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rhythmic state of animals, providing the opportunity to correlate health
outcomes with the degree and timing of circadian disruption among animals.
Further, it remains unclear how disease states in arrhythmic clock gene models
(i.e.,
bmal1
) are affected by dif-
ferent entrainment and free-running conditions (e.g., LD versus DD condi-
tions). Finally, the health consequences of circadian disruption can be further
studied in rhythmic clock gene models (e.g.,
per2
mutant) held under both
24 h LD cycles and LD cycles with a period closer to the inherent period
of the mouse model. In this manner, research can address the relative conse-
quences of misalignment versus arrhythmia, determine whether having the
right clock for the environment is corrective, and whether there are situations
where a broken clock may be advantageous.
69,267
In conclusion, there is compelling evidence that circadian disruption is
detrimental to health, and there is an increasing appreciation of the factor of
circadian timing in the manifestation of disease states. In most of the research
within this review, it would appear that the organism can compensate for
circadian disruption when environmental conditions are devoid of challenge
or stress; however, severe health consequences manifest when circadian reg-
ulation is compromised in the face of adversity. Collectively, this would sug-
gest that circadian disruption
per se
does not cause disease, but can interact
with disease states to increase outcome severity and/or accelerate disease
progression. Uncovering the mechanistic relationships that underlie these
synergistic and modulatory effects of circadian disruption on health are
important areas for future research.
/
,
clock
mutant, double
per
/
or
cry
/
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