Next Article in Journal
Identification of Phosphorylated Amino Acids in Human TNRC6A C-Terminal Region and Their Effects on the Interaction with the CCR4-NOT Complex
Previous Article in Journal
HMGA2 as a Critical Regulator in Cancer Development
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Article

Effects of Gene-Environment Interaction on Obesity among Chinese Adults Born in the Early 1960s

Chinese Center for Disease Control and Prevention, National Institute for Nutrition and Health, Beijing 100000, China
*
Author to whom correspondence should be addressed.
Genes 2021, 12(2), 270; https://doi.org/10.3390/genes12020270
Submission received: 9 December 2020 / Revised: 29 January 2021 / Accepted: 9 February 2021 / Published: 13 February 2021
(This article belongs to the Section Human Genomics and Genetic Diseases)

Abstract

:
The prevalence of obesity has been increasing sharply and has become a serious public health problem worldwide. Gene–environment interaction in obesity is a relatively new field, and little is known about it in Chinese adults. This study aimed to provide the effects of gene–environment interaction on obesity among Chinese adults. A stratified multistage cluster sampling method was conducted to recruit participants from 150 surveillance sites. Subjects born in 1960, 1961 and 1963 were selected. An exploratory factor analysis was used to classify the environmental factors. The interaction of single nucleotide polymorphisms (SNPs) and environmental factors on body mass index (BMI) and waist circumference were analyzed using a general linear model. A multiple logistic regression model combined with an additive model was performed to analyze the interaction between SNPs and environmental factors in obesity and central obesity. A total of 2216 subjects were included in the study (mean age, 49.7 years; male, 39.7%, female, 60.3%). Engaging in physical activity (PA) could reduce the effect of MC4R rs12970134 on BMI (β = −0.16kg/m2, p = 0.030), and also reduce the effect of TRHR rs7832552 and BCL2 rs12454712 on waist circumference (WC). Sedentary behaviors increased the effects of SNPs on BMI and WC, and simultaneously increased the effects of FTO rs9939609 and FTO rs8050136 on obesity and central obesity. A higher socioeconomic status aggravated the influence of SNPs (including FTO rs9939609, BNDF rs11030104, etc.) on BMI and WC, and aggravated the influence of SEC16B rs574367 on central obesity. The MC4R rs12970134 association with BMI and the FTO rs8050136 association with central obesity appeared to be more pronounced with higher energy intake (β = 0.140 kg/m2, p = 0.049; OR = 1.77, p = 0.004, respectively). Engaging in PA could reduce the effects of SNPs on BMI and WC; nevertheless, a higher socioeconomic status, higher dietary energy intake and sedentary behaviors accentuated the influences of SNPs on BMI, WC, obesity and central obesity. Preventative measures for obesity should consider addressing the gene–environment interaction.

1. Introduction

The prevalence of obesity has tripled over the past three to four decades and has become a serious public health issue and global health challenge [1]. In 2016, at least one third of the world’s adults were suffering from overweight or obesity [2]. The prevalence of overweight and obesity was lower, but was increasing faster in developing countries than in developed countries [3]. In 2010–2012, according to the Chinese criteria of weight for adults, the prevalence of obesity among residents aged 18 years and above was 11.9%, and among children and adolescents aged between 6–17 years, it was 6.4% [4]. Obesity is in relation to an increased risk of numerous chronic diseases, such as hypertension, coronary heart disease and stroke, as well as excess mortality [3,5,6]. However, obesity has a negative impact not only on health, but also on psychology and socioeconomics [7,8,9,10,11,12]. The median of mean total annual healthcare costs increased 12% and 36% for overweight and obese individuals, respectively, compared with the individuals with a healthy weight [12]. The medical costs of obesity was about USD 150 billion, accounting for almost 10% of all medical spending in the United States [8,10]. In 2010, the economic burden of major chronic diseases caused by overweight and obesity was about USD 12.85 billion, responsible for 42.9% of the economic burden of major chronic diseases in China [13]. The serious public health issues and economic burden caused by overweight and obesity made it imperative to understand their genetic and environmental factors.
Previous studies have found that the differences in the prevalence of overweight and obesity among different ethnic groups may be related to allele frequencies of obesity; in addition, environmental factors may regulate the expression of obesity genes and increase or decrease the susceptibility of people to obesity [14]. One study found that reduced outdoor activities may increase the risk of obesity in people carrying FTO rs9939609-A among Kazakh school-aged children [15]. Similarly, studies among Danes and Chinese school-aged children showed that low physical activity accentuated the effect of FTO rs9939609 on body fat accumulation [16,17]. Another study did not find an interaction between FTO rs9939609 and physical activity on obesity [18]. Several studies have shown that the genetics associated with obesity appeared to be more pronounced with greater intake of high-energy foods, such as fried foods, sugar-sweetened beverages and protein [19,20,21]. The effect of genes on obesity may also interact with socioeconomic status. The British Biobank’s research showed that a low socioeconomic status would aggravate the effect of the FTO gene on obesity [22]. Education level, as an aspect in determining socioeconomic status, worked together with genes to influence the occurrence of obesity. For example, the HELENA study found that a low education level increased the risk of obesity caused by genes [23]. A study of the Mediterranean population found that a low education level increased the FTO rs9939609 risk for obesity [24].
Despite comprehensive studies conducted on the interaction of genes and the environment on obesity, little is known about the effect of the gene–environment interaction among Chinese adults. A comprehensive study that evaluates environmental factors in conjunction with genetic contributions among Chinese population is imperative. The current study aimed to explore the effect of the gene–environment interaction on body mass index (BMI), waist circumference (WC), obesity and central obesity among Chinese adults born in the early 1960s.

2. Materials and Methods

2.1. Study Design and Subjects

This study was based on the 2010–2012 China Nutrition and Health Surveillance (CNHS). CNHS was a nationally representative cross-sectional study covering all 31 provinces, autonomous regions and municipalities directly under the central government of China (except Taiwan, Hong Kong and Macao). A stratified and multistage cluster random-sampling method proportional to population was employed to conduct the survey in 150 surveillance sites, with urban and rural areas divided into four stratums, including 34 metropolis surveillance sites, 41 small to medium urban surveillance sites, 45 general rural surveillance sites and 30 poor rural surveillance sites. Six neighborhood (village) committees were sampled from each surveillance site and 75 households were sampled from each neighborhood (village) committees. Subjects born in 1960, 1961 and 1963 were selected. The exclusion criteria were incomplete information (such as lack of weight or height, waist circumference, dietary data, etc.), unqualified blood samples, failure of DNA extraction or abnormal gene detection results, and those with liver, kidney or heart diseases, or cancer. Finally, a total of 2216 subjects were included in the current study. The study protocols were approved by the Ethics Committee of NINH, China CDC (No. 2013-010). All the permanent residents in the selected households were the respondents and signed the informed consent. The surveillance content included a dietary survey, a medical physical examination, an inquiring survey and a laboratory test. The data for the current study included basic household information, individual dietary behaviors (including a 24 h dietary-inquiry survey for 3 consecutive days and weighing of household seasonings), physical activity behaviors, individual health status, height, weight and waist circumference.

2.2. Genotyping and SNP Selection

The genotype of 16 obesity-related single nucleotide polymorphisms (SNPs) were detected by Mass ARRAY (Agera, San Diego, CA, USA). SNPs exclusion criteria: (1) detection rate < 80%; (2) deviation from the Hardy-Weinberg equilibrium p < 0.001; and (3) a minor allele frequency of each SNP < 5%. Finally, a total of 12 SNPs were involved in the present study. The association of the 12 SNPs with obesity had been indicated; however, whether these SNPs interacted with environment was still unclear.

2.3. Definition and Standards

According to the “Criteria of weight for Chinese adults,” obesity is defined as ≥ 28.0 kg/m2, so obesity was defined as BMI ≥ 28.0 kg/m2. The central obesity was defined as WC ≥ 90 cm for males and WC ≥ 85 cm for females. Environmental factors included economic level, education level, leisure-time physical activity, transportation mode, housework time, leisure sedentary behavior, daily energy intake, etc.

