Re: (loss of cell mass) ((( and all)))

[Guest guest]

Essentially, the domino effect. It makes sense.

Does anyone take protein supplement?

<Matsumura_Clan@...> wrote:

Int J Cardiol. 2002 Sep;85(1):89-99.

Cachexia in rheumatoid arthritis.

Walsmith J, Roubenoff R.

Nutrition, Exercise Physiology, and Sarcopenia Laboratory, Mayer USDA

Human Nutrition Research Center on Aging, Tufts University, Boston, MA

02111, USA.

Rheumatoid arthritis is a debilitating, chronic, systemic, autoimmune

disease of unknown etiology that causes destruction of joint cartilage and

bone. It generally occurs between the fourth and sixth decades of life, and

affects two to three times more women than men. It is characterized by joint

stiffness, pain, and swelling, and is accompanied by a loss of body cell

mass. This loss of cell mass, known as rheumatoid cachexia, predominates in

skeletal muscle, but also occurs in the viscera and immune system. Thus,

rheumatoid cachexia leads to muscle weakness and a loss of functional

capacity, and is believed to accelerate morbidity and mortality in

rheumatoid arthritis. Currently there is no established mechanism for

rheumatoid cachexia, but it is accompanied by elevated resting energy

expenditure, accelerated whole-body protein catabolism, and excess

production of the inflammatory cytokines, tumor necrosis factor-alpha and

interleukin-1beta. Tumor necrosis factor-alpha is probably the central

mediator of muscle wasting in rheumatoid arthritis, and is known to act

synergistically with interleukin-1beta to promote cachexia. In general,

tumor necrosis factor-alpha and interleukin-1beta are thought to alter the

balance between protein degradation and protein synthesis in rheumatoid

arthritis to cause muscle wasting. The precise mechanism by which they do

this is not known. Reduced peripheral insulin action and low habitual

physical activity are important consequences of rheumatoid arthritis, and

have also been implicated as mediators of rheumatoid cachexia. Insulin

inhibits muscle protein degradation. Consequently, reduced peripheral

insulin action in rheumatoid arthritis is thought to be permissive to

cytokine-driven muscle loss. The cause of reduced peripheral insulin action

in rheumatoid arthritis is not known, but tumor necrosis factor-alpha has

been shown to interfere with insulin receptor signaling and is probably an

important contributor. Low habitual physical activity has consistently been

observed in rheumatoid arthritis and is an important consequence of, and

contributor to, muscle wasting. In addition, low physical activity

predisposes to fat gain and is believed to precipitate a negative

reinforcing cycle of muscle loss, reduced physical function, and fat gain in

rheumatoid arthritis, which leads to 'cachectic obesity'. To date, there is

no standard treatment for rheumatoid cachexia. However, physical exercise is

currently believed to be the most important and clinically relevant

countermeasure against rheumatoid cachexia. In general, a combination of

skeletal muscle strength training and aerobic exercise is recommended, but

must be prescribed with the patient's disease status, overall health, and

safety in mind. Future studies should investigate the safety, efficacy, and

required dose of anti-cytokine therapy for the treatment of rheumatoid

cachexia. In this review, we outline the current definition of rheumatoid

cachexia, and discuss the etiology, pathogenesis, and treatment of

rheumatoid cachexia.

PMID: 12163213

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=PubMed & list_uids=1\

2163213

Not an MD

I'll tell you where to go!

Mayo Clinic in Rochester

http://www.mayoclinic.org/rochester

s Hopkins Medicine

http://www.hopkinsmedicine.org