Mood Disorders PDF

Mood Disorders Learning Objectives 1. Distinuish between the two most common depressive disorders, major depressive disorder and persistent depressive disorder 2. Differentiate between the cognitive, interpersonal, and biological theories of depression 3. Apply diathesis-stress models to depressive...

Mood Disorders Learning Objectives 1. Distinuish between the two most common depressive disorders, major depressive disorder and persistent depressive disorder 2. Differentiate between the cognitive, interpersonal, and biological theories of depression 3. Apply diathesis-stress models to depressive disorders 4. Identifiy the biopsychosocial factors that distinguish unipolar from biopolar depressive disorders 5. Apply biopsychosocial model to bipolar disorder Extra Resources if needed: 2-Minute Neuroscience: HPA Axis In this video, I discuss the hypothalamic-pituitary-adrenal (HPA) axis, which plays an important role in our stress response. I describe the components of the HPA axis (hypothalamus, pituitary gland, adrenal https://neuroscientificallychallenged.com/posts/2-minute-neuroscien ce-hpa-axis 2-Minute Neuroscience: Selective Serotonin Reuptake Inhibitors (SSRIs) SSRIs are the most widely-used treatment for depression, and have been since their introduction to the market in the late 1980s. They were formulated based on the hypothesis that depression is caused by low levels of the neurotransmitter https://neuroscientificallychallenged.com/posts/2-minute-neuroscience-sele ctive-serotonin-reuptake-inhibitors-ssris Practice Questions How are anxiety disorders and depressive disorders related? Why are treatment/prevention efforts particularly important for depressive disorders? Why do we typically not see improvement in depressive symptoms following treatment with SSRIs until after levels of 5-HT have reached homeostasis? Mood Disorders 1 Mood disorders are characterized by major changes in emotion Major Depressive Disorder (MDD) Characterized by intense sadness to be diagnosed you need 1 of the following Sad depressed mood loss of interest/pleasure Is accompanied by the following symptoms: Sleep difficulties lethargy or agitation appetite problems/weight loss or gain extreme fatigue loss of sexual desire feelings of worthlessness and guilt difficulty concentrating recurrent thoughts of death or suicide Prevalence of MDD In Canada 11% lifetime prevalence and 4.5% 1 year prevalence 80% who experience 1 episode → go on to experience more average number of episodes is 4 the average duration of an episode is 3-5 months 12% of episodes last for > 2 years → Many people assume you are lazy when you are unable to function/do day-to-day tasks which is difficult. The gender ratio is 2:1 (women: men)→ emerges consistently in mid-adolescence and carries across the lifespan Kindling Hypothesis each depressive episode provides more kindling for the next episode Meaning the more episodes you’ve had, the more likely you are to fall into another episode when something goes bad. Chronic Depression Mood Disorders 2 Persistent Depressive Disorder (PDD) Has to go on for at least (>2 years) chronic low-grade depression The average duration is 4-5 years There are intermittently normal moods You don’t require as many symptoms but it can still be quite debilitating as it continues for so long. “Double Depression” Frequent periods of MDD superimposed on PDD Experience PDD between episodes of Major depression Biological Bases of MDD Etiology Genes Heritability estimates 35% 1st-degree relatives are at 3x higher risk of developing MDD in contrast to someone who does not have a 1st-degree relative with MDD Mood Disorders 3 Genetic transmission can be influenced by a depressogenic reaction to stress when people are stressed they are likely to act a certain way, and their response can make them more predisposed to developing MDD. One gene that plays a big role is the 5-HTT allele the serotonin transporter gene, in depression, means there is a dysfunction in the serotonin system. → this is highly linked to temperament (neuroticism). This gene is hyperresponsive to adverse stimuli and stress which can lead to a vulnerability for depression and anxiety (shows why people often experience both depression and anxiety together). Neurotransmitters’ Function in MDD Syptoms (For reference 5-HT (serotonin) DA (dopamine) NE (norepinephrine)) Sad, depressed mood, (obsessive grief) → (-) decrease in 5-HT Loss of interest/pleasure → (-) decrease in DA as DA is responsible for motivation Psychomotor retardation → (-) decrease in NE moving very slowly → described as a war inside body as what