Why some mid-thoracic subluxations become chronic: The liver T4 to T10 - Part 2

Why some mid-thoracic subluxations become chronic: The liver T4 to T10 - Part 2

Last month, I started the discussion about the liver and its various functions that can cause and perpetuate spinal subluxations, structural misalignments, and loss of joint range of motion. Now I begin with the liver’s role in the maintenance of adequate glucose levels. The goal is to relate structure, function, and symptoms to subluxation patterns we encounter in practice every day.

The Liver under stress

Let’s start with the effects of sympathetic stimulation. If you accept that the vast majority of your patients suffer from the accumulated effects of chronic stress then you’ll readily recognize the appearance of muscle contraction within the entire Trapezius muscle related to the liver’s inability to fulfill its role in the maintenance of homeostasis.

Instead of dividing the Trapezius into its anatomical divisions of upper, middle, and lower sections consider the role of liver dysfunction (stress, not disease) with its spinal innervation from T4 to T10 on the Trapezius as a whole.

• Its origin is from the base of the occiput (external occipital protuberance, nuchal ligament and medial superior nuchal line) and the spinous processes of C7 to T12.
• It inserts on the posterior lateral surface of the clavicle, acromion process and spine of the scapula.

Association of liver dysfunction to postural deviations such as head tilt and low shoulder now becomes quite obvious. Also, the loss of the normal posterior kyphotic curve of the thoracic spine can be readily palpated, as can fixations of lateral bending and subluxations from C7 to T12 and specifically from T4 to T10.

The question should then be what are the specific functions of the liver during any acute stress reaction and how do they manifest themselves in patients suffering from chronic stress? To answer, recall that the body’s first reaction to the effect of any stress is to ascertain if it has adequate glucose to meet the challenge to normal function. Obviously, this includes not only the amount of glucose in the blood, but that stored primarily in the liver and muscles as glycogen.

Once the brain (hypothalamus) determines that it lacks an adequate energy supply to fight or run (flight) it activates the sympathetic stress cascade.

First on the list is to decrease digestive secretions and reduce peristalsis within the alimentary canal. This includes stomach acid and bile.

The biliary system (T4 to T8)

Sympathetic stimulation relaxes the muscles and contracts sphincter, thus reducing the flow of bile. Chronic stress therefore results in biliary stasis and the inability to properly emulsify lipids, regardless of whether the patient still has their gallbladder. The consequences of this are profound and I’ve dealt at length with them previously.

It’s commonly overlooked that cholesterol is normally drained from the body in bile. Chronic stress effectively decreases cholesterol secretion into bile and results in elevated blood levels. How many of your patients are taking statin drugs to reduce the liver’s production of cholesterol? How many have chronic recurring subluxations throughout the cervical and thoracic spine accompanied by headaches and/or shoulder problems?

If these postural deviations and symptoms are accompanied by muscle contraction in the right abdomen below the rib cage (where you would palpate for an enlarged liver) and if your patient is taking a stain drug, perhaps it’s time to suggest testing for “the simple liver tests” mentioned in the drug ads before the appearance of systemic muscle soreness (myositis) and liver damage.

Once available glucose levels are not sufficient to maintain normal function while under stress, the sympathetic system stimulates the adrenal medulla, pancreas, and the liver to elevate glucose levels as follows:

• Adrenal Medulla (T5 to T10) Response - This gland immediately releases epinephrine and norepinephrine which increase glucogenolysis (the conversion of glycogen to glucose) in the liver and releases the glucose to the body. It also has a lipolytic effect on adipose tissue thereby increasing fatty acid levels.
• Pancreas (T5 to T9) Response - reduces insulin secretion to prevent glucose absorption by the cells and increases glucagon secretion, which generally elevates the amount of glucose in by promoting gluconeogenesis and glucogenolysis.

The endocrine system also is stimulated during the stress reaction because moderate quantities of glucose can be formed from amino acids and from the glycerol portion of fat. This process is called gluconeogenesis.

The adrenal cortex response (celiac and renal plexus) - increased cortisol secretion mobilizes proteins from essentially all cells of the body, making these available in the form of amino acids in the body fluids. A high proportion of these immediately become deaminated in the liver and provide ideal substrates for conversion into glucose. Because of this, during chronic stress your patient will show evidence of protein deficiency.

The thyroid response (middle and inferior cervical ganglion) - Thyroxine increases the metabolic rate (until it becomes exhausted), increases release of protein from the cells thus contributing to gluconeogenesis, and increases the release of fat from adipose tissue.

The net effect is to return the glucose concentration to normal. I’ll continue the discussion of this very important subject next time.

(Dr. Loomis can be reached by mail at 6421 Enterprise Lane, Madison, WI 53719-1116 or by phone at 800-662-2630. Visit his website at http://www.loomisenzymes.com.)