Venlafaxine, Phenibut and Choline for Cyclothymia (“Bipolar Lite”)
Update 24/10/2014: A few weeks after writing this, I was able to beat my depression for good, without drugs. I wrote up this method here: How I Beat Depression — Forever
The following post is still worth a read however, especially for an introduction to my “Neanderthal mood model”. If you “cycle” a lot, particularly into downtime during winter, this post on modafinil is also worth a read: Modafinil for Seasonal Affective Disorder (SAD)
- Neanderthal Origin Hypothesis of Bipolar Conditions
- Psychological Feedback Loops
- Further Reading
This is a very long post. It covers my baby model of bipolar conditions and their proposed relationship with Neanderthal genes, sleep-wake cycles, diet, and the psychological mechanisms which amplify the emotional states at each end of the bipolar spectrum. It also discusses a possible link to schizophrenia.
It’s all very unscientific. The model is based on many assumptions which are currently unfalsifiable. You can skip to the Summary at the end if you want to have a look at those, and the conclusions I reached from them.
But the model also thinks outside the box and connects the dots in ways I haven’t seen before. I’m hoping it will give ideas to researchers who are in a position to develop it further. It’s also a response to my general disillusionment with what I see as the rigid, sloppy and uninspired way the mainstream medical and psychiatric professions think about mental conditions. I’d eventually like to put a wrecking ball through all that, and this is one of my baby steps towards that.
Disclaimer: This is not science. I am not a doctor. I am basically making this up as I go along. The pharmaceutical treatment I arrived at as a result of this model is based on a data set of one (me). It works very well — for me. But that does not prove any of what I wrote, or that the treatment arises as a result of the model. I cannot conscientiously recommend anyone tries these drugs, especially if you have more extreme forms of bipolar. I won’t be held responsible for anything anyone does as a result of this post. It’s an idea I’m exploring, that is all.
I self-diagnosed as cyclothymic about three months ago. Cyclothymia has the nickname “bipolar lite” as it is a less extreme form of full-blown bipolar disorder. Many people with this condition never get diagnosed, because the symptoms often aren’t severe enough for the individual to seek help, or for a doctor to recognize them and make the diagnosis.
I became aware of the cyclothymia classification after watching Stephen Fry’s documentary The Secret Life Of The Manic Depressive, in which he discusses his cyclothymia diagnosis. The symptoms match how I’ve been experiencing life for at least ten years (I am 30 now):
An individual with cyclothymia may feel stable at a baseline level but experience noticeable shifts to an emotional high during hypomanic episodes, with symptoms similar to those of mania but less severe, and emotional lows involving depressive symptoms that do not meet the criteria for a major depressive episode.
Cyclothymia is similar to bipolar II disorder in that it presents itself in signature hypomanic episodes. Because hypomania is often associated with exceptionally creative, outgoing, and high-functioning behavior, both conditions are often undiagnosed. As with most of the disorders in the bipolar spectrum, it is the depressive phase that leads most sufferers to get help.
So this post is about cyclothymia which I feel I have experience of. It’s still very conjectured. The bits where I talk about the more extreme forms of bipolar, and schizophrenia, should definitely be taken with a large pinch of salt.
I developed a model of bipolar conditions which is what this post describes. As a result of this model, I have developed a treatment regimen that has literally eliminated the symptoms — for me. I’ve been stable on this regimen for two months now. It was the amazing, almost magical success of this drugs regimen (for me) which inspired me to write this post and share it, in the hope others could benefit. It has literally been life-changing for me, and it began to work very, very quickly — i.e. overnight reduction of symptoms, followed by stable productivity and happiness within a few days.
You can skip this rant if you want to get straight to the model.
I had to self-diagnose cyclothymia for the following reasons. I have put myself in for voluntary mental health assessment three times over the last several years, because obviously I felt something was wrong. These health assessments basically consist of someone ticking boxes on a form then giving you the diagnosis their little score box tells them. They found nothing wrong with me each time. Cyclothymia is difficult to diagnose anyway because the symptoms are often not extreme enough for the individual to keep pushing for a diagnosis, nor for them to appear on the radar of a form-filling exercise. For example, sometimes I’d start feeling fine again and forget why I even made the appointment.
