Cannabis for Bipolar Disorder: Why It's Not a Good Option (5 Studies) I wanted to get to the bottom of this, so I went on a hunt for studies. The Connection Between Cannabis and Bipolar Disorder . 5 drops in the am 5 drops in the PM before bed. You have no idea how nice it is to not have to suffer from bipolar symptoms like raging and be able to have a. Although cannabis use is common in bipolar disorder and may . To the authors knowledge there are no published studies that have used . I am 'full of energy', ' high', ' full of good ideas' and the depression . Table 5. Effect of cannabis use on mood/ BD symptoms. .. Add to FavoritesView more options.
a (5 Studies) Cannabis It’s Not Good Option Disorder: for Bipolar Why
It makes sense that sleep problems would accompany bipolar disorder. Manias are associated with days of unfatigued sleeplessness, excessive activity and substance abuse, which eventually catches up with them and disrupts their sleep.
On the other hand, the depressive symptoms associated with bipolar disorder are the same experienced by those diagnosed with clinical depression , which is associated with sleep issues of is own.
In fact, for many people with bipolar disorder, the emergence of sleep issues can be a warning sign that an episode is coming on.
Likewise, a period of sleep deprivation or even a bout of jet lag can trigger a manic episode. Researchers have charted the interplay between bipolar disorder and sleep: Common sleep problems associated with bipolar disorder include insomnia, reduced need for sleep, hypersomnia, sleep apnea, delayed sleep phase syndrome, and fatigue.
Insomnia describes difficulty falling or staying asleep. A person with insomnia may take an hour or more to fall asleep. Once they finally do fall asleep, the sleep they experience is low-quality. Their energy remains unabated for days, despite not getting sufficient levels of sleep or any at all. People with mania draw sheep and make a collage! Many of the effects of sleep deprivation may sound familiar to you, considering their overlap with the bipolar symptoms listed above.
Moodiness, poor judgement, irritability, depression, anxiety, and lack of focus are all symptoms of bipolar disorder. Since these are also caused by sleep deprivation, the negative impact is only compounded for individuals with bipolar disorder. Much research has linked sleep deprivation with a relapse of bipolar symptoms. In particular, sleep loss has a pronounced negative impact on women with bipolar disorder, significantly increasing their risk for a manic episode. Hypersomnia is the opposite of insomnia.
It describes over-sleeping, and it affects one-third of individuals with bipolar disorder. Hypersomnia is common during periods of depression for anyone with bipolar disorder. However, it is more prevalent among younger individuals and those with bipolar I, while insomnia is more common among those with bipolar II.
People with bipolar disorder tend to experience one of two subtypes of hypersomnia: Sleep apnea describes a form of sleep-disordered breathing where the individual momentarily stops breathing during sleep, typically due to a blockage or narrowing of their airways, as often happens with obesity.
Because obesity is linked with insomnia as well as bipolar disorder particularly due to the weight gain during depression or varied appetite needs between episodes , sleep apnea frequently coexists with bipolar I disorder. The recommended form of treatment for severe cases of sleep apnea is CPAP therapy , whereby an individual wears a mask connected to a machine that regulates their breathing during sleep and keeps their airways open. Unfortunately, one study of individuals with comorbid sleep apnea and bipolar disorder found that while CPAP improved their apnea symptoms, as expected, it actually triggered symptoms of mania.
Sleep apnea affects as many as a third of individuals with comorbid bipolar disorder. Individuals with bipolar disorder are two to three times more likely to develop sleep apnea than individuals without any mood disorder, according to a large scale study of over 5, individuals. Individuals with extreme forms of bipolar disorder may disrupt their sleep-wake cycles to such an extent that they develop a circadian rhythm disorder like delayed sleep phase syndrome DSPS.
Delayed sleep phase syndrome describes people who have significantly shifted sleep-wake cycles. In turn, DSPS causes insomnia and daytime fatigue. Even when not in a manic or depressive stage, research shows that individuals with bipolar I disorder are more likely to have more irregular sleep-wake cycles , as well as wake up later and sleep longer.
