Inflammation is an immune response; a response to an infection, an irritation, or an injury. Immune cells are called to the site through the blood stream. The blood vessels near the site become miraculously permeable and the site becomes warm and red due to the increased blood flow (warm, hence inflammation).
Neutrophils and macrophages engulf microorganisms and phagocytes are called in. Some immune cells try to “eat” the invaders; others excrete hydrogen peroxide (and other oxidative chemicals) trying to kill them so they can be cleaned up by the phagocytes and friends.
Inflammation is a part of the body’s natural defense system against injury and disease.
Chronic inflammation, on the other hand, is a disease. The system has gotten hung up, and instead of protecting the organism (our bodies) it starts to kill the organism, slowly but surely.
Today modern medicine is starting to admit that chronic inflammation is the main contributing factor to all chronic degenerative diseases, and the root cause of the two greatest killers in America: Cancer and Heart Disease. In deed, chronic inflammation might just be the root cause of all degenerative disease.
Accepting this would certainly simplify preventive medical practices (even as non existent as they presently are), but I find it interesting that once in our early history medicine tried to create a theory that reduced all disease into one or two categories. History does, it seems, repeat itself.
Pro-inflammatory cytokines are the part of our immune systems that attack and kill cells with oxidative chemicals. If they don’t stop their attacks, they will start killing cells our bodies need. The inflammation in a joint can eat away at our cartilage and you’ve got a serious case of arthritis. Unchecked inflammation in an organ, say the pancreas, can cause diabetes. Unchecked inflammation is now thought to be responsible for cardiovascular disease and cancers. The elderly are especially vulnerable to this sort of unchecked inflammation since the body looses the ability to “down-regulate” inflammation with age.
You do not have to be old to have chronic inflammation. You can have it and not know it, until it is too late. Thus we are going to spotlight those tests for having chronic inflammation or being at risk for chronic inflammation.
After that, we will outline the therapies to bring down chronic inflammation and how to avoid it in the first place, for you will soon find that inflammation begins on the end of your fork.
Does anyone recall the headlines in the New York Times about blood vessels bursting like popcorn? The article told us that the latest theory on the cause of heart disease is inflammation. One of the doctors who made this discovery was Dr Paul Ridker. The results of his studies in the early 1900s landed on the front pages of the New York Times right around the turn of the century. We’ve covered this in our book, Bypassing Bypass, but we must tell you a little about it right now.
Microorganisms cause inflammation within our blood vessels, and the inflammation attacks the inside of the arteries. Besides immune cells being sent to the site to fight the inflammation, lipoprotein(a) is sent to form a sticky patch over the damaged area; a patch that that can grab onto cholesterol (supposedly bad cholesterol) and a cholesterol bandage is created over the site. However, the inflammation is inside now. The patch grows and bulges. The inflammation grows and bulges. Eventually, “blood vessels explode like popcorn.”
The reason I called the cholesterol “supposedly bad” is that it tried to save your life. If the inflammation continued without being patched by cholesterol, the artery would eventually open and you’d bleed out.
However, because the inflammation was not halted, the bandaged area has burst and the body must quickly respond because your artery is about to open wide. How is this patch formed? By a blood clot.
A clot is formed at the site to patch up the damage. Eventually, lipoprotein(a) will come along and form a sticky patch and attract cholesterol to form a better bandage, but there is a problem, and it has to do with our diet and lifestyle, our hypercoagulable lifestyles. Our blood tends to clot “too” much. The clot formed is usually bigger than it need be, and being such, the chances of it breaking loose increase. If it does break loose and it goes to your brain, you suffer a stroke. If it goes to your heart, you suffer a heart attack.
This sums up a good deal of what we have to say in Bypassing Bypass (which we are rewriting) but there is a lot more to learn (so if you want a copy, go get it here: Bypassing Bypass, and keep in mind that you are eligible to get the updated online version free when it is released).
Knowing you have a problem is the first step to fixing the problem.
