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1.
JAMA ; 322(12): 1150-1151, 2019 Sep 24.
Artigo em Inglês | MEDLINE | ID: mdl-31550012
2.
Adv Food Nutr Res ; 89: 1-52, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31351524

RESUMO

Beverages make important contributions to nutritional intake and their role in health has received much attention. This review focuses on the genetic determinants of common beverage consumption and how research in this field is contributing insight to what and how much we consume and why this genetic knowledge matters from a research and public health perspective. The earliest efforts in gene-beverage behavior mapping involved genetic linkage and candidate gene analysis but these approaches have been largely replaced by genome-wide association studies (GWAS). GWAS have identified biologically plausible loci underlying alcohol and coffee drinking behavior. No GWAS has identified variants specifically associated with consumption of tea, juice, soda, wine, beer, milk or any other common beverage. Thus far, GWAS highlight an important behavior-reward component (as opposed to taste) to beverage consumption which may serve as a potential barrier to dietary interventions. Loci identified have been used in Mendelian randomization and gene×beverage interaction analysis of disease but results have been mixed. This research is necessary as it informs the clinical relevance of SNP-beverage associations and thus genotype-based personalized nutrition, which is gaining interest in the commercial and public health sectors.

3.
Eur J Nutr ; 2019 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-31154491

RESUMO

PURPOSE: Coffee is widely consumed and implicated in numerous health outcomes but the mechanisms by which coffee contributes to health is unclear. The purpose of this study was to test the effect of coffee drinking on candidate proteins involved in cardiovascular, immuno-oncological and neurological pathways. METHODS: We examined fasting serum samples collected from a previously reported single blinded, three-stage clinical trial. Forty-seven habitual coffee consumers refrained from drinking coffee for 1 month, consumed 4 cups of coffee/day in the second month and 8 cups/day in the third month. Samples collected after each coffee stage were analyzed using three multiplex proximity extension assays that, after quality control, measured a total of 247 proteins implicated in cardiovascular, immuno-oncological and neurological pathways and of which 59 were previously linked to coffee exposure. Repeated measures ANOVA was used to test the relationship between coffee treatment and each protein. RESULTS: Two neurology-related proteins including carboxypeptidase M (CPM) and neutral ceramidase (N-CDase or ASAH2), significantly increased after coffee intake (P < 0.05 and Q < 0.05). An additional 46 proteins were nominally associated with coffee intake (P < 0.05 and Q > 0.05); 9, 8 and 29 of these proteins related to cardiovascular, immuno-oncological and neurological pathways, respectively, and the levels of 41 increased with coffee intake. CONCLUSIONS: CPM and N-CDase levels increased in response to coffee intake. These proteins have not previously been linked to coffee and are thus novel markers of coffee response worthy of further study. CLINICAL TRIAL REGISTRY: http://www.isrctn.com/ISRCTN12547806 .

5.
Hum Mol Genet ; 28(14): 2449-2457, 2019 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-31046077

RESUMO

Except for drinking water, most beverages taste bitter or sweet. Taste perception and preferences are heritable and determinants of beverage choice and consumption. Consumption of several bitter- and sweet-tasting beverages has been implicated in development of major chronic diseases. We performed a genome-wide association study (GWAS) of self-reported bitter and sweet beverage consumption among ~370 000 participants of European ancestry, using a two-staged analysis design. Bitter beverages included coffee, tea, grapefruit juice, red wine, liquor and beer. Sweet beverages included artificially and sugar sweetened beverages (SSBs) and non-grapefruit juices. Five loci associated with total bitter beverage consumption were replicated (in/near GCKR, ABCG2, AHR, POR and CYP1A1/2). No locus was replicated for total sweet beverage consumption. Sub-phenotype analyses targeting the alcohol, caffeine and sweetener components of beverages yielded additional loci: (i) four loci for bitter alcoholic beverages (GCKR, KLB, ADH1B and AGBL2); (ii) five loci for bitter non-alcoholic beverages (ANXA9, AHR, POR, CYP1A1/2 and CSDC2); (iii) 10 loci for coffee; six novel loci (SEC16B, TMEM18, OR8U8, AKAP6, MC4R and SPECC1L-ADORA2A); (iv) FTO for SSBs. Of these 17 replicated loci, 12 have been associated with total alcohol consumption, coffee consumption, plasma caffeine metabolites or BMI in previous GWAS; none was involved in known sweet and bitter taste transduction pathways. Our study suggests that genetic variants related to alcohol consumption, coffee consumption and obesity were primary genetic determinants of bitter and sweet beverage consumption. Whether genetic variants related to taste perception are associated with beverage consumption remains to be determined.

