People who exercise regularly are far less likely to suffer dementia and had less than half the risk of death during the 17-year study period, compared to those who do not exercise (Medicine & Science in Sports & Exercise, February, 2012).
Researchers followed 45,000 men and 15,000 women, ages 20 to 88 years, in the United States for an average of 17 years. Six times as many people in the low fitness group suffered from dementia, compared to those who exercised regularly. While deaths in the United States associated with heart disease, breast cancer and stroke have declined in recent years, deaths related to dementia and Alzheimer's disease rose 46 percent between 2002 and 2006.
Another exciting study, from Japan, shows that many of the benefits that exercise provides to muscles are also provided to your brain (The Journal of Physiology, February, 2012;590(Pt 3):607-16).
THE STUDY: Adult male rats exercised to exhaustion at moderate intensity on a treadmill. Glycogen, sugar stored in muscles, was depleted by 82-90 percent. One day later, the rats' muscles could store 43-46 percent more than they could originally, In a like manner, brain glycogen levels decreased by 50-64 percent with exhaustive exercise, and were able to store 29-63 percent more on the next day. The greater the depletion of sugar in muscles and brain, the greater the ability to store more sugar after the rats were fed. The brain filled with sugar before the muscles did and after four weeks of training, the rats' brains could store significantly more glycogen.
EXPLANATION: Sugar is the most efficient source of energy for your muscles during intense exercise. Sugar is the most efficient source of energy for your brain ALL the time. When you exercise regularly, you increase the ability of your muscles to store sugar so you can move faster and longer. This study suggests that exercise also increases the energy supply to your brain, which will help you to think and reason better.
Rheumatoid Arthritis Patients Benefit from Cortisone Injections
Author :
Kristie
Cortisone-type injections into joints control painful rheumatoid arthritis by blocking protein changes that damage joints (Arthritis Research & Therapy, published online Feb. 2012).
REACTIONS THAT CAUSE RHEUMATOID ARTHRITIS: Rheumatoid arthritis (RA) is characterized by the production of PAD enzymes that convert an amino acid, arginine, into citrullinated proteins. Then the victim's immunity makes highly specific anti- citrullinated protein antibodies that attack the synovium and cause it to swell, thicken, and hurt.
WHY CORTISONE INJECTIONS WORK: Injecting cortisone-type drugs into the joints blocks the production of the PAD enzymes that produce citrullinated proteins, and this decreases the thickness of the synovium, and the resultant pain.
THE STUDY: The authors biopsied the swollen knees of patients with rheumatoid arthritis and normal controls. One group was given methotrexate, a common RA treatment used for more than 40 years. The other group was given cortisone-type injections (40 mg triamcinolone hexacetonide) into the knee joint.
Antibodies to citrullinated proteins were found in 86 percent of biopsy samples from the RA patients and in none of the healthy tissue samples. After eight weeks, those receiving the cortisone- type injections had far less swelling of their synovia, far less evidence of inflammation under the microscope, and lower levels of cutrullinated proteins and PAD enzymes. Methotrexate had no effect on citrullinated proteins, PAD enzymes or inflammation in the synovium, although these patients did feel better.
CONCLUSION: This study explains why cortisone-type injections are such an effective treatment for rheumatoid arthritis. However, the effects of the injections do not last and a few months later, the patient may need another injection that may increase risk for diabetes, osteoporosis, and other side effects.
REACTIONS THAT CAUSE RHEUMATOID ARTHRITIS: Rheumatoid arthritis (RA) is characterized by the production of PAD enzymes that convert an amino acid, arginine, into citrullinated proteins. Then the victim's immunity makes highly specific anti- citrullinated protein antibodies that attack the synovium and cause it to swell, thicken, and hurt.
WHY CORTISONE INJECTIONS WORK: Injecting cortisone-type drugs into the joints blocks the production of the PAD enzymes that produce citrullinated proteins, and this decreases the thickness of the synovium, and the resultant pain.
THE STUDY: The authors biopsied the swollen knees of patients with rheumatoid arthritis and normal controls. One group was given methotrexate, a common RA treatment used for more than 40 years. The other group was given cortisone-type injections (40 mg triamcinolone hexacetonide) into the knee joint.
Antibodies to citrullinated proteins were found in 86 percent of biopsy samples from the RA patients and in none of the healthy tissue samples. After eight weeks, those receiving the cortisone- type injections had far less swelling of their synovia, far less evidence of inflammation under the microscope, and lower levels of cutrullinated proteins and PAD enzymes. Methotrexate had no effect on citrullinated proteins, PAD enzymes or inflammation in the synovium, although these patients did feel better.
CONCLUSION: This study explains why cortisone-type injections are such an effective treatment for rheumatoid arthritis. However, the effects of the injections do not last and a few months later, the patient may need another injection that may increase risk for diabetes, osteoporosis, and other side effects.
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