PROBLEMAS DE ORDEN CONSTITUCIONAL

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Social Class

Nutritional Status Severe

Thinness(n)(%)

Thinness (n)(%)

Normal (n)(%)

Overweight (n)(%)

Obesity (n)(%)

Total (N)(%)

I 0(0.0) 0(0.0) 3(75.0) 0(0.0) 1(25.0) 4(100.0)

II 0(0.0) 4(9.1) 33(75.0) 7(15.9) 0(0.0) 44(100.0)

III 1(0.8) 23(17.6) 97(74.0) 10(7.6) 0(0.0) 131(100.0)

IV 1(0.9) 41(35.3) 68(58.6) 5(4.3) 1(0.9) 116(100.0)

V 0(0.0) 12(37.5) 16(50.0) 4(12.5) 0(0.0) 32(100.0)

Total 2(0.6) 80(24.5) 217(66.3) 26(8.0) 2(0.6) 327(100)

Likelihood ratio Chi square = 41.27 ; df=16 ; p=0.000

Mean 2-Hour Postprandial Blood Glucose Values of the Study population according to

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Age (years) Gender

Male

(mean±SD)

Female (mean±SD)

6-<7 83.97±14.27 83.89±14.05

7-<8 85.12±13.33 85.16±13.07

8-<9 84.23±12.43 84.89±12.79

9-<10 83.38±14.70 83.40±14.67

10-<11 82.83±15.84 83.18±15.33

11-<12 86.38±17.17 86.19±16.62

Total Mean 83.91±15.54 84.38±13.20 t test p=0.383

2-Hour Postprandial Blood Glucose Profile according to Age

In this study, impaired glucose tolerance (IGT) was found in the 7-<8 and 11-<12 age groups.

Prevalence of IGT in the 11-<12 years age group was 3.3%, while the prevalence in the 7-<8 years age group was 1.9%. There was statistical significant difference in the blood glucose values of different age groups. p=0.024 (Table XV).

Table XV: 2-Hour Postprandial Blood Glucose Levels according to Age Age(years) Blood glucose values

<50mg/dl(%) 50-<140mg/dl(%) ≥140mg/dl(%) p value

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6-<7 0(0.0) 79(100.0) 0(0.0) 0.024

7-<8 0(0.0) 104(98.1) 2(1.9)

8-<9 0(0.0) 127(100.0) 0(0.0)

9-<10 0(0.0) 90(100.0) 0(0.0)

10-<11 0(0.0) 121(100.0) 0(0.0)

11-<12 0(0.0) 119(96.7) 4(3.3)

Likelihood ratio Chi square= 7.892; df=5; p=0.024

2-Hour Postprandial Blood Glucose Profile according to Gender

From this study, all the subjects with IGT were males. There was statistical difference in the frequency of IGT between males and females, p<0.001 (Table XVI).

Table XVI: 2-Hour Postprandial Blood Glucose Levels according to Gender Gender Blood glucose value

<50mg/dl(%) 50-<140mg/dl(%) ≥140mg/dl(%) p value

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Male 0(0.0) 275(97.9) 6(2.1) <0.001

Female 0(0.0) 365(100.0) 0(0.0)

Likelihood ratio chi χ²= 11.187, p< 0.001

2-Hour Postprandial Blood Glucose Levels and Nutritional Status

Out of the 6 subjects (0.9%) that had IGT, 2 were thin, 1 was overweight while 3 had normal weight. Therefore, 1.8%, 0.7% and 1.3 % of thin, normal weight and overweight subjects respectively had IGT. There was no statistical difference in the prevalence of IGT of the various nutritional states, p=0.372 (Table XVII).

Table XVII: 2-Hour Postprandial Blood Glucose Levels and Nutritional Status

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Nutritional Status

Blood Glucose Status

IGT (%) Normal Glucose Level (%) Total (%) p value

Severe Thinness 0(0.0) 2(100) 2(100.0) 0.372

Thinness 2(1.8) 107(98.2) 109(100.0)

Normal 3(0.7) 444(99.3) 447(100.0)

Overweight 1(1.3) 78(98.7) 79(100.0)

Obesity 0(0.0) 9(100.0) 9(100.0)

Total 6(0.9) 640(99.1) 646(100)

Likelihood ratio Chi square = 5.14; df= 4; p= 0.372

2-Hour Postprandial Blood Glucose Levels and Social Class

From this study, 0.5%, 1.8% and 4.1% of subjects from social class II, IV, V respectively had impaired glucose tolerance. There was a significant difference in the 2-hour postprandial blood glucose levels of the various social classes, p=0.034 (Table XVIII).

