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Probiotics As Targeted Antibiotics

By Karl Seddon, Founder & Director, Elixa Ltd.

The rise of public awareness of the bacteria living in our guts has occurred rapidly enough that it seems only a few years ago that probiotics were not much more than yoghurt drinks for your stomach, and when asked if they work, the typical response was a happy-go-lucky ‘Erm, not sure. Maybe … Well, they taste good! I have one at breakfast!’

Well ‘having one at breakfast’ was about the extent of the incentive for why people continued to purchase them, but fortunately, probiotics have come a long way since then.

Let me paint a picture of where probiotic supplements could go next. This will sound familiar to a lot of you who’ve given consideration to this and been following the topic. It makes a tonne of sense on paper, and you’ll be nodding to yourself, saying ‘Yup, this is what we’re after. Now we wait!’ Then, I’ll explain why I think that path is not the next step for probiotics and where I believe that it will go instead, in the shorter term (i.e., the direction I am pursuing with Elixa). Both ideas make sense and will have portions of truth in them.

The first scenario goes like this:

Whatever problem we have (of gut origin) is due to a lack of specific useful microorganisms. The future of probiotics is about offering the exact species; nay, the exact strains that will supplement those gaps. They will then colonise their niche in the gut and plug up the missing portion of a strong microbiotic profile. Sort of like curing a vitamin deficiency.

In this scenario, the way forward for probiotics is identifying these strains that are commonly deficient in the modern human. This could either be presented as different blends for different conditions or deficiencies: analogous to taking just Vitamin B6 or just Zinc, etc.

Or as an all-in-one formula tailored to the statistical average: analogous to taking a multivitamin containing RDA amounts.


‘Good Day Mrs. Health Store Owner. I’m found to be lacking in Bacteroides Thetaiotaomicron.’ (She consults her alphabetized shelf full of probiotics)

‘Ah yes, we have just the thing.’ (Hands you a bottle of capsules filled with that species.)

Ideally, you could even use some quantitative method to assay your microbiome beforehand. Thus being able to feed in this data and have a personalised blend for your needs.

Sounds good and a lot of truth in it, perhaps.

A slightly different take on this would be a probiotic that didn’t superimpose onto your native microbiota to make up for deficiencies, but moreover replaced large portions of microbiota. Think of the first scenario as pasting text into select places in a paragraph and the second scenario as pasting it with the current paragraph highlighted, i.e. replacing the entire paragraph of highlighted text with a better paragraph. The ultimate form of this would be a probiotic equivalent of a fecal microbial transplant (“FMT”) from a pure gut, whereby some think the aim is to replace the entire microbiota with a superior profile of microbes.

I don’t disagree with these scenarios in any sensationalistic, ‘complete baloney!!’, kind of way. And I think the probiotic equivalent of an FMT is going to be the quintessential probiotic, eventually. Just not in the short term. And I don’t think the supplementation model is going to be the intermediate stepping stone, nor do I think the current FMTs work via the mechanism of supplementing deficiencies.

I base my current R&D strategy on the hunch that probiotics‘ fundamental mode of operation is different.

Preface

First, I should explain a hunch I have that may differ from the norm.

The profile of the flora in our guts is assumed to be the cause of the majority of gut-related conditions. I should mention that there are other gut attributes to be considered, such as gut hyperpermeability or damage and inflammation to the gut lining causing, for example, malnutrition. But let’s go back to the gut flora (aka. the microbiota) because I think it’s likely that it is the main culprit and is linked to the other two items. The microbiota is a diverse community of microorganisms within our large intestine. They’re all bugs, but the taxonomic differences between some of these bugs are greater than the gap between you and your pet dog (and far more exotic organisms).

We assign most of the blame for gut-related conditions to a lack of some species in your gut. E.g., ‘I am deficient in Akkermansia Muciniphila; therefore, I am at greater risk of becoming obese from a similar diet to someone who is not deficient.’

Or, a more general example: ‘I have eczema due to lack of bacteria X.’

I think that the cause of the vast majority of these conditions is not a lack of good species, but instead an excess of harmful bacteria.

‘Huh, what’s the difference? Too much bad, not enough good … imbalance … balance … we need to ‘balance’ the gut …. the same thing right?’

The difference is simple but fundamental: It’s not condition Y due to lack of bacteria X. It’s condition Y due to the presence of non-beneficial bacteria Z in my opinion, in the majority, but not all, of cases.

Why do I think that? Mostly based on one observation.

