How to control lithium side-effects and use a safer lower dose 
How to use Low-Dose Lithium Orotate 
for 
Bipolar Syndrome & 
Recurrent Depression 

In this article I'll tell you:
- how to increase the effectiveness of low-dose lithium so that you can reap the benefits of lithium without the toxic side effects caused by high doses. 
- how to combine low-dose lithium with other natural remedies to treat bipolar syndrome

 
How to make low-dose lithium More Efficient  

Lithium counteracts the Brain Shrinkage caused by bipolar and chronic depression

Its now understood that people with bipolar syndrome and chronic depression have hyperactivity of one of the body stress pathways (the HPA-axis) the consequence of this can be increased production of the stress hormone cortisol which causes chronic inflammation and degradation of brain cells, opposing  this degradation is a protein the brain naturally produces called BDNF and lithium boosts BDNF production.  

Brain cells grow branches called dendrites that connect to neighbouring neutrons, the branches connected to little stumps called dendritic spines that grow on the sides of the dendrites, the connections are the synapses across which neurotransmitters are passed; the ability of the brain to grow new connections is called neuroplasticity.  The new theory is that the combination of the long-term low-grade inflammation caused by overactivity of the HPA-axis together with the inadequate levels of BDNF seen in bipolar syndrome results in shrinkage or loss of dendrites, dendritic spines and therefore a loss of synapses.  Loss of synapses in the key structures of the brain that control mood at least contributes to bipolar syndrome and recurrent depression and may possibly be a central cause of it in the first place.  I've had several patients that would suffer a bout of depression whenever they were under the period of heightened stress, for example they would start a new job (increased stress) and become so depressed they would have two stop working then after a period of rest and recuperation the depression would subside allowing them to gain a new job and start the cycle over again.  To me it looks like some of us have delicate brains that break down too easily under stress and if we are to live healthier lives, to be able to cope with stress and fulfil our ambitions we need to compensate for our exaggerated stress responses and the apparent inability of our brains to cope our stress responses c

There is debate over how much of the over activity in the HPA-axis stress response is due to psychological factors such as a stressful conditioning childhood, a genetically inbuilt hyper active HPA-axis or even caused by the stress of living with the condition, I'm convinced it will turn out to be a mixture of all of these, however in terms of treatment I'm less concerned with who’s the chicken and who’s the egg but how can I fix it, dampen down overactivity in the HPA-axis, boost BDNF levels and grow more synapses. 

In the illustration opposite on the left you see a healthy normal brain cell with a good level of dendrites and dendritic spines, in the centre you see the condition of someone with chronic long-term depression (it would be the same with bipolar syndrome) with a significant loss of dendrites and dendritic spines, and on the right you see the effects of BDNF boosting lithium treatment with a significant regrowth and regeneration of the dendrites and dendritic spines.

In 2012 I saw this illustration and wanted to apply it to my own brain unfortunately the impressive results shown in the illustration were obtained by the use of high doses of lithium carbonate which would involve exposing myself to an unacceptably high risk of toxic side-effects including kidney damage.

In 2012 I developed a treatment protocol based entirely around the BDNF hypothesis which consists of training the brain to counteract over activity in the HPA-axis with relaxation response brain training exercises and boosting BDNF not with high dose lithium carbonate but with low-dose lithium orotate and other natural remedies, for more on this see treatment see: How to Regenerate your Broken Brain 

 Tip # 1 To make low-dose lithium effective:
Overcome overactivity in your HPA-axis that's undermining your neuroplasticity  so that low-dose lithium stand a chance at repairing, do this by first completing 100 days of relaxation response brain training exercises, then 100 days of mindfulness meditation to train your prefrontal cortex to remain still and choose what it pays attention to, mindfulness training also diminishes the size and overactivity in the amygdala.  If necessary supplement this training with psychological therapies (psychotherapy, cognitive hypnotherapy etc) to remodel stress provoking traumatic memories.


Lithium counteracts imbalanced fat metabolism in the bipolar brain

Another discovery is that people with bipolar mismanage specific fats in the brain which results in damaging inflammation and interferes with brain function.  Specifically bipolar brains release an excessive amount of the omega-6 fat called arachidonic acid that promotes inflammation and a deficiency (real or relative to arachidonic acid) of the omega-3 fat called DHA which is anti-inflammatory. 