Ultimately though I believe the British NHS is so overstretched and under-equipped that you can only receive significant attention if you’re likely to harm yourself or others. I never got to that point so I was basically fobbed off each time.
The last time I went through the system, I was given a phone number to call for a chat with an assessor. I didn’t even get to see a mental health professional face-to-face. To my disappointment, the first phone call was just to set up the appointment. There was a three-week wait for the next available slot, which is absolutely ridiculous in my opinion — in three weeks anything could change in the circumstances of someone with a mood disorder. I asked if I would be listened to quicker if I was suicidal, to which they said, “Yes, you would get on a quicker list. Are you, though?” No, I said, because I’m not a liar. So three weeks it was.
They phoned me at the arranged time three weeks later and their phone system malfunctioned and cancelled the call after one ring. I gave them ten minutes to call me back before phoning them. They told me they phoned and no one answered, and because ten minutes had passed they had cancelled my appointment. I asked them why I couldn’t be put through now, and simply have 20 minutes instead of 30. They said it didn’t work like that and I’d have to rebook. Being depressed at this point, this kind of “care” did not help. It wouldn’t surprise me if that mental health service actually causes declines in mental state as a result of their apparent lack of care. It certainly made me feel a lot worse.
I rebooked the appointment for the next day and their automated system sent me a text to confirm. Then another one. Then another. I received no less than 31 copies of the same text. I had to phone them up from a different phone to tell them to knock it off, because my mobile was being pulverized.
The doctor, who gave the impression to me of being a glorified admin and form-filler, didn’t seem too bothered about my case. It was probably his tenth phone call of the day, and I suppose without direct face-to-face interaction his empathic faculties struggled to engage. His advice was basically, “Don’t worry about it, and let’s see how it goes.” I told him I was coming off a lengthy tramadol addiction (self-medication with inappropriate drugs is common in people with mood disorders) and he asked why I had been taking it. I told him I was self-medicating with it as an antidepressant. He said tramadol does not have any antidepressant effects, and is only a painkiller. This misunderstanding of the link between the endogenous opioid system and emotional affect aside, I pointed out that tramadol has serotonin- and norepinephrine-raising effects (the two major foci of modern antidepressants) and that it was currently in trials as an antidepressant. His words, and I quote: “Oh well, you learn something new every day.”
He told me to just see how I feel in a week, and if I don’t feel better then he might try me on pills. I said I was taking St. John’s Wort for the depression, and he said, “Oh yeah, take that as much as you want.” He was still working from medical guidelines from 20 years ago which said that St. John’s Wort was inactive and a placebo at best (it has since been proved as a potent raiser of serotonin, norepinephrine, dopamine and BDNF, all important neurochemicals in the pathology of depression). That’s typical when dealing with people in the medical profession. They don’t update their knowledge, and they talk to you as if you’re a moron. Another chat was scheduled for a couple of weeks later, but I cancelled it because I really didn’t see the point. As with most things in my life, I simply vowed to get the job done myself, and I’m glad I did for what I ended up discovering. Always find a way to appreciate your challenges in life!
I’m going to end this rant with the observation that the NHS is no longer fit for purpose, and hasn’t been for some time. This wouldn’t be a problem if I could get my contributions from the last 12 years back and invest in a decent medical care provider, but I can’t. The NHS is a sacred cow and it’s time to have a barbecue.
In the end, I self-diagnosed by keeping a journal for several months and matching symptoms as objectively as possible to a wide range of mental disorder diagnostic criteria until I found one that fit, and that was cyclothymia. I would urge anyone who feels they are being overlooked by an overstretched system to do the same, but to take time with it to avoid jumping to premature conclusions.
So, on to the backbone of my model…
I first became obsessed with the Neanderthals after reading Koanic’s fascinating face-reading guide which says Neanderthal genes not only live on but create individuals with significant Neanderthal physical and behavioural traits. I was massively sceptical about his ideas for a long time, but it became a reality tunnel I was unable to shake off. The world started to make a lot more sense when viewed through this lens. I recommend you read the rest of my post before venturing onto his guide, as it’s very long and I don’t want you to be put off via scepticism at this stage. I started researching everything that is known about the Neanderthals, from many different sources, and I’ve also begun to develop my own Neanderthal model which I’ll be writing about a lot over the next few months.