6.
JAMA ; 321(11): 1081-1095, 2019 03 19.
Artigo em Inglês | MEDLINE | ID: mdl-30874756

RESUMO

Importance: Cholesterol is a common nutrient in the human diet and eggs are a major source of dietary cholesterol. Whether dietary cholesterol or egg consumption is associated with cardiovascular disease (CVD) and mortality remains controversial. Objective: To determine the associations of dietary cholesterol or egg consumption with incident CVD and all-cause mortality. Design, Setting, and Participants: Individual participant data were pooled from 6 prospective US cohorts using data collected between March 25, 1985, and August 31, 2016. Self-reported diet data were harmonized using a standardized protocol. Exposures: Dietary cholesterol (mg/day) or egg consumption (number/day). Main Outcomes and Measures: Hazard ratio (HR) and absolute risk difference (ARD) over the entire follow-up for incident CVD (composite of fatal and nonfatal coronary heart disease, stroke, heart failure, and other CVD deaths) and all-cause mortality, adjusting for demographic, socioeconomic, and behavioral factors. Results: This analysis included 29 615 participants (mean [SD] age, 51.6 [13.5] years at baseline) of whom 13 299 (44.9%) were men and 9204 (31.1%) were black. During a median follow-up of 17.5 years (interquartile range, 13.0-21.7; maximum, 31.3), there were 5400 incident CVD events and 6132 all-cause deaths. The associations of dietary cholesterol or egg consumption with incident CVD and all-cause mortality were monotonic (all P values for nonlinear terms, .19-.83). Each additional 300 mg of dietary cholesterol consumed per day was significantly associated with higher risk of incident CVD (adjusted HR, 1.17 [95% CI, 1.09-1.26]; adjusted ARD, 3.24% [95% CI, 1.39%-5.08%]) and all-cause mortality (adjusted HR, 1.18 [95% CI, 1.10-1.26]; adjusted ARD, 4.43% [95% CI, 2.51%-6.36%]). Each additional half an egg consumed per day was significantly associated with higher risk of incident CVD (adjusted HR, 1.06 [95% CI, 1.03-1.10]; adjusted ARD, 1.11% [95% CI, 0.32%-1.89%]) and all-cause mortality (adjusted HR, 1.08 [95% CI, 1.04-1.11]; adjusted ARD, 1.93% [95% CI, 1.10%-2.76%]). The associations between egg consumption and incident CVD (adjusted HR, 0.99 [95% CI, 0.93-1.05]; adjusted ARD, -0.47% [95% CI, -1.83% to 0.88%]) and all-cause mortality (adjusted HR, 1.03 [95% CI, 0.97-1.09]; adjusted ARD, 0.71% [95% CI, -0.85% to 2.28%]) were no longer significant after adjusting for dietary cholesterol consumption. Conclusions and Relevance: Among US adults, higher consumption of dietary cholesterol or eggs was significantly associated with higher risk of incident CVD and all-cause mortality in a dose-response manner. These results should be considered in the development of dietary guidelines and updates.