Our body makes some arachidonic acid from the omega-6 oil (linoleic acid) found in nuts and most seed oils but we can also consume a lot of arachidonic acid directly in animal foods especially red meats and pork. Our body makes some  DHA from the oil found in a few vegetarian sources including linseeds, hemp and Chia seeds but unfortunately we only convert about 1% these vegetarian omega-3s DHA but this is not enough to obtain the therapeutic levels needed by the bipolar brain and we need to consume DHA directly by eating oily fish or taking fish oil.  

Lithium supplementation counteract the inflammation caused by the excessive arachidonic acid and deficient DHA seen in the bipolar brain {doi: 10.1194/jlr.M002469}.  

People that eat a diet containing a lot of arachidonic acid (duck, chicken, eggs) and only a little DHA (fish and fish oils) are giving the lithium they take a huge obstacle to overcome and may not obtain satisfactory results from low-dose lithium; I believe a diet low in arachidonic acid and high in DHA containing fish oil is one of the key things that enables my us to obtain effective therapeutic effects from a low dose of lithium orotate.   

This understanding shed light on something I had intuitively worked out, over several years of experimentation I became convinced that I could make my low-dose lithium supplements work better by altering the ratio of omega 6 to omega-3 in my diet.  I would cut down on foods high in omega 6 including nuts and seeds, stopped eating red meat and cut down on white meat and eggs and increased my consumption of omega-3 fish oils;  basically I ate a more plant-protein based diet low on omega 6 containing nuts and rich in fish oils.  When I was on this diet I felt that even a microbe dose of 0.1 mg of lithium from two capsules of Lithinase would have a healthy effect on my bipolar brain, it wasn't quite mood stabilising nor did I notice it improving my neuroplasticity however it was certainly capable of correcting my wayward bipolar sleep cycles. 

To me it felt like the omega-3 oils were helping the lithium to work and I cut down on omega-6 oils because  they compete with omega-3’s, I was close but it's the other way around it's the lithium that is correcting an oil imbalance in the bipolar brain and what I was doing was correcting the oil imbalance as much as I could buy the oils I ate so that even a very low dose of lithium was now capable of doing the rest so to speak.  I believe that high doses of lithium carbonate used in psychiatric medicine could probably be reduced significantly for anyone prepared to eat a healthy diet low in arachidonic acid and high in omega-3 DHA.  

 Tip # 2 To make low-dose lithium effective:

Eat a diet containing lots of DHA (800-1500 mg) and as little arachidonic acid as possible by eating little or no meat and obtaining most of your protein from from plant sources (beans and lentils) and fish.   

Low-dose aspirin assists low-dose lithium

Aother thing you can do to eke out as much from your low-dose lithium as possible is take a low dose of aspirin daily. Aspirin blocks the conversion of arachidonic acid to the inflammatory prostaglandin E2 {Prostaglandins Leukot Essent Fatty Acids. 2015 May;96:25-30. doi: 10.1016/j.plefa.2015.01.002. Epub 2015 Jan 13. Low-dose aspirin (acetylsalicylate) prevents increases in brain PGE2, 15-epi-lipoxin A4 and 8-isoprostane concentrations in 9 month-old HIV-1 transgenic rats, a model for HIV-1 associated neurocognitive disorders.
Blanchard HC1, Taha AY1, Rapoport SI2, Yuan ZX1.} and remember in the bipolar brain we already have to much arachidonic acid. There is some evidence that the addition of aspirin does indeed improve the treatment of bipolar with lithium {Prostaglandins Leukot Essent Fatty Acids. 2010 Jan;82(1):9-14. doi: 10.1016/j.plefa.2009.10.007. Epub 2009 Nov 25. Is aspirin useful in patients on lithium? A pharmacoepidemiological study related to bipolar disorder. Stolk P1, Souverein PC, Wilting I, Leufkens HG, Klein DF, Rapoport SI, Heerdink ER}.

I take aspirin daily but be advised however that daily consumption of aspirin dose come with some risks and may not be suitable for everyone. 

 Tip # 3 To make low-dose lithium effective:
Take a low dose enteric coated aspirin once a day. 

