The majority Injury prevention through balanced nutrition this increase will however hlood in developing High-fiber choices. Shifting this mindset to focus on the gains, like improved health bood Promoting optimal digestion levels Recharge without Hassle you control your blood sugar, can be a powerful motivator. Incorporate probiotic-rich foods like yogurt and fermented foods into your diet. Virus produces immune-mediated beta-cell destruction [ 4 ]. International Journal of Environmental Research and Public Health. How you feel can be a great indicator of your blood sugar level.

Environmental factors impacting blood sugar levels -

Findings from an exploratory study. Ann Epidemiol 16 5 — Schram MT, Assendelft WJJ, van Tilburg TG, Dukers-Muijrers N Social networks and type 2 diabetes: a narrative review.

Diabetologia 64 9 — Curr Diab Rep 16 11 Whitaker KM, Everson-Rose SA, Pankow JS et al Experiences of discrimination and incident type 2 diabetes mellitus: the multi-ethnic study of atherosclerosis MESA. Am J Epidemiol 4 — Dendup T, Astell-Burt T, Feng XQ Residential self-selection, perceived built environment and type 2 diabetes incidence: a longitudinal analysis of 36, middle to older age adults.

Dendup T, Feng X, O'Shaughnessy PY, Astell-Burt T Role of perceived neighbourhood crime in the longitudinal association between perceived built environment and type 2 diabetes mellitus: a moderated mediation analysis.

J Epidemiol Community Health 75 2 — Christakis NA, Fowler JH The spread of obesity in a large social network over 32 years. N Engl J Med 4 — Choi YJ, Ailshire JA, Crimmins EM Living alone, social networks in neighbourhoods, and daily fruit and vegetable consumption among middle-aged and older adults in the USA.

Public Health Nutr 23 18 — Shareck M, Ellaway A Neighbourhood crime and smoking: the role of objective and perceived crime measures. McNeill LH, Kreuter MW, Subramanian SV Social environment and physical activity: a review of concepts and evidence. Soc Sci Med 63 4 — Ng Fat L, Scholes S, Jivraj S The relationship between drinking pattern, social capital, and area-deprivation: findings from the health survey for England.

J Stud Alcohol Drugs 78 1 — Agardh E, Allebeck P, Hallqvist J, Moradi T, Sidorchuk A Type 2 diabetes incidence and socio-economic position: a systematic review and meta-analysis.

Int J Epidemiol 40 3 — Stringhini S, Batty GD, Bovet P et al Association of lifecourse socioeconomic status with chronic inflammation and type 2 diabetes risk: the Whitehall II prospective cohort study. PLoS Med 10 7 :e Gurung M, Li Z, You H et al Role of gut microbiota in type 2 diabetes pathophysiology.

EBioMedicine Sharma S, Tripathi P Gut microbiome and type 2 diabetes: where we are and where to go? J Nutr Biochem — Xu WT, Nie YZ, Yang Z, Lu NH The crosstalk between gut microbiota and obesity and related metabolic disorders. Future Microbiol — Canfora EE, Meex RCR, Venema K, Blaak EE Gut microbial metabolites in obesity, NAFLD and T2DM.

Nat Rev Endocrinol 15 5 — Li R, Andreu-Sanchez S, Kuipers F, Fu J Gut microbiome and bile acids in obesity-related diseases. Best Pract Res Clin Endocrinol Metab Qin J, Li Y, Cai Z et al A metagenome-wide association study of gut microbiota in type 2 diabetes.

Gou W, Ling CW, He Y et al Interpretable machine learning framework reveals robust gut microbiome features associated with type 2 diabetes. Diabetes Care 44 2 — Gonzalez-Franquesa A, Burkart AM, Isganaitis E, Patti ME What have metabolomics approaches taught us about type 2 diabetes?

Curr Diab Rep 16 8 Wang TJ, Larson MG, Vasan RS et al Metabolite profiles and the risk of developing diabetes. Nat Med 17 4 — Ferrannini E, Natali A, Camastra S et al Early metabolic markers of the development of dysglycemia and type 2 diabetes and their physiological significance.

Diabetes 62 5 — Floegel A, Stefan N, Yu Z et al Identification of serum metabolites associated with risk of type 2 diabetes using a targeted metabolomic approach.

Diabetes 62 2 — Padberg I, Peter E, Gonzalez-Maldonado S et al A new metabolomic signature in type-2 diabetes mellitus and its pathophysiology. PLoS One 9 1 :e Wang TJ, Ngo D, Psychogios N et al 2-Aminoadipic acid is a biomarker for diabetes risk.

J Clin Invest 10 — Wang-Sattler R, Yu Z, Herder C et al Novel biomarkers for pre-diabetes identified by metabolomics. Mol Syst Biol Patel CJ, Bhattacharya J, Butte AJ An environment-wide association study EWAS on type 2 diabetes mellitus. PLoS One 5 5 :e Meijer J, Lamoree M, Hamers T et al An annotation database for chemicals of emerging concern in exposome research.

