I have a friend that is trying to get off antidepressants for a second time. When she stops taking them she gets what she calls 'brain zaps', a sort of periodic electrical tingling in her head. The first time she went off them she had these zaps for 5 years, hence the return to the drugs a second time. She is in fairly good shape, in her mid 50's, has been a vegetarian for most of her adult life, is a little on the high blood pressure side and says she feels issues with her kidneys and is a little gouty. She doesn't drink and isn't into cannabis.
Does anyone have any suggestions? I really appreciate it.
Location: North Georgia / Appalachian mountains , Zone 7A
posted 6 years ago
She ruled out the one thing that saved ME from depression.
I'm not even sure if I would be alive today if it were not for "the-miracle-plant-that-must-not-be-mentioned"
To those that have never experienced the endless torture of depression,
its not just feeling down, it is like having a gorilla sit on you on the bottom of an ocean.
Good luck to your friend.
J W Richardson
Location: Council, ID
posted 6 years ago
I'm totally with you on that one! I was on and off Welbutrin a couple times myself, while I was living in the city and going through menopause/ 2008 business crashing/bad relationship. I guess mine was situational! Back living on the land now. and feeling alive and worth something again. Never had these brain zaps, just a facial tic for a while that could have been related, I guess.
My friend isn't depressed now, but these electrical pulses drive her crazy and she can't figure out how to get rid of them.
since you mentioned brain zaps, I assume the antidepressant in question is an SSRI. I suggest your friend get a prescription for the drug in liquid form and slowly reduce the dose over a period of months rather than just quit taking pills all at once. if her current doctor won't prescribe the liquid, find a different doctor.
I like Morgan's valerian suggestion, too. passionflower is another option I'm familiar with that might help get her through the weaning period.
probably also a good idea to make sure she's got another plan for handling the depression. I think quitting antidepressants is a good move, but not if nothing else is done to address the issue. whether that's counseling, diet or lifestyle changes, medicinal herbs, acupuncture, or something else, just doing nothing doesn't strike me as a viable solution.
I guess these zaps are a fairly common part of what they are calling antidepressant discontinuation syndrome. The idea of getting back on and then reducing them slowly makes a lot of sense to me, plus the herbs to assist.
I talked to her again and got more details. She was taking Efflexor, first went cold turkey for a couple of days and had major issues that felt like she should go to the hospital. She started taking them again and did the slow detox, but the zaps never went away for 5 years. Got back on them, did slow detox, but still the zaps. I wonder about taking St. John's Wort since they stop when on an SSRI.
Symptoms described as "brain zaps", "brain shocks", "brain shivers", "brain pulse-waves", "head shocks", "pulses", "flickers", or "cranial zings" are withdrawal symptoms experienced during discontinuation (or reduction of dose) of antidepressant drugs. These result from a global downregulation of serotonin in response to increased levels of serotonin in the synaptic cleft, but the specific mechanism through which this creates symptoms is not understood. Common responses to dose reduction or cessation include dizziness, electric shock-like sensations, sweating, nausea, insomnia, tremor, confusion, nightmares, and vertigo. The MedDRA "preferred term" for coding these types of symptoms in adverse drug reaction reports (for use in pharmacovigilance databases such as under the Yellow Card Scheme) is paraesthesia.[
Sounds like fun.
Location: woodland, washington
posted 6 years ago
might be a long shot, but I've just read that more muscular folks produce more serotonin because muscles use up most amino acids, but not tryptophan. a high ration of tryptophan to other amino acids increases serotonin in the body.
I don't know that trying to fudge serotonin levels is going to be the solution, though. it could work, but an extreme example of that is what led to the brain zaps in the first place.
There is the other one i was looking for .... damiana.
usually from the health food store for tea. they sell in Mexico for libido, but seems to have good brain chem function. Especially if you buy the Liqueur...
Would also try first is soaking feet in epsom salts.
Magnesium shortages allow the calcium and potassium to swing really wide. I like "magnesium oil" for deodorant better, easier to absorb, as it is still only mag and water.
Best buy at Swanson Vitamins.
In Germany the classic herb against depression is St. Johns wort. Just the tea. I don't know how the healthcare system over there works, but
I would suggest get a decent psychologist to clear up the underlying cause. That might not be an option because it is expensive.
Mindfull meditation might be helpful too, just ask at the next Buddhist center around here they are very cheap.
It seems like messing with serotonin levels with the heavy artillery is pretty fraught with problems. .
Depression isn't an issue any more for either of us - I think menopause hits some people really hard because your body is telling you that if you can no longer reproduce, what good are you? It's a phase on the way to finding a different worth as a crone, I think.
We were talking today and it sounds like she could use a good cleansing diet along with some of these suggestions. I'm a big fan of magnesium myself - I'll have to check out the deodorant!
