Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.
As I’ve discussed in my last few videos, it seems that current therapies for the most common forms of shoulder pain—from the simplest and most conservative to the most invasive and expensive—show no consistent differences in clinical outcomes, even when tested against placebos or simply doing nothing. In light of this lack of good treatment options, it’s worth focusing more attention on prevention.
Modifiable risk factors for rotator cuff disease include type 2 diabetes, high blood pressure, and high cholesterol. Comparing the tendons of mice, rats, and monkeys with low versus high cholesterol, researchers found decreased elasticity and increased stiffness in the tendons from animals with high cholesterol, and a similar relationship is apparent in people. Those with even mildly elevated cholesterol have been found to have significantly stiffer tendons. What does that mean in terms of clinical outcomes?
The increase in the likelihood of tendon tears seen in animals with high cholesterol is corroborated in people with high cholesterol, who have a sixfold higher odds of retear after surgical repair. This may be due to the role high cholesterol plays in delaying the healing process; indeed, those presenting with pain from the most commonly injured rotator cuff tendon appear to heal significantly slower if they have hyperlipidemia, meaning, for example, high LDL cholesterol or high triglycerides.
Just as oxidized LDL can get lodged in our artery walls and trigger inflammation, it can also get trapped in our tendons and disrupt the integrity of the connective tissue. The fact that those with high cholesterol taking cholesterol statin drugs may only have as little as half the risk of developing rotator cuff disease, compared to those with high cholesterol not taking statins, bolsters the case that those with high cholesterol should try to lower it to prevent shoulder disorders.
The same dietary approach to lowering cholesterol would also lower exposure to another tendentious tendon culprit: advanced glycation end-products (AGEs). Appropriately acronymed, AGEs are considered “gerontotoxins,” meaning aging agents (from the Greek geros for “old age,” as in geriatric) and they are implicated in a wide spectrum of age-related diseases. AGEs have been found to adversely affect virtually all tissues and organs, but mainly accumulate in collagen, which is the main component of the rotator cuff. About 95 percent of the dry weight of tendons is straight collagen.
Based on studies on human and animal rotator cuff tendons removed from surgery, AGEs were found to cause age-related degenerative rotator cuff changes, including a significant drop in tensile strength of tendons upon mechanical testing. The good news is that although some AGEs are produced endogenously, our greatest exposure to them is through our diet and therefore is under our control.
The same foods that can raise our blood cholesterol tend to be the same foods most concentrated in AGEs: cooked animal products. So whole food, plant-based diets can therefore lower both LDL cholesterol and AGE intake. Plant foods may average thirty times fewer AGEs, and the AGEs they do have appear to be less toxic than AGEs from animal foods.
Now the way animal products are cooked can also make a difference. Moist-heat methods, like boiling or steaming, produce fewer AGEs, explaining why a single meal of broiled chicken can cause a “profound impairment” of artery function within hours compared to eating the same amount of boiled chicken. Boiled chicken still impairs arterial function within 2 hours of consumption, but significantly less than when the chicken is broiled. An “AGE Less” diet would emphasize lower AGE foods, such as fruits and vegetables, while avoiding the worst of the worst, such as bacon and hot dogs.
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