symptoms, and the BB group showed improved memory discrimination (p = 0.04), indicating that supplementation improved cognition. Cognitive benefit in the BB group was associated with the presence of urinary anthocyanins reflecting recent BB intake but not with anthocyanin metabolites. However, combined FO + BB treatment was not associated with cognitive enhancement as expected. KEYWORDS: Aging; Anthocyanins; Blueberries; Dementia; Memory; Omega-3 fatty acids Perfluoroalkyl substances, glucose homeostasis, and gestational diabetes mellitus in Chinese pregnant women: A repeat measurement-based prospective study. Wang H, Yang J, Du H, Xu L, Liu S, Yi J, Qian X, Chen Y, Jiang Q, He G. Environ Int. 2018 Feb 16;114:12-20. doi: 10.1016/j.envint.2018.01.027. [Epub ahead of print] PMID: 29459131 Abstract BACKGROUND: Exposure to perfluoroalkyl substances (PFASs) can affect glucose homeostasis and has been suggested as a potential risk of diabetes mellitus, but data are limited for pregnant women. OBJECTIVES: We aimed to explore the associations of exposure to PFASs with glucose homeostasis and gestational diabetes mellitus (GDM) in Chinese pregnant women. METHODS: The current study was conducted in Hebei Province of Northern China between 2013 and 2014 and 560 pregnant women were recruited in their early term of pregnancy and two representative serum PFASs, perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS), were measured. In 385 pregnant women who completed oral glucose tolerance test (OGTT), the associations of serum PFOA and PFOS concentrations with fasting blood glucose (FBG), fasting insulin (FIns), and homeostasis model assessment of insulin resistance (HOMA-IR) in the early, middle, and late terms of pregnancy and occurrence of GDM were examined using linear and Cox proportional hazard regression models. The reproducibility of serum PFASs during pregnancy was assessed in 230 pregnant women. RESULTS: The intraclass correlation coefficients of serum PFASs, covariates, and outcomes based on averaged repeat measurement (0.35-0.96) were higher than those based on single measurement (0.16-0.92). Serum PFOA was positively associated with averaged FIns and HOMA-IR in the early, middle, and late terms of pregnancy and averaged blood glucose level at 1 h and 2 h of OGTT, but serum PFOS tended to be negatively associated with averaged FBG and OGTT blood glucose. The adjusted hazard ratios of GDM associated with serum PFOA and PFOS were 1.98 (95% confidence interval: 0.70-5.57; p-value: 0.197) and 0.71 (0.29-1.75; 0.453), respectively. CONCLUSIONS: Our data raised a possibility that exposure to PFASs might have different influences on glucose homeostasis and GDM in Chinese pregnant women. More lab and human studies are needed to further test the hypothesis and investigate potential mechanisms. KEYWORDS: Chinese pregnant women; Gestational diabetes mellitus; Glucose homeostasis; Perfluoroalkyl substances; Prospective study; Repeat measurement Body mass index and age at natural menopause: an international pooled analysis of 11 prospective studies. Zhu D, Chung HF, Pandeya N, Dobson AJ, Kuh D, Crawford SL, Gold EB, Avis NE, Giles GG, Bruinsma F, Adami HO, Weiderpass E, Greenwood DC, Cade JE, Mitchell ES, Woods NF, Brunner EJ, Simonsen MK, Mishra GD. Eur J Epidemiol. 2018 Feb 19. doi: 10.1007/s10654-018-0367-y. [Epub ahead of print] PMID: 29460096 Abstract Current evidence on the association between body mass index (BMI) and age at menopause remains unclear. We investigated the relationship between BMI and age at menopause using data from 11 prospective studies. A total of 24,196 women who experienced menopause after recruitment was included. Baseline BMI was categorised according to the WHO criteria. Age at menopause, confirmed by natural cessation of menses for ≥ 12 months, was categorised as < 45 years (early menopause), 45-49, 50-51 (reference category), 52-53, 54-55, and ≥ 56 years (late age at menopause). We used multinomial logistic regression models to estimate multivariable relative risk ratios (RRRs) and 95% confidence intervals (CI) for the associations between BMI and age