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March 2019 -
Volume 17, Issue 2

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From the Editor




Dr. Abdulrazak Abyad
DOI: 10.5742/MEWFM.2019.93623

Original Contribution

Self-monitoring of Blood Glucose Among Type-2 Diabetic Patients: An Analytical Cross-Sectional Study
Ahmed S. Alzahrani, Rishi K. Bharti, Hassan M. Al-musa, Shweta Chaudhary
DOI: 10.5742/MEWFM.2019.93624

White coat hypertension may actually be an acute phase reactant in the body
Mehmet Rami Helvaci, Orhan Ayyildiz, Orhan Ekrem Muftuoglu, Mehmet Gundogdu, Abdulrazak Abyad, Lesley Pocock
DOI: 10.5742/MEWFM.2019.93625

Case Report

An Unusual Persistent Mullerian Duct Syndrome in a child in Abha city: A Case Report
Youssef Ali Mohamad Alqahtani, Abdulrazak Tamim Abdulrazak, Hessa Gilban, Rasha Mirdad, Ashwaq Y. Asiri, Rishi Kumar Bharti, Shweta Chaudhary
DOI: 10.5742/MEWFM.2019.93628

Population and Community Studies

Prevalence of abdominal obesity and its associated comorbid condition in adult Yemeni people of Sana’a City
Mohammed Ahmed Bamashmos
DOI: 10.5742/MEWFM.2019.93626

Smoking may even cause irritable bowel syndrome
Mehmet Rami Helvaci, Guner Dede, Yasin Yildirim, Semih Salaz, Abdulrazak Abyad, Lesley Pocock
DOI: 10.5742/MEWFM.2019.93629

Systematic literature review on early onset dementia
Wendy Eskine
DOI: 10.5742/MEWFM.2019.93627

Middle East Quality Improvement Program

Chief Editor -
Abdulrazak Abyad MD, MPH, MBA, AGSF, AFCHSE


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Lesley Pocock
medi+WORLD International

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March 2019 - Volume 17, Issue 3

Prevalence of abdominal obesity and its associated comorbid condition in adult Yemeni people of Sana'a City

Mohammed Ahmed Bamashmos

Mohammed Ahmed Bamashmos (MD),
Associate Professor of Internal Medicine, Faculty of Medicine,
Sana'a University

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Objective: Abdominal obesity is a metabolic problem that has become increasingly common worldwide over the past several decades. Its prevalence is increased in both advanced and developing countries including Yemen. The aim of this cross sectional study was to investigate the prevalence of Abdominal obesity in a sample of Yemeni adult individuals and its association with other comorbid conditions namely, hypertension, diabetes, dyslipidemia (high triglyceride, low high density lipoprotein) and metabolic syndrome (MS).

Methodology: A sample of 1118 adult Yemeni people equal to or over 18 years was randomly chosen to represent the population living in Sana'a City during a period of two years from April 2016 to April 2018. All the study group underwent full clinical history and examination which included measurement of BP and waist circumference and the following laboratory investigations (FBS, serum TG, HDL, and LDL).

Results: The prevalence of abdominal obesity in this study was 24.5% (7.9% male and 44.2% female). Central obesity in this study was significantly correlated with age and sex. The highest prevalent comorbidity in patients with abdominal obesity was high BP (41.3%), followed by high serum TG (40 %), higher prevalence of MS (40%), low serum HDL (37.8%) high LDL (20.1%) raised fasting blood glucose (22.1%) than those without abdominal obesity (5.5%, 31.3%, 16.6%, 8.5%, 12.5% and increased FBS 10% respectively).

Conclusion: Hypertension, diabetes, dyslipidemia and MS are strongly correlated with abdominal obesity.