CAUTION 
Aspirin carries a small but real risk of causing ulceration and bleeding in the stomach, in rare cases this can be fatal.  So with due diligence I must recommend that you consult with your doctor before you start taking low-dose aspirin.  The risk of gastric bleeding is however very low when consuming a low-dose (75-81 mg) and the risk is further reduced when the aspirin tablet is encapsulated in a coating to protect the walls of the stomach, this is known as enteric-coated. Low-dose enteric-coated aspirin very cheap and sold without prescription as a protection against cardiovascular disease. 


Reduce vanadium to assist lithium
Lithium orotate the sale UK
Vanadium is a trace element that we naturally ingesting our diet, vanadium levels are observed to increase in the the blood during periods of both bipolar mania and bipolar depression; furthermore detoxifying excess vanadium with vitamins C has been shown to effectively reduce vanadium levels and improve symptoms.  I've been unable to establish whether or not vanadium and lithium are mineral antagonists i.e. as the level of one goes it displaces and decreases the level of the other, but I suspect it might (are there any biochemists out there that know whether vanadium and lithium are in fact mineral antagonists?).

Even if vanadium does not antagonise and compete with lithium I would still recommend taking 3 g of cheap cheerful vitamins C in a single dose every day to reduce the vanadium level and give your low-dose lithium less work to do to stabilise your condition.
low-dose lithium orotate for bipolar depression
P.S. You can take more vitamins C and better quality then ascorbic acid in addition if you want to, but for the purposes of eliminating vanadium we want a single dose of 3 g to temporarily elevate ascorbic acid levels in the blood and flush out excess vanadium. I uses three tablets of Now Foods vitamins C 1000 mg with breakfast or dinner and 1000 mg of ascorbyl palmitate a special oil soluble form of vitamins C at night at the same time I take my give three fish oils, ascorbyl palmitate delivers antioxidant activity into the oily parts of our body including the brain and in theory will protect the delicate omega-3 oils as they go to work, I can't say I noticed any significant improvement in my health when I added the ascorbyl palmitate I just do anyway.  

 Tip # 4 To make low-dose lithium effective:
Take 3 g of vitamins C every day in a single dose.


Is low-dose lithium strong enough for bipolar type I or is it just for bipolar II ?

CAUTION
We have to accept that low-dose lithium even with the assistance of the above techniques may not be sufficient to control all cases of extreme bipolar syndrome type I with hyper-mania.   remember the first rule of medicine is first do no harm so be safe and only experiment with low-dose lithium orotate as an alternative mood stabiliser when it's the right time in your life to do so and you have the appropriate support and supervision or at least knowledge in place. Having said that I do believe that if you get your diet just right, if you apply darkness therapy, either take or at least halved to the ready the appropriate anti-mania amino acids etc etc it is possible to use natural remedies and gain control over even severe cases of mood disorders.  


Lithium saves lives
Lithium is one of the few substances that specifically targets Suicide 

Lithium is also one of the very few substances known to be capable of reducing the risk of death from suicide. This affect intrigues me because although lithium is an effective mood stabiliser (anti-mania) remedy it is not particularly effective at alleviating depression and yet it has a specific anti-suicidal affect.

When you're suicidally depressed the thoughts of suicide seemed to be because of the depression so it's strange the way lithium reduces thoughts of suicide without significantly reducing the depression.  I've been suicidal many times during bouts of bipolar depression, sometimes I thought of suicide every day I had the depression however on some occasions I experienced something different I was depressed for some time without thoughts of suicide then very rapidly I became suicidal it was like a specific switch was switched on in my mind that had been switched off before.   

The speed with which the suicidality can be switched on can be surprising, once in my early 30s I foolishly stopped all my treatments to see how I would get on without them, for several weeks I was seemingly fine until in the course of half a day I went manically high then imploded then walked off into the Welsh mountains where I was on vacation climbed over a cliff sat down on a ledge and tried to overcome my fear of falling. 

The neurophysiological mechanisms of suicide perplexes me, the survival instinct is so deeply and powerfully ingrained into every living creature, when threatened people will display extreme and extraordinary behaviours to survive so what happens in the brain of a suicidal person to switch this off and override the survival instinct?  There are other very painful conditions people live with that do not drive them to suicide without the comorbid presence of depression, to me it seems there’s a very specific survival switch that gets switched off or overridden in the brains of people with depression and bipolar syndrome and lithium appears to restore or preserves that function in the brain

If you have mental health problems and thoughts of suicide recognise that you have a serious illness that's trying to kill you, it's altering your brain function and messing with your mind, the voice telling you to kill yourself is the illness speaking start taking lithium straightaway.  For more anti-suicidal treatments also see: my BDNF Boosting Treatment.  


