Alzheimer hastalığında demans düzeyinin vücut kompozisyonuna ve bazal metabolizma hızına etkisi

Year 2021, Volume: 14 Issue: 1, 201 - 207, 04.01.2021

Hülya Özkan , Ayten Üstündağ

https://doi.org/10.31362/patd.749681

Cited By: 1

Abstract

Amaç: Alzheimer hastalığı (AH), bilişsel fonksiyonların geri dönüşümsüz kaybı ile karakterize ilerleyici nörodejeneratif ve multifaktoriyel etyolojiye sahip bir hastalıktır. Bu hastalarda gelişen beslenme bozuklukları kognitif yıkımın artmasına, dolayısıyla demansın ilerlemesine neden olabilmektedir. Biz bu çalışmada, AH hastalarında hastalığın evrelerine göre kilo, vücut kütle indeksi (VKİ), yağsız vücut kütlesi ile bazal metabolizma hızı (BMH) arasındaki ilişkiyi araştırmak ve BMH üzerine etkili olabilecek klinik ve laboratuvar bulgularını incelemeyi amaçladık.
Gereç ve Yöntem: 108 (44 erkek, 64 kadın) AH hastasının klinik ve demografik özellikleri kayıt edildi. Hastalar Klinik Demans Evrelendirme Ölçeğine göre hafif ve hafif-orta evre AH (Grup 1, n=84) ile orta ve ağır evre AH (Grup 2, n=24) olmak üzere iki gruba ayrıldı. Hastaların kilo, boy, bel çevresi ölçümleri ve laboratuvar tetkikleri kayıt edildi. Hastaların VKİ Quetelet indeksine, yağsız vücut kütlesi Hume denklemi ve BMH düzeyleri de Harris-Benedict denklemine göre hesaplandı.
Bulgular: Hastaların ortalama yaşı 71.6±8.2 yıl, ortalama VKİ 30,6±39,8 kg/m2 ve ortalama demans süresi 33,8±29,4 ay olarak saptandı. Grup 1 ve Grup 2 arasında cinsiyet, yaş, VKİ, bel çevresi, demans süreleri açısından fark tespit edilmedi, buna karşın orta ve ağır evre AH hastalarında, hafif evre grubuna göre yağsız vücut kütlesi ve BMH düzeylerinin daha düşük olduğu saptandı (p<0.05). AH hastalarında VKİ düzeyinin, bel çevresinin ve yağsız vücut kütlesinin BMH ile pozitif ilişkili olduğunu saptadık. Yağsız vücut kütlesinin BMH’nı etkileyen bağımsız faktör olduğu tespit edildi (β=0,732, p<0,001, OR=11,06, CI %95 11,07-15,9).
Sonuç: İleri evre AH hastalarında kilo kaybının özellikle yağsız vücut kütlesindeki azalmanın hastaların yaşam kalitesini olumsuz etkileyebileceğini, hastalığın başlangıç döneminden itibaren doğru beslenme ve egzersiz programlarının uygulanmasının önemli olduğunu düşünmekteyiz.

Keywords

Alzheimer hastalığı, demans, bazal metabolizma hızı

The effect of dementia level on body composition and basal metabolic rate in Alzheimer’s disease

Abstract

Purpose: Alzheimer's disease (AD) is a progressive
neurodegenerative disease characterized by irreversible loss of cognitive
functions and has multifactorial etiology. Nutritional disorders
in Alzheimer's disease (AD) patients may lead to an increase in cognitive
impairment and subsequent progression of dementia. In this study, we
aimed to investigate the relationship of basal metabolic rate (BMR)
with weight, body mass
index (BMI), lean body mass in AD patients and to clarify the clinical and
laboratory findings that may affect BMR.

Materials and Methods: The clinical and demographic characteristics
of 108 patients (44 male, 64 women) were recorded. Patients were divided into
two groups according to Clinical Dementia Rating Scale as mild and
mild-moderate AD (Group 1, n=84) and moderate and severe AD (Group 2, n=24).
Weight, height, waist circumference measurements and laboratory tests were
recorded.

Results: The mean age of the patients was 71.6±8.2 years, the mean BMI
was 30.6±39.8 kg/m2 and the mean
dementia was 33.8±29.4 months. No
difference was found between Group 1 and Group 2 in terms of gender, age, BMI,
waist circumference, dementia duration, whereas lean body mass and BMR levels
were found to be lower in moderate and severe AD patients compared to
mild stage group (p<0.05).  BMI, waist
circumference and lean body mass were positively correlated with BMR in AD patients. Lean body
mass was found to be an independent factor affecting BMR (β=0.732, p<0.001, OR=11.06, CI 95%11.07-15.9).

