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And so it goes, a recent study (King et al., University of Chicago, published in JAMA) has established statistical link between the length of sleep and rate of calcification of the coronary arteries. According to study authors, in about 500 adult study participants, one extra hour of sleep, assumed averaged over the 5-year period between 2000/2001 and 2005/2006, decreased the estimated risk of calcification by 33%. They just don't know why.

The three possible explanations, according to them, are:

#1, there may be factors connecting sleeping time with cardiovascular disease that they are not aware of (no kidding!);

#2, some hormones with anti-inflammatory effects, like cortisol, may be more efficiently released with the prolonged sleeping time, suppressing the process of arterial plaque build up (thus, also, calcification), and

#3, blood pressure is lower during sleep (so what?).

Cortisol could have beneficial effect, but why limit consideration to this single factor? It is known that the entire body metabolism slows down during sleep. Direct consequence of it is lower rate of oxidation of tissues, including arterial lining. Less oxidation, less cellular damage and inflammation, less plaque formation and calcification. At the same time, the repair process is more efficient, one of the effects being also reduction in plaque formation.

Simply put, we need sleep to last longer. Slower rate of calcification is only one among many health benefits of getting good night's sleep.

But this generalized, common sense explanation becomes less obvious when we look at the typical sleep pattern. So called slow-wave, delta, or deep sleep, when brain activity - and metabolism - fall at their lowest level is entirely contained within the first three hours (stage 3 and 4 at the plot). This is the time when most of repair and regenerative work is done. Last 1-2 hours of sleep are comprised of so called "rapid eye movement" (REM) and light sleep (stage 1), when metabolism (heart rate, blood pressure, etc.) is not significantly lower, and the brain is nearly as active as when we are awake.

In fact, the entire second half of a complete sleep cycle is dominated by REM sleep, mainly used by the brain to re-wire and re-adjust, processing memories and relieving tensions (most of dreams occur during this stage of sleep). Doesn't seem as if taking out an hour, or so, at the end of this second half should significantly affect restorative effect of your sleep on the inner lining of your arterial walls. 

What it would affect is your mental state. Experiments have shown that individuals deprived of significant amount of REM sleep become irritable, anxious, depressed, with their cognitive function (ability to concentrate, or learn) deteriorating. This obviously injects more stress in one's life, and with it - among other undesirable effects - the likelihood of elevated blood pressure.

Why would elevated blood pressure contribute to arterial calcification? Because it increases

friction between blood and arterial walls,

especially where they are branching out (which is where most of the plaque buildup is taking place). The thicker, stickier blood - due to chronic dehydration, or overconsumption of animal fats, for instance - or the stiffer, less elastic vessel walls due to the lack of nitric-oxide, silica, MSN, chondroitin, glucosamine sulfate, etc. - the more so. And the more it interferes with the repair process, and even directly aggravates inflamed tissue. As a result, both inflammatory damage and resulting arterial calcification worsen.

It is possible, though, that one more hour of sleep does significantly add to the body's restorative function, if it takes place at a separate time; for instance, an afternoon nap. Most of that hour will be spent in deep sleep, which becomes especially important if your deep sleep stage during the night-time sleep is, for any of possible reasons, significantly reduced. It can be plain insomnia, when you just can't fall asleep, or when you are asleep some, or even most of the time, but don't wake up rested because you haven't gotten enough of deep, restorative sleep. Such sleep inefficiency can be caused by psychological factors, food substances, drinks containing caffeine, or alcohol, overeating before bed time, a wide variety of prescription drugs, and other factors.

Thus, compensating for the shortage of deep sleep with an afternoon nap can make a difference. Not only that it helps reduce oxidative damage, it is also needed for proper glandular function. Availability of some important hormones - such as human growth hormone, which is, among other things, beneficial for cardiovascular health - are directly dependant on the amount of deep sleep that you get.

Add to it that sleep strengthens your immune system. A recent small study (Cohen et al., Archives of Internal Medicine, 2009) has found that those with 8 or more hours of sleep are 3 times less likely to get cold (from rhinovirus) than those with 7 hours or less. But sleep efficiency matters even more: those with less than 92% sleep efficiency were 5.5 times more likely to develop cold.

An important factor influencing sleep efficiency is how full is your stomach when you go to bed. Remember that at least 50% of your immune system is in and around your digestive tract. That is, if it functions properly; if not, more. I you look at the above sleep pattern, you see that period of active digestion of close-to-bed-time meals overlaps with the period of deep, restorative sleep. That will significantly reduce therapeutic effect of sleep, not only in regard to your immune system, but the entire body as well.

As a result, your body will need more sleep and - even if you do fulfill that requirement - will likely be less well restored by it.

So, what the Universe looked like 2 seconds after the Big Bang? Doesn't matter. Just make sure you go to bed light, and have your Lullaby early enough to give you good night's sleep... R