Assuntos
Doenças Cardiovasculares/etiologia , Colesterol na Dieta/efeitos adversos , Ovos/efeitos adversos , Mortalidade , Adulto , Idoso , Dieta , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Inquéritos Nutricionais , Estudos Prospectivos , Fatores de Risco , Autorrelato
7.
PLoS One ; 14(3): e0213948, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30883587

RESUMO

OBJECTIVES: Age-related cognitive decline is a well-known phenomenon after age 65 but little is known about earlier changes and prior studies are based on relatively small samples. We investigated the impact of age on cognitive decline in the largest population sample to date including young to old adults. METHOD: Between 100,352 and 468,534 participants aged 38-73 years from UK Biobank completed at least one of seven self-administered cognitive functioning tests: prospective memory (PM), pairs matching (Pairs), fluid intelligence (FI), reaction time (RT), symbol digit substitution, trail making A and B. Up to 26,005 participants completed at least one of two follow-up assessments of PM, Pairs, FI and RT. Multivariable regression models examined the association between age (<45[reference], 45-49, 50-54, 55-59, 60-64, 65+) and cognition scores at baseline. Mixed models estimated the impact of age on cognitive decline over follow-up (~5.1 years). RESULTS: FI was higher between ages 50 and 64 and lower at 65+ compared to <45 at baseline. Performance on all other baseline tests was lower with older age: with increasing age category, difference in test scores ranged from 2.5 to 7.8%(P<0.0001). Compared to <45 at baseline, RT and Pairs performance declined faster across all older age cohorts (3.0 and 1.2% change, respectively, with increasing age category, P<0.0001). Cross-sectional results yielded 8 to 12-fold higher differences in RT and Pairs with age compared to longitudinal results. CONCLUSIONS: Our findings suggest that declines in cognitive abilities <65 are small. The cross-sectional differences in cognition scores for middle to older adult years may be due in part to age cohort effects.

8.
Nutrients ; 11(2)2019 Feb 16.
Artigo em Inglês | MEDLINE | ID: mdl-30781466

RESUMO

Coffee is one of the most widely consumed beverages in the world and is also a major source of caffeine for most populations [...].


Assuntos
Bebidas/efeitos adversos , Cafeína/efeitos adversos , Café/efeitos adversos , Humanos
9.
JAMA Intern Med ; 178(12): 1726-1727, 2018 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-30508056
10.
Nutrients ; 10(12)2018 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-30513727

RESUMO

Coffee is widely consumed and contains many bioactive compounds, any of which may impact pathways related to disease development. Our objective was to identify individual lipid changes in response to coffee drinking. We profiled the lipidome of fasting serum samples collected from a previously reported single blinded, three-stage clinical trial. Forty-seven habitual coffee consumers refrained from drinking coffee for 1 month, consumed 4 cups of coffee/day in the second month and 8 cups/day in the third month. Samples collected after each coffee stage were subject to quantitative lipidomic profiling using ion-mobility spectrometry⁻mass spectrometry. A total of 853 lipid species mapping to 14 lipid classes were included for univariate analysis. Three lysophosphatidylcholine (LPC) species including LPC (20:4), LPC (22:1) and LPC (22:2), significantly decreased after coffee intake (p < 0.05 and q < 0.05). An additional 72 species mapping to the LPC, free fatty acid, phosphatidylcholine, cholesteryl ester and triacylglycerol classes of lipids were nominally associated with coffee intake (p < 0.05 and q > 0.05); 58 of these decreased after coffee intake. In conclusion, coffee intake leads to lower levels of specific LPC species with potential impacts on glycerophospholipid metabolism more generally.

11.
Sci Rep ; 8(1): 16414, 2018 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-30442986

RESUMO

Consumption of coffee, tea and alcohol might be shaped by individual differences in bitter taste perception but inconsistent observational findings provide little insight regarding causality. We conducted Mendelian randomization analyses using genetic variants associated with the perception of bitter substances (rs1726866 for propylthiouracil [PROP], rs10772420 for quinine and rs2597979 for caffeine) to evaluate the intake of coffee, tea and alcohol among up to 438,870 UK Biobank participants. A standard deviation (SD) higher in genetically predicted bitterness of caffeine was associated with increased coffee intake (0.146 [95%CI: 0.103, 0.189] cups/day), whereas a SD higher in those of PROP and quinine was associated with decreased coffee intake (-0.021 [-0.031, -0.011] and -0.081 [-0.108, -0.054] cups/day respectively). Higher caffeine perception was also associated with increased risk of being a heavy (>4 cups/day) coffee drinker (OR 1.207 [1.126, 1.294]). Opposite pattern of associations was observed for tea possibly due to the inverse relationship between both beverages. Alcohol intake was only negatively associated with PROP perception (-0.141 [-1.88, -0.94] times/month per SD increase in PROP bitterness). Our results reveal that bitter perception is causally associated with intake of coffee, tea and alcohol, suggesting a role of bitter taste in the development of bitter beverage consumption.

