Micronutriënten en inflammatie

11 Jun, 2018

Door: Brigitte Baumeister

De meeste fysiologische processen opereren binnen nauwe grenzen, die door homeostatische mechanismen worden bewaakt. Inflammatie is een beschermende reactie ter verdediging en herstel van fysiologische functies, wanneer de homeostatische mechanismen ontoereikend zijn. Na een succesvolle inflammatie volgt de oplossingsfase, die leidt tot het herstel van de homeostase.

In tegenstelling tot het eiwitmetabolisme kan het vet- en glucosemetabolisme zich aanpassen aan veranderingen in aanbod uit de omgeving, functionele behoefte en biologische prioriteiten. Dit kan echter leiden tot langdurige veranderingen in vet- en/of glucosewaarden met als gevolg een verhoogde kans op verstoringen van de homeostase in de vorm van inflammaties. Als deze conditie blijft bestaan, is de kans groot dat een eenmaal ontstane inflammatie niet oplost, waardoor weefsels beschadigen en herstel uitblijft. Deze situatie die draagt bij aan de ontwikkeling en instandhouding van ziekten als obesitas en diabetes mellitus, die worden gekenmerkt door chronische inflammaties. Andere chronische inflammatoire ziekten die kunnen ontstaan zijn cardiovasculaire (CVD’s) en neurodegeneratieve ziekten, kanker en aandoeningen van de luchtwegen, darmen, huid en gewrichten (zie figuur 1).^1-5

Gedurende de afgelopen eeuw is er, met name in de geïndustrialiseerde landen, een verschuiving ontstaan naar deze ziekten, met opvallend veel overeenkomsten qua cellulaire en moleculaire disregulaties.^4,6 Mogelijke evolutionaire verklaringen hiervoor zijn antagonistische pleiotropie, waarbij genen geselecteerd worden die vroeg in het leven gunstig zijn voor voortplanting, maar op latere leeftijd de gezondheid juist schaden.⁷ Daarnaast is er sprake van een mismatch tussen de moderne leefomgeving en het menselijke genoom, dat gericht is op bescherming tegen bedreigende factoren als verhongering, infecties, verwondingen en vijanden.⁸

Van meerdere micronutriënten is bewezen dat ze een beschermende werking hebben bij chronische inflammatoire ziekten, vanwege hun antioxidatieve, anti-inflammatoire en/of immuunmodulerende en mogelijk andere, nog onbekende, beschermende eigenschappen. Voorbeelden hiervan zijn omega 3 langketenige meervoudig onverzadigde vetzuren (long-chain polyunsaturated fatty acids’; LCPUFA’s), vitamine C, D en E, en fytonutriënten, waaronder β-caroteen.

