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For many years since the concept first came up, many people in the medical profession have come up to support the hypothesis that the fat mass of the body is subject to homeostatic regulation. To understand this hypothesis better, one has to find answers to these two questions; what are the molecular and physiological mechanisms involved in matching food intake and energy expenditure to promote body fat content stability? And how can obesity be so common and yet fat mass is subject to homeostatic regulation? Arguments have been raised that body systems that control energy homeostasis evolved basically to protect bodies against loss of weight but not weight gain. This essay therefore looks at how nutrition, obesity and Atherosclerotic Cardiovascular Disease are related.
The ease with which people gain weight seems to contradict the concept that there is a system that controls body weight. Perhaps this can be explained better from an evolutionary perspective, where by one can say that the ability for individuals to reproduce and survive in habitats with scarce food resources led to the strong selection bias that was tilted more in favor of the regular systems that protected against deficits in body fat. Changes in the body fat stores generate homeostatic responses that involve the two sides of the energy balance equation. These persist until there is complete recovery of the body fat content. For instance, in times of energy deficit, there will be an increase in hunger as the rate of metabolism reduces. This combination makes sure that there is fast and efficient recovery of the weight that was lost as soon access to food is restored. These metabolic responses and adaptive feeding engage brain pathways that detect changes in the energy stores of the body and generate powerful and opposing reactions aimed at energy balancing. Those pathways that stimulate the intake of food and promote weight gain are called anabolic effector pathways and those that enhance anorexia and the exhaustion of the body fats are called catabolic effector pathways. These two pathways are always regulated in a reciprocal manner whereby an increase in the activity of one, is accompanied by a decrease in the other. For instance, whn a person is fasting, there is an inhibition in the catabolic pathways and activation in the anabolic pathways. This allows the body to effectively alter both sides of the energy balance equation. It is established that these pathways sense changes in the body with the help of leptin and insulin hormones which circulate the body in proportions that are equal to the body fat mass and enter the brain. It is in the brain that they bind to and also activate there respective receptors on the target neurons’ plasma membrane. Low concentrations of these hormones increase energy intake reducing energy expenditure at the same time. There are many neurons involved in theses processes. The neuronal systems are hard-wired in their functions in generating a state of positive balance in energy and also weight gain. As it has been shown, this bias towards body weight gain by the body activities causes increased body mass in many individuals. This in turn contributes to a large extent in the many cases of atherosclerotic cardiovascular disease, not forgetting the nutritional habits of individuals (Lopaschuk, Folmes & Stanley 2007)
Cardiovascular diseases that majorly affect the world today are atherosclerosis and hypertension. These two are affected to a large extent by diet and they can be looked at basing on the nutrition of individuals. But looking at nutrition as a cause of cardiovascular disease is not an easy task as it involves different groups of people each with different dietary habits. Atherosclerosis is a chronic disease that inflames the hemodynamically determined areas in the large and medium size arteries. It is usually characterized by accumulation of cholesterol and esters in the walls of the vessel. Obesity on the other hand is a nutritional disorder that arises from an imbalance in the body energy intake and consumption; it is also as a consequence of reduced physical activity. It is closely associated with increased mortality and morbidity from various diseases including cardiovascular diseases such as atherosclerosis. The many risk factors point to the fact that it is caused by metabolic syndrome (Getz & Reardon 2007)
A cross-sectional study was carried out to evaluate the association bbetween the circulating insulin level and the angiographic characteristics of coronary artery in 507 patients who went through coronary angiography for known or suspected coronary atherosclerosis.
The coronary arteries were first cannulated using the Judkins technique with 5F catheters. This was recorded on a Kodak 35-mm cine-film at a rate of 30 frames per second. Angiograms were then obtained and reviewed by experienced cardiologist that had no information on the patients. The evaluation of the cinefilms was then done using the Gensini score system that describes the extent and severity of the alterations of the vessel wall. Habits of alcohol intake and cigarette smoking were also tested in form of a questionnaire. People were then grouped as smoking (former and current) and never smoking, drinking (former and current) and never drinking.
Anthropometric were done twice and the average used in the analysis. Height, weight together with body mass index and blood pressure measurements were also done.
Blood samples of 12 hour fasting were drawn and plasma stored at -700C . This was done immediately after centrifugation until they were analyzed.
The analysis of data was done using SPSS for windows. The patients were then put into three categories with high, middle and low Gensini score using tertile values as cut of points making sure that each group had an equal or near equal number of patients to avoid bias in statistical analysis.
Patients in the groups showed an increasingly higher Gensini score, the gender and smoking distribution was different but the drinking status was similar in the three tertiles. The distribution level of BMI, SBP, TCH, TG, and fasting LDL-C, among the three groups was similar, but age, diastolic blood pressure, FBG, fasting HDL-C and TI was different in the groups (Schwartz & Niswender 2004)