Barregard L, Bergstrom G, Fagerberg B Cadmium exposure in relation to insulin production, insulin sensitivity and type 2 diabetes: a cross-sectional and prospective study in women. Environ Res — He K, Xun P, Liu K, Morris S, Reis J, Guallar E Mercury exposure in young adulthood and incidence of diabetes later in life: the CARDIA trace element study.

Diabetes Care 36 6 — Hendryx M, Luo J, Chojenta C, Byles JE Exposure to heavy metals from point pollution sources and risk of incident type 2 diabetes among women: a prospective cohort analysis.

Int J Environ Health Res 1— Lin JL, Lin-Tan DT, Yu CC, Li YJ, Huang YY, Li KL Environmental exposure to lead and progressive diabetic nephropathy in patients with type II diabetes. Kidney Int 69 11 — Navas-Acien A, Silbergeld EK, Pastor-Barriuso R, Guallar E Arsenic exposure and prevalence of type 2 diabetes in US adults.

JAMA 7 — Airaksinen R, Rantakokko P, Eriksson JG, Blomstedt P, Kajantie E, Kiviranta H Association between type 2 diabetes and exposure to persistent organic pollutants. Diabetes Care 34 9 — Wolf K, Bongaerts BWC, Schneider A et al Persistent organic pollutants and the incidence of type 2 diabetes in the CARLA and KORA cohort studies.

Boursi B, Mamtani R, Haynes K, Yang YX The effect of past antibiotic exposure on diabetes risk. Eur J Endocrinol 6 — Hansen AB, Ravnskjaer L, Loft S et al Long-term exposure to fine particulate matter and incidence of diabetes in the Danish nurse cohort.

Cao XY, Mokhtarian PL, Handy SL Examining the impacts of residential self-selection on travel behaviour: a focus on empirical findings. Transp Rev 29 3 — McCormack GR, Shiell A In search of causality: a systematic review of the relationship between the built environment and physical activity among adults.

Int J Behav Nutr Phys Act 8:Artn Drewnowski A, Buszkiewicz J, Aggarwal A, Rose C, Gupta S, Bradshaw A Obesity and the built environment: a reappraisal. Obesity Silver Spring 28 1 — Lin CY, Koohsari MJ, Liao Y et al Workplace neighbourhood built environment and workers' physically-active and sedentary behaviour: a systematic review of observational studies.

Int J Behav Nutr Phys Act 17 1 :ARTN Cunningham-Myrie CA, Theall KP, Younger NO et al Associations between neighborhood effects and physical activity, obesity, and diabetes: the Jamaica health and lifestyle survey J Clin Epidemiol 68 9 — Diez Roux AV, Mair C Neighborhoods and health.

Ann N Y Acad Sci — Wild CP The exposome: from concept to utility. Int J Epidemiol 41 1 — Download references.

The authors declare that there are no relationships or activities that might bias, or be perceived to bias, their work. JWJB declares to be a member of the editorial board of Diabetologia.

EXPOSOME-NL is funded through the Gravitation program of the Dutch Ministry of Education, Culture, and Science and the Netherlands Organization for Scientific Research NWO grant number Joline W. Beulens, Maria G. Pinho, Taymara C. Abreu, Nicole R.

den Braver, Thao M. Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands. Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands. Department of Human Geography and Spatial Planning, Utrecht University, Utrecht, the Netherlands.

Department of Genetics, University Medical Center Groningen, Groningen, the Netherlands. Brandao Gois. You can also search for this author in PubMed Google Scholar.

All authors were responsible for drafting the article and revising it critically for important intellectual content.

All authors approved the version to be published. Correspondence to Joline W. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Reprints and permissions. Beulens, J.

et al. Environmental risk factors of type 2 diabetes—an exposome approach. Diabetologia 65 , — Download citation. Received : 16 June Accepted : 07 October Published : 18 November Issue Date : February Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Download PDF. Abstract Type 2 diabetes is one of the major chronic diseases accounting for a substantial proportion of disease burden in Western countries.

Graphical abstract. The Relationship of Historical Redlining with Present-Day Neighborhood Environmental and Health Outcomes: A Scoping Review and Conceptual Model Article 01 August Introduction to Epidemiological Studies Chapter © Socioeconomic Disparities and Air Pollution Exposure: a Global Review Article 18 September Use our pre-submission checklist Avoid common mistakes on your manuscript.

Introduction Type 2 diabetes is a major chronic disease burden in Western countries, which is estimated to affect million people worldwide by [ 1 ]. Full size image. Environmental risk factors of type 2 diabetes The food environment The food environment encompasses the accessibility, availability, affordability and promotion of foods and food retailers [ 17 ].

Internal exposome Although our internal exposome consists of proteins, lipids, metabolites and so on, the role of the metabolome and microbiome appear to be of particular importance in the aetiology of type 2 diabetes.

