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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 7 to 31 of 31. Go back in thread:
Posted by linkadge on March 11, 2016, at 21:24:49
In reply to Re: Trying methylfolate, posted by SLS on March 11, 2016, at 17:19:30
Hi SLS.
Methylation is a complicated process, of which I know little! Methyl donors such as folic acid, b12, b6, trimethylglycine, choline, can increase SAMe production which has effects on the three primary monoamines as well as membrane function. The antidepressant effect of folates could thus be related to improved SAMe synthesis. However, I remember reading that SAMe can really lead to profound increases in dopamine vs. other monoamines. This might wreak havoc on dopamine stabilization in bipolar.
I remember reading a study in which mice were fed high levels of several methyl donors at a time. They ended up developing 'schizophrenic like' symptoms, which could be reversed by HDAC inhibitors like valproate. SAMe is notorious for exacerbating mania in bipolar, possibly due to its strong dopaminergic effect.
One issue with deplin could be the dose. It may be possible to have a folate deficiency that is overwhelmed by 7.5-15mg of methylfolate. Lower doses could prove more effective.
The OTC supplement I purchased has only 1mg in it and I am only starting with a fraction of a capsule. I can definitely notice the effect.
Linakdge
Posted by linkadge on March 11, 2016, at 21:32:34
In reply to Re: Trying methylfolate, posted by SLS on March 11, 2016, at 17:19:30
I understand that overmethylation can reduce the expression of the reelin gene. Reelin has effects on neurogenesis, synaptic density and cell to cell connections.
From Wikipedia:
"Reelin has been suggested to be implicated in pathogenesis of several brain diseases. The expression of the protein has been found to be significantly lower in schizophrenia and psychotic bipolar disorder, but the cause of this observation remains uncertain as studies show that psychotropic medication itself affects reelin expression. "
Valproate can reduce some of the hypermethylation of the reelin gene that may be present in certain models of schizophrenia / bipolar.
Article: Reelin promoter methylation in Schizophrenia...
http://www.ncbi.nlm.nih.gov/pubmed/15961543
Linkadge
Posted by linkadge on March 11, 2016, at 21:36:24
In reply to Re: Trying methylfolate, posted by linkadge on March 11, 2016, at 21:32:34
Hypermethylation of the reelin gene can decrease the expression of GAD 67, which presumably lowers levels of gabaergic signalling and possibly inducing mood symptoms in bipolar and/or schizophrenia.
In other words SAMe / deplin might reduce gaba levels over time, relative to monoamines - which could help some depressions but worsen others?
Linkadge
Posted by SLS on March 12, 2016, at 5:23:23
In reply to Re: Trying methylfolate, posted by linkadge on March 11, 2016, at 21:32:34
> I understand that overmethylation can reduce the expression of the reelin gene. Reelin has effects on neurogenesis, synaptic density and cell to cell connections.
You're hurting my brain.
:-)
- Scott
Posted by stan_the_man70 on March 12, 2016, at 8:06:42
In reply to Trying methylfolate, posted by linkadge on March 10, 2016, at 17:41:25
---------------------quote reference
http://www.ceu-usa.com/courses/Wc001/test_drive/methylation_cycle.htm
---------------------end quotePlease read this on the website to see all the pretty diagrams.
Nutrition and Mental Health: Professional Issues and Ethics
The Methylation Cycle
The second Key. So far we have reviewed some specific supplements that help relieve depression. We discussed each in isolation. But we haven't talked about that second Golden Key yet. This Key brings many of the puzzle pieces solidly together, making things simpler. It explains why certain vitamins, minerals, and other nutrients can reduce depression.
What is this concept? It's called the Methylation Cycle, and it's a rather complex topic. Fortunately, we can vastly oversimplify it and still gain all the understanding we need! With the goal of simplification in mind we now present ...
A Mickey Mouse explanation of the Methylation Cycle. As we have seen, the body makes different neurotransmitters out of particular amino acids. To do this, it usually changes the amino acid slightly. It does this mostly by sticking one or more methyl groups onto the amino acid. This is called Methylation.