Back to bipolar. The mainstream basically has no clue what bipolar is and why it exists. Some scientists view it simply as faulty genes. However I refuse to believe that nature would be so cruel as to issue something as debilitating as bipolar without those genes having served some original beneficial purpose. Nature simply does not allow genes to propagate unless they help the organism in some way.
I first made the link between bipolar and Neanderthal genes while reading this article about gene DRD4-7R which is believed to have come from the Neanderthals and is associated with bipolar, OCD, ADHD and schizophrenia — all of which I’ve long suspected are various expressions of the same phenomenon. These conditions are also prevalent in highly creative people (think of how many genius-level artists and scientists are also completely nuts) and I don’t think it’s a coincidence. Genius and madness appear to be two sides of the same coin: madness can be viewed simply as creativity turned inwards.
I’m researching other genes associated with these mental conditions, including COMT and NRG1 variants, to see if they came from the Neanderthals too, but it’s hard work since it’s not something you can simply type into Google at this stage — it’s all breaking ground. However, I am not the only one to propose a link between bipolar and the Neanderthals. (That link goes to a paper behind a pay-wall. Click here for a critique by another author which shows some excerpts.)
I’ll do a post on candidate genes for bipolar and their possible links to Neanderthals soon when I’ve finished the research, but for now let’s move forward under the assumption that bipolar is a Neanderthal trait. In that case, what “is” bipolar, and why did they have “it”?
My idea is that bipolar, at its root, is nothing more than a Neanderthal sleep-wake cycle. Its maladaption to a modern human circadian rhythm, combined with creative psychological story-writing mechanisms (covered later), are what propels an underlying “sleep” or “awake” state into depression or mania, respectively.
I first came up with this idea after practising meditation for years and noticing that, after stripping away the story — the internal narrative and false meanings I applied to my depressive phase — the state was indistinguishable from simple tiredness. When you’re depressed, the most appealing thing in the world is bed, or a sofa and a television. What if depression is literally a sleep phase? What if, when you are depressed, you are supposed to be asleep? The parallels are easier to see if you compare the anxiety, lack of motivation, and general difficulty performing basic tasks (especially social skills) while physically fatigued, to the similar state of affairs when one is depressed. Tiredness makes things difficult.
In contrast, the best description for my hypomanic phase is: awake. Colours are brighter, I’ve got tons of energy, and everything is easier. My creative abilities are turned up to ten and creating is pure joy. Anxiety diminishes significantly and I am inspired to socialize rather than feeling withdrawn.
So, to simplify:
- Depressed = asleep = difficult.
- (Hypo)manic = awake = easy.
Now, I know full-blown mania is a lot more serious than the simplification I’ve just made. It can lead to psychosis and breaks from reality, as well as hugely problematic personal and social behaviour. I’ve never had mania to this degree; my phases are limited to hypomania, a highly creative, productive and energetic sub-manic state. It is my hope that the ideas spawned in this post can help people who hit extreme mania and depression too, but in truth I just don’t have those reference points, and messing around with new drugs (covered later) could potentially be disastrous for such individuals.
So, to clarify, in this post I’m using a data set of one (me), for mild-to-moderate depression and hypomania. This isn’t science; it is ideas, and a treatment I arrived at that worked with, from what I can tell, complete effectiveness for a data set of one (me). But ideas are the start of progress. So, for now, let’s push on with the model that bipolar conditions are actually a manifestation of a sleep-wake cycle, and see where that leads us.
But what has sleep-wake cycles got to do with the Neanderthals?
My idea is that Neanderthals lived in very different conditions to how we live today. They evolved in frozen Ice Age Europe, and they actually lived in caves.