The first test you should know about is called the C Reactive Protein test. If your CRP test is positive, you have are three times more likely to die of a heart attack, no matter how many cholesterol drugs you are on, or if your cholesterol is normal. [NEJM, 1997]
Please note that there are two CRP tests. The one that is needed MUST BE specified to the lab as H.S.C.R.P., which is high-sensitivity cardiac reactive protein test. This is crucial as it is measured in mg/L with a range of 3.0 mg/L being a high relative risk. Now, the regular test, CRP, is measured in ml’s. Thus if your results came back showing that your result is 3 you look great and are considered low risk. But, if the lab measured CRP and not hs-CRP than the number is actually 3.0 which is not good.
Since many MDs are still unsure of their positions on chronic inflammation, they often order the wrong test without realizing it. So, be on your toes and always try to know more than your doctor
If you have Vulnerable Plaque (the popcorn popping arteries described above) you have an 800% greater chance of a heart attack.
In July of 2001, JAMA published a study on chronic inflammation and the risk of diabetes. Another test they used, besides the CRP, was an inflammatory marker test, the IL-6. The study concluded that your chances of developing type two diabetes are easily predicted by the outcome of the CRP and IL-6 tests together. The ultimate test would be the Inflammatory Cytokine Profile consisting of the two mentioned plus TNF (tumor necrosis factor), interleukins -1 beta and 8.
What is at stake?
Depression, asthma, pancreatitis, Parkinson’s, lupus, anemia, kidney failure, psoriasis, and fibrosis might just be the start. All of these diseases have a suspected root cause of chronic inflammation.
Seemingly unrelated illnesses often exhibit excess levels of pro-inflammatory markers:
-Allergy — Inflammatory cytokines induce autoimmune reactions
-Alzheimer’s — Chronic inflammation destroys brain cells
-Anemia — Inflammatory cytokines attack erythropoietin production
-Aortic valve stenosis — Chronic inflammation damages heart valves
-Arthritis — Inflammatory cytokines destroy joint cartilage and synovial fluid
-Cancer — Chronic inflammation causes many cancers
-Congestive heart failure — Chronic inflammation contributes to heart muscle wasting
-Fibromyalgia — Inflammatory cytokines are elevated
-Fibrosis — Inflammatory cytokines attack traumatized tissue
-Heart attack — Chronic inflammation contributes to coronary atherosclerosis
-Kidney failure — Inflammatory cytokines restrict circulation and damage nephrons
-Lupus — Inflammatory cytokines induce an autoimmune attack
-Pancreatitis — Inflammatory cytokines induce pancreatic cell injury
-Psoriasis — Inflammatory cytokines induce dermatitis
-Stroke — Chronic inflammation promoted thromboembolic events
-Surgical complications — Inflammatory cytokines prevent healing
Lets take a closer look at some diseases and their inflammatory connection.
-Cancer: in an article entitled “Chronic Inflammation and Cancer,” by Emily Shacter, PhD published in Oncology, she sums up her findings thus:
A substantial body of evidence supports the conclusion that chronic inflammation can predispose an individual to cancer, as demonstrated by the association between chronic inflammatory bowel diseases and the increased risk of colon carcinoma. Chronic inflammation is caused by a variety of factors, including bacterial, viral, and parasitic infections, chemical irritants, and nondigestible particles. The longer the inflammation persists, the higher the risk of associated carcinogenesis. This review describes some of the underlying causes of the association between chronic inflammation and cancer. Inflammatory mediators contribute to neoplasia by inducing proneoplastic mutations, adaptive responses, resistance to apoptosis, and environmental changes such as stimulation of angiogenesis. All these changes confer a survival advantage to a susceptible cell. In this article, we discuss the contribution of reactive oxygen and nitrogen intermediates, prostaglandins, and inflammatory cytokines to carcinogenesis. A thorough understanding of the molecular basis of inflammation-associated neoplasia and progression can lead to novel approaches to the prevention and treatment of cancer. [ONCOLOGY 16:217-232, 2002]
Click on the picture to the right to view an interesting 10 minute video from the company that produces immune26 to help control inflammation and their recent pilot study on the reduction of C-Reactive Protein.