Fatty Liver Disease Overview:
There are 2 main forms of fatty liver disease. Non alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFLD). It is a spectrum of diseases starting from the least severe (seatosis), and increasing in severeity (steatohepatitis, fibrosis, cirrhosis).
NAFLD is most often caused by metabolic syndrome, while AFLD is specifically caused by chronic alcoholism. Both conditions eventually lead to end stage liver disease (cirrhosis).
+ Alcoholic Fatty Liver Disease (AFLD)
Small amounts of alcohol is generally well tolerated in the human body, and fails to result in damage to the liver. In excess, however, serious complications can arise.
The detoxification of alcohol involves 3 separate pathways, each leading to the conversion of alcohol to acetaldehyde.
- Catalase (Peroxisomes)
- Alcohol dehydrogenase (ADH)
- Cytochrome P450 2E1
The main pathway that causes alcoholic fatty liver disease is the alcohol dehydrogenase pathway. This pathway requires NAD+, which is converted to NADH during the process. With less NAD+, and more NADH, the liver is forced to produce MORE fatty acids, and oxidise less, leading to increased fat storage in the hepatocytes (steatosis).
+ Non-Alcoholic Fatty Liver Disease (NAFLD)
This is the liver manifestation of metabolic syndrome. It results from the loss of sensitivity to insulin, dysfunctional blood glucose regulation, high blood lipid levels, abdominal adiposity, and the accumulation of free fatty acids in the hepatocytes.
Fatty deposits form when the synthesis of fatty acids exceeds the ability to export or metabolise them. This causes oxidative stress, hepatic stenosis, and inflammation in the liver.
With insulin resistance, fat storage increases, fatty acid oxidation decreases. This causes the formation of fat droplets to grow inside the hepatocytes of the liver. Over time, this begins to push the nuclei to the edges of the cell. This is called steatosis.
These accumulated fatty acids begin to degrade, creating water and unstable fatty acid radical molecules, which itself reacts with other fatty acids and cascading lipid membrane dysfunction. This can lead to mitochondral dysfunction and cell death. As these cells die, it causes inflammation. This is called non-alcoholic steatohepetitis (NASH).
As inflammation continues, stellate cells in the liver begins to lay down fibrotic tissue. This is called fibrosis.
As fibrosis continues, the architechture of the liver changes permenantly, eventually leading to failure. This is called cirrhosis.
Enlarged blood vessels just beneath the skin
Enlarged breasts (Men)
Liver Function Testing Considerations:
|Parameter||Reference Range||Common Findings|
|AST (Aspartate Aminotransferase)||10-35 U/L||High|
|ALT (Alanine Aminotransferase)||5-30 U/L||High|
|Alkaline Phosphatase||25-120 U/L||High|
|GGT (Gamma Glutamyltransferase)||Males - <50 U/L
Females - <30
|High (Especially in AFLD)|
|Lactate Dehydrogenase||80-240 U/L||High|
|MCV (mean Corpuscular Volume)||80-100fL||High|
|Uric Acid||Male - 0.20-0.45 mmol/L
Female - 0.15-0.40 mmol/L
1. Reduce Xenobiotic Load
- Diet (Elimination of alcohol, dietary fat, caffeine, refined carbohydrates)
2. Increase Transit Time Of The Digestive Tract
- Dietary Fiber
3. Protect Hepatocytes
- Hepatic Trophorestoratives (Cynara scolymus, Silybum marianum, Shisandra chinensis)
4. Improve Hepatobiliary Function
- Cholagogues & Choleretics (Taraxicum officinale, Cynara scolymus)
5. Reduce hepatic Inflammatory Changes
- Inhibit TNF-a and NF-kB (Curcuma longa)
6. Reduce Oxidative Damage
- Antioxidants (Curcuma longa, Camellia sinensis, Schisandra chinensis, Rosmarinus officinalis)
7. Reduce Blood Lipids
- Hypolipidaemics (Trigonella foeniculumgraecum)
- Metabolic syndrome
- Renal failure
- Chronic alcoholism
- Metabolic syndrome
The Sunlight Experiment
Updated: May 2018
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