Stephen Buhner - Official covid19 advise

[godlovesatrier]

Hi all,

Looks like Stephen published this recently. So this lists all of the things that are in his book with maybe a few other recommendations.

https://www.stephenharrodbuhner.com/wp-content/uploads/2020/03/coronavirus.txt.pdf

In the UK you buy these from Baldwins in Scotland (internet orders) or Bristol Botanicals.co.uk. Or your herbalist of choice outside of the UK.

Short summary of primary herbs, Buhner does recommend exactly which ones to take, what they do and their respective dosages:

Kudzu root
Rhodiola Rosea for oxygen utilisation
Cordyceps
Astragalus
Chinese skullcap
Red root Americanus
Bidens pilosa
Houttouynia Cordata
Isatis

Others were mentioned, but this was my main take.

 

[Hip]

In that document, Stephen Buhner says:

Plants specifically antiviral for the SARS-group of viruses; the strongest known so far are

Scutellaria baicalensis (Chinese skullcap root),
Houttuynia spp, Isatis spp,
Glycyrrhiza spp (licorice),
Forsythia suspensa (the fruit),
Sophora flavescens,
Lycoris radiata (extremely potent).

Lonicera japonica and Polygonum cuspidatum are also effective as antivirals for coronaviruses as a group.

Usually antiviral studies on a herb are in vitro, and even if a herb is a potent antiviral in vitro, this tells you nothing about whether the herb works as an antiviral in vivo (and it usually doesn't work in vivo). I am not sure if Stephen Buhner understands the difference between in vitro and in vivo antiviral testing, and that success in the former does not imply it will work in the latter.

 

[godlovesatrier]

Hi Hip,

Well I've read all his books and he definitely understands the difference. Whether he's drawing the right conclusions or not I'm not sure. However I think personally that he is. But that's based on what other Chinese Traditional Medicine doctors have also been saying about the right things to take. For example juniper berries freshly squeezed into a tincture or tonic and fresh ginger juice are two things Buhner recommends for upper respitory. Of course these are a total arse to make up in reality. But the recommendations he mentions were mirrored by ctm doctors.

 

[pamojja]

Usually antiviral studies on a herb are in vitro, and even if a herb is a potent antiviral in vitro, this tells you nothing about whether the herb works as an antiviral in vivo (and it usually doesn't work in vivo).

I think modern herbalist use in-vitro evidence only additional to millenia of clinical experience. I know for example in Ayurveda if one uses a single herb powder, often up to 10 grams per day have to be ingested. Not many would comply with. But if the right mix of each other potentiating herbs are taken, additionally in something agreeable, like fermented herbal wines, much less of the original herbs become much more effective.

Similar but not equal of pepper-extract increasing the absorbtion of cucurmin. Hundreds other potentially effective phytonutrients may synergize, where the whole becomes more than its parts. As in your experience, in which you found the whole herb of turmeric more effective, than its curcumin extract alone.

 

[IThinkImTurningJapanese]

Usually antiviral studies on a herb are in vitro, and even if a herb is a potent antiviral in vitro, this tells you nothing about whether the herb works as an antiviral in vivo

You're talking about herbs that have been used for centuries quite successfully, in vivo.

Why would anyone spend fortunes testing them in vivo to prove their effectiveness, when they can only be sold for fractions of the cost of modern pharmaceuticals?

 

[Hip]

I am not saying that herbs in general are not useful. I appreciate that many herbs do have clinical effects.

But specifically, when you look at in vitro studies of the antiviral potency of a herb, or for that matter in vitro studies on the effect of a herb on ACE2 or ACE, you cannot assume that herb which is potent in vitro will also be potent in vivo.

The reason is that high concentrations of the herb are typically added to cell lines in vitro; but it is often not possible to get anywhere near that high concentration in vivo, when you take the herb orally.



You might like to look at my comprehensive list of herbs which are potent inhibitors of enterovirus in vitro.

There are lots of herbs on the list which are antiviral for coxsackievirus B in vitro (CVB is the virus I have). But when I tried many of these herbs for my coxsackievirus B ME/CFS, I notice no benefit.

Only later when I learnt more about pharmacokinetics did I understand that the high concentrations of the herb used in vitro are usually not reproducible in vivo. I went through my entire list of antiviral herbs, performing the appropriate pharmacokinetic calculation on each one, and almost all of them turned out to have little or no antiviral effect in vivo, sadly.

