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4 Metabolic Syndrome and Type 2 Diabetes

4 Metabolic Syndrome and Type 2 Diabetes

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Sleeplessness



Concerning type 2 diabetes, the great majority of 6-hour sleepers

sleeping in this manner over many years, with undisturbed sleep, are still

unlikely to develop diabetes. For example, in the 10-year Nurses Health

Study, described earlier (Sect. 4.3), the incidence of diabetes in 6-hour

sleepers was 3.2 % compared with 2.5 % for 7- and 8-hour sleepers [26],

which might be construed as a worryingly 30 % greater relative incidence

for the former group, but if we again look at those who are symptom free,

at 96.8 % and 97.5 % respectively, this apparently greater risk is very

small. By the way, for those sleeping fewer than 5 hours and over 9 hours

the incidences of diabetes were 4.0 % and 4.2 % respectively.

Even when the incidence of diabetes is higher, as was found in another

large, long-term prospective study [27] reporting a doubling of the onset

of diabetes in those sleeping fewer than 6 hours, at an incidence of 10 %,

compared with 5 % for 7-hour sleepers, the onset was associated with up

to 14 years of sleeping in this manner, and still with 90 % of these shorter

sleepers remaining asymptomatic. Again, it cannot be established to what

extent short sleep itself was even ‘a’ cause, rather than ‘the’ cause.

Finally, whilst a recent meta-analysis [28] encompassing 10 different

studies concluded that ‘short sleepers’ have a 30 % increased risk of developing diabetes, it is quite clear from the findings of the individual studies

that were incorporated, that much of this assertion only really applies to

those sleeping fewer than 5 hours.



4.5



Overview: Unlikely Bedfellows?



The evidence behind the apparent link between habitual short sleep, obesity, metabolic syndrome and diabetes in adults does not point to short

sleep as having more than a minor effect at best, although for those habitually sleeping fewer than 5 hours, this outcome might be somewhat more

likely. Besides, there are various problems underlying many of these findings. Remember, sleep estimates are usually confounded by ‘time in bed’

and daytime naps, whilst largely ignoring sleep quality. There are wide

categorisations of ‘short sleep’ still leading to claims and advocacy (cf.

[29]) that less than 7 hours’ sleep is associated with obesity and related illnesses, which stem mostly from generalisations from 5-hour sleepers who



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comprise about 6 % of adults. Other evidence comes from more extreme

and unrealistic acute sleep restriction studies in healthy non-obese young

adults, where the extent of the accompanying sleepiness would have been

of a far greater immediate danger had they been outside the laboratory

than the extent of their increases in appetite and insulin resistance. By

far the majority of obese people are not short sleepers and for those very

short sleepers, excessive daytime sleepiness may well be of much greater

concern than obesity, especially if they suffer from undiagnosed obstructive sleep apnoea syndrome (cf. Sect. 9.3).

In terms of greater clinical importance are the statistically significant

epidemiological findings of a greater body weight gain in 5-hour sleepers.

Even then, any such weight gains accumulate slowly over years; these are

more easily redressed by a better diet and relatively short daily exercise

exposures, contrasting with the huge accumulation of ‘lost’ sleep. No

study has really compared both interventions, and there is little evidence

supporting ‘more sleep’, alone, as an effective treatment for obesity and

these related disorders. Impaired sleep quality and quantity are symptoms

of many deeper underlying physical and psychological disorders, as can

be obesity.

Advocating more sleep could again heighten the anxieties of those with

insomnia who might otherwise worry about becoming fat or developing

diabetes as a result of insufficient sleep, thus heightening their use of sleep

aids including hypnotics in order to lengthen sleep and seemingly offset

obesity. But such interventions are unlikely to increase sleep duration

by more than 30 minutes. So why not use this time for a healthier brisk

walk, instead?

Of course, it could still be countered that the accumulated yearly

health risk associated with ‘short sleep’, albeit small, is still a serious

issue from an epidemiological perspective and, statistically, for example,

might even be comparable to the year-on-year increased risk of smokers developing cardiovascular disease. However, excluding excessive daytime sleepiness, my conclusion here is that, irrespective of any causal link

between short sleep and these disorders having yet to be established, and

that a considerable amount of accumulated ‘lost’ sleep is required before

any such association is seen, any such risk must be weighed against the

lack of therapeutic effectiveness of extending sleep versus the benefits of



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more worthwhile behavioural countermeasures, especially exercise and a

weight-reducing diet. Moreover, this healthier regimen will often lead to

improved sleep and reduced daytime sleepiness in those overweight or

moderately obese [30].