A methyl group is one carbon (C) atom with two hydrogen (H) atoms stuck on it. The result looks a bit like Mickey Mouse -- a big round thing (the face) with two smaller round things (the ears) at the top. The body can't make methyl groups out of nothing. So it has to have a supply of these units to work with. The Methylation Cycle is the body's way of supplying these methyl groups. The diagram below is a simplified view of the Methylation Cycle. Let's see how it works.From A to B. The Methylation Cycle carries methyl groups around the body like railcars on a circular track. Because the track goes around in a circle, we could start anywhere. But let's start at the bottom, at point A. There a methyl group is attached to a molecule called SAM. The SAM molecule carries the methyl group to the place where it will be used -- point B. When it gets there methylation happens. Methylation is just a word meaning that the methyl group is popped off the SAM molecule and stuck on an amino acid to make a neurotransmitter.
From B to C. What happens to the SAM molecule when the methyl group is taken off? When the methyl group is gone, the molecule is not SAM anymore. It turns into a different molecule called Homocysteine. Now we've moved from point A all the way to point C.
From C back to A. Here's where things get tricky. The body normally recycles Homocysteine back into SAM -- from point C back to point A. A new methyl group is added to turn the molecule back into SAM again. Then the cycle is complete. The molecule goes round and round -- A-B-C-A-B-C-A-B-C, etc -- carrying methyl groups where they are needed. That's why we call it a Cycle. But that can happen only if there's enough of certain vitamins and nutrients around -- vitamin B12, folic acid, and a nutrient called TMG. These things enable the recycling. They have to be present, or the Homocycteine can't be changed back into SAM.
A depressing shortage. So what happens if the required nutrients just aren't there? Look at the diagram to the right. The Homocysteine doesn't get recycled. Instead, it simply piles up at point C unchanged. Big dollops of it accumulate. Because Homocycteine isn't being changed back into SAM, a shortage of SAM soon develops. And when there is a shortage of SAM, not as many neurotransmitters are made. So soon there is a shortage of neurotransmitters, too. The shortage includes Serotonin and Norepinephrine, those anti-depression neurotransmitters. A "chemical imbalance" -- the very kind the antidepressant ads talk about -- has appeared. The individual gets depressed.
Insight! Now we see why deficiencies of specific vitamins and minerals can lead to depression. The shortages tied to depression are of the very nutrients required to keep SAM circulating. When they aren't there, the SAM dries up. That's why supplementing with those vitamins and minerals can help with depression.
Why SAMe works. Understanding the Methylation Cycle also helps us understand why the supplement SAMe can help relieve depression.
SAMe is a special form of SAM designed to be taken orally. Taking SAMe increases the available supply of SAM in the body. That leads to increased methylation, and so to increased production of neurotransmitters. It quickly revs up the methylation process to bring neurotransmitter production back up. That can quickly relieve depression.
SAMe doesn't help with recycling Homocysteine, though. That substance continues to build up. Even so, supplementing with SAMe can provide a band-aid solution. It can power up methylation until something can be done to bring Homocysteine recycling back to normal.
The real fix. If SAMe is just a band-aid solution, what's the real fix? The only way to restore the Methylation Cycle to normal is to provide adequate vitamins and nutrients to recycle all the homocysteine that's lying around. Is this hard to do? Not at all! The individual just needs to take therapeutic amounts of vitamins B-12, Folic Acid, and TMG. There is no particular hazard associated with use of these supplements. Improvement may take a couple of months, but that's how it's done.----------------------------------------------------
Copyright (c) 2005 by Thomas Whitehead, All Rights ReservedNOTE: For purposes of our discussion we have drastically simplified the Methylation Cycle. We kept the basic idea, but eliminated all the messy details. In fact, we left out most of the steps in the Cycle! If you're interested, you can view a more realistic diagram of the Methylation Cycle here. Readers who wish to go beyond our "Mickey Mouse" presentation may find the following book helpful.
Further reading: For a more complete -- but still pretty simple -- exploration of the topic of methylation, read Craig Cooney's book Methyl Magic: Maximum health through methylation. Book is out of print, but used copies are still available at low cost.
Posted by stan_the_man70 on March 12, 2016, at 8:18:01
In reply to Mickey Mouse Cycle, posted by stan_the_man70 on March 12, 2016, at 8:06:42
---------------------------quote reference
http://ihateticks.me/2014/10/06/methylation-for-dummies/
---------------------------end quoteMethylation for Dummies
VH / October 6, 2014pretty picture:
https://ihateticks.files.wordpress.com/2014/09/yasko-methylation.jpg
Posted by SLS on March 12, 2016, at 10:57:51
In reply to Nice Diagram, posted by stan_the_man70 on March 12, 2016, at 8:18:01
Thank you. Very interesting stuff.