2.4. Statistical Analysis

The exploratory factor analysis was used to classify the environmental factors. First, a Kaiser–Meyer–Olkin (KMO) test and a Bartlett’s spherical test were performed to determine whether factor analysis was suitable. Factor analysis generally can be done when KMO ≥ 0.5, and Bartlett’s spherical test when p < 0.05, while KMO ≥ 0.6 would be more suitable [15,25]. In this study, we adopted KMO ≥ 0.5, which was used in a previous study [15]. Second, according to the results of factor analysis, the factor with eigenvalue > 1 and cumulative contribution rate > 70% was selected as the initial common factor. After orthogonal rotation, the variable with factor load ≥ 0.50 was considered as the main component of the factor. Finally, according to the 50th percentile of the factor score, each factor was divided into two categories of variables, and the single SNPs were divided into two categories according to whether they carried risk alleles. The interaction of SNP, genetic risk score and environmental factors on BMI and waist circumference was analyzed by general linear model. The model included genetic and environmental factors, and was adjusted for age and gender. A multiple logistic regression model combined with an additive model was performed to analyze the interaction between single SNPs and environmental factors on obesity and central obesity. The odds ratio (OR) is generally used to assess the risk. Let OR (GE) be the risk of interaction of SNPs and environmental factors, OR (G) be the risk when SNPs act alone, and OR(E) be the risk when environment acts alone. When the two factors were combined, the proportion attributed to interaction was AP(G*E) = (OR(GE) − OR (G) − OR (E) + 1)/OR (GE). A two-tailed p < 0.05 was considered statistically significant.

3. Results

3.1. Subjects Characteristics

Basic characteristics of the study subjects are presented in Table 1. The average age of the 2216 subjects was 49.7 years. The prevalence of central obesity in males was 27.5%, which was lower than that in females (33.0%, p < 0.05). There also were significant differences between obesity and non-obesity, and central obesity and non-central obesity in BMI and WC (p < 0.001).

3.2. Results of the Exploratory Factor Analysis

The results of exploratory factor analysis are shown in Table 2. This analysis was conducted for 7 variables, including leisure-time physical activity, housework, transportation mode, economic level, education level, energy intake and leisure-time sedentary behavior (LTSB). The KMO test value was 0.558, and the Bartlett’s spherical test value was 690.09 (df = 21, p < 0.0001), so it was suitable for exploratory factor analysis. After this analysis, four common factors were finally extracted. Factor 1 (including leisure-time physical activity, housework and transportation mode) was defined as physical activity (PA). Factor 2 (including economic level and education level) was defined as socioeconomic status. Factor 3 was LTSB. Factor 4 was dietary energy intake.

3.3. Interaction of Genes and Environment in BMI and WC

As shown in Table 3, engaging in PA could reduce the effect of MC4R rs12970134 on BMI (β = −0.16 kg/m2, p = 0.030), and reduce the effect of TRHR rs7832552 and BCL2 rs12454712 on WC (β = −0.426 cm, p = 0.044; β = −0.450 cm, p = 0.048, respectively). A high socioeconomic status appeared to increase the effect of most SNPs on BMI and WC. A high dietary energy intake accentuated the effect of MC4R rs12970134 on BMI (β = 0.140 kg/m2, p = 0.049). LTSB increased the influence of SEC16B rs574367 and MC4R rs12970134 on BMI (β = 0.140 kg/m2, p = 0.044; β = 0.214 kg/m2, p = 0.003, respectively), and increased the influence of BNDF rs11030104 and MC4R rs12970134 on WC (β = 0.459 cm, p = 0.041; β = 0.562 cm, p = 0.007, respectively).

3.4. Interaction of Genes and Environment in Obesity and Central Obesity

None of the SNPs was found to interact with PA in obesity or central obesity (Table 4).
Significant evidence for interaction with SEC16B rs574367 was seen for socioeconomic status (p = 0.020), with a larger effect of SEC16B rs574367 in high socioeconomic status (OR = 1.39, 95%CI:1.05–1.82) on central obesity. When a high socioeconomic status and SEC16B rs574367 coexisted, the incidence of obesity was attributable to the interaction ratio of 2.74%. No interaction was found between socioeconomic status and any SNP’s effect on obesity (Table 5).
A significant interaction was found between dietary energy intake and FTO rs8050136 (p = 0.004), in which participants with a higher dietary energy intake had a more obvious effect of FTO rs8050136 on obesity compared to those with a lower dietary energy intake (OR = 1.77, 95%CI:1.20–2.62). The proportion of obesity attributed to this interaction was 19.84%. No interaction was found between dietary energy intake and any SNP’s effect on central obesity (Table 6).
LTSB interacted together with SNPs on obesity and central obesity. FTO rs9939609’s association with obesity and central obesity appeared to be more pronounced with a long-time LTSB (OR = 1.63, 95%CI:1.09–2.45; OR = 1.49, 95%CI:1.09–2.02). Interaction accounted for 2.88% and 21.62% of the occurrence of obesity and central obesity when a long-time LTSB existed with FTO rs9939609. Interaction with obesity and central obesity was also observed between FTO rs8050136 and LTSB. A long-time LTSB accentuated the effect of FTO rs8050136 on obesity and central obesity (OR = 1.27, 95%CI:1.05–2.36; OR = 1.44, 95%CI:1.06−1.97). When the two factors existed together, the proportion attributed to interaction was 1.59% and 20.82%, respectively. Significant interaction was also identified between LTSB and SEC16B rs574367 (p = 0.005). A higher effect on central obesity for SEC16B rs574367 was observed in participants with a long-time LTSB (OR = 1.39, 95%CI:1.06−1.97). The proportion attributable to the interaction was 1.23% when both factors were present (Table 7).

