This page sets out a model we find compelling for how gut dysbiosis may begin. Parts of it rest on well-established microbiome science, and we say so where they do. Other parts are our own working hypothesis, connecting established findings in a way the literature has not yet directly tested. We present it openly as a theory, because we think it's a useful and honest way to explain why we make the yoghurt we do. It is not medical advice.
The gut is home to the microbiome, a vast community of bacteria and other microbes that functions as an organ in its own right. Rather than being made of human cells, it's made of microbes we pick up from our environment, largely inherited at birth from our mother's microbiome.
We have co-evolved with these microbes. They help digest our food, train the immune system, and resist invading pathogens, and in return we feed them. As they break down what we eat, they produce metabolites the body relies on, including short-chain fatty acids (such as acetate, propionate and butyrate), B vitamins, vitamin K2, and compounds involved in mood and hormones.
The microbiome lives along the lining of the intestines, called the epithelium. This lining is thin and constantly renewed, which keeps it working but also leaves it vulnerable. When it's damaged it can become more permeable, sometimes described as a "leaky gut."
Microbes compete for food, and that competition naturally keeps their populations in check. In a healthy, balanced state, the most beneficial microbes tend to be strong producers of butyrate. Butyrate matters because it is the main energy source for the cells of the large intestinal lining, so a steady supply helps keep that lining healthy. This part is well established in the literature.
That balance depends on the right conditions, and one of the most important is pH. Different segments of the gut sit at different, carefully regulated levels of acidity. Research shows that gut pH influences which microbes thrive. Our hypothesis builds on this: we propose that when the gut is pushed towards alkaline, beyond its normal range, the environment begins to favour microbes that produce propionate over those that produce butyrate.
If butyrate falls, the lining loses its main fuel. Our proposed consequence is an energy shortfall in the epithelium, leaving it weakened.
This next step draws on a recognised model in microbiome research. A healthy gut lining keeps the inside of the gut largely free of oxygen, which favours the beneficial microbes that prefer oxygen-free conditionsc called obligate anaerobes. Other microbes, called facultative anaerobes, examples include E. coli and Salmonella, can cope with oxygen and actually thrive when it's present.
When the lining is weakened and oxygen leaks from the blood into the gut, the balance tips. Facultative anaerobes can bloom, beneficial anaerobes are crowded out, and the microbiome shifts into dysbiosis, a disrupted, less healthy balance. In our model, this is the point at which a manageable imbalance becomes a self-reinforcing one.
So what starts the chain? Our hypothesis points to an alkalising agent in the stomach, and the most common candidate is Helicobacter pylori.
H. pylori is a very common stomach bacterium. It survives the stomach's strong acid using an enzyme called urease, which produces ammonia. Ammonia is alkaline, and by generating it, H. pylori neutralises the acid around itself to create a more comfortable environment. This urease mechanism is well established science.
The stomach normally sits at a very low, very acidic pH, which both helps break down food and kills many incoming microbes. The fluid that leaves the stomach for the small intestine, called chyme, carries a particular acidity that contributes to the pH balance further along the gut.
Here is the heart of our hypothesis: we propose that by raising stomach pH, H. pylori can leave chyme less acidic than it should be, and that this nudges gut pH towards the alkaline, setting off the chain described above, from a shift away from butyrate, to a weakened lining, to the oxygen tipping point, and finally to dysbiosis. We also reason that because H. pylori tends to persist, the alkalising pressure persists with it, which is why the resulting imbalance may not simply resolve on its own.
To be clear: the link between gut pH and microbial balance, the role of butyrate, and the oxygen model of dysbiosis are all grounded in published research. The specific idea that H. pylori-driven alkalinity carries downstream to initiate this whole cascade is our own theory, and the direct evidence for it is limited. We find it compelling, but we hold it as a hypothesis, not a settled fact.
Diet shapes the environment all of this plays out in. Ultra-processed foods and heavily refined seed oils undergo extensive chemical processing and heating, and research has associated diets high in these foods with poorer gut health and a higher burden on the gastrointestinal tract. Our view is that such diets can help create the conditions in which microbes like H. pylori establish themselves, and that the effects build quietly over time rather than all at once.
This theory is the reason we ferment with the strains we do. We use L. reuteri DSM 17648, which has been studied in connection with H. pylori, and L. reuteri DSM 17938, researched for its role in supporting microbial balance further along the gut. Our interest in where dysbiosis may begin is exactly why these two strains, rather than a generic culture, are the ones we chose.
You can read more about the strains and the research behind them on our about page, or browse the yoghurt in our shop.
This page presents a mixture of established microbiome science and our own working hypothesis, clearly distinguished, for educational and explanatory purposes. It is not medical advice, and it is not a claim that any food or product treats, cures or prevents infection or disease. If you have ongoing digestive symptoms or think you may have an H. pylori infection, please speak to a qualified healthcare professional, who can arrange appropriate testing and care.