Chronic Inflammation and Chronic Disease

We have looked at why chronic inflammation occurs, what contributes to it and how we can help relieve it in other articles. Here, we want to look at the reasons for why it is so important to get rid of it.

Some diseases caused by Chronic inflammation happen fairly soon. Many take a long time, often ten to twenty years or more. Reducing inflammation can delay or even prevent many chronic diseases! Most of these diseases are far more preventable than curable – so it makes a lot of sense to make some effort to reduce chronic inflammation.

Here are some diseases with strong evidence currently being researched.

Alzheimer’s                     Dermatitis                       Multiple Sclerosis
Arthritis                          Diabetes Insipidus Myalgias
Arthritis, Rheumatoid Eczema Nephritis
Asthma, Allergies            Fibromyalgia (FM)            Osteoarthritis
Atherosclerosis                Inflammatory Bowel Parkinson’s
Autoimmune                   Interstitial Cystitis            Psoriasis
Cardiovascular                Irritable Bowel Syn. Sarcoidosis
Colitis                           Joint pain Sjögren’s Syndrome
Crohn’s                         Lupus Erythematous Ulcerative Colitis

Following is a little further discussion of some of these diseases, in alphabetical order:

Alzheimer’s, Dementia, Cognitive Decline

Medical specialists are becoming interested in Alzheimer’s and inflammation these days. In the journal Neurology in 1997, neurologists presented research that people who had been regularly taking anti-inflammatory medicine like Ibuprofen had much lower rates of Alzheimer’sdisease. In the New England Journal of Medicine in 2001, a study showed an 80% reduction in risk of Alzheimer’s among those taking anti-inflammatory medicines daily for two years.

Linda Van Eldik, neurobiologist at Northwestern University School of Medicine, explains that whenever the brain is injured or irritated, glial cells pump out cytokines. These are chemical signals to begin the inflammatory process. However, “in chronic neurodegenerative diseases like Alzheimer’s, these glial cells are activated too high or too long or both,” says Van Eldik.

Now, the path to Alzheimer’s disease is being strongly linked to discrete inflammation in the area of the brain Alzheimer’s affects. Inflammation begins with an immune response to a very specific threat (insoluble amyloid beta fibrils). However, new research suggests delay or prevention of Alzheimer’s may be possible with anti-inflammatory treatments.

Several observational studies have linked chronic low-level inflammation in older adults to cognitive decline and dementia, including vascular dementia and Alzheimer’s disease (Singh et al. 2011). One study found that people with the highest CRP and IL-6 levels (> 2.4 pg/mL) had a ~30-40% increased risk of cognitive decline compared to those with the lowest levels (< 1.4 pg/mL). (Yaffe et al. 2003). Inflammatory markers can be elevated before the onset of cognitive dysfunction, indicating their potential relevance as a prognostic tool in high-risk individuals (Singh et al. 2011).

Not surprisingly, chronic inflammation has also been linked to depression with higher circulating levels of IL-6 and CRP. Whether inflammation leads to depression or whether depression leads to inflammation is still being debated.

Autoimmune Disorders

Among the best-known autoimmune diseases are: rheumatoid arthritis, lupus, multiple sclerosis, insulin-dependent (type 1) diabetes, Crohn’s disease, and ulcerative colitis. Rheumatoid arthritis, in particular, has been studied closely for links with chronic inflammation and its characteristic biomarkers. Both TNFa and IL-6 are elevated in patients with rheumatoid arthritis.

People with systemic lupus erythematosus also show elevated levels of IL-6 and TNFa, making it is clear that inflammation has a role.

Inflammatory Bowel Diseases, such as Crohn’s disease or ulcerative colitis, are another example of autoimmune disorders where inflammation plays a key role. In fact, doctors are debating about whether IBDs are really autoimmune diseases or whether they should be put in another, relatively new category known as “auto-inflammatory” diseases. In both cases, blocking TNFa or IL-6 can be an effective treatment for patients who do not respond to more conventional treatments.

Cancer

Several studies have established links between chronic low-level inflammation and many types of cancer, including lymphoma, prostate, ovarian, pancreatic, colorectal and lung (Aggarwal et al. 2006).(Kundu et al. 2008) There are several mechanisms by which inflammation may contribute to carcinogenesis, including alterations in gene expression, DNA mutation, epigenetic alterations, promotion of tumor vascularization, and the expression of pro-inflammatory cytokines that have roles in cancer cell proliferation (Kundu et al. 2008, Balkwill 2009)

Researchers in the journal Cell presented their findings about what could be the long-elusive mechanism through which inflammation can promote cancer. “There is plenty of evidence that chronic inflammation can promote cancer” says Alexander Hoffmann, at U.C. San Diego, who led a study. “We have identified a basic cellular mechanism that we think may be linking chronic inflammation and cancer.”

Cancer is much like Alzheimer’s in that it does not necessarily begin with inflammation. However, inflammation can greatly accelerate the development of cancer once it has begun. NFkB helps cells, which have gone through DNA transformation (cancerous cells, in this case), avoid death. This allows them to continue to proliferate.

In addition, NFkB plays a role in the angiogenesis of cancerous tumors. (This is when they develop their own blood supply, and the metastasis of cancer.) NFkB activity is turned up by the pro-inflammatory messengers, including TNFa and IL-6. In people suffering from chronic inflammation, the risk of certain cancers can be much higher.

