What is Inflammation?

Inflammation is classically defined as a localized tissue response in reaction to injury or destruction of tissues as a result of a variety of stimuli (e.g., infectious, chemical, mechanical, photo-electric, radiation, temperature etc.). The inflammatory process is directed at containing, destroying, or diluting the injurious agent and the injured tissue and restoring it to normal function. Acute inflammation is a self-limiting process in which the inflammatory process along with other interventions restores homeostasis.

Chronic inflammation is a state of prolonged activation of the immune response which results in chronic symptomatology;

Acute inflammation and chronic inflammation involve a series of cellular, molecular, genetic mechanisms which compromise function and create symptomatology which varies with tissue(s) involved and the severity of the immune response.

What are the causes of inflammation?

Broadly speaking, inflammation is caused by bad inputs—external factors -bad bacteria/viruses, bad air (mold), bad food, bad relationships bad thoughts, and physical trauma, too much exercise. On the other hand inflammation can be caused by internal diseases such as cancer, and autoimmune diseases.

What are the symptoms of inflammation?

Symptoms of Chronic inflammation are organ specific but include:

• Pain
• Fatigue
• Fever
• Reduced cognitive function/emotional regulation
• Restriction of function of organs involved
• Restrictions of function of musculoskeletal system
• Psycho-social dysfunction

What diseases are linked to inflammation?

Chronic inflammation is known to be a major underlying mechanism in the majority of chronic illnesses affecting western societies: these illnesses include, but are not limited to:

• All “-itis” disorders (e.g., arthritis, sinusitis, prosatitis, cystitis, thyroiditis, cholecystitis, etc)
• Chronic skin conditions such as acne vulgaris, cystic acne, drug induced acne (e.g., lamotirigine) , folliculitis
• Some chronic pain syndromes, such as sciatica, costochondritis, fibromyalgia,
• Diabetes
• Cardiovascular disease
• Mood disorders
• Cognitive disorders
• Auto-immune disorders
• Chronic infectious diseases
• Environmentally caused disorders (e.g., mold induced Sick Building Syndrome)
• Cancers
• Others

What are the traditional medical ways of dealing with inflammation?

Current anti-inflammatory approaches, (and analgesic approaches, which are included here because one of the cardinal signs of inflammation is “dolor”-i.e. pain) for chronic conditions are broken, primarily, into two broad categories: Steroidal and Non-steroidal medicines.

Steroidal medications are associated with long-term dangers including diabetes, osteoporosis, fracture, glaucoma, dependence etc.

Non-steroidal approaches include:

• Prostaglandin Inhibitors (acetaminophen),
• COX 1 and 2 inhibitors (e.g., ibuprofen, celocoxib),
• Salicylates (e.g. aspirin),
• Narcotics (e.g., codeine),
• Cannabinoids (e.g., marinol, medical marijuana),
• Interleukin 1 inhibitors (e.g., Rilonacept, an orphan drug)
• Cys-LT-inhibitors (Monteleukast-used specifically for asthma, as these receptors are present in the lung)

Chronic use of all of the above compounds are associated with a significant potential for serious side effects such as: 

• Hepatic injury(acetaminophen),
• Renal dysfunction COX 1 and 2 inhibitors (e.g., ibuprofen, celocoxib),
• Ulcers and hemorrhage (e.g. aspirin, ibuprofen),
• Addiction (e.g., codeine),
• Cognitive dysfunction (e.g., medical marijuana, narcotics),
• Infection (Rilonacept)

Natural systemic substances and their mechanisms which are used to reduce chronic inflammation include:

• Omega 3-EFA’s: EPA and DHA act by enhancing the conversion of COX to prostaglanding E3 (PG-E3), a natural anti-inflammatory which inhibits production of the strong pro-inflammatory molecule tissue damage in chronic inflammation.
• White Willow Bark: a non selective inhibitor of COX-1 and Cox 2 enzymes
  • Turmeric: A Cox 1 and 2 inhibitor, NF-Kappa Beta inhibitor, however, absorption in significant quantities is a challenge
  • Green tea: Polyphenolic compounds called catehcins; One of these, called epigallocatechin-3- galate (E3G) inhibits  Interleukin 1b, and reduces the activation of NF-Kappa B-NF-Kappa B mediated signal transduction has been implicates in the regulation of viral replication, auto-immune diseases, the inflammatory response, tumorigenesis and cell death (apoptosis); E3G also type II collagen breakdown and , like Omega 3-EFA’s inhibit  enzyme actions of aggrecanase (a proteoglycan degrading enzyme), which breakdown cartilage. Thus green tea is anti-inflammatory and protects cartilage. Green tea extract dosage: 300-400mg per day (or 3-4 cups per day). Can cause stomach irritation; contains caffeine (but can be decaffeinated).
  • Pycnogenol (pine bark): Contains polyphenols which inhibits TNF-alpha (which can induce NF-Kappa B activation) activation caused by bacteria, and MMP activity. Pycnogenol dosage: 100-200mg/day: this should not be used by those being treated with immune-suppressants or steroids; can cause diarrhea or upset stomach.
  • Boswellia: Boswellic acids (11-keto-Beta-boswellic acid is the most potent of all boswellic acids) inhibit Leukotriene B4, synthesis by inhibiting 5-LOX, thereby reducing inflammation; It reduce the white blood count in joints (a measure of inflammation) , and inhibits an enzyme (leukocyte esterase) which is elevated in rheumatoid arthritis.
  • Resveratol: Polyphenolic compounds in plant skins (e.g. red wine grapes) are potent inhibitors of TNF-alpha and (Il1B induced) NF-Kappa-Beta activation. This should not be taken if blood clotting issues are an issue;
  • Cat’s Claw (Uncaria tomentosa): once again, polyphenols inhibit activation of NF-Kappa Beta and inhibits TNF-alpha production; May cause nausea, and two case reports of acute renal failure have been reported; Doses are 20-60mg per day.
  • DrHRejoint: a combination of stinging nettle, boswellia, horsetail, garlic and celery. Very effective due to the synergistic combination of the ingredients.