4. Discussion

The occurrence of obesity was affected by genetic and environmental factors and their interactions. The polymorphism of obesity genes was different in different races; in addition to being related to heredity, the environmental factors may also affect the gene expression. In the present study, we analyzed the interaction between obesity-related genes and environmental factors. Several environmental factors were identified that influence the effect of SNPs on BMI, WC, obesity and central obesity.
Many studies have shown that regular PA can reduce the effect of genes on obesity [16,19,20,21]. In contrast, the genetic association with BMI was accentuated with increasing prolonged television-watching [26]. A study conducted among children in Beijing found that the association between BDNF rs6265 and obesity risk was only identified in children with moderate to low levels of PA or sedentary behavior [27]. Consistent with the above results, our results indicated that the interaction associated with PA attenuated the effect of MC4R rs12970134 on BMI, and the effect of TRHR rs7832552 and BCL2 rs12454712 on WC. LTSB increased the effects of SEC16B rs574367 and MC4R rs12970134 on BMI, and of BNDF rs11030104 and MC4R rs12970134 on WC. Nevertheless, no interaction was found between PA and any SNP’s effect on obesity and central obesity. A meta-analysis and other studies also identified no SNP interaction with PA for WCadjBMI or obesity [18,28]. This may be due to the bias inherent in self-reported estimates and measurement errors of PA [29]. Further studies should be done with relatively high accuracy and precisely measured PA to reveal the interactions of PA and SNPs in obesity and central obesity. Simultaneously, LTSB increased the effects of FTO rs9939609 and FTO rs8050136 on obesity and central obesity. So, engaging in PA and less LTSB could mitigate the impact of risk alleles on a genetic predisposition to obesity.
One of our novel findings was that MC4R rs12970134 interacted with dietary in BMI. High-energy dietary intake aggravated the influence of MC4R rs12970134 on an increased BMI. A study of the interaction between the FTO gene and dietary intake showed that the association between FTO and BMI was more pronounced in those with a dietary intake of high fat and low carbohydrates and fiber [30]. The inactive/high intake women had a 39.0% greater risk of obesity associated with each A allele in FTO carried when compared with the non-carriers [31]. Diet intervention could change the association between FTO and body-weight changes with a significant body-weight reduction [32]. Our results indicated that FTO rs8050136 increased the risk of obesity by 77% (OR = 1.77, 95%CI 1.20–2.62) among the participants with a high dietary energy intake. The specific mechanism of increasing energy intake that made FTO more pronounced in obesity is still unclear. One study found that the FTO gene was positively correlated with the percentage of energy derived from fat, and negatively correlated with the percentage of energy from carbohydrates [33], indicating that the association between the FTO gene and obesity may be regulated by energy intake. This conjecture needs to be confirmed in further studies.
To our knowledge, this is the first study that found that a high socioeconomic status aggravates the role of genes in obesity among Chinese adults. Some researchers believe that people of low social class are at a disadvantage in terms of economic level and education [34]. The gene–obesogenic environment interactions showed that a low socioeconomic position accentuated the risk of obesity in genetically susceptible adults [22]. A similar conclusion was reached in studies among European-American and African-American adolescents, as obesity-candidate genes carriers had a higher percentage of body fat with low socioeconomic status [35]. The above studies indicated that in developed countries, low socioeconomic status aggravated the genetic susceptibility to obesity. Contrary to the results in developed countries, our results indicate that high socioeconomic status aggravated the effect of SNPs on obesity. In developed countries, the people with a high socioeconomic status were more likely to choose a healthy lifestyle in developed countries. However, with rapid economic growth and changes in lifestyle in China, the people with a high socioeconomic status had more opportunities to choose food, and were more likely to eat high-energy food [36]. The people with a high socioeconomic status also were more likely to travel using transportation that lacked PA, such as private cars, taxis, motorcycles, etc. [37]. Research also showed that the family per capita annual income was positively correlated with obesity in China [38]. This might be why a high socioeconomic status aggravates the effect of genes on obesity in China.
The limitation of this study lies in its use of self-reported measurements, which could lead to spurious interaction. In addition, long-term changes in environmental factors, such as diet and exercise after birth, were unobtainable, which limited the ability to identify long-term genetic influences. The narrow age range also made it unclear whether this gene–environmental interaction occurred when younger, so further experiments will need to be done to reveal whether this kind of gene–environment effect occurs in younger people or elder adults.

5. Conclusions

In conclusion, a low level of PA, a high socioeconomic status, a long-time LTSB and a high dietary energy intake aggravated the predisposition of SNPs to BMI, WC, obesity and central obesity among Chinese adults. Our results reinforced that postnatal environment factors could change the influence of risk alleles on genetic predisposition to obesity. It was suggested that we should pay more attention to the influence of environmental factors on gene expression.

Author Contributions

Data curation, W.G. and H.L.; Formal analysis, W.G. and H.L.; Methodology, W.G.; Project administration, A.L.; Supervision, A.L.; Writing—original draft, W.G.; Writing—review and editing, C.S., F.Y., Y.M., Z.C., R.W., H.F. and A.L. All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by National Natural Science Foundation of China, grant number 81372990.

Institutional Review Board Statement

The study protocols were approved by the Ethics Committee of NINH, China CDC (No. 2013-010).

Informed Consent Statement

Informed consent was obtained from all subjects involved in the study.

Acknowledgments

We acknowledge all the participants in our study and the staff responsible for producing the China National Nutrition and Health Survey 2010–2012.

