Assessment of cognition in obese young adults
Umayal C C 1, Sasirekha G 2,Suganthapriya S 3, Viji Devanand 4, Niveditha P 5
1Professor and Head, Department of Physiology, Thiruvarur Medical College ,2AssistantProfessor, 3 Postgraduate, 4 Professor and Head, 5 Assistant Professor, Department of Physiology, Stanley Medical College, Chennai-600 001, Tamilnadu
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Abstract
Background: Obesity is abnormal or excessive accumulation of fat that has adverse effects on health. Obese individuals are at risk of several life threatening diseases and complications such as Type-2 Diabetes Mellitus, Hypertension, Metabolic syndrome, Cardiovascular diseases, Stroke, Cancers, and Psychosocial disorders. Apart from these, it also leads to neurological disorders like impairment in cognition, motor skills and higher executive functions. Aim: To assess the cognition in young adult obese males. Materials and methods: 80 male participants of which 40 obese males and 40 normal weight healthy subjects in the age group of 18 to 35 years were recruited from the Non Communicable Disease Outpatient Department, Body Mass Index(BMI),Waist Circumference(WC) and Waist Hip Ratio(WHR) were the obesity indices used to assess the obesity. Montréal Cognitive Assessment Score (MoCA score) was used to assess the cognition. Results: The data was analysed using Statistical Package for Social Sciences(SPSS) version 20. The study group were with the mean age of 34.02 + 3.20 yrs, mean BMI of 32.06 +3.47,mean WHR of 0.86 + 0.08, mean WC of 98.37 +5.35 and mean MoCA score of 26.09+0.49.Among the study group 28% of the participants had cognitive impairment with the score between 23-25. Negative correlation was observed between the obesity indices and MoCA score, among which BMI had better negative correlation with the MoCA score. Conclusion: Cognition was impaired in obese individuals and it was inversely related to the obesity indices. This shows that they are at the risk for early onset of dementia. Hence, early diagnosis and appropriate interventions may prevent severe impairment in cognition in obese individuals.
Key words: obesity, cognition, dementia, metabolic syndrome
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Corresponding Author
Dr. G. Sasirekha, Assistant Professor, Department of Physiology, Stanley Medical College,
Chennai-600001, Tamil Nadu
Telephone: +91 9629266730 E-mail: [email protected]
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Introduction
Obesity and overweight are defined as abnormal or excessive fat accumulation that may impair the health of the individual.Overweight and obesity result from an energy imbalance that occurs due

to over eating of too much of calories and inadequate physical activity to use up those calories.
Obesity is associated withvarious comorbidities such as metabolic syndrome, glucose intolerance, hyper-lipidemia, hypertension and hence it can lead to the development of Type-2 diabetes mellitus, coronary artery disease, heart failure,respiratory diseases such as obstructive sleep apnoea, gastrointestinal, and musculoskeletal disorders, thromboembolism, stroke and cancer.1
In addition, many studies have shown that obesity is associated with cognition impairment and early onset of dementia.Neuroinflammation,vascular inflammation, altered metabolites are the causal mechanism for cognitive decline in obesity. The ongoing inflammatory process in obesity couldhave been triggered by multiple factors such as insulin resistance, leptin dysregulation, altered gut brain axis and enhanced systemic mediators of inflammation.2
Recent evidences show that consumption of high fat diet and unbalanced diet alters the gut brain axis,leading to impaired cognition.The bacteriallipopolysaccharide(LPS) is a pro-infammatory neurotoxin released from the gut microbiome. Itcrosses thephysiological barrier to access the hippocampus, leading to cognitive impairments,such as memory disturbances.3
The incidence of obesity is increasing among the younger age group. Mild cognition impairment that occurs at the early stage in obese individuals remain unnoticedand itmay lead to severe cognitive decline as well as early onset of dementia. Most of the studies showed cognitive impairment in obese individuals aged above 45yrs.
Hence, inthis study we have taken younger age group to provide an insight into the earlier onset of impairment in cognitionin obese individuals. This shall pave way for early diagnosis and prompt interventions in order to prevent further impairment in cognition and a better quality of life.