People who undergo a total colectomy do not suddenly develop all these myriad conditions that result from a dysbiosis. If everyone who had their (entire) large intestine removed, suddenly developed depression, dermatitis, acne, diabetes, allergies, etc., then it would be common knowledge!

3 - Total Colectomy

Total and subtotal colectomies can indeed wreak havoc on the functional capability of the digestive tract, but they do not cause all these conditions of dysbiosis to present.

Without a large intestine (total colectomy) you don’t have any large-intestine bacteria because you don’t have a large intestine. So if a deficiency in beneficial species were the cause of the majority of symptoms of dysbiosis, then a total colectomy would result in the acquisition of the majority of problems (benign and severe) from the entire spectrum of dysbiosis-related conditions.

It’s simple logic that you can mull over yourself and make up your mind on your own. Don’t assume I’m right. That’s why I explained it all. So you can pick it apart. Think about it and let me know if I’m making a glaring error. To play devil’s advocate: Perhaps the Ileum undergoes significant adaptation and takes up some of the microbiotic ‘slack’?

Beneficial bacteria are clearly useful for something – extremely helpful, in my opinion. Both directly and indirectly. They play vital roles, and a sterile gut is not a healthy gut. They are the best defence from acquiring an overgrowth of other harmful microbes. That alone is worth their existence. Plenty of rodent experiments have demonstrated the serious consequences of having a sterile gut. They use Gnotobiotic rodents. Gnotobiotic means known life, i.e. the microbiota is fully known to the scientist. In this case, it is known to be non-existent – there’s no gut flora whatsoever. This can be achieved by using antibiotics from birth and keeping the rodent in a sterile environment.

They develop problems. Behavioural and immune and more. This demonstrates that good bacteria do play a role in maintaining a healthy organism. However, it also proves that lack of good bacteria is not responsible for the majority of dysbiotic conditions. Otherwise, the rodents would develop the majority of all medical conditions linked to gut dysbiosis. Not just a few.

Probiotics as targeted antibiotics

Mainstream awareness of probiotic supplements (post-yoghurt era) began a little like this:

(Cue sarcasm)

So you’re looking through the list of ingredients on the plethora of probiotics available online and on the shelves, and you recognise some names of species that featured in a study or an article, and you recall that this species was an important one which you would do well to supplement with, because it is very likely that you’re deficient in that one and it’s a good’un after all. At least according to the article and study you recall. What was the outcome of the study? Not really sure but it was studied, and the study was a science one. I read the first line of the Abstract, and it probably went on to conclude something very significant otherwise it wouldn’t have been a study, now would it?

With so many bacterial genera and species in our gut, it seems handy that there are these golden ones which are readily available in a supplement.

Take Lactobacillus Acidophilus. Good old Acidophilus. The tried and tested old-timer whom everyone knows is a beneficial species. Never lets us down. It’s in all the probiotics, and it’s likely one of the very first species of probiotic you ever heard about.

Don’t ask why it’s good. Everyone knows. No need to ask. Everyone’s heard of it. And look – here’s Lactobacillus Casei. Oh boy, it has the same L-word so it must be another home run!

Then things get advanced. Now there’s this new kid on the block – It’s called Bifidobacterium. Wow. Doesn’t even have Lactobacillus in the name. Variety …  yeah, I like that. Variety is good. It means we fill a greater variety of deficiencies. GREAT!

Then probiotics with 5 strains and 6 strains and 10 strains (and so on) came out. Wow. That’s a wide spectrum probiotic right there! That’s the profile I want my gut to be. If I take enough of this probiotic, my gut will have this perfect ratio of these potent probiotic species. The special ones. No room for the non-special ones that I’ve not heard of.

(/Sarcasm)

The reality (as I’m sure many reading this blog are aware) is that there are tonnes of species in the large intestine. And the majority of probiotics currently available only contain a handful of species from two genera! And guess what – Lactobacillus isn’t that special! It’s no coincidence that it is straightforward to manufacture and has been churned out by the bucketload due to the dairy industry, where it’s used as a starter culture.

Ok, so I take that back. It is special because it is a beneficial genus which we can manufacture right now. A decent probiotic that is available is much better than an amazing probiotic that is not commercially available – obviously.

Bifidobacterium is a little bit different. It’s towards the ‘more beneficial but harder to culture’ side of the spectrum.