at menopause. The mean (standard deviation) age at menopause was 51.4 (3.3) years, with 2.5% of the women having early and 8.1% late menopause. Compared with those with normal BMI (18.5-24.9 kg/m2), underweight women were at a higher risk of early menopause (RRR 2.15, 95% CI 1.50-3.06), while overweight (1.52, 1.31-1.77) and obese women (1.54, 1.18-2.01) were at increased risk of late menopause. Overweight and obesity were also significantly associated with around 20% increased risk of menopause at ages 52-53 and 54-55 years. We observed no association between underweight and late menopause. The risk of early menopause was higher among obese women albeit not significant (1.23, 0.89-1.71). Underweight women had over twice the risk of experiencing early menopause, while overweight and obese women had over 50% higher risk of experiencing late menopause. KEYWORDS: Age at menopause; Obesity; Prospective studies; Underweight Alcohol consumption and risk of hematological malignancies: A meta-analysis of prospective studies. Psaltopoulou T, Sergentanis TN, Ntanasis-Stathopoulos I, Tzanninis IG, Tsilimigras DI, Dimopoulos MA. Int J Cancer. 2018 Feb 20. doi: 10.1002/ijc.31330. [Epub ahead of print] PMID: 29460427 Abstract Current convincing evidence suggests that alcohol intake increases the risk of several carcinomas, which might subsequently lead to a recommendation towards limiting alcohol consumption. However, there are accumulating data worth meta-analyzing that show a different effect on the risk of hematological malignancies. Eligible cohort studies were sought in PubMed database up to August 31, 2016. Separate analyses were performed by subtype of hematological malignancy (non-Hodgkin lymphoma [NHL] and subtypes, Hodgkin lymphoma [HL], leukemia and subtypes), time status (ever, current, former), level of consumption (light, moderate, heavy), alcoholic beverage (total alcohol, beer, liquor, wine), and gender. Moderate and heavy alcohol consumption were significantly associated with reduced risk of NHL (relative risk [RR]=0.85, 95% confidence interval [CI]: 0.80-0.90 and RR=0.73, 95%CI: 0.60-0.89, respectively); a protective trend was also shown for light alcohol intake (RR=0.93, 95%CI:0.87-1.00). Specifically, beer consumption was associated with reduced NHL risk (RR=0.88, 95%CI: 0.81-0.95). However, the association regarding other alcoholic beverages seemed null. The beneficial effects of alcohol mainly pertained to Diffuse Large B-Cell Lymphoma (DLBCL) (RR=0.83, 95%CI:0.77-0.89) and Follicular Lymphoma (FL) (RR=0.85, 95%CI:0.78-0.93). There was also no association between alcohol consumption and risk of HL or leukemias. In contrast to most solid malignancies, alcohol seems to confer a protective effect on NHL risk, especially on DLBCL and FL subtypes, with beer being notably beneficial. KEYWORDS: Alcohol; Hodgkin lymphoma; leukemia; meta-analysis; non-Hodgkin lymphoma Chilli intake is inversely associated with hypertension among adults. Shi Z, Riley M, Brown A, Page A. Clin Nutr ESPEN. 2018 Feb;23:67-72. doi: 10.1016/j.clnesp.2017.12.007. Epub 2017 Dec 26. PMID: 29460816 Abstract BACKGROUND & AIMS: This study aimed to examine the association between chilli intake and the incidence of hypertension in a Chinese adult population. METHODS: Adults aged 20-75 years in the China Health and Nutrition Survey were followed from 1991 to 2011. Dietary data were collected during home visits using a 3-day food record in 1991, 1993, 1997, 2000, 2004, 2006, 2009 and 2011. Cox regression was used in the analysis. Blood pressure was measured at each data collection point. RESULTS: 13,670 adults were followed for a median of 9.0 years. During 132,089 person years of follow-up 4040 subjects developed hypertension. Chilli consumption was inversely associated with the incidence of hypertension. The incidence rate of hypertension was 30.5, 33.4, 31.9, and 24.0 per 1000 person years among those who consumed no chilli or 1-20, 20.1-50, ≥50.1 g/day respectively. Adjusting for age, gender, energy intake, sodium and fat intake, smoking, alcohol consumption and physical activity, those with increasing