Fatigue is a common experience for individuals with bipolar disorder. The extreme shifts in mood and energy are exhausting on the body. Fatigue also often results depression or insomnia. Even more unfortunately, the continuation of these sleep problems increases the severity and frequency of symptoms during both manic and depressive episodes, especially for women with bipolar disorder.
Good, regular sleep is essential to living a manageable life with bipolar disorder. Follow these tips to enjoy quality sleep, avoid triggering a manic episode, and better manage your bipolar symptoms. Organize your day and set aside time at night for you to get at least 7 hours of sleep. Go to sleep and wake up at the same time every day.
A quick nap will refresh you for an afternoon energy boost, without making it challenging to fall asleep at night. CBT-I, short for cognitive behavioral therapy for insomnia , is a form of psychotherapy that helps patients recognize the negative thoughts and behaviors they have around sleep and replace them with healthier ones. CBT-I the recommended treatment for insomnia, and multiple studies have shown it to be helpful for individuals with bipolar disorder, too.
A small study found that sleep restriction and stimulus control, as delivered as part of CBT-I, improved sleep for bipolar individuals. Another study found that a CBT-I program of stimulus control, sleep hygiene education and cognitive therapy proved effective for resolving or minimizing the sleep problems associated with bipolar disorder. During a depressive episode, the routine also gives your mind something to focus on instead of your worries and anxiety.
Because individuals with bipolar disorder are more sensitive to stimulation — from bright lights to heated even if fun conversations with family or roommates — aim to introduce a sense of calm at least 2 hours before bed, even before your bedtime routine.
Engage in relaxing activities, like reading a book or listening to music. Legal and illegal substances alike disrupt sleep. Caffeine and stimulants like cocaine wake up your mind, keeping you alert and preventing sleep. Avoid all of the above for a calmer mind and more restful sleep. Exercise energizes the body and makes you feel alert, so avoid doing it before bedtime. However, a regular exercise routine, when undertaken during the early part of the day, can energize the body during the day, counteracting the effects of fatigue, and tire you out by the time bedtime arrives.
Writing your racing thoughts down in a journal can help you sort them out during mania, and writing out your worries can help calm you during depression.
Consider keeping a sleep diary , as well. For example, melatonin is a natural supplement that helps many reset their circadian clock. Light therapy uses special lightboxes, available for purchase online, that artificially mimic the strength of sunlight. You sit in front of the box in the morning for 30 minutes or so or have it sit nearby on your desk to give you an alertness boost in the morning. Be thoughtful about getting natural sunlight, too.
The more natural sunlight your brain perceives during the day, the better attuned your sleep-wake cycles will become to the day-night cycle. Exercise outside in the morning, go for a walk on your lunch break, or position your desk near a window. For manic episodes, it can calm you down into a feeling of tiredness. During depression, it forces your brain to think about something other than your worries. Try practicing meditation, visualization, deep breathing exercises or progressive muscle relaxation techniques.
You might consider including one or more of these in your bedtime routine! A bedroom that is cool and dark is a bedroom that promotes sleep.
Set your bedroom thermostat to somewhere in the mid degrees Fahrenheit. Keep your bedroom as dark as possible at night, using blackout curtains or an eye mask if necessary. Table 1 shows the frequencies of sociodemographic, substance use, and psychopathological variables in the final sample stratified by sex.
Alcohol and cannabis use was significantly associated: Any and at least 2—3 times weekly cannabis use were very strongly related to other drug use ie, amphetamines, hallucinogens, or cocaine: We accordingly conducted a collinearity diagnosis. Variance inflation factors VIFs and tolerance values did not indicate an issue with multicollinearity in the logistic regressions.
The results of the logistic regressions weighted for the predictors of attrition are reported in table 2. In unadjusted analysis Model A , both any and at least 2—3 times weekly cannabis use were significantly associated with hypomania at 22—23 years, and demonstrated a dose-response relationship, ie, a stronger association for use at least 2—3 times weekly.
