Colds and the immune system

The New York Times recently printed a timely op-ed about the common cold, arguing that the remedies people take for them are generally useless and that the disease itself is misunderstood:

Here was a new insight in cold science: the symptoms are caused not by the virus but by its host — by the body’s inflammatory response. Chemical agents manufactured by our immune system inflame our cells and tissues, causing our nose to run and our throat to swell. The enemy is us.

Indeed, it’s possible to create the full storm of cold symptoms with no cold virus at all, but only a potent cocktail of the so-called inflammatory mediators that the body makes itself — among them, cytokines, kinins, prostaglandins and interleukins, powerful little chemical messengers that cause the blood vessels in the nose to dilate and leak, stimulate the secretion of mucus, activate sneeze and cough reflexes and set off pain in our nerve fibers.

So susceptibility to cold symptoms is not a sign of a weakened immune system, but quite the opposite. And if you’re looking to quell those symptoms, strengthening your immune system may be counterproductive. It could aggravate the symptoms by amplifying the very inflammatory agents that cause them.

I always find it a bit weird that whole industries exist to sell products that are either useless or actively harmful. While that is understandable enough when it comes to harmful-but-fun products like alcohol and tobacco, it is more ethically dubious in the case of things like cold medications that do not stand up to scientific scrutiny. Quite probably, they should bear warning labels from some kind of consumer protection agency saying: “As far as science has been able to establish, this product is useless for reducing the duration of colds.”

Author: Milan

In the spring of 2005, I graduated from the University of British Columbia with a degree in International Relations and a general focus in the area of environmental politics. In the fall of 2005, I began reading for an M.Phil in IR at Wadham College, Oxford. Outside school, I am very interested in photography, writing, and the outdoors. I am writing this blog to keep in touch with friends and family around the world, provide a more personal view of graduate student life in Oxford, and pass on some lessons I've learned here.

4 thoughts on “Colds and the immune system”

  1. The existence of snake oil cures is problematic, but is restricting them really a legitimate role for government? I can see the case for restricting things that are actually dangerous, but should the government be chasing down Halls because their cough drops don’t actually do anything?

  2. I’d like to see a SINGLE piece of science about this rather than an op-ed piece. The idea that some bodies are able to kill cold viruses without showing symptoms because they don’t make the same amount of inflammatory agents is very intriguing. It could have huge implications for cold sufferers everywhere. But the whole article is just speculation, by a non-scientist. This is just terrible journalism about bad science. Hell, it’s not even bad science, it’s just made up (or very poorly referenced, if she is basing it on any kind of actual research).

  3. I should definitely do some research into whether there is any meaningful empirical basis to the claims in this editorial.

  4. Light and Scanning Electron Microscopy of Nasal Biopsy Material from Patients with Naturally Acquired Common Colds

    As our knowledge of the histopathology of common colds is very limited, we have undertaken a blind quantitive examination by scanning electron microscopy and light microscopy of 56 nasal biopsies, taken from 29 volunteers with naturally acquired colds. In agreement with earlier reports we found evidence of sloughing of epithelial cells, but in contrast to in vitro experiments, this did not result in a destruction of the epithelial lining, which by and large remained continuous, with structurally normal cell borders. There was a significant increase in the number of neutrophils, both in epithelium and in lamina propria, already on the 2nd day of the disease, and the hypothesis is advanced that the virus infection itself is the cause of the local neutrophilia. The only other abnormality demonstrated was an increased number of extracellular erythrocytes in the acute stage. The histological picture was not suggestive of an involvement of epithelial mast cells in the inflammation.

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