Table XVIII: 2-Hour Postprandial Blood Glucose Levels and Social Class

Social Class Blood

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Glucose(mg/dl)

IGT (n)(%) Normal (n)(%) Total (N)(%) p value

I 0(0.0) 15(100) 15(100) 0.034

II 1(0.5) 186(99.5) 187(100)

III 0(0.0) 228(100) 228(100)

IV 3(1.8) 164(98.2) 167(100)

V 2(4.1) 47(95.1) 49(100)

Total 6(0.9) 640(99.1) 646(100)

Likelihood ratio Chi square = 8.912; df=4; p=0.034

Relative Risk of Developing IGT in Overweight Subjects.

Subjects who are overweight are 1.9 times more likely to have IGT than those with normal weight (Table XIXa).

Table XIXa: Relative Risk (RR) of Developing IGT in Overweight Subjects

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Nutritional Blood Glucose Levels Status

IGT Normal Blood Glucose Levels Total

Overweight 1 78 79

Normal Weight 3 444 447

Total 4 522 526

Relative Risk (RR) = 1.9 (RR>1 is significant) RR= a/(a+b)/c/(c+d)

RR = 1/(1+78)/3(3+444) = 1.9

Relative Risk of Developing IGT in Thin Subjects.

Subjects who were thin were 2.7 times more likely to have IGT than those with normal weight (Table XIXb).

Table XIXb: Relative Risk (RR) of Developing IGT in Thin Subjects.

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Nutritional Blood Glucose Levels Status

IGT Normal Blood Glucose Levels Total

Overweight 2 107 109

Normal Weight 3 444 447

Total 5 551 556

Relative Risk (RR) = 2.7 (RR >1 is significant) RR= a/(a+b)/c/(c+d)

RR = 2/(2+107)/3(3+444) = 2.7

Relationship between the BMI z score and 2-Hour Postprandial blood glucose levels of thin and severely thin subjects.

Figure 3a shows the Pearson’s correlation between the BMI z score and 2 hour Postprandial blood glucose levels of thin and severely thin subjects. There was no correlation between the

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BMI z score and 2 hour Postprandial blood glucose levels of thin and severely thin subjects, r

= -0.0319 (Figure 1a).

Figure 1a: Pearson’s correlation between the BMI z score and 2-Hour Postprandial Blood Glucose Level of Thin and Severely Thin subjects.

Relationship between BMI z score and 2-Hour Postprandial Blood Glucose of Overweight and Obese Subjects.

There was no correlation between BMI z score and 2-Hour Postprandial blood glucose levels in Overweight and Obese subjects, r = 0.0267 (Figure 1b).

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Figure 1b: Pearson’s correlation between the BMI z score and 2-Hour Postprandial Blood Glucose Levels in Overweight and Obese subjects.

Relationship between BMI z score and 2-Hour Postprandial blood glucose levels in subjects with normal weight..

There was no correlation between BMI z score and 2 Hour Postprandial blood glucose levels of all subjects with normal weight r = - 0.0375 (Figure 1c).

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Figure 1c: Pearson’s correlation between the BMI z score and 2-Hour Postprandial Blood Glucose levels in Subjects with Normal Weight.

DISCUSSION

From this study, the mean weight and height of urban (Asaba) subjects were higher than that observed for the rural (Illah) subjects. Kolekar and Sawant¹¹⁴ observed the same trend in their study. The trend seen for the mean weight and height in the urban and rural communities was

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also observed for the mean BMI in these communities. The mean BMI for the urban community was higher than that of the rural community. These observations may be due to the socioeconomic differences between the rural and urban communities observed in this study. Majority of pupils in the urban community belong to the higher social class, while majority of pupils in the rural community belonged to the lower class. High socioeconomic status is associated with greater incomes at household level with more resources invested in food consumption, access to clean water, good hygiene and health care.¹¹⁵

The mean body mass index of the total study population was similar to what Nwaiwu and Ibe,¹¹⁶ and Ansa et al¹¹⁷ reported. This similarity may be because their studies were carried out in children and some early adolescents like the present study. However, the mean body mass index in this study is lower than the mean reported by Ahmad et al^118. The reason for this could be because Ahmad et al¹¹⁸ did their work solely in adolescents, and adolescents are heavier than children, hence the difference in mean BMI from both studies.

