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Lifestyle causes of type 2 diabetes

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A number of lifestyle factors are known to be important to the development of type 2 diabetes including: obesity, physical activity, diet, stress, and urbanization.[1] Excess body fat underlies 64% of cases of diabetes in men and 77% of cases in women.[2] A number of dietary factors such as sugar sweetened drinks[3][4] and the type of fat in the diet appear to play a role.[5][6]

In one study, those who had high levels of physical activity, a healthy diet, did not smoke, and consumed alcohol in moderation had an 82% lower rate of diabetes. When a normal weight was included, the rate was 89% lower. In this study, a healthy diet was defined as one high in fiber, with a high polyunsaturated to saturated fat ratio, lower trans fats consumption, and a lower mean glycemic index.[7]

Dietary

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The composition of dietary fat intake is linked to diabetes risk; decreasing consumption of saturated fats and trans fatty acids while replacing them with unsaturated fats may decrease the risk.[5][8] Sugar sweetened drinks appear to increase the risk of type 2 diabetes both through their role in obesity and potentially through a direct effect.[3][4] A higher proportion of ultra-processed food in the diet was associated with a higher risk of type 2 diabetes in a large ten-year study published in 2019.[9]

Obesity

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Obesity has been found to contribute to approximately 55% of cases of type 2 diabetes;[10] chronic obesity leads to increased insulin resistance that can develop into type 2 diabetes,[11] most likely because adipose tissue (especially that in the abdomen around internal organs) is a source of several chemical signals, hormones and cytokines, to other tissues. Inflammatory cytokines such as TNFα may activate the NF-κB pathway which has been linked to the development of insulin resistance.[12] Gene expression promoted by a diet of fat and glucose, as well as high levels of inflammation related cytokines found in the obese, can result in cells that "produce fewer and smaller mitochondria than is normal," and are thus prone to insulin resistance.[13][unreliable medical source?] Fat tissue has also been shown to be involved in managing much of the body's response to insulin and control of uptake of sugar.[14] It secretes RBP4 which increases insulin resistance by blocking the action of insulin in muscle and liver.[15][16] Fat cells also secrete adiponectin which acts in an opposite way to RBP4 by improving the action of insulin, however, engorged fat cells secrete it in lower amount than normal fat cells.[14] The obese therefore may have higher level of RBP4 but lower level of adiponectin, both of which increase the risk of developing diabetes.[16][17]

However, different fat tissues behave differently. Visceral fat, which is found around organs such as the intestines and liver, releases signalling molecules directly into blood heading into the liver where glucose is absorbed and processed, while subcutaneous fat under the skin is much less metabolically active.[14] The visceral fat is located in the abdomen in the waist region, large waist circumference and high waist-to-hip ratio are therefore often used as indications of an increased risk of type 2 diabetes.[18][19]

The increased rate of childhood obesity between the 1960s and 2000s is believed to have led to the increase in type 2 diabetes in children and adolescents.[20]

Sleep

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Studies[21][22] have shown that a reduction in sleep is associated with a significant increase in the incidence of type 2 diabetes. This could account for the increased incidence of diabetes in developed countries in the last decades, since "the causes of this pandemic are not fully explained by changes in traditional lifestyle factors such as diet and physical activity",[21] and "one behavior that seems to have developed during the past few decades and has become highly prevalent, particularly amongst Americans, is sleep curtailment".[21]

In addition, it has been shown that certain minority populations, such as Native Hawaiians/Pacific Islanders[23] or American Indians/Alaska Natives,[24][25] report higher rates of suboptimal sleep, potentially leading to higher rates of type 2 diabetes.

Prenatal environment

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Research also suggests intrauterine growth restriction (IUGR) or prenatal undernutrition (macro- and micronutrient) as another probable factor.[26] Studies of those who were small or disproportionately thin or short at birth, or suffered prenatal exposure during period of famine such as the Dutch Hunger Winter (1944–1945) during World War II, have shown that they are prone to higher rates of diabetes.[27]

Other

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Environmental toxins may contribute to recent increases in the rate of type 2 diabetes. A weak positive correlation has been found between the concentration in the urine of bisphenol A, a constituent of some plastics, and the incidence of type 2 diabetes.[28]

