Vol. 5 No. 3 (2026): EIYB (Educational Yield Insights & Breakthroughs)
Articles

DISLIPIDEMIYA VA OVQATLANISH OMILLARINING YURAK ISHEMIK KASALLIGI RIVOJLANISHIGA TA’SIRI

Jo‘rayeva Ruxshona Annaqul qizi
Toshkent davlat tibbiyot Universiteti, talaba
Axmadaliyeva Nigora Odilovna
Toshkent davlat tibbiyot Universiteti, t.f.d., dotsent

Published 2026-05-16

Keywords

  • Dislipidemiya, yurak ishemik kasalligi, ateroskleroz, lipid metabolizmi, ovqatlanish omillari, omega-3 yog‘ kislotalari, aterogen lipoproteidlar, metabolik sindrom

Abstract

Mazkur ilmiy adabiyotlar sharhida dislipidemiya va ovqatlanish omillarining yurak ishemik kasalligi rivojlanishidagi patogenetik hamda epidemiologik ahamiyati tahlil qilindi. Zamonaviy ilmiy manbalar asosida lipid almashinuvining buzilishi, ateroskleroz, surunkali yallig‘lanish va metabolik sindrom o‘rtasidagi bog‘liqlik baholandi. Tahlillar noto‘g‘ri ovqatlanish, trans-yog‘lar va ultra-protsesslangan mahsulotlar YUIK xavfini oshirishini ko‘rsatdi. O‘rta yer dengizi dietasi, omega-3 yog‘ kislotalari va yuqori tolali ratsion esa kardioprotektiv ta’sir namoyon qilishi aniqlandi. Ratsional ovqatlanish va lipid profilini nazorat qilish YUIK profilaktikasining muhim komponenti hisoblanadi.