patient is experiencing people don’t see. Feelings of worthlessness and guilt (obsessive) → (-) decrease in 5-HT Recurrent thoughts of death or suicide → (-) decrease 5-HT Greater look at Neurotransmitters Decrease (-) 5-HT Levels (seretonin) indirect effects “Permissive theory” Regulates other neurotransmitters (e.g. NE and DA) It’s like the boss saying you have to do this and this and NE and DA follow instructions. But when the boss leaves (AKA, depression 3-5 month episode), the NE and DA go wild, and do whatever they want. → decreased 5-HT levels leads to → Decreased NE and DA = lead to Depression → decreased 5-HT levels leads to → Increased NE and DA = Lead to mania Direct Effects Trypotophan → 5-HT pre-curser (used to put seretonin together) Mood Disorders 4 When there is a depetion in this → relapse in depression episode 5-HT Mysteries 1. If you give someone someone SSRI’s where you are blocking the reuptake of seretonin → so there is more seretonin activity in the synapse → which should increase seretonin functioning within a very short period of time (days at most). However medication doesn’t work for 3-12 weeks, once it returns to homeostasis before symptoms improve. At 3-12 weeks we expect those receptors to have downregulated and our bodies to reach homeostasis again, and yet the symptoms don’t improve until then. Explanation for this: your body/neurons wants to stay in a state of homeostasis, if we throw in chemicals to increase neurotransmitter functioning (e.g. of seretonin), our neurons will decrease the amount of receptors they have (”i don’t need all that seretonin thankyou, i’ll catch seretonin with one hand and not two”) → some receptors close down so amount of seretonin functioning can return to how it was BEFORE medication. → we see symptoms improve when you return to your prior levels (before medication) which is still a mystry as to why. 2. Metabolite levels (when a neurotransmitter breaks down it becomes little metabolite pieces) not consistently found. we don’t see these metabolite levels to be reduced. More often this is the case with suicidal ideation and behaviour Remember: Again any seretonin dysfunction is going to be much for likely related to suicidal ideation and behaviour then other symptoms. Neuroendocrine System and MDD HPA Axis increases cortisol (fight or flight hormone) Hypothalamus sends CRH/CRF → to Pituitary sends ACTH → Adrenal Cortex which releases cortisol → cortisol goes into bloodstream and the receptors on the P and H, which determines how much cortisol is needed. This is a Negative feedback loop HPA axis loop in a typical (person not expereincing MDD): stress → goes to release of CRH (CRF) from hypothalamus → Release of corticotropin (ACTH) into circulation → Release of cortisol from Adrenal cortex into blood → cortisol inhibts release of ACTH from pituitrary (”stop no more cortisol”) and also → cortisol inhibits release of CRH from Hypothalamus → Increase in energy release (increase Mood Disorders 5 blood glucose) which supresses inflammatory and immune response = Coping with stress HPA axis loop in indivudal with Depression: Cortisol Suppression: Faulty Feedback The message that usually inhibits ACTH (saying we don’t need more cortisol) is weak and misinterpreted → the pituitrary releases more then hypothalamus releases more CRH (CRF) = the body is flooded with cortisol. On the outside the person with depression looks like their tired and don’t want to move, but on this inside you are running away from 5000 bears at once. note: look at arrow size difference from a normal subject compared to patient with MDD Mood Disorders 6 Stress and Relapse Stressful event which onsets MD (major depressive) episode once you have had 4-5 episodes in your life → the depression begins to develop it’s Own Cycle. It no longer requires a stressful life event (SLE) to cause a depressive episode. this means once you’ve had a certain number of depressive episodes (Reference to Kindling Hypothesis) → you have kindled the fire enough where it has it’s own rythem/cycle in which it will just start to develop MD epsidoes without a major life event, and do it on it’s own. This is really important → she doesn’t say why but ask in chat if it’s because it shows how important early intervention is? Excessive cortsiol depletes DA (DA allows you to work towards something/motivation) → leading to anhedonia. Brain Activity in Depression Note → these are observations in patients with depression as a whole, not every individual has everyone of these decreased activity in the Left PFC → less activation to approach things, reglating emotions and turning