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While good bone health is readily acknowledged as necessary for high quality of life, bones are of little use without healthy joints to move them. Osteoarthritis, or the loss of joint cartilage, was once considered a disease of excessive wear and tear. Because it’s a common occurrence in obesity, many physicians assumed it was a simple consequence of joints carrying around too much weight for too long. However, it is increasingly considered a metabolic disease. Like so many tissues, even our joints are sensitive to metabolic signals, including insulin.

Out of a broad range of overweight individuals researchers studied, those with osteoarthritis were most likely to have the highest insulin levels. An essential component of the joint is the cartilage: the smooth, flexible connective tissue lining the ends of the bones that articulate a joint. The main cells in cartilage are called chondrocytes and, of course, they are insulin responsive. They are responsible for creating and maintaining the cartilage lining, known as a matrix; this is made largely of collagen and substances that the chondrocytes need glucose to create. And, the chondrocytes need insulin to take in that glucose; an insulin-resistant chondrocyte can’t maintain that matrix, and, ultimately, the cartilage weakens.

Another essential component of a joint, beyond its lining, is the “grease” for the joint—synovial fluid. Synovial fluid is made from specialized cells called synoviocytes, which, just like the chondrocytes, play an essential role in helping the joint work well. When synoviocytes are exposed to high levels of insulin, they experience an invasion of immune cells that ramp up inflammation in the joint and reduce synovial fluid production. Without this grease, the gears just grind. Osteoarthritis shouldn’t be confused with rheumatoid arthritis, which is a chronic inflammatory joint disease. Likely because of the inflammation it creates, rheumatoid arthritis increases the likelihood of developing insulin resistance (we’ll discuss the role of inflammation in insulin resistance later).

In fact, the severity and activity of the disease can wax and wane over time, and the accompanying insulin resistance similarly will become more or less severe. FIXING ONE PROBLEM BUT CAUSING ANOTHER Many people with joint pains take glucosamine in some form, which may improve joint health and reduce joint pain, though evidence is equivocal. However, while it may improve your joints, the glucosamine is very likely making you more insulin resistant. The evidence isn’t equivocal at all—across humans and rodents, glucosamine makes a body less insulin sensitive.

Gout is a type of inflammatory joint disease where the joint accumulates uric acid crystals and the inflammation that accompanies them. The joints most commonly affected are those in your limbs, including your feet (especially the big toe), ankles, fingers, and wrists. Uric acid is normally excreted by the kidneys into the urine (as the name suggests) and eliminated from the body. However, insulin resistance changes this process, making the kidneys accrue uric acid rather than excrete it. Uric acid then builds up in the blood and settles in the joints just mentioned, initiating a local inflammatory reaction that causes the redness and swelling typical of gout.

Our muscles, bones, and skin have a common theme—they “connect” the body, allowing it to act as one unit. This connective tissue requires insulin’s actions to maintain its strength and integrity, though this isn’t unique to these bulky (muscle and bone) and stretchy (skin) tissues. Now that we’ve looked at the tissues that cover and move us, in the next series of videos we’ll dive back into the body to see how insulin resistance alters the tissues that nourish and clean us.

From Dr. Benjamin Bikman’s Book - [ Ссылка ]

Highly recommend Dr. Ted Naiman’s book P:E Diet - [ Ссылка ]

A Great Podcast with Dr. Ted Naiman - [ Ссылка ]

My Personal P:E Spreadsheet feel free to download or copy and make your own! - [ Ссылка ]

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