cumulative average chilli intake were less likely to develop hypertension: 0, 1-20, 20.1-50 and ≥50.1 g/day had a hazard ratio (HR) for hypertension of 1.00, 0.80 (95%CI 0.73-0.88), 0.81 (0.73-0.89) and 0.65 (0.57-0.75) (p for trend <0.001) respectively. The association was independent of overall dietary patterns and BMI. There was no significant interaction between chilli intake and gender, income, education and residence (urban/rural) in relation to the risk of hypertension. CONCLUSIONS: Chilli intake is inversely associated with the risk of developing hypertension in Chinese adults. KEYWORDS: Chilli intake; Cohort study; Hypertension The relation between dietary intake and glaucoma: a systematic review. Ramdas WD. Acta Ophthalmol. 2018 Feb 20. doi: 10.1111/aos.13662. [Epub ahead of print] Review. PMID: 29461678 Abstract PURPOSE: A common question of patients to their physician is what they can do themselves against glaucoma, except taking their daily medication. However, for ophthalmologists, it is often hard to give their patients an advice on their dietary intake. To help ophthalmologists in answering this question, an overview of the current scientific literature on the association of nutrients with glaucoma is presented. METHODS: A comprehensive systematic review was conducted in which articles published up to September 2017 were identified in PubMed and reference lists. Nutrients were categorized into minerals and trace elements, nutrition with antioxidative properties and omega-fatty acids. RESULTS: The literature search revealed a total of 407 articles of which a total of 46 met the inclusion criteria. Most of these articles studied the effect of nutrients on open-angle glaucoma. Many trace elements have been investigated in the literature, but the most interesting are selenium and iron (both may increase the risk of glaucoma). Investigated nutrients with antioxidative properties and omega-fatty acids included glutathione, nitric oxide, carotenoids, flavonoids, and omega-3 and omega-6 fatty acids. Of these, glutathione, nitric oxide, and flavonoids had a significant protective effect on glaucoma. CONCLUSION: Intake of selenium and iron may increase the risk of glaucoma, though, only few studies have been done on this topic. Nitric oxide present in other dark green leafy vegetables seems to have a beneficial effect on glaucoma. However, the evidence for an association of dietary intake with glaucoma is still not strong. More (longitudinal and randomized clinical trials) studies are required to make the presented findings clinically applicable. KEYWORDS: antioxidants; dietary intake; fatty acids; glaucoma; glutathione; minerals; nitric oxide; trace elements Regular Yogurt Intake and Risk of Cardiovascular Disease Among Hypertensive Adults. Buendia JR, Li Y, Hu FB, Cabral HJ, Bradlee ML, Quatromoni PA, Singer MR, Curhan GC, Moore LL. Am J Hypertens. 2018 Feb 15. doi: 10.1093/ajh/hpx220. [Epub ahead of print] PMID: 29462263 Abstract BACKGROUND: High blood pressure (HBP) is a major cardiovascular disease (CVD) risk factor. Clinical trials including Dietary Approaches to Stop Hypertension (DASH) have demonstrated beneficial effects of dairy consumption on risks of HBP and CVD. Yogurt, a fermented dairy product, may independently be related to CVD risk. OBJECTIVE: To evaluate the association between yogurt consumption and CVD risk among hypertensive individuals in 2 large cohorts and to determine whether the association differs among those whose eating pattern more closely resembles the DASH diet. METHODS: Overall, 55,898 female Nurses' Health Study (NHS) and 18,232 male Health Professionals Follow-Up Study (HPFS) participants with prevalent HBP were included. Cumulative average estimates of yogurt intake from validated food frequency questionnaires were related to verified self-reported CVD outcomes using Cox proportional hazards models. Hazard ratios and 95% confidence intervals (CI) were adjusted for CVD risk factors, medications, and diet covariates. RESULTS: Yogurt intake was inversely associated with CVD risk (myocardial infarction and stroke) among hypertensive