Key words: central obesity, hypertension, dyslipidemia, MS


Obesity is a worldwide epidemic. Beyond the fat mass per se, the pattern of fat distribution has a profound influence on cardiometabolic risk. Visceral abdominal fat (VAF) is metabolically active and pro-inflammatory and presents a higher cardiometabolic risk association and calcification of the coronary arteries than the body mass index (BMI) and has more impact on health than subcutaneous fat, presenting a risk factor for increased incidence of metabolic syndrome (1, 2). Abdominal obesity (AO) is directly associated with increased VAF, and it is also associated with endothelial dysfunction, inflammation, insulin resistance, diabetes mellitus, hypercholesterolemia, metabolic syndrome [MetS], and cancer (1, 3). There are several methods available to measure AO. Waist circumference (WC) provides an indicator of central adiposity that is the most practical and easiest method used in large-scale epidemiological studies (4). It is a good predictor of cardiometabolic morbidity and mortality, and it has also a positive association with visceral abdominal fat. However, WC does not allow us to differentiate between visceral fat and subcutaneous fat; methods such as absorptiometry by dual energy X-ray (DEXA), impedance, or densitometry can be used to handle this differentiation (5-7). WC measurement requires correct and standardized procedures, which depend mainly on training and adequate equipment. A standardized technique requires that the person being measured removes bulky or tight garments, as well as shoes with heels, empties their bladder then stands in the upright position, with arms loosely positioned to the side. The tape is passed around the body and positioned mid-way between the iliac crest and costal margin of the lower rib, ensuring that it is Population Organization Recommended waist circumference threshold for abdominal obesity Men Women Europid IDF >94 cm >80 cm Caucasian WHO >94 cm [increased risk] >102 cm [still higher risk] >80 cm [increased risk] >88 cm [still higher risk] United States AHA/NHLBI [ATP III] >102 cm >88 cm Canada Health Canada >102 cm >88 cm European European cardiovascular societies >102 cm ?88 cm Asian [including Japanese] IDF >90 cm >80 cm Asian WHO >90 cm >80 cm Japanese Japanese obesity society >85 cm >90 cm China Cooperative task force >85 cm >80 cm Middle East, Mediterranean IDF >94 cm >80 cm Sub-Saharan African IDF >94 cm >80 cm Ethnic Central and South American IDF >90 cm >80 cm. Waist circumference cutoffs are recommended for the diagnosis of abdominal obesity according to ethnicity and gender (8,9). In 2009, a method to standardize the diagnosis of metabolic syndrome was established, upon discussions held by the International Diabetes Federation (IDF) and the American Heart Association/National Heart, Lung, and Blood Institute. In this context, it was suggested that ethnicity and gender should be considered for the diagnosis of AO (9)

In decades past, many clinicians were taught in medical school that the adipose cell is a vehicle for energy storage and nothing more. Today, there is a different perception of the adipose cell; specifically, it is an active endocrine organ that communicates with gut hormones and a master regulator in the brain to control appetite and satiety. It also exerts pathologic effects on other organs and critical metabolic and immunologic processes .Four major hormones-ghrelin, insulin, peptide YY (PYY) from the gut, and leptin from fat tissue-participate in appetite and satiety regulation in communication with each other and the central control of energy balance, the arcuate nucleus in the hypothalamus. Ghrelin is a short-term appetite hormone, the "hunger hormone", that brings on feelings of hunger at mealtimes. Secreted in the gastric fundus, ghrelin rises immediately before meals and falls as insulin levels rise in response to the meal(10,11). It also increases during weight loss, which may be a factor in making successful weight loss so difficult. However, ghrelin levels decrease in persons who have had gastric bypass surgery, which may aid in maintaining weight loss (10). Insulin, in addition to its multiple other metabolic functions, acts as a satiety signal to the brain, causing feelings of fullness. PYY, secreted in the distal small intestine in response to food, signals satiety to the hypothalamus to counteract the influence of ghrelin. Levels of PYY are significantly lower in obese versus normal-weight persons,(8) but are elevated after gastric bypass(11). Leptin was the original "satiety factor," discovered to much excitement by Friedman and coworkers in 1994(12). This hormone is produced in adipose tissue in proportion to body fat; the more fat present, the more leptin secreted. Initially, it was hoped that exogenous leptin administration would be a "magic bullet" for curing obesity and establishing the condition as a metabolic disorder instead of a personal failing(9). Despite its effectiveness in mice with a genetic defect in the leptin molecule, exogenous leptin does not produce meaningful weight loss in obese humans, apparently because the brain becomes resistant to it. However, leptin is one of many neuro hormonal pathways that have evolved genetically to prevent starvation and ensure survival. In addition, the hypothalamus contains neurons that can either stimulate or inhibit food intake, and many of the gut hormones exert actions on both sides of the equation(13). The possibilities for routes to intervention among this wealth of pathways remain promising and rational in the search for weight control treatments. Current thinking now holds that fat tissue is an active participant in weight regulation. In one current theory, it is the basis of adiposopathy, defined by Bays and colleagues as pathogenic adipose tissue whose toxicity may be worsened by fat accumulation and a sedentary lifestyle in genetically susceptible individuals(14). This dysfunctional tissue releases increased amounts of free fatty acids (FFAs) and abnormal amounts of inflammatory factors such as cytokines from macrophages. Such changes can promote insulin resistance in skeletal muscle and the liver, increased insulin secretion, dyslipidemia, hypertension, and type 2 diabetes, all components of the metabolic syndrome, which increases the risk of atherosclerosis (14-16). Muscle biopsies in obese patients show that deposits of fat are stored in liver when fat can no longer be stored subcutaneously, with some cases resulting in steatohepatitis and eventually fibrosis. Excess fat may be associated with androgen elevations in women (or decreases in men); increases in plasminogen-activator inhibitor 1, which encourages thrombosis; and asthma, as a consequence of pro inflammatory changes. Even osteoarthritis may be an outcome of increased inflammation, although it is also mediated by the mechanical load of excess weight on the joints(17,18). Not everyone who is obese has metabolic syndrome or type 2 diabetes-although these are perhaps the most prevalent complications of obesity. Genetic susceptibility is yet another confounding component of obesity. The ability to differentiate genetically susceptible humans is not yet within reach. Better predictors of who will and will not respond to adiposity with endocrine and other consequences are still needed. In the meantime, ongoing research on appetite and satiety regulation has made it clear that obesity is a disease largely beyond an individual's control(19) rather than a function of inadequate willpower. The development and availability of medications and procedures that address the underlying pathobiology of obesity heralds a new approach to stemming the tide of the obesity epidemic.


