Saturday, December 10, 2011

What are Cytokines?

Cytokines are proteins that signal cells to act throughout the body. They are inflammatory in nature and are classified as proteins, peptides, and polypeptides (a nice pictorial of cellular immunity at work). One commonly known cytokine, interferon type I is used to treat hepatitis B and C.


There is debate in the scientific community whether or not cytokines are hormones. This may be due in part to their anatomy, origin, and level of concentration in the body. Cytokines can be concentrated 1,000s times greater during trauma or infection. Hormones are generally secreted by localized organs/glands such as the pancreas while cytokines can be generated from nearly every nucleated cell in our body including macrophages (WBCs), endothelial cells (interior of our body) like those that line our blood vessels, and epithelial cells (surface of our body) like our skin.


Here is a video representation courtesy of nucleusinc.org:






Just thinking about the structure of cytokines brings to light the fact that they are all highly dependent upon adequate levels of cholesterol since cell membrane structural integrity and intracellular communication are all reliant on cholesterol. In addition, WBCs act immunoprotectively with cholesterol in the blood to bind to and inactivate toxins such as bacteria, viruses, fungi, and free radicals. Here is a good site with practical application tips to reduce inflammation while enhancing the body's immunoprotective abilities naturally without dependence drugs which are partly responsible for iatrogenic disease and death. This also highlights one way cholesterol plays a role in immunity and how it may relate to other diseases such as cancer (McCully, Ravnskov & Rosch, 2011).  

Cytokines are active in both acute and chronic inflammation. This is a two edged sword since they actively facilitate immune responses in our body. Chronic inflammation can have detrimental long-term impact on our health and should be minimized since inflammation is a contributory factor in cardiovascular disease. This may be how statins are protective by reducing C-reactive protein (CRP) an inflammatory marker, needless to say the harm associated with statin's cholesterol lowering effect is greater than its documented benefits.


There are many factors that stimulate chronic inflammation and this is the underlying issue we should seek to correct when considering any level of prevention. Addressing these health abnormalities through a symptomatic response (pharmaceuticals) can have untold long-term consequences including cancer.


The greatest benefit of acute inflammation occurs when we have an infection. Inflammation stimulates cholesterol production. The bad news is that as chronic inflammation continues it inhibits nitric oxide (NO), a potent vasodilator, increases blood pressure and places the lining of our blood vessels at increased risk through atherosclerosis. The mechanisms responsible for atherosclerosis are very complex and the presence of cholesterol does not necessarily indicate cause. One of statins' benefits comes from inflammation reduction. According to Chris Masterjohn, (he describes the process in great detail here), statins can provide a co-occurring negative impact by reducing Coenzyme Q10 production which works in conjunction to NO to improve cardiovascular function and negate the effects of atherosclerosis. Statins are also known to cause muscle degeneration. Think about your heart. It is a muscle.


We need cytokines to keep us healthy when we get sick. We also need to understand how chronic inflammation occurs and to moderate the its effects by our lifestyle choices. When trying to mitigate these risks, understanding what causes inflammation and how to prevent it can reduce the risk of health problems down the road. We should approach it though our diet and lifestyle not a drug . . . unless you want to take that risk.


References

McCully, K., Ravnskov, U., and Rosch, P. (2011). The statin-low cholesterol-cancer conundrum. Quarterly Journal of Medicine. doi: 10.1093/qjmed/hcr243

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