The following are notes taken from the book Beyond Aspirin by Thomas M. Newmark (President of New Chapter) & Paul Schulick (Founder of New Chapter).
COX-2 inhibitors refer to compounds, both synthetic and natural, that have the ability to inhibit an enzyme in the body referred to as cyclooxygenase-2. A growing body of science is demonstrating that COX-2 inhibition prevents or reverses a number of currently life-threatening cancers.
Examples of synthetic COX-2 inhibitors are Celebrex and Vioxx, also referred to as “Safe Aspirin.” These two drugs have fewer side effects than NSAIDS. The Safety of “Safe Aspirin”: Are they safe for all people? Are they ideal for anyone on a long-term basis? In the Journal of the American Medical Association, over 100,000 people a year die from side effects from taking prescription pharmaceuticals. While there can be a time and a place for synthetic options, integrating traditional herbal COX-2 inhibitors are safe and have been used for thousands of years. This blog post will explain that COX-2 inflammation lies at the root of many diseases, including cancer, Alzheimer’s disease and many forms of arthritis.
The pain intervention of choice has been the long-term use of potentially dangerous nonsteroidal anti-inflammatory drugs (NSAIDS) like aspirin, ibuprofen and naproxen. There are serious long-term side effects such as kidney damage, peptic ulcers and associated severe hemorrhaging and perforation.
It is estimated that as many as 16,500 people died last year from serious complications from NSAID-induced bleeding. To put that number into perspective, it is almost identical to the number of people whose deaths last year were attributed to AIDS-related conditions.
Pain from arthritis is often caused or exacerbated by inflammation. Contrary to commonly held belief, it is not an inevitable condition of aging. It is a disease condition in which joints and their connective tissue degenerate; joints, cartilage and bone become tender and painful. Free-radical stress and pain-receptor sensitivity, for example, can significantly aggravate the osteoarthritis (OA) condition. The inflammatory processes stimulate bone deterioration and can impede bone and cartilage repair.
Pain is nature’s way of telling us that something is wrong.
Our quarrel is not with inflammation, but with excessive inflammation. There is supposed to be a perfect balance between the salvage and re-creation of cartilage. If the body does not create enough new cartilage to take the place of the old, the bones lose their soft protection, resulting in weakness, pain and loss of flexibility.
Not all inflammation is bad.
As we age, our bodies have a hard time repairing itself, such as responding to joint imbalances and wound-healing. We need allies. Herbal COX-2 inhibitors support the aging body.
Osteoarthritis (OA) affects 70% of the elderly population. Rheumatoid arthritis (RA) affects fewer individuals, but is far more disabling. RA is more a disease of the young, verses the older profile of the OA sufferer. RA’s distinguishing symptom is generalized inflammation. Once again, an over-stimulated COX-2 enzyme lies at the core of the problem. Cartilage comes and goes; cartilage maintenance works until the inflammation process accelerates the disintegration of the tissue. The bones lose their protective tissue, bone can rub against bone, and joints can lock up. Typically, when the joints become heated and swollen, people reach for the aspirin bottle.
It was discovered that aspirin decreased the production of inflammatory hormones, or chemicals, called prostaglandins. Prostaglandins were known to be created by the cyclooxygenase (COX) enzyme. Inhibiting COX inhibited the creation of inflammatory prostaglandins. All too often the chronic use of NSAIDS caused severe bleeding and kidney damage – even death. These dire consequences arose because NSAIDS, some worse than others, disrupted the formation of inflammatory prostaglandins, but also inhibited the balancing and protective features of the COX enzyme. COX is essential for proper kidney function and for protecting the stomach. You risked damaging critical organ systems in the body.
The Discovery of COX-2
In 1991 it was discovered that the COX enzyme was two enzymes, not just one. Both COX enzymes had the ability to burn a particular fat in the body. The enzyme that came to be known as COX-1, however, was the one responsible for maintaining homeostasis in our kidneys and stomach. COX-2 was identified as the one responsible for the creation of inflammatory prostaglandins out of the fat called arachidonic acid (AA).
Scientists at Monsanto located a highly specific COX-2 inhibitor called celecoxib, or Celebrex. Another selective COX-2 inhibitor is Vioxx. They showed substantial promise as a NSAID that could often reduce pain and inflammation without the side effects assoicated with other NSAIDS.
COX-2 & Cancer
Imbalanced inflammation contributes to the growth of cancers in various organs. As COX-2 activity increases, cancers increase. We are coming to understand that cancer cells use inflammation, born of COX-2, as a mechanism for survival and growth.
Scientists have observed an unexplained relationship between long-term use of NSAIDS for arthritis pain relief and a lower incidence of colon cancer. As stated earlier, the COX-2 enzyme metabolizes a type of fat AA. Scientists have also discovered that when AA is metabolized by 5-lipoxygenase (a type of enzyme), the by-product feeds cancer cells of the prostate.
Cancer proliferation involves platelets. Platelets circulate throughout the body. If a cancer cell can stick onto a blood platelet, it will be carried to another site of potential growth in the body. With inflammation we normally see an increase of blood flow and platelets in the inflamed region.
One of the hormones made by COX-2 from AA is a blood vessel growth stimulator named “thromboxane.” This is produced when our tissue is damaged and new blood vessels are stimulated to grow new tissue. If the body is chronically inflamed and this hormone is consistently making new blood vessels, then cancer tumors might be present. This process of stimulating new blood vessel growth is called “angiogenesis.”
It is natural that the body tries to heal itself. The body strives for homeostasis. COX-2 metabolites can inhibit apoptosis, which means programmed cell death (cellular suicide). This is natural, the body clears out the debris to make room for new and healthy cells. However, during inflammation the body keeps the old cells to heal the wound, creating substances that prevent apoptosis. This is a good thing for healthy cells, but is bad for malignant cells. One of the ways our body can turn off apoptosis is through COX-2 expression.
When a tissue is injured (infection, trauma), it releases chemical signals like cytokines and chemokines. Their role is to send white blood cells to the damaged area. This leads to swelling of inflammation. One way that they work is by sending free radicals of oxygen. They steal electrons to heal the damaged tissue or invading//foreign substances. If there is too much inflammation and too many cells are destabilized, DNA mutation and cancer cell growth may occur.
Nitric oxide (NO) is a type of free radical molecule. NO goes in and out of existence very rapidly, it is concentrated in inflamed areas, and is thought to play a role in the formation of diseases, including cancers (Viagra also creates NO). The preventative power of herbs, I like to call them herbal allies, are the approaches of choice compared to conventional protocols.
Science Meets Traditional Medicine
Using the silver bullet approach is not bad, but the approach is to use one synthetic molecule compared to the complex phytochemicals of plants. We now understand that Homo Erectus used plants perhaps even 800,000 years ago (See Urban Moonshine’s blog post on Paleolithic Herbalism ). The methodology for selecting the COX-2 inhibiting herbs by Thomas & Paul was done carefully. They looked at the traditional use of anti-inflammatory herbs, then weeded out some herbs that are either endangered or aren’t available in a high-quality form. Then they looked at the herbs with two perspectives: the observed pharmacological effect of the whole herb VS the principal “phytochemical” constituents of each herb. For example, you have vitamin C compared to an orange. Curcumin compared to turmeric or ginger. (See previous post on synthetic vs natural https://healthylivingmarket.com/nutrients/) Thomas and Paul relied on the USDA Phytochemical Database and the University of Illinois Napralert Database for their consideration of COX-2 inhibiting herbs.
Next week we will look in depth at each herb that they selected. Stay tuned!