Conflicts of Interest

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

References

  1. Wolfenden, L.; Ezzati, M.; Larijani, B.; Dietz, W. The challenge for global health systems in preventing and managing obesity. Obes. Rev. 2019, 20 (Suppl. 2), 185–193. [Google Scholar] [CrossRef]
  2. Seidell, J.C.; Halberstadt, J. The global burden of obesity and the challenges of prevention. Ann. Nutr. Metab. 2015, 66 (Suppl. 2), 7–12. [Google Scholar] [CrossRef] [PubMed]
  3. Ng, M.; Fleming, T.; Robinson, M.; Thomson, B.; Graetz, N.; Margono, C.; Mullany, E.C.; Biryukov, S.; Abbafati, C.; Abera, S.F.; et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: A systematic analysis for the Global Burden of Disease Study 2013. Lancet 2014, 384, 766–781. [Google Scholar] [CrossRef] [Green Version]
  4. National Health and Family Planning Commission’s Disease Prevention and Control. Report on Chinese Residents’ Chronic Diseases and Nutrition 2015; People’s Medical Publishing House: Beijing, China, 2016. [Google Scholar]
  5. Field, A.E.; Coakley, E.H.; Must, A.; Spadano, J.L.; Laird, N.; Dietz, W.H.; Rimm, E.; Colditz, G.A. Impact of overweight on the risk of developing common chronic diseases during a 10-year period. Arch. Intern. Med. 2001, 161, 1581–1586. [Google Scholar] [CrossRef]
  6. Must, A.; Spadano, J.; Coakley, E.H.; Field, A.E.; Colditz, G.; Dietz, W.H. The disease burden associated with overweight and obesity. JAMA 1999, 282, 1523–1529. [Google Scholar] [CrossRef] [PubMed]
  7. Sarwer, D.B.; Polonsky, H.M. The Psychosocial Burden of Obesity. Endocrinol. Metab. Clin. N. Am. 2016, 45, 677–688. [Google Scholar] [CrossRef]
  8. Kim, D.D.; Basu, A. Estimating the Medical Care Costs of Obesity in the United States: Systematic Review, Meta-Analysis, and Empirical Analysis. Value Health 2016, 19, 602–613. [Google Scholar] [CrossRef] [Green Version]
  9. Hammond, R.A.; Levine, R. The economic impact of obesity in the United States. Diabetes Metab. Syndr. Obes. 2010, 3, 285–295. [Google Scholar] [CrossRef] [Green Version]
  10. Von Lengerke, T.; Krauth, C. Economic costs of adult obesity: A review of recent European studies with a focus on subgroup-specific costs. Maturitas 2011, 69, 220–229. [Google Scholar] [CrossRef] [PubMed]
  11. Tremmel, M.; Gerdtham, U.G.; Nilsson, P.M.; Saha, S. Economic Burden of Obesity: A Systematic Literature Review. Int. J. Environ. Res. Public Health 2017, 14, 435. [Google Scholar] [CrossRef]
  12. Kent, S.; Fusco, F.; Gray, A.; Jebb, S.A.; Cairns, B.J.; Mihaylova, B. Body mass index and healthcare costs: A systematic literature review of individual participant data studies. Obes. Rev. 2017, 18, 869–879. [Google Scholar] [CrossRef]
  13. Juan, Z.; Xiao-Ming, S.; Xiao-Feng, L. Economic costs of both overweight and obesity among Chinese urban and rural residents, in 2010. Chin. J. Epidemiol. 2013, 34, 598–600. [Google Scholar] [CrossRef]
  14. Rask-Andersen, M.; Karlsson, T.; Ek, W.E.; Johansson, Å. Gene-environment interaction study for BMI reveals interactions between genetic factors and physical activity, alcohol consumption and socioeconomic status. PLoS Genet. 2017, 13, e1006977. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  15. Min, L.; Tao, Z.; Akenayi, S.; Pei-Ru, X. Interaction between FTO gene polymorphism and life style may contribute to obesity in Kazakh schoolchildren. J. Med. Postgrad. 2014, 27, 1281–1285. [Google Scholar]
  16. Andreasen, C.H.; Stender-Petersen, K.L.; Mogensen, M.S.; Torekov, S.S.; Wegner, L.; Andersen, G.; Nielsen, A.L.; Albrechtsen, A.; Borch-Johnsen, K.; Rasmussen, S.S.; et al. Low physical activity accentuates the effect of the FTO rs9939609 polymorphism on body fat accumulation. Diabetes 2008, 57, 95–101. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  17. Bo, X.; Mei-xian, Z.; Yue, S.; Xiao-yuan, Z.; Xing-yu, W.; Jie, M. Impact on the risk of obesity due to interactions between fat mass- and obesity-associated gene rs9939609 variants and behavioral factors, in the Chinese school-aged children. Chin. J. Epidemiol. 2010, 31, 737–741. [Google Scholar]
  18. Lappalainen, T.J.; Tolppanen, A.M.; Kolehmainen, M.; Schwab, U.; Lindström, J.; Tuomilehto, J.; Pulkkinen, L.; Eriksson, J.G.; Laakso, M.; Gylling, H.; et al. The common variant in the FTO gene did not modify the effect of lifestyle changes on body weight: The Finnish Diabetes Prevention Study. Obesity 2009, 17, 832–836. [Google Scholar] [CrossRef] [PubMed]
  19. Kilpeläinen, T.O.; Qi, L.; Brage, S.; Sharp, S.J.; Sonestedt, E.; Demerath, E.; Ahmad, T.; Mora, S.; Kaakinen, M.; Sandholt, C.H.; et al. Physical activity attenuates the influence of FTO variants on obesity risk: A meta-analysis of 218,166 adults and 19,268 children. PLoS Med. 2011, 8, e1001116. [Google Scholar] [CrossRef] [PubMed]
  20. Li, S.; Zhao, J.H.; Luan, J.; Ekelund, U.; Luben, R.N.; Khaw, K.T.; Wareham, N.J.; Loos, R.J. Physical activity attenuates the genetic predisposition to obesity in 20,000 men and women from EPIC-Norfolk prospective population study. PLoS Med. 2010, 7. [Google Scholar] [CrossRef] [Green Version]
  21. Oyeyemi, B.F.; Ologunde, C.A.; Olaoye, A.B.; Alamukii, N.A. FTO Gene Associates and Interacts with Obesity Risk, Physical Activity, Energy Intake, and Time Spent Sitting: Pilot Study in a Nigerian Population. J. Obes. 2017, 2017, 3245270. [Google Scholar] [CrossRef]
  22. Tyrrell, J.; Wood, A.R.; Ames, R.M.; Yaghootkar, H.; Beaumont, R.N.; Jones, S.E.; Tuke, M.A.; Ruth, K.S.; Freathy, R.M.; Davey Smith, G.; et al. Gene-obesogenic environment interactions in the UK Biobank study. Int. J. Epidemiol. 2017, 46, 559–575. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  23. Pigeyre, M.; Bokor, S.; Romon, M.; Gottrand, F.; Gilbert, C.C.; Valtueña, J.; Gómez-Martínez, S.; Moreno, L.A.; Amouyel, P.; Dallongeville, J.; et al. Influence of maternal educational level on the association between the rs3809508 neuromedin B gene polymorphism and the risk of obesity in the HELENA study. Int. J. Obes. 2010, 34, 478–486. [Google Scholar] [CrossRef] [Green Version]