In sum, it is argued that the presumed effects of short sleep on obesity

are not of such critical, clinical importance when put into these more

realistic contexts. Unfortunately, it is all too tempting for press releases

and the media to exaggerate the outcomes from the many reputable studies which themselves exercise caution in the interpretation of their own

findings (cf. [31]).



References

1. Knutson KL et al 2007 The metabolic consequences of sleep deprivation.

Sleep Med Rev 11: 163–178.

2. Spiegel K et al 1999. Impact of sleep debt on metabolic and endocrine function. Lancet 354, 1435–1439.

3. Leproult R, Van Cauter E. 2010 Role of sleep and sleep loss in hormonal

release and metabolism. Endocrol Devel 17, 11–21.

4. Flegal KM, Kit BK, Graubard BI. 2013. Association of all-cause mortality

with overweight and obesity using standard body mass index categories: a

systematic review and meta-analysis’ J Amer Med Assoc 309:1681–1682.

5. Patel SR et al 2006. Association between reduced sleep and weight gain in

women. Amer J Epidemiol 164, 947–954.

6. Hairston KG et al 2010 Sleep duration and five-year abdominal fat accumulation in a minority cohort: the IRAS family study. Sleep 33, 289–295.

7. Watanabe M et al 2010 Association of short sleep duration with weight gain

and obesity at 1-year follow-up: a large-scale prospective study. Sleep 33,

161–167.

8. Stranges S et al 2008 Cross-sectional versus prospective associations of sleep

duration with changes in relative weight and body fat distribution: the

Whitehall II Study. Amer J Epidemiol 167, 321–329.

9. Lauderdale DS et  al 2009 Cross-sectional and longitudinal associations

between objectively measured sleep duration and body mass index: the

CARDIA Sleep Study. Amer J Epidemiol 170, 805–813.



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10. Anic GM et al 2010 Sleep duration and obesity in a population-based study.

Sleep Med 11: 447–451.

11. Nielsen LS, Danielsen KV. 2010 Short sleep duration as a possible cause of

obesity: critical analysis of the epidemiological evidence. Obes Rev 12:78–92.

12. Cappuccio FP, et al 2008 Meta-analysis of short sleep duration and obesity

in children and adults. Sleep; 31: 519–626.

13. Magee L, Hale L. 2012 Longitudinal associations between sleep duration

and subsequent weight gain: a systematic review. Sleep Med Rev. 16:

231–241.

14. Vgontzas AN 2008 Short sleep duration and obesity: the role of emotional

stress and sleep disturbances. Int J Obesity (London) 32, 801–809.

15. Meiseninger C 2007 Sleep duration and sleep complaints and risk of myocardial infarction in middle aged men and women from the general population: the MONICA/KORA Augsburg cohort study. Sleep 30, 1121–1127.

16. Simon GE 2006 Association Between Obesity and Psychiatric Disorders in

the US Adult Population. Arch Gen Psychiat 63, 824–830.

17. McIntyre RS 2006, Obesity in bipolar disorder and major depressive disorder: results from a national community health survey on mental health and

well-being. Canada J Psychiatr 51, 274–280.

18. Dallman MF 2009 Stress-induced obesity and the emotional nervous system. Trend Endocrin Metab 21, 159–165.

19. Markwald RR 2013. Impact of insufficient sleep on total daily energy expenditure, food intake, and weight gain. Proc Natl Acad Sci U S A.

110:5695–5700.

20. Haba-Rubio J et al. 2015. Objective sleep structure and cardiovascular risk

factors in the general population: the HypnoLaus study. Sleep, 38: 391–400.

21. Spaeth AM 2013 Effects of experimental sleep restriction on weight gain,

caloric intake, and meal timing in healthy adults. Sleep 36:981–990.

22. Hall MH et al 2008 Self-reported sleep duration is associated with the metabolic syndrome in midlife adults. Sleep 31, 635–643.

23. Bryant PA et  al 2004. Sick and tired: does sleep have a vital role in the

immune system? Nature Rev Immunol, 457–467.

24. Rechtschaffen A et al 2002. Sleep deprivation in the rat: X. Integration and

discussion of the findings -1989. Sleep; 25, 68–87.

