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Sleep Deprivation For Depression: A Potent, Short-Term Treatment

We’ve all heard the media-driven dogma that everyone needs at least 8 hours of sleep per night for optimal neurophysiological performance.  Striving for 8 hours of sleep is generally a healthy rule of thumb [for most people], but shouldn’t be considered a utopian amount for everyone.  Many individuals diagnosed with major depressive disorder (MDD) sleep excessively, often exceeding 12 hours per night with intermittent naps throughout the day.

While you may think that the extra sleep would promote vigor and possibly aid in combating depression, it turns out that in many cases, the opposite is true.  Too much sleep perpetuates an imbalance of the circadian rhythm, and generally promotes or exacerbates depressive states.  It turns out that among individuals with major depression, sometimes deliberate [self-induced] sleep deprivation can elicit potent antidepressant effects.

Although most professionals don’t go around recommending sleep deprivation as an intervention for everyone, research since the 1970s has demonstrated the antidepressant potential of sleep deprivation.  There is even some evidence to suggest that when combined with certain pharmaceutical antidepressants, sleep deprivation acts synergistically, reducing depression more than either intervention as a standalone option.

Sleep Deprivation For Depression: A Potent, Short-Term Treatment

Under normative circumstances, chronic sleep deprivation is known to detrimentally affect both physical and mental health.  Those who frequently get a poor night’s sleep may suffer from excessive daytime sleepiness, anxiety, chronic fatigue, impaired cognitive performance, and a noticeable decline in motor skills.  However, among the depressed populace, strategic sleep deprivation (or restriction) can rapidly improve mood – sometimes quicker than any other intervention.

Hypothesized Mechanisms of Sleep Deprivation’s Antidepressant Effect

There are numerous hypothesized mechanisms behind the antidepressant effect associated with sleep deprivation.  Most recently, researchers suggest that increased glial signaling of adenosine (A1) receptors is largely responsible for the mood boost derived from sleep deprivation.  Others speculate that cumulative adjustments of: adenosine receptors, arousal, circadian rhythm, reduction of time spent in bed, and altered “microsleep” – may synergistically promote mood improvement.

Glial signaling: A study published in 2013 investigated the antidepressant mechanism of sleep deprivation.  It was discovered that glial signaling promotes the antidepressant effects derived from deprivation of sleep.  Specifically, when astrocytes (star-shaped glial cells) signal to A1 (adenosine) receptors, depressive moods (and behaviors) are significantly reduced.

A1 (Adenosine) receptors: Glial cells facilitate increased activation of synaptic A1 (adenosine) receptors.  Researchers were able to confirm the involvement of A1 receptors by deliberately administering the drug CCPA, an A1 adenosine receptor agonist.  Upon administration of CCPA, mood significantly improved.

Note: It was suggested that the mechanisms associated with sleep deprivation may be useful to target in the development of newer pharmaceutical antidepressants.  Drug developers could develop a compound that selectively modulates glial (astrocyte) signaling.

  • Source: http://www.nature.com/tp/journal/v3/n1/full/tp2012136a.html

Arousal alterations: A study published in 1992 suggested that total sleep deprivation produces antidepressant effects via alteration of arousal.  A total of 23 individuals with major depression were deprived of a full night’s sleep twice on a weekly basis for 2 consecutive weeks.  Arousal was assessed with the Thayer’s Activation Deactivation Adjective Check List (AD ACL).  Relief from depressive symptoms was directly associated with arousal assessment scores.  Evidence suggested that sleep deprivation enhances certain aspects of arousal, while decreases subcortical arousal.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10607054

Circadian rhythm: Many people with major depression have circadian rhythm abnormalities that perpetuate and/or exacerbate their depression.  Inability to normalize the circadian rhythm can have detrimental long-term consequences for both physical and mental health.  It appears as though sleep deprivation therapy may combat depression via modulation of the circadian rhythm, correcting various abnormalities and altering activation of specific genetic biomarkers.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/22906517

Cortisol increases: A study published in 2004 noted that just one night of sleep deprivation can significantly reduce depressive symptoms in up to 60% of patients.  In this study, researchers explored the role of the HPA (hypothalamic-pituitary-adrenal) axis in the attenuation of depressive symptoms.  They specifically recorded levels of cortisol (a stress hormone) prior to, during, and following one night of sleep deprivation.

