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a large number of studies that together included 2.88 million adults, of
whom around 270,000 had died, the investigation undertook a series of
discerning analyses to produce ‘hazard ratios’ (HRs—similar to relative
risks—see Sect. 3.2) of the chances of dying if one is overweight or obese.
By using the ‘traditional BMI boundaries’ of 25 and 30, compared with
the normal range, the outcome from this study was surprising, as being
‘overweight’ was not associated with a greater likelihood of death, but
marginally safer, with a HR of under 1 (HR: 0.94). For what the investigators called ‘grade 1 obesity’ (BMI between 30 and 34) this outcome
was still no different (HR: 0.95), but rose (HR: 1.29) for BMIs of 35 and
above. Needless to say the paper caused a furore. I will avoid this debate
but simply note that being overweight, even somewhat obese, is not necessarily a health hazard for everyone as they can be ‘fat and fit’. In fact, for
elderly people there is what is called ‘paradoxical obesity’ where moderate
obesity can enhance survival with certain disorders such as cardiovascular
Nevertheless, this issue of BMI cut-offs points to differences in medical opinion about the clinical relevance of what can be small differences
in BMI. More to the point, the findings relating BMI to habitual durations of sleep are often claimed to be of much greater clinical relevance
than might otherwise be the case.
There are two broad categories of studies, here. A ‘case-control’ study
takes a ‘snapshot’ of the present status of a large population and, for
example, assesses each participant’s estimated sleep duration with their
BMI, including various other factors apart from age and gender, such as
socio-economic status, education, etc. It would then compare the various sleep durations in terms of BMI. The second type of investigation
is a ‘prospective cohort’ study which takes similar measures, but follows
individuals for some years to see how BMI might change over time in
comparison with their sleep. These two approaches are not exclusive, as
by taking snapshots during the course of a cohort study and comparing
these sleepers, both aims are achieved.
There are many findings to choose from [cf. 4], but as the conclusions are similar I will select those that illustrate key points. The prospective ‘Nurses Health Study’ I mentioned earlier (Sect. 3.4), also measured
 body weights (but not BMIs) over a 16-year period, in 68,183 female
nurses, and found for each year measured, that those who reported sleeping fewer than 5 hours consistently weighed more than those sleeping
longer than this amount. In the first year of the study, those categorised as
sleeping fewer than 5 hours, or 6, 7 and 8 hours were all similar in weight,
weighing respectively 69.7 kg, 68.4 kg, 67.1 kg and 67.8 kg, although the
shortest sleepers were somewhat the heaviest. Sixteen years later, despite
all groups gaining weight and the shortest sleepers remaining heavier,
the latter group’s overall weight gain was only 2.8 kg more than for the
7-hour sleepers, and 3.2 kg more than for the 8-hour sleepers (the actual
weight increases being 7.6 kg, 5.9 kg, 4.8 kg and 4.4 kg respectively).
These differences were despite what might well have been a 10,000-hour
potential accumulated difference in sleep durations between the 5- and
7- or 8-hour sleepers over the 16 years. Moreover, the apparently minor
effect of short sleep as a possible cause of weight gain is further evident in
the small but albeit highly statistically significant 0.9 kg greater weight of
the 5-hour sleepers compared with those sleeping 8 hours, found at the
start of the study, when presumably all had been sleeping in this manner
for some years before then.
Three other recent, large prospective cohort studies are also noteworthy. The first  undertook a 5-year follow-up of 522 men and women.
For those originally aged under 40 years, who habitually slept fewer than
5 hours, and compared with 6–7 hour sleepers, there was a 1.8 greater
increase in BMI over this period. Comparison between 6–7 hour sleepers
and those sleeping over 8 hours, found a 0.9 greater increase in BMI for
these ‘longer’ sleepers. However, for those who were originally aged over
40 years, no such overall effects were found. A 1.8 greater BMI equates
roughly to about 6 kg (presumably mostly fat) for the typical man, which
is about 1.2 kg per year, here. It is roughly comparable in energy content from eating, each month, just one cheeseburger with French fries
(approx. 1000 calories—and assuming an approximate 70 % conversion
of this energy into fat).
The second of these prospective studies  monitored 31,447 men
and 3770 women for a year. For both groups there was no change in BMI
for those habitually sleeping 7–8 hours, and almost zero BMI change
for each of the three male groups sleeping 5–6, 6–7, and 8–9 hours.
However, for men sleeping outside the range 5–9 hours there were significant but slight BMI gains of 0.07, which amounts to about a 200 g
increase in body weight. None of the female groups showed any changes.
Thirdly, a UK study  of 3619 men and 1422 women initially compared BMIs and waist circumferences of habitually 7-hour sleeping
adults with those sleeping (by self-estimates): fewer than 5 hours, at 6,
8, and over 9 hours. The shortest sleeping group had a small but statistically significantly greater BMI of 0.82, and a larger waist circumference of 1.9 cm. However, the investigators concluded that these minor
differences were not sufficient enough to presume that short sleep was
of particular importance to these differences. A subsequent follow-up,
some 4–5 years later, found no relationship between short sleep and BMI
changes. More interesting, was the finding that within the shortest sleepers, 25 % of the men and 33 % of the women were depressed, compared
with values ranging between 8 % and 14 % for both men and women
for the other hourly sleep categories, including for those sleeping longer
than 9 hours.
