Friday, 5 February 2016

Propranolol, Autism and Sodium Ion Channels Nav1.1, Nav1.2, Nav1.3 and Nav1.5

When writing this blog I frequently wonder what happened to all the very clever people; why are these full-time paid researchers often missing the obvious?

Boy with severe headache and ASD, awaiting Propranolol

The answer is, with a few notable exceptions (Catterall, Ben-Ari etc), the clever ones do not study autism, they study things that are much better defined, rare things like Angelman Syndrome and, recently, Pitt-Hopkins Syndrome.  These researchers seem much more rigorous.  For example:-

David Sweatt (Pitt Hopkins)

Pitt–Hopkins Syndrome: intellectual disability due to loss of TCF4-regulated gene transcription

Edwin Weeber (Angelman syndrome)

So autism is left to what might be termed the Baron Cohen brigade.


Propranolol is a medication of the beta blocker type.  It is used to treat high blood pressure, a number of types of irregular heart rate, thyrotoxicosis, performance anxiety, and essential tremors. It is used to prevent migraine headaches, and to prevent further heart problems in those with angina or previous heart attacks.

It is a nonselective beta blocker which works by blocking β-adrenergic receptors.

While once a first-line treatment for hypertension, they do not perform as well as other drugs, particularly in the elderly, and evidence is increasing that the most frequently used beta blockers at usual doses carry an unacceptable risk of provoking type 2 diabetes.

Beta blockers block the action of endogenous catecholamines epinephrine (adrenaline) and norepinephrine(noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response. Some block all activation of β-adrenergic receptors and others are selective.

It is occasionally used to treat performance anxiety.   Given the effect (above) on the fight or flight response this is logical.

The sympathetic nervous system's primary process is to stimulate the body's fight-or-flight response. It is, however, constantly active at a basic level to maintain homeostasis.

Evidence to support the use in other anxiety disorders is poor.

But what the ever useful Wikipedia almost glosses over is the part I find more interesting:-

Now we have to hope that cardiologists prescribing Propranolol are fully aware of the role of Nav1.5 in the heart and its role in heart rate.  This has nothing to do with it being a beta blocker.

Hopefully neurologists prescribing it for certain severe headaches understand the role of Nav1.1 in the brain.

It would not surprise me if they did not.

Propranolol earlier in this Blog

Earlier in this blog there are comments regarding the use of low doses of Propranolol to treat anxiety in autism.

Some people report it works wonders, while for others it did nothing.


Propranolol in Autism Research

A study was published recently and a reader drew my attention to it, but there have also been a few others.

Blood pressure medicine may improve conversational skills of individuals with autism

An hour after administration, the researchers had a structured conversation with the participants, scoring their performance on six social skills necessary to maintain a conversation: staying on topic, sharing information, reciprocity or shared conversation, transitions or interruptions, nonverbal communication and maintaining eye contact. The researchers found the total communication scores were significantly greater when the individual took propranolol compared to the placebo.
"Though more research is needed to study its effects after more than one dose, these preliminary results show a potential benefit of propranolol to improve the conversational and nonverbal skills of individuals with autism," said Beversdorf


Effect of propranolol on verbal problem solving in autism spectrum disorder

Effect of Propranolol on Functional Connectivity in Autism Spectrum Disorder—A Pilot Study

Back to Channelopathies

There are 24,000 human genes, but a much more manageable number of ion channels.  For each ion channel or transporter, there is a gene that expresses it.

When ion channels malfunction, it is called a channelopathy.  Channelopathies are quite well researched and very common in autism.  Early on in this blog I simplified idiopathic classic autism with the following chart.

I suspect that people with channelopathies (Nav1.1, Nav1,2, Nav1.3) caused by dysfunctions in the genes SCN1A, SCN2A, SCN3A are the ones that will most benefit from Propranolol.

I suspect those people will already suffer terrible headaches and/or seizures.

These three channelopathies have been known to be associated with autism for ten years.

Nav1.1 / SCN1A

Migraine, other headaches

Regular readers will know that Professor Catterall is the expert on sodium channels and here he is again below

Nav1.2 / SCN2A

Epileptic encephalopathy, early infantile, 11 (EIEE11): An autosomal dominant seizure disorder characterized by neonatal or infantile onset of refractory seizures with resultant delayed neurologic development and persistent neurologic abnormalities. Patients may progress to West syndrome, which is characterized by tonic spasms with clustering, arrest of psychomotor development, and hypsarrhythmia on EEG

Nav1.3 / SCN3A

neuronal hyperexcitability and epilepsy 

         Novel SCN3A variants associated with focal epilepsy in             children.

