Non-Alcoholic Tumor Disease

Ideal cardiovascular health consists of seven factors, and very few individuals in the U.S. population actually meet all seven factors. The liver is also a critical organ in that it is essential for metabolic activities, and metabolic complications of the liver related to obesity result in non-alcohol-related fatty liver disease in both child and adult

According to the Merck Manual (2013), hyperlipidaemia is the increased synthesis of hepatic lipoproteins. Marieb (2012) explains that lipoproteins enable fat, fatty acids and cholesterol to circulate in the blood stream. They cannot do this alone due to their insolubility so they use lipoproteins as a type of transport. Nelson (2013) highlights four different varieties of lipoproteins which are chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL).

As discussed in the research by Birkenfeld, the accumulation of fatty deposits decreases the metabolic capacity of the liver, and causes inflammation of the hepatic tissue, causing hepatomegaly. This deposit of triglycerides in the liver instead of the adipose tissue is thought to be caused by altered levels of cellular products involved in the uptake of fatty acids. While the concentrations of enzyme lipoprotein lipase, fatty acid transport proteins, and FAT/CD36 are typically high enough in the muscle to cause lipid uptake into adipose tissue, it is inhibited in insulin-resistant NAFLD patients. Insulin plays a key role in the action of lipoprotein lipase. Without insulin the normal uptake of lipids to adipose decreases, and their uptake in the liver increases. This is shown by the disproportionally high level of lipoprotein lipase, fatty acid transport proteins, and FAT/CD36 in the liver to the bodily adipose tissue. (3)

The World Gastroenterology Organization (WGO) has recently declared NALFD as most common cause of liver disease. Obesity is an increasing problem not only in the UK but worldwide. An estimated 26% of the adults in the UK are considered to be obese 1, 2. Obesity induced metabolic syndrome may lead to NAFLD, which can progress to Nonalcoholic Steatohepatitis (NASH), and in turn to advanced fibrosis and an increased risk of Hepatocellular Carcinoma (HCC) 2, 3.

Obesity also affects insulin resistance by having an elevated number of free fatty acids (McCance & Huether, 2014). When these levels are elevated it causes a chain reaction with the body being able to get insulin and making tissues not sensitive to insulin (McCance & Huether, 2014). These alterations can cause not only changes to

Giving the fact that NAFLD is usually an asymptomatic disorder, it is often unrecognized in everyday clinical practice. Namely, most patients with NAFLD have no symptoms, and aminotransferase levels which are used as a marker of liver damage, are within normal values in almost half of all patients. NAFLD is strongly associated with type 2 diabetes mellitus (T2DM) and has been linked to increased cardiovascular disease (CVD) risk. It is characterized by insulin resistance and mitochondrial dysfunction6. Indeed, there is a gradual increase in the severity of insulin resistance in the range of NAFLD which may contribute to the evolution of liver damage. Also, it is associated with an increased risk of kidney disease in subjects with multiple CVD

Considering this fact, Rowena has both forms of risk factors; she is 48 years (Non-modifiable), morbidly obese and has a history of heavy smoking which are both examples of the modifiable risk factors of NIDDM. Secondly, overweight and obese patients with abdominal fat accumulation suffer from systemic low-grade inflammation. This type of inflammation is characterised by, elevated levels of fatty acids and circulating pro-inflammatory cytokines. These can mimic with normal functions of insulin and in effect cause insulin resistance according to (Van Greevenbroek, Schalkwijk, & Stehouwer, 2013).

Early initiation of lipid-lowering therapy and lifestyle measures might modify the clinical outcome. These treatment initiatives have especially improved the prediction of HeFH. All of the medications used for heterozygous FH are also used to treat homozygous FH, such as bile acid absorbing resins, drugs “Shatins” are used. People with homozygous FH often undergo LDL apheresis, a process by which blood is removed through the patient’s vein and LDL is filtered out before the blood is passed back into a different vein, similar to dialysis. Some successful cases for homozygous FH patients undergo a liver transplant in order to normalize LDL levels, but homozygous FH is still harder to be treated. Therefore the nutrition therapy (lower cholesterol foods) is very important for the FH patients to focus on, which can manage the healthy lifestyle to avoid the bad cholesterol was

ALD signifies a series of clinical illness that range from fatty liver to hepatic inflammation and necrosis (alcoholic hepatitis) to progressive fibrosis (alcoholic cirrhosis).3 Furthermore, excessively drinking alcohol increases the chance of other liver diseases progressing, such as virus-related chronic hepatitis, increasing the threat of hepatocellular carcinoma.6-8

Deposition of lipid within the liver represents part of an abnormal lipid partitioning pattern, most commonly associated with increased intra-abdominal fat. The typical obese child with NAFLD will usually manifest other components of the insulin resistance syndrome such as dyslipidemia, hypertension and altered glucose metabolism. As liver steatosis itself is usually asymptomatic, a high index of suspicion for its presence should be present in obese insulin resistant kid who present with dislipidemia or altered glucose metabolism or manifest anamnesttic or physical signs that suggest the presence of insulin

Fatty Liver Disease – This condition causes a buildup of extra fat in the liver, making it harder for the organ to process and

Fatty liver: Fatty liver is strongly linked with insulin resistance. Accumulation of fat in the liver is an appearance of the chaotic mess of lipids that occurs with

MetS was found among 30(13.6%; 95%CI: 9.5-18.2) study participants. Of the total study participants, 185(84.1%) had at least one abnormal component of MetS. Reduced HDL-c was the most prevailing abnormal components of MetS, 151(68.6%). However, elevated FBG was the least, 19(8.6%), Table 3.

Four different clinical trials were selected for this paper. First trial focuses on the management of fatty liver disease with vitamin E and C combined compared to usrodeoxycholic acid treatment. Second trial focuses on only vitamin E, pioglitazone, or placebo on NAFLD patients. Third trials focuses on the treatment of nonalcoholic steatohepatitis with vitamin E and vitamin C combined. Final trial focuses on pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis, similar to the second trial.

This disease was uncommon in the old days because it was unusual to accumulate enough fat to hurt livers. However, many people in the United States are now suffering from NAFLD and NASH. Before 1998, there was no case of NASH heard. In contrast, a statistics from a website called "Partners In Liver Wellness" provides an alarming information. The site says, “As a consequence of the on-going obesity epidemic in the U.S., fatty liver is a very common disorder with an estimated two thirds of obese adults and half of obese children having fat accumulation in the liver”8. It also mentions that up to 20% of those who are obese may suffer from NASH. This is a frightening number if this happened at, for example, West Anchorage High School. In high