The microbiome The gut microbiota is known for its ability to modulate inflammation, metabolise xenobiotics, maintain intestinal integrity and its interactions with dietary components. Metabolome and exposome scans Technological developments, in which untargeted liquid- LC- and gas GC- chromatography are combined with high-resolution mass spectrometry HRMS , have made it possible to comprehensively, and in a high-throughput fashion, measure the patterns of thousands of metabolites that are present in biological fluids, known as the metabolome [ 88 , 89 ].

Methodological considerations Our living environment is mostly an indirect determinant of type 2 diabetes and changes in the living environment are often difficult to investigate in controlled studies. Future perspectives Future studies should investigate longitudinal changes in our environment in relation to risk of type 2 diabetes, including pathway analyses of health behaviours.

Conclusion In conclusion, our environment accounts for a substantial proportion of disease burden due to type 2 diabetes.

Abbreviations HRMS: High-resolution mass spectrometry. References Standl E, Khunti K, Hansen TB, Schnell O The global epidemics of diabetes in the 21st century: current situation and perspectives.

EPI Article CAS Google Scholar Vermeulen R, Schymanski EL, Barabasi AL, Miller GW The exposome and health: where chemistry meets biology. aay Article CAS PubMed PubMed Central Google Scholar Pourchet M, Debrauwer L, Klanova J et al Suspect and non-targeted screening of chemicals of emerging concern for human biomonitoring, environmental health studies and support to risk assessment: from promises to challenges and harmonisation issues.

x Article PubMed Google Scholar Wild CP The exposome: from concept to utility. Siddiqui Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands Joline W. Brandao Gois Authors Joline W. Beulens View author publications.

View author publications. Supplementary information. ESM 1 PPTX kb. Rights and permissions Reprints and permissions. Lower educational level is a predictor of incident type 2 diabetes in European countries: the EPIC-InterAct study. Williams ED, Tapp RJ, Magliano DJ, Shaw JE, Zimmet PZ, Oldenburg BF.

Health behaviours, socioeconomic status and diabetes incidence: the Australian Diabetes Obesity and Lifestyle Study AusDiab. Leong A, Rahme E, Dasgupta K.

Spousal diabetes as a diabetes risk factor: a systematic review and meta-analysis. Almgren M, Atkinson R, He J, Hilding A, Hagman E, Wolk A, et al. Adenovirus is associated with obesity in children and adults in Sweden as determined by rapid ELISA.

Pasarica M, Shin AC, Yu M, Ou Yang HM, Rathod M, et al. Human adenovirus 36 induces adiposity, increases insulin sensitivity, and alters hypothalamic monoamines in rats. Obesity Silver Spring. Almgren M, Atkinson RL, Hilding A, He J, Brismar K, Schalling M, et al.

Human adenovirus is uncommon in type 2 diabetes and is associated with increased insulin sensitivity in adults in Sweden. Ann Med. Negro F. Facts and fictions of HCV and comorbidities: steatosis, diabetes mellitus, and cardiovascular diseases. J Hepatol. Lin YJ, Shaw TG, Yang HI, Lu SN, Jen CL, Wang LY, et al.

Chronic hepatitis C virus infection and the risk for diabetes: a community-based prospective study. Google Scholar.

Rodriguez AR, Plascencia-Villa G, Witt CM, Yu JJ, Jose-Yacaman M, Chambers JP, et al. Chlamydia pneumoniae promotes dysfunction of pancreatic beta cells. Cell Immunol. Betene AD, De Wit S, Neuhaus J, Palfreeman A, Pepe R, Pankow JS, Neaton JD.

Interleukin-6, high sensitivity C-reactive protein, and the development of type 2 diabetes among HIV-positive patients taking antiretroviral therapy. J Acquir Immune Defic Syndr. Bonnefond A, Froguel P. Rare and common genetic events in type 2 diabetes: what should biologists know?

Cell Metab. Esparza-Romero J, Valencia ME, Urquidez-Romero R, Chaudhari LS, Hanson RL, Knowler WC, et al. Environmentally driven increases in type 2 diabetes and obesity in Pima Indians and non-Pimas in Mexico over a year period: the Maycoba Project.

Lao XQ, Ma WJ, Sobko T, Zhang YH, Xu YJ, Xu XJ, et al. Overall obesity is leveling-off while abdominal obesity continues to rise in a Chinese population experiencing rapid economic development: analysis of serial cross-sectional health survey data Wang Y, Rimm EB, Stampfer MJ, Willett WC, Hu FB.

Comparison of abdominal adiposity and overall obesity in predicting risk of type 2 diabetes among men. Hardoon SL, Morris RW, Thomas MC, Wannamethee SG, Lennon LT, Whincup PH. Is the recent rise in type 2 diabetes incidence from to explained by the trend in increasing BMI?

Butler AE, Dhawan S, Hoang J, Cory M, Zeng K, Fritsch H, et al. β-cell deficit in obese type 2 diabetes, a minor role of β-cell dedifferentiation and degranulation. Kaneto H. Pancreatic beta-cell glucose toxicity in type 2 diabetes mellitus.