  24. Corella, D.; Carrasco, P.; Sorlí, J.V.; Coltell, O.; Ortega-Azorín, C.; Guillén, M.; González, J.I.; Sáiz, C.; Estruch, R.; Ordovas, J.M. Education modulates the association of the FTO rs9939609 polymorphism with body mass index and obesity risk in the Mediterranean population. Nutr. Metab. Cardiovasc. Dis. 2012, 22, 651–658. [Google Scholar] [CrossRef] [Green Version]
  25. Liu, D. Study on Relationship between Nutrition, Family Economic Factors and Childhood, Adult Obesity. Doctor, Chinese Center for Diseases Control and Prevention. 2019. Available online: https://kns.cnki.net/KCMS/detail/detail.aspx?dbcode=CDFD&filename=1019196179.nh (accessed on 8 December 2020).
  26. Qi, Q.; Li, Y.; Chomistek, A.K.; Kang, J.H.; Curhan, G.C.; Pasquale, L.R.; Willett, W.C.; Rimm, E.B.; Hu, F.B.; Qi, L. Television watching, leisure time physical activity, and the genetic predisposition in relation to body mass index in women and men. Circulation 2012, 126, 1821–1827. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  27. Xi, B.; Wang, C.; Wu, L.; Zhang, M.; Shen, Y.; Zhao, X.; Wang, X.; Mi, J. Influence of physical inactivity on associations between single nucleotide polymorphisms and genetic predisposition to childhood obesity. Am. J. Epidemiol. 2011, 173, 1256–1262. [Google Scholar] [CrossRef] [PubMed]
  28. Graff, M.; Scott, R.A.; Justice, A.E.; Young, K.L.; Feitosa, M.F.; Barata, L.; Winkler, T.W.; Chu, A.Y.; Mahajan, A.; Hadley, D.; et al. Genome-wide physical activity interactions in adiposity—A meta-analysis of 200,452 adults. PLoS Genet. 2017, 13, e1006528. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  29. Helmerhorst, H.J.; Brage, S.; Warren, J.; Besson, H.; Ekelund, U. A systematic review of reliability and objective criterion-related validity of physical activity questionnaires. Int. J. Behav. Nutr. Phys. Act. 2012, 9, 103. [Google Scholar] [CrossRef] [Green Version]
  30. Lappalainen, T.; Lindström, J.; Paananen, J.; Eriksson, J.G.; Karhunen, L.; Tuomilehto, J.; Uusitupa, M. Association of the fat mass and obesity-associated (FTO) gene variant (rs9939609) with dietary intake in the Finnish Diabetes Prevention Study. Br. J. Nutr. 2012, 108, 1859–1865. [Google Scholar] [CrossRef] [Green Version]
  31. Ahmad, T.; Lee, I.M.; Paré, G.; Chasman, D.I.; Rose, L.; Ridker, P.M.; Mora, S. Lifestyle interaction with fat mass and obesity-associated (FTO) genotype and risk of obesity in apparently healthy U.S. women. Diabetes Care 2011, 34, 675–680. [Google Scholar] [CrossRef] [Green Version]
  32. Razquin, C.; Martinez, J.A.; Martinez-Gonzalez, M.A.; Bes-Rastrollo, M.; Fernández-Crehuet, J.; Marti, A. A 3-year intervention with a Mediterranean diet modified the association between the rs9939609 gene variant in FTO and body weight changes. Int. J. Obes. 2010, 34, 266–272. [Google Scholar] [CrossRef] [Green Version]
  33. Park, S.L.; Cheng, I.; Pendergrass, S.A.; Kucharska-Newton, A.M.; Lim, U.; Ambite, J.L.; Caberto, C.P.; Monroe, K.R.; Schumacher, F.; Hindorff, L.A.; et al. Association of the FTO obesity risk variant rs8050136 with percentage of energy intake from fat in multiple racial/ethnic populations: The PAGE study. Am. J. Epidemiol. 2013, 178, 780–790. [Google Scholar] [CrossRef] [Green Version]
  34. Johnson, W.; Kyvik, K.O.; Mortensen, E.L.; Skytthe, A.; Batty, G.D.; Deary, I.J. Education reduces the effects of genetic susceptibilities to poor physical health. Int. J. Epidemiol. 2010, 39, 406–414. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  35. Lagou, V.; Liu, G.; Zhu, H.; Stallmann-Jorgensen, I.S.; Gutin, B.; Dong, Y.; Snieder, H. Lifestyle and socioeconomic-status modify the effects of ADRB2 and NOS3 on adiposity in European-American and African-American adolescents. Obesity 2011, 19, 595–603. [Google Scholar] [CrossRef]
  36. Jiguo, Z. Changes in Dietary Patterns and Their Associations with General and Central Obesity among Adults in China (1991–2009). Doctor, Chinese Center for Disease Control and Prevention. 2013. Available online: http://cdmd.cnki.com.cn/Article/CDMD-84501-1013352061.htm (accessed on 8 December 2020).
  37. Gong, W.; Yuan, F.; Feng, G.; Ma, Y.; Zhang, Y.; Ding, C.; Chen, Z.; Liu, A. Trends in Transportation Modes and Time among Chinese Population from 2002 to 2012. Int. J. Environ. Res. Public Health 2020, 17, 945. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  38. Yajie, P.; Aling, Y.; Li, X.; Haoran, Z.; Qingqing, W. Research on the relationship between overweight and obesity and socioeconomic status. J. Jilin Med. Univ. 2018, 39, 168–171. [Google Scholar] [CrossRef]
Table 1. Basic characteristics of the 2216 study subjects.
Table 1. Basic characteristics of the 2216 study subjects.
CharacteristicsTotalObesitypCentral Obesityp
Total2216295 (13.35%) 682 (30.9%)
Age (year)49.7 (48.7,51.3)50.1 (48.8,51.4)0.04850.1 (48.8,51.4)0.324
Gender (n, %) 0.072 0.006
Male879 (39.7%)102 (11.6%) 242 (27.5%)
Female1337 (60.3%)193 (14.5%) 440 (33.0%)
Education level (n, %) 0.951 0.460
Illiterate or primary *787 (35.5%)107 (13.6%) 232 (29.6%)
Junior school951 (42.9%)126 (13.3%) 293 (30.9%)
SHS and above **478 (21.6%)62 (13.0%) 157 (32.9%)
Economic status (n, %) 0.745 0.961
Low1146 (51.7%)150 (13.1%) 349 (30.5%)
Middle834 (37.6%)114 (13.7%) 260 (31.2%)
High157 (7.1%)18 (11.5%) 47 (30.3%)
No answer79 (3.6%)13 (16.5%) 26 (32.9%)
Housework (n, %) 0.144 0.198
≤P30653 (29.7%)74 (11.4%) 190 (29.1%)
P30–P60474 (21.5%)64 (13.5%) 139 (29.3%)
≥P601074 (48.8%)157 (14.7%) 350 (32.7%)
Transportation modes (n, %) 0.228 0.506
Inactive976 (44.3%)140 (14.4%) 308 (31.7%)
Active1225 (55.7%)155 (12.7%) 371 (30.3%)
Physical activity (n, %) # 0.107 0.076
No1909 (86.7%)247 (13.0%) 576 (30.2%)
Yes292 (13.3%)48 (16.4%) 103 (35.4%)
Sedentary behaviors (n, %) 0.124 0.965
No392 (17.8%)62 (15.9%) 121 (31.0%)
Yes1808 (82.2%)233 (12.9%) 558 (30.9%)