I've been collecting roots and herbs lately, using TCM tonic/liver roots to make scrumptious broths for soup bases. I'll look into damiana. She has some St. John's Wort, which might be a better alternative if nothing else works.\
It's amazing what tweaks to the diet can do to one's head space - I'm in this tiny town, and there are several folks who have gone off gluten and seen huge differences in mood.
It takes several weeks for the St. John's Wort to be effective. I've found it to be just fine as a preventative, although in reality my depressive episodes end when the stress that was causing it ends. Really, that is the truth. SSRIs can be less difficult to get off of if you titrate down by fooling the body's natural cycle. I can't remember exactly but it works something like this: take a full dose, the next day take half a dose the next day take a full dose and then cut your full dose in half. Repeat process until the full dose is next to nothing, a fingernail full of powder, then a few grains. You can take as long as you like to do this.
I will mention make sure that backing off the medicine is slow - they are not designed for fast withdrawal. You can add herbs to help build support while you are backing them down. The gouty stuff seems to happen in the early spring anyway, so that might be an issue - now that it is after full moon it could be easier to start, since toxins flow out easier with waning moon. Start further research here: http://www.herballegacy.com/Depression.html and as far as using St. John's Wort (which I love), I know that it doesn't "play well" with many pharmaceuticals, changing their actions. If you can, look up any interactions (Jonathan Treasure's work is the best reference for this).
St. Johnswort does speed up one of the liver detoxification pathways, increasing the effective dose of pharmaceuticals (because the drug is cleared from your body faster). I believe most trials on this, including those listed in Treasure's work, used standardized extracts of St Johns. The tea will not have as strong an effect in this regard, but it's probably still a good idea to ask your doctor if you're on any life-dependent drugs, e.g. blood thinners or blood pressure regulators, before beginning a regimen with St Johns (also note that it may affect the dose of oral contraceptives!)
I would want to know more about the depression, diet, lifestyle, etc before recommending other herbs that could help. One thing you could try, however, is supplementing with the mood chemical precursors. I've found that supplementing with 5-HTP (precursor to serotonin and melatonin, metabolized from tryptophan) and Tyrosine (precursor to dopamine, adrenaline, noradrenaline, thyroid hormones, etc) helps withdrawal symptoms for those experiencing haziness and depressed mood after long-term cannabis use. It's worth a shot. Tulsi/Holy Basil is also a great herb for bringing clarity to the mind and opening the lungs (increased respiration = more connection with heart-centered consciousness). Try a tea of Tulsi and Rose petals to help bring calm to mind and heart.
Meditation and removing all possible stressors will also help.
I've attached Treasure's work on St Johns if anyone is interested in reading through the full scientific explanation.
Yum, Holy Basil (Tulsi) I also thought of another herb to consider other than St. John's Wort or Kava Kava - and that is Mimosa (Albizzia julibrissen) which has heart action, but is a specific for depression. It could be a good match for your situation. If other heart-type herbs are desired, I would also look into Hawthorne (heart food) and Motherwort (can be strong for some people but if it is a good match, it is great).
Lisa Allen MH (AstroHerbalist)
posted 6 years ago
Yes to all of those! I do love Albizzia for relaxing into the heart space. Also, call upon some Linden Flower to remind the heart of the joy in life.
Location: San Diego, CA USA
posted 6 years ago
Oh super-yum - Linden Flowers! I think I will go get a cup of tea myself hehe!
Antidepressant epigenetic action of a common fitness supplement
A short note on the history of antidepressant research: From MAOIs/SSRIs to ketamine and BDNF
Traditional antidepressants, like Prozac, don’t work too well. Back in the 50s, researchers thought that depression was caused by a depletion of a group of neurotransmitters in the brain known chemically as the monoamines (i.e. serotonin, noradrenaline, dopamine). Hence, the reasoning goes, upping monoamine levels should treat depression. Unfortunately, even first-line drugs (such as Prozac) are effective for only ~40% of Major Depression cases. They also have a delayed onset time of weeks to months, and are accompanied by a slew of nasty side effects. In 2006, the field of antidepressant research was shocked by the discovery that ketamine – a dissociative club drug – has fast-acting antidepressant & anti-suicidal affects lasting longer than the duration of the drug. Ketamine works on the glutamate system, which is the main excitatory neurotransmitter in the brain, and results in a rapid increase of a protein called Brain-Derived Neurotropic Factor (BDNF). BDNF increases the formation of new synapses and reverses neuronal abnormalities in the prefrontal cortex. On the circuit levels, this leads to functional “rewiring” or “resetting” of connection between neurons, which may underlie rapid behavioral changes seen with ketamine administration. This discovery led to the “synaptogenic” hypothesis, which stipulates depression is not due to lack of monoamine neurotransmitters per se, but the inability to maintain normal synapse formation. It seems like the antidepression field is going through a paradigm shift, placing BDNF and the glutamatergic system front and central as targets for new generation antidepressant targets. Exciting times!
