Date:   4/2/2013 7:09:50 AM ( 11 y ago)
Hits:   17,865
URL:   https://www.curezone.org/forums/fm.asp?i=2051320

"Cannabis suppresses your immune system."

Where did you come up with this idea? On the contrary.

Truth is...

"Recent published research on CD4 immunity in AIDS patients found no compromise to the immune systems of patients undergoing cannabis therapy in clinical trials.[11]"

americansforsafeaccess.org/article.php

Ethan Russo, M.D.

Patients have long told us that cannabis has been helpful to them in the treatment of their arthritic conditions. Science has now demonstrated that the THC component of cannabis is a very effective analgesic (pain killer), and that the CBD (cannabidiol) component has unique immunomodulatory benefits as an antagonist of tumor necrosis factor-alpha, supporting benefits in treatment of rheumatoid arthritis, as well as Crohn's disease and psoriasis. It appears that cannabis-based medicines will likely be an important component of arthritis treatment in the 21st century.

...Cannabis has also been shown to have powerful immune-modulation and anti-inflammatory properties,[23-26] suggesting that it could play a role not just in symptom management but treatment of arthritis. In fact, one of the earliest records of medical use of cannabis, a Chinese text dating from ca. 2000 BC, notes that cannabis "undoes rheumatism," suggesting its anti-inflammatory and immune modulating effects were known even then.[27]

Modern research on cannabidiol (CBD), one of the non-psychoactive cannabinoid components of cannabis, has found that it suppresses the immune response in mice and rats that is responsible for a disease resembling arthritis, protecting them from severe damage to their joints and markedly improving their condition.[28-29]

...The immuno-modulatory properties of a group of fats found in cannabis, known as sterols and sterolins, have been used as natural alternatives to conventional rheumatoid arthritis treatments that employ highly toxic drugs to either suppress the entire immune response of the body or to palliate pain and the inflammatory process without correcting the underlying immune dysfunction.

Cytokines play a role in either fuelling or suppressing the inflammation that causes damage in rheumatoid arthritis and some other diseases. The release of selected cytokines is impaired by cannabis, but the findings differ by cell type, experimental conditions, and especially the concentration of the cannabinoids examined.[38-41] A sterol/sterolin combination has been experimentally demonstrated to reduce the secretion of the pro-inflammatory cytokines controlled by the TH2 helper cells and to increase the number of TH helper cells that regulate the secretion of antibodies from the B cells. This selective activation and inhibition of the immune system results is an effective control of the dysfunctional auto-immune response.

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The cannabinoid system and immune modulation

Studies on the effects of marijuana smoking have evolved into the discovery and description of the endocannabinoid system. To date, this system is composed of two receptors, CB1 and CB2, and endogenous ligands including anandamide, 2-arachidonoyl glycerol, and others. CB1 receptors and ligands are found in the brain as well as immune and other peripheral tissues. Conversely, CB2 receptors and ligands are found primarily in the periphery, especially in immune cells. Cannabinoid receptors are G protein-coupled receptors, and they have been linked to signaling pathways and gene activities in common with this receptor family. In addition, cannabinoids have been shown to modulate a variety of immune cell functions in humans and animals and more recently, have been shown to modulate T helper cell development, chemotaxis, and tumor development. Many of these drug effects occur through cannabinoid receptor signaling mechanisms and the modulation of cytokines and other gene products. It appears the immunocannabinoid system is involved in regulating the brain-immune axis and might be exploited in future therapies for chronic diseases and immune deficiency.

http://www.jleukbio.org/content/74/4/486.full

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