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Why your brain needs you to eat healthy and sleep well
by
Alicia Jones
on
December 3, 2012
| Resilience | Stress & Burnout |

Photo by Terisa Folaron

"In developed societies this [engagement of allostatic systems with worry, social conflict and overwork] all occurs in an environment of ...fast food or other high calorie consumables but with less and less physical activity. Coupled with an always-on-the-go society, where the sleep-wake cycle has almost been completely separated from the solar day…..there is no doubt that many of us live in a state of high allostatic load or even overload. The physical and mental health costs of this lifestyle are only now being appreciated...” (Psychobiological allostatis: resistance, resilience and vulnerability, Karatsoreos and McEwen, 2011)

First, a quick review on allostatic load.  As you may remember from Galen’s article on resilience, allostatic load is the wear and tear on the brain as a result of negative adaptation to stress in response to events in daily life. After a stressful event all manner of biochemical, hormonal and even neural and tissue related reactions occur. All this to say, there are many things happening inside your body that you can’t control. But there is another piece that you can control.  

Two researchers (Karatsoreos and McEwen) have observed that individual, behavioral responses to stress either assist a return to allostasis (getting back to normal) or interfere – contributing to allostatic load (bad). Some of the health damaging behaviors that can have a negative affect on the brain’s adaptive response to stress are: smoking, alcohol consumption, lack of sleep, and poor diet. For example, we all knew that eating too much sugar and carbohydrates would make us gain weight. But did you know it may also be related to your brain’s ability to bounce back from stress? Restricting food has been found to assist brain plasticity in rats, opening a window of opportunity for positive changes in the brain. (Spolidoro, M. et al. Food restriction enhances visual cortex plasticity in adulthood, 2011)

Karatsoreos and McEwen hypothesize that underlying all the systems that help your body modulate stress is sleep. Nearly all systems that help with allostasis are affected by the sleep-wake cycle (circadian rhythms), which hints at an important relationship between disrupted sleep and allostatic load. Here’s a few things Karatsoreos and McEwenhave already observed about sleep deprivation:

  • Shrunken medial temporal lobes (may be correlated with PTSD)
  • Increased reaction time
  • Compromises formation of new memories
  • Increases the amygdala’s response to negative stimuli (higher reactivity)
  • Impulsivity
  • Neural circuits become more vulnerable to stress
  • Allostatic responses that might otherwise help are compromised
  • Throws off the metabolism (weight gain, etc.)
  • Sleep deprivation elevates cortisol, glucose, insulin and insulin resistance

In other words, after a stressful experience, your body will try to return to a steady state, using a variety of processes. But it’s possible for us to trip up these processes by not sleeping.  So get some sleep! I’ll leave you with one more quote from Karatsoreos and McEwen:

“We propose that underlying allostasis and the capacity for resilience in response to stressors is a well functioning circadian timing system. The circadian system in mammals is centered in the suprachiasmatic nucleus with both neural and hormonal projections throughout the brain and body, impacting many of the systems involved in mediating allostasis. We hypothesize that disruption of the circadian system places the organism in a state of high allostatic load and eventually overload.”  

References:

Mood Disorders and Allostatic Load, Bruce McEwan, Society of Biological Psychiatry, 2003

Psychobiological allostasis: resistance, resilience and vulnerability, Ilia N. Karatsoreos and Bruce S. McEwan, Trends in Cognitive Sciences, December 2011 V. 15, N. 12

Food restriction enhances visual cortex plasticity in adulthood, Spolidoro, M. et all (2011)  Nat. Commun. 2, 320 DOI: 10.1038/ncomms1323

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