Strength Training Likely to Help Fatty Liver

By: Byron J. Richards, Board Certified Clinical Nutritionist
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The problem of fatty liver was previously limited to alcoholics and those with liver infections. The epidemic of obesity has now created an epidemic of fatty liver problems that induce high LDL cholesterol as well as a five-fold increased risk1 for developing type 2 diabetes. A new study explains how growth hormone is altered2 in fatty liver problems and opens the door for a fitness-based solution as part of a strategy to solve fatty liver problems.

The initial production of growth hormone occurs in the brain based on a signal called GHRH (growth hormone releasing hormone). It travels to the liver where it activates a gene signaling pathway based on JAK2, in turn producing biologically active growth hormone known as IGF-1. IGF-1 helps burn fat and build muscle anywhere in the body.

The researchers found that in situations of fatty liver the JAK2 system was not working and therefore IGF-1 was not being produced. Even worse, once the JAK2 system was not working then other signals turned on that specifically caused fat to build up in the liver. Various experiments proved that activating JAK2 and boosting IGF-1 could solve fatty liver. This is an important new angle in understanding the problem and it leads to an expanded approach to solving it.

You can’t just take a vitamin to boost up JAK2, as this is a complex signaling molecule involved with many aspects of health and disease, and thus it is neither “good” or “bad.”  Like so may health problems today, its function has become inefficient. It is also part of the inflammatory response and thus reducing inflammation may be the best strategy to help get JAK2 functioning better within the liver to help reduce fatty liver. This may be one reason why anti-inflammatory nutrients such as quercetin, curcumin, and green tea have been shown to help fatty liver.

It is also not a good idea to take IGF-1 in a drug form, as the results are highly unpredictable with an increased risk for type 2 diabetes likely as well as possible cancer. Once again, this is because IGF-1 is typically working inefficiently in people with insulin resistance and fatty liver. Thus, you want to stimulate the production of IGF-1 in the context of health. There is a very simple way to do this – its called strength training exercise. This form of exercise induces muscle tissue breakdown and thereby stimulates IGF-1 activation – helping to turn the system on by a process of use (use it or lose it).  Ironically, the more out of shape a person is the easier it is to activate IGF-1.  In other words, you don’t have to overdo strength training just do it.  Even though the IGF-1 you release may be to help a muscle recover, the IGF-1 released in systemic in function and will also help your liver. By building muscle over time you will also remove fat from those muscles making you much healthier as time goes by.

This now gives us multiple strategies to help improve fatty liver.
1)  Anti-inflammatory nutrients to help JAK2 work normally.
2)  Strength training to optimize the production of IGF-1.
3)  Reduced calorie intake and aerobic exercise to help clear stagnant fat in general which has also been shown to help fatty liver.
4)  Improve digestive issues so inflammatory signalling to the liver from the gut is reduced.
5)  Liver activating nutrients like whey protein and liver lipotropic nutrients like pantethine, choline, DHA, acetyl-l-carnitine, and tocotrienols –
    which accelerate the process of clearing fat sludge from the liver.

This topic is of vital importance to every overweight person to prevent a slide into serious health problems.

Referenced Studies:
  1. ^ Fatty Liver and Risk for Type 2 Diabetes   Journal of Clinical Endocrinology & Metabolism,  K.-C. Sung, S. H. Kim.
  2. ^ Low IGF-1 Associated with Fatty Liver  Journal of Clinical Investigation  Brandon C. Sos, Charles Harris, Sarah M. Nordstrom, Jennifer L. Tran, Mercedesz Balázs, Patrick Caplazi, Maria Febbraio, Milana A.B. Applegate, Kay-Uwe Wagner and Ethan J. Weiss.

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