Nav1.5 / SCN5A

Mainly heart conditions, since this ion channel is expressed mainly in the heart.

Autism and Nav1.1, Nav1.2, Nav1.3

For many years it has been known that the hundreds of variations in the genes SCN1A, SCN2A and SCN3A are associated with autism.  So we can consider them pretty well established autism genes.

Clearly any drug affecting expression of those genes, or affecting the ion channels they express, should be a target autism drug.


Some people with autism and severe headaches, or epilepsy, have an underlying sodium channelopathy.  Sodium channel blockers are not as well understood/ developed as calcium channel blockers.

In some cases, but maybe not all, this should be detectable by genetic testing of the genes SCN1A, SCN2A and SCN3A.

If you live in a country that does not bother with genetic testing, you might want to fall back on trial and error and discuss Propranolol with your doctor.

Did all the people with Asperger’s, in the recent study, who became more conversational after a single dose of Propranolol, have problems with Nav1.1, Nav1.2 or Nav1.3 ?  I doubt it.  The other commonly known effects of Propranolol should also play a role.

But for a sub-set of people with Strictly Defined Autism, Propranolol might be hugely beneficial.  Perhaps Professor Catterall should investigate?


  1. Peter, I've checked the Sfari gene database for the genes you mention.
    They have a scoring system that classifies the genes according to the evidence for its link with autism.
    They have scored SCN1A as syndromic (in the same level as Fragile X) and SCN2A as strong evidence.
    Here is the link, if someone wants to check what are the references that support the classification and other stuff related to these genes.


  2. It seems that intracellular increase of Na is necessary for cessation of seizure, and conventional AEDs prolong seizure duration by blocking it.

    Ionic dynamics mediate spontaneous termination of seizures and post-ictal depression state

  3. I know a mother who has a child (now adult) with severe autism who benefited greatly (at least cognitively) from beta blockers (no idea if it was propranolol) but had to discontinue treatment due to its side effects. By benefited greatly I mean some of the worst behaviors were reduced, the kind that require full-time care if you know what I am saying. The irony with propranonol is that it is known as a memory dampener (hence its interest with PTSD) which you would think would make it act as cognitive dampener overall, but some of these cognitive studies (including the ones on autism) suggest otherwise.

    I do think you have to be careful with this stuff though. I have been using agmatine sulfate in my son for a variety of reasons the last several weeks and have had good success with decreasing hyperexcitability, sibbing, and other things (I must note we have had a lot of big wins in the last several months with various other interventions so agmatine has helped quite a bit on top of all the other progress), but what I have found is dosage is super important because of its various effects, including one being as a selective NMDA receptor antagonist (my interest initially in agmatine was its role in the opioid system). While there is evidence of NMDA receptor issues in autism leading to hyperactivity, too much dampening is going to lead to mental processing problems, the kind associated with high dose benzos or that of risperidone. I took a large dose of agmatine myself to test it out (agmatine is most popular for its vascularizing effects with bodybuilders) and it is safe, but nevertheless potent and did make me feel a little slow (probably from NMDA receptor antagonism) until I lowered the dose a bunch.

    Now I think low-dose propanolol might be a good adjunct from what you are saying here, just you are going to have a hard time convincing a doctor to take a panoply of low-dose drugs/supplements to treat a channelopathy. The benefits of many low-dose drugs/supplements that work in the extracellular space probably has a bit to do with the idea of stochastic resonance which is the idea that if you have a weak signal, you can boost it to a threshold value with random noise (such as systemic application of a drug or supplement). The key of course is not to overdo things or else the noise will overwhelm all the signals and then you just have random perturbations of the system. Also, for more selective medications they often have side effects that are intolerable at doses where the medication exerts an effect all on its own. Perhaps low-dose application of a non-selective beta blocker like propanolol that may address channelopathies might be better if there were another similar medication (at low dose) that was more selective towards targeting these sodium channels. I am not an expert on beta blockers (I know what they generally do but the details elude me at this time), but that is just how I would approach the problem here. Cancer research for many decades focused on finding silver bullet solutions to no avail and then a lot of success was finally made when combinatorial treatments were attempted.

