FODMAP Prebiotic Arms Dealing, Probiotic Mercenaries, and Uganda
Based on the emails I receive, I’d say that the average person interested in probiotics and gut health are well-read on the topic. Due to the relatively recent emergence of majority access to the internet and mainstream awareness of the microbiome, there’s a huge amount of crowd-sourced research and shared information regarding probiotics, the microbiome, and prebiotics—or what I prefer to call FODMAPs.
Self-experimentation, anecdotal meta-analysis (collating 2nd hand reports), and scientific experiments are all legitimate means to increase our understanding of how the gut bacteria affect us and how to manipulate this understanding to our advantage.
Although I am the developer and manufacturer of Elixa Probiotic, this article does not directly concern probiotic supplementation. There is plenty to discuss about the individual attributes of Elixa, however I would prefer to start chronologically by detailing some of the R&D that came before. Hopefully this will be a brief insight into some of the thoughts and work performed during the 3+ years of development that has occurred since I graduated.
With a science-based, academic background, most people will assume: Oh, so you learned this stuff at university, right?
As it happens …No. And I would be a bit worried about the security of my intellectual property if that were the case, since there were at least 50 fellow students on my degree course!
But it has provided me with the tools to scientifically analyse and test, in addition to the manufacturing engineering knowledge I would subsequently expand upon to begin my business.
But First – To Uganda!
Entebbe International Airport, Uganda
My primary reason for taking a one way ticket to Uganda was that I felt like doing some humanitarian work while things were ticking along with my uncharted venture into probiotic R&D. Like writing a book, progress in research is not linear. Filling the lulls with other activities keeps you sane.
However, as many of you will know, when you’re obsessed with a scientific concept, you will always have some theory ticking over in your mind. You’ll catch yourself considering it in all situations you come across, attempting to apply it to these situations via a form of mental simulation. Since my plan was to take a taxi bus straight from Entebbe airport to a rural town (Kiboga), I felt that there’d be ample opportunity to make some observations and throw in a little bit of cold, hard science as a side-hobby to my primary intentions.
Skip forward almost a year and many, many things had happened and I had blown past all my expectations over what I’d intended to achieve there (in the domain of scientific investigation, as well as my original goals).
Looking back down on Kiboga Town after wandering up a mountain
The view in all other directions
The Local Ugandan Diet
Food is about the first thing on the list of things to do when you enter a new country. Anything you eat in these villages has been cooked a few hours or minutes before you eat it. Not only that, but much of it has—just minutes prior to cooking—been grazing around and enjoying the warm Ugandan sun…unaware that a Rwandan cattle herder is sharpening his panga, with an eye to retail old Bessy for 7,000 shillings per kilo.
No denying the meat is free-range
I made a few immediate observations about the dietary habits of Ugandans in non-urbanised settlements outside of the main cities. (Rwandans were slightly different. More on that another time.)
- They eat very substantial portions
- With lots of carbs
- And lots of red meat. With the subcutaneous fat still attached
But they’re not all obese, diabetic, and suffering from heart failure. In fact, they’re quite the opposite. I won’t spin you the fairytale that they’re all 6’6”& 250lbs of lean muscle with glowing skin and flowing hair. But healthy they certainly do appear.
Some of my friends. An accurate representation of the typically healthy men in Kiboga
This isn’t new news. Nobody reading this article is thinking that carbohydrates are automatically unhealthy, or that fatty meat will unquestionably predispose you to coronary heart disease. But first hand observation is certainly worth a thousand hours of reading 2nd hand reports.
So what’s the diet like, and why it is an extremely healthy diet in my opinion?
As grass-fed and organic as you can get. The best meat I’ve ever eaten
This is the typical range you will find in each meal. It’s usually served with carbohydrates on the plate, and the meat in a bowl of its own cooking soup. This was all served on a dish so I could carry it up to my hostel room to snap a photo.
The carbohydrates include (2-3 in the same meal):
- Green Banana (Matoke) – Steamed in banana leaves and mashed.
- Plantain – Grilled over charcoal or Boiled
- Cassava – Boiled
- Sweet Potato (of both the orange and white variety) – Boiled
- Rice (long-grain white or pilau) – Boiled
Less often would be:
- Posho (Maize/Corn flour boiled in water like rice)
- Beans (cooked into a half solid, half soup state)
- Groundnuts (Aka. Purple-skinned peanuts. Cooked into a thick paste.)
It’s an unimaginably vast array of naturally sourced and naturally prepared prebiotics/FODMAPs conspicuously lacking virtually all of the rabbit-food greens various Western diets tout above all else.