participants (P <0.01 in both cohorts). Among participants consuming ≥2 servings/week of yogurt, NHS women had a 17% (95% CI: 0.74-0.92) lower risk while HPFS men experienced a 21% (95% CI: 0.66-0.96) lower CVD risk compared to those who consumed <1 serving/month. Regular yogurt consumers with higher DASH diet scores had 16% (95% CI: 0.73-0.96) and 30% (95% CI: 0.57-0.85) CVD risk reductions in the 2 cohorts, respectively. CONCLUSION: Hypertensive men and women who consumed ≥2 servings/week of yogurt, especially in the context of a healthy diet, were at lower risk for developing CVD. Prediagnostic Serum Vitamin D Levels and the Risk of Crohn's Disease and Ulcerative Colitis in European Populations: A Nested Case-Control Study. Opstelten JL, Chan SSM, Hart AR, van Schaik FDM, Siersema PD, Lentjes EGWM, Khaw KT, Luben R, Key TJ, Boeing H, Bergmann MM, Overvad K, Palli D, Masala G, Racine A, Carbonnel F, Boutron-Ruault MC, Tjønneland A, Olsen A, Andersen V, Kaaks R, Kühn T, Tumino R, Trichopoulou A, Peeters PHM, Verschuren WMM, Witteman BJM, Oldenburg B. Inflamm Bowel Dis. 2018 Feb 15;24(3):633-640. doi: 10.1093/ibd/izx050. PMID: 29462382 Abstract BACKGROUND: A low vitamin D status has been put forward as a potential risk factor for the development of inflammatory bowel disease (IBD). This study investigated the association between prediagnostic circulating vitamin D concentrations and dietary intakes of vitamin D, and the risk of Crohn's disease (CD) and ulcerative colitis (UC). METHODS: Among 359,728 participants of the European Prospective Investigation into Cancer and Nutrition cohort, individuals who developed CD or UC after enrollment were identified. Each case was matched with2 controls by center, gender, age, date of recruitment, and follow-up time. At cohort entry, blood samples were collected and dietary vitamin D intakes were obtained from validated food frequency questionnaires. Serum 25-hydroxyvitamin D levels were measured using liquid chromatography-tandem mass spectrometry. Conditional logistic regression was performed to determine the odds of CD and UC. RESULTS: Seventy-two participants developed CD and 169 participants developed UC after a median follow-up of 4.7 and 4.1 years, respectively. Compared with the lowest quartile, no associations with the 3 higher quartiles of vitamin D concentrations were observed for CD (p trend = 0.34) or UC (p trend = 0.66). Similarly, no associations were detected when serum vitamin D levels were analyzed as a continuous variable. Dietary vitamin D intakes were not associated with CD (p trend = 0.39) or UC (p trend = 0.83). CONCLUSIONS: Vitamin D status was not associated with the development of CD or UC. This does not suggest a major role for vitamin D deficiency in the etiology of IBD, although larger studies are needed to confirm these findings. The Quest to Define Individual Risk After Living Kidney Donation. Poggio ED, Reese PP. Ann Intern Med. 2018 Feb 20;168(4):296-297. doi: 10.7326/M17-3249. Epub 2018 Jan 30. No abstract available. PMID: 29379960 Living-donor kidney transplantation has been a cornerstone treatment for patients with end-stage renal disease (ESRD) since the first living donation in the mid-1950s. In the United States, approximately 140 000 living persons have chosen to donate a kidney since 1988 and their kidneys currently account for about one third of all kidney transplants. Primary care physicians and other internists should have insight into donor outcomes because patients with kidney disease and potential donors may seek their advice. Despite more than 6 decades of living kidney donation, large and high-quality studies of ESRD and other relevant outcomes after donation have been completed only in the past decade. O'Keeffe and colleagues (1) report a meta-analysis that concludes that living kidney donors face elevated relative risks for ESRD, preeclampsia, and high diastolic blood pressure. Unfortunately, the field is still a long way from offering precise estimates to potential donors about donation-related risk. Determining the health consequences of kidney donation poses major methodological