    This is of course very unorthodox reasoning as most physicians who are content to prescribe megadoses of SSRI's to their patients to treat depression, but would cry in horror at the idea of using many small interventions to tackle big problems because it is more work for them and having to explain to their patients that they need to fill 10 low-dose prescriptions for one medical issue.

  4. My 8yo has been taking a low dose of propranolol for the past 7-8 months to help with anxiety and panic attacks. He does not have Aspergers. He has more of an atypical classic autism, if that makes sense. He does not have migraines or seizures. It has been helpful. However, during this past week he had a resurgence of awful, awful anxiety, which makes his autism worse. The propranolol didn't even seem to be working. It did seem to improve a bit when I added in 5ml of claratyne. His doctor ordered all new blood work so I hope we can find out what's going on.

    1. Nina, would your doctor be willing to consider trying verapamil or another calcium channel blocker to help anxiety? Especially since cl seems to help...

      There is SOME evidence base for this, but if nothing else helps why not try?

      "... The role of calcium in the etiology of anxiety has been proposed for several decades. Calcium channel blockers profoundly influence calcium metabolism and the transport of calcium. Even though the evidence for the role of calcium remains weak, drugs affecting calcium might be useful in the treatment of anxiety disorders. One of these compounds, verapamil, has been used to treat mood disorders. Calcium channel blockers have also been tried in other indications such as premenstrual syndrome, irritable bowel syndrome, schizophrenia, tardive dyskinesia, and Tourette's syndrome. However, the number of articles on the use of calcium channel blockers in the treatment of anxiety disorders is low. Three reports (two open, one double-blind) described some success in the treatment of panic disorder with verapamil, diltiazem, or nimodipine and one open-label study described unsuccessful treatment of anxiety and phobia with nifedipine in patients with various anxiety disorders."

    2. Thanks Nat, that's interesting. I have an appointment coming up in two weeks so I'll mention it then.
      Strangely enough, he's had a really good day today. So sometimes I just can't pick it. Sometimes I wonder if something as simple as not getting enough sleep could be a contributor to it.

    3. I found out the cause of my son's flare up. A chest infection was causing breathing problems which resulted in an asthma like attack. Two days in hospital. Paed at hospital is treating it like an asthma attack even though it's presentation is atypical. No previous signs of asthma before.

      Anyway, he is on antibiotics and oral steroids and his behaviour has much improved. Calm, happy, relaxed, cheerful, long attention span, keen to listen and learn. Phew.

  5. Thanks for this Peter! While Wikipedia only glosses over propranolol's action on sodium channel, it doesn't even mention possible effects of beta blockers on potassium and calcium channels.

    This paper is especially interesting since BKCa expression is messed up in autism!
    “β2AR can simultaneously interact with both BKCa and L-type Ca2+ channels (Cav1.2) in vivo, which enables the assembly of a unique, highly localized signal transduction complex ...
    Our findings reveal a novel function for G protein-coupled receptors as a scaffold to couple two families of ion channels into a physical and functional signaling complex to modulate β-adrenergic regulation of membrane excitability."

    1. It is surprising nobody clever thinks to publish a study called "Treatable Channelopathies in Autism"

  6. Hi Peter, Carnitine trial day 7th and I can see stable improvement in my son's energy levels and mood. I also noticed less inflammation, less muscle pain and better movement. I would give it the second best grade after Nac.
    Simvastatin looks a very clever idea and so does Propranolol. I am sure that if I need a "drastic solution", I have to trial them as well as other effective medication, such as Bumetanide/Diamox, Verapamil, but still I am worried because lowering cholesterol drugs and beta blockers are supposed to harm mitochondrial function. First I have to see how far I can possibly go with the treatment approach for mitochondrial dysfunction.
    Apart from the long list of vitamins, minerals, amino acids that help mitochondria, would you recommend other medication for complex I activity?
    Thank you

    1. Hi Petra, I would just use those supplements suggested by Dr Kelley for regressive autism secondary to mitochondrial disease.