12.
Nutrients ; 10(11)2018 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-30445721

RESUMO

Coffee, tea, caffeinated soda, and energy drinks are important sources of caffeine in the diet but each present with other unique nutritional properties. We review how our increased knowledge and concern with regard to caffeine in the diet and its impact on human health has been translated into food-based dietary guidelines (FBDG). Using the Food and Agriculture Organization list of 90 countries with FBDG as a starting point, we found reference to caffeine or caffeine-containing beverages (CCB) in 81 FBDG and CCB consumption data (volume sales) for 56 of these countries. Tea and soda are the leading CCB sold in African and Asian/Pacific countries while coffee and soda are preferred in Europe, North America, Latin America, and the Caribbean. Key themes observed across FBDG include (i) caffeine-intake upper limits to avoid risks, (ii) CCB as replacements for plain water, (iii) CCB as added-sugar sources, and (iv) health benefits of CCB consumption. In summary, FBDG provide an unfavorable view of CCB by noting their potential adverse/unknown effects on special populations and their high sugar content, as well as their diuretic, psycho-stimulating, and nutrient inhibitory properties. Few FBDG balanced these messages with recent data supporting potential benefits of specific beverage types.

13.
Nutrients ; 10(10)2018 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-30241358

RESUMO

Habitual coffee and caffeine consumption has been reported to be associated with numerous health outcomes. This perspective focuses on Mendelian Randomization (MR) approaches for determining whether such associations are causal. Genetic instruments for coffee and caffeine consumption are described, along with key concepts of MR and particular challenges when applying this approach to studies of coffee and caffeine. To date, at least fifteen MR studies have investigated the causal role of coffee or caffeine use on risk of type 2 diabetes, cardiovascular disease, Alzheimer's disease, Parkinson's disease, gout, osteoarthritis, cancers, sleep disturbances and other substance use. Most studies provide no consistent support for a causal role of coffee or caffeine on these health outcomes. Common study limitations include low statistical power, potential pleiotropy, and risk of collider bias. As a result, in many cases a causal role cannot confidently be ruled out. Conceptual challenges also arise from the different aspects of coffee and caffeine use captured by current genetic instruments. Nevertheless, with continued genome-wide searches for coffee and caffeine related loci along with advanced statistical methods and MR designs, MR promises to be a valuable approach to understanding the causal impact that coffee and caffeine have in human health.

15.
Nat Commun ; 9(1): 2536, 2018 06 29.
Artigo em Inglês | MEDLINE | ID: mdl-29959320

RESUMO

We have been alerted that in our recent Article the calculations used to transform the heritability from the observed scale to the liability scale did not take into account the individuals in category 2 of the baldness scale, who were removed in our original analysis. This led to an overestimation of the heritability on the liability scale, which should have been 0.62 instead of 0.94. Moreover, in the Title and in the Abstract, we report that we can explain 38% of the risk, while in fact that is the proportion of heritability explained by the loci we discovered. These errors do not substantially change the paper or its conclusions apart from the statement MBP is therefore probably one of the most heritable complex traits. Genome-wide significant associations and pathway analyses are not affected in any way and male-pattern baldness remains less genetically complex than other complex traits. We wish to thank Yap et al. for bringing this to our attention.