Screen Shot 2013-04-02 at 4.36.39 PM
Depression literally wilts your brain. In patients suffering from major depressive disorder (MDD) and rats undergoing chronic stress, their neurons are fewer, smaller, and host shrunken dendrites with malfunctioning synaptic connections. MDD patients also generate fewer new neurons, effectively cutting off the supply chain. All these morphological and functional changes lead to disrupted neuronal communication in the cognitive-emotional circuitry, leading to depressive symptoms. Tranditional antidepressants, like Prozac, can block or reverse these deficits – but only in ~40% MDD patients. They also require weeks to months to work, and often come with intolerable side effects. Not good!
In search for fast-acting antidepressants, researchers stumbled upon ketamine, the notorious dissociative club drug, which amazingly reverses depressive symptoms only hours after administration. Ketamine’s magic lies in its ability to act on the excitatory glutamate neurotransmitter system, causing an increase in the “nurturing” protein Brain-Derived Neurotropic Factor (BDNF), which leads to formation of new synapses. Unfortunately, although valuable, ketamine’s psychoactive effects and addictive potential lowers its potential as an antidepressant pill.
Is this the answer? Soooo many brands available OTC.
…And somehow, researchers find a fitness supplement.
Nasca et al. 2013. L-acetylcarnitine causes rapid antidepressant effects through the epigenetic induction of mGlu2 receptors.PNAS 110 (12):4804–4809.
L-acetyl carnitine (LAC) is an amino acid derivative involved in energy metabolism and fatty acid oxidization, and is frequently sold as an energy-enhancing fat-loss supplement in fitness stores. Clinically, it is used to treat pain by acting on the epigenome – changing the expression of certain genes. Namely, LAC increases the expression of a glutamate receptor, mGlu2. Since mGlu2 is lowered in a genetically depressed line of rats (named FSL), the authors hypothesized that LAC may have anti-depressive effects through an epigenetic mechanism.
To test this, the authors got ahold of two strains of rats: the spontaneously depressive FSL, and the depression-resilient FRL. They also pitted LAC against a traditional SSRI antidepressant, chlorimipramine (CLO). Now, how do you tell is a rat is depressed? Here, the authors used two main tests, the forced swim test, and the sucrose preference test. The former measures how much a rat is willing to fight for its life (depressed rats give up faster) while the later measures whether a rat takes pleasure in sweet tasting food (depressed rats show lower desire for sugar). FSL rats treated daily with LAC showed improved symptoms after only 3 days of treatment, while CLO took 14 days to see such an effect. LAC-treated rats also showed increased levels of BDNF, which as mentioned before, is crucial for the generation of new synaptic connections.
Forced swim test: depressed rats are less willing to swim.
Forced swim test: depressed rats are less willing to swim.
When researchers stopped giving the drugs (look at “days of withdrawal”), depressive symptoms rapidly came back in the CLO-treated group, but the effect of LAC persisted for at least 2 weeks after the treatment stopped. Unsurprisingly, none of the drugs affected the depression-resilient FRL rats. The authors further verified LAC’s antidepressant effects with a mice model of chronic stress exposure, which is thought to be a primary environmental cause of depression in humans.
Now we have a “black box”: in goes LAC, out comes happier rat. What’s happening inside the box? Well, the effect of LAC was abolished when coadministered with a mGlu2/3 blocker, suggesting that LAC is acting through mGlu2/3 to exert its effect. As mentioned before, mGlu2 levels in the hippocampus and prefrontal cortex are lower in the depression-prone FSL rats; LAC treatment increased both mGlu2 mRNA and protein levels to that of the FRL controls. Further analysis with pharmacological inhibitors showed that a transcription factor called NF-kappaB is involved in the upregulation of mGlu2 induced by LAC. A transcription factor acts as a “messenger”, mediating interactions between the environment and gene expression by directly binding to promotors on certain genes. Finally, LAC also changed the conformation of the histone proteins that the mGluR & BDNF gene is wrapped around, leading to a more “open” conformation that allows easier access to transcription factors to enhance gene expression. Essentially, all of the above shows that LAC can increase expression of mGlu2 and BDNF through an epigenetic mechanism, and (maybe) lead to formation of new synapses down the road.
Acetylcarnitine (the “AC” part of “LAC”) is produced naturally in the body, and can be acquired through diet by eating meat and diary (vegetarians are often deficient). Interestingly, the authors found that endogenous LAC levels were reduced by 40-60%in the prefrontal cortex and hippocampus of FSL rat, which may be one of the reasons they respond to LAC treatment. The authors didn’t further pursue this point – does low endogenous LAC predispose a person to depression? Is supplementing LAC “rectifying” this deficiency? LAC is heavily involved in fat metabolism – can a metabolic shift also promote an antidepressant effect?