      The drug most likely to be helpful is Baclofen. It seems that in Asperger's more than half of people respond to it (less anxiety and other benefits). The UK pediatrician using it who left comments elsewhere on this blog found no side effects. Maybe mention this to your new doctor, since you will need a prescription. It is an off-label use, so he may never have used it for autism. The more potent version, Arbaclofen, is a research drug used in autism, but trialed on the "wrong" sub-type it appears.

    2. Petra,

      I just thought to mention our experience with (acetyl-l) carnitine here, in case it can be of any use now or in future. It was great for our son to start with, and one of the things we decided very early on was a definite keeper, but after a while it became problematic. It took as a long time to figure it out - precisely because it was so great to start with we didn't consider it a suspect. It was only when we ran out at one point that his irritability and impulsive/aggressive behaviours reduced a lot, and came back after we reintroduced carnitine, that we finally put two and two together.

      As for myself, carnitine caused chronic lower back pain, that kicked in after a month or two of use. The pain was very similar (but stronger) to lower back pain in period pains. It was getting progressively worse... also took me many weeks and months to put two and two together. The pain started subsiding as soon as I stopped carnitine, and appeared again later when I experimentally tried restarting it. Twice. I suspect it started raising prostaglandins after a certain time, hence similarity to period pains.

    3. Nat, Thank you very much for sharing your experience with carnitine. I don't know what to say, I haven't trialed it for myself yet. May I ask how long you had been using it before you noticed aggressive behaviour and how much? We use it for 10 days and raised the dose to 2gr/day. I also combine it with Nac for irritability and seems to work.
      Once again thank you for keeping me informed.

  7. Dear Peter,
    You might also be interested in mentionning one more interesting thing about propranolol: it is an anti-angiogenesis (which is why it is used in infantile hemangioma and thus considered as a safe pediatric drug)
    This is of considerable interest in certain types of ASD-
    It is also an PI3K/Akt/enos/vegf inhibitor (This is actually the mechanism involved in its anti-angiogenesis properties)

    We have been using it at 30 mg/day as part of our personalized translational home treatment for my 8 year old son with ASD.
    I work in a medical Faculty in Europe and read and compile the ASD, CNS and neuro-inflammation, mitochondria and oncology litterature during my free hours ( night....) in order to find solutions to help my son, 8 years old with ASD.
    I am a great admirer of your work and understand so deeply your quest and motivation to accelerate translation in ASD. I agree with you it is just not happening....and have come to the conclusion that if I wanted effective evidenced based treatments for my son; I just had to search basic litterature and do translation myself in a N=1 scheme.
    Our current personalized treatment consists of various mtor pathway inhibitors -including brain penetrant longvida curcuma - which we recently replaced with J147 (fully brain penetrant curcumin derivative)due to habituation and probable mtor inhibition resistance loop mechanisms and two other compounds which are downstream inhibitors of mtor. Longvida curcumin was our "cognitive enhancing" revelation last year ( probably works through mtor inhibition associated with p53 upreg/ Nestin inhibition//sirt1-sirt3 activation)... Curcumin just hits so many pathways involved in ASD....but resistance is unfortunately a big problem.

    1. Peter,

      Can you comment on J147? Alli describes its precursor curcumin as being 'revelatory' as a cognitive enhancer.

      If Bumetinide does not yield a significant response as a cognitive enhancer/awareness promoter then is J147 worth a try and at what dosage?


    2. Hi Peter,

      Have you come across J147? Alli appears to have had a 'cognitive enhancing' revelation with its precursor curcu in. I see parallels with your Bumetinide revelation.

      Has anyone else tried Longvidia Curcumin? Is it worth a trial?


    3. Hi D&G, J147 is an experimental drug.

      Curcumin is interesting, it is available in many forms that try to improve its bioavailability. It is worth a trial and many people with ASD do take it.

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    7. Alli, so where are you acquiring your J147 ? If it works in autism, tell the Simons Foundation, they are not profit seeking. Also according to Nat, there is another very wealthy donor interested to fund autism.