Energy intake/day (Kcal)1379.8 (1051.1,1720.8)1315.4 (1028.7, 1679.4)0.8841315.4 (1028.7,1679.4)0.259
Energy intake/day (n, %) 0.693 0.286
≤P25431 (25.0%)63 (14.6%) 136 (31.6%)
P25–P50432 (25.0%)51 (11.9%) 120 (27.8%)
P50–P75431 (25.0%)57 (13.3%) 129 (29.9%)
≥P75432 (25.0%)56 (13.0%) 145 (33.7%)
BMI (kg/m2)24.0 (21.9,26.4)23.5 (21.6,25.4)<0.00129.7 (28.8,31.1)<0.001
Waist circumference (cm)82.0 (75.2,88.8)95.5 (91.1,100.4)<0.00195.5 (91.1,100.4)<0.001
* Illiterate or primary school; ** Senior high school and above; # Leisure time physical activity.
Table 2. Factor analysis of obesity-related environmental factors.
Table 2. Factor analysis of obesity-related environmental factors.
Environmental FactorsFactor 1 *Factor 2 *Factor 3 *Factor 4 *
Leisure-time physical activity0.681
Housework0.639
Transportation mode0.618
Education level 0.720
Economic level 0.634
Everyday energy intake 0.951
Leisure-time sedentary behavior 0.974
Eigenvalues1.4971.1711.0000.964
Contribution rate (%)0.2140.1670.1430.138
Cumulative contribution rate of variance (%)0.2140.3810.5240.662
* Only displays factor-loading values > 0.45, which was considered as the principal component of the factor.
Table 3. Interaction of genes and environment on BMI and waist circumference.
Table 3. Interaction of genes and environment on BMI and waist circumference.
SNPsGenePhysical ActivitySocioeconomic StatusDietary Energy IntakeSedentary Behavior
βpβpβpβp
BMI
rs9939609FTO **0.0820.3200.2030.0100.0770.3140.1450.062
rs11030104BDNF **0.0830.3160.2130.0070.0880.2530.1350.079
rs6265BDNF **0.0690.4080.2020.0120.0670.3950.1380.078
rs16892496TRHR **−0.0140.8540.1030.162−0.0030.9660.0600.424
rs7832552TRHR **−0.1310.099−0.0010.988−0.0980.183−0.0460.534
rs25689581p31−0.1320.4380.3430.015−0.0750.5960.1690.230
rs7561317TMEM18−0.1370.4340.3400.020−0.1090.4500.1290.372
rs574367SEC16B0.0890.2240.1950.0050.0900.1970.1400.044
rs12454712BCL2−0.0710.4000.0900.269−0.0210.7900.0370.640
rs12970134MC4R−0.1640.0300.270<0.0010.1400.0490.2140.003
rs8050136FTO **0.0400.6180.1770.0230.0770.3130.1270.099
rs2237892KCNQ1−0.1220.2760.0720.507−0.0550.613−0.1060.336
WC *
rs9939609FTO **0.2020.3970.6100.0070.2410.2860.4140.065
rs11030104BDNF **0.2690.2640.7250.0020.3300.1420.4590.041
rs6265BDNF **0.2450.3120.6810.0040.2870.2070.4390.052
rs16892496TRHR **−0.0930.6760.3110.144−0.0090.9660.1380.525
rs7832552TRHR **−0.4260.0440.0280.900−0.2790.195−0.1640.447
rs25689581p31−0.2270.6481.3010.0020.0980.8100.6700.102
rs7561317TMEM18−0.6460.2030.9760.021−0.2940.4830.2810.503
rs574367SEC16B0.1760.4070.5330.0080.2140.2880.3610.074
rs12454712BCL2−0.4500.0480.0520.824−0.2690.245−0.1190.605
rs12970134MC4R0.3700.0910.737<0.0010.3670.0770.5620.007
rs8050136FTO **0.1310.5780.5520.0140.2140.3310.3430.124
rs2237892KCNQ1−0.3170.3270.2810.369−0.1430.647−0.3510.267
* Waist circumference. ** The two SNPs on the same gene are in linkage disequilibrium.
Table 4. The interaction between physical activity and SNPs in obesity and central obesity.
Table 4. The interaction between physical activity and SNPs in obesity and central obesity.
Environmental Factor *SNPsObesityOR (95%CI)pAP (%)Central ObesityOR (95%CI)pAP (%)
Physical activityrs9939609 −54.57% −15.19%
T104 (12.7%)1 267 (32.3%)1
+T99 (12.4%)1.14 (0.80, 1.61)0.464 228 (28.7%)0.96 (0.75, 1.24)0.762
A48 (19.5%)1.67 (1.15, 2.44)0.008 90 (36.6%)1.21 (0.90, 1.62)0.218
+A27 (12.7%)1.17 (0.71, 1.92)0.532 63 (29.7%)1.01 (0.71, 1.45)0.939
Physical activityrs11030104 −25.18% 13.98%
G26 (11.6%)1 67 (29.9%)1
+G24 (11.8%)1.19 (0.64, 2.23)0.578 46 (22.6%)0.79 (0.50, 1.25)0.308
A122 (14.9%)1.34 (0.85, 2.11)0.203 278 (33.9%)1.2 (0.87, 1.66)0.257
+A94 (12.1%)1.23 (0.74, 2.03)0.426 232 (29.9%)1.15 (0.81, 1.65)0.438
Physical activityrs6265 −29.51% 5.18%
T25 (11.3%)1 63 (28.4%)1
+T24 (12.4%)1.29 (0.69, 2.43)0.424 45 (23.2%)0.85 (0.53, 1.36)0.497
C125 (15.0%)1.39 (0.88, 2.19)0.162 288 (34.4%)1.32 (0.96, 1.83)0.093
+C99 (12.6%)1.30 (0.78, 2.15)0.311 241 (30.6%)1.24 (0.86, 1.77)0.250
Physical activityrs16892496 0.93% 12.91%
A36 (12.6%)1 101 (35.1%)1
+A30 (11.4%)1.02 (0.59, 1.78)0.945 77 (29.2%)0.86 (0.58, 1.26)0.430
C113 (14.5%)1.15 (0.77, 1.72)0.491 253 (32.4%)0.88 (0.66, 1.17)0.380
+C97 (13.0%)1.18 (0.75, 1.86)0.465 216 (29.0%)0.84 (0.61, 1.16)0.300
Physical activityrs7832552 28.97% 9.10%
T42 (17.0%)1 85 (34.4%)1
+T32 (12.6%)0.84 (0.49, 1.43)0.520 72 (28.5%)0.87 (0.58, 1.30)0.494
C109 (13.1%)0.74 (0.50, 1.10)0.133 274 (32.7%)0.93 (0.69, 1.26)0.638
+C96 (12.5%)0.82 (0.53, 1.27)0.367 222 (28.8%)0.88 (0.63, 1.23)0.451
Physical activityrs12454712 −34.08% −28.49%
C25 (11.4%)1 72 (32.9%)1
+C24 (13.1%)1.34 (0.72, 2.50)0.358 60 (32.8%)1.11 (0.72, 1.73)0.629
T130 (14.8%)1.34 (0.85, 2.12)0.209 292 (33.1%)1.01 (0.74, 1.38)0.958
+T103 (12.3%)1.25 (0.76, 2.07)0.380 230 (27.5%)0.87 (0.62, 1.24)0.453
Physical activityrs12970134 6.25% −2.87%
G100 (14.0%)1 233 (32.4%)1
+G83 (12.2%)1.00 (0.69, 1.44)0.985 192 (28.2%)0.91 (0.70, 1.20)0.517
A47 (14.3%)1.02 (0.70, 1.49)0.901 113 (34.2%)1.09 (0.83, 1.44)0.542
+A40 (13.1%)1.09 (0.70, 1.69)0.708 90 (29.5%)0.98 (0.70, 1.35)0.886
Physical activityrs8050136 −90.90% −20.85%
C105 (12.5%)1 272 (32.4%)1
+C103 (12.8%)1.19 (0.84, 1.68)0.319 230 (28.7%)0.96 (0.75, 1.24)0.759
A53 (19.9%)1.74 (1.21, 2.50)0.003 96 (36.1%)1.18 (0.88, 1.58)0.259
+A24 (11.1%)1.01 (0.61, 1.69)0.966 61 (28.2%)0.95 (0.66, 1.36)0.759
Physical activityrs574367 13.42% 13.52%
G95 (14.3%)1 218 (32.8%)1
+G75 (12.0%)0.95 (0.65, 1.38)0.785 171 (27.3%)0.87 (0.66, 1.15)0.338
T54 (14.0%)0.98 (0.68, 1.41)0.911 133 (34.1%)1.07 (0.82, 1.39)0.632
+T47 (13.2%)1.07 (0.70, 1.64)0.746 112 (31.7%)1.09 (0.79, 1.49)0.603
Physical activityRs2237892 66.27% 16.44%
C69 (14.7%)1 156 (33.1%)1
+C53 (12.2%)0.92 (0.58, 1.46)0.725 127 (29.3%)1.03 (0.74, 1.45)0.850
T7 (7.3%)0.45 (0.20, 1.01)0.054 30 (31.3%)0.91 (0.57, 1.46)0.685
+T16 (14%)1.1 (0.57, 2.11)0.773 35 (30.7%)1.13 (0.69, 1.84)0.637