Aim
To evaluate cognition in obese males in comparison with the control group.
Objectives
1. To assess cognition by using Montreal Cognitive Assessment (MoCA) Score in all the participants.
2. To measure the waist circumference, hip circumference and to calculate Body Mass Index andWaist Hip Ratio in them.
3. To find out the association between obesity indices and MoCA score in obese males.
Materials and methods
This is an analytical cross-sectionalstudy. Institutional ethical committee clearance was obtained. 40 obese maleswere recruited, based on the revised consensus guidelines for India (Normal weight – BMI 18 – 22.9, Overweight – BMI 23 – 24.9, Obese – BMI > 25)4 from Non communicable disease outpatient department.Inclusion criteria were obese males (BMI > 25) of age 18 -35 years with minimum educational qualification8th standard.
Exclusion criteria included subjects with established diagnosis of dementia, co-morbid conditions that affect cognitive function such asneurological disorders, psychiatric disorders, history of acute / chronic illness, patients on any other chronic medications for and those with history of smoking, tobacco and alcohol abuse. 40 apparently healthy, age matched and gender matched subjects were included in the control group. All the subjects were explained about the study and written informed consent was obtained from each of them. A brief history was taken and clinical examination was done. The height was measured in metres (m) on barefoot using stadiometer and weight inkilograms by using a standardized weighing machine for all the participants.Body Mass Index was calculated using Quetelet’s Index (Weight / Height2).Their waist circumference was measured in centimetres at the level of umbilicus or midway between the lower ribcage and pubic symphysis. Hip circumference was measured as widest circumference at the level of greater trochanter using inch tape. Then Waist-Hip Ratio was calculated using waist and hip circumference.
Cognitive function of all the participants was assessed by Montreal Cognitive Assessment Score (MoCA score). It includes several questions grouped into seven categories, representing different cognitive domains such as Orientation, Delayed Recall, Language, Abstraction, Attention, Naming and Visuospatial. Duration of the test was 10 minutes. The subjectswere made comfortable and scoring for each question was done immediately on asking it in an orderlylisted way.

S.No.
Variable
Control group
(n=40)
Mean+S.D Obese group
(n=40)
mean +S.D p value
1.
Age (years)
33.04+2.43 34.02+3.20 0.72
2. Obesity Indices
BMI (Kg/m2)
WHR
WC (cm)
22.33 + 1.07
0.83 + 0.43
78.34 + 3.52
32.06 +3.47
0.86 + 0.08
98.37 + 5.35
0.04*
0.53
0.02*
3. MoCA score
1. Orientation (6)
2. Naming (3)
3. Attention (6)
4. Delayed recall (5)
5. Language (3)
6. Visuospatial (5)
7. Abstraction (2)
Total (30)

5.91 + 0.12
2.88 + 0.23
5.7 + 0.61
4.85 + 0.47
2.76 + 0.32
4.98 + 0.41
1.83 + 0.39
28.91 + 0.36

5.62 + 0.49
2.84 + 0.37
5.30 + 0.76
3.88 + 0.85
2.60 + 0.49
4.76 + 0.43
1.72 + 0.39
26.09 + 0.49

0.46
0.82
0.75
0.3
0.86
0.5
0.64
0.8
Table -1 Comparison of age, obesity indices and MoCA scores between obese and control group.
*p value < 0.05 significant, MoCA score – Montreal Cognitive Assessment Score.

The maximum total score is 30 and the score of 26 or above is considered as normal. The data obtained wereanalysedusing SPSS, version 20.An Independent Student’s t-test was used to compare the means of variables. Pearson ҆s test was used to find out the correlation between the variables,p value < 0.05 was considered significant.Correlation between obesity indices and MoCA score is given in Table-2. A significant negative
correlation was observed between BMI, WC and MoCA score. Though negative correlation was observed between WHR and MoCA score, it was not statistically significant. Among the obesity indices, BMI was found to have greater negative correlation with the MoCA score than WHR and WC.
Among the 40 obese males, 11 persons (28%) were found to have MOCA score between 23-25. Though 29 persons had normal MoCA scoring, there was a significant reduction in the scores of delayed recall domain and attention domain among them.
The distribution of cognitive impairment among the study population is shown in Fig-1

Figure -1 Distribution of cognitive impairment among the obese group.

Table-2 Correlation between obesity indices and MoCA score in the obese group.