    8. Another organization that funds autism research (in Canada):


  8. We also use FRAX486 as a PAK1/WNT pathway inhibitor. This has had disease modifying effects (Developpment of new intrests with no specific intervention, less repetitive behavior & awakness.I tried it on myself first for 6 months- animal toxicology was good- I had virtually no side effect (blood checks ok...except hair wightening due to Wnt inhibition... but it is totally reversable and manageable.
    To moderate Cytokine related autism flare ups- usually related to sickness in my son, I found by investigating neuroinflammation litterature that a substance found in Garlic - fruarg- was a very effective modulator of neuroinflammatory response in Bv2 microglial cells (on top of being a known antiviral). The litterature says that Aged garlic should work but fresh works better with my son. Clinically, it is particularly effective and almost totally prevents cognitive decline that was usually associated with infections. I reserve it for flare-ups otherwise habituation kicks in.
    I also use ibudilast which is a Pde4 inhibitor as a modulator of microglia. It is more effective than NSAID for cytokine flare-ups and does not have their nasty side effects.
    We do not use Nrf2 upreg as sulfarophane -which we tried when the Hopkins publication came out- & kiwi skin (!!) make my son aggressive and substancially worsens his cognition).
    We also use Biogaia gastrus ( which contains Lactobacillus reuteri 17938 and ATCC PTAt 6475 which down regulate TH1 and upregulate IL-10) - We have done cytokine panels which indicate chronically upregulated TH1- and proportionally low IL10-
    Bumetamide or low dose clonazepam do not work for us ( my son was on Bnx for 1.5 year as of 4 as we personally know E.Lemonnier) but Sodium Butyrate 500 mg/day- C is 25kg- is effective in improving his awareness and is a GABA regulator.... What is interesting is going up to 1G creates a negative effect...but this was also reported in the litterature.
    L-Theanine regulates hyperactive behavior and possible aggressiveness which appears as side effects of curcumin (also upregs Nrf2-but is such a cognitive inhancer on the other hand that the only left side effect is aggressivness)
    We also use synthocinon to improve social awarness.It works to some degree.

    For information, we have tried 5-Loxin but bioavailability seems low and passage of botsewelia through the BBB is documented as limited. PEA did not work for us. Oral administration is also documented not to result in high brain levels.

    I would be interested in having further exchanges if you are interested in exchanging litterature and usefull findings.


    1. Alli, thanks for sharing your strategies. Please continue to share them and exchange your findings.

      Curcumin is indeed interesting and in vitro it has been shown to have a wide range of beneficial effects. I thought it should help people with type 1 mitochondrial disease, but we do not have that issue.

      Ibudilast looks interesting and is being trailed for several conditions. The Japanese have some interesting drugs. Did you ever try Montelukast to see if it gave a similar protective effect?

      I am glad someone finds Sodium Butyrate useful, I was just discussing this with a doctor/parent a few days ago.

    2. Sodium Butyrate is very interesting. I used to do that for my son but switched to a combination of inulin, potato starch, and barley flour in a shake I give my son everyday with the idea of the gut bacteria producing the butyrate via the various sources of soluble fiber. My son won't do pills and sodium butyrate literally smells and tastes like puke so it is hard to mask. Do you do the sodium butyrate because it is an HDAC inhibitor or else is it supplemented to help keep the gut healthy?

      L-Theanine paradoxically (pre-Bumetanide) caused extreme mood swings and aggression. My best guess was that the glutamic acid that it metabolizes to was tipping the scales with regards to excess glutamate (normally the excitatory amino acid transporter in the BBB keeps influx rates pretty low) as theanine rapidly crosses the BBB but once in the brain it can be metabolized back to glutamic acid.

  9. Just a side note: they first did research on propranolol for autism in 1987. I think this is the biggest problem with our researchers. Oh, look at that. That actually worked. I'm bored now and just going to put this on a shelf. If there had been some follow through on the research, we'd probably have at least as many treatments for autism as there are for multiple sclerosis. Also, don't forget about curemark's cm-at. I think there is a lot of potential there, at least for kids with low chymotrypsin. It passed the clinical trial for kids with low chymotrypsin. Biomarker/corresponding treatment found. At least 99 left to go. Sigh.

    1. Nobody seems in a hurry to get to a conclusion.

      The latest trials for CM-AT are scheduled to finish in October 2018. They started in 2009. They have not published anything in the literature. They have hundreds of kids in trials. Since they have patents, why not share the results?

    2. Aren't they finishing phase III for autism this year? Btw they are recruiting for a manufacturing director, according to their website 'hoping to start large scale production' soon. As their autism trial will be the first one to cross the finish line this is saying to me they are willing to bet good money on CM-AT getting FDA approval.