Overall, this study identifies LAC as a potential fast-acting antidepressant with notably fewer side effects than existing options. While I’m not very convinced its action is mainly through epigenetic regulation of BDNF, it does support the idea of targeting epigenetic mechanism to develop new generation antidepressants (on the other hand, epigenetics is so hot these days EVERYONE wants a bite of it). For me, this study nicely illustrates the intricate interaction between foodstuff and cellular signaling beyond metabolism (see “The complicated science of a simple pleasure”).
I wonder if LAC will now be promoted as “fat metabolizer, nootropic and antidepressant all in one”.
Nasca C, Xenos D, Barone Y, Caruso A, Scaccianoce S, Matrisciano F, Battaglia G, Mathé AA, Pittaluga A, Lionetto L, Simmaco M, & Nicoletti F (2013). L-acetylcarnitine causes rapid antidepressant effects through the epigenetic induction of mGlu2 receptors. Proceedings of the National Academy of Sciences of the United States of America, 110 (12), 4804-9 PMID: 23382250
Posted on 04/02/2013 by Shelly Fan. This entry was posted in Research and tagged antidepressant, depression, epigenetics, neuroscience. Bookmark the permalink.
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I am so relating!
I have 2 things to add. First, especially since this person is a vegetarian, nutrition is of supreme importance! Low blood sugar is a real issue and can have similar symptoms to depression & anxiety. Also watch the caffeine because it, too, can exacerbate the symptoms of withdrawal from the meds.
I was a vegetarian who took Prozac for 20 years. Finally I began to investigate if my mental & emotional struggles could be nutrition-related. (They were, indeed.) Going off Prozac has been miserable but after a year now I think my system is finally regulating itself & the vertigo, etc. is subsiding. For me, abundant protein is the key.
...Peace is Joy at rest. Joy is Peace in action...
Location: Verde Valley, AZ.
posted 6 years ago
Just posted this in the blood/brain thread, but it appears mannitol sweetner will open the blood brain barrier, for a half hour.
May allow more of the LAC to get thru.
Your friend will doubtless reject this advice, but I would suggest that she start eating meat, drop the grains, cut out the legumes and let her brain heal. The antidepressants are likely covering up significant underlying derangement of brain metabolism caused by years of too little high-quality protein, too little animal-source fat and too much grain.
All this discussion of specific drugs and specific herbal remedies are focusing on bits and pieces, not the whole system. Just as in permaculture we look to nature to giving us guidance on how to design functional systems for humans, I think your friend would be wise to look to nature to design a functional lifestyle for her brain.
Before I found permaculture, I found the paleo/primal lifestyle. It is the only approach to eating (and exercising and sleeping and playing and simply living) that has ever made complete sense to me as a veterinarian, biochemist and virologist by training. Just as many of us here at permies have recognized that grains are not a ruminant's natural diet (grass is), the paleo/primal folks have recognized that much of what is on the grocery store shelves is not a natural diet for humans. Basically, there are very few humans or domestic animals in North America who are eating a species-appropriate diet. Since adopting the species-appropriate primal lifestyle, my husband and I have felt better in so many ways, including mental health and resilience to stress. And my 13-year-old dog has gotten over her arthritis and storm anxiety and now runs like a puppy when we take walks.
Here is some recommended reading on a diet that supports mental health, with links to further reading on exercise, sleep, sunshine and other facets of lifestyle as they pertain to depression. The same website features primal success stories every Friday. It is amazing how many people mention overcoming mental health issues (including dependence on antidepressants) simply through adopting a few basic lifestyle changes.
I would also strongly, emphatically advise that she have her thyroid function screened. There is an epidemic of hypothyroidism in North America, particularly among women over 40, and it can produce all kinds of psychiatric signs, from clinical depression to schizophrenia. I know, because I suffered clinical depression for years due to hypothyroidism and have been reading extensively on the issue since I was diagnosed. The main driver of this epidemic is Hashimoto's thyroiditis, which may well be triggered by the body's response to gluten. I have not touched grains since I found out about this link, but my thyroid gland was already toast. Fortunately, thyroid hormone replacement is effective for most people. If she does test positive for hypothyroidism, let me know. It is tough to get most doctors to understand just what constitutes effective treatment.
Another issue is Vitamin D, essential to brain function and strongly anti-depressive in action. She should get that checked too. This is really, really important. We have all been avoiding sunshine to prevent skin cancer, but it is depriving our bodies of this essential vitamin. Supplements can make a huge difference if she does not want to simply get out in the sunshine (a wonderful antidepressant in and of itself).
I wish her all the best. Depression is the pits.
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