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Obesity and its effects on cardiovascular system

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Obesity and its effects on cardiovascular system

Obesity is quite a complex disease that involves excessive amounts of body fats. It is indicated by a high Body Mass Index(BMI). Body mass index is a division of weight against height, used to determine if a person is within an appropriate weight bracket according to their age, gender and height. According to BMI rates, the average is between 18.5 and 24.9, below that, is considered underweight. Between 25 and 29.9 is a symptom of excess weight. A body mass index that goes over thirty is a sign of obesity. Other factors that can be used to determine the health of a person’s weight and shape are waist-to-hip size ratio and waist-to-height ration. Obesity is caused by several factors and bears several health effects. In this study, I intend to discuss obesity, its causes and the impact it has on the cardiovascular system.

The first cause of obesity is the consumption of foods enriched with excess amounts of calories which get stored into the body as fats. Some of the foods that are listed include; fast foods, fried foods, processed foods and foods with high sugar levels. The second cause is living a sedentary lifestyle like working in offices instead of manual works, playing computer games instead of engaging in physical outdoor games and always using cars to go places instead of working or cycling. The fewer the movements a person makes, the fewer the calories get burned in the body. The third cause is lack of enough sleep. Research shows that deprivation of sleep hours leads to changes in hormones by increasing ghrelin that increases appetite and reducing the production of leptin which is responsible for the suppression of appetite. The fourth cause can be some medications which lead to weight gain. Like glucocorticoids, some antidepressants, anticonvulsants especially gabapentin and medicines related to hypoglycemia like colbutamide. The fifth cause of obesity is gene-related. A faulty gene is known as the fat-mass, and obesity-related gene (FTB) is behind some obesity cases. Research indicates a connection between the gene and obesity, behaviours leading to obesity, increased food intake, craving for high-calorie foods and satiety, which is an inability to feel satisfied. The last cause connected to obesity is that it is self-perpetuating. According to research, the longer the period a person maintains an overweight lifestyle, the harder it is to lose weight. Usually, the more the body carries the fat, the less possible it becomes to burn fat due to a gene-protein named SLR 11.

First, obesity is a risk factor of Atherosclerosis. In previous medical terms, both conditions were considered as disorders related to lipid storage with accumulation of triglyceride in fat tissues and presence of cholesterol esters in the Atherosclerotic  plaques. In recent research terms, both diseases are said to be chronic inflammatory disorders marked by activation of adaptive and nonspecific immune occurrence. The pathogenesis processes of obesity and Atherosclerosis are based on some common factors. For both cases, they are triggered by lipids and free fatty acids that activate the process of inflammation. Inflammatory processes are behind the steps leading up to Atherosclerosis, from the beginning of endothelial dysfunction to the complications of atherosclerotic plaques,  and is connected to obesity and diabetes mellitus from insulin resistance. Fatty tissues produce adipocytokines responsible for insulin resistance, hypercoagulability, endothelial failure and systemic inflammation, hence activating atherosclerotic process. In the case of visceral obesity, this inflammatory adipocytokines are at their highest levels. So basically, obesity accelerates the process of inflammations and eventually Atherosclerosis.

The second risk factor brought about by obesity is coronary Heart Disease. Research indicates that Atherosclerosis starts some decades before the manifestation of coronary heart disease. In people with high body mass index, the atherosclerotic vascular lessons are more advanced in comparisons to those with an average body mass index. Further research shows that at least two decades of living an obese lifestyle is somewhat an independent risk in the causation of coronary heart disease. An increase of ten kilograms of the bodyweight increases a coronary heart disease possibility by twelve per cent. Coincidentally, systolic blood pressure rises by 3mm Hg as well as diastolic blood pressure by 2.3mm Hg. When it comes to Non-Stegment Elevation Myocardial Infarction (NSTEMI) which occurs in people who are obese, being overweight is a vital risk factor. The higher the boy mass index, the sooner NSTEMI starts to develop. A similar relationship is present in the case of Stegment Elevation Myocardial Infarction (STEMI). Obesity is an independent risk factor in the occurrence of STEMI. An increase in body mass index by a single unit causes an increase in the possibility of Ischemia by four percent and a rise of haemorrhagic strokes by up to six percent. The pro-thrombic condition in obese people is a contribution to the onset of acute coronary heart disease.

