Fungi including Candida albicans are natural members of our gut microbiota. Unlike most fungi, Candida can overgrow under the certain conditions and even assume an invasive hyphal form that can cause tissue damage.
These are the things you can do to protect yourself against SIBO:
Avoid antibiotics when possible. Antibiotis is the biggest reason people end up with yeast overgrowth. Your best defense against SIFO is having a robust (mostly bacterial) microbiota. Gut bacteria help keep the small intestine acidic which helps keep Candida in check.
Avoid acid reducing drugs including PPIs and H2 blockers that also reduce the acidity in your small intestine.
Stay healthy, get rest and address any medical conditions you may have or medicines you are taking that negatively impact your immune system. Most fungal infections occur when people have compromised immune systems.
Simple carbs to resolve challenging SIBO symptoms. These strategies are also applicable for Candida but the emphasis is now on simple carbohydrates – Specifically:
- Limit sucrose, fructose and oligosaccharides containing fructose. All of these are likely to increase the amount of simple carbohydrates, especially fructose in the small intestine.
- Limit other sugars, even those that are easy to digest including glucose, galactose and maltose.
- Limit all starches, even easy-to-digest (low FP) starches.
Once symptoms are under control, easy-to-digest low FP starches and low FP sugars can be added back gradually.
Intestinal control of Candida
- Ketones altering the killing of Candida by neutrophils is irrelevant in controlling intestinal Candida overgrowth.
- As for Candida using ketones for energy in the GI tract, you mentioned the TCA cycle. But this requires oxygen, which is pretty scarce in the intestines. This recent report suggests that dysbiosis may involve a shift to higher O2 levels. Perhaps this is something to explore, but otherwise, I don’t see adequate O2 levels for aerobic respiration via the TCA cycle.
Systemic control of Candida (tissue or blood infections)
These are the highlights from the Saeed paper you cited (Production of Pyruvate by Candida albicans: Proposed Role in Virulence) :
- Focuses on the role of myeloperoxidase (MPO), the enzyme that helps neutrophils (phagocytic white blood cells) kill Candida (in tissue, not the gut).
- MPO is inhibited by acetoacetate, one of the ketone bodies increased during ketosis.
- It is suggested that prolonged ketosis may be a risk factor for (systemic) Candidiasis because Candida albicans can produce lots of pyruvate, a metabolite that may be converted to acetoacetate.
It has not been proven that Candida’s ability to use ketones efficiently for fuel in the GI tract. I will rethink this if increased GI oxygen levels (in dysbiosis?) needed to support the TCA cycle can be proven. Both ketones and glucose appear to repress cellular immunity to Candida. Other research suggests that increased blood glucose levels alone can induce a Candida protein which helps Candida evade the immune response regardless of ketone concentrations. I am not convinced that ketones per se are the only potential mechanism to help Candida evade the immune response.