Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online: 464
  • Home
  • Print this page
  • Email this page

 Table of Contents  
EDITORIAL
Year : 2018  |  Volume : 5  |  Issue : 1  |  Page : 1-3

Metabolic-cognitive syndrome: Is this understanding useful?


Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Web Publication27-Jun-2018

Correspondence Address:
Sandeep Grover
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jgmh.jgmh_14_18

Rights and Permissions

How to cite this article:
Grover S. Metabolic-cognitive syndrome: Is this understanding useful?. J Geriatr Ment Health 2018;5:1-3

How to cite this URL:
Grover S. Metabolic-cognitive syndrome: Is this understanding useful?. J Geriatr Ment Health [serial online] 2018 [cited 2018 Nov 20];5:1-3. Available from: http://www.jgmh.org/text.asp?2018/5/1/1/235362



Metabolic syndrome (MetS) is conceptually understood as a clinical syndrome, which can help in detecting people at risk of developing diabetes mellitus, hypertension, and dyslipidemia. It is considered as a state of chronic low-grade inflammation as a consequence of complex interplay between genetic and environmental factors. There are different definitions of MetS.[1],[2],[3],[4],[5],[6] These definitions have included factors such as glucose intolerance (impaired glucose tolerance test or present of diabetes mellitus)/raised fasting blood sugar levels (mg/dl), increased blood pressure (mm Hg), raised triglycerides (mg/dl) levels, low high-density lipoprotein (HDL) (mg/dl) levels, obesity as measured in the form of increased waist circumference (in cm) or increased waist-hip ratio, high urinary albumin excretion (μg/min) and 2-h postglucose challenge. Among these factors, the five factors which have been included in most of the recent definitions include increased waist circumference (population/ethnic-specific), raised blood pressure (≥130 or ≥85 mm of Hg or diagnosed with hypertension), fasting blood glucose levels of ≥100 mg/dL or diagnosed with diabetes mellitus, triglyceride levels ≥150 mg/dL or receiving lipid-lowering agents, HDL levels <40 for men and <50 for women or receiving lipid-lowering agents.[1],[2],[3],[4],[5],[6] To consider someone as having MetS, there is a need to fulfill at least 3 out of the 5 given criteria.[1],[2],[3],[4],[5],[6] There is also some consensus on considering the ethnic/population specific waist circumference while defining MetS.[6]

It is suggested that MetS is an outcome of genetic risk factors, lack of exercise, and excessive intake, all of which lead to insulin resistance, visceral obesity, dysregulation of the hypothalamo-pituitary axis, and dyslipidemia. These factors lead to increase in the pro-inflammatory cytokines which lead to the development of MetS.[7]

It is now increasingly recognized that central obesity, diabetes mellitus, hypertension, and dyslipidemia play a crucial role in the development of dementia.[8],[9],[10],[11],[12],[13],[14],[15] These factors contribute to increased cerebral vascular resistance, decreased capillary density, and decreased cerebral autoregulation. These changes lead to the development of white matter hyperintensities and cerebral atrophy. There is evidence to suggest that obesity, diabetes mellitus, hypertension, and dyslipidemia are related to the development of mild cognitive impairment (MCI) and dementia.[8],[9],[10],[11],[12],[13],[14],[15] It is considered that the besides these factors acting as risk factors for cognitive decline, these factors also possibly share some of the risk factors, i.e., genetic factors and lifestyle factors, which are reported to be associated with the development of cognitive decline and dementia.[8],[9],[10],[11],[12],[13],[14],[15]

However, it is important to remember that, once these diagnoses are established, it is too late to intervene to prevent the development of cognitive decline. Accordingly, it can be said that MetS, which is considered as risk factor for the development of diabetes, hypertension, dyslipidemia, and coronary artery disease can also act as an important risk factor for the development of dementia. This understanding has given rise to the concept of Metabolic Cognitive Syndrome (MCS).

The concept of MCS was first given by Frisardi et al. in 2010.[16] They used this term to describe a state which included the presence of MetS and cognitive impairment of degenerative or vascular origin. They hypothesized that this entity could help us in improving our understanding about the clinical and neuropathological features of these cognitive disorders.[16] It was further suggested that the term MCS should not be considered as a clinical label but rather must be considered as pathophysiological model which can help in identifying patients with MetS plus cognitive impairment of degenerative or vascular origin, and help in understanding the neuropsychological and neuropathological features of these predementia or dementia syndromes associated to MetS.[17]

