Hemorrhoids Inflammation

Inflammation Swelling

Overwhelming scientific evidence shows that the brain, nerves, and immune system interact, generating a new area of investigation called psychoneuroimmunology, or simply mind/body medicine. Although most of us recognize that extremely stressful events or unremitting stress can cause people to become more accident prone or lead to flare- ups in normally benign conditions, scientists

STRESS AND INFLAMMATION

Stress causes the brain and nerves to release peptides (small proteins, composed of two or more amino acids), neurohormones(are active in or produced by the brain to carry out activities), and neurotransmitters(chemicals that transmit messages between brain and nerve cells), that stimulate immune cells to release a cascade of inflammatory mediators, causing swelling, pain, and reduced mobility. The immune response can be localized to one area or generalized throughout multiple body systems. If the inflammatory response continues for extended periods of time, scarring and deformity can result. Although normally associated with aging, chronic inflammation can occur in younger individuals and is, in fact, accelerated aging brought on by stress.

THE INFLAMMATORY PROCESS

There are two phases of inflammation: acute and chronic. Acute inflammation is nature's way of protecting us from injury or infection. When traumatic injury is suffered or a foreign substance enters the body, large engulfing cells (macrophages), smaller scavenging white blood cells (phagocytes), and blood platelets are attracted to the site of the injury. They move into a frenzied state of activity as they engage the infectious agent damaged tissue.

Macrophages begin releasing signaling chemicals, called cytokines, that increase capillary permeability, allowing fluids and red blood cells to flow into the area. Macrophages signal other immune cells to produce various inflammatory mediators. Pain centers in the brain begin releasing neurohormones and neurotransmitters. The damaged site becomes inflamed and immobilized by swelling and pain. This prevents further injury and seals off the damaged area, thus confining the infectious agent. During this kind of inflammatory response, dead cells accumulate. All of this has to be cleaned up, and the damaged tissue repaired.

The acute phase lasts between 24 and 48 hours. Then the cleanup and recovery process begins, which may take anywhere from a few days to several months as the cellular debris is removed from the site of injury and healthy replacement tissue grows. During acute inflammation, large numbers of free radicals are generated by phagocyte activity. More free radicals are released during the enzymatic destruction of microbes and necrotic tissue. If these radicals are not neutralized by antioxidants, they will lead to chronic inflammation.

Chronic inflammation, unlike the acute phrase, is not self-limiting and is more prolonged. It is caused by persistent irritants, including free radicals, severe stress, environmental agents, or microbes that are resistant to the immune system's attack. Severe pain, continuing tissue damage, immobility, and formation of scar tissue result.

Chronic inflammation fuels its own progressive tissue destruction by recycling inflammatory mediators: pro-inflammatory prostaglandin 2 (PGE-2) and the cytokines interleukin 1 (IL-i), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNFa). TNFa is particularly insidious because it activates a protein, called nuclear fraction kappa B (NP-kB), that prompts joint-damaging proteolytic enzymes. These enzymes destroy connective tissue in chronic inflammatory conditions such as rheumatoid arthritis. They also cause tissue destruction in other chronic conditions, including inflammatory bowel disorders (Crohn~s and ulcerative colitis), hypertension, coronary artery disease, psoriasis, and asthma.

Fortunately, a number of nutritional therapies are effective. Prostaglandin PGE-2 produces prostanoids called cyclooxygenases 1 and 2 (COX-1 and -2) and leukotrienes. While COX-1 has important regulatory functions (like maintaining the stomach lining), COX-2 promotes inflammation. The trick is to block COX-2 but not COX-1.

Widely prescribed for inflammation, aspirin and naproxen sodium (Aleve) are nonsteroidal anti-inflammatory drugs (NSAIDs) that block both COX-1 and -2, resulting in gastric pain and ulcers. While newer drugs such as Celebrex and Vioxx block only COX-2, they are costly and may exacerbate heart problems.

The good news is that researchers have found several natural COX-2 inhibitors, including horse chestnut, gotu kola, bioflavenoid complexes, omega-3 fatty acids, and green tea catechins.

The active ingredient in horse chestnut seeds is aescin, a substance shown to promote circulation of the blood through the veins. It also acts as an anti-inflammatory, and has been shown to reduce swelling and edema following injury, particularly following surgery or head injuries.

It is reported that gotu kola is to have a positive effect on tissues, improving soft tissue inflammation, infection and venous insufficiency. The bioflavenoids found in proanthocyanidins such as grapes , red wine, lemons are powerful antioxidants that also suppresses production of PGE-2s. In animal studies these bioflavenoids blocked the release of arachidonic acid from cell membranes, the first step toward production of COX-2.

Omega-3 fatty acids are available in flaxseeds, walnuts, fish and algae oils. Two long-chain polyunsaturated omega-3 fatty acids, eicosapentaenoic (EPA) and docosahexaenoic (DHA) produce anti- inflammatory PGE-3 prostaglandins that effectively block the production of COX-2 in both acute and chronic inflammation. Two published studies show that people taking essential fatty acids for rheumatoid arthritis experienced symptom improvement and reduced dependence upon NSAIDs. Further research suggests omega-3 fatty acids are effective in other inflammatory conditions such as Crohn's and ulcerative colitis, both of which increase the risk of cancer.

There have been three recent animal and in vitro studies to have anti-inflammatory action. The results of one investigation suggest that green tea may be effective in treating inflammatory bowel disease and reducing swelling.