Obesity indices

Correlation
co-efficient
( r value) p value

1. Body Mass Index (BMI)
(Kg/m2)

2. Waist Hip Ratio (WHR)

3. Waist Circumference (WC) ( Cm)

-0.69

-0.03

-0.63
0.03*

0.49

0.05*
*p value < 0.05 significant

Results
Out of the total 80 participants, 40 were obese and 40 were normal weight subjects. Data are represented as mean+standard deviation. Table-1 shows the comparison of age, obesity indices and MoCA scores between obese and control groups. It shows thatthe mean age of the obese and control groups were 34.02 yearsand 33.04 years. Both groups were age matched. There was a significant difference(p value <0.05) in the mean levels of BMI and Waist Circumference between obese and control groups.WHR was higher in obese subjects when compared to controls which were not statistically significant. There was a slight decline in the mean MoCA score in the obese groupin comparison with control group which was not statistically significant.While considering the scores of individual domains, there was decline in scores of attention and delayed recall among the obese group but not statistically significant.
Discussion
In our study,80 participants were recruited. Obesity indices such as waist circumference, hip circumference were measured, then BMI and Waist-Hip ratio (WHR) were calculated. Cognition assessment was done using MoCA score. Kannaiyiram et al reported that MoCA appears to be a better screening test than MMSE for screening and diagnosing mild cognitive impairment.5
The mean age of our study group was 34.02 years.Most of the studies demonstrated cognitive decline among obese and overweight individuals in the age group of 40 to 55 years.6This age group was selected in our study to demonstrate early onset of cognitive impairment in obese subjects. Also only obese males without any co morbidities were recruited in order to prove that obesity is an independent risk factor for cognitive dysfunction.
Themean MoCA score was reduced in obese males when compared tothat of normal subjects which was not statistically significant. The overall prevalence of cognitive impairment among obese subjects was 28%. The lower prevalence observed in our study could be due to smaller sample size.We observed agreater decline in the scores of attention and delayed recall which were consistent with the results obtained byJohn Gunstad et al. John Gunstad et al showed that obesity is linked to reduced cognitive function,with more impact on attention and executive function.7Studies also have shown diminished performance on various measures of cognition such as executive function, motor speed, short term memoryamong the obese individuals.8,9
In our study, we obtained a negative correlation between BMI, WC, WHR and MoCA Score. Among the obesity indices, BMI was found to have greater negative correlation with the MoCA score than WHR and WC. Manystudies have shown that both BMI and WC were inversely related to cognitive decline.10 Few studies have shown similar findings like that of our study.11 On the contrary, WC was found to have better negative correlation than BMI in other studies.12
The probable cause for cognitive decline noted in obese individuals could be the following. The leptin receptor mRNA are highly expressed in brain regions including hippocampus, amygdala, brain stem, cerebellum and substantia nigra. It regulates the higher functions in those regions. Leptin modulates synaptic functions, neuronal excitability in hippocampus and enhances learning and memory.13Chen et al revealed elevated levels of leptin and C-reactive protein (CRP) in obesity.Elevated CRP binds to leptin and prevents itsbinding to its receptor attributing to leptin resistance, resulting in cognitive decline in obese individuals.14
The inflammatory mediators such as C-reactive protein, IL-6 and visceral adipocyte derived factors are elevated in obesity. They may be neurotoxic causing slow deterioration of the higher functions of CNS leading to dementia later in life.15In another study, Raji et al reported that BMI>30kg/m2 was associated with atrophy in frontal lobes, anterior cingulate gyrus, hippocampus and thalamus as compared to normal weight individuals, leading to deterioration of higher functions.16In addition to the above factors, deficiency of micronutrients such as , zinc, biotin, iodine , magnesium, vitamin B-12 , vitamin D and antioxidant vitamin C, vitamin E were observed in obese and were found to be associated with cognitive decline.17,18Since obesity is associated with cognitive decline which remains unnoticed, our study mainly focused on early identification of cognitive decline in young obese adults.Moreover,cognitive impairment is reversible with earlyinterventions like life-style modifications, health education, increased physical activity, meditation.19 Increasing physical activity is simple, beneficial, which can reverse the mild cognitive decline as well as other neurological disturbances. It is the best treatment until the development of therapeutic options to treat cognitive deficits or to prevent cognitive decline in obesity are available.20

Conclusion

Our study concludes that the young obese individuals do have mild impairment in cognition which was assessed by MoCA scoring even at the early stages. Obesity in later life may lead to severe impairment in cognition and progressive dementia. Hence early interventions such as life style modifications, increased physical activity along with micronutrient supplementation can reverse this impairment in cognition.
Limitations
Our present study was conducted in smaller sample size and only among males. Significant cognition impairment could have been demonstrated if women were included in the study. Age group included in our study was between 18 to 35 years, wide range in selection of age group including the middle age group could be done in future studies for assessing the impairment of cognition.
Acknowledgements: Nil
Conflict of interest: Nil
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