The plot thickens. How simple it once was for endocrinologists to identify a few organs, like the thyroid, measure their hormones, and then prescribe hormone replacement when seemingly lacking in them. While this method may have been easier, it was often not very helpful in
solving the obvious thyroid problems that many experience.
In 1994 that simplicity changed forever. With the discovery of the hormone leptin and the fact that the adipocyte, fat cell, was busy not only making leptin but also making many other hormonal signals, this picture takes on even more complexity. It is now clear that your muscle cells,
myocytes, are also making hormonal signals that cross-talk with your fat cells and your thyroid. Anyone for a game of chess?
Insulin resistance comes in many shapes and sizes. At the cellular level, cells that are having too many calories stuffed into them shut the door to keep calories out; this is a key method of self-preservation. Slamming the door means taking down the receptor for insulin on the surface of
the cell, which prevents the taxicab known as insulin from dropping off its passengers (sugar).
Insulin resistance can happen at the site of a major organ such as the liver, causing such drastic problems that Type 2 diabetes is likely to occur. Over the past few years it has been proven that this type of insulin resistance is caused by a decrease in a hormone produced in fat cells
called adiponectin Protein hormone that modulates metabolism including glucose and fatty acid catabolism. High levels are associated with low body fat. As leptin goes up (because of leptin resistance from overeating), adiponectin Protein hormone that modulates metabolism including glucose and fatty acid catabolism. High levels are associated with low body fat. is adversely depressed.
Besides your white adipose tissue (which makes leptin and adiponectin Protein hormone that modulates metabolism including glucose and fatty acid catabolism. High levels are associated with low body fat. ), your muscles are the other largest organ mass in your body. It has now been found that as body weight goes up your muscles make more of a hormonal signal called myostatin, which adversely inhibits muscle growth and promotes insulin resistance.
Additionally, both muscle and fat cells make various inflammatory signals, such as IL-6, which cross-talk to each other. For example, IL-6 coming from muscles to fat can break down fat to provide fuel to muscles. Whereas IL-6 going from inflamed fat to muscles actually induces
The newest data indicates that these cross-talking metabolic signals, when in a condition of poor health, inhibit the conversion of basic thyroid hormone T4 to active T3 in muscle, thereby causing muscle fatigue and poor muscle fitness (a classic sign of hypothyroid that is now being understood for the first time).
This data indicates that by improving the fitness of your fat you will have more muscle energy and better thyroid function. It means that
if you do something to improve your thyroid function, then your fat will work better and so will your muscles. It also means that if you improve your muscle function you will have better fat function and thyroid function.
Maybe this sounds complex, so let me give you one of many potential take-home messages. If you have symptoms of low thyroid then get
yourself on a consistent strength training program and gradually work to improve your muscles. The improvement in muscles will directly improve your thyroid health and help you lose weight. This will also help unravel insulin resistance and help prevent accelerated aging and Type 2 diabetes.
Byron Richards, CCN