The occurrence of chronic inflammation is associated with an increased risk of cardiovascular disease [3]. Low-level chronic inflammation disrupts cardiovascular function and it can even accelerate atherosclerosis [7]. According to the INSPIRE ME IAA Study, increased abdominal circumference associated with visceral fat is strongly associated with cardiovascular disease [8]. Epicardial adipose tissue is visceral fat deposited in the chest cavity, which covers the coronary arteries and muscular tissue of the heart. Epicardial adipose tissue is linked with high-risk plaques and atherosclerosis [9]. It has been found that individuals who suffer from coronary artery disease (CAD) have increased epicardial adipose tissue thickness and volume, as compared to individuals devoid of CAD [9].

Hyperinsulinemia and insulin resistance are both associated with an increased risk of type 2 diabetes mellitus [10]. In the body, visceral fat is a source of lipids. These lipids are transported to the liver via the hepatic portal vein. The accumulation of these lipids interferes with insulin signaling in liver cells [6]. This occurs because excess FFAs can alter blood glucose levels through several mechanisms, including excess of acetylcoenzyme A, as well as a reduction of nicotinamide adenine dinucleotide, ATP and citrate [4]. Increased levels of adipokines and cytokines are also linked to visceral fat. The latter increased levels of cytokines can deter insulin receptor kinase activity, thus disrupting insulin signaling by inhibiting the transmission of chemical responses within cells [7]. In addition, obesity causes a decrease in insulin sensitivity of the liver and thereby leading to insulin resistance [10]. Thus, the liver extracts less insulin than usual. Furthermore, visceral fat causes an increase in the amount of secreted insulin which enters the blood. The decrease in extracted insulin by the liver and increase in the amount of secreted insulin entering the blood can cause hyperinsulinemia.

The metabolism of lipoproteins is controlled by hepatic triglyceride lipase (HTGL) [11]. When the concentration of post-hepatic HTGL is high, then the serum concentration of high-density lipoprotein (HDL) cholesterol is low. In visceral adipose tissue there is high HTGL activity. Thus, visceral fat causes low levels of HDL cholesterol (also referred to as “good cholesterol”). Visceral fat also contains high levels of triglycerides. The abundance of triglycerides is linked with high concentrations of very-low-density lipoprotein (VLDL) as well as lowdensity lipoprotein (LDL). Thus, visceral fat can cause increased concentrations of VLDL and LDL in the blood.

Hypertension is a condition in which there is elevated systemic blood pressure. Adiponectin is an adipokine that is secreted by adipocytes; however, in obesity, there are decreased levels of adiponectin [12]. Adiponectin is a vasodilator and it helps to regulate blood pressure. In obese individuals, subcutaneous adipose tissue expresses a greater amount of adiponectin than in visceral adipose tissue. Thus, excess visceral adipose tissue is a factor which can lead to the development of systemic hypertension through low-level chronic inflammation and decreased levels of adiponectin.

Obesity is associated with an environment that promotes inflammation and thrombosis [13]. This type of environment can lead to the development of stroke. Specifically, it has been shown that an increase in abdominal obesity leads to an increased risk of cerebral thrombosis. In the human body, the carotid arteries provide the majority of blood to the brain. The Multicultural Community Health Assessment Trial (M-CHAT) Study demonstrated that increased abdominal girth, in particular, visceral adipose tissue is associated with the development of carotid atherosclerosis [14].

As we previously discussed, obesity is associated with low-level chronic inflammation. In this environment, macrophages are triggered and these macrophages are able to enter tumors. When the macrophages enter tumors, they produce cytokines, prostaglandins and angiogenic factors, which in turn aid tumor growth [15]. Plasminogen activator inhibitor-1 (PAI-1) is a protein that is made in visceral white adipose tissue. Increased PAI-1 levels can lead to the formation of new blood vessels, which can promote tumor cell growth and cause the tumor cells to metastasize [15].

Despite a heritability of 48% - 57% for visceral fat [6], there are several methods to maintain low-levels of abdominal fat. Exercise is a critical way of reducing abdominal fat. Intense physical activity can improve overall health [2]. It is recommended that individuals partake in at least 30 minutes of high-intensity physical activity daily. Additionally, resistance strength training is important, because it helps maintain muscle mass when an individual is trying to lose weight via diet [2]. Moreover, a well-rounded low-glycemic diet is effective in combating obesity. Effective diets are diets that reduce the total energy intake and result in the most weight loss. Converting from a diet that includes refined grain foods to a diet that includes whole grain foods has shown to decrease visceral fat [16]. It has been found that two drugs are effective in reducing belly fat: Sibutramine and Orlistat [2]. Sibutramine prevents the reuptake of certain neurotransmitters, which results in decreased food intake. On the other hand, Orlistat decreases the absorption of triglycerides in the small intestine. In severe cases of obesity, gastric bypass surgery can be performed. In this type of surgery, the stomach is stapled and this creates a small pouch. This reduces food intake, and since a portion of the stomach and a portion of the small intestine are bypassed, certain nutrients cannot be absorbed.

Hormonal deficiencies can also be the root of abdominal fat. Adults with acquired human growth hormone (HGH) deficiency have increased visceral adipose tissue [17]. As the extent of obesity increases in adults, growth hormone secretion decreases within the body. Even in nonobese individuals, abdominal fat has shown to decrease growth hormone secretion [17].

In men, testosterone is vital in order to decrease fat and to preserve muscle. Therefore, testosterone deficiency can lead to obesity. In addition, low levels of testosterone can lead to the development of metabolic syndrome and type 2 diabetes mellitus [18]. This occurs because low levels of testosterone lead to increased adipokine release by the adipocytes, which in turn can lead to the chronic low-level inflammatory state associated with obesity. When testosterone is restored to an adequate level, it reduces triglyceride storage and lipoprotein lipase (LPL) activity [18].

Dehydroepiandrosterone (DHEA) is a hormone secreted by the adrenal gland. Decreased levels of DHEA sulfate are associated with obesity. It has also been found that DHEA sulfate stimulates adiponectin gene expression in visceral fat [19]. Therefore, DHEA sulfate deficiency can lead to decreased levels of adiponectin, and subsequently abdominal obesity [19].