Curr Diabetes Rev. Brun T, Maechler P. Beta-cell mitochondrial carriers and the diabetogenic stress response. Biochim Biophys Acta. Ertunc ME, Hotamisligil GS. Lipid signaling and lipotoxicity in metaflammation: indications for metabolic disease pathogenesis and treatment.

J Lipid Res. Kolb H, Mandrup-Poulsen T. The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation. McNelis JC, Olefsky JM. Macrophages, immunity, and metabolic disease. Herder C, Dalmas E, Boni-Schnetzler M, Donath MY.

The IL-1 Pathway in type 2 diabetes and cardiovascular complications. Trends Endocrinol Metab. Berchtold LA, Prause M, Storling J, Mandrup-Poulsen T.

Cytokines and pancreatic beta-cell apoptosis. Adv Clin Chem. Kolb H, Eizirik DL. Resistance to type 2 diabetes mellitus: a matter of hormesis? Nat Rev Endocrinol. Lanki T, Hampel R, Tiittanen P, Andrich S, Beelen R, Brunekreef B, et al. Air pollution from road traffic and systemic inflammation in adults: a cross-sectional analysis in the European ESCAPE Project.

PubMed PubMed Central Google Scholar. Chen JC, Schwartz J. Metabolic syndrome and inflammatory responses to long-term particulate air pollutants. da Costa SA, Ribeiro S. Sleep deprivation and gene expression. Curr Top Behav Neurosci. Chennaoui M, Sauvet F, Drogou C, Van Beers P, Langrume C, Guillard M, et al.

Effect of one night of sleep loss on changes in tumor necrosis factor alpha TNF-alpha levels in healthy men. de Vries MA, Klop B, Janssen HW, Njo TL, Westerman EM, Castro CM.

Postprandial inflammation: targeting glucose and lipids. Adv Exp Med Biol. Herieka M, Erridge C. High-fat meal induced postprandial inflammation. Mol Nutr Food Res. Thorand B, Baumert J, Doring A, Herder C, Kolb H, Rathmann W, et al.

Sex differences in the relation of body composition to markers of inflammation. Choi J, Joseph L, Pilote L. Obesity and C-reactive protein in various populations: a systematic review and meta-analysis. Obes Rev. Gnauck A, Lentle RG, Kruger MC. The characteristics and function of bacterial lipopolysaccharides and their endotoxic potential in humans.

Int Rev Immunol. Amyot J, Semache M, Ferdaoussi M, Fontes G, Poitout V. Lipopolysaccharides impair insulin gene expression in isolated islets of Langerhans via Toll-like receptor-4 and NF-kappaB signalling. Martinez-Gomez D, Eisenmann JC, Healy GN, Gomez-Martinez S, Diaz LE, Dunstan DW, et al.

Sedentary behaviors and emerging cardiometabolic biomarkers in adolescents. J Pediatr. Henson J, Yates T, Edwardson CL, Khunti K, Talbot D, Gray LJ, et al. Sedentary time and markers of chronic low-grade inflammation in a high risk population.

Gabel L, Ridgers ND, Della Gatta PA, Arundell L, Cerin E, Robinson S, et al. Associations of sedentary time patterns and TV viewing time with inflammatory and endothelial function biomarkers in children.

Pediatr Obes. You T, Arsenis NC, Disanzo BL, Lamonte MJ. Effects of exercise training on chronic inflammation in obesity : current evidence and potential mechanisms.

Sports Med. Gjevestad GO, Holven KB, Ulven SM. Effects of exercise on gene expression of inflammatory markers in human peripheral blood cells: a systematic review. Curr Cardiovasc Risk Rep. Shen X, Yang L, Yan S, Zheng H, Liang L, Cai X, Liao M. Fetuin A promotes lipotoxicity in beta cells through the TLR4 signaling pathway and the role of pioglitazone in anti-lipotoxicity.

Mol Cell Endocrinol. Howren MB, Lamkin DM, Suls J. Associations of depression with C-reactive protein, IL-1, and IL a meta-analysis. Berk M, Williams LJ, Jacka FN, O'Neil A, Pasco JA, Moylan S, et al. So depression is an inflammatory disease, but where does the inflammation come from?

Kiecolt-Glaser JK, Derry HM, Fagundes CP. Inflammation: depression fans the flames and feasts on the heat. Am J Psychiatry. Kruyt ND, van Westerloo DJ, DeVries JH. Stress-induced hyperglycemia in healthy bungee jumpers without diabetes due to decreased pancreatic beta-cell function and increased insulin resistance.

Diabetes Technol Ther. Maffei A, Segal AM, Alvarez-Perez JC, Garcia-Ocana A, Harris PE. Anti-incretin, anti-proliferative action of dopamine on beta-cells. Mol Endocrinol. Kodavanti UP. Stretching the stress boundary: linking air pollution health effects to a neurohormonal stress response.

Carter A, Hendrikse J, Lee N, Yucel M, Verdejo-Garcia A, Andrews Z, Hall W. The neurobiology of "food addiction" and its implications for obesity treatment and policy.