The mean body mass indices of the studied subjects were found to increase with age for both genders in both communities. This is in agreement with what was found by Nwaiwu and Ibe,¹¹⁶ and Ahmad et al.¹¹⁸ Normally in children, muscle mass, bone mass and adiposity increase with increasing age,³⁹ thus the reason for this observation.

The prevalence of overweight in the entire study population was higher than the global prevalence of overweight as reported in the State of the World Children³. There is no composite data in Nigeria on the prevalence of overweight and obesity in school aged children, although regional prevalence has been described.4,8,23,49,116 However, the National Demographic and Health Survey (NDHS)¹¹⁹ reported a lower prevalence of 4.0% for overweight in under five children. The high prevalence of obesity and overweight in this study may be due to the widespread urbanization and westernization in developing countries,

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with attendant changes in lifestyle to the sedentary and changes in eating habit to more energy dense fast food observed in these countries.⁶ The prevalence of overweight/obesity in this study is low compared to the prevalence reported by Margellos et al¹²⁰ among children in Chicago, United State of America. The lower obesity/overweight rates seen in this study as compared to that obtained by Margellos et al, is possibly because, unlike in the United States of America, where children especially those in the low income category consume cheap foods with high calories, which predispose them to overweight and obesity, children in developing countries consume less calorie dense diets, thus reducing the incidence of overweight and obesity.¹²¹

The prevalence of thinness in the entire study population was high compared to what was observed in the study by Bovet et al.¹²² While this study comprised mainly preadolescent population with little contribution by early adolescent group (10-<11years, 11-<12years), the study by Bovet et al¹²² had significant contribution by the early and mid adolescent age groups. Sex hormones secretions in early and mid adolescents have been shown to contribute significantly to increased body weight in this age group.¹²³ Furthermore, Bovet et al¹²² did their study in Seychelles where the economic situation is better compared to Nigeria.³ Better economy invariably connotes better nutrition and better growth and development.

The prevalence of thinness in this study was also higher than that obtained by Ene-Obong et al ⁸and Ani et al²³. Although all the studies were conducted in Southern Nigeria, higher prevalence in this study was possibly due to the continued increase in malnutrition and disease states occasioned by poor economic growth, poverty and poor access to affordable health care. The high prevalence of thinness in this study shows that, regardless of the growing prevalence of overweight and obesity, undernutrition is still a significant problem in our society. This creates a double burden of malnutrition in Nigerian children.

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In this study, the prevalence of overweight in Asaba was similar to what was reported by Mogre et al⁵¹ in Tamale, Ghana. Both studies utilized almost the same age group and the same growth reference, these may account for the similarity in the prevalence. Nigeria and Ghana have almost similar economic status as shown by their Gross National Income reported in the 2016 State of the World’s Children,³ this may also account for the similarities in the findings. Goon et al¹²⁴ conducted a study in Markudi, in 2011, and reported very low prevalence for obesity and overweight compared to the index study. Geographical location of study sites with differences in culture, diets, beliefs and genetic differences may be the reasons for the variation observed. The increase in incidence of overweight and obesity in children over the years, may also have contributed to the higher prevalence seen in the index study.

In Asaba, prevalence of overweight was highest in the 9-<12 years age bracket. A similar trend was reported in the USA by the state of obesity foundation.¹²⁵ A plausible explanation that can be adduced to this observation is the effect of sex hormones in early adolescence, which have been shown to contribute to adiposity.¹²³

The prevalence of thinness and severe thinness in Asaba were low compared to overweight and obesity. Most of the subjects in Asaba belonged to the upper and middle social classes.

Relative affluence and luxury that come with these classes can promote achievement and maintenance of normal weight or promote development of overweight and obesity. This trend could even be seen amongst the urban lower classes. This may explain the reason for lower prevalence of thinness in Asaba in this study.