The third risk factor of obesity is Atrial fibrillation which is a branch of arrhythmia. An increase of BMI by one unit adds to the potential risk of development of Atrial fibrillation by four percent. Obesity causes the dilation of the left atrial and its eventual dysfunction. Increase in the close diameter of left atrial by a 5mm length is enough to put one at risk of paroxysmal atrial fibrillation by an odd of 1.39. Further studies indicate a relationship in an increase of epicardial fat tissue and atrial fibrillation. The epicardial fat leads to the development of atrial interstitial fibrosis. Infiltration of the myocardium, with connection to adipocytes, epicardial fat increase and fibrosis,  combine to form different atrial pulse which causes endocardial an epicardial electrical detachment. These processes combined, foresee to the growth of atrial re=occurrence, which is the electro=physiological foundation of atrial fibrillation in obese persons, atrial fibrillation reduces the refractory time of occurrence for the atrial and pulmonary vein myocardial cells. Diet=induced obesity is associated with lengthened atrial conduction period and heterogenous pulse occurrence. The main reason behind atrial fibrillation is connected to low-grade inflammation as a result of obesity.

The fourth risk factor of obesity is ventricular tachycardia, another form of Arrhythmia and Sudden Cardiac Death (SOD). Increase in intracellular lipid content leads to impairment of repolarization from decreased potassium channel protein production levels, hence the SDC and ventricular tachycardia. Adipocytokines produced from epicardial fat tissues causes a decrease in the delayed rectifier outward currents so that they prolong duration and trigger activity of depolarization. Obese persons have an increased occurrence of premature contractions of the ventricular system in comparison to healthy persons. Aside from changes in wave intervals, other electro-cardio graphic changes tend to occur in people with obesity including; increased heart rate patterns, modified QRS voltage, flattening of T waves, prolonged QT interval durations and the leftward shifts of P waves.  Most of this Electro-cardio graphic (ECG) abnormalities can be reversed by a substantial loss of weight. Obese persons have increased heart rate and low variability from the defects caused by sympathovagal balance, which are factors connected to increased potential risk in myocardial infarction and SCD (Sudden Cardiac Death).

Lastly, obesity is related to heart failure. A recent study shows that an increase of Body Mass Index by one unit adds to the potential of heart failure occurrence by five percent in men and seven percent in women. For obese and overweight people, heart failure occurs ten years earlier than people with average body weight. The period of morbid obesity is closely connected to heart failure because, after twenty years of an obese lifestyle, potential of heart failure prevalence is increased by seventy percent. After thirty years, it is at ninety percent. Functional and structural changes of the heart in obesity contributes to the deterioration of myocardial function, known as obesity cardiomyopathy. Obese lifestyle causes heart failure by direct and indirect processes. Being overweight causes haemodynamic changes. Increase in cardiac output and blood pressure is observed because of an increase of five kilograms weight increases by 5mm Hg the systolic blood pressure. Obesity adds aldosterone levels and mineralocorticoid receptor expression, which is an agent of interstitial cardiac fibrosis, endothelial dysfunction and aggregation of the platelet. An increased volume of blood tends to cause venous backflow leading to preload of the ventricular system, which causes ventricular wall tension hence dilatation. Inflammatory cytokines that are known to increase obesity play a vital role in the development of heart failure. The inflammatory mediators alongside acute-phase proteins, lead to myocardial fibrosis that causes dilation hence diastolic and systolic heart failure. Triglyceride accumulation in cardiac muscles is mainly found in obese patients and is responsible for the generation of toxic metabolites like diacylglycerol and ceramide, which enhances apoptosis of cardiomyocytes. Obesity is an independent potential risk factor of heart failure.

In conclusion, excess weight is a background factor of cardiovascular diseases as a consequence of obesity itself and associated medical conditions like hypertension, sleep apnoea syndrome, insulin resistance and type 2 diabetes. In people who have an already established cardiovascular disease, mortality tends to be lower for obese people than those with average body weight, which is termed as the obesity paradox. In consideration of the increased rates of cardiovascular risk, frequent cardiology screening tests for obese individuals is imperative for early diagnosis and eventual treatment of subclinical health conditions.

Work cited

  1. Ng, T. Fleming, M. Robinson “Global, regional, and national prevalence of overweight and obesity in children and adults during 1980–2013: a systematic analysis for the Global Burden of Disease Study 2013,” The Lancet, vol. 384, no. 9945, pp. 766–781, 2014.
  2. Poirier, T. D. Giles, G. A. Bray “Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism,” Circulation, vol. 113, no. 6, pp. 898–918, 2006.
  3. Z. Rocha and P. Libby, “Obesity, inflammation, and atherosclerosis,” Nature Reviews Cardiology, vol. 6, no. 6, pp. 399–409, 2009.
  4. E. Shoelson, L. Herrero, and A. Naaz, “Obesity, inflammation, and insulin resistance,” Gastroenterology, vol. 132, no. 6, pp. 2169–2180, 2007.
  5. W. F. Wilson, R. B. D’Agostino, L. Sullivan, H. Parise, and W. B. Kannel, “Overweight and obesity as determinants of cardiovascular risk: the Framingham experience,” Archives of Internal Medicine, vol. 162, no. 16, pp. 1867–1872, 2002.

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