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Metabolic Syndrome and Osteoarthritis
Metabolic syndrome is a condition where we begin to lose our blood sugar and blood insulin control. It is considered a prelude to diabetes and it is characterized by elevated blood sugar, elevated blood insulin, increased belly fat, high blood fats, and high blood pressure.
There are many doctors and scientists who now think that joint inflammation is part of the natural progression of the metabolic syndrome, which worsens as metabolic syndrome gets worse. Consider the importance of this. Doctors had thought for a long time that joint problems and osteoarthritis were due to aging or wear and tear. A growing body of research later showed that people who were overweight or who had diabetes had a much greater risk to osteoarthritis. With modern genetic and biochemical tools, it is becoming clear that osteoarthritis might be one of the expected outcomes of blood sugar abnormalities.
Doctors writing in the journal Medical Hypothesis have suggested a series of events that might be simplified in the following ways:
1) Weight and belly fat increase
2) White blood cells travel to belly fat
3) White blood cells take up residence in belly fat
4) While in the belly fat, white blood cells produce immune chemicals that circulate through the bloodstream and reach distant tissues
5) These immune chemicals act to damage joint tissue
These doctors write, “The fatigue and muscle weakness induced by insulin resistance and inflammation in obese patients with metabolic syndrome increase the frequency and the intensity of traumatic events of peripheral or axial joints that result in stretch and breaking of teno-periosteal junction and abrasive damage of cartilage and therefore in these patients with metabolic syndrome and pro-inflammatory state the reparative process of cartilage and peri-articular tissues would be severely modified by the growth factor activity in presence of high levels of insulin.”
This statement is a bit of a mouthful. To simplify it just a bit, they suggest that insulin resistance and inflammation are linked processes. Because of this changing body chemistry, there is increasing trauma to parts of the joint where tendons attach to bone and where cartilage attaches to bone. When people have high blood sugar and high insulin levels, repairing cartilage becomes difficult due to the biochemical “soup” bathing the joints.
[Rojas-Rodríguez, J, Escobar-Linares, LE, Garcia-Carrasco, M, et al. The relationship between the metabolic syndrome and energy-utilization deficit in the pathogenesis of obesity-induced osteoarthritis. Med Hypotheses. 2007;69(4):860-8.]
One recent study in dogs illustrates this point.
Scientists at Washington University in St. Louis, Missouri fed dogs a diet that was either sharply restricted in calories or one that contained normal amounts of calories over a period of 12 years. From ages 9 to 12, these researchers tested the dogs’ blood sugar, insulin response, time to development of arthritis, and time to death. They discovered that dogs with the lowest blood glucose and best insulin sensitivity were those who were the least likely to develop arthritis.
When they looked at what caused the better blood sugar and insulin control, it became clear what the major influence was—lower calorie intake. Imagine, better blood sugar and insulin control delays the development of arthritis.
This study has some very important implications. It could mean that keeping your calorie intake low, controlling your blood sugar, and controlling your weight might stave off the development of joint problems. It may also mean that anyone with osteoarthritis who is overweight, who has insulin resistance, metabolic syndrome, or diabetes can take charge of her joint health by gaining control of her blood sugar. This is an extraordinary opportunity.
Low Calories = Better Blood Sugar Control = Delayed Development of Arthritis
[Larson, BT, Lawler, DF, Spitznagel, E, Kealy, RD. Improved Glucose Tolerance with Lifetime Diet Restriction Favorably Affects Disease and Survival in Dogs. J. Nutr 2003;133:2887–2892.]




