- Scott
Posted by Larry Hoover on March 12, 2016, at 13:51:40
In reply to Re: Trying methylfolate, posted by linkadge on March 11, 2016, at 16:12:51
> Hi Larry,
>
> Thanks for the reply. You are certainly the person to confirm the authenticity of my supplement's contents.
>
> It says each cap contains:
>
>
> L-Methylfolate (calcium L-5-methyltetrahydrofolate) 1mg
>
> Vitamin B12 (methylcobolamin) 2.8 mcg
>
> Vitamin B6 (pyridoxal-5'-phosphate) 2mg
>
> Is this the real deal?
>
> LinkadgeYes, it is.
I compared it to Deplin, on the basis of dose. Deplin has two doses, 7.5 and 15 mg. The same company also produces a 1 mg dose, but they don't call it Deplin.
Your supplement is great, as it also has small amounts of other B-vitamins. B-vitamins interact considerably, so if you were just taking a single B-vitamin, the increased demand for other B-vitamins that participate in the same enzymatic pathway would have to met from other sources. Whoever made your supplement anticipated the amount of other B-vitamins that were needed by your body to not substitute one deficiency condition for another.
In case you might consider increasing your dose in the future, it would be perfectly safe to do so.
Best,
Lar
Posted by Larry Hoover on March 12, 2016, at 14:01:49
In reply to Re: Trying methylfolate, posted by linkadge on March 11, 2016, at 16:25:37
The over/under methylation concern in bipolar disorder is not settled science. The following text is one doctor's perspective on the subject.
"Bipolar disorder is not a single condition, but an umbrella term which includes a number of very different biochemical abnormalities. Im bothered by any attempt to generalize over the bipolar phenotypes & to blindly recommend any formulation or therapy for all of them. The key is to determine a patients biochemical individuality, and to provide focused appropriate treatment. In our database of 1,500 bipolar patients, about 25% are overmethylated, 35% are undermethylated, and the remaining 40% do not exhibit a methylation disorder.
The three primary biochemical classifications of bipolar disorder are the following:
A. Undermethylation: This condition is innate & is characterized by low levels of serotonin, dopamine, and norepinephrine, high whole blood histamine and elevated absolute basophils. This population has a high incidence of seasonal allergies, OCD tendencies, perfectionism, high libido, sparse body hair, and several other characteristics. They usually respond well to methionine, SAMe, calcium, magnesium, omega-3 essential oils (DHA & EPA), B-6, inositol, and vitamins A, C, and E. They should avoid supplements containing folic acid. In severe cases involving psychosis, the dominant symptom is usually delusional thinking rather than hallucinations. They tend to speak very little & may sit motionless for extended periods. They may appear outwardly calm, but suffer from extreme internal anxiety.
B. Overmethylation: This condition is the biochemical opposite of undermethylation. It is characterized by elevated levels of serotonin, dopamine, and norepinephrine, low whole blood histamine, and low absolute basophils. This population is characterized by the following typical symptoms: Absence of seasonal, inhalent allergies, but a multitude of chemical or food sensitivities, high anxiety which is evident to all, low libido, obsessions but not compulsions, tendency for paranoia and auditory hallucinations, underachievement as a child, heavy body hair, hyperactivity, nervous legs, and grandiosity. They usually respond well to folic acid, B-12, niacinamide, DMAE, choline, manganese, zinc, omega-3 essential oils (DHA and EPA) and vitamins C and E, but should avoid supplements of methionine, SAMe, inositol, TMG and DMG.
C. Pyrrole Disorder: This condition, also called pyroluria, is a genetic stress disorder associated with severe mood swings, high anxiety, and depression. The biochemical signature of this disorder includes elevated urine kryptopyrroles, a double deficiency of zinc and B-6, and low levels of arachidonic acid. Pyrolurics are devastated by stresses including physical injury emotional trauma, illness, sleep deprivation, etc. Symptoms include sensitivity to light and loud noises, tendency to skip breakfast, dry skin, abnormal fat distribution, rage episodes, little or no dream recall, reading disorders, underachievement, histrionic behaviors, and severe anxiety. They usually respond quickly to supplements of zinc, B-6, Primrose Oil, and augmenting nutrients.