References

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  1. ^ Melmed S, Polonsky KS, Larsen PR, Kronenberg HM, eds. (2011). Williams textbook of endocrinology (12th ed.). Philadelphia: Elsevier/Saunders. pp. 1371–1435. ISBN 978-1-4377-0324-5.
  2. ^ Visscher TL, Snijder MB, Seidell JC (2009). "Epidemiology: Definition and Classification of Obesity". In Kopelman PG, Caterson ID, Dietz WH (eds.). Clinical Obesity in Adults and Children (3rd ed.). Wiley-Blackwell. p. 7. ISBN 978-1-4443-0763-4.
  3. ^ a b Malik VS, Popkin BM, Bray GA, Després JP, Hu FB (23 March 2010). "Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk". Circulation. 121 (11): 1356–1364. doi:10.1161/CIRCULATIONAHA.109.876185. PMC 2862465. PMID 20308626.
  4. ^ a b Malik VS, Popkin BM, Bray GA, Després JP, Willett WC, Hu FB (November 2010). "Sugar-sweetened beverages and risk of metabolic syndrome and type 2 diabetes: a meta-analysis". Diabetes Care. 33 (11): 2477–2483. doi:10.2337/dc10-1079. PMC 2963518. PMID 20693348.
  5. ^ a b Risérus U, Willett WC, Hu FB (January 2009). "Dietary fats and prevention of type 2 diabetes". Progress in Lipid Research. 48 (1): 44–51. doi:10.1016/j.plipres.2008.10.002. PMC 2654180. PMID 19032965.
  6. ^ Gaeini, Zahra; Bahadoran, Zahra; Mirmiran, Parvin (November 2022). "Saturated Fatty Acid Intake and Risk of Type 2 Diabetes: An Updated Systematic Review and Dose–Response Meta-Analysis of Cohort Studies". Advances in Nutrition. 13 (6): 2125–2135. doi:10.1093/advances/nmac071. PMC 9776642. PMID 36056919. S2CID 252046318.
  7. ^ Mozaffarian D, Kamineni A, Carnethon M, Djoussé L, Mukamal KJ, Siscovic D (April 2009). "Lifestyle Risk Factors and New-Onset Diabetes Mellitus in Older Adults: The Cardiovascular Health Study". Archives of Internal Medicine. 169 (8): 798–807. doi:10.1001/archinternmed.2009.21. PMC 2828342. PMID 19398692.
  8. ^ Salmerón J, Hu FB, Manson JE, Stampfer MJ, Colditz GA, Rimm EB, Willett WC (June 2001). "Dietary fat intake and risk of type 2 diabetes in women". American Journal of Clinical Nutrition. 73 (6): 1019–1026. doi:10.1093/ajcn/73.6.1019. PMID 11382654.
  9. ^ "Ultraprocessed Food Consumption and Risk of Type 2 Diabetes Among Participants of the NutriNet-Santé Prospective Cohort". JAMA Internal Medicine. 16 December 2019. Retrieved 23 March 2020.
  10. ^ Eberhart MS, Ogden C, Engelgau M, Cadwell B, Hedley AA, Saydah SH (19 November 2004). "Prevalence of Overweight and Obesity Among Adults with Diagnosed Diabetes – United States, 1988–1994 and 1999–2002". Morbidity and Mortality Weekly Report. 53 (45): 1066–1068. PMID 15549021. Retrieved 19 July 2008.
  11. ^ Brooks NA (Mar 2009). "Type 2 Diabetes: Lifestyle Changes and Drug Treatment". AMA Journal of Ethics. 11 (3): 237–241. doi:10.1001/virtualmentor.2009.11.3.cprl1-0903. PMID 23194906. Retrieved 5 Oct 2020.
  12. ^ Shoelson SE, Lee J, Goldfine AB (July 2006). "Inflammation and insulin resistance". Journal of Clinical Investigation. 116 (7): 1793–1801. doi:10.1172/JCI29069. PMC 1483173. PMID 16823477.
  13. ^ "The origin of diabetes: Don't blame your genes". Economist. 3 September 2009.
  14. ^ a b c Powell K (31 May 2007). "The Two Faces of Fat". Nature. 447 (7144): 525–527. Bibcode:2007Natur.447..525P. doi:10.1038/447525a. PMID 17538594. S2CID 28974642.
  15. ^ Yang Q, Graham TE, Mody N, Preitner F, Peroni OD, Zabolotny JM, Kotani K, Quadro L, Kahn BB (21 July 2005). "Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes". Nature. 436 (7049): 356–362. Bibcode:2005Natur.436..356Y. doi:10.1038/nature03711. PMID 16034410.
