Changes in the use of online and blended learning

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Data from the National Health and Nutrition examination survey showed a remarkable and linear relationship between rise in BMI and systolic, diastolic, and pulse pressures in the American population. In regression models corrected for age-related rise in BP, a BMI gain of 1.7kg/m² in men and 1.25kg/m² in women or an increase WC of 4.5cm for men and 2.5cm for women corresponds to an increase in SBP of 1mmHg.²⁹ Obesity by itself possibly accounts for 78% and 65% of essential hypertension in men and women, respectively, according to data from the Framingham cohort.²⁹

Approximately 80% of people with hypertension in US are overweight or obese.⁴¹ Fadupin et al in Ikeja using BMI ≥ 25 reported a prevalence of 78.2% (50.5% were females against 27.6% male subjects) among adults attending Lagos state Hospital.⁷¹ Amodu et al in a hospital based study in Abuja found that 71.6% of 109 female hypertensive were obese as against 50.5% of 184 men. The study used BMI value ≥ 30.⁷²

Obesity is associated with activation of Renin Angiotensin System (RAS), increased sympathetic nervous system (SNS) activity and hyperinsulinaemia, all of which may contribute to sodium re-absorption and associated fluid retention and may therefore contribute to renal obese hypertension.^29,73 Persistent obesity causes renal injury and functional nephron loss, contributing to elevated BP, which in turn leads to further renal injury, thereby setting off a vicious cycle of events leading to further elevated BP and renal injury.²⁹

Intra abdominal fat which is lipolytically more active than the fat elsewhere, releases large amounts of free fatty acids (FFA) into the blood stream and then to the liver through the portal vein.^8,25,74 In the liver, it activates hepatic afferent pathways that may lead to sympathetic activation leading to raised BP.⁸ The increased FFA also results in the generation of oxidant stress molecules, depression of Nitric oxide (NO), production and impairment of endothelial relaxation function,

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hyperinsulinaemia which all promote atherogenesis and atherosclerosis.²⁵ FFA levels in obese subjects are approximately two-fold higher than in lean subjects.²⁹ Visceral fat is resistant to the antilipolytic effects of insulin, which may contribute to postprandial hyperlipidaemia and hyperglycaemia and in turn, to insulin resistance.⁷⁴ Acute exposure of skeletal muscle to elevated levels of FFA induces insulin resistance, whereas chronic exposure of the pancreas to elevated FFA impairs β-cell function.⁷⁴ Observational evidence suggested a two fold increase in the Ischaemic heart disease association with elevated plasma FFA after correction for non-lipid risk factors.⁷⁴

The systemic RAAS (Renin Angiotensin Aldosterone system) seems to be activated in obesity despite a state of volume expansion and sodium retention.⁷³ Elevated serum aldosterone levels have been reported in the obese and it is postulated that a yet unidentified factor (possibly a fatty acid) derived from adipose tissue causes the release of a hepatic factor that in turn, steps up aldosterone synthesis.²⁹ Also it is becoming increasingly evident that adipose tissue possesses a local RAAS that plays an important role in adipose tissue function. Studies suggest that adipose tissue angiotensinogen mRNA expression is higher in abdominal than subcutaneous adipose tissue and therefore may be associated with increased cardiovascular risk.²⁹ Fat cells possess the capability to synthesize all components of the RAAS.²⁹ Despite the fact that expression of the Angiotensinogen gene is lower in the obese, the high Angiotensin II levels in circulation may be derived from the huge fat cell mass, resulting in hypertension.²⁹

The presence of both obesity and hypertension in a patient results in a mixed pattern of cardiac hypertrophy, caused by an elevation in both cardiac preload and afterload.²⁹ Obesity results in increased preload due to an expanded vascular volume while the high after load can be accounted for by the presence of hypertension and SNS activation.²⁹ After adjustment for established risk

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factors, the risk of heart failure increases by 5% in men and 7% in women for each BMI increment of one (Kencharah et al 2002). Compared to subjects having a BMI below the obesity range, obese subjects have doubled the risk of heart failure, after adjustment for co-morbid risk factors.²⁹ Autopsy data from the Mayo Clinic reveal that the average cardiac mass is 467g in obese hypertensive subjects, compared with 367g in obese individuals without heart disease and 272g in non-obese-hypertensive subjects. Since left ventricular hypertrophy itself is a major risk factor for sudden death and death due to progressive cardiac decompensation, it may partially explain the increased incidence of cardiovascular morbidity and mortality in the obese. Mononuclear cell infiltration in and around the sino atrial node, with fat deposition all along the conduction system is present in the myocardium of obese individuals. Lipomatous hypertrophy of the inter atrial septum also has been noted in obesity.²⁹ All these changes make the myocardium in the obese-hypertensive an ideal substrate for cardiac arrthythmia and sudden death.²⁹

Adipose tissue in general and central adiposity in particular is recognized as a rich milieu and source of inflammatory cytokines, such as TNF-α (Tumour necrosis factor-alpha), IL-6(interleukin) and CRP(C-reactive protein), and Plaminogen activator inhibitor (PAI-1).^29,70,74 TNFα is a paracrine mediator in adipocytes and appears to act locally to reduce the insulin sensitivity of adipocytes and appears to act locally to reduce the insulin sensitivity of adipocytes.⁷⁰ This action would tend to exacerbate FFA release, inducing an atherogenic dyslipdaemia.^29,70 TNFα also increase the secretion of other inflammatory mediators. IL-6 is a systemic adipokine, which not only impairs insulin sensitivity but is also a major determinant of hepatic production of C-reactive protein, the most important source of this inflammatory maker.⁷⁰ Circulatory levels of C-reactive protein are elevated in subjects with abdominal obesity, and conversely subjects with elevated C-reactive protein tend to have intra-abdominal adipose C-reactive protein concentration

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is associated with cardiovascular risk.⁷⁰ It is a marker of increase risk of CHD or stroke. PAI-1 is secreted from intra-abdominal adipocytes, although mainly from platelets and the vascular endothelium.^29,70 This acute phase protein is elevated in inflammatory states and promotes a pro-coagulation state by inhibiting tissue plasminogen activator, thus increasing the risk of an intravascular thrombus, Plasma PAI-1 levels are increased in abdominal obesity subjects and are predictive of adverse cardiovascular outcomes.⁷⁰ As such, obesity has been suggested to be a low-grade inflammatory condition important in the causation and progression of hypertension and atherosclerosis. Increased risks for thrombosis may contribute to a high incidence of heart disease and stroke in obesity.²⁹ Obesity is associated with polycythaemia and evidence exist that hypercoagulation and impaired fibrinolysis activity are related to BMI or WHR.²⁹

Hyperinsulinaemia, hyperleptinaemia, hypercortisolaemia, renal dysfunction, altered vascular structure and functions, enhanced sympathetic and RAS activity and blunted natriuretide peptide activity stand out as major contributory mechanism to obesity hypertensive syndrome.²⁹

These responses individually and interdependently, lead to a substantial increase in cardiovascular disease morbidity and mortality, including hypertension, CHD, congestive heart failure, sudden cardiac death, stroke and end stage renal disease.^29,34,75