So I now appreciate that herbs which are potently antiviral in vitro usually have little or no potency when they are actually taken. This is the sad reality, because I've searched high and low for any unusual substances that might be antiviral for coxsackievirus B.



I've seen herbalists quote in vitro studies as evidence for the antiviral potency of a herb, but you just cannot rely on in vitro studies to determine clinical effectiveness. You can make use of the in vitro result, but you have to apply pharmacokinetics to that result, to work out whether when you take the drug orally, you get the same high concentration in the blood. If you cannot achieve the high concentration used in vitro when you take the herb orally, then unfortunately it will not work in the body.

Why would anyone spend fortunes testing them in vivo to prove their effectiveness, when they can only be sold for fractions of the cost of modern pharmaceuticals?

You do not necessarily have spend any money to prove in vivo effectiveness: you can just use a pharmacokinetic calculation to see whether you can obtain the same high concentration of the herb in the blood, to match the concentration used in vitro in the cell line.

If your pharmacokinetic calculation shows that you cannot achieve that high concentration when you take the herb orally, then the herb will not work in the body.



You can often also test substances cheaply in animal studies to get in vivo data. I've seen some antiviral herbs tested on rodents to demonstrate their virus-fighting ability in vivo.

These animals studies are a good approach, because sometimes a herb may fight infections by an immune-stimulating effect, rather than an antiviral effect.

In vitro antiviral studies in cell lines only measure the antiviral effect of a herb, but they cannot measure any systemic immune-stimulating effect the herb may have, which may also be effective against the virus.

One example is oxymatrine: the antiviral effect of oxymatrine for enterovirus is negligible in vivo, but it can still fight the virus via an immune-stimulating effect.

 

[godlovesatrier]

Potency is absolutely important. No two ways about it. For example the same dose for differnet things does not owrk at all. You have to find, understand or know the right dose for the right herb for it to even work and if you load the body too much while sick that could be just as bad as not even bothering. It's tricky stuff.

It's a shame we don't know and understand the potency better really.

 

[godlovesatrier]

One thing I want to know is what research papers show that Lycoris radiata (extremely potent) is extremely potent. As I have never seen this mentioned in his books.

https://www.sciencedirect.com/science/article/pii/S0166354205000690

More than 200 Chinese medicinal herb extracts were screened for antiviral activities against Severe Acute Respiratory Syndrome-associated coronavirus (SARS-CoV) using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium inner salt (MTS) assay for virus-induced cytopathic effect (CPE). Four of these extracts showed moderate to potent antiviral activities against SARS-CoV with 50% effective concentration (EC50) ranging from 2.4 ± 0.2 to 88.2 ± 7.7 μg/ml. Out of the four, Lycoris radiata was most potent. To identify the active component, L. radiata extract was subjected to further fractionation, purification, and CPE/MTS assays.

It's in vitro. So bit misleading can't know how it would be once it got into the body. Very hard to find online too, so I wonder if that's due to efficacy and overall safety/effectiveness. Or rather adverse side effects. Like Lomatium or Andrographis for example, which both had severe side effects in some cases.

 

[Hip]

It's in vitro. So bit misleading can't know how it would be once it got into the body.

I will give a quick demo of how you can use pharmacokinetics to calculate the oral dose needed to get a clinical antiviral effect from the Lycoris radiata herb, based on the info from the in vitro study you quoted. We don't have all the data necessary to do the calculation, but we can use some guesses.



So the paper you quoted says the in vitro EC50 concentration of the most potent Lycoris radiata herbal extract used is 2.4 μg/ml (a concentration of 24 micrograms of the extract per ml).

The EC50 is a standard measure of antiviral efficacy. But to have useful clinical antiviral effects, you need to achieve blood concentrations that are at least 5 times the EC50 value. So we would want to achieve at least 5 x 2.4 = 12 μg/ml of the herbal extract in the blood.

Now the body has around 50 liters = 50,000 ml of fluids, so even if we had 100% bioavailability, you would need an oral dose of 12 x 50,000 = 600,000 μg = 600 mg of the extract, because whatever dose you ingest, it will be diluted in those 50 liters of body fluid (the blood and the fluids in and around the cells in the tissues).

Unfortunately, we don't know how much of the extract is present in the Lycoris radiata herb, but typically it might be say 33%, so now we need to multiply our 600 mg by 3 to get the actual dose of the herb required. So the oral dose of the herb required may be around 1800 mg = 1.8 grams.