25. Horne JA. 1988 Why we sleep. Oxford: University Press.

26. Ayas NT et al 2003. A prospective study of self-reported sleep duration and

incident diabetes in women. Diabetes Care 26, 380–384.



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27. Yagg HK et al. 2006. Sleep duration as a risk factor for the development of

type 2 diabetes. Diabetes Care 29, 657–661.

28. Holliday EG et al 2013 Short sleep duration is associated with risk of future

diabetes but not cardiovascular disease: a prospective study and metaanalysis. PLoS One 25;8(11):e82305.

29. Watson NF et al 2015. Recommended amount of sleep for a healthy adult:

a joint consensus statement of the American Academy of Sleep Medicine

and Sleep Research Society. Sleep 38: 843–844.

30. Verhoef SPM et  al. 2013. Concomitant changes in sleep duration, body

weight and body composition during weight loss and 3-mo weight maintenance. Am J Clin Nutr, 98: 25–31.

31. Sumner P et al 2014. The association between exaggeration in health related

science news and academic press releases: retrospective observational study.

BMJ Dec 9;349:g7015. doi: 10.1136/bmj.g7015.



5

Childhood and Adolescence



Sleep is but one of the many needs of children, and it is foolish to make it the scapegoat for all kinds of physical and mental evils as hygienists have so often done. It is

possible that the quantity of sleep is less important than its quality, and that when

disturbances of the latter occur they are more likely to be the effect of ill-health than

its cause … sleep cannot be accurately measured in units of time alone …

Terman & Hocking 1913.



5.1



Kids: Too Little Sleep?



Much is being said about today’s children not having enough sleep, often

blamed on lax bedtimes, excessive evening TV, video-gaming, etc. Plus ỗa

changea hundred or so years ago things were just as bad, even worse,

when excessive homework was the culprit. For example, in 1884 the

British Medical Journal reported that a Dr Crichton-Browne had testified to Parliament that, “I have encountered many lamentable instances of

derangement of health, diseases of the brain, and even death resulting from

enforced evening study in young children, with the nervous excitement it so

often induces … it implies a maximum of effort with a minimum result”.

© The Editor(s) (if applicable) and The Author(s) 2016

J. Horne, Sleeplessness, DOI 10.1007/978-3-319-30572-1_5



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Albeit wise but ignored words, he remained persistent, as in 1908 [1]

the now knighted Sir James Crichton-Browne, in his presidential address

to the Child Study Society bemoaned that, “the evil of insufficient sleep

in children is widespread”. He was responding to the talk by Dr Alice

Ravenhill who had just described her three-year-long investigation into

the sleep of elementary schoolchildren. Ten thousand forms had been

issued of which 6180 “were properly filed up, and gave particulars as to

3500 boys and 2680 girls”. Having previously “consulted the best authorities” who had apparently advocated 13 hours’ sleep for the younger group

and 11 hours’ for the older ones, she had calculated a sleep deficiency

ranging from 2.75 to 3.25 hours, depending on the age. For example,

for the 3–5 year group she found the average sleep obtained was 10.75

hours versus the recommended standard of 14 hours, and at 13 years the

average was only 8 hours against the recommended 10.30 hours. Both

of these actual findings are somewhat less than those of today, as will be

seen. Nevertheless, Sir James went on to comment that this represented

“a loss equivalent to one night in four in the youngest children, and one night

in five among those of intermediate ages”.

There are two more studies of note, appearing around the same time,

from different countries. In 1907, a Dr L Bernhard published [2] a similar study on 6551 German children aged between 6 and 14 years. And in

1913 came the still renowned report from the USA by Drs Lewis Terman

and Alice Hocking [3] on, ‘The sleep of schoolchildren: its distribution

according to age and its relation to physical and mental efficiency’.

Bernhard’s findings point to children’s bedtimes being later then than

today, but with similar morning rising times. Further details of his findings are given in the table below, including those of Ravenhill and, more

importantly, from the remarkably thorough and still unique study by

Terman and Hocking, that I will now describe.

It was based on 2692 Californian children and, most importantly,

avoided asking parents to complete the questions on behalf of their children, but rather asked the children themselves about their sleep, with the

children having received very clear and impartial guidance from their

teachers. It might be argued that younger children are not really able to do

this, but the study was so well organised and, remember, it was a hundred

years ago when reading and writing skills were as good as, and arguably



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