bipolar disorder

Free Gift with Depression – A Tale of Anxiety

→ March 29, 2010 - 4 Comments

Anxious and DepressedAnxiolytic Isn’t Even in the Dictionary

I grit my jaw. I bite the skin around my nails. I pull at my hair. I bunch my fists. My breaths are shallow. I twitch and clench erratically.

I tell myself not to grit, bite, pull, bunch, twitch and clench. I tell myself to intake more air. Those instructions are followed. For moments. And then they’re not. While I wasn’t looking I started gritting, biting, pulling, bunching, twitching, and clenching all over again.

Anxious. Anxiety.

These are tiny, little words. The barely seem to warrant entries in dictionaries bloated with words like crunk (a type of hip-hop or rap music) and yogilates (a combination of Pilates and yoga), and yet somehow they have achieved great significance in my life.

Anxiety and Depression, Like Peas and Carrots

Anxiety and depression always come in pairs. The each cover half a sphere. How much you feel of each of them depends on your point of view of the sphere.

I was never an anxious person before. Or at least, I was never inordinately anxious, I think. But then came the psych meds and so the anxiety. Anxiety – the side effect that’s it’s own mental illness.

And now I worry. And I’m overwhelmed. Frozen with the fear of things not getting done . . . leading to the very obvious result of things not getting done.

Anxiety. A self-replicating organism.

Anticonvulsants as Calcium Antagonists in Mood Stabilization

→ March 20, 2010 - 2 Comments

This is a paper I wrote for a psychology course I am taking so the level of discourse is quite high, sorry about that. I promise though, it is comprehensible. What I’m basically talking about is calcium-channel blockers and other calcium antagonists (they turn calcium down). This refers to calcium in your brain and not calcium in your blood.

Mood Stabilizers and Bipolar Disorder

Because inadequate response, poor compliance, chronic recurring symptoms, and functional disability are constant challenges is the treatment of bipolar disorder, (Gitlin, 2006) efforts have been made to search out new mood stabilizing medication and determine new methods of action. There has been an effort to treat bipolar disorder with a class of medication termed “mood stabilizers”, most notably consisting of some anticonvulsants (also known as antiepileptics) in addition to the traditional lithium.[1] [push]I will show that these anticonvulsants, stabilize mood in bipolar disorder, at least partially, through their ability to act as calcium antagonists.[/push]

While anticonvulsants are widely used in the treatment of mood disorders, their method of action in mood stabilization is mostly unknown.[2] Recent research has indicated that disrupted calcium homeostasis is present in bipolar disorder, and that anticonvulsants and lithium effect calcium channels and concentration in the brain (Amann, 2005). The mood-stabilizing effects of calcium channel blockers like Nimodipine (Levy, 2000) further add to the evidence that calcium antagonism is useful in the treatment of bipolar disorder. I will show that these “mood stabilizers”, anticonvulsants, stabilize mood in bipolar disorder, at least partially, through their ability to act as calcium antagonists.

Bipolar Disorder and Calcium Levels

A review of hypercalcemia and hypocalcemia shows links from calcium blood levels to depression, irritability, delirium, and psychosis – symptoms that are similar to a bipolar disorder. Additional to calcium’s powerful abilities in the blood, it also plays a vital role both as primary and secondary messengers in the brain and according to Gargus (2009), is known to regulate “physiological systems at every level from membrane potential and ion transporters to kinases and transcription factors”. Calcium also plays a role in long-term changes to the architecture of a neuron (Amann, 2005). Disruption of intracellular calcium homeostasis is now thought to underlie many diseases such as Autism, Migraine, Seizures, and psychological disorders like bipolar (Gargus, 2009). Additionally, atrophy and glial death now found in mood disorders may be avoided by increasing cellular plasticity, accomplished through reducing intracellular calcium concentrations (Landmark, 2008).[pull]Atrophy and glial death now found in mood disorders may be avoided by increasing cellular plasticity, accomplished through reducing intracellular calcium concentrations.[/pull]

In some studies, the bipolar population has been found to have abnormally elevated intracellular calcium, elevated basal platelet and lymphocyte calcium concentrations, and elevated B-lymphoblast calcium (Silverstone, 2005). Found more consistently the bipolar population, both in the manic and depressed phase, is an enhanced calcium response to agonist stimulation (Silverstone, 2005). This may partially be explained by the enhanced platelet intracellular calcium mobilization found after stimulation by serotonin in bipolar disorder (Suzuki, 2003). This research suggests that not only are calcium levels elevated, and calcium activities dysregulated, but this may become worse if the patient is treated with a selective serotonin reuptake inhibitor (SSRI), which is often the case.

