BASICS
- Non Alcoholic Fatty Liver Disease on the increase.
- Cirrhosis on the increase.
- Obesity is a risk factor for liver failure
- Up to 38% of obese children have Non Alcoholic Fatty Liver Disease
IDEAS
Obesity is a bigger risk factor than alcohol for the development and acceleration of cirrhosis.
Inflammation
The consumption of Sugar and Polyunsaturated Seed Oils combine in our diet to create inflammation in every blood vessel wall and in every tissue in every organ of the body. The inflammatory process makes everything susceptible to damage and disease.
Fructose consumption is implicated in the basic pathway.
MORE INFORMATION
Liver Tissue Damage
Fructose is metabolised down an aldehyde pathway in the liver, which is the same concept as producing alcohol. In the outside world we ferment fruit to make alcohol and the liver does the same thing via a fructose pathway. The aldehyde effects on the liver means inflammation can occur within the liver.
The alcohol production within the substrate causes a cross linkage of proteins in its own low-grade inflammation. Over time this can result in fibrosis and the ultimate situation of cirrhosis and liver failure.
There is direct fat accumulation within the liver due to an inability to excrete fat when the body is already saturated with fat storage.
Tissue oxidative stress from ATP depletion.
Non-Alcoholic Fatty Liver Disease
There is an increasing incidence of non-alcoholic fatty liver disease in society. On CT scan and ultrasound scanning of livers it is now common place and is almost being considered a normal finding.
The cause of non-alcoholic fatty liver disease has been well associated with fructose metabolism. The aldehyde pathway (alcohol production) promotes a degree of damage within the liver. Excess fat is also not excreted which creates a build up and then there is the ongoing low-grade chronic inflammation in the blood vessel walls associated with the by-products of fructose and polyunsaturated oils.
The ongoing chronic inflammatory state can provoke fibrosis and scarring leading to cirrhosis of the liver.
Read about the Damage Process
Read about the Metabolism
Read about other Health Issues
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ARTICLES
The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome.
Nature Reviews Gastroenterology Hepatology . 2010 May;7(5):251-64. doi: 10.1038/nrgastro.2010.41. Epub 2010 Apr 6.
Lim JS, Mietus-Snyder M, Valente A, Schwarz JM, Lustig RH.
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most frequent liver disease worldwide, and is commonly associated with the metabolic syndrome. Secular trends in the prevalence of these diseases may be associated with the increased fructose consumption observed in the Western diet. NAFLD is characterized by two steps of liver injury: intrahepatic lipid accumulation (hepatic steatosis), and inflammatory progression to nonalcoholic steatohepatitis (NASH) (the ‘two-hit’ theory). In the first ‘hit’, hepatic metabolism of fructose promotes de novo lipogenesis and intrahepatic lipid, inhibition of mitochondrial beta-oxidation of long-chain fatty acids, triglyceride formation and steatosis, hepatic and skeletal muscle insulin resistance, and hyperglycemia. In the second ‘hit’, owing to the molecular instability of its five-membered furanose ring, fructose promotes protein fructosylation and formation of reactive oxygen species (ROS), which require quenching by hepatic antioxidants. Many patients with NASH also have micronutrient deficiencies and do not have enough antioxidant capacity to prevent synthesis of ROS, resulting in necroinflammation. We postulate that excessive dietary fructose consumption may underlie the development of NAFLD and the metabolic syndrome. Furthermore, we postulate that NAFLD and alcoholic fatty liver disease share the same pathogenesis.
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Pediatric non alcoholic fatty liver disease: old and new concepts on development, progression, metabolic insight and potential treatment targets.
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in children. NAFLD has emerged to be extremely prevalent, and predicted by obesity and male gender. It is defined by hepatic fat infiltration >5% hepatocytes, in the absence of other causes of liver pathology. It includes a spectrum of disease ranging from intrahepatic fat accumulation (steatosis) to various degrees of necrotic inflammation and fibrosis (non-alcoholic steatohepatatis [NASH]). NAFLD is associated, in children as in adults, with severe metabolic impairments, determining an increased risk of developing the metabolic syndrome. It can evolve to cirrhosis and hepatocellular carcinoma, with the consequent need for liver transplantation. Both genetic and environmental factors seem to be involved in the development and progression of the disease, but its physiopathology is not yet entirely clear. In view of this mounting epidemic phenomenon involving the youth, the study of NAFLD should be a priority for all health care systems. This review provides an overview of current and new clinical-histological concepts of pediatric NAFLD, going through possible implications into patho-physiolocical and therapeutic perspectives.
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Prevalence of fatty liver in children and adolescents.
Abstract
OBJECTIVE:
Fatty liver disease is diagnosed increasingly in children, but the prevalence remains unknown. We sought to determine the prevalence of pediatric fatty liver as diagnosed by histology in a population-based sample.
METHODS:
We conducted a retrospective review of 742 children between the ages of 2 and 19 years who had an autopsy performed by a county medical examiner from 1993 to 2003. Fatty liver was defined as > or = 5% of hepatocytes containing macrovesicular fat.
RESULTS:
Fatty liver was present in 13% of subjects. For children and adolescents age 2 to 19 years, the prevalence of fatty liver adjusted for age, gender, race, and ethnicity is estimated to be 9.6%. Fatty liver prevalence increases with age, ranging from 0.7% for ages 2 to 4 up to 17.3% for ages 15 to 19 years. Fatty liver prevalence differs significantly by race and ethnicity (Asian: 10.2%; black: 1.5%; Hispanic: 11.8%; white: 8.6%). The highest rate of fatty liver was seen in obese children (38%).
CONCLUSIONS:
Fatty liver is the most common liver abnormality in children age 2 to 19 years. The presence of macrovesicular hepatic steatosis in approximately 1 of every 10 children has important ramifications for the long-term health of children and young adults. The influence of the risk factors identified should be taken into consideration in the development of protocols designed to screen at-risk children and adolescents.
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Radiologic Assessment of Liver Fibrosis – Present and Future
By Luca Macarini and Luca P. Stoppino
More to follow.