In the rural community (Illah), the prevalence of overweight was higher than the prevalence (1.5%) reported in a rural community by Olumakaiye et al,¹²⁶ and the prevalence (4.2%) obtained in another rural community by Ani et al²³. The prevalence of overweight in the

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rural area in this study was almost twice that reported by Ani et al²³and five times that described by Olumakaiye et al.¹²⁶ This further gives credence to the fact that incidence of overweight and obesity are increasing in our society due to changes in our diets and adoption of sedentary life style.⁶ This study shows that even the rural areas are not left out of this paradigm shift.

In this study, thinness is the major problem in the rural community. Looking at the socioeconomic status, majority of the subjects in the rural community belonged to the lower class (Classes IV and V). Lower social class means low earning power which begets suboptimal nutrition, unsafe water supply, unclean environment, increase susceptibility to diseases and poor access to health care. All these have suboptimal growth and development as the final pathway.

In both the urban and rural communities, thinness had higher prevalence in subjects in the younger age groups. This finding agrees with findings by Ene-Obong et al⁸, van Niekerk et al¹²⁷ and Ani et al²³, who found the same trend of thinness in younger age groups. This is probably because children in these age groups are more prone to malnutrition, since they are unable to look for food by themselves even when they are hungry and they depend solely on their caregiver for sustenance. Children in this age group are also prone to infections and infestations which can hinder their growth and development.¹¹⁹

This study also describes the 2 hour postprandial blood glucose profile of primary school children in Asaba (urban) and Illah (rural) communities of Delta State. Studies on blood glucose profiles especially in children are very few. The mean blood glucose level of children in this study was similar to the mean described among children in China by Cao et al¹²⁸ but lower than the mean reported by Oluwayemi et al¹²⁹ among adolescents in Ado Ekiti, Nigeria.

While this study and that by Cao et al¹²⁸ consisted of both young children and some early

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adolescents, Oluwayemi et al¹²⁹ predominantly studied adolescent population. The differences in study population may account for this dissimilarity because adolescents have been shown to have higher blood glucose levels due to the effects of growth hormone and sex steroids which are high in this stage of development.¹³⁰ These hormones can cause insulin resistance, an effect that is however attenuated to a great extent in normal subjects by increase in insulin output.

Although the difference was not significant, the mean blood glucose of female subjects in this study was higher than that of males. This finding is similar to that by Cao et al¹²⁸ and Oluwayemi et al.¹²⁹ The reasons for higher mean blood glucose levels in females may be due to the fact that, women have a smaller lean mass of muscle than men and therefore less muscle is available for uptake of glucose.¹³¹ This could predispose females to having higher blood glucose levels than males.¹³¹

In this study, the prevalence of impaired glucose tolerance (hyperglycemia) was low compared to the prevalence of IGT reported among adolescents in India by Ranjani et al.¹³² Oluwayemi et al¹²⁹ in Ado Ekiti, Nigeria, also reported a higher prevalence of impaired fasting blood glucose compared to the index study. These disparities may be explained by the different study populations used. While children comprised majority of the study population for this study, Ranjani et al¹³² and Oluwayemi et al¹²⁹ conducted their study exclusively in adolescents. Blood glucose level in adolescents can be increased by hormones such as growth hormones and sex hormones like oestrogen, progesterone and testosterone. The increased release of these hormones during puberty and adolescence, leads to increased insulin resistance, which can result in impaired glucose tolerance. Differences in methods used in measuring the blood glucose levels might also be reason for the differences in prevalence reported. While this study used 2-hour postprandial in estimating the blood glucose levels of subjects, Ranjani et al¹³² and Oluwayemi et al¹²⁹ used OGTT and fasting blood glucose

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respectively. Different sensitivities have been reported for these methods of blood glucose measurements.¹⁰¹

In this study, impaired glucose tolerance was found exclusively amongst males. This finding is at variance with findings from several studies in which prevalence of IGT in females were higher.129,132,133 This is rather surprising because from the study, obesity and thinness which are risk factors for abnormal glucose regulation were more predominant in females. Although overweight which is also a risk factor was commoner in males, however, only one male subject with overweight had hyperglycemia. Reasons for these findings are unclear.

