Wednesday 4 November 2015

Circadian Rhythms

Thought I'd try the circadian rhythms topic from the other half of the course next. There are still two schizophrenia topics left to write up - psychological therapies, and diagnosis, classification & validity - these should be finished sometime in the next fortnight. IDAs (issues, debates and approaches) are much more important on this side of the course, I'll try and clearly signpost them as I go. I will try and write this in the style of a response to an exam question into this topic, but if people are interested, I can write an additional post including more studies than necessary so you can pick and choose your favourites.

Black: AO1 - Description
Blue: AO2 - Evaluation - studies
Red: AO2 - Evaluation - evaluative points/IDAs


Control of circadian rhythms - EPs and EZs


Circadian rhythms are biological rhythms with a cycle length of roughly 24 hours. They are controlled by both external factors (exogenous zeitgebers, or EZs) and internal factors (endogenous pacemakers, or EPs.) The two main EZs that affect the sleep/wake cycle, the best example of a circadian rhythm, are light (either natural or artificial) and social cues such as the sleep/wake cycles and behavior of those around us. The two main EPs that affect the sleep/wake cycle are the SCN (suprachiasmatic nucleus) and the pineal gland. The SCN is located within the brain, just behind the eye, and detects changes in light levels. When a decrease is detected, it stimulates the pineal gland, also in the brain, to release melatonin, a hormone that induces tiredness. When an increase is detected, the SCN stimulates the pineal gland to cease melatonin release, which helps wake us up when the sun rises in the morning. Thus, the hormone melatonin helps us regulate the sleep/wake cycle.

Stephan and Zucker (1972) provide supporting evidence for the role of the SCN in controlling circadian rhythms. They compared a control group of healthy rats to a group of rats that had undergone surgery to destroy their suprachiasmatic nuclei. Whilst before, the rats had maintained constant and reliable patterns of eating and movement, these patterns disappeared in the group that had had their SCN removed - being replaced with unpredictable and patternless behavior, the rats unable to maintain a steady circadian rhythm due to the brain damage. Even though the rats were kept in the exact same environment, those with damaged SCNs lost their circadian rhythms, demonstrating that the SCN is a crucial EP in the control of circadian rhythms.

In some respects, this study was highly scientific, taking place in a controlled laboratory environment and using a control group for causal establishment. This would normally mean that the study is highly generalisable, but despite its scientific replicability, care must be taken when generalising to humans, due to the nature of the sample. There are likely to be large physiological and neuroanatomical differences between the mechanisms that control the sleep/wake cycle in rats and in humans, and it is overly anthropomorphic to confidently extrapolate results from this study onto humans.

Another important issue is raised by the use of non-human animals in this study, and that is one of ethics. The levels of harm the rats were subjected to is not at all insignificant - 14 of the 25 rats died during surgery or as a result of complications, meaning the study is ethically questionable, even when factoring in the (small) scientific and social benefits of the results. Also, the severity of the surgery calls the experiment's validity into question - as over half of the sample died from it, it is highly possible that the surgery affected the rats' brains in some way unrelated to the SCN that could explain the elimination of circadian rhythms.

Further supporting evidence for the role of EPs in the control of circadian rhythms comes from Morgan (1995), who removed the SCN from hamsters. The hamsters without an SCN had their circadian rhythms eliminated, but the rhythms were restored when the SCN cells were transplanted back in. This study clearly demonstrates the role of the SCN as an EP in circadian rhythm control.

Generalisability to humans may be an issue, as there are definite physiological differences between the brains of humans and hamsters. Additionally, humans do not live in isolation as the hamsters did in this study, so other factors proven to have an influence on circadian control such as social cues affect the human sleep/wake cycle in ways that this study ignored.

Again, the validity of this study may be called into question, as the major operation may have contributed to the change in behaviour, weakening the supporting evidence for the role of EPs in controlling circadian rhythms.

However, a 1975 study by Siffre challenged the importance of EPs in the control of circadian rhythms. Siffre spent 179 days underground in a cave with no natural light or social cues to act as EZs, only artificial light on demand. During his stay, he recorded body temperature (another circadian rhythm), heart rate, blood pressure and sleep/wake pattern. His sleep/wake circadian extended from 24 to between 25 and 32 hours despite a fully functional SCN and pineal gland- his days became "longer."  On the 179th day, by his terms it was only the 151st day. This study demonstrates the importance of EZs such light and social cues in the control of circadian rhythms, proving that EPs such as the SCN alone are not enough - EZs are required as well in order to keep the sleep/wake cycle at a steady 24 hours. However, it does demonstrate that EPs can provide some regulation to circadian rhythms without light or social cues, as once the rhythms had increased to 25-32 hours, they remained fairly constant throughout.

Being a case study, an issue with Siffre's research is that it lacks generalisability, only studying one man. This means that results are likely to be unrepresentative of the general population, and care should be taken when applying them as such. Only studying a male is also problematic, as hormonal or neurological sex differences could mean that the mechanisms that control circadian rhythms in males and females function slightly differently, so it would be beta gender bias to apply Siffre's results to women too.

Luce and Segal studied circadian rhythms in the indigenous population of the Arctic Circle, where it is light all through the summer months, and dark all through the winter months, meaning light will not function properly as an EZ. Despite this, people who live there keep up a steady sleep/wake cycle of roughly 7 hours per night, due to the function of social cues as an EZ. This study supports the role of social cues as an EZ, but suggests that light is not as crucial as otherwise thought.

Cultural or ethnic differences in the indigenous people of the Arctic Circle could mean that these results cannot be accurately generalised to the global population, and it would be imposing an etic to attempt this. Having grown up and lived all their lives accustomed to this annual pattern of light, it is possible that they have developed biological or social mechanisms that allow them to function normally using only social cues as an EZ rather than light, and we shouldn't assume that the sleep/wake cycle of non-natives would regulate itself in the same way if exposed to the same patterns.


Conclusion


In conclusion, it seems that both exogenous zeitgebers and endogenous pacemakers are required for the healthy regulation of circadian rhythms - it is overly reductionist to study one in isolation, or to claim that EPs such as the SCN and pineal gland are responsible for controlling such complicated processes as the sleep/wake cycle and body. This theory ignores cognitive and social factors that play a role in the control of human sleep behaviour. Humans are able to make appraisals of situations and of the behaviour of others, and these factors play an important role in the control of circadian rhythms. Sleep is not purely a biological behaviour, and other approaches should not be completely ignored.


Additionally, claiming that human sleep behaviour is only a result of EPs and EZs is too deterministic, as humans generally have the free will to decide when we want to sleep or choose to partake in activities that will influence our sleep/wake cycle, thus altering the rhythm ourselves. This is demonstrated by everyone who alters their own sleep/wake cycles in order to participate in shift work. Born et al found higher ACTH levels in the blood of people who made themselves get up earlier, suggesting that even biological processes and factors can be influenced by free will.

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