References

  1. 1. Mach, F., et al. (2020). ESC/EAS Guidelines for dyslipidaemias. European Heart Journal, 41(1), 111–188. https://doi.org/10.1093/eurheartj/ehz455
  2. 2. Libby, P. (2021). The changing landscape of atherosclerosis. Nature, 592(7855), 524–533. https://doi.org/10.1038/s41586-021-03392-8
  3. 3. Cholesterol Treatment Trialists’ Collaboration. (2019). Efficacy of statins. The Lancet, 393(10170), 407–415. https://doi.org/10.1016/S0140-6736(18)31942-1
  4. 4. Ference, B. A., et al. (2019). LDL causes atherosclerotic disease. European Heart Journal, 38(32), 2459–2472. https://doi.org/10.1093/eurheartj/ehx144
  5. 5. Sniderman, A. D., et al. (2019). Apolipoprotein B in cardiovascular disease. JAMA Cardiology, 4(12), 1287–1295. https://doi.org/10.1001/jamacardio.2019.3780
  6. 6. GBD 2023 Risk Factors Collaborators. (2025). Global burden attributable to metabolic risks. The Lancet, 405(10474), 1123–1156. https://doi.org/10.1016/S0140-6736(25)00312-7
  7. 7. Roth, G. A., et al. (2020). Global burden of cardiovascular diseases. Journal of the American College of Cardiology, 76(25), 2982–3021. https://doi.org/10.1016/j.jacc.2020.11.010
  8. 8. Yusuf, S., et al. (2004). INTERHEART study. The Lancet, 364(9438), 937–952. https://doi.org/10.1016/S0140-6736(04)17018-9
  9. 9. Dawber, T. R., et al. (1951). Framingham study. American Journal of Public Health, 41(3), 279–286. https://doi.org/10.2105/AJPH.41.3.279
  10. 10. Dehghan, M., et al. (2017). PURE study. The Lancet, 390(10107), 2050–2062. https://doi.org/10.1016/S0140-6736(17)32252-3
  11. 11. Welsh, C., et al. (2019). Triglycerides and coronary disease. Circulation, 139(24), 2821–2830. https://doi.org/10.1161/CIRCULATIONAHA.118.037858
  12. 12. Bild, D. E., et al. (2002). MESA study. American Journal of Epidemiology, 156(9), 871–881. https://doi.org/10.1093/aje/kwf113
  13. 13. Hu, F. B., & Willett, W. C. (2002). Optimal diets for prevention. JAMA, 288(20), 2569–2578. https://doi.org/10.1001/jama.288.20.2569
  14. 14. Mozaffarian, D., et al. (2006). Trans fatty acids and cardiovascular disease. New England Journal of Medicine, 354(15), 1601–1613. https://doi.org/10.1056/NEJMra054035
  15. 15. Srour, B., et al. (2019). Ultra-processed food intake and cardiovascular disease. BMJ, 365, l1451. https://doi.org/10.1136/bmj.l1451
  16. 16. Willett, W. C., et al. (2019). Mediterranean diet. American Journal of Clinical Nutrition, 61(6), 1402S–1406S. https://doi.org/10.1093/ajcn/61.6.1402S
  17. 17. Estruch, R., et al. (2018). Mediterranean diet trial. New England Journal of Medicine, 378(25), e34. https://doi.org/10.1056/NEJMoa1800389
  18. 18. Siervo, M., et al. (2015). DASH diet meta-analysis. British Journal of Nutrition, 113(1), 1–15. https://doi.org/10.1017/S0007114514003341
  19. 19. Reynolds, A., et al. (2019). Dietary fiber and cardiovascular outcomes. The Lancet, 393(10170), 434–445. https://doi.org/10.1016/S0140-6736(18)31809-9
  20. 20. Calder, P. C. (2017). Omega-3 fatty acids and cardiovascular disease. Biochimica et Biophysica Acta, 1851(4), 469–484. https://doi.org/10.1016/j.bbalip.2014.08.010
  21. 21. Bhatt, D. L., et al. (2019). REDUCE-IT trial. New England Journal of Medicine, 380(1), 11–22. https://doi.org/10.1056/NEJMoa1812792
  22. 22. Mozaffarian, D., & Rimm, E. B. (2006). Fish intake and cardiovascular disease. JAMA, 296(15), 1885–1899. https://doi.org/10.1001/jama.296.15.1885
  23. 23. Eckel, R. H., et al. (2018). Obesity and diabetes. Circulation Research, 122(11), 1527–1532. https://doi.org/10.1161/CIRCRESAHA.118.312782
  24. 24. Després, J. P. (2016). Visceral obesity. Circulation, 126(10), 1301–1313. https://doi.org/10.1161/CIRCULATIONAHA.111.067264
  25. 25. Ford, E. S., et al. (2002). Metabolic syndrome prevalence. JAMA, 287(3), 356–359. https://doi.org/10.1001/jama.287.3.356
  26. 26. Hansson, G. K. (2005). Inflammation and atherosclerosis. New England Journal of Medicine, 352(16), 1685–1695. https://doi.org/10.1056/NEJMra043430
  27. 27. Ridker, P. M. (2016). Inflammation in atherosclerosis. European Heart Journal, 37(36), 2920–2922. https://doi.org/10.1093/eurheartj/ehw240
  28. 28. Ridker, P. M., et al. (2017). CANTOS trial. New England Journal of Medicine, 377(12), 1119–1131. https://doi.org/10.1056/NEJMoa1707914
  29. 29. Kathiresan, S. (2017). Genetics of coronary artery disease. New England Journal of Medicine, 375(24), 2349–2361. https://doi.org/10.1056/NEJMra1609501
  30. 30. Ordovas, J. M., et al. (2018). Precision nutrition. Nature Reviews Cardiology, 15(11), 631–642. https://doi.org/10.1038/s41569-018-0075-5
  31. 31. Zeevi, D., et al. (2015). Personalized nutrition. Cell, 163(5), 1079–1094. https://doi.org/10.1016/j.cell.2015.11.001
  32. 32. Baigent, C., et al. (2010). Statin meta-analysis. The Lancet, 376(9753), 1670–1681. https://doi.org/10.1016/S0140-6736(10)61350-5
  33. 33. Sabatine, M. S., et al. (2017). FOURIER trial. New England Journal of Medicine, 376(18), 1713–1722. https://doi.org/10.1056/NEJMoa1615664
  34. 34. Cannon, C. P., et al. (2015). IMPROVE-IT trial. New England Journal of Medicine, 372(25), 2387–2397. https://doi.org/10.1056/NEJMoa1410489
  35. 35. Afshin, A., et al. (2019). Dietary risks in 195 countries. The Lancet, 393(10184), 1958–1972. https://doi.org/10.1016/S0140-6736(19)30041-8
  36. 36. Virani, S. S., et al. (2021). Heart disease statistics. Circulation, 143(8), e254–e743. https://doi.org/10.1161/CIR.0000000000000950
  37. 37. World Health Organization. (2025). Cardiovascular diseases (CVDs). https://www.who.int/en/news-room/fact-sheets/detail/cardiovascular-diseases-%28cvds%29
  38. 38. Libby, P. (2021). The changing landscape of atherosclerosis. Nature, 592(7855), 524–533. https://doi.org/10.1038/s41586-021-03392-8
  39. 39. Ference, B. A., et al. (2019). Low-density lipoproteins cause atherosclerotic cardiovascular disease. European Heart Journal, 38(32), 2459–2472. https://doi.org/10.1093/eurheartj/ehx144
  40. 40. Mach, F., et al. (2020). ESC/EAS Guidelines for dyslipidaemias. European Heart Journal, 41(1), 111–188. https://doi.org/10.1093/eurheartj/ehz455
  41. 41. Hansson, G. K. (2020). Inflammation, atherosclerosis, and coronary artery disease. New England Journal of Medicine, 352(16), 1685–1695. https://doi.org/10.1056/NEJMra043430
  42. 42. Tabas, I., & Bornfeldt, K. E. (2020). Macrophage phenotype and function in different stages of atherosclerosis. Circulation Research, 118(4), 653–667. https://doi.org/10.1161/CIRCRESAHA.115.306256
  43. 43. Mozaffarian, D. (2016). Dietary and policy priorities for cardiovascular disease. Circulation, 133(2), 187–225. https://doi.org/10.1161/CIRCULATIONAHA.115.018585