So why all this talk about Lactobacillus? Why all the studies focused on that genus? Well, it’s simple. You may think that a microbiologist established the healthy species of bacteria necessary for optimal human health and then went about manufacturing them. However, it was somewhat the reverse of that: What was sold was determined by what was possible to manufacture – already established by existing industries. The demand was stimulated in a targeted manner based on what is available to sell. There’s no use promoting the benefits of some species which we can’t even put in a pill yet. But I don’t think there’s anything conspiratorial about this. It’s just a case of dealing with what’s to hand versus waiting until perfection has been achieved. Let’s leave the ‘big pharma’ conspiracies at the door and appreciate that industry got things rolling in the first place.

Since the mainstream understanding of probiotics was molded by the contemporaneous technology and understanding, it means a little bit of unlearning may be required. Firstly: I do not believe that the species in Elixa are ones that everyone is ‘deficient’ in. And I do not think the ratios of the formula are proportional to the desired ratios in the gut. And I do not think that it is designed to supplant your pre-existing flora and shift the gut towards a pitifully non-diverse, 12-species, 2 genus profile!

So if it’s not working to plug up the deficiencies in select species, then what’s it doing?

This is the point of this article.

I think that the primary mechanism by which probiotics work is better thought of as targeted (intra-luminal / non-systemic) antibiotics. NOT as a multi-vitamin that plugs deficiencies.

Let’s look at what I mean by this.

‘Intra-luminal / non-systemic’ – Ok, this is pretty simple so forgive me for I have, at the least, used unnecessarily long words. It just means a substance whose direct action takes place within the gastrointestinal tract and does not enter the bloodstream. The only reason to make this distinction is because most antibiotics enter the bloodstream. Simple enough.

Antibiotic – In this analogy, it is referring to the capacity to destroy microbial populations. Simple.

Targeted – This would be the holy grail of antibiotics. The ability to target only bad species and ignore the good ones. Well … guess what – beneficial gut bacteria do exactly that. They have adapted to do so during the millions of years they have co-existed within mammalian guts. If they treated other beneficial bacteria in the same way that they treated non-beneficial bacteria, then the gut would always revert to one (or 2-3, if separated by significant distance) dominant species / genus / strains in the gut. And if it were not true that they counteract the proliferation of non-beneficial bacteria then all the evidence for competitive exclusion would not exist (i.e., the ability of a gut filled with healthy bacteria to be more resilient against an invasion of non-beneficial bacteria, e.g., c. Difficile).

So – just like Richard’s prescient title for the article I did back in April – probiotics really can be seen as mercenaries! So if you thought that was only a play on the Uganda theme (as I did when I first saw it!) consider the following similarities between probiotics and mercenaries:

  • They are best utilised temporarily (at least that is my stance on probiotics).
  • Mainly when there is a problem to resolve (i.e. not in times of peace/good gut health).
  • They do not in any way represent the operational diversity of a fully functioning army (or in this case, a healthy microbiota).
  • They come with weapons (chemical weapons – bacteriocins, fungicins, pH modulating byproducts, etc.).
  • They can cause a tonne of disruption and evict a belligerent.
  • And finally, they can be decommissioned once sufficient change has been made such that the regular microbiota can handle things from there on out.

Sticking with the analogy – some of these mercs may stick around to join the regular military (military = the vast ranging, self-sustaining, permanent gut flora in our large intestine), especially if some of them possess skills which were deficient in the regular army, i.e. they have an available niche to fill in a gut ecosystem (because, yes, you may well need an increase in Bifidobacterium Infantis, for example).

I didn’t always think this. A lot of it was due to the success that Elixa V1.0 had. I knew that version 1 was nowhere near representative of the full range of a healthy microbiota (in the way that, perhaps, an FMT is). It was still helping people immensely. That’s why I started to care less about specific strains and more about overarching modes of action at the species and genus level. For example, the ability to create lactic acid thus lowering pH. This was not a strain-specific mechanism. And perhaps it didn’t require a range of 5 Lactobacillus species to accomplish (although I am sure that there will be some variation between the bacteriocins that those 5 separate species produced and other differences in competitive exclusion mechanisms) – any Lactic Acid Bacteria could have done the trick.

It would not even surprise me if Elixa could generate a benefit in someone who already had those 12 species in abundance because you are still jacking up the overall chemical warfare going on in the gut. And that chemical warfare is targeted. Perhaps more so than any antibiotic could be. Take pH modulation for example. When lactic acid bacteria create d-lactate and lower the pH of the intestinal environment, this doesn’t just benefit themselves. A lower pH has been found to be optimal for beneficial bacteria and generally sub- optimal for non-beneficial bacteria.

It doesn’t take much to imagine that the bacteriocins which beneficial bacteria produce will selectively target only non-beneficial species. So the ‘targetedness’ probably spans across their entire armament. Whether the probiotic course causes a permanent or long-lasting increase in the quantity of those particular species in your microbiota will be dependent on whether there was a gap in that niche to begin with – and I do not think it’s even important. In fact, I would not be surprised if a ‘Lact/Bif’ probiotic, that caused significant resolution of a gut problem, left behind a substantial (and sustained) increase in an entirely different genus. One that may have previously been repressed by whichever set of bad microbes were overgrown in your gut. Said bad bacteria having now been evicted by the probiotic species.

Rock, paper, scissors

(with the twist that Rock has no conflict with Scissors)

Paper (a bad species) is well adapted to suppress Rock (a good species). Rock is poorly suited to counteract Paper.

Scissors (the species in the probiotic) comes along and gets rid of Paper with ease. Rock is free to flourish, now that Paper is gone.

Scissors leaves (i.e., the probiotic course ends)

Paper’s population is so diminished that Rock has no problem keeping its foothold now that it has been allowed to regain its former population size.

Net result:

  • Paper has gone
  • Rock flourishes
  • No net change in Scissor population

Had it been a different bad species, Rock may have had no problem regaining its foothold by itself. Hence, why sometimes people bounce back easily from antibiotic-associated diarrhoea (for example).

The natural, healthy microbiota is so diverse that they will all be working together, handling different tasks that benefit each other. One species may breakdown substrate X and product metabolic byproduct Y as a result. Another species may utilise byproduct Y but would not have been able to produce Y itself. Mutual co-existence.

So … probiotics as targeted antibiotics versus probiotics as deficiency solvers. Mull it over.

This last point is for another time, but I’ll briefly touch upon it. A separate mechanism by which probiotics can exert an effect involves a beneficial immune response to the presence of the probiotic bacteria – even if they are dead!

I mention this because I think it is the best explanation for why some people have reported skin improvements within 24-36 hours. I don’t see that the competitive exclusionary actions of probiotics could show a change that rapidly. So I would suspect it is some effect on the immune system which causes that lowering of inflammation in the skin resulting in improved texture and complexion (for some) to begin with, followed by additional benefits once the probiotic has had time to evict significant numbers of the bad microbes in your gut.

Karl Seddon is the UK-based biotech entrepreneur who created and manufactures Elixa Probiotic in his own facility.

Richard Nikoley

I'm Richard Nikoley. Free The Animal began in 2003 and as of 2021, contains 5,000 posts. I blog what I wish...from health, diet, and food to travel and lifestyle; to politics, social antagonism, expat-living location and time independent—while you sleep—income. I celebrate the audacity and hubris to live by your own exclusive authority and take your own chances. Read More

34 Comments

  1. Tim Steele on March 24, 2016 at 11:35

    Lots to chew on!

    “an effect involves a beneficial immune response to the presence of the probiotic bacteria – even if they are dead!”

    This, I think, may be a key piece top the whole probiotic puzzle.

    Regarding colectomies. there is an interesting twist. Sometimes they do not remove the large intestine, but bypass it for a while in the hopes of salvaging it. When they bypass the colon, it quickly begins to deteriorate. Guess what helps it survive? Resistant starch suppositories!

    Read some experimentation here: http://gut.bmj.com/content/61/Suppl_2/A93.1

    • Karl S on March 25, 2016 at 16:54

      Hi Tim!
      Yes, indeed. I believe it was on your blog where I read about that study into butyrate ‘nourishing’ an atrophying colon back to health (or another blog I was reading a while back, if not yours). Definitely valid for medical situations.
      I think the further we try and ‘skip steps’ in the chain, the more likely errors will be made (as I’m sure you’ll already agree). The idea of ‘post-biotics’ (i think they’re called?) is an example of that – whereby the metabolic byproducts (e.g butyrate) are supplied ready-formed. Skipping steps like this for anatomically normal adults always sets up the potential for some other vital step being missed out. It goes back to the paleo principle that by replicating what we are evolved to consume, we can be most sure that we are not causing some unforseen damage due to mechanisms we don’t yet know about. So, like your blog espouses – achieving the metabolic byproducts via the natural mechanism is optimal. The exception comes when we deal with dysbioses too far gone to be treated by regression to healthy eating [that’s where it gets interesting (!) with probiotics and refined forms of prebiotics, etc.. 🙂 ] The prevalence of ‘too far gone’ dysbioses may be commonplace by now (in Western countries).

      Another point relating to changes in intestinal structure is the cecal enlargement found in germfree mice. Hypothesised as the cecum adapting to increase its surface area to compensate for loss of nutrient absorption that is usually being facilitated by the no-longer-present microbiota.
      Most of the studies are extremely old though.
      Thanks,
      -Karl (Elixa)



  2. James on March 24, 2016 at 14:44

    Thank you, Karl and Richard, for all of the research and hard work you’ve done to share this vital information with the rest of us!
    My mom has suffered with IBD (Crohn’s Disease) for at least 2 decades. She’s been in an out of the hospital over the years and has suffered tremendously with this illness.
    It has always loomed like a dark cloud over our family–“will she get sick again, will she be able to come to the wedding, will she lose her job because of taking too many sick days, will she have to get her colon removed…?”
    During my own crazy health quest, I’ve had her try many things. She came to the raw food retreat I lived and worked at in my early 20’s in Puerto Rico. She’s done all manner of supplements that I’ve sent her. She followed me down the Primal path for awhile (which helped for a little bit).
    Well, I keep trying to help her, and I sent her some Elixa about 2 months back and so far so good (fingers crossed!). No more pain, no more bloody diarrhea, no more vomiting after eating simple meals.
    I think we’re all cautiously waiting to see if this success continues. I hope it does continue, but even if this is just a temporary vacation from her illness, it still means the world to me to see her have some relief. Thanks for everything, guys! I’ll keep you updated.

    • Karl S on March 25, 2016 at 17:05

      Hi James!
      I’m happy to hear of the progress your mother has made!
      I hope that things remain on an improving trajectory.
      Please send me an email to let me know how things go over the next few weeks.
      I’ve heard from a number of people regarding Crohn’s and it would be an interesting condition to get more feedback on. Thanks for sharing this here.
      Kind Regards,
      Karl (Elixa)



  3. Robert on March 25, 2016 at 05:10

    Hi Karl,

    I wrote to you regarding d-lactate worries due to previous lobotomy style side effects from probiotics and fermented goods containing lactobacillus(cfs/m.e). You responded at length saying that you didn’t think it would be a problem with Elixa and you were absolutely right. The delivery system did get around the trouble I’d been having with other probiotics.

    I noticed that 6 hours after taking the pills, I would get a flush to my cheeks and nose and with vastly improved skin tone. The first day I took the pills, my bowel system came to a standstill and saw no action until day 6, though at no time did I experience anything like the discomfort that I would have if I’d been experiencing a bout of constipation. When everything started moving again, it was all perfectly formed stools.

    What could I say had changed for the better over the course? Nothing noticeable. What I did notice was obvious improvements in bowel health over a period of months. I’d read your thoughts on the Elixa lowering the ph, creating a positive environment for beneficial changes and took these changes as that exact thing having happened. So yes, I think you could be correct about it’s action.

    • Karl S on March 28, 2016 at 08:47

      Hi Robert,
      Thank you for sharing this feedback!
      Just goes to show that people’s introductory response to Elixa can vary drastically.
      Glad to hear it didn’t cause you the problems that you were experiencing with other probiotics and fermented foods!
      Kind Regards,
      Karl (Elixa)



  4. Doug on March 25, 2016 at 07:59

    I find this very interesting, but feel I am not very knowledgeable in this area at all.

    My questions is we talk about good microbes and bad microbes, but is it possible that the bad…could be good?

    My example: If one studied blood cells at various points in time they would see a “healthy” person with lots of red blood cells. Red is good. In a another study they noticed white blood cells and that a person was sick. White is bad. Eventually someone figured out that the sickness caused white blood cells to proliferate to attack the illness.

    • Karl S on March 28, 2016 at 08:26

      Hi Doug,
      Well I think you could perhaps say that an excessive population size and/or an abnormal location along the GI tract, could flip the definition of species X from good to bad.
      The model/mechanism in your example would – in our context – equal a set of bacteria being high as a result of a negative physiological condition, as opposed to the negative physiological condition being a result of the high population of that particular set of bacteria. Well, I can’t say how prevalent that is but there has certainly been some discussion as to which way round the relationship is between the profile of gut flora in an obese person and their diet. I.e. whether the diet caused the obesity directly AND incidentally affected the gut microbiota. OR whether the diet affected the gut microbiota and that was the primary method that the person became obese.

      Kind Regards,
      Karl (Elixa)



  5. solver on March 25, 2016 at 13:04

    Richard, with your interest in economics, I thought you may be able to shed some light on this question for me: I often see bumper stickers in Texas declaring that “Jesus Saves” but what is happening to all Jesus’ savings with interest rates near zero for nearly a decade? Surely he would have been better off borrowing and investing? Maybe he should have invested in stocks and gold, no?

    • Richard Nikoley on March 25, 2016 at 14:46

      LOL. You just sent me down meme hell rabbit holes. In an instant.

      Jesus saves. LOL. It’s all in the context.



  6. Drully on March 26, 2016 at 01:18

    Surprised that no one has made mention of rifamaxin which has become a game changer in the treatment of IBS. This antibacterial uniquely targets intestinal bacteria. I don’t think it targets “bad” bacteria. Perhaps the benefits of “good” bacteria is that they cancel out the bad and they are not positive in themselves?

    • Karl S on March 28, 2016 at 08:35

      Hi Drully,
      Rifaximin is useful in SIBO. But SIBO (which is far less prevalent than the internet community would imply) is an overgrowth of bacteria. Whereas a dysbiosis is an unhealthy profile of bacteria. Total count of bacteria is not the issue in the latter.
      As far as I’m aware, Rifaximin doesn’t have any reputation as being good for treating IBS. In fact I would say it was one of the worst things you could take if you have a dysbiosis.
      It interferes with RNA transcription. So there’s no good vs bad differentiation, as far as I can see.
      I agree with your latter statement that the exclusionary action of good bacteria is a large part of their benefit (although not their entire benefit).
      Kind Regards,
      Karl (Elixa)



  7. Antonio on March 28, 2016 at 07:39

    Some overlap with Woo’s opinion on ‘broad spectrum antiseptics’ function:
    “In a nutshell: My belief is most of the fiber/probiotic science is nonsense and the majority of people with GI dysbiosis are better served to consume broad spectrum antiseptics. These indiscriminately target all microbiota populations, so inhibition is parallel to overgrowth. Long term effect is regulation and diversity.
    OTOH, take any sort of fiber, you are bound to make dysbiosis worse. You have no clue what might grow from that. Antiseptics, in contrast, reliably inhibit bacteria parallel to excess.”
    http://itsthewooo.blogspot.com.es/2015/03/broad-spectrum-antiseptics-are-ideal.html

    • Richard Nikoley on March 28, 2016 at 08:12

      You mean the person with the post at the top of the blog about her taking high dose lithium?

      Perhaps she doesn’t know as much about the microbiome as she seems to think.

      https://www.sciencenews.org/article/microbes-can-play-games-mind



    • Karl S on March 28, 2016 at 08:44

      Hi Antonio,
      There’s some overlap… if by ‘overlap’ you mean ‘exact opposite’. 😉
      My article is about probiotics being *targeted* equivalents to *indiscriminate* antibiotics.
      The quote in your post, advocates *indiscriminate* antiseptic use…I.e. the exact opposite.
      Kind Regards,
      Karl (Elixa)



  8. Kevin Moore on March 28, 2016 at 22:11

    Karl xifaxan was approved last year for treatment of IBS

    • Karl S on March 29, 2016 at 10:12

      Hi Kevin,
      It has its place for treatment of diarrhoea and has been prescribed as such for a long time. Rifaximin has been around for a while, prescribed both on- and off- label (especially in Eastern Europe) for GI conditions. Sometimes prescribed for rosacea without even a confirmation of SIBO (according to one doc I met!).
      It’s so easy to get a hold of (or prescribed) in Europe, that if it reliably cured IBS (even just one variety; IBS-D) I would imagine that people would be aware of it by now, since it is not a new option.
      Some can get lucky (and I really do mean *luck*… until accurate microbiome assaying is used beforehand) but chances are that most people will have their condition worsen.
      The interesting thing to remember is that removing a pathogen that causes diarrhoea does not mean that the overall gut has been improved in health, because other gaps will have been created putting you at a huge chance of worsening your gut flora profile. That’s why it’s used for traveller’s diarrhoea, where the pros outweigh the cons (of using any ABX).
      I imagine it will be prescribed quite a lot more in the USA now it has been approved by the FDA. We’ll wait and see what the effect is. Although it’s been a year already and I think the internet would be lit up with it by now if it had a high success rate.
      I think using antibiotics for large intestinal dysbioses is like playing roulette. Once the microbial massacre has begun, there’s a lot of luck involved in what bacteria subsequently go on to prosper in the aftermath.
      I’d wager that AAD is a lot more common than IBS-D resolved via Rifax 😉
      Kind Regards,
      Karl (Elixa)



  9. Antonio on March 28, 2016 at 08:20

    Don’t know. I’m just pointing about the overlap to Karl Seddon who knows better.

  10. Antonio on March 28, 2016 at 08:55

    Hi Karl. I think it’s not that way but more a defence for ‘broad spectrum’ antiseptics, not indiscriminate use.
    If the quote can be misleading (not for me but could be) the link is more elaborate.
    BTW, I’m one of your customers, from Spain. Regards.

    • Karl S on March 28, 2016 at 09:07

      Hi Antonio!
      Let me be a bit more specific with my word order, because ‘indiscriminate’ can be a bit ambiguous the way I’ve used it.
      I don’t mean the indiscriminate usage of antiseptics. I meant the usage of indiscriminate antiseptics. I.e. an antiseptic that does not discriminate good from bad.
      As with any antibiotic or antiseptic, there are always some microbes that can survive. THAT is the problem with antibiotic usage. The species that they do NOT kill off. Because now those species have free reign to colonise your gut, because all their opposition has been wiped out. And rarely do you have an antibiotic that coincidentally wipes out ONLY bad microbes, except… probiotics! 🙂 (In my opinion)
      In fact, with the ‘unnaturalness’ of the survival pressure that antibiotics are – it would be credible that the surviving profile of flora are also unnatural, in the context of what is natural to thrive in the human gut.
      I think if broad-spectrum was ‘100% spectrum’ then they would cause less issues. As it stands, that is not the case.
      Kind Regards,
      Karl (Elixa)



  11. Antonio on March 28, 2016 at 09:37

    From my part I could also explain better the ‘overlap’ part, which is not to be taken as some sort of equivalence, but I think it’s ok like that. Thinking about controlling/restraining the microbiota instead of promoting it is quite a change of direction.
    Good enough Karl. Thanks for your work and insights.

  12. GT on March 31, 2016 at 00:39

    Thanks for all your work Karl, I am slowly getting my head around the concepts you and others are bringing forward.
    I have had a severely compromised gut and have been slowly getting it more healthy with various pre and probiotics over the last year or so.
    I tried one round of Elixa a few weeks ago and mostly felt quite irritated whilst on it. So assume that the ‘scissors’ were doing their work! Unfortunately I just recently had to take antibiotics for a tooth infection, but will do another round or two once that has settled down.
    I wanted to ask you about a butyrate producing probiotic, Clostridium butyric. (a Japanese product called Miyarisan has it). There are some on a Chronic Fatigue forum who have been trialling it, with at times very strong reactions on really small quantities of it. It seems to have quite a different role to the Bifidos and Lactobacs I have tried. And interestingly I had also tried the AOR Probiotic-3 (which has it along with two other species) before it and noticed nothing at all.
    Any thoughts? I know it is difficult to comment on one specific strain, but am more curious as to other species/strains out already there that you think might be useful.

    • Karl S on April 16, 2016 at 13:18

      Hi GT!
      Apologies for the late reply. I must have missed your comment when it was originally posted!
      Thank you for the kind words.

      I would guess that the amount of butyrate producing bacteria in those products produce a change in butyrate output that would be absolutely dwarfed to insignificance when compared to the variation in butyrate production caused by the average person’s variation in dietary intake of raw or retrograded starch, or certain non-starch polysaccharides.

      Kind Regards,
      Karl (Elixa)



    • GT on April 17, 2016 at 16:49

      Thanks Karl! Given what you have said to Michael, do you think that taking a probiotic that amps up the amount of butyrate (like C Butyric) is not ideal? The best probiotics still being ones like bifido? Or am I misunderstanding?



    • Karl S on April 24, 2016 at 12:16

      Hi GT,
      If it DOES, in fact, noticeably increase butyrate production in the L.I. then i’d imagine it to be a good thing – assuming no other detrimental metabolites or bacteriocins are produced by that species and that the species does not competively exclude some other more beneficial species out of its niche.
      But my point was that the supplementation of that amount of CFU of whichever species you choose, would LIKELY make no dent in comparison to the upregulation in butyrate production by increasing RS intake.
      However, the advantage with probiotics is they allow you to control which populations increase. That’s the pro. The con is that the increase provided exogeneously won’t compare with the potential increases brought about indirectly by diet/prebiotic interventions.
      The difference with lactic acid bacteria (particularly in Elixa) is that they can be supplied in amounts that will be significant. My general stance is that most probiotics are wayyy under-dosed; and that is probably a good thing in the case of certain species/strains that are perhaps not natural in our guts at all. I.e. best to take something potentially useless/harmful at a low dose, than at a high dose!
      When the clinical theory is still thin on the ground, the fastest way to find the answer is to experiment and observe any changes.
      Kind Regards,
      Karl (Elixa)



  13. Michael on April 1, 2016 at 06:56

    Also interested in your thoughts on butyrate (I saw above comment in response to Tim). It’s not in the Elixa formulation. Do you recommend it for certain profiles of people (e.g. longterm Crohn’s)? Good for all? I saw you thought it was better to get naturally than from skipping steps in the process via direct supplementation, if a good idea, what would be a good natural source? Could taking it cause problems (would it feed anything bad?)

    Thanks~
    Michael

    • Karl S on April 16, 2016 at 13:37

      Hi Michael!
      Sorry for the slow reply!
      I think that looking at overall SCFA production gives a very zoomed out representation of the gut flora.
      While an increase in butyrate is a good thing, it is a byproduct of many bacteria’s fermentation processes and so looking purely at butyrate production would not explain all the finer details of different types of IBS, skin conditions, mental conditions, etc.
      So while PS may cause person A and person B to have a similar increase in intestinal butyrate production, for person A PS may also cause gas, pain, and headache. Whereas for person B PS may cause deep sleep and well-formed bowel movements. Because it also matters what all the other byproducts these butyrate producing bacteria (and non-butyrate-producers that still feed on RS) are creating. Which, imo, is determined by the exact type of bacteria that are feeding on the RS.
      I think looking at the ratio of intestinal production of SCFAs is similar to looking at the [Firmicutes:Bacteriodetes] ratio, insofar as it doesn’t explain the differences in the myriad symptoms/conditions of dysbiosis – skin, mental, digestive, immune, etc..
      Kind Regards,
      Karl (Elixa)



  14. Michael Ede on April 13, 2016 at 08:19

    Curious as to where pro-biotics would fit into fasting, fasting for 36 hours once a week with fat loss as the main goal. Skip the Elixa on fast days? or take the dose?

    • Richard Nikoley on April 13, 2016 at 08:29

      I’ll defer to Karl but I think you could look at it two ways.

      1. It costs money and since no food is coming down the pike to feed your new babies, you might be wasting it.

      2. Since no food is coming down the pike to feed the pathogens, they are weakened and Exlixa can do a more effective job in the role of antibiotic.

      Karl?



    • Karl S on April 16, 2016 at 13:03

      Hi Michael,
      I think you could make sense on paper arguing either way, i.e. lack of FODMAP/prebiotic content of diet (when fasting) will not allow the Elixa bacteria to thrive – OR – lack of FODMAP/prebiotic content of diet would lower total count of bacteria in the large intestine and make the size of the Elixa dosage *comparatively* larger vs the incumbent microbiota waiting for it in the large intestine.
      In practice I think the latter is far more relevant, even more so when considering that the capsule excipient is a prebiotic in itself (and directly in contact with Elixa when the whole thing rehydrates.
      For your scenario I would recommend not interrupting the course during the fast.
      Kind Regards,
      Karl (Elixa)



  15. Adrian on April 28, 2016 at 21:16

    Hi Karl,

    You explain above, “SIBO (which is far less prevalent than the internet community would imply) is an overgrowth of bacteria. Whereas a dysbiosis is an unhealthy profile of bacteria.”

    Could you clarify further on the different impacts Elixa is likely to have on Dysbiosis versus on SIBO?

    Love your work

  16. Adrian on April 29, 2016 at 16:07

    Hi Karl, Just checked out your website and you have answered that question there. Thanks

    • Karl S on May 3, 2016 at 12:54

      Hi Adrian,
      Good to hear!
      If you have any further questions about the topic, feel free to shoot me an email. I’ll be happy to help 🙂
      Kind Regards,
      Karl (Elixa)



  17. […] Probiotics As Targeted Antibiotics (33 Comments) […]

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