Seasonally, what if they were “awake” during spring and summer, highly active and stockpiling food, but “asleep” during winter, hibernating in their caves? This accounts for long-phase bipolar (months spent in “mania” followed by months spent in “depression”). It also explains seasonal affective disorder (which I also get pretty bad). Depression certainly feels like a hibernation state to me.
For shorter-phase bipolar (days in mania followed by days in depression) we can model this as a few days’ hunting followed by a few days’ sleep. Whatever the scale, we can model bipolar as a long-phase sleep-wake cycle using just a little imagination.
Culturally, the Neanderthals would likely have had rituals set up for both hibernation and active periods. Perhaps hunts would have been interspersed with short naps — long enough for non-REM sleep, but not long enough to trigger REM sleep which, later in the post, I propose as being the hibernation trigger. Hibernation would literally have consisted of days spent asleep or resting in an extreme low-energy state, huddled together in caves. This makes sense if you consider that the most appealing thing while in a depressed state is a bed and someone to cuddle.
There is no cultural framework present in modern-day human society to support such a long-phase cycle. Such a cycle is very misaligned with the modern human circadian rhythm of eight hours’ sleep at night followed by sixteen hours of activity. Perhaps this fundamental misalignment is really at the root of the psychological suffering experienced by bipolar-spectrum individuals. Trying to be active while actually in a physiological sleep state is extremely difficult and demoralizing, and very much sums up my experience of the “depressive” phase of bipolar. I liken it to trying to walk through treacle.
The manic phase on the other hand is more like flying. Perhaps the Neanderthals would have had a cultural framework in which to turn this highly energetic state into group productivity.
Yes, this is a lot of speculation. But I find it a lot more inspiring and ultimately workable than “you have faulty genes and you’re broken”.
It was about ten years ago I first found I was far more functional in just about every area of life when I’d missed one night’s sleep. Paradoxically, these days were like truly being awake. Not being the sort of person to ignore such things, I began researching it diligently. I found that this phenomenon was not just restricted myself, and is actually known as “wake therapy”:
Sleep deprivation can exert antidepressant effects in humans in less than 24 h, making it the fastest acting antidepressant treatment. However, it is rarely used clinically because the effect disappears once the subject goes back to sleep.
Many neurotransmitter systems have been implicated in and hypothesized about in regard to why sleep deprivation is such an effective and rapid antidepressant. These include: serotonin, norepinephrine, dopamine, opioids, GABA, glutamate and BDNF. Over the next ten years I became dedicated to finding out which neurotransmitter systems were responsible for making me feel so well on those sleep-deprived days, and I bought drugs (both legal and not-so-legal) which could activate those systems together or in isolation in order to find out. I now believe I have found the answer, and my new treatment regimen makes me feel that way every day.
During REM sleep, the serotonin and norepinephrine systems are turned off completely in the brain.
Scientifically, it is still not well understood why SSRIs work. Besides the assumed mood-lifting effect of increased serotonin, they also suppress REM sleep and increase BDNF. I’m going to join the dots.
I hypothesize that serotonin itself is a key regulator of mood. SSRIs also suppress REM sleep which in turn raises BDNF. So SSRIs work through all these factors, in my opinion.
Bringing this back to my model, I believe REM sleep is the hibernation trigger for individuals expressing Neanderthal genes. Suppress REM sleep, and individuals stay in the “awake” mode. I believe it is no coincidence that both SSRIs and sleep deprivation are known mania triggers.
My idea was therefore to intentionally suppress REM sleep so my hibernation cycle was not triggered by going to bed. I got my hands on an SSRI (sertraline). Patients who are given SSRIs are told by doctors that it typically takes six weeks of daily use for their antidepressant effects to begin working. I had the idea that a low dose (25mg) taken before bed would keep the serotonin system turned on enough to partially suppress REM sleep, and bring about an instant sleep deprivation–style antidepressant effect. This worked. I awoke willfully at 7:30am (unheard of without treatment, for me) feeling alert, knocked out a few hours of work, went for a swim, came back and wrote my novel, did some more work — and essentially fitted three days’ productivity into one day.
That mood however still did not quite reach the clarity of the full sleep-deprived state I had been aware of for the last ten years. That’s because there is another neurotransmitter which is switched off during REM sleep: norepinephrine.