Among those who experienced an antidepressant effect, cortisol levels were significantly elevated during the night of sleep deprivation as well as the following day.  Those who didn’t respond to sleep deprivation didn’t experience clinically significant changes in cortisol levels.  Researchers speculate that significant elevations in post-sleep deprivation cortisol (compared to baseline) may predict antidepressant responses.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/15285966

Decreased sleep fragmentation: Excessive sleep is associated with increases in sleep fragmentation or lack of deep (slow-wave) sleep.  It appears as though acute sleep restriction may decrease sleep fragmentation, ultimately increasing the amount of deep, restorative sleep that is attained.  Perhaps normalization of the circadian rhythm with sleep deprivation is what trains the body to adapt to sleeping during a specific chunk of time.  As the body comes to learn that it must sleep during a shorter allotted timeframe, it may decrease fragmentation.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/15144959/

Microsleep minimization: “Microsleeps” may influence the antidepressant effect of sleep deprivation.  These are considered ultrashort, unintentional episodes of attention loss that last 5 to 10 seconds.  It appears as though individuals undergoing partial-sleep deprivation as a treatment for depression experience greatest improvement when microsleep is minimized compared to those who experience high amounts of microsleep.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/9611673/

Neurotransmission: A publication from 2014 analyzed changes in plasma metabolites among 12 sleep deprived individuals.  They used liquid chromatography to determine alterations in plasma metabolites that were specifically altered as a result of sleep deprivation.  They discovered that 27 metabolites increased – perhaps most notably tryptophan, serotonin, and taurine.

It has long been known that increasing serotonin can elicit an antidepressant response, and past-research suggests that among depressed individuals, taurine levels are generally altered.  Therefore, it is important to consider that increases in levels of tryptophan, serotonin, and taurine could contribute to the antidepressant efficacy of sleep deprivation.

  • Source: http://www.pnas.org/content/111/29/10761.abstract

Reduction of “time in bed”: It is well known that people with depression are unable to summon up the motivation to get out of bed and/or get things done.  Despite the fact that energy may be low among those with depression, spending excess time in bed as a result of oversleeping can promote grogginess and lethargy as a result of this habit.  By reducing the time spent in bed with sleep deprivation, individuals break the psychological crutch of staying in bed all day and may feel less fatigued – contributing to an antidepressant effect.

REM reduction: Individuals with depression often experience REM sleep earlier in the night and an overall increase in rapid-eye movement compared to those with normative moods.  Sleep deprivation has been hypothesized to alter the amount of REM (rapid-eye movement) that a person experiences during their sleep cycle, potentially contributing to a therapeutic antidepressant response.  In addition, some believe that the antidepressant effect from REM reduction is a result of REM-restricted increases in BDNF levels.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/26146031

Sleep Deprivation for Depression Treatment (Research)

Researchers have known that sleep deprivation can be used as a potent intervention for depression since the 1970s.  Nearly every study has suggested short-term efficacy of sleep deprivation as a short-term treatment for a majority (up to 60%) of those with major depression.  In addition to improving mood, sleep deprivation may provide an added benefit of enhancing executive performance and potentiating antidepressant responses.

2014: A study published in 2014 aimed to determine the effect of sleep deprivation on EEG (electroencephalograph) and executive functions among individuals with depression.  Researchers recruited 18 individuals with a diagnosis of depression and 21 healthy non-depressed individuals.  They used a polysomnography to assess changes before and after sleep deprivation, and the Visual Analogue Scale (VAS) to measure depression.

Executive performance was measured with the Wisconsin Card Sorting Test (WCST), an assessment used to determine cognitive flexibility.  Results indicated that sleep deprivation significantly improved mood and cognitive function among those with depression.  This was evidenced by the decrease in depression scores from “6.7” to “2.9” and reduced errors in various measures of the WCST.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/25266518

2010: A paper published in 2010 reported that sleep deprivation as a treatment for depression is effective for 40% to 60% of all patients.  Despite the significant short-term efficacy of sleep deprivation as an antidepressant, it is estimated that nearly 4/5 (80%) of all individuals experience a relapse of depressive symptoms within several days.  Still, authors note that sleep deprivation is highly-effective despite its mysterious, unknown mechanism of action.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/20586691

2003: A publication from 2003 notes that acute sleep deprivation for one night or partial sleep deprivation (in the second half of the night) significantly improves mood of approximately 60% of individuals with depression for the following day.  Authors of this publication mention the fact that sleep deprivation yields the most rapid antidepressant response, even more rapid than ECT (electroconvulsive therapy).

