The evolution of sleep

Why do we sleep? How much is enough? What happens when we don’t get enough. These questions will be the topic of next Tuesday’s October 18th Evolutionary Medicine class.

Sleep is one of the last frontiers in the study of lifestyle-related risk factors for chronic diseases. For instance, it has been well established that smoking reduces lifespan and increases the risk of chronic inflammatory diseases and cancer. Same goes for certain diets. The opposite is true for exercise. Now we can add disrupted sleep to the list of risk factors for chronic disease and shortened lifespan. Read Disruption of Circadian Clock Linked to Obesity, Diabetes and Heart Attacks. The question is, why?

Sleep via Jawbone

The sleep and activity tracker Jawbone (I have no financial interest in this company) released some data showing the ideal amount of sleep for a happy mood (above). This result, from a large sample makes it appear that sleep duration has a prominent effect on mood.

More about the Jawbone data here.

Work done here at the University of New Mexico by Gandhi Yetish PhD tried to answer the question: how much sleep are we evolved to need? He compared sleep in  modern industrialized populations in comparison to diverse hunter gatherer populations.

Read Yetish et al Current Biology 2015 here.

Other evolutionary work has centered on the uniquely human habit of nesting on comfortable beds, unlike other primates. We seem to prioritize sleep more than our closest relatives? Why?

Nunn, C. et al. 2016 Shining evolutionary light on human sleep and sleep disorders.

The discussion of sleep would be incomplete without the microbiome, of course. A landmark study showed that sleep deprivation, if long enough, is fatal. Death happens because microbes escape from the gut, causing abscesses and sepsis. Sleep seems to be important in preventing microbes gone amok.

Everson and Toth  Am J Physiol Regul Integr Comp Physiol 2000

screen-shot-2016-10-13-at-3-43-42-pm

Bacterial overgrowth after sleep deprivation (solid bars) in rats

Until recently, little evidence has linked sleep with gut microbiota in humans. One major finding was that gut microbiota have a circadian rhythm, with gene expression and population numbers that cycle in circadian fashion:. For example Lactobacillus populations expand and contract in the gut microbiome, depending on the time of day:

Thaiss et al. Transkingdom control of microbiota diurnal oscillations promotes metabolic homeostasis. Cell 2014. 159 (3) 514-529

This group showed that the gut microbiota follows a circadian rhythm, just like host cells. Moreover, they showed that healthy cycling microbiotas require a host that follows a normal circadian pattern of eating and sleep. When the mouse sleep and eating pattern is disrupted, their microbes lose their rhythm. When this “jet-lagged” microbiota is transplanted into germ free mice, the inoculated mice become fat and lose glucose control, that is, they exhibit a pre-diabetic state

The investigators also studied humans who suffered jet lag. Two subjects with 10-12 hour time change gave fecal samples before, during, and after resolution of jet lag. The samples were inoculated into germ free mice. Lo and behold, the mice receiving jet-lagged poop became obese and pre-diabetic, exhibiting glucose intolerance:

Jet lagged human microbiota causes metabolic changes

These findings mean that all our body’s activities, and those of our microbiota, have evolved to be on a timer. Mistimed sleep and eating has real consequences, increasing the risk of obesity, diabetes and many other diseases.

Thaiss-et-al-2014-transkingdom-control-of-microbiota

Sleep is a thread that is tightly woven in the fabric of metabolism, diet, activity level, inflammation, and obesity. Teasing out the cause and effect relationships between these features is a fascinating challenge for science and for evolutionary medicine.

Writing assignment for Tuesday: Why do we sleep? Use the readings to defend your answer.

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