To me, a bipolar patient who becomes well with greatly-reduced medication requirements may have achieved complete success. I dont believe that medication doses need to go to zero, as long as side effects are absent and long-term effects are minimal or absent.
Incidence of bipolar depression (diagnosis during lifetime):
TOTAL POPULATION OF ADOPTEES INCIDENCE = 4.5%
FRATERNAL TWINS SEPARATED AT BIRTH . Concordance = 32%
IDENTICAL TWINS SEPARATED AT BIRTH . Concordance = 80%We have seen more than 1,500 patients diagnosed with bipolar disorder, including a few hundred who presented with a diagnosis of rapid-cycle bipolar disorder. Many of the rapid cycle patients exhibited a severe pyrrole disorder as their primary imbalance. The key lab test is urine kryptopyrroles. Most pyrolurics are prone to high anxiety, severe mood swings, depression, and may be famous for their temper. Classic symptoms include aversion to eating breakfast, poor dream recall, sensitivity to bright lights & loud noises, abnormal fat distribution, poor short-term memory (often coincident with good long-term memory), and very poor stress control. (Feb 27, 2003)
We have worked with more than 1500 bipolar patients & found that most have an atrocious diet. I remember one young man whose only dietary intake for the past month consisted of Pepsi and potato chips.
In our experience, best results are achieved with a two-step procedure: (1) biochemical treatment followed by (2) life-style changes including a better diet. We learned the hard way that most bipolars are incapable of life-style changes until after their chemical imbalances have been corrected (or at least lessened). Once real biochemical progress has been made, the patient is more functional and real dietary improvements can be achieved. Trying to everything at once tends to overwhelm the patient, and they usually give up. (March 6, 2003)
About 20% of patients labeled as bipolar have a pyrrole disorder (genetic) which is associated with (a) fatty acid abnormalities, especially depressed arachidonic acid, (b) strikingly weak immune function, and (c) severe metal oxidative stress. The definitive test for the pyrrole disorder is urinalysis for kryptopyrroles (Direct Healthcare Access is the lab, 847/299-2440). These patients might benefit greatly from therapy concentrating on zinc, B-6, and primrose oil (or borage oil). Omega-3 oils can make things worse because of the competition for Zn & B-6 between delta-5 desaturase and delta-6 desaturase.
If a patient has a pyrrole disorder he/she likely would have at least half of the following symptoms:
Poor stress control
Sensitivity to bright lights and/or loud noises
Preference for spicy or heavily flavored foods
Significant growth after age 16
Morning nausea
Tendency to skip breakfast
Poor dream recall
Emotional outbursts
Poor short-term memory, perhaps coincident with excellent L.T. memory
Diagnosis of rapid-cycle bipolar
Much higher capability & alertness in the evening, compared to mornings
Dry skin
Reading disorder. (March 27, 2003)From http://www.alternativementalhealth.com/commentary-on-nutritional-treatment-of-mental-disorders-2/
Lar
Posted by TriedEveryMedication on March 13, 2016, at 15:52:27
In reply to Trying methylfolate, posted by linkadge on March 10, 2016, at 17:41:25
not sure if 1mg is enough.
I have the mutation and I'm currently taking 15mg/day
not sure it's doing anything, though.
btw, you can get deeply discounted real deplin from "brand direct health" (which I think is affiliated with Nestle medical who makes deplin).
Also a decent generic l-methylfolate that comes in 7.5 and 15mg doses is called "Methyl-pro" or something like that.
Posted by linkadge on March 13, 2016, at 18:33:35
In reply to Re: Trying methylfolate » linkadge, posted by Larry Hoover on March 12, 2016, at 13:51:40
I tend to be sensitive to supplements (especially B vitamins). I am currently taking about 0.5mg of the methylfolate.
I have noticed some improvement in mood and energy, but a bit of restlessness as well. I will give it a few more days then possibly try a higher dose.
Linkadge
Posted by linkadge on March 13, 2016, at 18:49:10
In reply to Re: methylation hypothesis, posted by Larry Hoover on March 12, 2016, at 14:01:49
Hi Larry,
Thanks for this. I gathered that the whole methylation thing is a bit on the alternative side. You don't hear mainstream science mention methylation too much in psychiatric disorders, but it has been welcomed with open arms by the alternative autism, bipolar, depression, schizophrenia, and personality disorder community.
Mainstream science does, however, acknowledge the antidepressant effects of agents like methylfolate and SAMe.