  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181780/

2002: A report from 2002 suggests that “total sleep deprivation,” or deprivation of sleep for an entire night, significantly improves mood in up to 60% of those diagnosed with depression.  Authors of the report suggest that responses are subject to significant individual variation, with certain individuals experiencing an increase in depression (up to 7%) and others experiencing full symptomatic remission.  They also mention that antidepressant responses to total sleep deprivation are noted during the night of the deprivation and/or throughout the following day.

In less common cases, up to 15% of individuals experience reductions in depression after brief “recovery sleep” the following day.  Unfortunately, up to 80% of those who experience a reduction in depressive symptoms from sleep deprivation end up experiencing symptomatic relapse (complete or partial).  In many cases, a return to the pre-deprivation sleep schedule triggers symptomatic relapse.

Authors report that antidepressant properties of sleep deprivation can often be maintained with antidepressant augmentation strategies (e.g. pharmaceutical drugs, light therapy, etc.).  Moreover, some sources suggest that “partial sleep deprivation” throughout the second half of the night is equal in efficacy to “total sleep deprivation” (no sleep for the entire night).  Whether partial deprivation is superior as an antidepressant to total deprivation remains unknown.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12531127

2002: Researchers in 2002 stated that partial sleep deprivation can significantly ameliorate depressive symptoms.  Despite fast-acting antidepressant relief from sleep deprivation, a majority of individuals engaging in partial sleep deprivation relapse in depressive symptoms within just one night.  In this study, researchers used repetitive transcranial magnetic stimulation (rTMS) to determine whether it could prevent relapse in depressive symptoms.

A group of 20 individuals with depression that responded to partial sleep deprivation were assigned to receive TMS or a sham-TMS.  They discovered that TMS significantly elongated the antidepressant response associated with sleep deprivation, thus it may be an effective way to inhibit relapse.  That said, it is important to consider that the TMS may be acting as a standalone antidepressant among responders to sleep deprivation rather than potentiating its effect.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/12002519

2001: Researchers noted that when used in conjunction with serotonergic and noradrenergic antidepressants, total sleep deprivation may enhance antidepressant response.  In addition, the combination of lithium and total sleep deprivation may also provide a sustained antidepressant effect.  A study published in 2001 suggested that total sleep deprivation may elicit an antidepressant effect via dopaminergic mechanisms.

This study aimed to test the hypothesis that total sleep deprivation (e.g. skipping sleep for an entire night) had dopaminergic effects contributing to its antidepressant efficacy.  A total of 28 individuals diagnosed with bipolar depression were assigned to total sleep deprivation with administration of the drug Survector (Amineptine) or a placebo.  Results indicated that total sleep deprivation significantly attenuated depressive symptoms, but the effect was not significantly enhanced by Survector by the end of the treatment.

It should be noted that despite no synergistic effects of total sleep deprivation and Survector (a dopamine reuptake inhibitor with a minor affinity for norepinephrine), the effect of total sleep deprivation in isolation provided significant therapeutic benefit.   This suggests that among individuals with severe bipolar depression, total sleep deprivation may be an advisable intervention.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/11728613

1999: A study published in 1999 discussed the therapeutic potency of sleep deprivation among individuals with bipolar depression.  Their goal was to test the efficacy of the drug Pindolol when administered synergistically with  intervention of total sleep deprivation.  Pindolol is a beta blocker that is nonselective, with some effects as a 5-HT1A (serotonergic) receptor weak partial agonist and antagonist.

A total of 40 individuals with bipolar depression were randomly assigned to receive Pindolol (7.5 mg) or a placebo for 9 days in conjunction with 3 sessions of total sleep deprivation.  Results indicated that administration of Pindolol potentiated the antidepressant effect associated with total sleep deprivation.  Further, it appears as though Pindolol administration provided a sustained antidepressant effect, thus preventing relapse.