Lithium and Calcium

Lithium has long been the standard therapy for bipolar disorder both for acute and maintenance treatment due to its quality and quantity of supporting evidence (Gitlin, 2006), (Levy, 2000). Part of lithium’s biological effects is to both inhibit the entry of calcium intracellularly acting as a calcium antagonist, and to block calcium channels directly. This, in turn, inhibits other cellular responses of subtypes adrenergic, serotonergic, and cholinergic (Levy, 2000). Moreover, adding Verapamil, a calcium channel blocker, to unresponsive lithium treatment, improves outcomes, (Mallinger, 2008) suggesting that both calcium itself and calcium channels benefit from antagonists.[3]

Calcium Channel Blockers as Mood Stabilizers

A number of calcium channel antagonists have been studied with varied results likely resulting from their specific affinities to different calcium channel subtypes and their individual ability to cross the blood-brain barrier. Verapamil, one of the most studied calcium channel blockers, is not the most lipophilic and is likely not as effective as other calcium channel blockers like nimodipine (Gitlin, 2006), although Verapamil has been shown effective in some studies and does work on calcium ions in a way similar to lithium (Levy, 2000).[pull]Nimodipine is not only a calcium channel blocker but has also been shown to have anticonvulsant properties and has shown great potential as a mood-stabilizer particularly for cycling forms of bipolar disorder.[/pull]

Nimodipine is not only a calcium channel blocker but has also been shown to have anticonvulsant properties and has shown great potential as a mood-stabilizer particularly for cycling forms of bipolar disorder (Goodnick, 2000). While its efficacy needs further study, there have been positive results shown for bipolars in manic, depressed, and rapid cycling states.

Anticonvulsants spawn a broad range of medication and methods of action. Useful actions for treatment of psychiatric disorders are thought to be: increases in GABAurgic transmissions, decreases in glutamate, inhibition of voltage-gates sodium and calcium channels, and interference with intracellular modulators (Landmark, 2008). For the treatment of bipolar disorder, specifically mood stabilization, carbamazepine and Lamotrigine, have been identified, and accepted as treatments through their inhibition of voltage-gated sodium and calcium channels (Landmark, 2008).[push]Anticonvulsants that work on calcium channel blockers are also known to be helpful in the treatment of neuropathic pain, which some researchers believe is closely tied to psychological pain, here in the form of bipolar disorder.[/push]

Carbamezapine and Lamotrigine have also been seen to positively affect mood while GABAurgic transmitting anticonvulsants have not. The general decreased excitability found with Carbamezapine and Lamotrigine may also be responsible for their role in preventing affective episodes (Landmark, 2008). Valproate is also considered an accepted treatment although likely functions more from the combined actions mentioned above, making it an anti-mania treatment as well as possibly useful for mood stabilization (Landmark, 2008). The effects of anticonvulsants are compared to the therapeutic effects of lithium on calcium, calcium channel blockers, and inositol concentrations, another secondary messenger indirectly acting on calcium signals (Berridge, 1993). Anticonvulsants that work on calcium channel blockers are also known to be helpful in the treatment of neuropathic pain (Landmark, 2008), which some researchers believe is closely tied to psychological pain, here in the form of bipolar disorder.

Lithium acts in the body as a complex agent, making it difficult for scientists to specify exactly how it stabilizes mood in the bipolar population, in spite of its being used for decades. It is clear; however, that part of its biological action is to antagonize calcium concentrations as well as calcium channels. This action is shown to have positive mood stabilizing effects as proven by successful treatments with calcium blocking agents like Verapamil and Nimodipine. These same mood stabilizing effects are seen with some anticonvulsants which also act as calcium antagonists. Therefore, it is reasonable to assume that part of the reason why some anticonvulsants stabilize mood is because of their ability to work on calcium, calcium channel blockers, and inositol, as seen in Lithium and calcium channel blockers.

_________________________

[1] There are several antipsychotics also in this list but are outside the scope of this paper.
[2] Treatment of bipolar disorder and mood stabilization in this paper will refer to non-acute treatment, although some of the drugs mentioned can be used in acute treatment also. No distinction will be made between types of bipolar.
[3] It should be noted that Mallinger (2009) posited that the positive effects of combining Lithium and Verapamil may also be due to the inhibition of protein kinase C (PKC) activity provided by the Verapamil.