The other big unknown for me (as I am not a geneticist by any stretch) is the connection between nutritional methylation and gene methylation. Individual genes can become 'hyper methylated' but I don't know whether this has anything to do with an excess or deficiency of methyl donors, or if this has more to do with individual genetic variation / life experiences (or none / all of the above).
Many psychiatric medications are HDAC inhibitors (i.e. imipramine, amitriptyline, citalopram, valproate, lithium), which I understand can lead to de-methylation. This enters epigenetics which is way out of my league. I'll wait for the "for dummies" book.
Linkadge
Posted by linkadge on March 13, 2016, at 19:33:20
In reply to Re: methylation hypothesis » Larry Hoover, posted by linkadge on March 13, 2016, at 18:49:10
I did a 20 min crash course on Wikipedia:
I gathered the following:
-Histones prevent gene transcription
-Acetylated histones are less able to bind less to DNA to prevent transcription
-Histone deacetylase HDAC removes acetyl groups from histone allowing them to more effectively prevent gene transcription
-HDAC inhibitors block histone deacetylase, which reduces histone deacetylation, which allows more acetyl groups on this histone, which makes the histones less able to bind to DNA to prevent gene transcription** Net effect of HDAC inhibitors is to enhance gene transcription
Methylation is related to deactylation in that they both result in more condensed DNA (which reduces gene transcription).
HDAC inhibitors can thus inhibit the reduction in gene transcription brought on by DNA methylation.
But, if methylation decreases gene transcription, how does this improve depression?
I know nothing.Linkadge
Posted by SLS on March 14, 2016, at 13:21:28
In reply to Re: methylation hypothesis, posted by linkadge on March 13, 2016, at 19:33:20
> But, if methylation decreases gene transcription, how does this improve depression?
BDNF is one example of a histone induced epigenetic change in gene transcription that results in a reduction in BDNF synthesis.
This is why I was curious as to whether there were a way to reduce methylation. Does desipramine do this? I'm taking desipramine and lithium.
- Scott
Posted by linkadge on March 14, 2016, at 19:35:00
In reply to Re: methylation hypothesis » linkadge, posted by SLS on March 14, 2016, at 13:21:28
Hi SLS,
From what I read, many antidepressants and mood stabilizers can counteract the effects of the hypermethylation in a certain brain region. For example, in schizophrenia there is a hypermethylation in the prefrontal cortex, which reduces expression of the reelin gene and gad 67. This would be expected to reduce connectivity and gaba levels in the prefrontal cortex. In animal models, valproate can reverse the changes to reelin and gad67.
From what I read, HDAC comes in different forms, depending on the location in the brain.
Some antidepressants can directly reduce the methylation in a widespread manner (ie amitriptyline) others inhibit HDAC which, can reverse some of the effects of the hypermethylation.
In one article I read, a common targets of antidepressants was to induce H7 acetylation in the nucleus accumbens, which functionally blocked the hypermethylation in this region induced by repeated social defeat. Animals that were resistant to the social defeat, didn't exhibit the hypermethylation. I am assuming the hypermethylation, functionally supresses activity of that particular region.
Like you say, hypermethylation of BDNF or the serotonin transporter are also present in some models of depression. This may be why SERT and BDNF are usually diminished in depression.
What I don't know, is whether "methylating agents" would functionally increase gene methylation in a nonspecific fashion.
How does this improve depression? Is it enhanced methylation of certain 'bad regions' aka increasing methylation of stress response systems might reduce stress reactions (?)
But yes, to answer your question, from what I have read, antidepressants and mood stabilizers (including lithium) tend to decrease gene methylation.
Linkage
Posted by linkadge on March 14, 2016, at 19:50:37
In reply to Re: methylation hypothesis » SLS, posted by linkadge on March 14, 2016, at 19:35:00
Here is an interesting study in which amitriptyline and valproate are shown to induce different degrees of gene demethylation (in different brain regions). Interestingly, valproate induced demethylation strongly at GLT-1 (glutamate transporter) whereas amitriptyline did not. This would be expected to result in increased activity of the glutamate transporter after valproate administration (functioning enhancing glutamate reuptake).
http://www.nature.com/npp/journal/v35/n3/full/npp2009188a.html
This is interesting. We know so little about the widespread effects of these drugs. Just because the drug directly affects one target, does not mean that other targets, modified more slowly by changes to gene transcription, are not the more active targets.