  16. ^ a b Graham TE, Yang Q, Bluher M, Hammarstedt A, Ciaraldi TP, Henry RR, Wason CJ, Oberbach A, Jansson PA, Smith U, Kahn BB (15 June 2006). "Retinol-binding protein 4 and insulin resistance in lean, obese, and diabetic subjects". New England Journal of Medicine. 354 (24): 2552–2563. doi:10.1056/NEJMoa054862. PMID 16775236.
  17. ^ Yang WS, Lee WJ, Funahashi T, Tanaka S, Matsuzawa Y, Chao CL, Chen CL, Tai TY, Chuang LM (August 2001). "Weight reduction increases plasma levels of an adipose-derived anti-inflammatory protein, adiponectin". Journal of Clinical Endocrinology & Metabolism. 86 (8): 3815–3819. doi:10.1210/jcem.86.8.7741. PMID 11502817.
  18. ^ Qiao Q, Nyamdorj R (January 2010). "Is the association of type II diabetes with waist circumference or waist-to-hip ratio stronger than that with body mass index?". European Journal of Clinical Nutrition. 64 (1): 30–34. doi:10.1038/ejcn.2009.93. PMID 19724291.
  19. ^ Schmidt MI, Duncan BB, Canani LH, Karohl C, Chambless L (July 1992). "Association of waist-hip ratio with diabetes mellitus. Strength and possible modifiers". Diabetes Care. 15 (7): 912–914. doi:10.2337/diacare.15.7.912. PMID 1516514. S2CID 44493450.
  20. ^ Rosenbloom A, Silverstein JH (2003). Type 2 Diabetes in Children and Adolescents: A Clinician's Guide to Diagnosis, Epidemiology, Pathogenesis, Prevention, and Treatment. American Diabetes Association. p. 1. ISBN 978-1-58040-155-5.
  21. ^ a b c Knutson KL, Spiegel K, Penev P, Van Cauter E (June 2007). "The Metabolic Consequences of Sleep Deprivation". Sleep Medicine Reviews. 11 (3): 163–178. doi:10.1016/j.smrv.2007.01.002. PMC 1991337. PMID 17442599.
  22. ^ Spiegel K, Leproult R, Van Cauter E (23 October 1999). "Impact of sleep debt on metabolic and endocrine function". The Lancet. 354 (9188): 1435–1439. doi:10.1016/S0140-6736(99)01376-8. PMID 10543671. S2CID 3854642.
  23. ^ Young MC (2018). "Neighborhood social cohesion and sleep outcomes in the Native Hawaiian and Pacific Islander National Health Interview Survey". Sleep. 41 (9). doi:10.1093/sleep/zsy097. PMID 29771373.
  24. ^ Nuyujukian DS (2016). "Sleep Duration and Diabetes Risk in American Indian and Alaska Native Participants of a Lifestyle Intervention Project". Sleep. 39 (11): 1919–1926. doi:10.5665/sleep.6216. PMC 5070746. PMID 27450685.
  25. ^ Nuyujukian DS, Anton-Culver H, Manson SM, Jiang L (2019). "Associations of sleep duration with cardiometabolic outcomes in American Indians and Alaska Natives and other race/ethnicities: results from the BRFSS". Sleep Health. 5 (4): 344–351. doi:10.1016/j.sleh.2019.02.003. PMC 6935393. PMID 30987947.
  26. ^ Christian P, Stewart CP (March 2010). "Maternal Micronutrient Deficiency, Fetal Development, and the Risk of Chronic Disease". The Journal of Nutrition. 140 (3): 437–445. doi:10.3945/jn.109.116327. PMID 20071652.
  27. ^ Godfrey KM, Barker DJ (May 2000). "Fetal nutrition and adult disease". American Journal of Clinical Nutrition. 71 (5 Suppl): 1344S–1352S. doi:10.1093/ajcn/71.5.1344s. PMID 10799412.
  28. ^ Lang IA, Galloway TS, Scarlett A, Henley WE, Depledge M, Wallace RB, Melzer D (17 September 2008). "Association of urinary bisphenol A concentration with medical disorders and laboratory abnormalities in adults". JAMA. 300 (11): 1303–1310. doi:10.1001/jama.300.11.1303. hdl:10871/37692. PMID 18799442.
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