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I have known that what is called Rapid Eye Movement (REM) sleep is related to dreaming.  I didn’t know until now that those of us who suffer from depression HAVE TOO MUCH REM sleep and not enough Non-REM sleep (NREM).  Because I woke up at 2:30 this morning and cannot go back to sleep, I thought perhaps this might be the time to take a look at this topic.

I have been thinking about this information regarding the link between depression and disturbances in dreaming from a ‘streaming’ Netflix film I watched.  I found this synopsis of the program which describes another blogger’s reaction to the movie.

From ‘Radiant Recovery’, posted by By:  Arwen, 3/18/2010:

“For anybody who watches Netflix, on instant view there is a documentary about sleep called “What Are Dreams?”. It’s a NOVA special. I watched it last night and heard this interesting tidbit. If you watch it the part I’m about to mention starts roughly about 12:30.

Researchers used to think that dreaming happened in REM sleep only (where your eyes are darting about under your eyelids.) It turns out that is not true, that we all also dream in non-REM sleep. They know this from waking dream study participants up during both REM and non-REM sleep and asking them if they had been dreaming, and if so, what they had been dreaming about.

Here’s the interesting part – when asked to describe their feelings coming out of both types of sleep, the words used to describe how they felt after non-REM sleep were positive. The words used to describe their feelings after REM sleep were negative.

The researcher describing this says that these results are surprisingly reliable and consistent among a variety of participants. He mentions that the amygdala, a part of the brain, is highly activated during REM sleep, and the amygdala specializes in processing negative emotions.

Now, here’s where I sort of sat up a little bit – he goes on to note that normally people fall asleep through non-REM sleep. But people with serious depression and depressive disorders – they invariably go right into REM. And “they stay in REM and they spend too much time in REM.”

I have no idea of the connections between the potato/serotonin and any sleep science. But I do know the difference between a potato-night and a non-potato night for me. On a non-potato night I feel like I fall like a heavy rock into a dark place. I feel like I’ve had a heavy sleep, but not necessarily a deep or a sound sleep. More like something has descended on me and I can’t move. But a potato night for me feels almost like I’ve been out running errands mentally, and for the first few minutes after I’m up I feel slightly, barely disoriented. Then I feel strong and vibrant.

Again, no idea if and how any of the stuff we talk about here fits together with any of this. I just thought it was a fascinating tidbit of research and wanted to share it.”

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Then, of course, I wanted to take a look at some research about this interruption in the sleep cycle related to depression and located the following:

Human regional cerebral glucose metabolism during non-rapid eye movement sleep in relation to waking (2002)

“Sleep is an essential human function. Although the function of sleep has generally been regarded to be restorative, recent data indicate that it also plays an important role in cognition. The neurobiology of human sleep is most effectively analyzed with functional imaging, and PET studies have contributed substantially to our understanding of both rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. In this study, PET [measures levels of brain activity] was used to determine patterns of regional glucose metabolism in NREM sleep compared with waking.

“Whole-brain glucose metabolism declined significantly from waking to NREM sleep. …The reductions in relative metabolism in NREM sleep compared with waking are consistent with prior findings from blood flow studies. The relative increases in glucose utilization in the basal forebrain, hypothalamus, ventral striatum, amygdala, hippocampus and pontine reticular formation are new observations that are in accordance with the view that NREM sleep is important to brain plasticity in homeostatic regulation and mnemonic [memory] processing.”

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Conditional corticotropin-releasing hormone overexpression in the mouse forebrain enhances rapid eye movement sleep

This 2009 study used mice that were genetically modified in regard to production of a hormone that is involved in sleep cycles and dreaming states:

“Impaired sleep and enhanced stress hormone secretion are the hallmarks of stress-related disorders, including major depression. The central neuropeptide, corticotropin-releasing hormone (CRH), is a key hormone that regulates humoral and behavioral adaptation to stress. Its prolonged hypersecretion is believed to play a key role in the development and course of depressive symptoms, and is associated with sleep impairment.

“To investigate the specific effects of central CRH overexpression on sleep, we used conditional mouse mutants that overexpress CRH in the entire central nervous system … or only in the forebrain, including limbic structures ….CRH hypersecretion in the forebrain seems to drive REM sleep, supporting the notion that enhanced REM sleep may serve as biomarker for clinical conditions associated with enhanced CRH secretion.”

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I found this link to a Text of PowerPoint slides used by Dr. Leibowitz that includes some basic facts about sleep and dreaming.