Over the past few years, attempts have been made to evaluate this entity and look at the association of MetS with cognitive decline.[18],[19] Studies have shown association of MetS with decreased capillary density, decreased cerebral arterial vasodilation response, thickening of intima-media, decreased cerebral blood flow, vasomotor reactivity, decreased cerebral blood flow in the medial and lateral aspects of frontal, and parietal lobe gray matters and increase in arterial thickness.[20],[21] In addition, evidence also suggests association of MetS with poor immediate memory, decreased fluid intelligence, reduced global cognitive functioning, impaired executive functions, poor attention, poor recall, and poor visuospatial performance.[21] MetS have also been shown to have detrimental effect on psychomotor speed, verbal memory and fluency, and attention.[20] Some of the data suggest that decrement in executive function (as well as information processing speed and verbal memory) is the most frequently reported cognitive impairment. Some of the available data from various cross-sectional studies also suggests that present of MetS is associated with higher risk of Alzheimer's dementia (AD), increased risk of developing vascular dementia, increased risk of progression from MCI to dementia.[20],[22] However, few studies contradict these associations. There are some data to suggest that in populations aged ≥75 years, having MetS was associated with a lower risk of developing AD, and associated with decelerated cognitive decline.[22] However, it is important to remember that the cross-sectional studies are not sufficient to establish a cause and effect relationship. To overcome this limitation, many population-based longitudinal studies have evaluated the cause and effect relationship of MetS with cognitive decline.[23],[24],[25],[26],[27],[28],[29],[30],[31] These studies suggest that during the follow-up period varying from 1 to 13 years, presence of MetS at the baseline is associated with increased risk of cognitive decline, higher risk of progression from MCI to dementia, higher level of cognitive and functional decline in activities of daily living and instrumental activities of daily living by 10 years. In terms of cognitive domains, presence of MetS has been shown to be associated with worst performance in the domains of information processing speed, attention, and executive functioning (inconsistently reported) and memory (inconstantly reported).[23],[24],[25],[26],[27],[28],[29],[30],[31] In terms of effect of age, available data also suggest that the MetS may be a risk factor for cognitive decline in the young and young-elderly, but the effect is not seen in those 80 or above possibly because of development of physical morbidities.[22],[23],[24],[25],[26],[27],[28],[29],[30] An interesting finding which has been noted in some studies suggests that cognitive decline may not be related to individual components of MetS, but is related to the MetS per se.[22],[23],[24],[25],[26],[27],[28],[29],[30] Occasional study also suggests the synergistic effect of MetS and Apoε4.[32] The strength of association of MetS with cognitive decline in some of these studies can be understood by the fact that, this association is present, even after controlling for confounding variables. However, these studies are criticized for not using the same set of cognitive test for assessing the association.[23],[24],[25],[26],[27],[28],[29],[30],[31] Although the exact pathophysiological mechanisms involved require further decoding, it is suggested that possibly the metabolic-hormonal changes which occur over the course of MetS may be detrimental for neuronal cells and are resultantly responsible for development of dementia.

In the last one decade or so, understanding about the concept of MCS has improved. This concept can have multiple implications, i.e., can help in prevention of dementia, early intervention and furthering the understanding about pathophysiological mechanisms associated with development of dementia. The current level of understanding suggests that the concept of MCS provides an important window for primary prevention of dementia. Changing the modifiable risk factors can reduce the incidence of dementia and also possibly delay the onset of dementia. Further, identification of a clinical profile of the MCS could be central in detecting in these patients a molecular profile of higher risk to develop predementia or dementia syndromes. The MCS model could also help us to explain the complex relationship between metabolic disorders and cognitive disturbances and the boundaries between normal and pathological conditions, with a better understanding of clinical and neuropathological features of these metabolic-based cognitive disorders.[18]

India is considered to be diabetes capital of the World [33] and recent data also suggest that the figures for hypertension in India may also be comparable to that of diabetes mellitus.[34] In the year 2013, it was estimated that 65.1 million people aged between 20 and 79 years were suffering from diabetes mellitus and it is estimated that this number is going to increase to 109 million by 2035.[35] Accordingly, in this country, there is an urgent need to prevent the development of these noncommunicable diseases (NCDs), to reduce the associated morbidity, mortality, and health-care costs. Considering the association of cognitive decline with these NCDs, it can be said that in the future, India, may also emerge as the world capital for dementia, if timely interventions are not done. At present, there is gross lack of data in terms of association of MetS and cognitive decline. There is an urgent need to study this association in community samples. Understanding the progress from MetS to overt NCDs and development of dementia can also help in identifying other associated risk and protective factors for development of dementia.



