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Sleep, obesity and the rhythm of life

We make ourselves and break ourselves day-by-day, hour-by-hour and minute-by-minute. The only time this stops is when we pop our clogs and die. The molecules that make up the chemicals that give form and function to your liver today will not be there next week. Some (Carbon & Oxygen) will leave the body to the atmosphere and some (Nitrogen & Hydrogen) will vanish down the loo. Next weeks liver will be today’s salami and tomorrows mushroom soup. This constant synthesis and degradation of all human organs has one enormous survival advantage. In times when food is short, the body can prioritise which organs are more precious than others such that they get priority for re-synthesis. Usually, the brain, the gut and the immune system get priority over muscle, fat and bone because they perform more vital functions. Why look like Arnold Schwarzenegger when your immune system is in trouble.

The constant making and breaking of the human body is cyclical and almost all biological systems operate in cycles and in rhythms. The most important is the circadian cycle, which is regulated by a part of the brain called the supra-chiasmatic-nucleus (SCN), which connects to the pineal gland, which in turn secretes melatonin into the blood stream.  Daylight is detected by photosensitive cells in the retina, providing a signal to the pineal gland to suppress melatonin secretion. As daylight fades and night time falls, melatonin levels in the blood begin to rise and we begin to wind down in preparation for sleep. No one really knows why we sleep but every living creature does so and among the popular theories of why we sleep is the repair of faulty wiring of nerves in the brain that occur as we process information throughout the day.

Once upon a time it was New York that boasted it was the “city that never sleeps” but today that is a global urban phenomenon. Light abounds and night time is getting busier. Moreover, we are spending a decreasing proportion of night time asleep. In the US, sleep duration was 8-9 hours in the 1960s. This fell to 7 hours in 1995 and to just 6 hours in 2005.  Whereas jet lag can temporarily disrupt our circadian cycles, the growth of urban light, the increasing proportion of the population engaged in shift work and shorter sleeping habits, all have long-term effects on our circadian cycles with a particular emphasis on obesity and its related disorders.
About 15% of our entire genome is involved in circadian cycles and this can go up to 25% in some tissues including fat.  Thus the gene for leptin, a protein that is centrally involved in feeding, peaks at night in humans. In contrast, two other hormones secreted by our fat tissues (adiponectin and lipocalin 2) show a trough at night time at about 04.00 hours and the scale of the trough is substantial (40% fall from the peak daytime value). Animal studies that either insert or delete genes that have a circadian rhythm also reveal major changes in energy metabolism involving both glucose and fat and also body temperature. Shift workers show higher levels of obesity, diabetes and cardiovascular abnormalities when compared to those who work by day and these studies corrected for all the relevant confounding factors of age, gender and social class. Whereas light is the main factor in driving the circadian rhythm, there is considerable interest in the role that meal patterns might have on these events. However, those few human studies that have been completed under strict experimental conditions fail to show any major difference in the circadian cycles of eating-related hormones (adiponectin and lipocalin 2) in the fed or the fasted state. Of course, the act of eating sets off a cyclic events which is characterised by transport of nutrients into tissues in the immediate postprandial phase followed by the transport of nutrients out of tissues such as adipose tissue in the later postprandial phase but these diet induced metabolic cycles do not drive the main biological clock in the SCN.
Interestingly, a group of researchers at Oxford measured the rate of flow of fats into and out of human abdominal fat when the subjects were fully fasted. The expected direction of traffic would be out of adipose tissue because they are in the fasted state. They measured these events every 2 minutes over an hour. Was the outflow steady over time?  It wasn’t. The researchers noted 7 peaks in the exit of fats, effectively indicating cycles of net inflow and net outflow, each lasting about 8 minutes. This isn’t surprising since the making and breaking genes are always switched on with one dominating over the other in cycles. However, what is fascinating is how these genes are switched up and down with such regularity.

Changing sleep patterns are beginning to attract great interest in obesity. Bring back the siesta, I say. 


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