In Model B, associations were only slightly attenuated after adjustment for psychotic and depression symptoms. In Model C, associations were further attenuated by adjustment for other drug and alcohol use, but remained robust. In Model D, associations were reduced further by adjustment for gender, family adversity, and experience of childhood abuse, but again remained significant.
All analyses weighted for gender, birthweight, family adversity, and maternal shouting; Model A: Bold signifies the positive results clear in the table. Path analysis fit indices indicated excellent model fit: Consistent with the adjusted logistic regression analysis, cannabis use at 17 years was significantly and independently associated with subsequent hypomania in the final model controlling for all pathways. Direct associations are shown in figure 1.
The association between cannabis use and hypomania was not significantly mediated by depression or psychotic symptoms. However, cannabis use significantly mediated associations of gender and abuse with subsequent hypomania table 3. Pathways from cannabis use to hypomania. Main direct effects in the final path model. Significant pathways signified by solid arrows; nonsignificant modeled pathways represented by dotted lines; Model fit: To the best of our knowledge, this is the first study to test the prospective association between adolescent cannabis use and hypomania in early adulthood, while controlling for a range of environmental risk factors, other substance use, and associated psychopathologies.
Our analysis indicated 3 pathways whereby cannabis use is associated with subsequent hypomania. First, adolescent cannabis use is independently associated with hypomania in early adulthood.
This effect was independent of other key risk factors or markers for hypomania, including other drugs use, hazardous alcohol use, psychotic symptoms, and depression in late adolescence. This finding is consistent with population data in adults suggesting the association between cannabis use and manic symptomatology is independent of psychotic symptoms. The logistic regression analysis implied a dose—response relationship in that the odds ratios for frequent use was greater than for any use.
Though we are tentative in our conclusions because of the observational nature of the data, our control for numerous confounders, the prospective association, and the dose—response findings are consistent with a causal role for cannabis use in the emergence of hypomania in young people. Second, male sex is significantly indirectly associated with hypomania through an increased likelihood of cannabis use. Harmful use of cannabis is more frequent in men than women, 2 and this study shows its use in men may be much more important in the pathway to hypomania.
Finally, childhood physical or sexual abuse is indirectly associated with hypomania through an increased likelihood of cannabis use. Both childhood abusive experiences and cannabis use in adolescence and adulthood have been shown to be connected to the expression of bipolar disorder psychopathology and to markers of its severity. It appears that cannabis use seems to be one response of an individual to traumatic childhood experiences that can lead to harmful psychopathology in young adulthood.
Our results align with those of Aas et al 18 in highlighting the importance of both cannabis use and childhood trauma in bipolar disorder symptomatology. The precise neurochemical mechanism by which cannabis might lead to hypomania is unclear, reflecting the incomplete knowledge of the biology of bipolar disorders in general. Neurobiological studies indicate the brain is particularly vulnerable to the effects of cannabis use during adolescence. It has the potential to adjust reward system sensitivity 38 and can interfere with mechanisms related to establishing axonal connections during development.
A recent systematic review of the literature highlights that converging evidence from imaging as well as pharmacological studies indicates a state of hyperdopaminergia in mania.
This study had several strengths. The prospective assessments and sampling adolescents at age 17 years reduces the risk of reverse causality. The path analysis also controls for all associations between correlated items, enabling an examination of simultaneous pathways and determining the specificity of associations. There are also study limitations. Our conclusions regarding the link between cannabis use and hypomania must remain cautious.
The HCL asks about a lifetime history of hypomania symptoms, and so in some cases the experience assessed at age 22—23 years may have preceded cannabis use. There may also be pre-existing psychopathology that could link to cannabis use and hypomanic symptoms that we did not account for.
The HCL was used as a measure of hypomania but this will not always equate with a clinical diagnosis of hypomania. Nevertheless, we used a well-recognized cut-off score for hypomania, amplified by measures of duration and impact on functioning.
This is likely to have improved the capacity of the HCL to identify clinical levels of hypomania. Experiences of physical and sexual abuse were reported by the mother rather than child, potentially leading to an under-reporting of these factors. Nevertheless, we still found a significant indirect association between abuse and hypomania via cannabis use suggesting this finding is relatively robust.