This finding is especially helpful for individuals with bipolar depression.  Researchers noted that the antidepressant response from the combination of total sleep deprivation and Pindolol could be maintained for 6 consecutive months (a longer term) with administration of lithium salts in approximately 65% of cases.  As was noted in newer research, authors suggest a serotonergic mechanism of total sleep deprivation, thus aiding in the reversal of depressive symptoms.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/10088139

1993: A study from 1993 indicated that an estimated 70% of all adults diagnosed with depression can experience antidepressant effects of sleep deprivation.  That said, it wasn’t known as to whether sleep deprivation would provide benefits among adolescents diagnosed with depression.  In this study, researchers recruited a total of 17 adolescents diagnosed with psychiatric disturbances and deprived them of sleep for 36 hours.

Prior to the sleep deprivation, assessments of both depression severity and subjective arousal were recorded.  These same assessments were also collected during the sleep deprivation and after a night of recovery sleep.  Results were interesting in that adolescents with severe depression experienced significant therapeutic benefit from sleep deprivation.

However, among patients considered “in remission” from depression, the 36 hours of sleep deprivation worsened their depressive symptoms and notably decreased their subjective arousal.  Authors noted that there are likely parallels in responses to sleep deprivation among adolescents and adults with severe depression.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/8340295

1992: In the early 1990s, a review of evidence of sleep deprivation as a treatment for depression was published.  This review incorporated all research investigating sleep deprivation for clinical purposes.  Researchers focused on 6 clinically relevant interventions of sleep deprivation including: enhancement of antidepressant medication efficacy, expediting an antidepressant’s therapeutic onset, as an inhibitor of mood cycling, as an alternative intervention to pharmaceutical antidepressants, usefulness as a diagnostic aid, and predicting responses to antidepressants.

The review drew evidence from a total of 36 published studies.  The review literature suggested that sleep deprivation may potentiate the efficacy of antidepressants.  In addition, sleep deprivation appeared to expedite antidepressant onset of action and aided in the distinguishing of dementia from pseudo-dementia stemming from depression.  It was unclear as to whether sleep deprivation could be used to successfully predict antidepressant responses.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1734735

1992: A study conducted in the early 1990s noted that sleep deprivation often demonstrated rapid antidepressant efficacy among certain individuals with depression.  Researchers in this study sought to distinguish differences in regional activation within the brain of those who respond to sleep deprivation from those who didn’t respond.  To accomplish this, a brain imaging technique called PET (Positron Emission Tomography) was utilized.

The PET scans were conducted pre-sleep deprivation and post-sleep deprivation in a group of 15 individuals with major depression.  It was noted that those who respond to sleep deprivation have significantly greater metabolism in the cingulate cortex region of the brain (following sleep-deprivation) compared to those who don’t respond.  Of the 15 patients, a total of 4 experienced greater than 40% reduction in depressive symptoms based on the Hamilton Rating Scale for Depression (HAM-D).

While this study proved that sleep deprivation is effective in a subset of those with depression, it appears as though not everyone responds.  Researchers speculated that among the responders, it appears as though the limbic system may have been overactive, and thus contributing to their depression.  Among the nonresponders, depressive symptoms may be non-limbic and as a result, they derived no substantial benefit from sleep deprivation.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/1554042

1982: In the early 1980s, researchers were reporting that sleep deprivation may elicit an antidepressant effect as a result of altering sleep latency, sleep fragmentation, and REM sleep.  Authors noted that sleep deprivation for one night contributes to a substantial antidepressant effect.  It was speculated that certain sleep-dependent processes associated with sleep regulation are impaired among the depressed populace.

Specifically, deficiencies in “Process S” are thought to contribute to abnormal sleep among those with depression.  Researchers noted that the antidepressant effect associated with sleep deprivation is likely a result of an increase in “Process S” as a result of extended waking periods.  Although in this report researchers were attempting to decipher the antidepressant mechanisms of sleep deprivation, they highlighted its efficacy as a short-term antidepressant intervention.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7185793

1980: A study from 1980 analyzed a sleep deprivation task as an intervention for depression.  A total of 14 individuals with depression were matched with 14 healthy controls.  This sleep deprivation task specifically focused on waking individuals to minimize REM (rapid-eye movement) phase sleep.

Among those with depression, REM sleep is often excessive compared to NREM (non-REM) sleep.  It was noted that prior to REM deprivation, those with depression had reductions in REM latency, greater REM frequency, and the temporal distribution of REM was considered abnormal – compared to the healthy controls.  Results indicated that REM deprivation provided therapeutic antidepressant benefit among those with depression, possibly by temporarily restoring an imbalanced circadian rhythm.