challenges, which include identifying an equally healthy group of nondonors for comparison. O'Keeffe and colleagues rated the quality of these comparison groups in the studies in their analysis and found that most comparison nondonors were probably not as healthy as living kidney donors. An additional challenge is that although a reduction in glomerular filtration rate of 25% to 40% and small perturbations in renal metabolism (such as higher levels of uric acid and fibroblast growth factor 23) are evident by the early postdonation period (2), clinically meaningful consequences of having a single kidney may not manifest for decades. The meta-analysis found no evidence of higher mortality or cardiovascular disease rates associated with kidney donation—an important finding because a higher risk for death among donors was reported in a Scandinavian cohort (3). However, on the basis of 3 studies, the meta-analysis found that living kidney donation was associated with a relative risk for ESRD of 8.83. Based on 2 studies, the relative risk for preeclampsia for donors who subsequently became pregnant was 2.12. The limited evidence related to key outcomes in kidney donors is concerning. Median follow-up in the 3 largest donor cohorts was less than 10 years. For studies with more than 100 donors, the longest follow-up was a mean of 24 years. Potential donors should be cognizant that the absolute rate of ESRD after nephrectomy was low (about 0.5 event per 1000 person-years). However, we must also recognize that a low ESRD rate reported for 8 years of follow-up (from a U.S. cohort) or 15 years of follow-up (from a Norwegian cohort) should not be particularly reassuring when advising a 25-year-old donor. The authors also correctly acknowledge that the findings may not apply to donors in low- and middle-income countries. Disclosure of the risks reported by O'Keeffe and colleagues should be standard practice when counseling potential kidney donors, and such disclosures are incorporated into some existing guidelines (4, 5). Similarly, potential donors should understand how complications of nephrectomy will or will not be addressed by transplant programs or the health system. For example, in some nations, prior living donors who develop ESRD are awarded substantial priority in allocation of deceased-donor kidneys (6). However, whether this counseling influences many donation decisions is unclear because most donors are already highly motivated by sympathy for a loved one. Many are young: 28% of U.S. donors in 2016 were younger than 35 years (7), and these persons may have difficulty imagining the possibility of ESRD or other problems far in the future. For those of us who counsel potential donors, there is reason for pessimism that we will soon be able to estimate individual risk with any precision. Three issues inhibit prediction (8, 9). First, because rates of ESRD are so low, only a handful among many donors with highly similar characteristics at donation will develop ESRD. Second, the risk for ESRD (or other complications) probably depends substantially on factors unexamined in current studies. If validated by future research, some of these risks might be uncovered during donor evaluation (such as an APOL1 high-risk genetic variant or low birthweight). However, other unforeseeable events many years after donation likely provide the “second hit” that predisposes a person to ESRD (for example, diabetes or acute kidney injury). A third barrier is that times change, which can undermine research relevance. Although we might need cohorts with 30-year follow-up to accrue sufficient events to identify at-risk subgroups, population demographics and medical practice will also evolve. For example, the prevalence of obesity—a risk factor for ESRD—has rapidly increased. One cohort from 3 large centers reported that obesity rates among living donors more than tripled from 8% in 1963 to 1974 to 26% in 1997 to 2007 (10). In the absence of precision risk prediction, the transplant field has some immediate opportunities. The first is orienting selection toward older donors. This orientation would have