1. Nasef NA, Mehta S, Ferguson LR. Susceptibility to chronic inflammation: an update. Archives of Toxicology. 2017;91(3):1131-41.
2. Hancock REW, Haney EF, Gill EE. The immunology of host defence peptides: beyond antimicrobial activity. Nature Reviews Immunology. 2016;16:321.
3. Medzhitov R. Origin and physiological roles of inflammation. Nature. 2008;454(7203):428-35.
4. Kotas Maya E, Medzhitov R. Homeostasis, Inflammation, and Disease Susceptibility. Cell. 2015;160(5):816-27.
5. Nathan C, Ding A. Nonresolving Inflammation. Cell. 2010;140(6):871-82.
6. Garn H, Bahn S, Baune BT, Binder EB, Bisgaard H, Chatila TA, et al. Current concepts in chronic inflammatory diseases: Interactions between microbes, cellular metabolism, and inflammation. Journal of Allergy and Clinical Immunology. 2016;138(1):47-56.
7. Williams GC. Pleiotropy, Natural Selection, and the Evolution of Senescence. Evolution. 1957;11(4):398-411.
8. Gluckman P, Beedle A, Buklijas T, Low F, Hanson M. Principles of evolutionary medicine: Oxford University Press; 2016.
9. Yehuda S, Rabinovitz S, Carasso RL, Mostofsky DI. The role of polyunsaturated fatty acids in restoring the aging neuronal membrane. Neurobiology of aging. 2002;23(5):843-53.
10. Serhan CN. Treating inflammation and infection in the 21st century: new hints from decoding resolution mediators and mechanisms. The FASEB Journal. 2017;31(4):1273-88.
11. Calder PC. Fatty acids and inflammation: the cutting edge between food and pharma. European journal of pharmacology. 2011;668:S50-S8.
12. Calder PC. Marine omega-3 fatty acids and inflammatory processes: effects, mechanisms and clinical relevance. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids. 2015;1851(4):469-84.
13. Fraga VG, Carvalho MdG, Caramelli P, de Sousa LP, Gomes KB. Resolution of inflammation, n−3 fatty acid supplementation and Alzheimer disease: A narrative review. Journal of Neuroimmunology. 2017;310(Supplement C):111-9.
14. Sorice A, Guerriero E, Capone F, Colonna G, Castello G, Costantini S. Ascorbic acid: its role in immune system and chronic inflammation diseases. Mini reviews in medicinal chemistry. 2014;14(5):444-52.
15. Oudemans-van Straaten HM, Spoelstra-de Man AM, de Waard MC. Vitamin C revisited. Critical Care. 2014;18(4):460.
16. Calder PC, Albers R, Antoine J-M, Blum S, Bourdet-Sicard R, Ferns G, et al. Inflammatory disease processes and interactions with nutrition. British Journal of Nutrition. 2009;101(S1):1-45.
17. Block G, Jensen CD, Dalvi TB, Norkus EP, Hudes M, Crawford PB, et al. Vitamin C treatment reduces elevated C-reactive protein. Free Radical Biology and Medicine. 2009;46(1):70-7.
18. Langlois M, Duprez D, Delanghe J, De Buyzere M, Clement DL. Serum vitamin C concentration is low in peripheral arterial disease and is associated with inflammation and severity of atherosclerosis. Circulation. 2001;103(14):1863-8.
19. Lykkesfeldt J, Poulsen HE. Is vitamin C supplementation beneficial? Lessons learned from randomised controlled trials. British journal of nutrition. 2010;103(9):1251-9.
20. European Food Safety A. Dietary Reference Values for nutrients Summary report. EFSA Supporting Publications. 2017;14(12):e15121E-n/a.
21. Wacker M, Holick MF. Vitamin D - effects on skeletal and extraskeletal health and the need for supplementation. Nutrients. 2013;5(1):111-48.
22. Garbossa SG, Folli F. Vitamin D, sub-inflammation and insulin resistance. A window on a potential role for the interaction between bone and glucose metabolism. Reviews in Endocrine and Metabolic Disorders. 2017:1-16.
23. Singer T. Nutrition: The vitamin D complex. Nature. 2012;489(7417):S10-S1.
24. Hyppönen E, Läärä E, Reunanen A, Järvelin M-R, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes mellitus: a birth-cohort study. The Lancet. 2001;358(9292):1500-3.
25. Munger KL, Zhang S, O’reilly E, Hernan M, Olek M, Willett W, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62(1):60-5.
26. Merlino LA, Curtis J, Mikuls TR, Cerhan JR, Criswell LA, Saag KG. Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women's Health Study. Arthritis & Rheumatology. 2004;50(1):72-7.
27. Jørgensen SP, Agnholt J, Glerup H, Lyhne S, Villadsen GE, Hvas CL, et al. Clinical trial: vitamin D3 treatment in Crohn’s disease – a randomized double‐blind placebo‐controlled study. Alimentary pharmacology & therapeutics. 2010;32(3):377-83.