Safety Taking Lithium 

Lithium the Thyroid and Iodine

Lithium antagonises iodine and may reduce you iodine levels, we need iodine for the proper functioning of the thyroid.  To prevent this problem I always recommend either supplementing iodine or eating lots of sea vegetables rich and iodine when taking lithium long-term.  You can supplement iodine either orally or by putting a dab of 2% iodine tincture on skin, if you do the latter is important to rotate the area of application to prevent irritating the skin.  

Lithium Sodium and De-hydration

Lithium also strongly antagonises sodium, it's known that on the high doses of lithium carbonate used in psychiatric medicine it is possible for people to become sodium deficient and so it is recommended that people on lithium carbonate include a little table salt in their diet.  It is unlikely that this would be such an issue with the very low doses of lifting from this imperative that I recommend however if over concerns of high blood pressure you have already put yourself onto a low-sodium diet it could be possible that even low doses of lithium could lead to sodium deficiency.  You can watch out for light headedness when you stand up and check for low blood pressure with a meter, if you experience either of these include a consistent amount of table salt in your diet.

The other concern with taking high doses of lithium carbonate is that it puts the kidneys and the string and it's imperative to avoid dehydration, I can't be sure but I had distinct impression when I began to take 10 mg of lithium from lithium or rotate the day that it did affect my hydration status, I sort by felt much worse than usual if I allowed myself to become dehydrated.

 Safety tip: So in summary if you going to take lithium consume plenty of iodine, adequate sodium and lots of water.

TEXT BELOW IS UNFINISHED DRAFT
How to use low dose 
In naturopathic functional medicine which I practice we are obsessive (some would say paranoid) about avoiding anything considered toxic and fear of lithium is toxicity put me off taking it myself and I wouldn't prescribe anything to my patients that I wouldn't take, but since delving deeper into lithium’s enormous benefits and discovering how to obtain the benefits without the toxicity I've completely changed my view and become a fan of lithium, I have to admit with the benefit of hindsight I regret my prior ignorance and wish I'd worked this out sooner…


Lithium is able to effectively put the brakes on the manic side of bipolar syndrome in the majority of people and smooth out bipolar mood swings. I believe that lithium administration may help reduce bipolar depression  mainly because it reduces bipolar mania and very often a bout a bipolar depression follows a bout of mania just like night follows day, so reducing the incidence of mania/hypomania events may reduce the rebound post-mania depressions but many of my patients on long-term high-dose pharmaceutical lithium complain that although it controls the ups and severe depression it leaves them suffering from unacceptable chronic low grade depression and emotional flatness. This and  worries about the toxicity of high-dose pharmaceutical lithium often leads people to discontinue its use.  

To experiences this first-hand I tried taking a relatively high doses of the lithium products I use, I quickly felt awful, drowsy and devoid of feelings, I was like an emotionless automaton going through the motions of human activities but without a heart or soul. It may help you in a crisis but for long-term use it can give you a life that is not worth living.

I would hate to have to live like that, it sounds crazy but I personally I felt I'd prefer to experience the pain of depression than to not be able to feel anything at all.  I don't want to put people off taking pharmaceutical lithium carbonate if they need to, it could be that after an initial adjustment period and by adjusting the dosage you would not have to live with such an emotionally flattened condition.

On the low-dose lithium I now take (10 mg a day) I do not experience any adverse side-effects whatsoever.  

I’d had obvious chronic depression for decades but for a long time I rejected the diagnosis of bipolar with the consequence that I did not manage the manic side of my condition and look after the health of my brain as well as I could have, bipolar especially untreated bipolar can take a tole on the health of the brain and by my late 40’s I began to see signs that my brain had been beaten up by the chronic mental health problems.   I first wanted to take receive the benefits of lithium (with other remedies) to boots the production of the protein BDNF and repair my brain, but resisted because of fear of the physical and emotionally numbing side effects I’d herd of.  

Discovering that it’s possible to obtain some powerful therapeutic effects from low-dose lithium without the side effects has helped me and the health of many of my patients. 