a strong ethical foundation: A 15-year ESRD risk horizon is more meaningful for a 55-year-old than a 25-year-old potential donor. The second is candid discussion with all potential donors about the limits of knowledge about long-term outcomes. The third opportunity is determining how best to counsel potential donors. We lack guidance about whether and how to consider the motives that drive an individual to donate a kidney. For many, kidney donation is affirming and meaningful. We need to hear what donors feel, think, want, and understand about excess risk and how they use this information to reconcile long-term medical risk with psychosocial health and quality of life while making the decision. The meaning an individual might find through donation is very difficult to quantify. Yet, the field must contend with these issues when determining acceptable risk thresholds that are based on highly uncertain estimates at the individual level (5). Finally, transplant programs and primary care physicians should help prior donors adopt healthy lifestyles to prevent and treat threats to kidney health after donation, such as diabetes, that may harm their kidneys later in life. O'Keeffe and colleagues have provided a definitive analysis of the known medical risks associated with donor nephrectomy in the medium-term after donation. However, a close look at the data reminds us that long-term outcomes are uncertain and that precision medicine has not arrived for risk prediction in kidney donors. In the meantime, we should do our best to protect potential donors with careful selection, candor about harms, open discussion about unknowns, and a commitment to their lifelong health after nephrectomy. Those goals give us plenty of work to do. >>>>>>>>>>>>>>>>>>>>>> Mid- and Long-Term Health Risks in Living Kidney Donors: A Systematic Review and Meta-analysis. O'Keeffe LM, Ramond A, Oliver-Williams C, Willeit P, Paige E, Trotter P, Evans J, Wadström J, Nicholson M, Collett D, Di Angelantonio E. Ann Intern Med. 2018 Feb 20;168(4):276-284. doi: 10.7326/M17-1235. Epub 2018 Jan 30. PMID: 29379948 Abstract BACKGROUND: Long-term health risks for adults who donate kidneys are unclear. PURPOSE: To summarize evidence about mid- and long-term health risks associated with living kidney donation in adults. DATA SOURCES: PubMed, Embase, Scopus, and PsycINFO without language restriction from April 1964 to July 2017. STUDY SELECTION: Observational studies with at least 1 year of follow-up that compared health outcomes in adult living kidney donors versus nondonor populations. DATA EXTRACTION: Two investigators independently extracted study data and assessed study quality. DATA SYNTHESIS: 52 studies, comprising 118 426 living kidney donors and 117 656 nondonors, were included. Average follow-up was 1 to 24 years. No evidence suggested higher risk for all-cause mortality, cardiovascular disease, hypertension, type 2 diabetes, or adverse psychosocial health outcomes in living kidney donors than in nondonor populations. Donors had higher diastolic blood pressure, lower estimated glomerular filtration rates, and higher risk for end-stage renal disease (ESRD) (relative risk [RR], 8.83 [95% CI, 1.02 to 20.93]) and preeclampsia in female donors (RR, 2.12 [CI, 1.06 to 4.27]). Despite the increased RR, donors had low absolute risk for ESRD (incidence rate, 0.5 event [CI, 0.1 to 4.9 events] per 1000 person-years) and preeclampsia (incidence rate, 5.9 events [CI, 2.9 to 8.9 events] per 100 pregnancies). LIMITATION: Generalizability was limited by selected control populations, few studies reported pregnancy-related outcomes, and few studies were from low- and middle-income countries. CONCLUSION: Although living kidney donation is associated with higher RRs for ESRD and preeclampsia, the absolute risk for these outcomes remains low. Compared with nondonor populations, living kidney donors have no increased risk for other major chronic diseases, such as type 2 diabetes, or for adverse psychosocial outcomes. Quote Link to comment Share on other sites More sharing options...
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