28. de Oliveira DL, Hirotsu C, Tufik S, Andersen ML. The interfaces between vitamin D, sleep and pain. Journal of Endocrinology. 2017;234(1):R23-R36.
29. Prentice A. Vitamin D deficiency: a global perspective. Nutrition reviews. 2008;66(s2).
30. Azzi A, Meydani SN, Meydani M, Zingg JM. The rise, the fall and the renaissance of vitamin E. Archives of Biochemistry and Biophysics. 2016;595(Supplement C):100-8.
31. Saboori S, Shab-Bidar S, Speakman JR, Yousefi Rad E, Djafarian K. Effect of vitamin E supplementation on serum C-reactive protein level: a meta-analysis of randomized controlled trials. European Journal Of Clinical Nutrition. 2015;69:867.
32. Hosomi A, Arita M, Sato Y, Kiyose C, Ueda T, Igarashi O, et al. Affinity for α-tocopherol transfer protein as a determinant of the biological activities of vitamin E analogs. FEBS Letters. 1997;409(1):105-8.
33. Zingg J-M, Azzi A. Non-antioxidant activities of vitamin E. Current medicinal chemistry. 2004;11(9):1113-33.
34. Zingg J-M, Han SN, Pang E, Meydani M, Meydani SN, Azzi A. In vivo regulation of gene transcription by alpha-and gamma-tocopherol in murine T lymphocytes. Archives of biochemistry and biophysics. 2013;538(2):111-9.
35. Zingg J-M, Kempna P, Paris M, Reiter E, Villacorta L, Cipollone R, et al. Characterization of three human sec14p-like proteins: α-Tocopherol transport activity and expression pattern in tissues. Biochimie. 2008;90(11):1703-15.
36. Traber MG, Stevens JF. Vitamins C and E: Beneficial effects from a mechanistic perspective. Free Radical Biology and Medicine. 2011;51(5):1000-13.
37. Singh U, Devaraj S, Jialal I. Vitamin E, oxidative stress, and inflammation. Annu Rev Nutr. 2005;25:151-74.
38. Schwab S, Zierer A, Schneider A, Heier M, Koenig W, Kastenmüller G, et al. Vitamin E supplementation is associated with lower levels of C-reactive protein only in higher dosages and combined with other antioxidants: The Cooperative Health Research in the Region of Augsburg (KORA) F4 study. British Journal of Nutrition. 2015;113(11):1782-91.
39. Bae S-C, Kim S-J, Sung M-K. Inadequate antioxidant nutrient intake and altered plasma antioxidant status of rheumatoid arthritis patients. Journal of the American College of Nutrition. 2003;22(4):311-5.
40. Milman U, Blum S, Shapira C, Aronson D, Miller-Lotan R, Anbinder Y, et al. Vitamin E supplementation reduces cardiovascular events in a subgroup of middle-aged individuals with both type 2 diabetes mellitus mellitus and the haptoglobin 2-2 genotype. Arteriosclerosis, thrombosis, and vascular biology. 2008;28(2):341-7.
41. Islam MA, Alam F, Solayman M, Khalil MI, Kamal MA, Gan SH. Dietary phytochemicals: Natural swords combating inflammation and oxidation-mediated degenerative diseases. Oxidative medicine and cellular longevity. 2016;2016.
42. Bahonar A, Saadatnia M, Khorvash F, Maracy M, Khosravi A. Carotenoids as Potential Antioxidant Agents in Stroke Prevention: A Systematic Review. International Journal of Preventive Medicine. 2017;8:70.
43. Cheng HM, Koutsidis G, Lodge JK, Ashor A, Siervo M, Lara J. Tomato and lycopene supplementation and cardiovascular risk factors: A systematic review and meta-analysis. Atherosclerosis. 2017;257:100-8.
44. Chandran B, Goel A. A randomized, pilot study to assess the efficacy and safety of curcumin in patients with active rheumatoid arthritis. Phytotherapy research. 2012;26(11):1719-25.
45. Arablou T, Aryaeian N, Valizadeh M, Sharifi F, Hosseini A, Djalali M. The effect of ginger consumption on glycemic status, lipid profile and some inflammatory markers in patients with type 2 diabetes mellitus mellitus. International journal of food sciences and nutrition. 2014;65(4):515-20.
46. Mahluji S, Ostadrahimi A, Mobasseri M, Attari VE, Payahoo L. Anti-inflammatory effects of Zingiber Officinale in type 2 diabetic patients. Advanced pharmaceutical bulletin. 2013;3(2):273.
47. Prasad AS. Zinc: role in immunity, oxidative stress and chronic inflammation. Current Opinion in Clinical Nutrition & Metabolic Care. 2009;12(6):646-52.
48. Liu H, Xu H, Huang K. Selenium in the prevention of atherosclerosis and its underlying mechanisms. Metallomics. 2017;9(1):21-37.
49. Gagné F. Chapter 6 - Oxidative Stress. Biochemical Ecotoxicology. Oxford: Academic Press; 2014. p. 103-15.
50. Currais A. Ageing and inflammation – A central role for mitochondria in brain health and disease. Ageing Research Reviews. 2015;21:30-42.