This was a cross sectional population based study conducted in Sana'a city for a period of 2 years between April 2017 and April 2018. A sample of 1,118 adult Yemeni people (508 male and 610 aged This was a cross sectional population based study conducted in Sana'a city for a period of 2 years between April 2017 and April 2018. A sample of 1,118 adult Yemeni people (508 male and 610 aged This was a cross sectional population based study conducted in Sana'a city for a period of 2 years between April 2017 and April 2018. A sample of 1,118 adult Yemeni people (508 male and 610 aged >18 years) was randomly selected. The data collection was from those attending Al-Kuwait University Hospital and Consultation Clinic. All the participants in this study underwent complete clinical history (regarding their age, occupation, habits, any history of hypertension, diabetes mellitus, dyslipidemia and medication). Anthropometric measurements included measurement of waist circumference and systolic and diastolic blood pressure. Waist circumference was manually measured on standing subjects with soft tape midway between the lowest rib and the iliac crest. WC was divided into abdominal overweight (85-95 cm in males and 80-90 cm in females) and abdominal obesity groups (WC > 95 cm in males and >90 cm in females) (20,21 ). WC >85 cm in males and >80 cm in females were defined as elevated WC. Two blood pressure recordings were obtained from the right arm of patients with standard mercury sphygmomanometer in a sitting position after 10 minutes of rest; measurements were taken in 3-5 minute intervals and the mean values were calculated. Blood pressure was classified as normotensive (SBP < 120 mmHg and DBP < 80 mmHg), pre-hypertensive (SBP: 120-139 mmHg and/or DBP: 80-89 mmHg) and hypertensive (SBP >140 mmHg and/or DBP ? 90 mmHg) by the Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (22,23); fasting blood glucose, total cholesterol, triglyceride, LDL and HDL cholesterol were measured.

The American Diabetes Association criteria was used to classify FBG as normal glucose (FBG < 5.6 mmol/L), impaired fasting glucose (IFG) (FBG >5.6 mmol/L <FBG < 7.0 mmol/L), and diabetic (FBG >7.0 mmol/L).

Type 2 diabetes mellitus was defined according to the American Diabetes Association (24) A1C >6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay or FPG >126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 hours. In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing or 2-hour plasma glucose > 200 mg/dl (11.1mmol/l) during an OGTT. The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water. In the absence of unequivocal hyperglycemia, result should be confirmed by repeat testing or in a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose 200 mg/dl (11.1mmol | l).

Dyslipidemia was classified according to ATP III, TG: Normal < 1.69 mmol/L, Borderline high 1.69-2.26 mmol/L, High 2.26-5.65 mmol/L, Very high >5.65 mmol/L; TC: Desirable < 5.17 mmol/L, Borderline high 5.17-6.24 mmol/L, High >6.24 mmol/L; HDL-C: High 1.56 mmol/L, Optimal 1.03-1.56 mmol/L, Low <l.03 mmol/L; LDL-C: Optimal <2.59 mmol/L, Near optimal 2.59-3.38 mmol/L, Borderline high 3.38-4.16 mmol/L, High 4.16-4.94 mmol/L, Very high >4.94 mmol/L.(25).