References

(I apologize for the departure from APA style, blog formatting issues.)

Amann, B., & Grunze, H. (2005). Neurochemical Underpinnings in Bipolar Disorder and Epilepsy. Epilepsia (Series 4), 4626-30.
doi:10.1111/j.1528-1167.2005.463006.x.
Retrieved from EbscoHost Mar. 14, 2010 AN = 17118993

Berridge, M. J. (1993). Inositol Trisphosphate and Calcium Signaling. Nature 361, 315-325.
doi:10.1038/361315a0
Available online: http://www.ncbi.nlm.nih.gov/pubmed/8381210

Farooq, M., Moore, P., Bhatt, A., Aburashed, R., & Kassab, M. (2008). Therapeutic Role of Zonisamide in Neuropsychiatric Disorders. Mini Reviews in Medicinal Chemistry, 8(10), 968-975.
Retrieved from Academic Search Complete database.
Retrieved from EbscoHost Mar. 15, 2010 AN = 34436130

Gargus, J. (2009). Genetic Calcium Signaling Abnormalities in the Central Nervous System: Seizures, Migraine, and Autism. Annals of the New York Academy of Sciences, 1151133-156.
doi:10.1111/j.1749-6632.2008.03572.x.
Retrieved from EbscoHost Mar. 14, 2010 AN = 35830926

Gitlin, M. (2006). Treatment-resistant bipolar disorder. Molecular Psychiatry, 11(3), 227-240.
doi:10.1038/sj.mp.4001793.
Retrieved from EbscoHost Mar. 14, 2010 AN = 19892243

Goodnick, P. (2000). The use of nimodipine in the treatment of mood disorders. Bipolar Disorders, 2(3), 165.
Retrieved from Academic Search Complete database.
Retrieved from EbscoHost Mar. 15, 2010 AN = 6500123

Landmark, C. (2008). Antiepileptic Drugs in Non-Epilepsy Disorders. CNS Drugs, 22(1), 27-47.
Retrieved from Academic Search Complete database.
Retrieved from EbscoHost Mar. 15, 2010 AN = 28088990

Levy, N., & Janicak, P. (2000). Calcium channel antagonists for the treatment of bipolar disorder. Bipolar Disorders, 2(2), 108-119.
Retrieved from Academic Search Complete database.
Retrieved from EbscoHost Mar. 14, 2010 AN = 5788405

Mallinger, A., Thase, M., Haskett, R., Buttenfield, J., Luckenbaugh, D., Frank, E., et al. (2008). Verapamil augmentation of lithium treatment improves outcome in mania unresponsive to lithium alone: preliminary findings and a discussion of therapeutic mechanisms. Bipolar Disorders, 10(8), 856-866.
doi:10.1111/j.1399-5618.2008.00636.x.
Retrieved from EbscoHost Mar. 14, 2010 AN = 35323933

Silverstone, P., McGrath, B., Wessels, P., Bell, E., & Ulrich, M. (2005). Current Pathophysiological Findings in Bipolar Disorder and in its Subtypes. Current Psychiatry Reviews, 1(1), 75-101.
doi:10.2174/1573400052953574.
Retrieved from EbscoHost Mar. 14, 2010 AN = 18882320

Suzuki, K., Kusumi, I., Akimoto, T., Sasaki, Y., & Koyama, T. (2003). Altered 5-HT-Induced Calcium Response in the Presence of Staurosporine in Blood Platelets from Bipolar Disorder Patients. Neuropsychopharmacology, 28(6), 1210-1214.
doi:10.1038/sj.npp.1300159.
Retrieved from EbscoHost Mar. 15, 2010 AN = 22436847

Caffeine and Mental Illness and Caffeine Disorders

→ February 21, 2010 - 13 Comments

Caffeine and Mental Illness and Caffeine Disorders

Caffeine is the world’s most popular psychoactive substance. So many of us love it a la Starbucks, Tim Hortons or just out or our home coffee machine. Me, I love coffee and I’m a fan of caffeine too. Coffee’s the nectar of the gods and nothing will convince me otherwise.

It seems though, caffeine can actually hurt you. I know, I never thought my beloved coffee could harm me, but I suppose anything that you abuse, will abuse you back. So, here is everything you ever needed to know about caffeine, caffeine disorders and caffeine and mental illness but were afraid to ask.

Read more

Causes of Mood Disorders – Serotonin, Dopamine, Norepinephrine

→ July 26, 2009 - 4 Comments

Today, I was watching a Comcast On Demand program about the causes of bipolar. I thought I’d watch and see how ridiculous it was because obviously, no one knows the cause of bipolar disorder.