    3. I seriously blame Baron-Cohen and the whole neurodiversity thing. They've set autism research back 10 years, at least. I like Jonathan Mitchell, but people say that he wants a cure because his parents "made him feel bad about his autism". Whatever. Don't get me started. Joan Fallon actually says in a video that they released that they passed all their endpoints for the low chymotrypsin trial. I think it's on a TedTalk, the Power of Disruption, they met their clinical endpoints for CM-AT, and they started the NDA. For some reason that I can't fathom, instead of having the FDA approve CM-AT for kids with low chymotrypsin, they are having to do ANOTHER clinical trial for all levels of chymotrypsin to see if it helps irritability. So, apparently this is what a fast track looks like...I remember seeing expectations that the "drug" would be approved by 2012. I really hope I don't get in trouble for this, but my kid is in that trial. Suffered through 3 months of getting placebo (they get burn reactions on their mouths that I'm having to counteract that he didn't have during that 3 months). He's been on "drug" since late December. And, admittedly, it's been a little like hotwiring a car. The cars lights come on and the engine starts to turn over, then the wire disconnects, and the car dies. But, I can call his name from anywhere in the house and he immediately responds. He has days when he is so connected with us. But, on the disconnected days he can be kind of frustrating because you've gotten to enjoy the good days. After a month on "drug", his chymotrypsin level is at a 10.4. Still considered low, even though she says in her TedTalk that anything above a 10 was considered in the "normal range". The clinical trial actually set the ceiling for low at 12.6. He is talking tons more. He can sit and play a game with his older brother and me. He wants me to play with him at the pool. The frustrating thing to me right now is no one is enrolling in this trial. Yeah, it's not a cure, but his behavior is tons better. So, that goes back to the neurodiversity movement and the whole "we don't want a cure" attitude. I just want the FDA to approve it so I don't have to worry about it going the way of Arbaclofen. To me, the better way to do this is to determine the side effects of the drugs, determine if they are, at least, relatively safe. Let doctors prescribe what's available and see what works for each individual kid. Maybe drug companies can start looking at the medical workups for the kids that respond to certain drugs and back into better solutions that way. I just think we need to start thinking outside the box.

    4. Thanks for the explanation.

      I took my data from the Clinical website.

      Faecal chymotrypsin was used as reliable index of exocrine pancreatic function. When I went to order the test, I was told the test is not so good and there is a more reliable one (elastase-1). I did the newer test and it was all normal.

      For years there has been an treatment for lack of pancreatic enzymes:-

      I wonder if CM-AT is any better than creon.

      It looks like no test is totally reliable, here they compare the older chymotrypsin with the newer elastase-1, that I used.

      Fecal elastase-1 determination: 'gold standard' of indirect pancreatic function tests?

      "Neither test is suitable for screening, as they provide a pathologic result in roughly half of 'non-pancreas' patients."

  10. Hey Peter,

    I really enjoy your blog and informative posts but there is also some gold in your comment section. The problem is it's really hard to search and navigate through previous comments. Maybe you might want to install a forum? It would make it a lot easier for readers to post, respond and keep track of messages.

    Keep up the good work!

  11. re: FRAX486
    question to: alli9 February 2016 at 17:27
    I wonder what are the safety data available for FRAX486?

  12. Peter, hmmm propranolol to treat PTSD?? I'm listening..... A few yrs ago, maybe a little more, a friend of mine got her son in to see Dr Frye. He then had a place for propranolol in his tx plan for mito - to first calm down the adrenals. Do you know if this is a standard practice in mito tx?

  13. Hi
    I tried .10g propranolol on my son
    It almost stopped potty accidents increased his attention span
    Though couldn't find any congnitive gains

    Do you have any idea about the optimal dosage for propranolol

    1. The limiting factor on the dosage is heart rate and blood pressure. This you can measure at home. You need to make sure these stay within the normal range.

  14. Hi again
    Someone on the FB posted
    "Low dose Propranolol has been the best intervention for us"

    She continues, "Resolved failure to thrive, anxiety and ocd significantly decreased, hypersexual behaviour almost completely stopped, immune markers improved and others"

    Will it be affective like 5mg of propranolol

    1. Riza, ask the lady what dose she uses. I would call 5mg a low dose.

      I think it will only benefit a small number of people.


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