I hypothesized that keeping the norepinephrine system on as well as serotonin would lead to a more full suppression of REM sleep. I took low-dose (about 10mg) venlafaxine, an SNRI, before bed and immediately got the effect I was looking for the next morning. However, taking the drug on the successive night made me wake up at about 3am and be unable to fall back to sleep, so I moved my administration time to early morning (6:30am) thereafter. I also increased the dose to 18.75mg, which is half the lowest clinical dose (37.5mg).
WARNING: Venlafaxine (and all SSRIs and SNRIs) are known potential triggers for mania.
I found that this dose gave the mood-lift I was looking for during the day, while still retaining enough of the drug in my system to suppress REM sleep that night without affecting non-REM sleep. In other words, I was able to fall asleep easily but still wake up with the alertness and clarity of an REM sleep suppression. I found what I was looking for.
I have not had to alter that dose since, and it causes me practically zero side effects. And that is coming from a drug known for its insane side-effect profile (at standard dose) which includes sleep disturbance, appetite suppression and sexual dysfunction. I will now talk about my ideas on why low dose is the key. I consider the doses recommended by doctors for both SNRIs and SSRIs as insanely high. Take this experience report from Erowid, for example:
I started taking effexor xr about 3 weeks ago. My doctor gave it to me to help with anxiety. He told me to take 37.5 the first day, 75 the second day, 112.5 the third day, then 150 the fourth day, and then stay at that dose.
In the short term, this is going to feel like something similar to ecstasy (depending upon the existing neurochemistry and emotional affect of the individual). However, having personally taken 37.5mg daily for about a week in the past, I quickly developed that “zombie” effect common to people on long-term antidepressants.
I think standard doses are far too high. The goal should be to reinforce the serotonin (and norepinephrine in the case of an SNRI) systems. Instead, standard doses overload it. They turn it up to ten, and leave it there. SSRIs and SNRIs are well-known for their blunting effect on mood, and the huge-pupilled zombie stereotype of long-term antidepressant users is culturally well-established.
The goal, in my opinion, should instead be to stabilize the baseline of mood to prevent deep downward spirals, while leaving room in the upper register for positive emotions. Clinical doses instead compress everything high into the upper register leaving no room for emotional dynamism.
The system needs to be left responsive. Not flatlined and zombified. I’ve found that my 18.75mg daily dose achieves that amazingly well. I also experience next to no side effects from this dose.
I believe night-owlism is another Neanderthal trait, and consequence of the Neanderthal sleep-wake cycle. People who are night owls become highly productive and creative towards the evening, and feel naturally inclined to stay up late, working on projects or simply enjoying the high-energy state. In contrast, in the day they tend to feel lethargic. I have always been a night owl, feeling more clear, happy and productive at night, but unfortunately the standard modern human day does not cater well for such individuals. This is one reason I became self-employed.
Take my standard (non-drug-controlled) sleep-wake cycle, for example. Given the choice, I’ll wake up at at least 10am. At this point I’m basically useless for the next few hours. I feel terrible, my thinking is really cloudy, I’m antisocial and annoyed at everything. This is the time when “normal” people are drinking coffee to wake up. Coffee for me, during this time, makes my thoughts race but adds no clarity or wakefulness. It’s muddy, useless, racing thoughts. Creativity is typically poor up until 2pm, as thinking hurts. Like clockwork, at 2:30pm there’s some sort of “wake-up wave” I feel passing through me, and I start to come to life. By 7pm I’m all systems go. By that point, most of the day has been lost to sub-standard psychological states, and it’s soon time to go to bed and start the cycle all over again.
I believe what is happening with night-owlism is that such individuals are on the Neanderthal longer-phase sleep-wake cycle — e.g. one day (or longer) asleep, followed by one day (or longer) awake — as opposed to eight hours asleep, sixteen hours awake as per the modern human cycle. In such individuals the serotonin and norepinephrine systems, turned off by REM sleep (hibernation), take longer to reactivate fully. When they finally turn back on they are set up to stay on for a long time. As a night owl, with all systems go in the early evening, you’d better have something to do, otherwise you’ll just be lying in bed or watching television, waiting for the sun to come up.