Linkadge
Posted by SLS on March 14, 2016, at 20:40:47
In reply to Re: methylation hypothesis » linkadge, posted by linkadge on March 14, 2016, at 19:50:37
Thanks.
I appreciate your hard work.
- Scott
Posted by Tomatheus on March 14, 2016, at 20:57:03
In reply to Re: methylation hypothesis » linkadge, posted by linkadge on March 14, 2016, at 19:50:37
Linkadge,
I've been learning a lot from reading the information that you've been putting forth about methylation on this thread. There are without question a lot of things to consider as far as methylation, hypermethylation, and demethylation are concerned, and I think it's interesting how different therapeutic agents can influence not only methylation itself, but also some of the effects of methylation. In particular, I think it's helpful to know about how psychiatric medications can influence methylation, because many of us who either take medications or have taken them don't always consider the extent to which medications might exert effects in the brain and elsewhere in the body that might not be so closely connected with the most commonly known pharmacological actions of the medications. As you said, there is a lot that we don't know about the widespread effects of these drugs, and it could very well be the case that some of the effects of psychiatric medications that aren't so well known might have more to do with their benefits than most of us think. So, thank you for your posts here. I hope that you're still noticing benefits in connection with your methylfolate trial, and I hope that you'll keep noticing methylfolate-related benefits as time goes by.
Tomatheus
Posted by linkadge on March 15, 2016, at 16:15:10
In reply to Re: methylation hypothesis » linkadge, posted by Tomatheus on March 14, 2016, at 20:57:03
The methylfolate is still providing some improvement, but I have noticed I noticed the need to take a periodic break. It seems to be fairly strong for me.
Linkadge
Posted by linkadge on March 16, 2016, at 19:12:58
In reply to Re: methylation hypothesis, posted by linkadge on March 15, 2016, at 16:15:10
http://www.karger.com/Article/PDF/337590
Linkadge
Posted by SLS on March 17, 2016, at 2:24:56
In reply to DHA on methylation, acetylation and neuoprotection, posted by linkadge on March 16, 2016, at 19:12:58
> http://www.karger.com/Article/PDF/337590
>
> LinkadgeBased on the article, is it bad to take in the zinc found in a multivitamin?
- Scott
Posted by linkadge on March 18, 2016, at 18:40:18
In reply to Re: DHA on methylation, acetylation and neuoprotection » linkadge, posted by SLS on March 17, 2016, at 2:24:56
Hmm. It could be the dose involved with the Zinc that caused the problems. I understand that sufficient zinc is needed for proper brain functioning but elevated levels can be neurotoxic. I don't know if it is related to NMDA hypofunction.
I understand that NMDA antagonists (in higher doses) like ketamine can induce 'dopamine agonist like' neuronal changes and behavioral modifications. Like stimulants, higher doses of NMDA antagonists can mimic a certain forms of schizophrenia and associated brain changes (i.e. decrease in neuroprotective BCL-2 protein). DHA appears very helpful in bipolar / schizophrenia and has many actions in common with mood stabilizers like valproate - especially in mood disorders associated with low BCL-2 and other neuroprotective factors.
Linkadge
Posted by linkadge on March 18, 2016, at 18:44:24
In reply to Re: DHA on methylation, acetylation and neuoprotection » linkadge, posted by SLS on March 17, 2016, at 2:24:56
To be honest, I probably have a bipolar genetic disposition which has been controlled by lower does of lithium and omega-3.
Linkadge
Posted by herpills on March 20, 2016, at 20:44:47
In reply to Re: Trying methylfolate, posted by SLS on March 11, 2016, at 6:56:21
>
> I just want to mention that a recent study of the combining of Lamictal and Seroquel (to be found in the Bipolar Network Newsletter) reported that there was a worsening of depression when methylfolate was added. It was an unexpected result. The study hasn't been published on the Internet yet. I experienced a worsening of my bipolar depression after the addition of methylfolate (Deplin) to Lamictal and several other drugs. I experienced a brief period of improvement during the first few weeks before feeling worse. After discontinuing the methylfolate, I felt better immediately. I don't know if my experience corroborates the results of the study.
>
>
> - Scott
>
>I always wondered if there was a misunderstood interaction between methylfolate and Lamictal.
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In reply to DHA on methylation, acetylation and neuoprotection, posted by linkadge on March 16, 2016, at 19:12:58
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This is the end of the thread.
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