The meat on offer is slow-cooked chicken and beef. And occasionally slow-cooked goat or pan-fried fish. The beef and chicken is ridiculously tasty. The beef, especially, will ‘melt’ apart in your mouth due to it being so soft. They’re cooked in a boiling broth of freshly prepared onions, green peppers, aubergine, tomatoes, and salt. Sometimes a bit of garlic for the phonetically spelled menu item: Gallick Chicken.
As you can see: a veritable prebiotic/FODMAP soup! It goes without saying: there’s no deep-frying in sight.
Steaming green banana, wrapped in banana leaf, on a charcoal stove
There’s an old adage: a calorie is a calorie. This is patently untrue. Eat 1,500 calories per day of doughnuts and french fries for just a few months and see how you fare versus the 100-year-old Japanese eating 1,500 calories of fish and rice. Your skin, waistline, and mental state will not thank you for the former, but may thank you for the latter.
So how about a calorie of macronutrient X is a calorie of macronutrient X? For example: A calorie of carbohydrate is a calorie of carbohydrate.
Sound better? Whether it does or doesn’t, it’s still untrue. Bread, Rice, Potatoes, Maize/Corn, Yams, etc., are not all created equal. A 100g plate of carbs from plantain would not generate the same response as would 100g of carbs from bread, if consumed regularly as your staple.
So what causes the difference? Is it the micronutrient content (i.e., the vitamins and minerals?), or is it perhaps something to do with the speed at which the substances are broken down and absorbed into the blood stream?
It’s All About The FODMAPs
It’s my belief that the most important factor to consider in a meal are the FODMAPs contained within. Before proceeding, I should define what I mean: Fermentable: Oligosaccharides, Disaccharides, Monosaccharides and Polyols.
Generally speaking, this correlates to Indigestible: Carbohydrates, Dimer Sugars (e.g., lactose), Monomer Sugars (e.g., glucose) and Sugar Alcohols (e.g., sorbitol, xylitol, etc.).
I should clarify that indigestible here refers to the inability of a human to digest the substance via our own digestive enzymes and processes. So, fermentable correctly implies the idea that microorganisms can digest these substances.
With my friends, the founders of Orphan Hope Centre, getting our RDA of sugar alcohol. Well…. alcohol, atleast
For purposes of this discussion: FODMAPs include anything we eat/drink which makes it all the way to the large intestine in a form that can be digested (or further digested) by the microorganisms colonising our gut.
The reason I believe the FODMAP content on your plate to be of such significance is because I happen to be entirely convinced that the profile of microorganisms in our gut microbiome plays an enormous role in our health, across a huge range of systems (neurological, dermatological, gastroenterological, immunological, etc.).
So it stands to reason that we should consider the microbiome’s daily diet just as much as our own (our own being the human-digestible portion of the meal). It has been comprehensively demonstrated that the profile of our gut bacteria can be manipulated via the use of prebiotics. Prebiotics are, of course, FODMAPs. I prefer to use the latter term because it does not bias the phrase towards symbolising something inherently good or inherently bad.
FODMAPs—fiber, prebiotics… whatever you choose to call them—have a context dependent response. Specifically, the profile of the eagerly awaiting population of gut microorganisms sitting there with mouths wide open, waiting for that next trickle of fermentable substrate to be passed from the latter portion of the small intestine (the ileum), through the ileocecal valve, into the first portion of the large intestine (the ascending colon)—where it will then make its way through the 100 trillion bacteria that reside between the IC valve and exit sphincter.
The resulting effect from consuming one FODMAP versus another is determined via 2 main mechanisms:
- The bacterial strains whose populations it increases/decreases
- The byproducts produced by the fermentation (a function of the bacteria metabolizing it and the substrate itself)
There’s already plenty of information on Richard Nikoley’s FreeTheAnimal site about the various byproducts produced by gut fermentation (especially among the Resistant Starch discussions). For now, I’ll discuss point number one.
How does the dietary FODMAP profile affect the populations of our microbiome?
Of Arms Dealers and Mercenaries
A whole article could be written about this, but the fundamental mechanism at play is the preferential feeding of certain strains over others. What this means is that certain strains of bacteria are better equipped to break down a particular substrate and use it to fuel their proliferation and survival. If there’s enough food (and room) to go around for everyone, all is well. But what happens when the food source is not a limiting factor and bacterial population growth occurs? The limiting factor in survival now becomes epithelial space, i.e., the surface area on the large intestinal wall for the bacterial populations to colonise. When populations expand into each other’s territory, competitive exclusion must occur to one or more belligerents. Who wins (in this example) is determined by who can best metabolise the food source, and this is determined by their metabolic pathways.