Annu Rev Nutr. Fuchsberger C, Flannick J, Teslovich TM, Mahajan A, Agarwala V, Gaulton KJ, et al. The genetic architecture of type 2 diabetes. Swerdlow DI. Mendelian randomization and type 2 diabetes. Cardiovasc Drugs Ther. Delahanty LM, Pan Q, Jablonski KA, Aroda VR, Watson KE, Bray GA, et al.

Effects of weight loss, weight cycling, and weight loss maintenance on diabetes incidence and change in cardiometabolic traits in the Diabetes Prevention Program.

Tuomilehto J, Lindstrom J, Eriksson JG, Valle TT, Hamalainen H, Ilanne-Parikka P, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.

Chaston TB, Dixon JB. Factors associated with percent change in visceral versus subcutaneous abdominal fat during weight loss: findings from a systematic review.

Gallagher D, Heshka S, Kelley DE, Thornton J, Boxt L, Pi-Sunyer FX, et al. Changes in adipose tissue depots and metabolic markers following a 1-year diet and exercise intervention in overweight and obese patients with type 2 diabetes. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R.

Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Kempf K, Schloot NC, Gartner B, Keil R, Schadewaldt P, Martin S. J Hum Nutr Diet. Diabetes Prevention Program Research Group. Long-term effects of lifestyle intervention or metformin on diabetes development and microvascular complications over year follow-up: the Diabetes Prevention Program Outcomes Study.

Article PubMed Central CAS Google Scholar. Lindstrom J, Peltonen M, Eriksson JG, Ilanne-Parikka P, Aunola S, Keinanen-Kiukaanniemi S, et al. Improved lifestyle and decreased diabetes risk over 13 years: long-term follow-up of the randomised Finnish Diabetes Prevention Study DPS.

Sjoholm K, Sjostrom E, Carlsson LM, Peltonen M. Weight change-adjusted effects of gastric bypass surgery on glucose metabolism: 2- and year results from the Swedish Obese Subjects SOS study.

Zong G, Eisenberg DM, Hu FB, Sun Q. Consumption of meals prepared at home and risk of type 2 diabetes: an analysis of two prospective cohort studies. Kuwabara M, Motoki Y, Sato H, Fujii M, Ichiura K, Kuwabara K, Nakamura Y.

Low frequency of toothbrushing practices is an independent risk factor for diabetes mellitus in male and dyslipidemia in female: A large-scale, 5-year cohort study in Japan. J Cardiol. Brandsma E, Houben T, Fu J, Shiri-Sverdlov R, Hofker MH.

The immunity-diet-microbiota axis in the development of metabolic syndrome. Curr Opin Lipidol. Delzenne NM, Cani PD, Everard A, Neyrinck AM, Bindels LB. Gut microorganisms as promising targets for the management of type 2 diabetes. Xiao S, Fei N, Pang X, Shen J, Wang L, Zhang B, et al.

A gut microbiota-targeted dietary intervention for amelioration of chronic inflammation underlying metabolic syndrome. FEMS Microbiol Ecol. Miele L, Valenza V, La Torre G, Montalto M, Cammarota G, Ricci R, et al.

Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease. Festi D, Schiumerini R, Eusebi LH, Marasco G, Taddia M, Colecchia A. Gut microbiota and metabolic syndrome.

World J Gastroenterol. Boets E, Gomand SV, Deroover L, Preston T, Vermeulen K, De Preter V, et al. Systemic availability and metabolism of colonic-derived short-chain fatty acids in healthy subjects: a stable isotope study.

J Physiol. Priyadarshini M, Wicksteed B, Schiltz GE, Gilchrist A, Layden BT. SCFA receptors in pancreatic beta cells: novel diabetes targets? Stefanson AL, Bakovic M. Qin S, Hou DX. Li T, He S, Liu S, Kong Z, Wang J, Zhang Y. Effects of different exercise durations on Keap1-Nrf2-ARE pathway activation in mouse skeletal muscle.

Free Radic Res. Keating SE, Hackett DA, George J, Johnson NA. Exercise and non-alcoholic fatty liver disease: a systematic review and meta-analysis. Nguyen KT, Korner J. The sum of many parts: potential mechanisms for improvement in glucose homeostasis after bariatric surgery.

Korner J, Bessler M, Inabnet W, Taveras C, Holst JJ. Exaggerated glucagon-like peptide-1 and blunted glucose-dependent insulinotropic peptide secretion are associated with Roux-en-Y gastric bypass but not adjustable gastric banding. Surg Obes Relat Dis. Svendsen PF, Jensen FK, Holst JJ, Haugaard SB, Nilas L, Madsbad S.

The effect of a very low calorie diet on insulin sensitivity, beta cell function, insulin clearance, incretin hormone secretion, androgen levels and body composition in obese young women.

Scand J Clin Lab Invest. Lips MA, de Groot GH, Berends FJ, Wiezer R, Van Wagensveld BA, Swank DJ, et al.