Metabolic syndrome was diagnosed by the presence of three or more of the following criteria (26).
• Fasting glucose ?100 mg/dL (or receiving drug therapy for hyperglycemia)
• Blood pressure ?130/85 mm Hg (or receiving drug therapy for hypertension)
• Triglycerides ?150 mg/dL (or receiving drug therapy for hypertriglyceridemia)
• HDL-C < 40 mg/dL in men or < 50 mg/dL in women (or receiving drug therapy for reduced HDL-C)
• Waist circumference >102 cm (40 in) in men or >88 cm (35 in) in women; if Asian American, >90 cm (35 in) in men or >80 cm (32 in) in women (The international diabetes federation [IDF] criteria allow the use of a body mass index [BMI] >30 kg/m2 in lieu of the waist circumference criterion.)

Statistical analysis was undertaken using the Statistical Package for the Social Sciences (Windows version 13.0; SPSS, Chicago IL USA). Differences between groups were tested statistically using the Chi square test for categorical and T test for numerical variables. Data were considered statistically significant when the p-value was < 0.05.


A study sample included 1,118 persons aged between 18-83; of them 508 (45.4%) were male and 610 (54.6%) were female . The Mean age ± SD was 47.4 ±10.2 years, with an age range of 30-77 years with no significant age difference between men and women.

The prevalence of abdominal obesity according to WC was 24.5%. The physical and metabolic characteristic of the study population by gender are shown in Table 1. Women have significantly higher prevalence of abdominal obesity, systolic and diastolic BP, high serum TG, high LDL, low serum HDL as well as high prevalence of MS.

Table 1: shows the clinical and laboratory characteristics of the study group

Table 2: The prevalence of both clinical and laboratory characteristics between obese and non-obese

The highest prevalent comorbidity in patients with abdominal obesity was high BP (41.3%), followed by high serum TG (40 %), high prevalence of MS (40%), low serum HDL (37.8%) high LDL ( 20.1% ) raised fasting blood glucose (22.1%) than those without abdominal obesity (5.5%, 31.3%, 16.6%, 8.5%, 12.5% and increased FBS 10% respectively).


The prevalence of abdominal obesity is increasing dramatically worldwide (27,28). In the United States, the overall age-adjusted prevalence of abdominal obesity increased significantly from 46.4% (95% confidence interval [CI], 42.1%-50.8%) in 1999-2000 to 54.2% (95% CI, 51.3%-57.0%) in 2011-2012 (27).

Obesity is a major risk factor for hypertension, type 2 diabetes, coronary heart disease, and certain types of cancer(29,30,31,32,33). Obesity is classified as general obesity (defined as body mass index > 30 kg/m2) and abdominal obesity (defined as waist circumference [WC] > 90 cm for men and WC > 80 cm for women), based on World Health Organization (WHO) recommendations for Asians(34,35). In particular, abdominal obesity has a close relationship with central fat localization and cardiovascular disease, independently of general obesity(36,37,38). The overall prevalence of abdominal obesity among the study population in the present study was found to be 24.5% which is comparable to that found in Nigeria (21.8%) [39] , Tanzania (24.8%)(40) and Brazil (30%) (41), lower than that was found in South Asia (68.9%) (42), USA (56%)(43) and Mexico (74%) (44). The prevalence of abdominal obesity in population-based studies from the Arab world was found to be variable and was in the range of 23 % to 46.5% (45,46).

In our study, there was significant gender difference which is consistent with the findings from Saudi Arabia (46) and Taiwan (23).

The highest prevalent abdominal obesity co morbidity in our study population was hypertension (41.3%)(47) followed by atherogenic dyslipidemia as high TG (40%) low serum HDL (37.8%) and high serum LDL ( 20.1%) (48), followed by higher prevalence of MS (41.3%) (49.50) and raised fasting blood glucose (22.1%) (51) than those without central obesity (5.5%, 31.3%, 16.6%, 8.5%, 12.5% and increased FBS 10% ) respectively .
This finding was in keeping with the existing knowledge that obesity is clearly linked to essential hypertension. Hypertension was also the most common comorbid condition in abdominal obese subjects (47, 48). The mechanism linking abdominal obesity with hypertension might be explained by the activation of the renin-angiotensin-aldosterone system which primarily leads to the activation of the sympathetic activity, promotion of the leptin resistance by increased pro-coagulatory activity. The cumulative effect of this cascade is endothelial dysfunction and inflammatory changes. Additional mechanisms include the enhanced renal sodium reabsorption with a resultant increase in volume expansion usually observed