  • Source: http://www.ncbi.nlm.nih.gov/pubmed/7362414/

Benefits of Sleep Deprivation for Depression

There are many benefits of strategically engaging in sleep deprivation for the treatment of depression.  Regardless of whether you’re using total sleep deprivation (skipping sleep for a full night), partial sleep deprivation (skipping sleep for part of the night), or specifically depriving yourself of REM (rapid-eye movement) – all serve as potent short-term antidepressants.

  • Adjunct treatment: Sleep deprivation has been documented as being highly effective when used as an adjunct treatment for depression. In other words, among those taking antidepressants (SSRIs or SNRIs), sleep deprivation may potentiate the antidepressant response and/or onset of action.  Further, sleep deprivation may provide someone with temporary relief from depressive symptoms while they are waiting for their pharmaceutical antidepressant to work.
  • Circadian rhythm modulation: Many individuals with depression are thought to have abnormalities of the circadian rhythm. In other words, their “biological clocks” are thrown out of balance, possibly due to the depression.  However, in some cases the direct cause of depression is likely a circadian rhythm abnormality.  Sleep deprivation is thought to modulate the circadian rhythm and correct disturbances.
  • Established efficacy: Sleep deprivation has been documented as an effective short-term intervention for depression since the 1970s. It has been suggested as an effective antidepressant for up to 60% of individuals with depressive disorders.  Moreover, it appears as though many types of sleep deprivation including: total-night, partial-night, and REM deprivation all provide substantial mood boosts among those with depression.
  • Executive improvement: Some research has suggested that both arousal and executive performance improve among those with depression who engage in sleep deprivation. Perhaps the noticeable executive improvement among those with depression contributes to the antidepressant effect.  After all, many individuals with depression complain of brain fog – which may exacerbate their depressive feelings.
  • Fast-acting: Among the most prominent benefits of sleep deprivation is the fact that it provides rapid antidepressant effects. Studies have documented that the antidepressant (mood boosting) effect associated with sleep deprivation is often noted to occur during the deprivation and is sustained throughout the following day.  This fast-acting effect may be beneficial for someone who is highly suicidal, feeling as if they want to die.
  • Limbic system modulation: Certain reports suggest that those who are most likely to benefit from sleep deprivation may have overactive limbic systems. Engaging in sleep deprivation tones down activity within the limbic region of the brain, and ultimately contributes to feeling less depressed.  Should you have depressive feelings stemming from the limbic regions (anterior cingulate), sleep deprivation may temporarily normalize the activity within these regions.
  • Neurotransmission: It appears as though sleep deprivation affects glial signaling to adenosine A1 receptors, increases serotonin (and its precursor tryptophan), and taurine. The specifics of alterations in neurotransmission as a result of sleep deprivation aren’t fully understood, but it may be that the sleep deprivation is having an impact on mood via serotonergic mechanisms. Fully elucidating the alterations in neurotransmission associated with sleep deprivation could help spur the creation of new antidepressants.
  • Potent antidepressant effect: Most people don’t question whether sleep deprivation is effective as a transient treatment for depression due to the fact that improvements are often significant. Reports suggest that it may be more effective as a short-term antidepressant than other approved options.  Although not everyone responds to sleep deprivation, those who do often experience substantial reductions in depressive symptoms.
  • Prevents oversleeping: Many individuals with depression have gotten into the habit of oversleeping. Though the depression may have caused fatigue, tiredness, grogginess, and brain fog – often times a person’s neurophysiology adapts to the new behavior of increased sleep.  The neurophysiological adaptations may be perpetuating and/or exacerbating depressive emotions.  Sleep deprivation prevents oversleeping, forcing a person to break their depressive neurophysiological patterns, which may contribute to the antidepressant effect.
  • Sustainability with pharmaceuticals: There is some evidence suggesting that the antidepressant effect resulting from sleep deprivation can be maintained long after the night of deprivation. While the antidepressant effect from sleep deprivation is generally considered transient, some papers document sustainability of up to 6 months with the right treatment.  Sustainability may be more pronounced among those with bipolar depression due to the fact that they are more sensitive to mood adjustments.  Antidepressants, mood stabilizers, and even repetitive transcranial magnetic stimulation (rTMS) have been shown to sustain sleep deprivation’s effect.
  • Synergistic effects: The antidepressant effect from sleep deprivation can often be enhanced in a synergistic manner with administration of specific pharmaceutical drugs. For example, one study cited that administration Pindolol (a beta blocker with a weak effect on the 5-HT1A receptor) potentiated the antidepressant responses from sleep deprivation.  Combining sleep deprivation with an SSRI or SNRI may generate a synergistic antidepressant response.  It has also been theorized that tricyclic antidepressants (TCAs) and certain MAOIs (e.g. Tranylcypromine) may act synergistically with sleep deprivation as a result of REM suppression.
  • Temporary contrast: Perhaps the most notable benefit of sleep deprivation among those with clinical depression is that it provides temporary contrast, allowing the individual to understand that they are capable of feeling less depressed. Many people stuck in depression for an extended period of time often assume that they’ve always felt depressed.  The antidepressant effect of sleep deprivation gives them some emotional contrast and may provide them with increased hope and/or optimism of improvement.