An inverse relationship was found between the prevalence of IGT and social class. Subjects in high social class (social classes I and II) had lower prevalence of IGT than subjects in lower social class (social classes IV and V). Studies^134,135 have described inverse relationship between social economic class and prevalence of impaired glucose tolerance. Income, education and employment are social determinants of health. Although this study did not look into factors that predispose children to IGT, some of the factors that have been reported to predispose to development of IGT and DM are recurrent infections (especially enteroviral infections) in genetically predisposed individuals and lack of exclusive breastfeeding.¹³⁶ Exclusive breastfeeding has been shown to be suboptimal in low social class ¹³⁶ and the risk of repeated infection is also higher in children in this class.¹³⁶ It is therefore possible that, these factors predisposed children in the lower class in this study to developing impaired glucose tolerance.

The prevalence of IGT in overweight children in this study is higher than the prevalence of IGT in children with normal weight. Although, there is no statistical significant difference, this finding underscores the fact that maintaining a normal weight is crucial to reducing the risk of developing impaired glucose tolerance. The prevalence of IGT in overweight subjects

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in this study is lower than that reported by Purusthotham et al⁹³. While this study utilized 2-hour postprandial blood glucose as means of assessing the blood glucose levels in the subjects, Purushotham et al⁹³ used oral glucose tolerance test. This difference in methods of blood glucose measurement may account for differences in prevalence obtained. Genetic differences may also have contributed to differences in prevalence obtained. Lower prevalence of IGT seen in this study may be connected with lower frequencies of human leucocyte antigen DR3, islet cell antibodies and other auto-antibodies that have been observed in black race.⁸⁷ This offers some protection against development of IGT and type 1 DM in blacks.

The prevalence of IGT in thin subjects was higher than the prevalence of IGT in overweight and normal weight subjects. Impaired glucose tolerance and diabetes mellitus have been described amongst thin/lean people. This has been linked to pancreatric atrophy which may occur in undernourished people.^11,12 Studies ^93,94,95 have documented prevalence of impaired glucose intolerance in overweight/obese children but there’s dearth of studies on the prevalence of impaired glucose tolerance in undernourished children. Undernutrition remains the most prevalent and worrisome nutritional problem in our environment. This may explain the marginally higher prevalence of IGT in the thin children of this study, compared to those that were overweight and normal weight subjects. Since the prevalence of IGT is lower in normal weight subjects compared to thin children, the importance of maintaining normal weight towards preventing problems like IGT cannot be overemphasized.

In subjects with normal BMI z score, the prevalence of IGT was lower than the prevalence reported by Jaja T and Okoh B¹³⁷ in PortHarcourt, Nigeria, in normal weight adolescents. A plausible explanation for this disparity is possibly because of the homogenous population of predominant adolescents used by Jaja and Okoh,¹³⁷ while this study used a heterogeneous population of children and adolescents. Growth hormones and sex hormones which have

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been shown to cause insulin resistance are higher in adolescents.¹³⁰ The effects of these hormones can trigger insulin resistance and impaired glucose tolerance in adolescents with background predisposing genetic and environmental factors.

There’s dearth of study on the correlation between blood glucose and BMI in children in Nigeria. In this study, using the Pearson’s correlation, no correlation was found between 2 hour postprandial blood glucose and body mass index in thin, overweight and normal weight subjects, although some studies^97,98 have documented correlation between blood glucose and BMI.

Absence of correlation between 2- hour postprandial blood glucose and obesity/overweight could be because none of the obese subjects and only 1.3% (1/79) of the overweight subjects had impaired glucose tolerance. In these subjects, absence of correlation suggests that, with increase in their body weight, there was no corresponding increase in their blood glucose level. Apart from overweight and obesity, insulin resistance is influenced by genetic and environmental factors like high calorie food, lack of exercise, and long hours spent watching television and playing video games. Although these factors were not explored in the study, if they were absent in these overweight/obese subjects, their sensitivity to endogenous insulin may have been preserved even in the face of overweight/obesity.

In thin and severely thin subjects, there was also no correlation between the 2-hour postprandial blood glucose and BMI z scores of the subjects. The low prevalence of 1.8%

(2/109) of IGT amongst thin subjects may have accounted for this finding. From literatures, undernourished children may have IGT if insulin production from the pancreatic beta cells is compromised due to insults from chronic undernutrition.^11,12 Most of the thin subjects in this study may not have suffered pancreatic insults from undernutrition that can compromise

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