 
  References Top

1.
Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: Diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med 1998;15:539-53.  Back to cited text no. 1
[PUBMED]    
2.
Balkau B, Charles MA. Comment on the provisional report from the WHO consultation. European group for the study of insulin resistance (EGIR). Diabet Med 1999;16:442-3.  Back to cited text no. 2
[PUBMED]    
3.
Zimmet P, Magliano D, Matsuzawa Y, Alberti G, Shaw J. The metabolic syndrome: A global public health problem and a new definition. J Atheroscler Thromb 2005;12:295-300.  Back to cited text no. 3
[PUBMED]    
4.
National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third report of the national cholesterol education program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult treatment panel III) final report. Circulation 2002;106:3143-421.  Back to cited text no. 4
[PUBMED]    
5.
Einhorn D, Reaven GM, Cobin RH, Ford E, Ganda OP, Handelsman Y, et al. American college of endocrinology position statement on the insulin resistance syndrome. Endocr Pract 2003;9:237-52.  Back to cited text no. 5
[PUBMED]    
6.
Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, et al. Harmonizing the metabolic syndrome: A joint interim statement of the international diabetes federation task force on epidemiology and prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation 2009;120:1640-5.  Back to cited text no. 6
[PUBMED]    
7.
Rochlani Y, Pothineni NV, Kovelamudi S, Mehta JL. Metabolic syndrome: Pathophysiology, management, and modulation by natural compounds. Ther Adv Cardiovasc Dis 2017;11:215-25.  Back to cited text no. 7
[PUBMED]    
8.
Bos D, Vernooij MW, de Bruijn RF, Koudstaal PJ, Hofman A, Franco OH, et al. Atherosclerotic calcification is related to a higher risk of dementia and cognitive decline. Alzheimers Dement 2015;11:639-470.  Back to cited text no. 8
[PUBMED]    
9.
Yang Y, Song W. Molecular links between Alzheimer's disease and diabetes mellitus. Neuroscience 2013;250:140-50.  Back to cited text no. 9
[PUBMED]    
10.
Hölscher C. Diabetes as a risk factor for Alzheimer's disease: Insulin signalling impairment in the brain as an alternative model of Alzheimer's disease. Biochem Soc Trans 2011;39:891-7.  Back to cited text no. 10
    
11.
Baumgart M, Snyder HM, Carrillo MC, Fazio S, Kim H, Johns H, et al. Summary of the evidence on modifiable risk factors for cognitive decline and dementia: A population-based perspective. Alzheimers Dement 2015;11:718-26.  Back to cited text no. 11
    
12.
Albanese E, Launer LJ, Egger M, Prince MJ, Giannakopoulos P, Wolters FJ, et al. Body mass index in midlife and dementia: Systematic review and meta-regression analysis of 589,649 men and women followed in longitudinal studies. Alzheimers Dement (Amst) 2017;8:165-78.  Back to cited text no. 12
[PUBMED]    
13.
Pedditizi E, Peters R, Beckett N. The risk of overweight/obesity in mid-life and late life for the development of dementia: A systematic review and meta-analysis of longitudinal studies. Age Ageing 2016;45:14-21.  Back to cited text no. 13
[PUBMED]    
14.
Meng XF, Yu JT, Wang HF, Tan MS, Wang C, Tan CC, et al. Midlife vascular risk factors and the risk of Alzheimer's disease: A systematic review and meta-analysis. J Alzheimers Dis 2014;42:1295-310.  Back to cited text no. 14
[PUBMED]    
15.
Hasnain M, Vieweg WV. Possible role of vascular risk factors in Alzheimer's disease and vascular dementia. Curr Pharm Des 2014;20:6007-13.  Back to cited text no. 15
[PUBMED]    
16.
Frisardi V, Solfrizzi V, Seripa D, Capurso C, Santamato A, Sancarlo D, et al. Metabolic-cognitive syndrome: A cross-talk between metabolic syndrome and Alzheimer's disease. Ageing Res Rev 2010;9:399-417.  Back to cited text no. 16
[PUBMED]    
17.
Frisardi V, Imbimbo BP. Metabolic-cognitive syndrome: Metabolic approach for the management of Alzheimer's disease risk. J Alzheimers Dis 2012;30 Suppl 2:S1-4.  Back to cited text no. 17
[PUBMED]    
18.
Panza F, Solfrizzi V, Logroscino G, Maggi S, Santamato A, Seripa D, et al. Current epidemiological approaches to the metabolic-cognitive syndrome. J Alzheimers Dis 2012;30 Suppl 2:S31-75.  Back to cited text no. 18
[PUBMED]    
19.
Panza F, Frisardi V, Capurso C, Imbimbo BP, Vendemiale G, Santamato A, et al. Metabolic syndrome and cognitive impairment: Current epidemiology and possible underlying mechanisms. J Alzheimers Dis 2010;21:691-724.  Back to cited text no. 19
[PUBMED]    
20.
Mellendijk L, Wiesmann M, Kiliaan AJ. Impact of nutrition on cerebral circulation and cognition in the metabolic syndrome. Nutrients 2015;7:9416-39.  Back to cited text no. 20
[PUBMED]    
21.
Yates KF, Sweat V, Yau PL, Turchiano MM, Convit A. Impact of metabolic syndrome on cognition and brain: A selected review of the literature. Arterioscler Thromb Vasc Biol 2012;32:2060-7.  Back to cited text no. 21
    