Why lithium is so fantastic for the brain

Without the side-effects lithium is a truly wonderful remedy for the brain of anyone with bipolar syndrome, chronic depression, cognitive impairment and recovering from stroke/brain injury; in this article I'll explain how to get the benefits of lithium without the side effects. 

I recommend lithium because it targets multiple aspects of brain health:-

-it regenerates brain the shrinkage/damage associated with bipolar, depression and cognitive decline/Alzheimer’s,
-it can also assist regeneration following stroke and traumatic brain injury,  
-it reduces the chances of bi or unipolar depression killing you,
-it treats the imbalance in the biological-clock part of the brain that causes the disturbed sleep cycles often seen bipolar syndrome, 
-it’s a mood stabiliser, what this means is firstly it can reduce the occurrence of bipolar manic events and because a manic phase often crashes into a depression lithium reduces the precipitation of depressions; furthermore by putting a ‘lid’ on the manic side lithium may enable you to use and receive the benefits of natural antidepressants at the same time without them flipping you up into another mania, I use this so-called combination treatment myself. 

lithium bipolar 2 Biochemical and Physiological Effects of Lithium Cellular Transport and the Inorganic Biochemistry of Lithium (N.J. Birch)
The chemistry of lithium is unusual. Lithium atoms are very small, highly polarized, and have a high charge density. The chemical and biochemical properties of lithium are similar to those of magnesium, with which it shares a “diagonal relationship” in the periodic table. Because magnesium plays a crucial role in the regulation of biochemical systems, it has been theorized that lithium influences magnesium-dependent processes
Lithium can be transported across membranes in five different ways. Of these, passive flux is important for the entry of lithium into cells, and sodium-lithium countertransport for the extrusion of lithium from cells. Lithium can presumably replace sodium in the sodium-sodium countertransport system, although the biological significance of the latter process is still unclear.
It appears that the concentration of lithium in cells does not reach the levels predicted by the Nernst equation. Rather, the intracellular lithium concentration is considerably lower than its concentration in blood or extracellular fluid. This is important for the models which have been proposed for its mechanism of action, as these must be able to explain the effects of lithium at intracellular concentrations of 0.1 mmol/l (i.e. similar to those seen in patients on lithium prophylaxis).
One hypothesis suggests that the biological effects of lithium are due to the role it plays at the cell periphery, where, for example, it may influence cell recognition, cell signaling mechanisms at the cell membrane, and certain immunological processes.
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Position of lithium in the Periodic System
Lithium as a Trace Element (K. Lehmann)
In humans endogenous serum lithium levels normally range from 0.14-8.6 micromol/l, with a maximum level of 15.8 micromol/l.
These lithium serum levels are 3 orders of magnitude lower than those necessary for therapeutic/prophylactic treatment.
Scientists suspect that endogenous lithium in the human body has a physiological function, although sufficient evidence of this is still lacking.
Daily lithium intake in humans is dependent on both diet and the use of medications that contain lithium. With the latter, a total of 15 micromol to 0.66 mmol of lithium may be administered per day.
Effects of Lithium on Neurotransmitters and Second Messenger Systems (D. van Calker)
Studies examining the effect of lithium ions on the synthesis and metabolism of neurotransmitters have, thus far, yielded inconsistent results, failing to shed any light on the mechanism of action of lithium in vivo.
Lithium ions prevent the development of functional supersensitivity to dopamine and acetylcholine receptor stimulation, most likely by influencing second messenger systems.
Lithium ions increase basal cAMP levels and inhibit the neurotransmitter-stimulated accumulation of cAMP in the brain and other tissues.
Acute administration of lithium inhibits the stimulation of adenylyl cyclase, most likely through direct competition with magnesium, whose hydrated ionic radius is similar to that of lithium. The effects of chronic lithium treatment, however, probably result from (a) the modification of gene expression among components of the adenylyl cyclase system, especially G protein subunits (G_i, G_s), as well as from (b) a stabilization of the inactive trimeric form of the Gi protein. Lithium has been found to increase basal cAMP levels, which is most likely due to attenuation of the Gi protein and an increase – probably resulting from the effects of lithium on gene transcription – in the levels of adenylyl cyclase type I and type II mRNA.
At therapeutically relevant concentrations, lithium ions inhibit the hydrolysis of inositol mono-phosphatase to inositol. This leads to a depletion of inositol and a strong increase in diacylglycerol (DAG) in susceptible cells and tissues, depending on species and tissue type. Susceptibility is determined by the activity of a high-affinity inositol transport system, as well as by the degree to which the inositolphospholipid (IP) second messenger system is hormonally stimulated. Pronounced inositol depletion can lead to an inhibition of the IP system in affected cells, which is probably a result of attenuated IP synthesis and/or the activation of protein kinase C (PKC) through the accumulation of DAG.
Lithium exposure facilitates the activation of certain PKC isozymes, chronic activation of which can result in a downregulation of PKC activity (i.e. a constitutive activation and redistribution in the cell nucleus). This process is probably responsible for the diverse effects of lithium on the release of neurotransmitters, the inhibition of receptor sensitization and certain membrane transport processes. By influencing transcription factors such as c-fos, this process could also be responsible for the lithium-induced changes in gene transcription which have been observed.
The inhibitory effects of chronic lithium treatment on the PI system have also been demonstrated in humans. Peripheral cells from manic-depressive patients show increased hormonal sensitivity in the phosphoinositide (PI) system. Thus, it appears that lithium ions might compensate for the hyperactivity of the PI system which is associated with illness in these patients.
The Effect of Lithium on Serotoninergic Function (B. Müller-Oerlinghausen)
In animal experiments, lithium administration results in a net rise in 5-HT activity, which is probably caused presynaptically by an increase in the release and transformation of 5-HT precursors, an increase in the release of 5-HT, and by the functional antagonism between lithium and inhibitory presynaptic 5-HT1A receptors.
However, there are considerable differences in the amount of time which elapses before each of the different effects occurs.
An increase in 5-HT uptake in the thrombocytes of depressive patients, but not in those of healthy test subjects, has been observed.
In several studies of patients and healthy volunteers on short-term lithium therapy, neuroendocrine stimulation (e.g. with fenfluramine or tryptophan) led to increased prolactine or cortisol responses via serotoninergic transmission.
The presumably adaptive mechanisms which tend to emerge after chronic lithium administration (e.g. a decrease in the number and sensitivity of postsynaptic 5-HT receptors) probably result in a stabilization of serotoninergic neurotransmission rather than a unidirectional increase in 5-HT activity.