There have been other case-control studies further pointing to little
real association between sleep and obesity, e.g. [9–11], including metaanalyses (see Sect. 3.5) that have combined the various findings. A substantial meta-analysis  concluded that a habitual sleep reduction
of 1 hour per day below 7 hours is associated with a 0.35 increase in
BMI, per year, which is only about 1 kg for the average (1.8 m) height
man. Again, it is apparent, as with other reviews , that any significant weight differences between short and ‘normal’ sleepers are small,
very slow to accrue, even after many years of sleeping in this manner.
Moreover, there remains no sound explanation for how short sleep might
be the cause of this very slow weight gain.
Obesity itself can create discomfort and disturbance during sleep,
apart from causing obstructive sleep apnoea (Sect. 9.3). Moreover, obese
people tend to report higher incidences of insomnia linked to chronic
emotional stress , although there appears to be no obvious difference
in self-reported sleep duration between those obese and non-obese individuals who are free of chronic stress . That is, emotional stress seems
to have a stronger relationship with reported sleep duration than BMI, to
the extent that short sleep in obese individuals might mostly be a sign of
emotional stress. Given that shortened sleep in the form of early morning
awakening is one of the diagnostic criteria for depression, then a disproportionate number of short sleepers would be expected to be depressed,
irrespective of obesity . An association between obesity and psychiatric problems has also been described by others as, for example, in a
survey  of 9125 respondents, obesity was linked to a 25 % greater
incidence of mood and anxiety disorders compared with the non-obese.
Indeed, outside the topic of sleep, there is a clear link between depression
and obesity , as well as with ‘comfort eating’ , but as the weight
gain in very short sleepers attributable to their sleep is generally slow to
develop, then the extent to which excess comfort eating is to blame, here,
must be small.
While acute sleep restriction to 4 or 5 hours a night for several nights
in healthy lean adults [1–3] increases appetite and hunger, one must bear
in mind that if food is freely available to sleep-deprived participants who
have little else to do, as has also been reported for other experimental
studies of this nature [18, 19], then participants might well eat or snack
more readily. Although such findings have been used to explain obesity in
habitually very short sleepers, the very slow weight gain in such sleepers
contrasts with that of these sleep restricted participants, who eat at least
300 calories a day in excess of the extra energy needed just by being awake
for longer [18, 19]. As we have seen, someone habitually sleeping only
5 hours a day could put on maybe up to 2 kg of fat over a year. Roughly
speaking, if this is converted back into calories at 9 calories per gram of
fat, which is about 50 calories a day, this is much less than that seen in
these acute experiments. It suggests that the increased food consumption
in these experimental studies further points to it being undertaken under
unusual conditions. However, there is a twist to my line of thinking, here,
as habitually short sleep might well alter not so much body weight itself,
but the regulation of energy balance in more subtle and hitherto unforeseen ways, to be covered in Sect. 12.3, concerning Rapid Eye Movement
Finally, rather than assess obesity levels in terms of sleep duration, it
would be worthwhile to reverse these same findings and present them
not as BMI for different sleep durations, but as mean sleep durations for
normal BMI, versus overweight 26–29, and 30–34 (grade 1 obesity).
Few studies focusing on obesity and sleep seem to have done this, however, the Swiss study  I mentioned previously (Sect. 3.5), which concentrated on cardiovascular disease, happened also to divide their 2162
patients into those whose BMI was either greater than or equal to 25 or
below 25. Average sleep durations differed by 3 minutes, being 402 and
399 minutes respectively, and it should be remembered that those sleep
durations were determined by EEGs, not by self-estimates.
Metabolic Syndrome and Type 2 Diabetes
Issues concerning the acute, severe sleep restriction studies on healthy
young adults that pointed to the development of the metabolic syndrome
were described at the beginning of this chapter. However, and in contrast,
there is little epidemiological evidence to show that healthy, habitually
6-hour sleepers are at any seriously greater risk for developing metabolic
syndrome. For example in a study  of 1214 participants aged 30 to
54 years, of whom 268 had the syndrome, 18 % of the 7–8 hour sleepers
had it compared with 24 % for 6–7 hour sleepers, 28 % for those sleeping fewer than 6 hours, and 24 % for the longer than 8-hour sleepers; all
of which seem to be similarly high incidences, but with only a 6 % difference between 6 and 8 hour sleepers. In terms of inverting these findings
from the perspective of those who are symptom free, the figures seem less
persuasive, being between 72 % and 82 % for all sleep groups.
Yet, as the metabolic syndrome and type 2 diabetes have been seen as
‘inflammatory responses’ , it could be argued that inadequate sleep
has an adverse effect on immunity; hence this response. However, it will
be remembered from Sect. 3.7 that short sleep or sleep loss leads only to
equivocal changes in human immune function, which are not necessarily
detrimental but may simply indicate heightened immunological activity (cf. ), and that one should exclude the animal studies in these
respects [24, 25].
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 ,
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  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  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.
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.
) that less than 7 hours’ sleep is associated with obesity and related illnesses, which stem mostly from generalisations from 5-hour sleepers who