It is conceivable that hypomania symptoms may have been secondary to continuing use of substances such as cannabis and stimulants between assessment at age 17 and 22—23 years, though we do not know the extent to which use continued over this period.
The HCL requires people to consider a period in their life when they were feeling high while not using drugs or alcohol. This caveat in the questions in the HCL reduces the risk that hypomanic symptoms were closely linked to periods when a young person was using cannabis, stimulants, or alcohol. Despite these limitations, we show adolescent cannabis use is an independent risk factor for future hypomania, and the nature of the associations found is suggestive of a causal link, though the gold standard for inferring causality of course remains intervention.
The study also identifies cannabis use as a candidate mechanism for explaining how childhood abuse may lead to hypomania in adulthood. This is important in the context of the push in many jurisdictions to legalize or decriminalize cannabis. Consistent with the stage specific model of mental disorders linking intervention to stage of illness, 46 our findings suggest frequent cannabis use is likely to be a suitable target for interventions that may allay the risk of young people developing bipolar disorder.
All other authors report no disclosures. We are extremely grateful to all the families who took part in this study, the midwives for their help in recruiting them, and the whole ALSPAC team, which included interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists, and nurses.
This publication is the work of the authors and Steven Marwaha and Catherine Winsper will serve as guarantors for the contents of this article. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Close mobile search navigation Article navigation.
Cannabis Use and Hypomania in Young People: A Prospective Analysis Steven Marwaha. View large Download slide. Prevalence of marijuana use disorders in the United States between — and — Cannabis use in adolescence and risk for adult psychosis: Developmental trajectories of psychotic-like experiences across adolescence: The association between cannabis use and depression: Comorbidity of mental disorders with alcohol and other drug abuse.
Prevalence of comorbid bipolar and substance use disorders in clinical settings, — Twelve-month outcome after a first hospitalization for affective psychosis. Risk for substance use disorders in youths with child- and adolescent-onset bipolar disorder. Cannabis use and cannabis use disorders and their relationship to mental disorders: Risk factors predicting onset and persistence of subthreshold expression of bipolar psychopathology among youth from the community.
Childhood sexual abuse, early cannabis use, and psychosis: Additive effects of childhood abuse and cannabis abuse on clinical expressions of bipolar disorders. Gestational influenza and risk of hypomania in young adulthood: School mobility during childhood predicts psychotic symptoms in late adolescence. The alcohol use disorders identification test. World Health Organization; Psychotic experiences and psychotic disorders at age 18 in relation to psychotic experiences at age 12 in a longitudinal population-based cohort study.
Measuring psychiatric disorder in the community: QSRR modeling for diverse drugs using different feature selection methods coupled with linear and nonlinear regressions. Childhood sexual abuse and adult psychiatric and substance use disorders in women: The dopamine hypothesis of bipolar affective disorder: Deltatetrahydrocannabinol effects in schizophrenia: Clinical correlates of age at onset distribution in bipolar disorder: Prediction of transition from common adolescent bipolar experiences to bipolar disorder: Prospective study of family adversity and maladaptive parenting in childhood and borderline personality disorder symptoms in a non-clinical population at 11 years.
Clinical staging in psychiatry:
Impact of Cannabis Use on Long-Term Remission in Bipolar I and Schizoaffective Disorder
Of note, he used high-cannabidiol (CBD) marijuana strains, and ostensibly Although evidence in bipolar disorder is less robust than in psychosis, there is Early evidence is promising, but more randomized, quality-controlled studies The information in this column is not intended as a definitive treatment ;5: Previous studies of bipolar disorder have found that cannabis use is more As this was an observational study, participants were not Diagnoses were confirmed by the Mini-International Neuropsychiatric Interview (MINI) version, . to achieve better therapeutic outcomes for bipolar spectrum disorders. There is no formal universal definition of treatment resistance; medication trials, incomplete or unsatisfactory response to treatment (usually Some of these factors can be successfully addressed, often resulting in a better prognosis. bipolar disorder as defined by DSM-5, should determine the choice of.