“Studies with animals have shown that a little inflammation is necessary for the normal development of the immune system and other organ systems,” explains Hoffmann. “But there can be too much of a good thing. In the case of chronic inflammation, the presence of too much p100 may over activate the developmental pathway, resulting in cancer.”

Heart, Coronary & Cardiovascular Disease

Inflammation also plays a role in heart disease! In fact, inflammation is so closely associated with heart disease that many doctors now use a test for inflammation called CRP (C-reactive protein) to assess a person’s risk of heart attack. Research shows that CRP can predict the risk of heart attack and stroke as well or better than cholesterol levels.

This is because the immune system attacks LDL “bad” cholesterol that has been embedded in arterial walls. Also, studies have shown that chronic inflammation directly leads to a damaged endothelium (the lining of our blood vessels). The ongoing inflammation eventually damages the arteries – which can cause them to burst. This, in turn, causes another round of plaque patching build-up.

Inflammation is an integral part of atherosclerosis (oxidized low-density lipoprotein cholesterol stimulates the inflammatory response). It is these circulating inflammatory cytokines that are predictive of peripheral arterial disease, heart failure, atrial fibrillation, stroke, and coronary heart disease (Singh et al. 2011, Emerging Risk Factors Collaboration et al. 2010).

That is why researchers have found that CRP is a moderate indicator of coronary heart disease. Total cholesterol levels, blood pressure and smoking still rules but CRP may play a role in their onset.

Inflammation is the match that starts the blaze in the development of heart diseases. Without an elevated level of CRP damaging the blood vessels, much less plaque would form – even if all other factors were present.

Diabetes

Recent research has linked inflammation, caused by increased fat tissue, with insulin resistance. In type 1 diabetes, the immune system attacks the cells that make insulin. As circulating pro-inflammatory messengers and macrophages increase, insulin resistance follows. While other factors can contribute to insulin resistance and diabetes, the link between chronic inflammation caused by obesity and diabetes is very strong.

The infiltration of macrophages into fat tissue and their subsequent release of pro-inflammatory cytokines into circulation occur at a greater rate in type II diabetics than in non-diabetics (Pickup et al. 2000, Nappo et al. 2002, Ortega Martinez de Victoria et al. 2009). Pro-inflammatory cytokines clearly decrease insulin sensitivity (Bastard et al. 2006).

Children who have allergies are less likely to develop type 1 diabetes. “Children with type 1 diabetes are less likely to get asthma, eczema, or hay fever,” says pediatrician Dr. Alan Greene, MD. “And the reverse is true, that those with asthma, eczema, or hay fever are less likely to get type 1 diabetes.”

“One possible explanation for this is the imbalance between two types of immune cells, T-helper 1 cells and T-helper 2 cells. In children with diabetes, the balance tends to favor T-helper 1 cells; in those with asthma, T-helper 2 cells. It’s difficult for one child to have both.”

Type II diabetes is also linked to inflammation, as chronic inflammation releases TNF (tumor necrosis factor), which makes cells more resistant to insulin. “No one would have thought these things were related, but they are” says Dr. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health.

Kidney disease (CKD)

The chronic, low-grade inflammation in CKD can lead to the retention of several pro-inflammatory molecules in the blood (including cytokines, AGEs, and homocysteine) (Glorieux et al. 2009). The reduced excretion of pro-inflammatory factors by the diseased kidney can accelerate the progression of chronic inflammatory disturbances elsewhere in the body, such as the cardiovascular system.

Osteoporosis

Inflammatory cytokines (TNF-α, IL-1β, IL-6) are involved in normal bone metabolism. Osteoclasts, the cells that break down (resorb) bone tissue, are a type of macrophage and can be stimulated by pro-inflammatory factors. Systemic elevations in pro-inflammatory cytokines push bone metabolism towards resorption, and have been observed to induce bone loss in persons with periodontal disease, pancreatitis, inflammatory bowel disease, and rheumatoid arthritis (Cao 2011). An increase in the levels of inflammatory cytokines is also a mechanism by which menopause stimulates bone loss.

(More diseases, and expanded descriptions, will be added as time permits.)

What to Do? – Take a Quality Anti-Inflammatory Supplement.

Our Infl-Mazing Plus relief formula contains concentrated anti-inflammatory compounds, such as Theracurmin and Meriva and 4 more herbs and nutrients! Of course, we should eat enough fresh fruits, vegetables, and spices to help moderate your immune response. However, everybody falls short and our current world environment doesn’t help, so a quality supplement to help with inflammation is a good idea.

We are not fond of taking non-steroidal anti-inflammatory drugs (NSAIDs) unless directed to do so by your doctor. All NSAIDs can have toxic side effects with prolonged use, such as liver damage, and are not meant to be taken for more than a short period of time. Herbal anti-inflammatory supplements can actually provide some of the same relief associated with NSAIDs, but without the risks of side effects!

It may have taken many years for inflammation to build up, but that doesn’t mean it has to take the same amount of time to reduce it. If it seems like too much to do everything all at once, start with one BIG, easy-to-do step – our anti-inflammation supplement.

As you begin to make lifestyle steps, increasing your spice intake and having a daily bowl of vegetables, etc. adds to lowering inflammation. As your body begin to fight inflammation, you’ll start to feel well enough to make another change, and then another, and then another.