But now we have to consider bioavailability, because for many herbs, the bioavailability can be low. We don't have any data for the actual bioavailability of the Lycoris radiata extract, but it could be anywhere in the range of 100% down to 1% or lower.

If it the bioavailability is low, say 1%, you now need an oral dose 100 times higher, which in this case would be an oral dose of 1800 grams = 1.8 kilograms!



The final pharmacokinetic factor you have to take into account is plasma protein binding: most substances (drugs or supplements) will bind to the proteins in the blood, and when they do this, they are lost (they no longer have an active effect in the body).

For many substances, the plasma protein binding can be high, like 90% or more of the substance binds to the proteins. So if the plasma protein binding of the Lycoris radiata extract were 90%, you would now have to multiply your oral dose by 10 to compensate, so that the oral dose now becomes 18 kilograms! Which is obviously far too high to be practicable.

Of course, we do not have the actual values for the bioavailability and protein binding of the Lycoris radiata extract, so in this case I have just entered pessimistic guesses. So this calculation of an oral dose of 18 kilograms is not accurate, but is given just to demonstrate how these calculations are done.



And this is what you usually get with many herbs: when you try to replicate the concentrations used in vitro, you find your required oral doses are in the kilogram range, which is just not viable.

 

[godlovesatrier]

Thank you Hip. This is really fascinating stuff for me. Bioavailability is certainly important as is binding, I am guessing there might be others too?

It does make me wonder if this is why certain herbs like houttuynia cordata can be taken in high doses of up to 30g a day, whereas others like andrographis are more like 15 to 18g a day. This is also assuming that the stated dose is actually relevant to an extract and not a powder. I also find that powder forms often give me more side effects than extract forms, nevermind constintuents like andrographolide. Because as you mention above dosage would be important, so if we used the constituent we could maybe get closer to the right dose without needing such massive quantities of the extract form. But would this then cause liver and kidney toxicity? Lots of variables.

I must admit if I find something I tolerate, i try to find the max dose in chinese traditional medicine and use that IF I am actually sick. When I am very ill I take lomatium, red root, etc half a teaspoon to a teaspoon every hour. Whilst it does have an effect, potency can sometimes be low, which might be where the diulution in the body of the substance is coming into effect.

So it seems the potency of Lycoris in this case is actually extremely subjective. I'll admit I have never heard of it before.

There's also the tincture/extract/constituent powder debate too. Basically is it much easier and indeed better to take 2 to 3 teaspoons of tincture to get the right dose, out of practicality if nothing else. Assuming there was no danger to organs or systems.

 

[Hip]

Thank you Hip. This is really fascinating stuff for me. Bioavailability is certainly important as is binding, I am guessing there might be others too?

Oral bioavailability and plasma protein binding are the two main factors which reduce the amount of an orally-taken substance which becomes available in the blood.

Some herbal extracts, like curcumin, have amazing effects in vitro, but unfortunately in vivo, the benefits of curcumin are severely curtailed because not only does curcumin have a very low bioavailability of 1%, but in addition, it's plasma protein binding is very high, at 98%, which means that 98% of the curcumin you take is lost because of protein binding.

So this double-whammy of low bioavailability and high protein binding makes it near impossible to get adequate amounts of curcumin the blood.

So all the amazing benefits of curcumin seen in vitro are unfortunately not available in vivo. Curcumin is one of the most researched herbal extracts, but it's never lived up to its promise because of a poor pharmacokinetic profile.

Curcumin is actually a potent antiviral for coxsackievirus B in vitro, so that's why I investigated its pharmacokinetics; but I calculated that even if you take high doses of the most bioavailable form of curcumin, you still do not get any significant antiviral effect in vivo. Sadly.

It does make me wonder if this is why certain herbs like houttuynia cordata can be taken in high doses of up to 30g a day, whereas others like andrographis are more like 15 to 18g a day.

Sometimes with herbs, it's their toxicity or side effects that limit the dose. So for some herbs there is a maximum safe dose which you should not go above. This max safe dose is another limiting factor on how much blood concentration you can achieve.

I was looking at trying some emodin (extract from Rheum palmatum, Chinese rhubarb), as in vitro is it a potent broad-spectrum antiviral for enterovirus. But with emodin, higher doses make you vomit, and they also can be toxic to the liver and kidneys, so in this case, it's the toxicity and side effects that limit the dose.