22.
Crichton GE, Elias MF, Buckley JD, Murphy KJ, Bryan J, Frisardi V, et al. Metabolic syndrome, cognitive performance, and dementia. J Alzheimers Dis 2012;30 Suppl 2:S77-87.  Back to cited text no. 22
    
23.
Reijmer YD, van den Berg E, Dekker JM, Nijpels G, Stehouwer CD, Kappelle LJ, et al. The metabolic syndrome, atherosclerosis and cognitive functioning in a non-demented population: The Hoorn study. Atherosclerosis 2011;219:839-45.  Back to cited text no. 23
[PUBMED]    
24.
Solfrizzi V, Scafato E, Capurso C, D'Introno A, Colacicco AM, Frisardi V, et al. Metabolic syndrome, mild cognitive impairment, and progression to dementia. The Italian longitudinal study on aging. Neurobiol Aging 2011;32:1932-41.  Back to cited text no. 24
    
25.
Solfrizzi V, Scafato E, Capurso C, D'Introno A, Colacicco AM, Frisardi V, et al. Metabolic syndrome and the risk of vascular dementia: The Italian longitudinal study on ageing. J Neurol Neurosurg Psychiatry 2010;81:433-40.  Back to cited text no. 25
    
26.
Overman MJ, Pendleton N, O'Neill TW, Bartfai G, Casanueva FF, Forti G, et al. Glycemia but not the metabolic syndrome is associated with cognitive decline: Findings from the European male ageing study. Am J Geriatr Psychiatry 2017;25:662-71.  Back to cited text no. 26
    
27.
Rouch I, Trombert B, Kossowsky MP, Laurent B, Celle S, Ntougou Assoumou G, et al. Metabolic syndrome is associated with poor memory and executive performance in elderly community residents: The PROOF study. Am J Geriatr Psychiatry 2014;22:1096-104.  Back to cited text no. 27
[PUBMED]    
28.
Ho RC, Niti M, Yap KB, Kua EH, Ng TP. Metabolic syndrome and cognitive decline in Chinese older adults: Results from the Singapore longitudinal ageing studies. Am J Geriatr Psychiatry 2008;16:519-22.  Back to cited text no. 28
[PUBMED]    
29.
McEvoy LK, Laughlin GA, Barrett-Connor E, Bergstrom J, Kritz-Silverstein D, Der-Martirosian C, et al. Metabolic syndrome and 16-year cognitive decline in community-dwelling older adults. Ann Epidemiol 2012;22:310-7.  Back to cited text no. 29
[PUBMED]    
30.
Viscogliosi G, Donfrancesco C, Palmieri L, Giampaoli S. The metabolic syndrome and 10-year cognitive and functional decline in very old men. A population-based study. Arch Gerontol Geriatr 2017;70:62-6.  Back to cited text no. 30
[PUBMED]    
31.
Muller M, van Raamt F, Visseren FL, Kalmijn S, Geerlings MI, Mali WP, et al. Metabolic syndrome and cognition in patients with manifest atherosclerotic disease: The SMART study. Neuroepidemiology 2010;34:83-9.  Back to cited text no. 31
[PUBMED]    
32.
Lai CL, Liou LM, Liu CK, Yang YH, Lin RT. Effects of metabolic syndrome, apolipoprotein E, and CYP46 on cognition among Taiwanese Chinese. Kaohsiung J Med Sci 2014;30:343-9.  Back to cited text no. 32
[PUBMED]    
33.
International Diabetes Federation: IDF Diabetes Atlas; 2014. Available from: http://www.idf.org/diabetesatlas. [Last accessed on 2016 May 16].  Back to cited text no. 33
    
34.
Mohan V, Deepa M, Farooq S, Datta M, Deepa R. Prevalence, awareness and control of hypertension in Chennai – The Chennai urban rural epidemiology study (CURES-52). J Assoc Physicians India 2007;55:326-32.  Back to cited text no. 34
[PUBMED]    
35.
Yesudian CA, Grepstad M, Visintin E, Ferrario A. The economic burden of diabetes in India: A review of the literature. Global Health 2014;10:80.  Back to cited text no. 35
    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
References

 Article Access Statistics
    Viewed518    
    Printed63    
    Emailed0    
    PDF Downloaded133    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]