Posts archived in Biological rhythms and sleep
March 11, 2013 by Cara Flanagan.
There are many theories about why we sleep and dream, and many of these involve memory in some way (including Freud’s theory of why we dream). A relatively recent theory has been gathering support, variously called synaptic renormalisation hypothesis or synaptic homeostasis hypothesis (aka ‘SHY’ – first proposed by Tononi and Corelli, 2003).
The basic principle is the suggestion that sleep provides a necessary opportunity for brain synapses to recover. During the day we are constantly forming new memories – when a new memory is formed essentially the synapse between the neurons involved becomes strengthened. Such strengthening can’t go on forever because of the energy required. So, according to SHY, slow wave sleep provides a slowing down of brain activity in order to allow all synapses to reduce activity. The relative differences in strengths between neurons remains, so the new memories aren’t lost.
Not everyone supports this idea. For example Frank (2013 here) argues that the underlying mechanisms have yet to be clearly defined and, until this happens, the hypothesis remains tentative.
Subscribers to the New Scientist can read about this hypothesis, and more, in a great piece on the Wonder of Slumber (2 February 2013).
July 30, 2012 by Cara Flanagan.
In our A2 Complete Companion we reported a study by Knutsson et al. (1986) who found that shift workers were three times more likely to develop heart disease than non-shift workers. A study just published by Hackam et al. (2012) confirms this, claiming a 24% increased risk of a coronary event and 5% increased risk of stroke. The study controlled for socioeconomic status, diet and general health of the workers.
It may be that problems arise because of poor day time sleeping and disruption to eating patterns and social routines. This might be improved by ensuring that shift workers have a minimum of two full nights’ sleep between after a period of night shifts, and should do both day and night shifts for alternate periods. See here for more detail.
May 27, 2012 by Cara Flanagan.
Henry Nicholls is a science writer and narcoleptic, a condition characterised by a frequent and overwhelming need to sleep. The current thinking is that narcolepsy develops in genetically vulnerable individuals when the immune system mishandles an infection.The outcome is an autoimmune attack on a region of the hypothalamus that produces the hormone orexin (aka hypocretin). Orexins are the ‘stay awake’ hormone, in other words they carry a message around the brain ‘stay awake’. In their absence the brain goes to sleep. So what Henry, and other narcoleptics, need is an orexin substitute.
So are drug companies researching this? No, they are trying to find ways of blocking the production of orexin rather than trying to find ways to produce it. Why? Because insomnia is a much bigger problem for people than narcolepsy (there are about 150 times more insomniacs than narcoleptics). In many cases insomnia might be due to an overactive orexin system. The drug company Merck are trialling a drug called Suvorexant which is due to be released in the US later this year. Narcoleptics are going to have to wait.
Henry’s article was published in the New Scientist (24 March 2012) but you can read it here. You can also read Henry’s blog here.
February 22, 2012 by Mike Cardwell.
Today’s BBC website carries a fascinating article that challenges the commonly held view that an eight-hour period of continuous sleep is natural for human beings.
We often worry about lying awake in the middle of the night – but it could be good for you. A growing body of evidence from both science and history suggests that the eight-hour sleep may be unnatural.
In the early 1990s, psychiatrist Thomas Wehr conducted an experiment in which a group of people were plunged into darkness for 14 hours every day for a month.
Read the rest of this entry »
July 25, 2011 by Cara Flanagan.
Juliette Massey-Smith wrote in the following query: I was wondering if you could help… I was re-reading about SAD in your AQA textbook and read on p.4 that in winter melatonin and serotonin are higher and this causes depression, but then also that LACK of serotonin causes it… What am I missing?
This error was corrected in the A2 Mini Companion (page 8): More darkness means more melatonin, and more melatonin means less serotonin (because melatonin is produced from serotonin). Low levels of serotonin are associated with depression.
May 27, 2011 by Cara Flanagan.
Early temporal isolation studies overlooked the fact that artificial light has an effect on circadian rhythms but more recent research showed that even fairly dim lighting may reset the SCN (suprachiasmatic nucleus). Even more recently research has found that blue light is particularly effective – for good and bad.