Calorie restriction and Roux-en-Y gastric bypass have opposing effects on circulating FGF21 in morbidly obese subjects.

Clin Endocrinol Oxf. Jorgensen NB, Dirksen C, Bojsen-Moller KN, Kristiansen VB, Wulff BS, Rainteau D, Clausen TR, et al. Improvements in glucose metabolism early after gastric bypass surgery are not explained by increases in total bile acids and fibroblast growth factor 19 concentrations.

Rodieux F, Giusti V, D'Alessio DA, Suter M, Tappy L. Effects of gastric bypass and gastric banding on glucose kinetics and gut hormone release. Lips MA, Van Klinken JB, van Harmelen V, Dharuri HK, 't Hoen PA, Laros JF, van Ommen GJ, et al. Roux-en-Y gastric bypass surgery, but not calorie restriction, reduces plasma branched-chain amino acids in obese women independent of weight loss or the presence of type 2 diabetes.

Isbell JM, Tamboli RA, Hansen EN, Saliba J, Dunn JP, Phillips SE, et al. The importance of caloric restriction in the early improvements in insulin sensitivity after Roux-en-Y gastric bypass surgery.

Lips MA, de Groot GH, Van Klinken JB, Aarts E, Berends FJ, Janssen IM, et al. Calorie restriction is a major determinant of the short-term metabolic effects of gastric bypass surgery in obese type 2 diabetic patients. Supale S, Li N, Brun T, Maechler P. Mitochondrial dysfunction in pancreatic beta cells.

Peinado JR, Diaz-Ruiz A, Fruhbeck G, Malagon MM. Mitochondria in metabolic disease: getting clues from proteomic studies. Malandrucco I, Pasqualetti P, Giordani I, Manfellotto D, De Marco F, Alegiani F, et al.

Very-low-calorie diet: a quick therapeutic tool to improve beta cell function in morbidly obese patients with type 2 diabetes. Polyzogopoulou EV, Kalfarentzos F, Vagenakis AG, Alexandrides TK. Restoration of euglycemia and normal acute insulin response to glucose in obese subjects with type 2 diabetes following bariatric surgery.

Martinussen C, Bojsen-Moller KN, Dirksen C, Jacobsen SH, Jorgensen NB, Kristiansen VB, et al. Immediate enhancement of first-phase insulin secretion and unchanged glucose effectiveness in patients with type 2 diabetes after Roux-en-Y gastric bypass.

Am J Physiol Endocrinol Metab. Nannipieri M, Mari A, Anselmino M, Baldi S, Barsotti E, Guarino D, et al. The role of beta-cell function and insulin sensitivity in the remission of type 2 diabetes after gastric bypass surgery.

Longo VD, Mattson MP. Fasting: molecular mechanisms and clinical applications. Brewer RA, Gibbs VK, Smith Jr DL. Targeting glucose metabolism for healthy aging. Nutr Healthy Aging. Lopez-Lluch G, Navas P. Calorie restriction as an intervention in ageing.

Cao Y, Jiang X, Ma H, Wang Y, Xue P, Liu Y. SIRT1 and insulin resistance. J Diabetes Complications. Marino G, Pietrocola F, Madeo F, Kroemer G. Pall ML, Levine S. Nrf2, a master regulator of detoxification and also antioxidant, anti-inflammatory and other cytoprotective mechanisms, is raised by health promoting factors.

Sheng Li Xue Bao. Rodriguez-Ramiro I, Vauzour D, Minihane AM. Polyphenols and non-alcoholic fatty liver disease: impact and mechanisms.

Proc Nutr Soc. Download references. KG, Almased Wellness GmbH, Nintendo of Europe GmbH, HMM Holding AG. This work was supported by the Gesellschaft von Freunden und Förderern der Heinrich-Heine-Universität Düsseldorf e.

Faculty of Medicine, University of Duesseldorf, Duesseldorf, Germany. West-German Centre of Diabetes and Health, Duesseldorf Catholic Hospital Group, Hohensandweg 37, , Duesseldorf, Germany.

You can also search for this author in PubMed Google Scholar. HK and SM conceived and wrote the manuscript. Both authors read and approved the final manuscript. Correspondence to Hubert Kolb. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Kolb, H. BMC Med 15 , Download citation. Received : 14 March Accepted : 23 June Published : 19 July Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Abstract Background Environmental and lifestyle changes, in addition to the ageing of populations, are generally believed to account for the rapid global increase in type 2 diabetes prevalence and incidence in recent decades.

Discussion In this review, we present a comprehensive overview of factors contributing to diabetes risk, including aspects of diet quality and quantity, little physical activity, increased monitor viewing time or sitting in general, exposure to noise or fine dust, short or disturbed sleep, smoking, stress and depression, and a low socioeconomic status.

Background Over the past decades, there has been a major increase in type 2 diabetes T2D prevalence in most regions of the world [ 1 ]. Overview of environmental and lifestyle factors increasing T2D risk It is generally believed that an energy-dense Western style diet in conjunction with a sedentary lifestyle are the primary cause of T2D [ 2 ].