Drawbacks of using sleep deprivation for depression

There are some potential disadvantages associated with using sleep deprivation as an intervention for depression.  The most notable disadvantage is that not everyone is guaranteed to respond, thus it could actually worsen depressive symptoms in a subset of individuals.  In addition, the biggest downfall associated with sleep deprivation is that it’s generally only effective for a short-term.

  • Adverse health effects: Sleep deprivation can cause a variety of adverse health effects and compromise your ability to drive or operate heavy machinery the following day. In fact, evidence has shown that those who are sleep deprived suffer from compromised driving performance to a greater extent than those who drive drunk.  Sleep deprivation increases risk of heart abnormalities (e.g. irregular beats), stroke, high blood pressure, and diabetes.
  • Daytime fatigue: Although one study suggested enhancement of executive function following sleep deprivation among those with depression, it cannot be assumed that everyone experiences this enhancement. In fact, some individuals may end up feeling more fatigued than usual, suffering from excessive daytime fatigue.  Daytime fatigue could significantly impair job (or school) performance.
  • Not universally effective: While estimates suggest that between 40% and 60% of those with major depression experience short-term benefit from sleep deprivation, it is clearly not universally effective. Some individuals derive no benefit from a night without sleep and may end up feeling fatigued and equally as depressed the following day.  Should you try sleep deprivation, there’s a chance you won’t notice any change in mood.
  • Short-term efficacy: Despite sleep deprivation’s proven efficacy as a treatment for depression, its antidepressant effect is generally considered extremely short-term and/or transient. Among the 60% of individuals who experience mood improvement, most end up experiencing a full relapse of depressive symptoms within a day or two.  That said, there are some medications that can be used to maintain a longer-term effect (up to 3 months).
  • Side effects: Even if sleep deprivation successfully reduces your depressive symptoms, there’s a chance that it may result in unwanted side effects including: anxiety, brain fog, cognitive impairment, emotional recognition difficulties, and lethargy. It is important to be cognizant of potential side effects associated with reduced sleep.  Sleep deprivation can trigger hypomania (or mania) among individuals with bipolar disorder, provoke psychotic symptoms, and increase seizure susceptibility.
  • Worsening of depression: One study estimates that of individuals with depression who try sleep deprivation as an antidepressant intervention, up to 15% experience a worsening of depressive symptoms. Any intervention that has the potential to worsen symptoms should be used with caution.  Individuals agreeing to test sleep deprivation for their depression may want to remind themselves that it could exacerbate their symptoms rather than alleviate them.

Who is most likely to benefit from sleep deprivation for depression? Factors to consider.

Clearly not everyone should use sleep deprivation as a treatment for depression.  Research has suggested certain factors can be used to predict whether you’re likely to benefit from sleep deprivation as a treatment for depression.