off amygdala note: Left PFC is in charge of Approach, emotion regulation, turns off amygdala alarm Increased activity in PFC which increases avoidance, inhibition, negative thoughts “negative nelly.” with these two differences, patients with depression have less apporach and more avoid happnening. (personal note: i imagine this can make it hard to reach out for help and effects behaviour) Hyperactive amygdala → leading to great increase in fear to the slightest amount of percieved threat. (again this is consisten with the expression of feeling a “war inside onself”) and because there is decreased activity in the Left PFC, the amydala isn’t able to be be quieted down → brain thinks “nothing is okay/fine” Decreased Anterior Cingulate Cortex (ACC) activity → leading to not being able to place attention to what is beneficial to you, lack of selective attention Mood Disorders 7 ACC is related to Error-related rewards and losses (selective attention), behaviourally it is related to where we place our attention. (”i will pay attention to this and not all the other negative thoughts”) Decreased Hippocampal volume (also seen in PTSD and anxiety) → leading less functioning in learning, memory, and approprioatly regulating ACTH. Hippocampus plays a role in learning, memory, and regulating ACTH (how much cortisol floods the body) Other Biological Factors that may play a role in the Development of Depression: Disruptions in the following: Sleep → if you are not getting enough sleep you are more vaulnerable to develop an epsiode Circadian rhythm → if you’re sleep rythem is off you are more vaulnerable to devleope an episode. Exposure to sunlight → the more exposure is protective against developing and episode and less exposure makes you vaulnerable. inflammatory response system → similar to when you are sick and have an inflammatory repsonse to response to foriegn virus/bacteria, an inflammatory response is also seen in depression. (shows that their is such a big physiological response to depression, responding to depression like it’s a virus). Psychological Facotors of Major Depressive Disorder (MDD) Psychological Etiology: 1. (chronic) stressful life events (stress) These can be either Independent or Dependent Independent → “I had no effect on this event happening” Dependent → “something I did was related to why this stressful life event happened” These then create a vaulnerability in response to stress (ask is it dependent that creates this or both independent and dependent). 2. Risk-Related Vulnerability factors (diathesis) Personality and cognitive diathesis Early adversity Mood Disorders 8 Becks Cognitive Theory Main idea: Negative interpretations of situations/events → lead to feelings of depression (they act like a loop/reciprocal) Evidence to this: People with depression lack a positivity bias Most people without depression have this positivity bias to some bit. → means they think good things about themselves People who are not optimistic will say “i’m not a pestimist im a realist” → this is actually true. People who are thought of as pestimistic just have realistic observations of things. However → what seems to be protective against depression, is having a slight positivity bias, meaning seeing yourself and other things as slightly better then they are. people with depression have a greater accessibility of negative content meaning there is more negative content/thoughts available to the brain, so when you ask that person a question they are more likely to respond with something negative then positive. Beck’s Cognitive Model: Depression → early experience → which leads to formation of dysfunctional beliefs → critical incident (something happens) → dysfunctional beliefs are activated → this leads to negative automatic thoughts → leads to symptoms of depression → these symptoms lead to more negative automatic thoughts → then symptoms depression etc. (loops between negative autonmatic thoughts and symptoms of depression). somatic → physical, cognitive → thoughts, affective → moods or emotion, motivational → “am i motivated to do anything”, Behavioural → the things I do Diathesis:→ Formation of dysfunctional beliefs because if you have the early experience but not the formaiton of dysfunctional beliefs then the beliefs won’t be later activated and depression symtoms won’t occur/be triggered. Stressor:→ Critical Incident(s) you can have the formation of dysfunctional beliefs but if you don’t have the critical incidence then the beliefs are unlikely to be activated. Mood Disorders 9 Negative Cogntive Triad This is a pattern of negative autonomatic thoughts These pessimistic