I know some night owls in real life who “self-medicate” by simply staying awake till they feel tired, going to bed whether it’s 3am or 5am, and only having a few hours’ sleep before getting on with a standard human day the next morning. They’d rather take the lack of sleep on the chin (perhaps intuitively suppressing their own REM sleep?) than feel like an insomniac by turning in early and lying awake in bed for hours. Needless to say, self-employment or night shifts are good ideas for night owls.
On my venlafaxine regimen, I can wake up at 6:30am and feel immediately fresh. At 2:30pm, my like-clockwork “wake-up wave” kicks in even more powerfully and noticeably than usual. Around 6pm however I typically get sleepy and have a half-hour nap, which reinvigorates me and means I can do whatever I like with the evening. In other words I’ve taken control of the cycle.
Once a week, usually on a Sunday-through-Monday, I come off all drugs completely and have what I call my “hibernation day”. This consists of relaxing, sleeping a lot to catch up on my REM sleep, and basically doing nothing till Monday morning when I start my regimen again and do a fully-productive week. I believe this recovery period is essential to maintaining the effectiveness of any drug, but especially an SNRI. It re-establishes a lower neurotransmitter baseline (thus allowing emotional dynamism), keeps tolerance at bay, and I believe this hibernation day is the reason my regimen has continued to work on the same dose for two months now. I am recreating a Neanderthal cave sleep-in to keep the system cycling on my terms.
The drugs formula is by no means complete at this point. We’ve covered mood-lifting via suppression of REM sleep. Now we need to look at mood stabilization.
The Neanderthals would have eaten a high-fat ketogenic diet based on hunting large game such as mammoths. It is known from those of us who have tried ketogenic diets (such as paleo and Atkins) that, after a few days, one begins to experience a calm, clear, euphoric high. It is proposed that this mental state is achieved by the body’s production of a ketone body called BHB, which is remarkably similar to recreational anti-anxiety drug GHB. It is proposed that BHB, like GHB, induces calm by agonizing GABA-B receptors. Modern mood stabilizers valproate, carbamazepine, and lithium also increase sensitivity to GABA-B via receptor upregulation.
Therefore, could the Neanderthals’ high-fat diet have stabilized their mood?
It has been established that GABA levels are significantly lower in people with mood disorders. If we push on with our assumption that mood disorders are caused by Neanderthal-Sapiens hybridization, and a failure to meet the lifestyle requirements of the expressed Neanderthal genes, perhaps low GABA levels are a Neanderthal trait ordinarily counterbalanced by GABA-agonizing ketones produced by their high-fat diets. Since dietary fat has been demonized by the mainstream for the last 50 years, perhaps the high-carb, low-fat “ideal” mainstream diet has been hurting those of us with Neanderthal traits even more. In contrast, no-grain, high-meat diets such as paleo are reported to treat a variety of health problems including mood disorders.
Phenibut is a GABA-B agonist. It also has the benefit of being available legally without prescription — you can even buy it on Amazon. I discovered phenibut over a year ago, and wrote about it plenty on the forum. Taking this substance, for me, was like turning a key, giving instant clarity, creativity, and a drastic reduction in anxiety.
Phenibut makes up the second half of my daily drugs regimen. I take 1.5g. Yes, that is grams, not milligrams. This is a moderate dose, as I’d already been taking the drug for close to a year before introducing the venlafaxine. I recommend anyone who wishes to try phenibut to start off with a much lower dose, e.g. 500mg.
WARNING: One of the main problems with phenibut is that it increases dopamine, so it is a mania trigger danger.
I fill up two size 00 capsules which is about 1.5g and take them at the same time as my 18.75mg venlafaxine. Like the venlafaxine, I have never had to increase the dose of phenibut. The effectiveness of these two drugs in combination has stayed consistent over the last two months. If that ever changes, rather than raising the dose, I will actually take a week off from both to reset the tolerance. I think raising doses is madness. If you’re at the ceiling, back down a bit so you’ve got room to move, rather than trying to punch your way through.