However, the spot had some interesting information on the brain, neurotransmitters and bipolar disorder, which I then transcribed so I could share it with you. (Yes, I really did transcribe the whole thing.)

It’s in fairly layperson terms, so give it a look. At the bottom is a bit more information about dopamine, norepinephrine, and serotonin. This, unfortunately, is not in layperson terms, but is interesting nonetheless.

Brain Chemistry and Bipolar Disorder

And for the info:

…but research has shown that chemical imbalances in the brain play an especially key role in the onset of the disease. Every adult has more than 90 billion brain cells, or neurons. These neurons communicate with each other through chemical messengers called neurotransmitters. Neurotransmitters help control a range of bodily functions such as thinking, reasoning, and mood. But when they don’t function properly then problems can occur.

Here’s how neurotransmitters work, each neurons is composed of an axon, a dendrite, and cell body. When a neuron fires, an electrical signal is sent to the axon, and down a long slender tube that functions like an antennae. At the end of the axon the signal is transferred to the neurotransmitters. These neurotransmitters then travel across a synapse, or gap, to a dendrite of another neuron which receives the chemical messages. Once the process is complete the neurotransmitters are pumped back into the releasing neuron.

Under normal circumstances, just the right amount of a neurotransmitter is sent across the gap to communicate with other neurons, but in cases of bipolar disorder levels of certain neurotransmitters are abnormally high or low which experts believe can trigger mood abnormalities. For example, bipolar depression has been linked to low levels of serotonin in the synaptic gap. Serotonin is a neurotransmitter that helps regulate moods. Manic episodes have been associated with high levels of norepinephrine; the neurotransmitter that contributes to our fight or flight response. And too much dopamine, a neurotransmitter effecting emotions and perceptions, is linked to psychotic symptoms such as hallucinations.

Breakthroughs in diagnostic imaging have revealed that the brain structure of those suffering from bipolar disorders also differs from those of healthy individuals. Using advanced MRI and PET scanning technologies, experts now have evidence that experiences of sever episodes of bipolar depression can lead to changes in different parts of the brain. For example, the brain has two hypocampii, each located in the temporal lobes. One of the functions of the hippocampus is to help control learning, emotions, and memory. In some bipolar patients the hippocampus appears to shrink over time. Other areas of the brain’s temporal regions may shrink as well.

Since bipolar disorder often runs in families, scientists are trying to identify the specific genes that cause the condition. But genes are likely not the only explanation. Studies on identical twins reveal that if one twin develops bipolar, the other twin has an 80% chanced of developing bipolar as well. This suggests that while genes are a primary cause, other factors may also be needed for the disease to manifest itself. People born with the possibility of bipolar may find that stressful events like divorce, job loss or emotional strain can trigger the illness…

Serontonin, the Brain and Bipolar Disorder

Serotonin can also do the following:

1. It gives us self-confidence, a feeling of safety and security.
2. It causes us to feel sleepy.
3. It increases our appetites.

The part of the brain where it does each of these 3 things is a different part of the brain from the part where the other 2 things occur. Thus, for example, increasing serotonin in the part of the brain where self-confidence is will increase your self-confidence, but not your sleepiness. Unfortunately, we have no medications to increase only the serotonin in one part of the brain. This explains why medications to increase serotonin in the brain can also cause increased appetite and sleepiness.

Medications which increase serotonin in the brain (SSRI’s such as citalopram, escitalopram, fluoxetine, paroxetine, and sertraline and SNRI’s such as venlafaxine and duloxetine) give us more self-confidence, and a feeling of safety and security.

By the way, serotonin also exists in our gastrointestinal tracts. In this location, it stimulates digestion. This is why such medications can cause gastrointestinal upset. But they can also help constipation.

Norepinephrine, the Brain and Bipolar Disorder

Norepinephrine is a catecholamine with dual roles as a hormone and a neurotransmitter.

As a stress hormone, norepinephrine affects parts of the brain where attention and responding actions are controlled. Along with epinephrine, norepinephrine also underlies the fight-or-flight response, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle.

However, when norepinephrine acts as a drug it will increase blood pressure by its prominent increasing effects on the vascular tone from α-adrenergic receptor activation. The resulting increase in vascular resistance triggers a compensatory reflex that overcomes its direct stimulatory effects on the heart, called the baroreceptor reflex, which results in a drop in heart rate called reflex bradycardia.