predictions center on 3 things 1. Self “I’m unlovable” 2. The World “No one loves me” 3. Future “no one will ever love me” Helplessness Theory Learned helplessness comes from a lack of percieved control over life events A Depressive Attribitional Style seems to come from Learned Helplessness Individual makes: internal attributions meaning negative outcomes are one’s own fault “it’s my fault” Stable Attribitions future negative outcomes will be one’s fault Global attribution negative events disrupt many life activities/across many domains This increases sense of hopelessness Helplessness theory orignoinally comes from an animal model Mood Disorders 10 shocking animals who can’t do anything about it/couldn’t escape → so next time they were shocked they didn’t even try to escape → lead to depression Uncontrollable event → sense of helplessness → emerging depression Helplessness theory reformulated learned helplessness (in human cognitive abilities) uncontrolable event → leads to attributions (certain negative ways of thinking) → this leads to sense of helplessness → emerging depression From this hopelessness theory was developed Hopelessness Theory uncontrollable event → attribution OR other cogntive factors (pessimistic thinking style or biases) → that lead to having a sense of hopelessness; no response or hope (being hopeless in present tense but also for the future) → emerging depresssion Hopelessness theory explains the increased comorbiditiy between anxiety and depression: Helplessness → leads to anxiety Persistent helplessness + no hope → leads to depression Helpnessness vs. Hopelessness Helplessness theory is comprised of a pessimistic attributional style = Diathesis having pessimistic view on things is a vaulnerability to developing depression Hopelessness theory takse pessimistic attributional style + one more negative life events → this will not lead to depression unless: → the person first experiences a state of hopelessness again hopelessness theory is very similar to helplessness theory but hopelessness says: helplessness explains the diathesis but not the stressor, and it’s not describing the required lack of hope in addition to the pessimistic attributional style. Attributions: Failed Math Test Remember → the most depressogenic attribution style is Internal, Global, and Stable. Internal = about me (individual themself) Stable = not going away (won’t change) Global = it effects be across all/many domains (not just this one event/incidence) Mood Disorders 11 Unstable = not going to last forever (just right now) (e.g something due to the state of mind your in, not because of your own trains/or lack thereof) external = about the event/incidence (not yourself) specific = directly about the one event (attribution is not across all domains) how could these different thought processes lead you to or make you more vaulnerable to a depression if a stressor were to occur? possibly if you failed another math test and already had these pessimistic attributional styles, and experience a sense of hopelessness afterwards leading to depression. And/Or: after another failed test you would have more internal, stable, global pessimistic attributions leading to depression? (I am stupid, i have no hope etc)? The Positive bias here would likely be “my math test was numbered 13” external, unstable, specific. Psychoanalytic Theory Freud: Depression is anger turned inward though there is not much data to support psychoanalytic theory, it IS worth considering the biology we mentioned. → intense fight or flight/stress (”war inside”) reaction which gives some accuracy to it, not emperically though. Mood Disorders 12 Psychosocial Etiology of MDD Interpersonal Theories: People who are depressed may act in ways: that genuinely have a negatively effect on others leading to alientating themselves from social support networks social support networks can be protective and helpful in working through depression, so by removing the social support can have negative impacts. Evidence for interpersonal deficits/theory: Poor social networks depressed people seem to have much more sparse social networks and tend to regard them as not providing all that much support/not being helpful. (as if all their eggs in few baskets) few postive social behaviours So when people are depressed they are showing alot fewer of positive social behaviours and more negative behaviours. Elicit negative reations from others they also illict negative reations from others → research shows college students with depressed roomates don’t enjoy interacting with them and feel more aggressive towards them. High marital discord