* Environmental factors were divided into binary variables with the P50 of the factor score as the cut-off value. Physical activity: “−“ = not taking part in physical activity often, “+” = taking part in physical activity often. The first subgroup was used as the reference group.
Table 5. The interaction between socioeconomic status and SNPs in obesity and central obesity.
Table 5. The interaction between socioeconomic status and SNPs in obesity and central obesity.
Environmental Factor *SNPsObesityOR (95%CI)pAP (%)Central ObesityOR (95%CI)pAP (%)
Socioeconomic statusrs9939609 −69.21% −34.86%
T88 (11.2%)1 224 (28.4%)1
+T115 (13.9%)1.34 (0.99, 1.81)0.055 271 (32.6%)1.28 (1.03, 1.59)0.024
A46 (19.0%)1.85 (1.25, 2.74)0.002 85 (35.1%)1.36 (1.00, 1.85)0.048
+A29 (13.4%)1.30 (0.83, 2.04)0.261 68 (31.5%)1.22 (0.88, 1.69)0.237
Socioeconomic statusrs11030104 −1.63% −15.89%
G23 (11.1%)1 47 (22.6%)1
+G27 (12.3%)1.16 (0.64, 2.10)0.625 66 (30.0%)1.52 (0.98, 2.34)0.062
A106 (13.3%)1.22 (0.75, 1.97)0.424 248 (31.0%)1.53 (1.07, 2.19)0.021
+A110 (13.8%)1.35 (0.84, 2.19)0.217 262 (32.9%)1.76 (1.23, 2.52)0.002
Socioeconomic statusrs6265 20.31% −11.39%
T25 (12.4%)1 45 (22.3%)1
+T24 (11.2%)0.91 (0.50, 1.65)0.756 63 (29.4%)1.48 (0.95, 2.31)0.082
C108 (13.3%)1.06 (0.67, 1.69)0.798 255 (31.3%)1.57 (1.09, 2.26)0.015
+C116 (14.3%)1.22 (0.77, 1.94)0.400 274 (33.8%)1.84 (1.28, 2.65)0.001
Socioeconomic statusrs16892496 −19.69% −40.87%
A30 (10.8%)1 78 (27.7%)1
+A36 (13.4%)1.33 (0.79, 2.23)0.283 100 (37.0%)1.59 (1.11, 2.29)0.011
C104 (13.8%)1.31 (0.85, 2.01)0.225 229 (30.4%)1.13 (0.83, 1.53)0.443
+C106 (13.7%)1.37 (0.89, 2.10)0.158 240 (31.0%)1.22 (0.90, 1.66)0.197
Socioeconomic statusrs7832552 13.87% 33.49%
T36 (15.3%)1 78 (33.3%)1
+T38 (14.3%)0.99 (0.60, 1.64)0.982 79 (29.7%)0.90 (0.62, 1.32)0.599
C100 (12.2%)0.78 (0.52, 1.18)0.243 233 (28.4%)0.80 (0.59, 1.09)0.160
+C105 (13.3%)0.90 (0.60, 1.36)0.622 263 (33.4%)1.06 (0.77, 1.44)0.728
Socio-economic statusrs2568958 −136.22% −30.68%
G1 (11.1%)1 1 (11.1%)1
+G2 (25.0%)2.94 (0.21, 40.86)0.421 2 (25.0%)2.84 (0.21, 39.36)0.436
A133 (12.9%)1.19 (0.15, 9.68)0.868 308 (29.8%)3.32 (0.41, 26.76)0.260
+A141 (13.6%)1.33 (0.16, 10.77)0.790 338 (32.6%)3.95 (0.49, 31.84)0.197
Socioeconomic statusrs7561317 95.64% 342.70%
A1 (25.0%)1 3 (75.0%)1
+A1 (12.5%)0.52 (0.02, 11.53)0.682 4 (50.0%)0.40 (0.03, 5.65)0.495
G130 (12.9%)0.50 (0.05, 4.85)0.550 299 (29.6%)0.16 (0.02, 1.50)0.107
+G137 (13.4%)0.55 (0.06, 5.36)0.607 331 (32.3%)0.19 (0.02, 1.79)0.145
Socioeconomic statusrs574367 2.28% 2.74%
G83 (12.8%)1 186 (28.7%)1
+G87 (13.6%)1.12 (0.81, 1.56)0.482 203 (31.6%)1.21 (0.95, 1.53)0.127
T47 (13.1%)1.03 (0.70, 1.52)0.868 113 (31.3%)1.14 (0.86, 1.51)0.357
+T54 (14.1%)1.18 (0.82, 1.72)0.373 132 (34.6%)1.39 (1.05, 1.82)0.020
Socioeconomic statusrs12454712 −39.84% −50.65%
C18 (9.5%)1 51 (26.7%)1
+C31 (14.6%)1.72 (0.93, 3.20)0.086 81 (38.4%)1.79 (1.17, 2.74)0.008
T117 (13.6%)1.51 (0.89, 2.55)0.124 258 (29.9%)1.18 (0.83, 1.68)0.365
+T116 (13.6%)1.59 (0.94, 2.70)0.083 264 (30.9%)1.30 (0.91, 1.86)0.144
Socioeconomic statusrs12970134 −6.63% −0.30%
G85 (12.4%)1 197 (28.7%)1
+G98 (13.7%)1.19 (0.87, 1.63)0.287 228 (31.9%)1.23 (0.97, 1.55)0.082
A43 (13.4%)1.10 (0.74, 1.63)0.636 97 (30.4%)1.10 (0.82, 1.46)0.543
+A44 (14.0%)1.21 (0.81, 1.79)0.350 106 (33.5%)1.32 (0.99, 1.76)0.061
Socioeconomic statusrs8050136 −68.42% −15.56%
C90 (11.4%)1 1
+C118 (14.0%)1.33 (0.99, 1.79)0.060 228 (28.7%)1.25 (1.01, 1.55)0.04
A48 (18.5%)1.76 (1.20, 2.58)0.004 274 (32.4%)1.21 (0.89, 1.63)0.226
+A29 (13.1%)1.24 (0.79, 1.94)0.354 85 (32.7%)1.26 (0.91, 1.74)0.161
Socioeconomic statusRs2237892 44.03% 39.44%
C52 (11.6%)1 131 (29.2%)1
+C70 (15.4%)1.46 (0.99, 2.16)0.057 152 (33.4%)1.3 (0.98, 1.73)0.071
T6 (5.6%)0.45 (0.19, 1.08)0.075 25 (23.2%)0.74 (0.45, 1.21)0.232
+T17 (16.7%)1.63 (0.89, 2.98)0.111 40 (39.2%)1.72 (1.09, 2.71)0.019
* Environmental factors were divided into binary variables with the P50 of the factor score as the cut-off value. Socioeconomic status: “−“ = low socioeconomic status, “+” = high socioeconomic status. The first subgroup was used as the reference group.
Table 6. The interaction between dietary energy intake and SNPs in obesity and central obesity.
Table 6. The interaction between dietary energy intake and SNPs in obesity and central obesity.
Environmental Factor *SNPsObesityOR (95%CI)pAP (%)Central ObesityOR (95%CI)pAP (%)
Dietary energy intakers11030104 2.80% 10.71%
G24 (10.3%)1 64 (27.5%)1
+G26 (13.3%)1.32 (0.73, 2.38)0.359 49 (25.1%)0.87 (0.56, 1.34)0.522
A92 (11.8%)1.17 (0.73, 1.89)0.509 248 (31.6%)1.23 (0.89, 1.71)0.210
+A124 (15.3%)1.54 (0.97, 2.45)0.070 262 (32.4%)1.23 (0.89, 1.70)0.207
Dietary energy intakers6265 9.71% 2.87%
T25 (11.1%)1 60 (26.7%)1
+T24 (12.6%)1.13 (0.62, 2.06)0.682 48 (25.1%)0.91 (0.58, 1.41)0.664
C98 (12.3%)1.13 (0.71, 1.80)0.606 261 (32.7%)1.35 (0.97, 1.87)0.079
+C126 (15.2%)1.40 (0.89, 2.21)0.150 268 (32.4%)1.29 (0.93, 1.79)0.132
Dietary energy intakers16892496 0.13% −1.79%
A27 (10.3%)1 85 (32.2%)1
+A39 (13.6%)1.32 (0.78, 2.23)0.298 93 (32.3%)0.98 (0.68, 1.40)0.900
C95 (12.2%)1.19 (0.76, 1.88)0.446 240 (30.8%)0.94 (0.69, 1.26)0.663
+C115 (15.3%)1.52 (0.97, 2.37)0.068 229 (30.6%)0.90 (0.66, 1.21)0.478
Dietary energy intakers7832552 13.84% −2.53%
T37 (13.9%)1 83 (31.2%)1
+T37 (15.7%)1.14 (0.69, 1.86)0.616 74 (31.6%)0.99 (0.68, 1.45)0.964
C85 (10.8%)0.76 (0.50, 1.14)0.183 243 (30.8%)0.98 (0.73, 1.33)0.909
+C120 (14.6%)1.03 (0.69, 1.54)0.875 253 (30.9%)0.95 (0.70, 1.28)0.737
Dietary energy intakers2568958 −174.49% −81.05%
G1 (10.0%)1 1 (10.0%)1
+G2 (28.6%)4.04 (0.29, 56.87)0.301 2 (28.6%)4.07 (0.29, 57.18)0.297
A123 (11.9%)1.28 (0.16, 10.20)0.818 326 (31.4%)4.27 (0.54, 33.90)0.169
+A151 (14.6%)1.57 (0.20, 12.54)0.669 320 (31.0%)4.06 (0.51, 32.20)0.185
Dietary energy intakers574367 22.64% 10.14%
G79 (12.2%)1 200 (30.8%)1
+G91 (14.2%)1.16 (0.84, 1.60)0.379 189 (29.4%)0.91 (0.72, 1.15)0.433
T41 (11.0%)0.90 (0.60, 1.34)0.604 121 (32.4%)1.08 (0.82, 1.43)0.566
+T60 (16.3%)1.37 (0.95, 1.97)0.095 124 (33.6%)1.11 (0.84, 1.45)0.474
Dietary energy intakers12454712 −16.26% −2.11%
C19 (9.5%)1 65 (32.3%)1