Conclusion: We found a significant weight loss, especially in lean body mass, that may adversely affect
the quality of life in advanced AD patients. It is important to
implement proper nutrition and exercise programs from the onset of the disease.

Keywords

Alzheimer’s disease, dementia, basal metabolic rate

References

• 1. Knopman DS, Boeve BF, Petersen RC. Essentials of the proper diagnoses of mild cognitive impairment, dementia, and major subtypes of dementia. Mayo Clin Proc 2003;78:1290–1308. hhtps://doi.org/10.4065/78.10.1290.
• 2. Prince M, Bryce R, Albanese E, Wimo A, Ribeiro W, Ferri CP. The global prevalence of dementia: a systematic review and metaanalysis. Alzheimers Dement 2013;9:63- 75. hhtps://doi.org/10.1016/j.jalz.2012.11.007.
• 3. Gao S, Hendrie HC, Hall KS, Hui S. The relationships between age, sex, and the incidence of dementia and Alzheimer disease. Arch Gen Psychiatry 1998;55:809-815. hhtps://doi.org/10.1001/archpsyc.55.9.809.
• 4. Williamson J, Goldman J, Marder KS. Genetic aspects of Alzheimer disease. Neurologist 2009;15:80-86. hhtps://doi.org/10.1097/NRL.0b013e318187e76b.
• 5. Cardoso B, Cominetti C, Cozzolino S. Importance and management of micronutrient deficiencies ın patients with alzheimer’s disease. Clin Interv Aging 2013;8:531-542. hhtps://doi.org/10.2147/CIA.S27983
• 6. Aliev G, Ashraf GM, Kaminsky YG, Sheikh IA, Sudakov SK, Yakhno NN, Benberin VV, Bachurin SO. Implication of the nutritional and non-nutritional factors in the context of preservation of cognitive performance in patients with dementia/depression and alzheimer disease. Am J Alzheimers Dis Other Demen 2013;28:660-670. hhtps://doi.org/10.1177/1533317513504614
• 7. Lopez OL, Dekosky ST. Clinical Symptoms in Alzheimer’s Disease. Handbook of Clinical Neurology Dementia 2008;89:207-216. hhtps://doi.or/10.1016/S0072-9752(07)01219-5.
• 8. McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology 1984;34:939-944. hhtps://doi.org/10.1212/wnl.34.7.939
• 9. Burns A, Marsh A, Bender DA. Dietary intake and clinical, anthropometric and biochemical indices of malnutrition in elderly demented patients and non-demented subjects. Psychol Med 1989;19:383–391. hhtps://doi.org/10.1017/s0033291700012423.
• 10. Diagnostic and statistical manual of mental disorders, fourth edition (DSM-IV). Washington, DC: American psychiatric association 1994;143-147.
• 11. Morris J. The clinical dementia rating (CDR): current version and scoring rules. Neurology 1993;43:2412-2414. hhtps://doi.org/10.1212/wnl.43.11.2412-a.
• 12. Gadzik J "How much should I weigh?"--Quetelet's equation, upper weight limits, and BMI prime. Conn Med 2006;70:81-88.
• 13. Hume R. Prediction of lean body mass from height and weight? J Clin Pathol 1966;19:389–391. hhtps://doi.org/10.1136/jcp.19.4.389
• 14. Harris JA, Benedict FG. A Biometric study of human basal metabolism. Proc Natl Acad Sci USA 1918;4:370-373. hhtps://doi.org/10.1073/pnas.4.12.370.
• 15. White H, Pieper C, Schmader K, Fillenbaum G. Weight change in Alzheimer's disease. J Am Geriatr Soc 1996;44:265-272. hhtps://doi.org/10.1111/j.1532-5415.1996.tb00912.x.
• 16. Wolf-Klein GP, Silverstone FA, Levy AP. Nutritional patterns and weight change in Alzheimer patients. Int Psychogeriatr 1992;4:103-118. hhtps://doi.org/10.1017/s1041610292000930.
• 17. Berlinger WG, Potter JF. Low Body Mass Index in demented outpatients. J Am Geriatr Soc 1991;39:973-978. hhtps://doi.org/10.1111/j.1532-5415.1991.tb04043.x.