The story starts with blind people – some blind have considerable difficulties with their circadian rhythms because their insensitivity to light means that their body rhythms are constantly fluctuating. However, this is not true of all blind people. It seems that the eye has special light receptors related to the circadian rhythm and these feed directly into the SCN (Czeisler et al., 1995). Other research has found that these special cells are particularly sensitive to blue light. For example Kayumov et al. (2005) found that volunteers doing simulated shift work had reduced melatonin production if they were exposed to bright light but not if they wore goggles that filtered out blue light. Dim lighting also did not result in reduced levels of melatonin.
You may ask ‘Where did the melatonin come in’? Light resets the SCN and also suppresses the production of melatonin (when it gets dark, melatonin levels rise making us sleepy). Suppression of melatonin has been linked to cancer, obesity, diabetes and cardiovascular disease. So shiftworkers doing night work with bright lighting are exposed to risks that could be prevented if the lighting was dim or blue light was filtered out. In fact the same is true for all of us, at night it is better to sit in dimly lit rooms and use lighting with less blue in it.
January 25, 2011 by Cara Flanagan.
In Chapter 1 (Biological rhythms and sleep) of our A2 Complete Companion there is a contradiction (kindly pointed out by Ruth Bailey of Akeley Wood School). On page 13 the text says that dolphins don’t have REM sleep whereas on page 14 the graph indicates a significant amount of REM sleep in dolphin. So which is correct?
The data for the graph was taken from a study Lyamin et al. (2004) of one dolphin, reported by the Phylogeny of Sleep Project (you can see the dolphin data here). As pointed out in our textbook much of the data about sleep is actually derived from very small samples and research conducted under poorly controlled conditions.
All of the other dolphin studies given by the Phylogeny of Sleep Project did not record the amount of REM sleep which is why we used the data from Lyamin et al. However this data is misleading as the general view appears to be that (REM) sleep is either absent in cetaceans (e.g. dolphins) or occupies an extremely small proportion of the day – an absolute maximum of 15 min each day (Manger et al., 2003). In fact a recent paper published by Lyamin et al. (2008) states that ‘We find that for cetaceans sleep is characterized by USWS [unihemispheric slow wave sleep] [and] a negligible amount or complete absence of rapid eye movement (REM) sleep’.
December 14, 2010 by Evie Bentley.
A small study of Canadian infants and toddlers found that those who slept most at night were making significantly more progress in executive functions than those who slept less at night, even if the latter group also had daytime sleep. These functions include impulse control, memory and mental flexibility. The researchers controlled for parents’ education and income and children’s general cognition, but the link between night-time sleep and development of cognitive skills remained. These finding support similar research findings on schoolchildren.
Might this also apply to older childern and adults? That would be interesting to know!
Annie Bernier, Stephanie M. Carlson, Stéphanie Bordeleau, Julie Carrier. Relations Between Physiological and Cognitive Regulatory Systems: Infant Sleep Regulation and Subsequent Executive Functioning. Child Development, 2010; 81 (6)
December 8, 2010 by Evie Bentley.
It’s been known for ages that information on light levels is passed from the two retinas via a special small nerve from each eye to the SCN, but the mechanism of this is now more clear. As well as rods and cones, cells which are sensitive to light and give us black-and-white and colour vision there is a third type of light-sensitive retinal cell. These are far less in number than rods and cones, and react to light by expressing the pigment melanopsin, so they are known as mRGCs (melanopsin-expressing retinal ganglion cells). Not only do these cells send information to the SCN but they also control pupil size. And now it seems they also contribute to our visual image formation as axons from the mRGCs have been traced onwards from the SCN to visual processing centres. What does this imply? It gives some idea of how seriously sight impaired people can still detect levels of brightness, plus the possibility in the future of engineering melanopsin-expressing cells to improve or restore sight.
Fred Rieke, Timothy M. Brown, Carlos Gias, Megumi Hatori, Sheena R. Keding, Ma’ayan Semo, Peter J. Coffey, John Gigg, Hugh D. Piggins, Satchidananda Panda, Robert J. Lucas. Melanopsin Contributions to Irradiance Coding in the Thalamo-Cortical Visual System. PLoS Biology, 2010; 8 (12)
October 29, 2010 by Adrian Frost.
A US researcher has said he plans to electronically record and interpret dreams.
Writing in the journal Nature, researchers said they have developed a system capable of recording higher-level brain activity.
“We would like to read people’s dreams,” says the lead scientist Dr Moran Cerf.
The aim is not to interlope, but to extend our understanding of how and why people dream.