Dopamine, the Brain and Bipolar Disorder

Dopamine

Dopamine has many functions in the brain, including important roles in behavior and cognition, voluntary movement, motivation and reward, inhibition of prolactin production (involved in lactation), sleep, mood, attention, and learning.

A common hypothesis, though not uncontroversial, is that dopamine has a function of transmitting reward prediction error. According to this hypothesis, the phasic responses of dopamine neurons are observed when an unexpected reward is presented. These responses transfer to the onset of a conditioned stimulus after repeated pairings with the reward. Further, dopamine neurons are depressed when the expected reward is omitted. Thus, dopamine neurons seem to encode the prediction error of rewarding outcomes. In nature, we learn to repeat behaviors that lead to maximize rewards. Dopamine is therefore believed to provide a teaching signal to parts of the brain responsible for acquiring new behavior. Temporal difference learning provides a computational model describing how the prediction error of dopamine neurons is used as a teaching signal.

 

Diet and Depression / Bipolar

→ July 20, 2009 - Comments off

I’ve written about this before, but due to the amount of misinformation on the internet on this topic, I feel compelled to write about it again.

  • Omega-3 and Depression
  • Folic Acid and Depression
  • Low-Carb Diets and Mood

Now, first off, I do not believe you can cure depression or bipolar using diet. Let me be clear, people who tell you this are mostly flakes. There are ways though that you can possibly improve your treatment plan using dietary components.

Omega-3 and Depression

Omega-3: This is the most well-known and probably well-studied supplement, and it shows a lot of promise. Omega-3 also has been studied for other reasons too and it appears to be good for your heart also, so there are actually a few good reasons to take it.

Omega-3 is, of course, a long chain monounsaturated fat found in a number of foods including fatty fish like salmon. However, understand that you cannot eat enough fish to actually get into a clinical range to help depression. Feel free to eat salmon all you like, but don’t expect it to make you better. Again, people suggesting that you “eat more fatty fish” just really don’t know the research.

Omega-3 Over-the-Counter Supplement

Omega-3 supplements over-the-counter are a little different. They can bump up your omega-3 intake by quite a bit. But don’t by fooled. The big number on the front of the bottle is NOT the amount of omega-3’s you actually get in each capsule. Turn the bottle around to see the ingredients and you’ll see that the amount you get in each capsule might be only a third or less than the number reported on the front. So you might be thinking you’re doing something good for yourself, but just not getting the benefit from it.

So what’s going on here? It’s simple really, supplements are not regulated by anyone and so you never really know what you’re getting. If you’re trying to treat a life-threatening illness, I don’t think this is OK.

Luckily, there is an easy way to solve this problem. There is a pharmaceutical grade omega-3 supplement available for purchase. You just need to go to your doctor or psychiatrist and ask for it. Keep in mind, you should be asked for at least 2 GRAMS of omega-3 because that’s what the studies used. 3 grams would be OK too (and is what I take). Bring in the study abstract for your doctor for review if you don’t think he would be up on it, but it’s pretty widely known. And make sure he knows about the possible side-effects from taking large amounts of omega-3s. Thinning of the blood is one that I know of and so omega-3s should always be stopped several days before surgery. Definitely make sure that your doctor discusses with you anything that may effect yoaffectsonal medical issues.

Assuming you don’t have any specific risks, I have seen no side effects. Yay!

Folic Acid and Depression

Folate / Folic Acid: to be clear, folate is the substance in the body, and folic acid is the supplement you find on the shelf (pregnent woman are generally advised to take it). Folate definitiancies have been studied in depressives along with several other nutrients like B12. However, it appears that folate itself is not the part that’s definitiancy, it’s actually l-methylfolate, which is a compound that is created from folate. And the key here, is that one study has found that no matter how much folic acid you consume, your body may not be able to create enough l-methylfolate to actually fix your deficiency. So by telling you to take folic acid you may be doing absolutely nothing.

Again, luckily there is an easy fix. Your doctor can prescribe you a cheap pharmaceutical grade l-methylfolate supplement. Keep in mind, the number of people who respond to this supplement is very low, but as there don’t seem to be any side-effects (talk to your doctor) there’s no real downside to trying it.

Both of these supplements can/should be taken in addition to your conventional treatment.

Low-Carb Diets and Mood

And one final note. There is some thought that a low carbohydrate diet (like Atkins or South Beach) may adversely affect the serotonin in your brain which may effect mood and cognition. However, there is also evidence suggesting that this is not that case. Personally, I think long-term extreme low-carb diets may be a concern, but over the short term, no difference will probably be noticeable. However, if you have a serious mood disorder, like me, that might affect your choice of diet even if the evidence isn’t clear.