Think of it like this: Imagine a group of primitive humans sitting in one corner of an enclosed field and a group of cows sitting in the other corner. These two species are analogous to two different species of bacteria. Now, for the sake of analogy, imagine that each of these cows is equally matched to the fighting capability of each of these humans. They peacefully coexist because they rarely cross paths and have no incentive to venture over to the other corner and start problems. Life goes on and all is good. Once per day, a crate of food is air-dropped in. It contains a small amount of food (just enough to maintain both populations at a fixed size) and it contains a range of food types. For the cows we have some nice grass and other plants. For the humans we have meat, yams, and some fruit. This crate represents the fermentable portion of your daily diet. The parts of the diet that make it all the way to the large intestine (the field). The average Westerner will eat only a small amount of FODMAPs and this is represented by there being a meagre one crate dropped per day.
However, one day the air-drops change. (This part is analogous to you making a dietary change in your FODMAP consumption.) Now the air-drop consists of 10 crates. 1 of them is identical to the previous daily air-drop but the other 9 are all filled with…. grass! ‘Oh great!’ say the cows, and they begin to feast. The humans continue to eat their previous diet but also attempt to eat some grass, because… you know… they’re hungry and when they see more food they want to eat it (bacteria, like most organisms, will at least attempt to eat anything food-like). The humans manage to extract some nutrition out of the grass but they’re very poorly equipped to digest and extract the calories from this grass. Nevertheless, in times of peace, this is sufficient for these humans to continue living as usual.
￼￼A few years go by (in the gut this would be equivalent to hours or days) and the population of the cows is booming, thanks to all the grass consumption, and they’re starting to occupy most of the field. In fact, they’re almost infringing on the human population’s area. The surface area of the field represents the surface area of the large intestine’s epithelium.
Another year goes by and the cows make their move! They need that land because they literally can’t fit on the field without that last corner. So the clash begins. As we’ve already contrived, a human here is equal to a cow in fighting capability. The Great War of Cow and Human ensues, but the cows outnumber the humans and all the cows are sinewy and energized…well-fed…on grass.
The humans attempt to increase their numbers and bolster their physiques by consuming grass (of which there is plenty to go around!) but, alas, they just can’t get anything out of it except green-specked bowel movements. Eventually the humans are outnumbered and overpowered by the cows. They’re killed off with no other place to procreate and colonise. They have now been competitively excluded.
And all because they didn’t have the necessary mechanisms to efficiently metabolise that grass!
A friendly Ugandan cow that I walked into, in the pitch black night. It, understandably, did not appreciate my use of camera flash to see what I had just bumped into
In case you hadn’t realised, the grass here represents the particular FODMAP that you have decided to dietarily (or via supplements) increase within your daily diet. This could be…. for example, resistant starch or inulin.
It’s a simplistic analogy, but acts as a good introduction to the idea of ONE of the modes by which a change in dietary FODMAP profile can change the bacterial profile: stimulating population growth to a degree which necessitates competitive exclusion by the better-adapted strains.
The reality is much more complex, with 100s of species present and dozens of fermentable substrates, most of which can be metabolised fairly easily by the vast majority of bacteria present. Bacteria are more omnivorous than one may be lead to believe by reading about prebiotics and their ‘selective’ ability to feed only ‘good’ bacteria.
Having said that, I previously stated that not all macronutrients are created equal and, by inference, this is because not all FODMAPs are created equal. Delving deeper should be kept outside the scope of this article, lest I stray completely off my point. But if you were to modify the Cow vs. Human analogy to say that the humans could metabolise the grass, let’s say… 80-90% as efficiently as the cows—instead of the 1-2% implied—you may be getting closer to reality.
The specific bacteria already residing within the gut (and the size of their populations) can determine the steady-state result arrived at after the transient ‘war’ that ensues soon after the point of introduction of the new FODMAP. Based on my own research and hypotheses I believe an example of one of these ‘wars’ would be the transient increase in flatulence after initial adoption of inulin. Or the transient predisposition to headaches after initial adoption of resistant potato starch. It credibly explains why the symptoms arise initially, yet subsequently resolve. The layman explanation—your body adapts to the increase in fiber—was a tad unscientific for my liking. Ultimately, the negative symptoms will settle out IF your pre-existing microbiome was sufficiently healthy and you possessed a critical threshold of beneficial bacteria.
Many variables (particularly the type of FODMAP itself) can affect whether your pre-existing microbiome will indeed be able to adapt in a positive direction. But it remains true that a hugely influential variable is the starting profile. Going back to my analogy (assuming we use the more representative model of humans being able to metabolise the grass at 80-90% the efficiency of the cows): If the starting population of humans was 10x that of the cows, to begin with, how do you think the results would turn out? Now, what about 2x? What about 1.1x?
Or, what about equal population size… but humans are actually superior (on a per capita basis) in fighting capability? What if they are just a little better? What if they’re a lot better?
This is what can lead to different results for the exact same FODMAP.
Take inulin, for example. Give it in high quantities to someone with IBS and they may experience the worst pain, flatulence, bloating, and diarrhoea imaginable. Give the same inulin to someone who has never suffered from gut issues and they may find they have deeper sleep, more sustained energy throughout the day, and cleaner bowel movements.
￼￼￼￼￼There is huge potential in prebiotics. But what about right now? How can we guarantee we’re feeding up the good and not feeding up the bad?
One obvious route is to omit the ‘feed-up’ altogether, and go for a more precise approach where the bacterial profile changes are determined more by the supplement than by the pre-existing state of your microbiome.
This is where Elixa Probiotic and the whole concept of beneficial probiotic bacteria enters the scene. The uncertainty of the pre-existing state of the gut microbiome is rendered practically irrelevant when you’re now able to determine the affected bacterial populations by incorporating them into the supplement itself!
But probiotics aren’t new, so what’s so revolutionary about Elixa?
The answer is quite simple. In fact, it almost seems trivial. The not-so-trivial part is the technological innovations of the manufacturing process that have been invented to create Elixa. There’s a big difference between theorising how a probiotic could be superior, versus developing the means to actually manufacture it in practice.
For starters, the CFU count of Elixa is 50x that of the average probiotic. This means it has approximately 50 times the number of bacteria compared to an average 10 Billion CFU probiotic. Getting a true factor of five times higher concentration of viable lactic acid bacteria, on a capsule for capsule basis, is no easy feat.
And this is not 50x too many. Or an ‘overdose’, ‘megadose’, or any other superlative. It’s actually a reasonable dose compared to perhaps insufficient doses in other products. Don’t take my word for it. Consider the number of bacteria in the large intestine. We’re talking approximately 100 trillion. If you take your 10 billion CFU average probiotic, you are consuming a pill containing one 10,000th of the residing population. It’s like a droplet of food-dye in a bucket of water. There simply isn’t enough to generate a noticeable change. And certainly not enough to initiate a reversal of a significant imbalance in an unhealthy microbiome. With the recommended starting point of a 6-day course of Elixa, you’d be consuming over 3 Trillion CFUs. Whew, finally into the trillions now! This is more like a whole bottle of food colouring poured into that same bucket of water.
And this is no ‘monochrome’ probiotic. We utilise 9 strains within the blend. The choice of the specific species and strains is based upon, in part, research performed in Uganda on raw-milk drinking Rwandans and several other population-sets in rural Africa. But that’s a story for another time! It suffices to say that all are adapted for colonisation of the human large intestine and from species that have undergone extensive scientific studies. And in addition to a fundamental leap in yield, our Fortress-5 technology produces Elixa in a more ‘protected’ supplement format than conventional formulations.
This is an oft-used description for probiotics. More stable; better protection; acid-resistant; etc. However, the reality (and as the inventor and manufacturer I feel I have good insight into this) is that surviving in the stomach acid and duodenum environment is fairly simple. There’s much more to the viability of the probiotic than surviving the brief exposure to less than optimal pH. Questions such as: what exactly occurs during lyophilisation? (freeze-drying) and what is the precise mechanism by which rehydration causes reanimation? (reviving the bacteria once in the gut) and what obstacles to epithelial binding are presented to a freshly reanimated bacteria in viscous suspension? and what aversion mechanisms/constructs have the—already-settled—bacteria got lying in wait for the new entrants into the neighborhood?
An elaboration on the answers would encroach upon revealing the gears and cogs underpinning our Fortress-5 technology, so I’ll allow the questions to remain rhetorical and stimulate an appreciation that the simplistic manufacturing & administration concept of: Grow bacteria. Dry bacteria. Encapsulate bacteria. Swallow bacteria. Hydrate bacteria. Reanimate bacteria. Done! is where Elixa differentiates itself.
I hope this article has been enlightening to novices and informative and stimulating to the more expert among you. Thank you for reading, and I look forward to expounding on some of the other topics I touched upon…such as the dietary, clinical, and physiological variations among rural Africans…and subsequent extrapolations to the field of the microbiome and human health.
The next logical step is to give an ultra high potency probiotic a try! I’ve been developing Elixa over the past 5 years and it has experienced an unbelievably positive reception ever since I first launched it. I now sell to customers in over 30 countries, have fulfillment warehouses in 2 countries (UK & USA), and the demand is rising every day. I look forward to hearing great feedback from you, if you decide to try it for yourself. Just get in touch via email if you have any questions. I’ll be happy to help!