• 18. Grundman M, Corey-Bloom J, Jernigan T, Archibald S, Thal LJ. Low body weight in Alzheimer's disease is associated with mesial temporal cortex atrophy.Neurology 1996;46:1585-1591.hhtps://doi:.org/10.1212/wnl.46.6.1585.
• 19. Morris MC. The role of nutrition in Alzheimer’s disease: epidemiological evidence. Eur J Neurol 2009;16:1-7. hhtps://doi.org/10.1111/j.1468-1331.2009.02735.x.
• 20. Kontush K, Schekatolina S. Vitamin E in neurodegenerative disorders: Alzheimer’s disease. Ann N Y Acad Sci 2004;1031:249-262. hhtps://doi.org/10.1196/annals.1331.025.
• 21. Vercruysse P, Vieau D, Blum D, Petersén Å, Dupuis L. Hypothalamic Alterations in Neurodegenerative Diseases and Their Relation to Abnormal Energy Metabolism. Front Mol Neurosci. 2018;19;11:2. hhtps://doi.org/ 10.3389/fnmol.2018.00002
• 22. Cunningham JJ. A Reanalysis of the factors influencing basal metabolic rate in normal adults. Amer J Clin Nutr 1980;33:2372-4. hhtps://doi.org/10.1093/ajcn/33.11.2372.
• 23. Psota T, Chen KY. Measuring energy expenditure in clinical populations: rewards and challenges. Eur J Clin Nutr 2013;67:436–42. hhtps://doi.org/10.1038/ejcn.2013.38.
• 24. Wang Z, Heshka S, Zhang K, Boozer CN, Heymsfield SB. Resting energy expenditure: systematic organization and critique of prediction methods. Obes Reas 2001;9:331–6. hhtps://doi.org/10.1038/oby.2001.42.
• 25. Da Rocha EEM, Alves VGF, Fonsenca RBV. Indirect calorimetry: methodology, instruments and clinical application. Curr Opin Clin Nutr Metab Care 2006;9:247–56. hhtps://doi.org/10.1097/01.mco.0000222107.15548.f5.
• 26. Henry CJ. Basal metabolic rate studies in humans: measurement and development of new equations. Public Health Nutr 2005;8:1133–52. hhtps://doi.org/10.1079/phn2005801.
• 27. Bosy-Westphal A, Eichhorn C, Kutzner D, Illner K, Heller M, Müller MJ. The age-related decline in resting energy expenditure in humans is due to the loss of fat-free mass and to alterations in its metabolically active components. J Nutr 2003;133:2356-62. hhtps://doi.org/10.1093/jn/133.7.2356.
• 28. Poehlman ET, Dvorak RV. Energy expenditure, energy intake, and weight loss in Alzheimer disease. Am J Clin Nutr 2000;71:650S-5S. hhtps://doi.org/10.1093/ajcn/71.2.650s.
• 29. Niskanen L, Piirainen M, Koljonen M, Uusitupa M. Resting energy expenditure in relation to energy intake in patients with Alzheimer's disease, multi-infarct dementia and in control women. Age Ageing 1993;22:132-7. hhtps://doi.org/10.1093/ageing/22.2.132.
• 30. Cova I, Clerici F, Rossi A, Cucumo V, Ghiretti R, Maggiore L, et al. Weight Loss Predicts Progression of Mild Cognitive Impairment to Alzheimer's Disease.PLoS One. 2016;18;11:e0151710. hhtps://doi.org/10.1371/journal.pone.0151710.
• 31. Burns JM, Johnson DK, Watts A, Swerdlow RH, Brooks WM. Reduced lean mass in early Alzheimer disease and its association with brain atrophy. Arch Neurol 2010;67:428-33. hhtps://doi.org/10.1001/archneurol.2010.38.
• 32. Santos TBND, Fonseca LC, Tedrus GMAS, Delbue JL. Alzheimer's disease: nutritional status and cognitive aspects associated with disease severity. Nutr Hosp 2018;35:1298-304. hhtps://doi.org/10.20960/nh.2067
• 33. Dulloo AG, Jacquet J, Miles-Chan JL, Schutz Y. Passive and active roles of fat-free mass in the control of energy intake and body composition regulation. Eur J Clin Nutr 2017;71:353-7. hhtps://doi.org/10.1038/ejcn.2016.256.