Choline has been shown to be an effective mood stabilizer. Food sources containing the most choline are eggs and — you guessed it — fatty meats. Score another hit for the Neanderthal diet and mood disorders hypothesis.
On the regimen I’ve discussed so far (18.75mg venlafaxine + 1.5g phenibut), I am generally stable, very happy, and highly productive. Occasionally however that does tip over into hypomania, especially following excess coffee consumption (I actually recommend tea with this regimen as the theanine enhances the phenibut’s calming action). In such cases, I use cholinergic drugs to take the edge off the mania.
The drug I use is a pre-prepared “stack” combination called Noo Day. Each capsule contains sulbutiamine, n-acetyl-l-tyrosine, choline, aniracetam and noopept. You’ll have to look those up yourself to find out the specifics. They are all “nootropics”, however (drugs which supposedly make you smarter). The most important ones with regard to our discussion are choline, sulbutiamine, aniracetam and noopept, which all promote cholinergic action in the brain.
I first came across the subduing action of cholinergic drugs almost a year ago. I had been experimenting with a noopept-plus-choline preparation and was finding that, instead of making colours brighter and thinking clearer as was purported by the literature and thousands of user reports on the internet, it actually took the edge off whatever mood I was in and made my thinking cloudier. In fact it brought me down so much I stopped using it after a few test runs. However, bearing its mood-dulling effects in mind, I kept it in order to test it on my next episode of hypomania, and found it effective at bringing me down a notch. It was only recently I discovered that it was the cholinergic action which was responsible for this effect.
I never found any of these “smart” drugs to particularly work the way they are supposed to. The effects they have on others are consistent with what I experience in my “awake” state anyway. In other words, the effects of any psychotropic drug seem to depend upon one’s existing neurochemical state and brain function.
When considering the effectiveness of my treatment plan you should also bear in mind I have close to six years’ mindfulness meditation practice under my belt.
I know when I’m in the depressive state. I know when I’m hypomanic. I know to not pay too much attention to the story — the internal narrative — the thinking mind writes when it attempts to explain these states.
I believe this kind of self-knowledge is hugely important in managing any mood oscillation, but particularly when dealing with the extremes of bipolar conditions.
I believe the thinking mind is always trying to interpret an underlying emotional state. I believe its interpretations are frequently wrong without lifelong awareness of and dedication to improving those interpretations.
In bipolar conditions, the shift to a depressive state is so intense that the thinking mind must come up with a whole bevy of nonsensical interpretations in order to explain it. That’s when you get internal scripts running such as, “I’m a complete loser” or “Everything is hopeless”. The mind writes a story consistent with the emotional state, and applies it both backwards in time, focusing on all past mistakes via the explanation of inherent unworthiness, and forwards, extrapolating those perceived failures far into the future to extinguish all hope.
In manic states, the sudden uplift in mood and energy similarly gets its own story. Past mistakes are seldom focused upon in this state, as they are not consistent with that emotional state or the story the thinking mind comes up with to explain it (memories seem to be linked in networks connected to the emotional state under which they were created, and different emotional states turn on different associated memory networks). In this state, past achievements tend to be highlighted in memory. This sense of energy, achievement and creativity is then extrapolated by the thinking mind far into the future, and this is where you get all the grandiose ideas, plans, and inflated self-image common to the manic state.
People with bipolar conditions frequently have many projects started but never completed, and it is the manic state with its grandiose future extrapolations which spawns this frantic project-starting. When cycling back to the depressed state, one comes to see those projects as a waste of time (since everything is pointless anyway) and they only serve as a reminder of one’s inherent loserdom. I remember I’ve actually deleted projects off my hard disk in the depressed state, in the days before meditation when I was not yet mindful of the effects of emotion upon the thinking mind. With meditation however I learned to spot the thinking mind’s story-writing process and let it fall away. Stripping back all the narrative, and just seeing the emotions for what they were, is how I came to realize that:
- Depressed = low energy = sleep.
- Manic = high energy = awake.
And hence this post.