  • Bipolar depression: Those with bipolar depression often derive significant benefit from using sleep deprivation as an antidepressant intervention. It is unknown as to why those with bipolar disorder may derive more benefit from sleep deprivation, but it is hypothesized that bipolar patients may be more sensitive to “switching” of moods.  Sleep deprivation may trigger a “switching” mechanism for an antidepressant response, which can be augmented with a mood stabilizer (e.g. lithium) for long lasting results.
  • Chronotype: Research demonstrates that those who are most likely to benefit from sleep deprivation tend to have specific circadian preferences. Those that derive the most benefit from sleep deprivation tend to prefer staying up later or have an “eveningness” preference.  Individuals with a “morningness” preference were more likely to experience a worsening of depression following sleep deprivation.
  • Depressive subtypes: The two depressive subtypes most likely to benefit from sleep deprivation include: endogenous depression (naturally occurring without external influences) and melancholic depression (characterized by anhedonia and lack of mood reactivity). It is unknown as to whether certain types of depression are more likely to worsen following sleep deprivation compared to others.
  • High arousal: Individuals with a higher baseline level of arousal tend to respond significantly more than those who have lower arousal. This could be due to the fact that those with higher arousal have a different neurophysiological signature associated with their depression compared to those with lower levels of arousal.  Greater arousal may be associated with faster-paced brain waves (e.g. beta waves) compared to slower ones (e.g. theta waves) and different neurotransmission.
  • “Limbic” depression: One study documented that those with high baseline metabolism within the anterior cingulate region of the brain responded better to sleep deprivation for depression than those with lower baseline metabolism. This suggests that individuals with depression characterized by overactivation within the limbic region may be more likely to respond to sleep deprivation.  PET scan data suggests that sleep deprivation may normalize metabolic activity within the anterior cingulate.
  • Mood swings: Individuals with significant mood swings or subject to significant variance in mood throughout the day or between multiple days are more likely to respond to sleep deprivation for depression. It is unclear as to why depression with mood swings makes an individual more likely to derive benefit from sleep deprivation, but it is an important factor that may help predict individuals that are more likely to respond.

Note: There are factors that seem to be non-predictive of responses to sleep deprivation for depression including: age, depression severity, duration of depression (or illness), number of prior antidepressant treatments, subjective expectation, and sex.

  • Source: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181780/

Strategies to Maintain the Antidepressant Effects of Sleep Deprivation

There are several proven strategies that potentiate the antidepressant effect of sleep deprivation.  While several involve co-administration of pharmaceutical drugs (antidepressants, beta blockers, mood stabilizers) – other interventions include: light therapy, sleep phase advance therapy, and repetitive transcranial magnetic stimulation.

  • Antidepressants: Administration of SSRIs and SNRIs may aid in sustaining the antidepressant effect of sleep deprivation. Perhaps more likely to sustain the antidepressant response is administration of a tricyclic antidepressant (TCA) or specific MAOI that suppresses REM (rapid-eye movement) sleep.  A decrease in REM sleep and increases in specific neurotransmitters resulting from the antidepressants may potentiate the effect of sleep deprivation.
  • Beta blockers: The drug Pindolol, a nonselective beta-blocker has been researched and cited as an effective adjunct to sleep deprivation. It appears as though administration of this drug can extend the antidepressant effect of sleep deprivation.  It is unclear as to whether any other beta blockers have this same effect as Pindolol – acting on the 5-HT1A receptor.
  • Light therapy: Administration of bright light therapy the morning after sleep deprivation can extend the antidepressant effect of the intervention. In one study, patients were divided into 2 groups: one received bright light therapy, while the other received no bright light therapy after the sleep deprivation.  The group that didn’t receive the bright light therapy experienced a depressive relapse within one day, whereas the group receiving bright light therapy maintained their antidepressant response for a week.
  • Mood stabilizers: Among those with bipolar depression, administration of lithium tends to extend the efficacy of sleep deprivation. In fact, those with bipolar disorder are significantly more likely to respond to sleep deprivation in the first place.  Lithium may help prevent a person’s mood from plummeting once they’ve managed to transition out of the depressed state.
  • Sleep phase advance: A study conducted in the 1990s documented that by “shifting” a person’s sleep schedule by one hour each day, they were able to maintain the antidepressant effect provided by sleep deprivation. Researchers scheduled individuals to sleep from 5 PM to 12 PM, then 6 PM to 1 AM, followed by 7 PM to 2 AM (and so on) – until the sleep phase had reached 11 PM to 6 AM.  This shifting significantly preserved improved mood derived from sleep deprivation.
  • Transcranial magnetic stimulation: Using repetitive transcranial magnetic stimulation (rTMS) has demonstrated preliminary efficacy in extending the antidepressant effect of sleep deprivation. The effect was noted to be maintained several days longer than the norm.  It is unclear as to how long the antidepressant effect can be maintained with consistent rTMS following sleep deprivation.