more mutual hostility and criticism between spouses critical comments from spouses can sometimes cause MD episodes to reoccur Overall, Couples with 1 spouse with depression tend to be less satisfied/happy. Insecurity in relationships e.g. frequent reassurance seeking → has negative impact on social network people with depression show a greater amoung of insecurity in relationship especiallly during MD episode, and overall more so then those without the disorder. Gender Ratio of MD Why 2:1? (women:men) Biological Reasons Mood Disorders 13 Cortisol → women have more cortisol then men, leading to susceptibility in developing MD Psychological Reasons Note: rumination is different and higher in women BUT also the notes on rumination relate to all gender unless specified Rumination → focus on distress and possible casues/consequences concept comes from cows chewing (chewing grass over and over) → in psychology you are doing this in your head. It is unproductive, repetive, and passive e.g. thinking “i can’t believe she did that and im so upset she did that etc.” or “this could go wrong and that etc.” → very unproducitve, there was no problem solving, and passive rather than active (i will make time to talk with her to do this). People who ruminate are 4x more likely to develop depression in contrast to those who don’t. Rumination Predicts (in addition to depression): low confidence in own solutions Failure to act on solutions the lack of confidences prefents you from actually acting on the solution (”what if’s spiral”) → so you don’t get anywhere in solving the problem. It drives others away depressed ruminators are more likely to stay depressed (alongside more likely to become depressed). going over thoughts repeatitively, not in a helpful way but in a way that perpetuates negative cognitive bias and negative mood. There is a focus on emotion women focus on sadness (more likely to lead to depression) → they are focus on a passive emotion that makes them want to withdraw from the world and curl up men focus on anger → whereas men are more likely to be active with anger (not great still) Anixety link? possible reason why people who experience depression also experience anxiety Mood Disorders 14 anxiety → greater rumination → blends itself nicely to negative/depressed thinking Social Reason Interpersonal (cost of caring) → a lot more relationships where there is greater caring to how the other is feeling, with the greater increase of friendships of people going through something difficult and having greater care for them can predispose women to developing MD. more relationships + more emotionally based those relationships are = the more vaulnerable they are to the negative effects of whatever is going on with their friends. Type of traumatic events → women are more likely to be traumatized by someone close to them They experience more betrayl within their trauma → so women more often experience trauma at the hands of someone they trust or someone they expect to not hurt them (more so then men) Chronic negative events things that are more common in women then men include: Poverty Sexual harrassment Lack of affirmation/power in intimate relationships (they have alot less say) Other Psychological Factors Neuroticism sensitivity to aversive events meaning → if you are highly sensetive to something going wrong and easily upset by it, you are more prone to developing depression Integrative Model Biological → genes, cortisol etc. psychological → ruminating, pessimistic cognitive style Stressful life event happens → activates: 1. stress hormones with wide ranging effects on neurotransmitters 2. negative attributions, snese of hoplessness, dysfunctional attitudes, negative schema Mood Disorders 15 3. problems in interpersonal relationships and lack of social support all then leading to developing Mood Disorder Treatment of MDD Biological Treatment Pharmacotherapy SSRI’s SNRI’s Take 3-12 weeks to work (depending on the person) pharmalogical treatment is described as “clarity pills” NOT “happy pills” “as if i have been wearing dirty glasses and took them off” Light therapy helpful for season depression/seasonal affective disorder (SAD) Treatment Resistance: Biological Options when none of the treatments seem to work, these are some other options (can be extreme, but if nothing is working, it’s could be worth a try). 