Impact of Obesity on Cardiovascular diseases

Obesity and Diet

The role of diet is crucial in the development and prevention of cardiovascular disease and is the key modifiable risk factor for heart diseases. The obesity is an epidemic which is spreading from low- to the middle-income countries as a result of new dietary habits and sedentary ways of life, fuelling chronic diseases and premature mortality.

This sneaky inflammation and the inflammatory factors when released increase the risk of developing atherosclerosis and the build-up of plaque in the walls of the arteries. Obesity also releases substances in the blood that can make plaque rupture, which then leads to heart attacks. The extra weight carrying does put the heart under increased stress, in particular during the relaxation phase of the cardiac cycle, which is known as the diastole. As the heart fills with blood, there’s higher pressure in the heart valves, which with over time, can lead to causing people to have heart failure symptoms.

Association between Obesity and Cardiovascular outcomes

As Obesity increases there are adverse cardiac events occurring in many ways, which may be indirectly mediated through risk factors associated with metabolic syndrome like diabetes, dyslipidemia, glucose intolerance, hypertension, and or effects from sleep disorders associated with obesity.  Metabolic syndrome is associated with central or abdominal obesity, which is associated with the distribution of fat predominantly in the abdominal viscera rather than the extremities in the body. Waist circumference or waist-hip ratio is useful ways of assessing this type of fat distribution and increased values confer additional cardiovascular risk. In abdominal obesity, there is an increase in the level of various inflammatory markers along with the occurrence of a prothrombotic state. The Obese patients have increased concentrations of many adipokines and other chemical mediators like interleukin-6, resistin, plasminogen activator inhibitor-1, tumor necrosis factor-alpha, retinol binding protein, acylation stimulating protein, lipoprotein lipase, cholesteryl ester transport protein, estrogens, leptin, angiotensinogen, and insulin-like growth factor-1, but these proteins have various adverse effects on the cardiovascular system by creating a pro-inflammatory and prothrombotic state as well as causing endothelial damage and vascular hypertrophy. There is also a higher incidence of sleep apnea/hypoventilation syndromes in obesity, which can also affect the heart in different ways.

Obesity also poses considerable challenges in making a precise cardiovascular diagnosis because of limitations in the physical examination as well as with various investigations like imaging studies, electrocardiograms (ECGs), and cardiac catheterization.

The direct effect of Obesity on the heart in obese individual results in cardiomyopathy which is also known as the adipositas cordis. Initially, it increases the fat content of the heart because of a metaplastic phenomenon and is not an infiltrative process. The various tissues of the heart, like the atrioventricular node, sinus node, right bundle branch, and the myocardium near the atrioventricular ring, are replaced by fat cells. The conduction defects can occasionally occur in the sinoatrial block, bundle branch block, and, rarely, an atrioventricular block which results in irregular bands of adipose tissue which may separate and cause pressure-induced atrophy in the myocardial cells. These adipose cells surrounding the heart valves may also secrete active molecules like adipokines, which indirectly cause injurious effects on the adjacent myocardial cells or the heart cells. Accumulation of triglycerides in nonfat cells like myocytes can also directly cause cell dysfunction due to lipotoxicity.

Heart Disease and Obesity Treatment

In addition to weight loss, the sodium restriction may be helpful in the treatment of heart disease, since high intake of sodium increases fluid retention in the body. There a number of series of medically supervised weight loss programs, starting from alterations in dietary and physical habits to pre-packed meals, pharmacotherapy and weight loss surgery, which can be used to make an impact on both cardiovascular diseases and obesity.

Childhood obesity starts in the womb?

The environmental pollutants which may also interfere with the fetal growth and influence health later, maternal exposure to especially traffic pollutants like as nitrogen dioxide, which can lead to babies being born with low birth weight may predispose the child to ill health to infant and adulthood.

Gestational diabetes

Gestational diabetes only happens during pregnancy. It means high blood sugar levels, but those levels were normal before pregnant. Sometimes after the baby is born, gestational diabetes usually goes away. Gestational diabetes makes more likely to develop type 2 diabetes, but it won’t definitely happen.

During pregnancy, the placenta makes hormones which can lead to a build-up of glucose in the blood. Usually, the pancreas can make enough insulin to metabolize. If not, the blood sugar levels in the blood will rise and can cause gestational diabetes. 

In any case, there are more deceptive impacts which aren't instantly known. There is an expanding theory that proves that the mothers eat less, weight and weight pick up in pregnancy, and complications of pregnancy such as gestational diabetes and preeclampsia can all affect the health of the child to be born. This happens in the longer term and to be a really imperative determinant of the risk of common infections like obesity and diabetes in later life.

