So now you are convinced that sugar is a main culprit of leaky gut as we are trapped in an addiction managed by processed food companies. But before we move on, it is better to know what the tiny thing, Candida, is. Why? Because this tiny thing is powerful and horrible, slowly eroding our health and deepening the misery of IBS.
Powerful that it is both a lover (romantic but toxic) and a team player that it can get into our bloodstreams and escape from the radars of our internal defenders. Horrible that it is related to diseases such as depression, multiple sclerosis, and even cancer (a message delivered by Ann Boroch, a passed naturopathic doctor in Los Angeles).
What (on earth) is Candida?
Most female IBS people know that Candida is a yeast that lives in vagina. Actually, Candida is a type of yeast (a kind of fungus) that also naturally resides in our digestive tracts (Mayer et al. 2022). As mentioned in post 1, it is a friendly bug when kept in small amounts.
Well, yeast might seem harmless, barely worth a second thought. But hold on, because what if I told you that fungi, a tiny creature, may have played a part in wiping out another creature that is really huge? Let me share with you a horrible theory mentioned by Keith Seifert (a fungi expert).
Fungi: the murder?
You know that a long time ago the earth was hit by a asteroid, a big, rocky marble from space. You also know that the hit killed off dinosaurs. But did you know that the asteroid lowered Earth’s temperature? And do you know what happened when dinosaurs were not able to increase their body temperature under such cold conditions? Their body could not fight against fungi that were pathogenic.
So what happened finally? Without the ability to fight off deadly fungal infections, dinosaurs’ days were numbered. (This concept—called fungal infection-mammalian selection—is explained in Chapter 7 of Seifert’s book.)
Now that you know what fungi might have done to dinosaurs, it is time to turn the focus to us, IBS people, to find out what they do in our guts.
Candida & sugar: The love that is romantic but toxic
In our guts there is a special bond between sugar and Candida, so special that they cannot live without each other. And because Candida loves sugar so much they will send this signal of love through the gut-brain axis to our brains. (Yes, some of you may have already known about the axis. Microorganisms, candida included, in our guts ‘talk’ to our brain through the axis, a piece of information explained by Steve Gundry in his book, Gut Check).
With that calling, you will look for, long for, and rush for, your favourite desserts and processed food. So, next time you crave desserts, remember it is actually not you wanting more sugar, but Candida in your gut. Candida ‘communicates’ with your brain, compelling you to grab sweets. In a way, Candida’s love for sugar hijacks both your mind and body.
As a result of the bonding, Candida will swim in our bloodstream and treat every part of our bodies as travel destinations (leaky gut mentioned in the previous post). In a word, the bonding and love between Candida and sugar is romantic, but toxic to us.
Team work of Candida VS our internal defenders
However, it is not just the romantic love between Candida and sugar you have to combat. Candida will go hand in hand with others to form a team, and worst of all, such a team can produce a shield (doctors call it biofilms). Such a shield acts as a protective layer, making it hard for medicines to reach teams of Candida, not to mention killing them. Making it hard? What does that mean?
a. weakening our big defenders
First, the teams of Candida weaken the power of a band of our internal defenders, the white blood cells doctors call macrophages. Macrophages? They are defenders of our bodies with three grand tasks: detecting, engulf and destroying harmful things. However, the protective shield of Candida is so thick that our great defenders cannot get through it, making the Candida undetectable.
Worst of all, the shield has the ability to prevent macrophages from becoming active and producing necessary signals, chemical messages telling other cells in the immune system to be on alert.
b. bravest fighters being tricked
Second, another band of our immune fighters is also blocked. Neutrophils. Who are they? They are not as powerful as the band of Macrophages but they are the bravest. Neutrophils live in our bodies for one and only one purpose. To fight and then die for us (Dettmer, 2021). They are skillful at attacking Candida when the fungal is in on their own, in a free-floating state. However, when Candida forms a team and hides behind its biofilm wall, the bravest defender struggles to get inside.
Even worse, Candida can trick neutrophils into making traps, which actually help make its wall stronger. How does this tiny, horrible creatures do it? It plays a trick. It makes Neutrophils build sticky webs, thinking they are catching Candida. But instead of stopping it, these webs help Candida grow stronger and build a tougher shield (information by Biology Insights).
References
Biology Insights. (2025). Candida Biofilm Formation and Host Interaction Dynamics. Retrieved from https://biologyinsights.com/candida-biofilm-formation-and-host-interaction-dynamics/
Boroch, A. (2020). The Candida Cure: The 90-Day Program to Balance Your Gut, Beat Candida, and Restore Vibrant Health (Revised Edition). HarperOne, New York, NY, USA.
Dettmer, P. (2021). Immune: A Journey into the System That Keeps You Alive. Hodder & Stoughton, London, UK.
Gundry, S. (2021). Gut Check: The Science Behind the Gut-Brain Connection and How It Affects Your Health. Harper Wave, New York, NY, USA.
Mayer, F.L., Wilson, D., & Hube, B. (2022). Interactions between Candida albicans and the resident microbiota. Frontiers in Cellular and Infection Microbiology, 12, 9531752. https://pmc.ncbi.nlm.nih.gov/articles/PMC9531752/
National Library of Medicine. (2021). Candida Biofilms: Formation, Structure, and Antifungal Resistance. In Biology Insights. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK560624/
Seifert, K. (2011). The Fungi: A Very Short Introduction. Oxford University Press, Oxford, UK.