Chronobiological Aspects of Lithium Prophylaxis (B. Pflug)
Repetitive variations with a periodicity of approximately 24 hours are part of the circadian system. This system can be found among single-celled organisms, plants, animals, and humans.
In humans the circadian system is based on a number of oscillators of varying strengths which exert mutual influence on one another. The main pacemaker of this multi-oscillatory system is the nucleus suprachiasmaticus.
Lithium ions are chronobiologically active. They influence the circardian system by modifying phase relationships and lengthening the free-running period.
During manic-depressive episodes a variety of circadian rhythm dysfunctions have been observed.
The chronobiological effects of lithium salts help explain their efficacy in the treatment of manic-depressive disorders.
The Psychological Approach to the Effects of Lithium Prophylaxis (W. Classen)
The main effect of long-term lithium treatment is based on the modification of behavior and perception. These effects can be explained within psychological models and need not be reduced to other, lower levels of explanation.
Over the last 25 years, animal studies, psychophysiological investigations in humans, and routine clinical observation have led to the development of models which help explain the psychological effects of lithium salts. The phenomenological model developed by Kropf integrates concepts of genetic disease, aspects of the illness described in psychological terms, as well as the acute and chronic effects of lithium.
Among healthy test subjects lithium can cause fatigue, apathy, irritability, alternation between increased and decreased susceptibility to external stimuli, and general feelings of illness along with negative thinking, dysphoria, and lethargy.
Depressive patients exhibit a rigid and non-regulable behavioral repertoire, both during acute episodes and over the long term. This indicates a change in mental functions, such as cognition, perception, emotions, and the ability to structure thoughts and process information. Lithium most likely modulates these processes by raising the perception threshold for various stimuli and improving information processing structures.
The aggression-dampening effect of lithium which has been observed in human and animal studies is probably due to changes in the perception of aggression-inducing stimuli, as well as to improved control over aggressive impulses accompanied by a reduction in the number of aggressive behavioral patterns. 
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