1. ECT How: Electric current induces a seizure Mood Disorders 16 Potential Benefits: Works quickly when it works Risks: confusion, memory, seziures aren’t generally good for the brain, but can be helpful in resitence to depression 2. TMS How: magnetic stimulation in select parts of brain Potential benefits: non-invasive, also seems to work a bit Risks: still relatively new in use Psychosocial Treament 1. Psychodynamic (freud) theory thinks of: imporance of early loss Attechment to mother/parent lack of sufficient nurturance/love → leads to low self-esteem Anger at self = is reinterpreted as anger at mother 2. Interpersonal Therapy it is eclectic but evidence based It does work particularly for depression “you make some gains working on relationships/your style of relating with other people 3. Family and Marital Therapy really helpful when having a negative interactions with family members/spouse → to address those negative interactions so that both parties needs are being met and it’s not perpetuating the disorder (e.g. criticism from spouse increasing liklihood of another MD episode) 4. CBT when looking at depression we are looking at a couple different skills including: Primary control → identifying where you have primary control (e.g. skills like problem solving) Secondary control → when you can’t do anything about the situation but you can change/work on how you think about the situation. addressing maladaptive cognitions (catastrophic or black and white thinking) Mood Disorders 17 Focusing Attention → on different areas (takes alot of work to learn this with depression, but is important). note: remember Anterior Cingulate Cortex → involved in focusing attention where you want to. → this area is less active in depression, making it much more difficult to rest your brain from negative cognitions and focus on something else. Behavioural Activation this is where you have to do stuff that you don’t want to do. e.g. with depression it is very difficult to get up out of bed, and brush teeth go to work etc. Despite not feeling like doing these things, this aspect of CBT works with you to help make sure those things happen. by doing those things you are going to decrease your stressful life events that you end up causing due to your disorder, as it works to make sure the disorder isn’t taking over your life. it also helps you have more relationships, social interactions, postive social interactions, better experiences → so that you are less likely to isolate and feel hopeless due to lack of “goodness in your life” note: primary and secondary control are the cognitve aspects and Behavioural control is the behaviour aspects. If there was 1 Key active ingredient in treating Depression, it would be Behavoural Activation. That is what you want, other stuff is really good too, but you have to have the behavioural activation if you want to address the depression. Bipolar Disorder Marked by periods of mania and depression Manic Episodes are charcaterized by: A marked increase in activity level (e.g. work, social, sexual etc.) Unusal talkativeness, rapid speech Flight of ideas or racing thoughts Less than the usual amount of sleep needed Inflated self-esteem and believe have special talents, powers, and abilities Distractability, attention is easily diverted Mood Disorders 18 Excessive involvement in pleasurable activities that are likely to have undesirable consequences (e.g. reckless spending, infedelity etc.) Bipolar I Disorder (BP) Comprised of Manic (or mixed) episodes + Major depressive episodes There is a very high suicide risk (highest suicide risk among all disorders) Associated problems with the disorder include: divorce domestic violence truancy occupational failure substance abuse episodic antisocial-behaviour Prevelence of BP I Lifetime prevalence of 0.4-2.2% of people meaning about 3 people in this class there is no gender difference in BP I, however men tend to have more manic episodes and women tend to have more depressive episodes. Tends to be a 3:1 Depressed:Manic days (much more often to be depressed days then manic) Course: Average age of onset is 18-22 years old many things tend to “set it off” so it’s important to take care of mental health Recurrent: more than > 50% of cases have 4 or more episodes it’s not very likely for someone to have just 1 episode, but to have them again and again. Etiology of Bipolar Disorder I Biological: Genes Mood Disorders 19 1st degree relatives have a much higher risk of devleoping a bipolar disorder But people wth bipolar disorder are more likely to have relatives that have a unipolar depressive disorder (persistant or major depressive disorder) rather than bipolar disorder. Twin studies strong amoung of genetic heritability MZ twins 85% concordance rate → if one twin has it 85% chance the other does too. DZ twins 14% shows substantial role of genes play in this disorder Neurotransmitters