The Fat Resistance Diet

Inflammation - Arthritis  E-mail


Inflammation is part of the body’s protective response to injury or infection. The ancient Greeks described it as an internal fire. The Romans recognized it by four attributes: redness, heat, swelling and pain. We see those attributes in medical conditions that end in "-itis": arthritis, tonsillitis, appendicitis. During the Nineteenth Century, scientists discovered that inflammation was produced by white blood cells that migrate from the blood stream and enter areas of infection or injury. Recent research has linked heart attacks and strokes to microscopic inflammation of the blood vessels. Although inflammation produces many of the symptoms associated with being sick or injured, it is a necessary part of healing. 

During the Twentieth Century, scientists uncovered the chemical basis of inflammation. It became clear that inflammation could exist without redness, heat, swelling or pain and without a migration of white blood cells. Today, in the Twenty-first Century, inflammation is seen as a chemical state that can exist in all or part of your body without necessarily producing symptoms. Its presence is most accurately determined by measuring the levels of inflammatory chemicals in the inflamed tissue, or sometimes in a blood sample. Many of the chemicals associated with inflammation actually cause damage to cells. They are referred to as "mediators" of inflammation. Other chemicals are just signals that indicate inflammation is present. They are "markers" of inflammation. 

The biochemical understanding of inflammation has allowed scientists to recognize that your body controls the degree of inflammation by producing anti-inflammatory substances that damp down the pro-inflammatory signals. This is the normal response of your body to all kinds of stress: a stimulus provokes a reaction and that reaction acts as a stimulus to a counter-reaction that slowly returns your body to the state that existed before the initial stimulus. The whole process is called homeostasis and the pattern involves negative feedback loops. Homeostasis requires that all components of the negative feedback loops are in working order. Chronic inflammation results from the failure of homeostasis.

How does fat itself cause inflammation? Many adipokines, even leptin itself, are mediators of inflammation. They promote and encourage the inflammatory response, wherever it might be occurring. The more fat in your body, the higher the levels of these mediators in your blood and the greater the level of inflammation in your body. Here’s a fascinating example:

We’ve known for a long time that being overweight is associated with the development of osteoarthritis, especially in the knees. Osteoarthritis is the commonest form of arthritis and is thought to result from wear and tear on the cartilage that lines joints. Osteoarthritis produces an overgrowth of bone that narrows the space in the joint and increases the likelihood of damage when the joint is moved. Doctors have thought that the reason osteoarthritis is associated with obesity is that being heavy increases the wear and tear on your knees, a simple physical explanation. Recent research has found a chemical connection. Joint fluid in the knees of overweight people contains high levels of leptin, which is produced by fat, not by the joints themselves. Leptin in the joints causes inflammation. Leptin also triggers the production of an anti-inflammatory chemical called TGF-beta (transforming growth factor-beta). TGF-beta is part of a negative feedback loop to damp down inflammation. But one of the effects of TGF-beta is to stimulate the growth of bone, in this case producing the bony overgrowth characteristic of osteoarthritis. So the relationship between obesity and osteoarthritis is not just created by how much you weigh. It is a hormonal relationship in which the body’s normal homeostatic mechanisms go awry and produce disease.


Everyone experiences trauma to their knees during the course of their lives. Lean people, like athletes, who experience extensive, repetitive trauma, are at risk for osteoarthritis because the stimulus to inflammation and counter-inflammation is so intense. People who are overweight develop osteoarthritis because excess body fat causes an excessive inflammatory response to minor injury, which then triggers an increase in the counter-inflammatory response. The result is that both inflammatory and anti-inflammatory mediators are increased in obesity. The end result is no longer homeostasis but disease, which develops because of the unbridled activity of chemical mediators that fail in their effort to heal. 

The plot gets even thicker. The inflammatory nature of fat is not only due to fat cells themselves. In addition to fat cells (adipocytes), fat also contains blood vessels and white blood cells. Fat specifically attracts a type of white blood cell called a macrophage. Macrophage literally means "large eater" and macrophages are large white blood cells that gobble up cellular debris. They are scavengers, sometimes called "garbage men of the immune system." The macrophages found in fat are major producers of inflammatory mediators, especially a substance called Tumor Necrosis Factor (TNF). TNF is well-known in medicine, because high levels of it produce much of the tissue damage and pain associated with rheumatoid arthritis and other autoimmune diseases. Fatty tissue can be laden with TNF-producing macrophages. In some animal studies, over 40% to 50% of cells found in adipose tissue were macrophages. 




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