In the last 20 or 30 years, researchers have followed up that the children born to those mothers and found that the experience of famine in utero was associated with quite significant defects on the health of the child such as increased obesity which in turn increases the risk of cardiovascular disease and abnormal blood lipids.

The emphases have now changed from the developed countries and are more likely recently to developing countries too, to the effects of maternal obesity, which is remarkably prevalent in the population. Any high-income country or a developed country now has the biggest man-made problem known as obesity. Those geographical reasons which are now showing the greatest rise obesity are those which historically have been undernourished or have suffered feminine. Countries like South Africa, for example, now have a new growing problem called maternal obesity, as the region transitions from dietary deprivation to dietary plenty.

Researchers have therefore been looking at the relationship between maternal obesity, the weight the mother puts on in pregnancy which leads risks to the child. The first thing to be noted is that there is an immediate and very obvious risk to the obese mother in relation to a heightened chance of developing diabetes in pregnancy. In turn, this can lead to a child being born too large or heavy.

Large for gestational age infants, as these babies are also known to have problems at delivery in that there a higher risk of the mother might not be being able to deliver the baby vaginally, with a greater chance for a cesarean section, and a higher risk of damage during delivery and of stillbirth and various other problems.

Babies that are born too large tend to become overweight adults and suffer from Obesity. There is a close association of adiposity at birth, that's the amount of fat, and adiposity in later childhood.

Children who are overweight at nursery school age tend to become obese adolescents, and obese adolescents have a higher risk of obesity in adulthood which leads to a variety of health conditions. Increasing evidence, therefore, suggests that being developed in the womb in the face of maternal obesity and maternal diabetes, the unborn has to experience a persistent effect of obesity and diabetes.

The mother is feeding the child the same diet as she might feed herself, so of course that's going to be the case, but the statisticians have adjusted for many of those socioeconomic and family environment factors, and still find that there is a relationship between development in utero in relation to obesity and excessive maternal weight gain and gestational diabetes in turn leading to the risk of obesity and diabetes developed in the offspring.

According to the few recent studies that mean the utero environment can definitely lead to obesity in the child, observational, longitudinal studies like these can never really conclusively recommend causality.

By Blocking Single Gene, Obesity Could Be Prevented

Obesity may be a major worldwide health epidemic that's evaluated to decrease life expectancy by 6–20 a long time, and is related with an increased risk for cardiovascular disease, type 2 diabetes, and cancer. The regulation of whole-body digestion system includes the integration of multiple organ systems, and disrupting this homeostatic balance underlies the developing epidemic in obesity, metabolic disease, and associated comorbidities.

Researchers have long worked to develop approaches that can boost non-shivering thermogenesis (NST)—the process by which calories are used as heat, rather than stored as fat—as a mechanism to burn excess calories and so offer assistance treat obesity. In any case, the body operates numerous feedback mechanisms that generally act to suppress unnecessary caloric consumption. In evolutionary terms, these forms have helped to preserve energy in times of hardship. Mammals have had to cope with pressures of limited nourishment resources and environmental exposure, developing mechanisms for both long-term storage of calories and their use for functions such as thermogenesis when required.

When a single gene called as the RCAN1 was removed in mice and in turn were fed, they failed to gain weight, even after gorging on high-fat foods for prolonged periods. A comparative approach that restrains this quality will too be compelling with people to combat corpulence and genuine diseases like diabetes. The study used a large genetic screen in rodents to identify novel genetic candidates which will cause obesity, potentially paving the way for new sedate therapies. We know a lot of individuals battle to lose weight or indeed control their weight for a number of different reasons. The discoveries in this study may mean creating a pill which would target the function of RCAN1 and may result in weight loss.

Obesity could be a major worldwide health plague, resulting in expanded hazard of genuine maladies like sort 2 diabetes, and heart infection, but roads for compelling helpful medications are lacking. There are two sorts of fat within the human body – brown fat burns vitality, whereas white fat stores vitality. Blocking RCAN1 makes a difference to convert undesirable white fat into brown

fat, showing a potential treatment method within the fight against obesity. We have already developed an arrangement of drugs that target the protein that this quality makes, and we are present in the handle of testing them to see on the off chance that they repress RCAN1 and whether they might speak to potential new anti-obesity drugs. In light of our results, the drugs we are developing to target RCAN1 would burn more calories whereas individuals are resting.

It implies the body would store less fat without the requirement for an individual to reduce food utilization or work out more. Brown fat tissue is especially inexhaustible in newborns and in hibernating mammals. It additionally shows and metabolically active in adult people, but its predominance diminishes as human’s age. Its primary work is thermoregulation. In expansion to warm created by shivering muscle, brown fat tissue produces heat by non-shivering thermogenesis. The researchers say these discoveries open up a potentially simple treatment but further considers are required to determine in case they translate the same comes about to people.