Physiological Causes of Depression – Surgeon’s General Report

→ July 6, 2009 - 2 Comments

I like to think I know almost all there is to know about mood disorders, but I was pretty shocked when I read this:

The Surgeon’s General Report

Differential Diagnosis
Mood disorders are sometimes caused by general medical conditions or medications. Classic examples include the depressive syndromes associated with dominant hemispheric strokes, hypothyroidism, Cushing’s disease, and pancreatic cancer (DSM-IV). Among medications associated with depression, antihypertensives and oral contraceptives are the most frequent examples. Transient depressive syndromes are also common during withdrawal from alcohol and various other drugs of abuse. Mania is not uncommon during high-dose systemic therapy with glucocorticoids and has been associated with intoxication by stimulant and sympathomimetic drugs and with central nervous system (CNS) lupus, CNS human immunodeficiency viral (HIV) infections, and nondominant hemispheric strokes or tumors. Together, mood disorders due to known physiological or medical causes may account for as many as 5 to 15 percent of all treated cases (Quitkin et al., 1993b). They often go unrecognized until after standard therapies have failed.

(bold mine)

I’m shocked. No one ever mentioned anything about birth control pills to me and I’ve been on them for years. YEARS. This is yet another reason why doctors so often get on my bad side.

This quote was taken from the Mental Health: A Report of the Surgeon General. The whole report is a good read, but very long. It’s everything you wanted to know but didn’t know you needed to ask.

I’m disgusted.

Mood Charting Depression, Anxiety, Mania, Irritation

→ August 16, 2008 - 4 Comments

I’m a geek. If you know me, I deny this, but it’s actually true. Not the Star Wars-watching, video-game drenched, mother-basement living, socially awkward,virgin type, but a geek nonetheless. I do, after all, make software for a living, understand math, and make logical arguments.

A Mood Chart

So, in the vein supportive numbers, I have been charting my mood for a while. I chart depression (obviously) along with mania, anxiety, and irritation. I’ve also added trend lines for anxiety and depression (the dotted ones):


The headline is the depression is dropping while the anxiety is increasing. Looking a bit closer, you can see that Jul. 16 when I added the Zyprexa/Celexa combo, the depression dropped substantially. It’s probably the best I have felt for over a year. I don’t have the numbers to prove it, but trust me, it’s true. (I’m scared to even write that because I feel like it will be taken away from me. I feel like a higher power will reach down into my life and destroy it. I suppose a higher power will reach into my brain and start squishing it like squishing whole tomatoes for a marinara sauce. Brain sauce. Yum.)

Mood charting has two main benefits.

One, you have objective record for what is happening to you. Your doctor is going to ask you “how are you feeling?” (which is the dumbest question ever) and you have to be able to answer it. It’s harder than it sounds. Are you more anxious, or less? What side effects have you noticed? How long have they been happening? What kind of pain? How depressed are you compared to last time? Irritation? Mania? Energy level? And it would be handy if you could answer all of that in 2 minutes or less.

Seriously? Yes, seriously. You only have a few minutes with your doctor. You don’t have time to “think about it”. Mood charting can help you maintain an objective view of what is really going on. Generally, I can remember all these things because I have been doing this forever, but you may not be so “experienced”.

Two, you’ll have historic record so when you switch doctors, you know what to tell the new guy. Think your new doc will sift through the records of the old one? Well, maybe, but maybe not. It’s so much better if YOU can answer their questions and be the record for them. Then you know it’s actually accurate and right. And trust me, you won’t remember 17 drugs from now what happened with THIS antidepressant and THIS mood stabilizer combination. You just won’t. At this point, all the goddamned drugs sound the same to me. Alprozylepin. Meh. Whatever.

Try charting the numbers with drug names, dosages, side-effects, and “other pertinent info”. If every time you eat an ice cream sundae you feel super, maybe note that. Or your menstrual cycle, or whatever makes sense for you. Generally I haven’t bothered doing this because I’m so depressingly constant. I know how I am, I’m depressed. Screw off already. It just so happens that something has changed. Unbelievably. Miraculously.

See, I have the numbers to prove it.

(Child says to God, “how do I know you’re God? Show me a miracle.” God points to a tree. The child says, “that’s not a miracle, that’s a tree!”, to which God says, “let’s see you make one”.

God should have pointed to me. Let’s see you fix her.)

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