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Depression deprives us of our Non-REM positive sleep stages and drops us into the highly negatively charged amygdala-driven (fear and stress response brain region) REM dream state for most of our sleeping time:

Post by Jen Robinson — “Oct 27, 2009 … Not only do most of our dreams occur in this stage, but REM dreams are also more vivid and emotionally wrought than non–REM dreams. … studies conducted during REM sleep also show increased activation of the amygdala…”

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Are trauma and abuse survivors continually called to TRY to process overwhelming emotional memories?

Emotional Memory Formation Is Enhanced across Sleep Intervals with High Amounts of Rapid Eye Movement Sleep (2001)

“Recent studies indicated a selective activation during rapid eye movement (REM) sleep of the amygdala known to play a decisive role in the processing of emotional stimuli.

“[Study] Results are consonant with a supportive function of REM sleep predominating late sleep for the formation of emotional memory in humans.”

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“Serotonin is thought to be intimately involved in the regulation of sleep and waking in humans….”

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REM-OFF & REM-ON NEURONS

“It is now well known that the visual-emotional hallucinatory aspects of dreaming occur during REM, whereas more thought-like and verbal ideational patterns are produced during NREM.”

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When the Brain Disrupts the Night

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Does amygdalar perfusion correlate with antidepressant response to partial sleep deprivation in major depression? (2006)

“One night of total sleep deprivation (TSD) or partial sleep deprivation (PSD) produces temporary remission in 40–60% of patients with major depression….”

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{I still believe that so-called depression is an immune system response to stressors.]

Stress and Depression: Preclinical Research and Clinical Implications (2008 – Italian and Swedish authors – excellent list of references at this link, many of the cited articles are available online)

“Major depression (MD) is a severe, life-threatening, and widespread psychiatric disorder having an incidence of about 340 million cases worldwide. MD ranks fifth among leading causes of global disease burden including developing countries, and by year 2030 it is predicted to represent one of the three leading causes of burden of disease worldwide [1], [2]. MD is also a risk factor for cardiovascular and metabolic diseases, and a major risk factor for suicide [3]. Despite extensive investigations, the exact mechanisms responsible for MD have not been identified…”

“Stress is usually defined as a state of disturbed homeostasis inducing somatic and mental adaptive reactions, globally defined as “stress response,” aiming to reconstitute the initial homeostasis or a new level of homeostasis after successful adaptation, i.e., allostasis [31]–[34]. There is wide consensus and support from preclinical and clinical data that stress exposure conceivably plays a causal role in the etiology of MD and depression-like disorders [11], [27], [31], [34]. However, no specific mechanism linking stress exposure and stress response to the occurrence of MD has yet been fully elucidated. Growing evidence indicates several classical candidates, including neurotransmitters and neuropeptides, as well as conceptually novel immune and inflammatory mediators, as likely intermediate links between stress exposure, depressive symptoms, and MD [9], [21], [34]–[38]. ….

“One of the hallmarks of the stress response has long been considered the activation of the HPA axis. Hypothalamic CRH activation is a pivotal signaling molecule in the regulation of the HPA axis in particular and of the stress response in general. Therefore, comprehension of the mechanism responsible for the negative feedback regulation of CRH is of paramount importance…..”

“Knowledge on the functioning of the HPA axis under acute or chronic challenge is also a key to understanding the intimate link between stress response and the pathogenesis of depression [40]. Indeed, in all MD syndromes, a certain degree of HPA-axis disturbance is often present, visible either at the baseline or with functional tests. Despite the fact that observed changes of HPA regulation are so far not specific for the diagnosis of depression or for any of its clinical syndromes [8], altered HPA-axis parameters are considered important biomarkers, particularly in preclinical studies. Increased circulating hormones such as adrenocorticotropic hormone (ACTH) and cortisol/corticosterone or increased adrenal gland weight are considered biomarkers of stress response in preclinical models [41], including in several papers in this Collection [19], [29], [42]–[46]. Despite the bulk of data available, surprisingly current knowledge has not yet been developed to a point where HPA-axis reactivity can be rationally exploited for targeted drug treatment, as opposed to the major achievements of drugs targeting the CRH receptors [47]….”

“The link between stress and depression is not novel, and several authors have aimed at identifying new subtypes of depression based on their functional link with stress exposure (e.g., [70]–[72]).”

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BBC film, “Why Do We Dream?”

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