16.
JAMA Intern Med ; 178(8): 1086-1097, 2018 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-29971434

RESUMO

Importance: Prospective cohorts in North America, Europe, and Asia show consistent inverse associations between coffee drinking and mortality, including deaths from cardiovascular disease and some cancers. However, concerns about coffee, particularly among people with common genetic polymorphisms affecting caffeine metabolism and among those drinking more than 5 cups per day, remain. Objective: To evaluate associations of coffee drinking with mortality by genetic caffeine metabolism score. Design, Setting, and Participants: The UK Biobank is a population-based study that invited approximately 9.2 million individuals from across the United Kingdom to participate. We used baseline demographic, lifestyle, and genetic data form the UK Biobank cohort, with follow-up beginning in 2006 and ending in 2016, to estimate hazard ratios (HRs) for coffee intake and mortality, using multivariable-adjusted Cox proportional hazards models. We investigated potential effect modification by caffeine metabolism, defined by a genetic score of previously identified polymorphisms in AHR, CYP1A2, CYP2A6, and POR that have an effect on caffeine metabolism. Of the 502 641 participants who consented with baseline data, we included those who were not pregnant and had complete data on coffee intake and smoking status (n = 498 134). Exposures: Total, ground, instant, and decaffeinated coffee intake. Main Outcomes and Measures: All-cause and cause-specific mortality. Results: The mean age of the participants was 57 years (range, 38-73 years); 271 019 (54%) were female, and 387 494 (78%) were coffee drinkers. Over 10 years of follow-up, 14 225 deaths occurred. Coffee drinking was inversely associated with all-cause mortality. Using non-coffee drinkers as the reference group, HRs for drinking less than 1, 1, 2 to 3, 4 to 5, 6 to 7, and 8 or more cups per day were 0.94 (95% CI, 0.88-1.01), 0.92 (95% CI, 0.87-0.97), 0.88 (95% CI, 0.84-0.93), 0.88 (95% CI, 0.83-0.93), 0.84 (95% CI, 0.77-0.92), and 0.86 (95% CI, 0.77-0.95), respectively. Similar associations were observed for instant, ground, and decaffeinated coffee, across common causes of death, and regardless of genetic caffeine metabolism score. For example, the HRs for 6 or more cups per day ranged from 0.70 (95% CI, 0.53-0.94) to 0.92 (95% CI, 0.78-1.10), with no evidence of effect modification across strata of caffeine metabolism score (P = .17 for heterogeneity). Conclusions and Relevance: Coffee drinking was inversely associated with mortality, including among those drinking 8 or more cups per day and those with genetic polymorphisms indicating slower or faster caffeine metabolism. These findings suggest the importance of noncaffeine constituents in the coffee-mortality association and provide further reassurance that coffee drinking can be a part of a healthy diet.

17.
Int J Epidemiol ; 47(2): 450-459, 2018 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-29186515

RESUMO

Background: Coffee consumption has been shown to be associated with various health outcomes in observational studies. However, evidence for its association with epithelial ovarian cancer (EOC) is inconsistent and it is unclear whether these associations are causal. Methods: We used single nucleotide polymorphisms associated with (i) coffee and (ii) caffeine consumption to perform Mendelian randomization (MR) on EOC risk. We conducted a two-sample MR using genetic data on 44 062 individuals of European ancestry from the Ovarian Cancer Association Consortium (OCAC), and combined instrumental variable estimates using a Wald-type ratio estimator. Results: For all EOC cases, the causal odds ratio (COR) for genetically predicted consumption of one additional cup of coffee per day was 0.92 [95% confidence interval (CI): 0.79, 1.06]. The COR was 0.90 (95% CI: 0.73, 1.10) for high-grade serous EOC. The COR for genetically predicted consumption of an additional 80 mg caffeine was 1.01 (95% CI: 0.92, 1.11) for all EOC cases and 0.90 (95% CI: 0.73, 1.10) for high-grade serous cases. Conclusions: We found no evidence indicative of a strong association between EOC risk and genetically predicted coffee or caffeine levels. However, our estimates were not statistically inconsistent with earlier observational studies and we were unable to rule out small protective associations.

