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The liver itself does not normally store fat since fatty infiltration interferes with the health and functioning of liver cells. A normal, healthy liver converts excess carbohydrates and proteins derived from the food you have eaten into fatty acids and triglycerides. These are products that can be exported out into the blood and ultimately stored as fat in peripheral adipose tissue. When the liver is overtaxed by detoxifying harmful substances in alcohol and drugs, its ability to get rid of these fatty acids is compromised.
The exact mechanisms involved are not fully understood, but a number of possible causes have been proposed. One of the more complex pathways involves the ratio of the oxidized form of nicotinamide adenine dinucleotide (NAD+) to the reduced form (NADH) in the liver. The enzyme that metabolizes alcohol, alcohol dehydrogenase, removes a hydrogen atom from alcohol and transfers it to a molecule of NAD. NAD is converted (or “reduced” in chemical terminology) to NADH. NADH participates in numerous other reactions and passes on the hydrogen to other compounds.
These chemical interactions are called REDOX (reduction-oxidation) and in balance are essential for normal physiology and health. However, when NADH builds up in excess, the passing on of hydrogen to other compounds can create oxidative stress. The alcohol-related surplus of NADH causes alterations in fatty acid metabolism, such as slowing down the breakdown or oxidation of fatty acids.
Alcohol also stops the action of an enzyme that breaks down a backbone structure of triglycerides. When the supply of this backbone is in abundance, more triglycerides are made and put into circulation. So, alcohol works to both increase the amount of fatty acids and to limit the breakdown of fatty acids.
Fatty acids are broken down to generate NADH ultimately to create energy (ATP generation) via the Kreb’s cycle. The alcohol drinker has an excess of NADH as a result of metabolizing the alcohol that is consumed. In fact, the excess NADH tells the liver that conditions are just right for making fatty acids rather than breaking them down. As a result, when NADH is abundant as a result of alcohol consumption, fatty acids (in the form of triacylglycerols) accumulate in the liver. All of these mechanisms favor fatty liver.
Nutrient therapies that benefit fatty acid metabolism in the liver include essential amino acids, caffeine, and omega-3 fatty acids along with a varied, nutrient-dense diet. Most importantly, honor the relationship between alcohol and the liver and give your liver a breather with mocktails every now and then.