The problem with the story-writing — a function of what we can loosely model as the “higher brain” — is that it can feed back into the lower brain. Positive feedback loops are formed this way.
If we take an underlying energy state of 10, and then feed it through the higher brain’s story-writing faculty, this 10 is then extrapolated into the future many times where it becomes grandiose plans and dreams, pumping the reward circuitry with each fantasy, raising the underlying energy state each time which then gets cycled into more stories. The 10 quickly becomes 100. I believe this is how mania arises so quickly and gets out of hand. A depressive state can similarly turn a -10 into a -100 via story-writing of loser scripts.
As a side note, I believe the paranoid delusions associated with schizophrenia come from the thinking mind’s attempts to interpret and narrate a persistent fear state (most likely an ongoing activation of the right amygdala, which is shown to be smaller in schizophrenics). A story is written to explain the fear, and that story is even more terrifying than the initial fear itself, feeding back to create more fear. It’s the same process as seen in mania and depression, but is based upon slightly different underlying physiological brain conditions. I believe this is one of the possible links between schizophrenia and bipolar, and these conditions tend to run together in families and share many associated genes (my eldest brother is schizophrenic, and I’ve seen his story-writing faculty in full swing on many sad occasions). In both cases an underlying physiologically-based emotional state of 10 can be turned up to 100 via this psychological feedback loop.
Treating such conditions then, in my opinion, absolutely relies on addressing both the underlying physiological conditions (and thus initial emotional states) via medication, and individuals training themselves to become aware of their own psychological mechanisms (story-writing) which amplify those states via positive feedback.
I promote daily mindfulness meditation as the “catch-all” method for brain-training. Shinzen Young’s course still stands out to me as being one of the best introductions to the practice. I also recommend other cognitive methods such as journalling, spirituality, and constantly refining one’s perspective of life and the world through introspection, reading, and gathering as much life experience as possible to feed back into that refinement process. The external must influence the internal and vice versa in an ongoing cycle of improvement. Medication and lifestyle improvements provide the physiological basis for a balanced and ultimately positive experience. One also cannot deny the effectiveness of regular exercise on improving mood.
Assumption 1: I am cyclothymic.
Assumption 2: Bipolar conditions come from Neanderthal genes.
Assumption 3: Bipolar conditions are manifestations of a Neanderthal longer-phase sleep-wake cycle (at least one day asleep (hibernation), at least one day awake) misaligned with modern human cycles (eight hours asleep, sixteen hours awake).
Outcome: Adjusting sleep patterns (“wake therapy”) can help.
Assumption 4: REM sleep is the Neanderthal “hibernation trigger”.
Outcome: Suppressing REM sleep via wake therapy or drugs can have a therapeutic effect by maintaining the “awake” mode. 18.75mg venlafaxine daily can achieve this (WARNING: mania trigger danger).
Assumption 5: Neanderthal diet of fatty meats has mood stabilizing properties via action of BHB ketone and choline on central nervous system.
Outcome: Replicate BHB GABA-B agonism with phenibut (500-1500mg daily) (WARNING: mania trigger danger). Replicate high-choline diet with choline supplementation and/or use of cholinergic drugs, e.g. the racetams or noopept.
Assumption 6: Bipolar mania and depressive symptoms are worsened via psychological feedback mechanisms (internal story-writing).
Outcome: Increase awareness of the story-writing process in order to break such feedback loops. Meditation and other cognitive interventions e.g. journal-writing recommended.
- How to read faces by Koanic. Establishes his Neanderthal theory and teaches how to spot individuals expressing Neanderthal genes via analysis of their facial features and skull shape.
- Evolutionary origin of bipolar disorder — revised by Julia A. Sherman. Paper proposing that bipolar disorder comes from the Neanderthals.
- Invalid Attribution by Illuminatus. Describes how the thinking mind is constantly interpreting emotional state and attributing shifts in that state to causes, frequently incorrectly. Useful in understanding how this process exacerbates emotional extremes in bipolar conditions.
- Interesting Self-Talk Tip via Journalling by Illuminatus. Describes how keeping a journal is an effective cognitive intervention for spotting psychological feedback mechanisms and long-term patterns.