18.
PLoS One ; 12(12): e0186456, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29236708

RESUMO

BACKGROUND: Regular fish and omega-3 consumption may have several health benefits and are recommended by major dietary guidelines. Yet, their intakes remain remarkably variable both within and across populations, which could partly owe to genetic influences. OBJECTIVE: To identify common genetic variants that influence fish and dietary eicosapentaenoic acid plus docosahexaenoic acid (EPA+DHA) consumption. DESIGN: We conducted genome-wide association (GWA) meta-analysis of fish (n = 86,467) and EPA+DHA (n = 62,265) consumption in 17 cohorts of European descent from the CHARGE (Cohorts for Heart and Aging Research in Genomic Epidemiology) Consortium Nutrition Working Group. Results from cohort-specific GWA analyses (additive model) for fish and EPA+DHA consumption were adjusted for age, sex, energy intake, and population stratification, and meta-analyzed separately using fixed-effect meta-analysis with inverse variance weights (METAL software). Additionally, heritability was estimated in 2 cohorts. RESULTS: Heritability estimates for fish and EPA+DHA consumption ranged from 0.13-0.24 and 0.12-0.22, respectively. A significant GWA for fish intake was observed for rs9502823 on chromosome 6: each copy of the minor allele (FreqA = 0.015) was associated with 0.029 servings/day (~1 serving/month) lower fish consumption (P = 1.96x10-8). No significant association was observed for EPA+DHA, although rs7206790 in the obesity-associated FTO gene was among top hits (P = 8.18x10-7). Post-hoc calculations demonstrated 95% statistical power to detect a genetic variant associated with effect size of 0.05% for fish and 0.08% for EPA+DHA. CONCLUSIONS: These novel findings suggest that non-genetic personal and environmental factors are principal determinants of the remarkable variation in fish consumption, representing modifiable targets for increasing intakes among all individuals. Genes underlying the signal at rs72838923 and mechanisms for the association warrant further investigation.


Assuntos
Ácidos Docosa-Hexaenoicos/administração & dosagem , Ácido Eicosapentaenoico/administração & dosagem , Estudo de Associação Genômica Ampla , Alimentos Marinhos , Adulto , Idoso , Estudos de Coortes , Europa (Continente) , Grupo com Ancestrais do Continente Europeu , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estados Unidos
19.
Nat Commun ; 8(1): 1584, 2017 11 17.
Artigo em Inglês | MEDLINE | ID: mdl-29146897

RESUMO

Male pattern baldness (MPB) or androgenetic alopecia is one of the most common conditions affecting men, reaching a prevalence of ~50% by the age of 50; however, the known genes explain little of the heritability. Here, we present the results of a genome-wide association study including more than 70,000 men, identifying 71 independently replicated loci, of which 30 are novel. These loci explain 38% of the risk, suggesting that MPB is less genetically complex than other complex traits. We show that many of these loci contain genes that are relevant to the pathology and highlight pathways and functions underlying baldness. Finally, despite only showing genome-wide genetic correlation with height, pathway-specific genetic correlations are significant for traits including lifespan and cancer. Our study not only greatly increases the number of MPB loci, illuminating the genetic architecture, but also provides a new approach to disentangling the shared biological pathways underlying complex diseases.


Assuntos
Alopecia/epidemiologia , Alopecia/genética , Predisposição Genética para Doença/genética , Estudo de Associação Genômica Ampla , Humanos , Masculino , Polimorfismo de Nucleotídeo Único/genética , Estudos Prospectivos , Risco , Inquéritos e Questionários
20.
Stat Sin ; 27(2): 785-804, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28649172

RESUMO

Case-control studies are designed towards studying associations between risk factors and a single, primary outcome. Information about additional, secondary outcomes is also collected, but association studies targeting such secondary outcomes should account for the case-control sampling scheme, or otherwise results may be biased. Often, one uses inverse probability weighted (IPW) estimators to estimate population effects in such studies. IPW estimators are robust, as they only require correct specification of the mean regression model of the secondary outcome on covariates, and knowledge of the disease prevalence. However, IPW estimators are inefficient relative to estimators that make additional assumptions about the data generating mechanism. We propose a class of estimators for the effect of risk factors on a secondary outcome in case-control studies that combine IPW with an additional modeling assumption: specification of the disease outcome probability model. We incorporate this model via a mean zero control function. We derive the class of all regular and asymptotically linear estimators corresponding to our modeling assumption, when the secondary outcome mean is modeled using either the identity or the log link. We find the efficient estimator in our class of estimators and show that it reduces to standard IPW when the model for the primary disease outcome is unrestricted, and is more efficient than standard IPW when the model is either parametric or semiparametric.

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