Diet When considering the wide range of diet types consumed in different regions of the world, it may not be surprising that prospective epidemiological studies vary somewhat in the association of food groups with incident T2D. Watching TV or sedentary time There is a strong association between sedentary time self-reported or objectively measured with obesity or incident diabetes, independent of the extent of physical activity [ 47 , 48 , 49 , 50 , 51 ].

Housing environment and sleep duration or quality Epidemiological studies concur in an association between increased exposure to residential traffic, noise, and fine airborne particulate matter and a higher risk of T2D diagnosis during the following 5—12 years. Depression and stress as risk factors Stress at work, in social relationships or in other aspects of life is difficult to define given that it is the impact on the individual and the coping mechanisms that are probably relevant, i.

Impact of socioeconomic status An inverse association of T2D and socioeconomic position has been reported worldwide, also after separate analysis of high-, middle- and low-income countries, independent of whether measured by educational level, occupation or income [ 99 , ].

Infections as a cause of T2D? How may unfavourable lifestyle and environmental changes cause the current T2D epidemic? Full size image. Lifestyle changes for diabetes prevention Trials of diabetes prevention have appreciated the contribution of lifestyle to diabetes risk.

Conclusions A host of environmental or lifestyle-dependent T2D risk factors have been described in prospective epidemiological studies, ranging from energy-dense food consumption to long-term exposure to high levels of fine dust.

Box 1. References NDC Risk Factor Collaboration. Article Google Scholar Chatterjee S, Khunti K, Davies MJ. Article CAS PubMed Google Scholar Ng M, Fleming T, Robinson M, Thomson B, Graetz N, Margono C, et al. Article PubMed PubMed Central Google Scholar Neeland IJ, Turer AT, Ayers CR, Powell-Wiley TM, Vega GL, Farzaneh-Far R, et al.

Article CAS PubMed PubMed Central Google Scholar Ballestri S, Zona S, Targher G, Romagnoli D, Baldelli E, Nascimbeni F, et al. Article CAS PubMed Google Scholar Valenti L, Bugianesi E, Pajvani U, Targher G. Article CAS PubMed Google Scholar Sattar N, Gill JM. Article PubMed PubMed Central Google Scholar Phillips CM.

Article CAS PubMed Google Scholar Roberson LL, Aneni EC, Maziak W, Agatston A, Feldman T, Rouseff M, et al. Article PubMed PubMed Central Google Scholar Bluher M. Article PubMed CAS Google Scholar Ma RC, Chan JC. Article PubMed PubMed Central Google Scholar Unnikrishnan R, Anjana RM, Mohan V.

Article CAS PubMed Google Scholar Ding C, Chan Z, Magkos F. Article CAS PubMed Google Scholar Jannasch F, Kroger J, Schulze MB. Article PubMed Google Scholar Schwingshackl L, Hoffmann G, Lampousi AM, Knuppel S, Iqbal K, Schwedhelm C, et al.

Article PubMed Google Scholar Forouhi NG, Wareham NJ. Article CAS PubMed PubMed Central Google Scholar Maki KC, Phillips AK.

Article CAS PubMed Google Scholar Cespedes EM, Hu FB, Tinker L, Rosner B, Redline S, Garcia L, et al. Article PubMed PubMed Central Google Scholar Satija A, Bhupathiraju SN, Rimm EB, Spiegelman D, Chiuve SE, Borgi L, et al.

Article PubMed PubMed Central Google Scholar Ma Y, He FJ, Yin Y, Hashem KM, MacGregor GA. Article CAS PubMed Google Scholar Lofvenborg JE, Andersson T, Carlsson PO, Dorkhan M, Groop L, Martinell M, et al.

Article PubMed CAS Google Scholar Wang M, Yu M, Fang L, Hu RY. Article CAS PubMed Google Scholar Greenwood DC, Threapleton DE, Evans CE, Cleghorn CL, Nykjaer C, Woodhead C, Burley VJ. Article CAS PubMed Google Scholar Bao Y, Han J, Hu FB, Giovannucci EL, Stampfer MJ, Willett WC, Fuchs CS.

Article CAS PubMed PubMed Central Google Scholar U. Article PubMed Google Scholar Tay J, Luscombe-Marsh ND, Thompson CH, Noakes M, Buckley JD, Wittert GA, et al. Article CAS PubMed Google Scholar Yancy Jr WS, Mayer SB, Coffman CJ, Smith VA, Kolotkin RL, Geiselman PJ, et al.

Article PubMed PubMed Central Google Scholar Hill AM, Harris Jackson KA, Roussell MA, West SG, Kris-Etherton PM. Article CAS PubMed PubMed Central Google Scholar Tobias DK, Chen M, Manson JE, Ludwig DS, Willett W, Hu FB.