+C30 (14.9%)1.63 (0.88, 3.00)0.119 67 (33.3%)1.01 (0.67, 1.53)0.963
T104 (12.0%)1.31 (0.78, 2.19)0.305 262 (30.2%)0.91 (0.65, 1.27)0.577
+T129 (15.2%)1.67 (1.00, 2.78)0.049 260 (30.6%)0.90 (0.65, 1.25)0.535
Dietary energy intakers12970134 −4.38% −9.15%
G83 (11.7%)1 215 (30.3%)1
+G100 (14.5%)1.23 (0.90, 1.68)0.203 210 (30.4%)0.97 (0.77, 1.22)0.795
A40 (12.7%)1.09 (0.73, 1.63)0.689 104 (32.9%)1.13 (0.85, 1.50)0.408
+A47 (14.7%)1.26 (0.85, 1.85)0.247 99 (31.0%)1.01 (0.76, 1.34)0.969
Dietary energy intakers8050136 19.84% −14.98%
C94 (11.3%)1 251 (30.0%)1
+C114 (14.1%)1.25 (0.93, 1.68)0.138 251 (31.2%)1.02 (0.82, 1.26)0.878
A32 (13.2%)1.17 (0.76, 1.80)0.471 82 (33.7%)1.17 (0.87, 1.59)0.305
+A45 (18.8%)1.77 (1.20, 2.62)0.004 75 (31.4%)1.04 (0.76, 1.41)0.828
Dietary energy intakeRs2237892 −10.66% 16.6%
C45 (10.1%)1 133 (29.8%)
+C77 (16.8%)1.78 (1.20, 2.63)0.004 150 (32.8%)1.12 (0.84, 1.48)0.447
T9 (8.2%)0.80 (0.38, 1.70)0.565 30 (27.3%)0.91 (0.57, 1.45)0.689
+T14 (14%)1.43 (0.75, 2.72)0.281 35 (35%)1.23 (0.78, 1.95)0.379
* Environmental factors were divided into binary variables with the P50 of the factor score as the cut-off value. Dietary energy intake: “−“ = low dietary energy intake, “+” = high dietary energy intake. The first subgroup was used as the reference group.
Table 7. The interaction between sedentary behavior and SNPs in obesity and central obesity.
Table 7. The interaction between sedentary behavior and SNPs in obesity and central obesity.
Environmental Factor *SNPsObesityOR (95%CI)pAP (%)Central ObesityOR (95%CI)pAP (%)
Sedentary behaviorrs9939609 2.88% 21.62%
T93 (11.6%)1 234 (29.1%)1
+T110 (13.5%)1.21 (0.90, 1.63)0.207 261 (32.0%)1.16 (0.94, 1.43)0.171
A35 (15.1%)1.37 (0.90, 2.09)0.140 67 (28.9%)1.00 (0.73, 1.39)0.981
+A40 (17.7%)1.63 (1.09, 2.45)0.018 86 (38.1%)1.49 (1.09, 2.02)0.012
Sedentary behaviorrs11030104 12.31% −12.31%
G26 (11.4%)1 52 (22.8%)1
+G24 (12.0%)1.05 (0.58, 1.89)0.881 61 (30.5%)1.48 (0.96, 2.28)0.078
A98 (12.6%)1.11 (0.70, 1.76)0.663 235 (30.2%)1.46 (1.03, 2.06)0.033
+A118 (14.5%)1.32 (0.84, 2.07)0.236 275 (33.7%)1.72 (1.22, 2.43)0.002
Sedentary behaviorrs6265 11.71% −10.57%
T26 (11.4%)1 53 (23.1%)1
+T23 (12.3%)1.09 (0.60, 1.98)0.779 55 (29.4%)1.38 (0.89, 2.15)0.149
C100 (12.6%)1.12 (0.71, 1.77)0.637 247 (31.2%)1.50 (1.07, 2.11)0.020
+C124 (14.9%)1.37 (0.87, 2.15)0.175 282 (33.9%)1.70 (1.21, 2.39)0.002
Sedentary behaviorrs16892496 32.91% 0.52%
A33 (12.7%)1 79 (30.2%)1
+A33 (11.5%)0.91 (0.54, 1.52)0.706 99 (34.1%)1.22 (0.85, 1.74)0.285
C94 (12.0%)0.94 (0.62, 1.44)0.789 222 (28.5%)0.92 (0.68, 1.26)0.613
+C116 (15.5%)1.27 (0.84, 1.92)0.264 247 (33.0%)1.15 (0.85, 1.56)0.381
Sedentary behaviorrs7832552 −0.61% −9.03%
T36 (13.9%)1 74 (28.5%)1
+T38 (15.8%)1.16 (0.71, 1.91)0.553 83 (34.6%)1.32 (0.90, 1.93)0.154
C95 (11.9%)0.83 (0.55, 1.25)0.375 232 (28.9%)1.01 (0.74, 1.38)0.948
+C110 (13.7%)0.99 (0.66, 1.48)0.943 264 (32.8%)1.22 (0.90, 1.66)0.209
Sedentary behaviorrs2568958 219.79% 8.00%
G2 (28.6%)1 1 (14.3%)1
+G1 (10.0%)0.24 (0.02, 3.36)0.288 2 (20.0%)1.32 (0.10, 18.23)0.838
A125 (12.1%)0.31 (0.06, 1.62)0.165 299 (28.9%)2.19 (0.26, 18.36)0.470
+A149 (14.4%)0.38 (0.07, 1.99)0.252 347 (33.5%)2.73 (0.33, 22.82)0.355
Sedentary behaviorrs7561317 203.14% 137.45%
A1 (33.3%)1 2 (66.7%)1
+A1 (11.1%)0.30 (0.01, 7.13)0.452 5 (55.6%)0.68 (0.04, 10.63)0.785
G122 (12.0%)0.31 (0.03, 3.49)0.344 293 (28.8%)0.22 (0.02, 2.43)0.215
+G145 (14.2%)0.38 (0.03, 4.28)0.435 337 (33.0%)0.27 (0.02, 2.97)0.283
Sedentary behaviorrs574367 −25.42% 1.23%
G75 (11.7%)1 180 (28.1%)1
+G95 (14.6%)1.30 (0.94, 1.80)0.117 209 (32.2%)1.21 (0.96, 1.54)0.114
T51 (13.7%)1.20 (0.82, 1.76)0.344 116 (31.1%)1.16 (0.87, 1.53)0.308
+T50 (13.5%)1.20 (0.82, 1.76)0.361 129 (34.9%)1.39 (1.05, 1.83)0.020
Sedentary behaviorrs12454712 −0.07% 19.96%
C23 (11.2%)1 67 (32.5%)1
+C26 (13.2%)1.23 (0.67, 2.24)0.504 65 (33.2%)1.04 (0.69, 1.58)0.857
T108 (12.6%)1.15 (0.71, 1.86)0.567 237 (27.6%)0.80 (0.58, 1.11)0.182
+T125 (14.6%)1.38 (0.86, 2.21)0.187 285 (33.2%)1.05 (0.76, 1.45)0.781
Sedentary behaviorrs12970134 −43.03% −4.32%
G78 (11.4%)1 191 (27.8%)1
+G105 (14.7%)1.36 (0.99, 1.86)0.056 234 (32.8%)1.28 (1.02, 1.61)0.037
A47 (14.4%)1.31 (0.89, 1.94)0.171 98 (30.1%)1.12 (0.84, 1.50)0.430
+A40 (13.0%)1.17 (0.78, 1.76)0.454 105 (34.0%)1.34 (1.01, 1.79)0.045
Sedentary behaviorrs8050136 1.59% 20.82%
C95 (11.7%)1 237 (29.1%)1
+C113 (13.7%)1.22 (0.91, 1.63)0.186 265 (32.0%)1.16 (0.94, 1.44)0.164
A38 (14.8%)1.33 (0.89, 2.00)0.170 73 (28.4%)0.98 (0.72, 1.34)0.895
+A39 (17.3%)1.57 (1.05, 2.36)0.029 84 (37.3%)1.44 (1.06, 1.97)0.021
Sedentary behaviorRs2237892 −1.93% 13.94%
C51 (12.1%)1 128 (30.4%)1
+C71 (14.7%)1.26 (0.86, 1.86)0.24 155 (32.1%)1.10 (0.83, 1.46)0.513
T11 (9.7%)0.79 (0.4, 1.58)0.51 32 (28.3%)0.93 (0.59, 1.48)0.766
+T12 (12.4%)1.03 (0.53, 2.03)0.922 33 (34%)1.20 (0.75, 1.92)0.451
* Environmental factors were divided into binary variables with the P50 of the factor score as the cut-off value. Sedentary behavior: “−“ = not engaging in sedentary behavior often, “+” = engaging in sedentary behavior often. The first subgroup was used as the reference group.
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Gong, W.; Li, H.; Song, C.; Yuan, F.; Ma, Y.; Chen, Z.; Wang, R.; Fang, H.; Liu, A. Effects of Gene-Environment Interaction on Obesity among Chinese Adults Born in the Early 1960s. Genes 2021, 12, 270. https://doi.org/10.3390/genes12020270

AMA Style

Gong W, Li H, Song C, Yuan F, Ma Y, Chen Z, Wang R, Fang H, Liu A. Effects of Gene-Environment Interaction on Obesity among Chinese Adults Born in the Early 1960s. Genes. 2021; 12(2):270. https://doi.org/10.3390/genes12020270

Chicago/Turabian Style

Gong, Weiyan, Hui Li, Chao Song, Fan Yuan, Yanning Ma, Zheng Chen, Rui Wang, Hongyun Fang, and Ailing Liu. 2021. "Effects of Gene-Environment Interaction on Obesity among Chinese Adults Born in the Early 1960s" Genes 12, no. 2: 270. https://doi.org/10.3390/genes12020270

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop