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CORRELATION OF VISCERAL FAT LEVEL AND POOR COGNITIVE

FUNCTION AMONG ELDERLY POPULATION IN DENPASAR


Erick Lios1, R A Tuty Kuswardhani2, IGP Suka Aryana2
1

PPDS-1 Internal Medicine, Udayana University, Denpasar


Internal Medicine Department Udayana University/ Sanglah Hospital Denpasar,
Geriatric Division

ABSTRACT
Visceral adipose tissue is more metabolically active and has stronger
influence on adipocytokyne production. One of the main characteristics of
visceral adipose tissue is its lipolysis ability which is stronger than others adipose
tissue so that the number of free fatty acid in portal circulation will be higher and
increasing risk of developing insulin resistance. Visceral adipose tissues
hormones is more proatherogenic . The aim of this research is to find out whether
visceral adipose tissue is corelates with poor cognitive performance and hopefully
could fill the gap between one to another research and to prevent poor cognitive
performance by controlling level of visceral adipose tissue regularly.
We used cross sectional analytical study. Sample were recruited using total
sampling method by collecting all elderly population in 3 nursing homes located
in Denpasar in July 2015. We obtained 87 samples. Visceral adipose tissue level
was measured using Omron HBF 510 Body Composition Monitor with Scale and
cogitive performance was measured using structured questionnaire Mini Mini
State Examination (MMSE). Correlation test result using gamma test showed
visceral adipose tissue was correlated moderately with poor cognitive
performance ( 0.413 and p 0.003).
Keywords : visceral adipose tissue, leptine, cognitive performance, elderly,
systemic inflammation.
Introduction
Obesity is one of major health problems in almost every country in the
world. Globalization development has influenced our lifestyle and the number of
obesity prevalence is increasing every year. World Health Organization (WHO)
reports there are at least 1,4 billion people in this world who catagorized as
overweight with Body Mass Index (BMI) around 25 29.9 kg/m2 while another
500 million has BMI 30.0 kg/m2 which means they suffered obesity. 1 High level
of adipose tissue has strong correlation with high risk of various metabolic
diseases such as cardiovascular diseases, type 2 diabetes melitus (T2DM) and
even several types of cancer. Obesity at individual level is an interaction between
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genetic and environmental factors where environment factors were suspected play
more important role than the others since fact showed that obesitys prevalence
has been increasing in the last 30 years as much as the globalization era grows.
Lately, some researches showed that obesity has adverse effect on brain structure.
Rajik et al (2010) found there was poor cogntive function in patient with high
visceral fat level.2,3
Human brain is vital organ that regulates homeostasis of energy. Brain
controls homeostatis level subconciously through hippothalamus while non
homeostasis circuit located in structure outside hippothalamus. 4 Those integrated
processes control our body weight so that it remains stable throughout our life.
Rapid development in medical imaging also has important effects in this case
since they helped us detecting the change of brains structure better than before.
Obesity was suspected related to poor grey matter density in prefrontal,
somatosensoric, insular, temporal and subcortical area compared to non obesity
subjects. 3,4
Most of studies were using BMI as parameter to define obesity objectively
while the remains measured waist circumference to define how much fat
accumulation in abdomen area. Visceral fat has emerged as the key pathogenic
depot and having stronger association with adypocytokines production and
insuline resistance so that it strongly correlates to various metabolic diseases and
poor cognitive function.5 BMI is the easiest parameter to measure obesity however
it seems less representative since people with normal BMI have possibility to have
high visceral fat level too.
Published data on the association of visceral fat level and poor cognitive
function among elderly still lack of evidences due to limited study about this
topic. Raschpiler et al (2013) found that poor grey matter density correlates to
high visceral fat level while Debette et al (2010) showed the opposite. Many
studies showed contradictive results compared to each other and theres only
limited study about this topic thus further study is needed. This study aims to
know whether high visceral fat levels correlate to poor cognitive function or not
and hopefully it could fill the gap in prior study. Last but not least, we hope this

study could help decreasing poor cognitive impairment among elderly patients
through better prevention.
Methods
This study is analitical study, using cross sectional design and aims to
study correlation between visceral fat level and cognitive function among elderly
population ( 60 years old) in Denpasar. Samples were enrolled using total
sampling method which means we took all elderly population from 3 nursing
homes in Denpasar from July 2015. We found 87 samples in total.
Visceral fat levels were measured using Omron HBF 510 Body
Composition Monitor with Scale. This device is similar to weigh scales however
we need to input sample personal imformations first such as age, gender and
height before using this device. When its done, sample can step on the main unit
barefoot. Right posture for measurement is standing barefoot with knees and back
straight and look straight ahead, raise arms horizontally and extend elbow straight
to form 90 degrees angles to body, hold the display unit with both of your hands.
Omron has higher accuracy compared to other similar devices and research
showed that omron accuracy has nearly similar with hydrodensitometry, Dual
Energy X-ray Absorptiometry (DXA) and Magnetic Resonance Imaging (MRI).
The results then classified in three catagories which is 0 means normal, + means
high and ++ means very high. If the scored was 1 9 so it considered as 0
catagory (normal), when the score was 10-14 so it considered as + (high) while
the score was 15 30 then it considered as ++ (very high).
Global cognitive function was measured objectively using structured
questionnaire called Mini Mini State Examination (MMSE). MMSE consists of
several questions to measured orientation, registration, attention, calculation,
memory and language ability. The result is ranging from 0 as minimum score and
30 as maximum score where higher score reflects better cognitive function. Those
scores then classified again into three catagories, 0 19 is definitely dementia
disorder, 20 24 is suspected dementian disorder and 25-30 is normal cognitive
function.

Results
Sample Characteristics
Table 1
Variable

Demographic Characteristics of Sample


Numbe Percenta
rs (n)

Variable

Mean (SD)

Range

ge (%)

Gender :

Age

69.23 7.90

60-98

Man

27

31

BMI

23.95 4.86

13.7-37.7

Woman

60

69

Body weight

57.25 12.05

32 81.6

1234.95 253.69

14 1760

33,04 8.26

14 45.8

Education

Resting

background :

Metabolism

Uneducated

35

40.2

Body

Elementary school

30

34.5

Percentage

Junior high school

10

11.5

High school

8.0

Bachelor

3.4

Others

Fat

1
1.1
Data from 87 samples of elderly (60 years old) are reported. Their mean

age (SD) was 69.23 years old where the smallest age was 60 years old and the
oldest one was 98 years old. Most of the samples were women (69%) and the
remaining 27 samples (31%) were men. We devided education background into
several catagories where uneducated was 35 samples (40.2%), elementary school
was 30 samples (34.5%), junior high school was 10 samples (11.5%), high school
was 7 samples (8%), bachelor was 3 samples (3.4%). Their average BMI was
23.95 kg/m2 ranging from 13.7 kg/m2 until 37.7 kg/m2. Sample characteristics
based on their resting metabolism level was 1234.95 in average where the smallest
and the biggest is 14 and 1760 respectively, while mean body fat level percentage
was 33.04% where the lowest and highest is 14% and 45.8%.
Correlation of Visceral Fat Levels and Poor Cognitive Function
As mentioned above, visceral fat levels in sample were measured using
Omron HBF 510 Composition Monitor and divided into 3 catagories as normal,
high and very high.

Picture 1. Visceral Fat Levels of Samples ( in %)


Statistical analysis towards visceral fat level showed 43 samples (49.4%)
has normal visceral fat level, 25 samples (28.7%) has high visceral fat level and
remaining 19 samples (21.8%) has very high visceral fat level (picture 1). MMSE
score as cognitive function parameter also catagorized in 3 different levels where
32 samples (36.8%) has normal cognitive function, 30 samples (34.5%) suspected
having cognitive impairment, and 25 samples (28.7%) has cognitive impairment
(picture 2).

Picture 2. MMSE Score Results ( in %)

Cross tabulation analysis showed 43 samples with normal visceral fat


level, most of them have normal cognitve funtion (51.2%) whereas only 12
samples (27.9%) suspected having cognitive impairment and only 20.9% has poor
cognitive function. Second group was high visceral fat level group consists of 25
samples in total. Sample with high visceral fat level tends to have poor cognitive
function according to MMSE test result. Total numbers of sample with high
visceral level was 25 sample, 11 samples (44%) were suspected having dementia
disorders, 8 samples (32%) definitely have dementia and only remaing 6 (24%)
have normal cognitive function. Next group was very high visceral fat level group
consisted of 19 samples in total where most of them (42.1%) definitely have
dementia, 7 samples (36.8%) suspected having dementia and only small number
from them (21.1%) have normal cognitive function.
Table 2

Crosstabulation of Visceral Fat Level and Cognitive Funtion


Normal

Visceral
Fat
Level

Normal
High
Very High

Total

Count
%
Count
%
Count
%
Count
%

22
51.2%
6
24.0%
4
21.1%
32
36.8%

MMSE Score
Suspected
Poor Cognitive
cognitive
Impairment
impairment
12
9
27.9%
20.9%
11
8
44.0%
32.0%
7
8
36.8%
42.1%
30
25
34.5%
28.7%

Gamma correlation test were performed to test the association between


visceral fat level and cognitve function among elderly population in Denpasar.
The gamma correlation test showed in Table 3, p value 0.003 which means
visceral fat level and poor cognitive function was significant clinically. Gamma
correlation score was 0.413 means that they have average correlation so that the
higher visceral fat levels, the poorer cognitive function.

Total
43
100%
25
100%
19
100%
87
100%

Table 3

Gamma Correlation Test Result

Discussion
According to research and analysis result that have been done above, it
showed that visceral fat level has average correlation with poor cognitive
function. Visceral fat is stored is abdominal cavity and several vital organs such as
hepar, pancreas, and intestines. Other fat storage was below our skin so that it
often called as subcutaneous fat.6 Compared to subcutaneous adipose tissue, the
visceral adipose tissue has been considered as a pathogenic adipose tissue
compartment. One of the mechanisms is the sustained exposure of the liver to an
increased flux of free fatty acid via the portal circulation from the visceral adipose
tissue may be antecedent to the disturbances in glucose and lipid metabolism and
it will increase the chance of insulin resistance. Hormons produced by visceral fat
tissue has proaterogenic effect. Visceral fat tissue is more metabolically active an
has stronger association towards adipocytokine production like adiponectine,
tumor necrosis factor (TNF) and plasminogen activator inhibitor type I. 7
Visceral fat effect on various metabolic and cardiovascular diseases have been
studied extensively, however study of visceral fat effect on poor cognitive
function in elderly still limited until now.
Study conducted by DH Yoon et al (2012) strongly support our hypothesis
in this study. They found that visceral fat and poor cognitive function were
associated each other. DH Yoon et al used CT Scan to measured visceral fat level
and they conclude visceral fat was an independent factor and strongly correlated
to poor cognitive function. They even excluded several comorbid factors of
cardiovascular disease yet visceral fat remains correlated to poor cognitive
function. Visceral fat can caused the development of lesion in brain white matter.

In transgenic animal models, leptin receptor deficient rodents were shown to have
impaired memory performances, long term potentiation of neurons in the
hippocampus. Leptin resistance in obesity is one of important keys in developing
poor cognitive function.8
The first followed 1.423 individuals in the Framingham Heart Study for 46 years and found that higher BMI was associated with worse cognitive function
scores in men alone.9 We prefer measured visceral fat using omron so that the
results we obtained is more accurate compared to those who using BMI to
measure visceral fat level. BMI often didnt represent the actual percentage of
visceral level since its possible having high visceral fat level while BMI still in
normal range. Some pilot studies that using BMI as parameter have shown no
correlation between BMI and poor cognitive function, this phenomenon can be
explained especially in elderly population (> 60 years old). Muscle mass in
elderly is decreasing as the age goes older, and it will be replaced with fat mass
therefore their body weight remains stable. That phenomenon is one of the reasons
why we didnt use BMI as visceral fat level parameter and prefer omron which
can give us more accurate data on visceral fat level.
The decreasing of cognitive function in elderly was strongly suspected due
to brain structure changing. Higher visceral fat was associated with regional
cortical thinning such as decreasing hippocampus volume, increasing ventricel
size, poor memory ability and also thinning several areas of brain cortical. All of
those changing contributed to poor cognitif function in human.

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Study from

Walther et al (2010) have shown reduced gray matter density with increasing
visceral fat in left inferior frontal, right posterior region, right precentral region,
right lingual using voxel-based morphometric. Underlying mechanism of those
facts still hasnt been understand clearly until now. Some of studies suggested
brain structure changing was strongly associated to obesity itself. T2DM is
strongly correlated to obesity and suspected to be one of underlying mechanisms
that cause brain structure changing. However that hypothesis remains speculative
because in the present dataset after excluded diabetic subjects but were still able to
show an independent effect of visceral fat on brain structure.11

Systemic inflammation could be another important mediator.Inflammation


is important mediator since obesity has been correlated to massive production of
inflammation markers. Cytokines such as interleukin 6 and tumor necrosis factor
alpha are produced in adipose tissue and induce hepatic production of CRP.
Adipose tissue itself basicly contained various infammatory cells such as
monocyte and macrophage that accumulates in obese people. Inflammation was
shown to predict a higher risk of dementia. In frammingham offspring study,
found that infflamation markers were inversely associated to brain total volume.
Persons on anti-inflammatory drugs show significantly smaller age-related
volume changes in regions of both gray and white matter compared to controls.
Other mechanism was probably through hypercortisolemia state, hyperlipidemia,
and decreasing physical activity. Hypercholesterolemia was contributed to
hippocampus atropy.
Similar study found that high level visceral tissue contribute to decreasing
grey matter density from cerebellum where this finding also consistent with other
study that used different parameter such as BMI or waist circumference. Newest
finding about cerebellum function shown that cerebellum plays role in motoric
process not only in cognitive process. Moreover, cerebellum showed greater
glucose metabolic activity and there was significant blood flow decrease to
cerebellum in obesity sample. Interestingly, the cerebellum expresses Fto gene,
which has been shown to be associated with both overall obesity and very recently
visceral adipose tissue.12
The adipocyte-derived hormone leptin may provide further explanations
for correlation of visceral fat and poor cognitive function in elderly. Leptin is
predominantly produced in white subcutaneous tissue, messages the switch
between the starved and fed states and serves as an essential factor for the
development of leptin sensitive, hypothalamic feeding circuits. Its signal is
conveyed via the long isoform of leptin receptors (Ob-Rb). This receptors mRNA
was shown to be present in the cerebellum. Moreover, Ob-Rb mRNA levels in
both rodents and humans exceed all other tissues investigated, including the
hypothalamus.13 Leptin also play a role in the relation between adipose tissue and
brain atrophy. In transgenic animal models, leptin receptor deficient rodents were
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shown to have impaired memory performances, and long term potentiation of


neurons in the hippocampus. Leptin has also been shown to reduce the
extracellular amyloid beta load and the level of tau phosphorylation in neuronal
cells.10 Frammingham cohort study has identified positive correlation between
leptin level in plasma and grey matter volume in right hippocampus. The higher
circulating leptin levels were significantly associated with a reduced risk of
incident dementia and brain atropy. Leptin was expressed more in subcutaneous
fat tissue compared to visceral fat tissue. Obesity people tends to have lower
leptin level and has increasing risk of poor cognitive function. Guftasin et al
(2008) has supported the idea about leptin roles in poor cognitive function where
leptin and other fat derived hormones has ability to cross blood brain barrier so
they may disturb brain cognitive function through various mechanism. 13
Conclusion
Visceral fat tissue has been considered as a pathogenic adipose tissue
compartment. It is more metabolically active an has stronger association towards
adipocytokine production like adiponectine, tumor necrosis factor (TNF) and
plasminogen activator inhibitor type I.7 Visceral fat is strongly correlated with
increasing risk of metabolic diseases and poor cognitive function. The result of
this study has shown significant correlation between visceral fat level and poor
cognitive performance. Underlying mechanism remains speculated, however some
suspected mehanisms are systemic inflammation, chronic exposure to free fatty
acid and leptin role. All of those mechanisms will directly influence brain volume,
brain structure in some brain regions so that they may caused poor cognitive
function later.
There were only limited published studies about this topic thus we need
more studies with larger sample and represent actual population, better design and
method with longer follow up time and also more accurate sample enrollment so
that sample will be more homogenous and exclude some confounding variables.In
this study we use MMSE as cognitive function parameter while visceral fat level
was measured using omron. We hope that further study will be done by better and
more accurate modality such as MRI to measure brain structure changing and CT
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scan to measure visceral fat level and therefore the results wil be more actual and
representative. We hope this study could help better prevention if dementia
prevalence in elderly by doing more physical activity and regular control of body
weight so that excessive visceral fat level can be avoided.
References
1. World Health Organization. Obesity and overweight [on-line]. URL :
http://www.who.int/mediacentre/factsheets/fs311/en/ Accessed September
2015.
2. Gunstad J, Paul RH, Cohen RA, Tate DF ,Spitznagel MB, Grieve S,
Gordon E. 2008. Relationship between Body Mass Index and Brain
Volume in Healthy Adults. Int. J. Neurosci 118 : 15821593.
3. Raji CA, Ho AJ, Parikshak NN, Becker JT, Lopez LO, Kuller LH, Hua X,
Leow AD, Toga AW, Thompson PM. 2010. Brain Structure and Obesity.
Hum.Brain Mapp 31: 353364
4. Shin AC, Zheng HY, Berthoud HR. An Expanded View of Energy
Homeostasis: Neural Integration of Metabolic, Cognitive, and Emotional
Drives to Eat. Physiol Behav 97:57280
5. Liu J, Fox CS, Hickson DA, May WD, Hairston KG, Carr JJ, Taylor,H.A.
2010. Impact of Abdominal Visceral and Subcutaneous Adipose Tissue on
Cardio Metabolic Risk factors. J. Clin.Endocrinol.Metab 95: 54195426.
6. Chen CH, Chen YY, Chuang CL, Ching LM, Chiao SM, Hsieh KC. 2014.
The Study of Anthropometric Estimates in the Visceral Fat of Healthy
Individuals. Nutrition Journal 46 : 1-8.
7. Kanaya AM, Lindquist K, Harris TB et al. 2009. Total and regional
adiposity and cognitive change in older adults: the Health, Aging and
Body Composition (ABC) study. Arch Neurol 66: 32935.
8. Fewlass DC, Noboa K, Pi-Sunyer FX, Johnston JM, Yan SD, Tezapsidis
N. 2004. Obesity-related leptin regulates Alzheimers Abeta. FASEB J 18:
18708.
9. Elias MF, Elias PK, Sullivan LM, Wolf PA, D'Agostino RB. 2005. Obesity,
diabetes and cognitive deficit: The Framingham Heart Study. Neurobiol
Aging 26:1116.
10. Debette S, Beiser A, Hoffmann U, Decarli C, Odonnell CJ, Massaro JM,
Au R, Himali JJ, Wolf PA, Fox CS, Seshadri S. 2010. Visceral fat is
11

associated with lower brain volume in healthy middle-aged adults.


Ann.Neurol. 68: 136144.
11. Jagust,W. 2007.What can imaging reveal about obesity and the brain?
Curr.AlzheimerRes. 4 : 135139.
12. London ED, Berman SM, Chakrapani S, et al. 2011. Short-term plasticity
of gray matter associated with leptin deficiency and replacement. J Clin
Endocrinol Metab 96:121220.
13. Burguera B, Couce ME, Long J, et al.2000. The long form of the leptin
receptor

(OB-Rb)

is

widely

expressed

in

the

human

brain.

Neuroendocrinology 71:18795.

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