NE, DA, 5-HT (all involved in mood states) Decrease NE & DA → depression Increase NE & DA → Mania again, NT’s return to homeostasis after several days of medication treatment (just as they do for major depressive disorder SSRI treatment) We don’t always find the expected metabolite levels (increase and decrese), these aren’t consistently found. Other Biological Factors Involved: Cortisol levels Disturbances in biological rhythms (e.g. circadian rhythm- even in remission/not experiencing either episodes) Shifting patterns of blood flow to L & R PFC right → avoid Left → approach There is this shifting between activation in either side, so one side is more active at one point then the other (vice versa) Psychosocial Etiology There is a pessimistic attributional style seems to predispose people to bipolar disorder Personality Mood Disorders 20 Neuroticism High levels of achievement striving Stressful life events (esp. Dependent) meaning → stressful events one is responsible for causing Low social support Biological Treatment for Bipolar Disorder Pharamatherapy Mood Stabilizers (e.g. Lithium (often the go-to), anticonvulsants) Antipsychotics → in a number of unipolar and bipolar disorders, psychotic features are sometimes observed. If that’s the case antipsychotics are also used Other Biological treatments used depending on how severe the disorder is and nonremitent (no recovery) it is: TMS ECT Lithium Relapse rate for Bipolar disorder is about 34% vs. 81% with placebo after 1 year course not a great relapse rate, but still a whole lot better again this is another great example of why it’s important when treating disorders to incorporate medication with other treatment methods, not sticking to just one Not effective over long haul/period of time (only continues to help 36% of people over 5 years) again why it’s important to utilize multiple forms of treatment methods alongside medication and not rely only only on medication. Prognosis (how well it will work for someone) Good: it works better when you have a family hx (history) of bipolar illness Poor: it is worse if you experience rapid cycling, multiple prior episodes, and if you have substance abuse. note: everything is always worse if you have substance use, that goes for any disorder/treatment. Mood Disorders 21 rapid cycling → presence of at least 4 mood episodes in the previous 12 months that meed the criteria for manic, hypomanic, or major depressive disorder. Psychological Treatment for Bipolar Disorder CBT How it works: Cognitive restructuring → rethinking how you percieve things, what you attribute events too. Behavioural activation → for depressive periods Mindfulness based cognitive therapy (MBCT) Aceptance of thoughts, emotions etc. is used for other disorders but is frequently used for bipolar disorder and tends to be quite helpful How it works: In this therapy there is less focus on changing things and instead focuses on acceptance of thoughts, emotions, physical sensations. And trying to maintain very present rather than thinking “everything that happened, is going to happen, or is happening is horrible.” this thinking increases misery. And if you have this cycling → you have periods where you have limited control over your behaviour, it can be frustrating. so just accepting where you are at in that moment is very helpful (mindfulness/staying present and acceptance) Interpersonal and Social Rhythm Therapy Interpersonal interactions can influence daily rhythms seems to make a difference for people in terms of setting themselves up for predictable rhythms, social rhythms that are most beneficial to that person Why it helps: people with bipolar disorder tend to be much more sensitive to predictable social rhythms (e.g. when your going to do this, or see someone, or behave a certain way in that place). so if you have a therapy that can help you with your interpersonal interactions in a way you can expect and predict it can help decrease the fluctuations of mood. Family and Marital Therapy Reduced criticism, hostility (expressed emotion: EE) Mood Disorders 22 as seen in other disorders, but especially in bipolar disorder, there is an expressed emotion (criticism and hostility) → you want to address the EE so stress is not being added and therefor not possibly sparking a relapse in episodes. How it works: Both parties needs to be met, and that they communicate in a way that is effective for them, and you want the person with the disorder to be communicating in a way where they don’t take on all the blame for everything that is wrong, but doesn’t also excuse them from the things they do cause. Mood Disorders 23