Sleep Deprivation and
the Shrinking Brain
Indeed, in Scotland,
a group of endocrinology and metabolic scientists are using retinal impairment as a
model for dementia
associated with diabetes – retinopathy. Here
again the problem is
that they consider type
2 diabetes as a major
risk factor for retinopathy, and not that incipient dementia of the
brain is the initiating
and driving causative
influence. They seem
to miss the correct
sequence of events –
from chronic cerebral
and retinal glucose
deprivation (hunger) to
increased consumption
of more high-energy
carbohydrate foods, in
a repeating cycle.
One of the most universal and pernicious
influences on modern
metabolic impairment
is that driven by the
myth that sleep is a low
energy protocol. This
has led to the notion,
promoted by diet gurus
and not opposed by
the health professions,
that it is unhealthy to
eat late. The impact of
this on metabolic health
has been profoundly
negative – it means
that after an early evening meal we retire to
bed with a depleted
liver, with insufficient
reserve energy supply
(liver glycogen) to provision the brain overnight.
This does not activate quality sleep and
recovery physiology,
but rather chronic nocturnal metabolic stress
and increased risk of
metabolic syndromes
– dementias/obesity/
diabetes and heart disease; note the seminal paper by Turek and
Bass in 2005:
“ ... However, while there is a growing awareness
among some sleep, metabolic, cardiovascular,
and diabetes researchers that insufficient sleep
could lead to a cascade of disorders, few in the
general medical profession or in the lay public
have yet made the connection ...”: Sleepless in
America: A Pathway to Obesity and Metabolic
Syndrome.
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