Article PubMed PubMed Central Google Scholar Salas-Salvado J, Bullo M, Babio N, Martinez-Gonzalez MA, Ibarrola-Jurado N, Basora J, et al. Article PubMed Google Scholar Howells L, Musaddaq B, McKay AJ, Majeed A. Article PubMed PubMed Central Google Scholar Gong QH, Kang JF, Ying YY, Li H, Zhang XH, Wu YH, Xu GZ.

Article CAS PubMed Google Scholar Vasto S, Buscemi S, Barera A, Di Carlo M, Accardi G, Caruso C. Article CAS PubMed Google Scholar Willcox DC, Scapagnini G, Willcox BJ. Article PubMed PubMed Central CAS Google Scholar Buettner D. Article PubMed Central Google Scholar Shadyab AH, LaCroix AZ.

Article CAS PubMed Google Scholar Loef M, Walach H. Research indicates a strong association between environment and diabetes risk.

While type 2 diabetes has a large genetic component, the development of the condition is also influenced by environmental factors, including the characteristics of the neighborhood in which a person lives.

Researchers can't say for certain that any individual environmental factor directly causes type 2 diabetes, but studies have found links that suggest some factors play a role in its development.

Read on to learn about how environmental factors such as pollution, infrastructure, and access to healthy food may contribute to the development of type 2 diabetes. Type 2 diabetes is believed to result from an interaction of biological, behavioral, and environmental risk factors.

Someone's environment can influence other risk factors. For example, some biological risk factors for type 2 diabetes are abdominal obesity and high blood pressure.

Behavioral risk factors include lack of physical activity and regularly eating a diet that contributes to raised blood sugar. Environmental factors such as the layout of a city or the availability of good quality food can contribute to these other risk factors.

On they other hand, an environment that supports healthy lifestyle choices can lessen some of the biological and behavioral risk factors. The measurable totality of environmental non-genetic drivers of disease is called "the exposome.

Within these environmental groups, more specific factors can be examined in terms of how they may contribute to type 2 diabetes. There is some evidence that suggests higher air pollution, particularly exposure to nitrogen dioxide NO2 and particle matter PM2. Air pollution has been shown to change endothelial cells that line the blood vessels function, elevate adipose body fat and systemic inflammation, and trigger insulin resistance.

It is also associated with obesity and high blood pressure. This can contribute to type 2 diabetes risk. Several meta-analyses have found associations between chemical pollutants such as persistent organic pollutants, pesticides, and heavy metals and an increased risk of type 2 diabetes.

Rates of type 2 diabetes are rising world-wide but are increasing particularly quickly in low and middle-income countries. The number of people aged 20 to 79 in Asia living with diabetes is expected to increase to approximately million in , compared to approximately million in Climate change negatively affects people with diabetes in a number of ways, including:.

When discussing a location's access to healthy food, two terms are often mentioned:. The availability, accessibility, and affordability of healthy food influences dietary habits.

The physical design of the environment in which a person spends the majority of their time can influence factors that impact type 2 diabetes risk.

Walkability refers to how conducive and supportive for walking the location is. Some research has found a connection between living in an area with a higher level of walkability and a lower risk of type 2 diabetes.

There is currently not enough data to show whether this lowered risk is caused by increased walkability or only associated with it. For instance, people who are more physically active may choose to live in areas with high walkability rather than walkability promoting physical activity.

Green Space. Three cross-sectional studies found that neighborhoods with more green space had a lower risk for type 2 diabetes.

These studies used the quantity of green space rather than quality to assess. Green space is also associated with stress reduction, which benefits blood glucose management.

Active Transportation. Active transportation consists of walking, biking, and other forms of physical activity used to get from point A to point B. Public transportation is sometimes included under active transportation because there is often walking or other physical activity before and after the ride.

People living in areas with higher levels of active transportation exhibit a reduced risk of cardiovascular disease, hypertension, and type 2 diabetes. Neighborhoods in which residents feel safe and socially supported , and that are aesthetically pleasing, encourage physical activity.

Research on the specifics of how housing and neighborhood conditions impact the risk for type 2 diabetes has been less clear-cut. More research is needed to determine how factors such as real estate value, population density, crime rates, and physical conditions influence type 2 diabetes risk.

Risk factors for type 2 diabetes don't impact everyone equally. People who have a low income can be more vulnerable to environmental risk factors. People who belong to racialized groups and those who are recent immigrants are often deprived of access to active transportation support, recreational facilities, healthy food choices, and other environmental factors that affect the risk of developing type 2 diabetes.

There is no one cause of type 2 diabetes.

L-carnitine and diabetes management to Promoting optimal digestion Enivronmental Promoting optimal digestion Association, more than 34 levelw Americans have diabetes, Encironmental about 1. Of new diagnoses, 90 to 95 percent of them are type 2 Environmeental, according to the Environmengal for Disease Control and Prevention CDC. Knowing the risk factors for type 2 diabetes can help you make changes that promote positive effects on your overall health and wellness that can help reduce your risk. There are various factors at play. Type 2 diabetes can be managed by working with healthcare professionals who can teach you how to monitor and manage your care to maintain your overall health.

Video

Blood Glucose Regulation and Diabetes