So again, the potent in vitro antiviral effect does not pan out in vivo.

So it seems the potency of Lycoris in this case is actually extremely subjective. I'll admit I have never heard of it before.

It's possible Lycoris might have some useful antiviral effect in vivo, but without knowing the bioavailability and protein binding of the extract, we can't accurately calculate its in vivo antiviral potency.

 

[Not_ME]

Hi all,

Looks like Stephen published this recently. So this lists all of the things that are in his book with maybe a few other recommendations.

I have had this for well over a month and I posted this on Saturday to this forum
My Post to Antivirals Effective Against Coronavirus

I do not think starting a new thread was necessary.

 

[IThinkImTurningJapanese]

If your pharmacokinetic calculation shows that you cannot achieve that high concentration when you take the herb orally, then the herb will not work in the body.

A human being's not a petri dish, it's illogical to assume that everything will function the same way as it did in vitro once you employ a substance in a different environment.

 

[Judee]

Oral bioavailability and plasma protein binding are the two main factors which reduce the amount of an orally-taken substance which becomes available in the blood.

But, @Hip, maybe herbals don't have to get to the blood in order to have an affect on the gut microbiome. Is it possible that the byproducts of that interaction communicate with the rest of the immunity?

I'm not sure if this is the right wording (my brain is overtired right now) but I think the microbiome creates peptides. I was reading something about this when trying to find out the half-life of licorice and in essence some of the papers basically said they don't know exactly because the metabolic byproducts of the licorice can recycle in the intestinal system for some time--there's a biological name for this but I can't find it at the moment.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799574/ kinda talks about this when it says, "All our epithelial surfaces participate in keeping up an effective barrier against microbes while not initiating ongoing inflammatory processes and risking collateral damage to the host. Major players in this scenario are antimicrobial peptides (AMPs). Such broad-spectrum innate antibiotics are in part produced by specialized cells but also widely sourced from all epithelia as well as circulating inflammatory cells." [bolding mine]

 

[JES]

Herbs may well work through other ways not yet known to us. I react strongly to almost any herb these days, but I suspect it's more due to immunomodulatory effects. I spent a couple of years trying to get past the "herx" phase of various herbals by continuing to take them, but I never reached the point where I would start to improve, so for me, this has mostly been an exercise in frustration. On the other hand, none of the herbs I trialed caused any long term damage whereas it happened a couple of times with drugs and one specific probiotic, so in my experience the safety record is pretty good.

I think the point @Hip makes is that claiming certain herbs are antiviral is quite questionable unless you have the results in vivo. "Antiviral" usually implies something where the active compound(s) are responsible for killing the virus. If the antiviral effect has only been confirmed in vitro, it would be a bit like saying desloratadine is antibacterial (against Lyme). Yes, it turns out to be (source), but you would need to take hundred times the standard dosage of desloratadine to achieve potential Lyme killing effect in vivo, so it wouldn't make sense to call it an antibacterial.

 

[Hip]

A human being's not a petri dish, it's illogical to assume that everything will function the same way as it did in vitro once you employ a substance in a different environment.

It's true that there's more complexity in the body than in a petri dish; but the in vitro approach is the way many pharmaceutical drugs are developed. During drug development, substances are synthesized, then often tested in cell lines first. If they show beneficial effects in the cell lines, then they may be tested in vivo.

But drug companies also have the same problems with pharmacokinetics: often a synthesized substance will have a potent effect in vitro, but because of its poor pharmacokinetic profile, you cannot obtain the same effects in vivo. In which case, the experimental drug has to be binned. Or sometimes the drug company might tweak the molecule in order to improve its pharmacokinetics.

So poor pharmacokinetics is a problem that the pharmaceutical companies face all the time.

But, @Hip, maybe herbals don't have to get to the blood in order to have an affect on the gut microbiome. Is it possible that the byproducts of that interaction communicate with the rest of the immunity.

If we are talking about a herb which might benefit a gut disorder like SIBO or IBS, then sure, you sometimes don't have to get into the blood, as it may be the local action of the drug at the gut lining which has the effect.

And there are some diseases where improving gut health can have systemic benefits in the disease.

But if we are talking about an antiviral, then that usually needs to get to every cell in the body in order to protect those cells from a viral infection.




The bottom line is that you cannot take an in vitro study showing that a herb is antiviral, and then assume that herb will also be antiviral in the body.