Note: It is unclear as to whether combining multiple strategies such as administration of Pindolol, using bright light therapy, sleep phase advance, and transcranial magnetic stimulation would significantly extend the antidepressant effect of sleep deprivation compared to using just one adjunct intervention.  Responses to these maintenance strategies are likely subject to significant individual variation.

How often should you use sleep deprivation for depression?

There are no definitive guidelines as to how often sleep deprivation should be used for those with severe depression.  Assuming an individual derives significant benefits from sleep deprivation, it may be used up to several times per week.  The goal isn’t to deprive an individual of sleep every night as this would result in adverse health effects.

Most people will want to work with a professional that has some experience with using sleep deprivation as an antidepressant.  By working with a professional, you can come up with a personalized frequency to maximize the benefit you derive from deprivation.  For example, you may benefit from 3 nights of sleep deprivation per week, whereas another person may find that they only benefit from 1 night of sleep deprivation per week.

Further, the specific type of sleep deprivation (e.g. total deprivation, partial deprivation, REM deprivation) may make a difference.  In addition to deprivation, coming up with a set sleep schedule or restricting sleep (to prevent oversleeping) may provide added benefit.  I’ve recommended tweaking sleep as a way to biohack your mental health and overcome depression with logic.

My interest in sleep deprivation as a treatment for depression

I became interested in sleep deprivation as an intervention for depression as a result of contrasting times in my life when I felt happy with times that I felt depressed.  When I was depressed, I ended up taking antidepressants – some of which made me feel extremely tired.  On these drugs I would sleep for 10 to 14 hours per night, wake up, only to sleep even more throughout the day.

In my experience, the antidepressants caused chronic fatigue, and exacerbated depression – both of which were maintained upon withdrawal.  I continued to have severe brain fog and fatigue as a result of an antidepressant-induced chemical imbalance.  My neurochemistry was a shambles and nothing seemed to fix it until I developed PTSD and severe hypochondria (health anxiety).

The combination of PTSD and hypochondria resulted in significant increases in adrenaline levels, which prevented me from getting the standard 10 to 14 hours of sleep that I was getting on antidepressants.  Now I was getting about 6 to 8 hours of sleep per night, possibly less than 6 a few nights of the week.  Reduction in sleep hours was due primarily to anxiety-induced insomnia and a state of hyperarousal.

As I overcame my PTSD and adrenaline addiction, I realized that my sleep hours began increasing and my mood went from being highly-anxious + happier to less anxious + more depressed.  I documented these subtleties and hypothesized that sleep deprivation may increase arousal and ultimately elicit an antidepressant effect.  Just like the research suggested, I found that temporary sleep deprivation improved my mood, but chronic deprivation and restriction impaired my executive functioning.

I believe that individuals with higher arousal are likely to be less depressed, and thus get more sleep compared to those with lower arousal – who may have less activating neurotransmission and neuroelectrical activity (e.g. beta wave deficiencies).  I think it would be interesting to analyze the neuroelectrical activity (brain waves) of individuals with depression that respond to sleep deprivation as an antidepressant intervention.

Theoretically, certain commonalities in the brain activation could be noted among those who experience an antidepressant effect, and these could be consciously trained via EEG neurofeedback and/or combined with decoded neurofeedback to target regional activation.  While the effects of sleep deprivation are more complex than neuroelectrical activity, it would be worth investigating.

Have you deliberately tried sleep deprivation for depression?

If you’ve engaged in sleep deprivation as a treatment for depression, feel free to share your experience in the comments section below.  To help others better understand your situation, mention whether you were assigned a specific sleep deprivation protocol by a professional (e.g. partial sleep deprivation) or whether you deliberately skipped sleep on your own as a treatment.  Discuss whether the sleep deprivation ended up being an effective short-term antidepressant or whether no noticeable response was noted.

If the sleep deprivation was effective, note when you noticed your mood shifting from depression to feeling less depressed, and how long you were able to sustain the antidepressant response before your mood relapsed.  Were you taking any medications and/or supplements that may have influenced (or potentiated) your response to the deprivation?

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