Shoes, Ships, and Sealing Wax

Like my metaphors?

So last week, the Situation looked like a runaway train. Actually, it looked like a runaway train full of hazardous chemicals about to plunge off a cliff...and onto a playground full of children and puppies. All I was doing was stressing and preparing my disaster response plan.

This week Situation seems to be snoozing in the corner. So I oughta relax, right? Except I'm not...I'm afraid Situation is a violent, unpredictable, drunken lout. I'm tip-toeing around and bracing myself for when it wakes up, not knowing if it's just gonna just want some pancakes or if it's going to come at me swinging a baseball bat.

This is actually related to Heart Month. The quote of the day (from this Post article):

"This is another in a long line of accumulating, well-documented effects of stress on the body," said Herbert Benson, a mind-body researcher at Harvard Medical School. "Stress must be viewed as a disease-causing entity."

I need to find a scientific citation for this*, but my understanding is that when your body reacts to stress, the chemical response includes changes to slow your bleeding in case you happened to be bitten by a tiger or stabbed. If you don't end up bleeding, well, you've gunked up your blood vessels just like you would if you ate crappy food. It's not going to hurt once in a while, but it's not something you want to be doing all the time.

If stress is as bad a cheeseburgers, I might as well be Morgan Spurlock on day 29 of the SuperSize Me experiment.

*Found one:

Black, P. Stress, inflammation and cardiovascular disease. Journal of Psychosomatic Research, Volume 52, Issue 1, Pages 1-23:

Stress, by activating the sympathetic nervous system, the hypothalamic-pituitary axis, and the renin-angiotensin system, causes the release of various stress hormones such as catecholamines, corticosteroids, glucagon, growth hormone, and renin, and elevated levels of homocysteine, which induce a heightened state of cardiovascular activity, injured endothelium, and induction of adhesion molecules on endothelial cells to which recruited inflammatory cells adhere and translocate to the arterial wall. An acute phase response (APR), similar to that associated with inflammation, is also engendered, which is characterized by macrophage activation, the production of cytokines, other inflammatory mediators, acute phase proteins (APPs), and mast cell activation, all of which promote the inflammatory process. Stress also induces an atherosclerotic lipid profile with oxidation of lipids and, if chronic, a hypercoagulable state that may result in arterial thromboses. Shedding of adhesion molecules and the appearance of cytokines, and APPs in the blood are early indicators of a stress-induced APR, may appear in the blood of asymptomatic people, and be predictors of future cardiovascular disease. The inflammatory response is contained within the stress response, which evolved later and is adaptive in that an animal may be better able to react to an organism introduced during combat. The argument is made that humans reacting to stressors, which are not life-threatening but are "perceived" as such, mount similar stress/inflammatory responses in the arteries, and which, if repetitive or chronic, may culminate in atherosclerosis.

Posted by Nic at February 10, 2005 11:22 AM