Malassezia have lost a gene* required to completely burn unsaturated fats—but they can burn saturated fats without issue. This means they can obtain energy to grow more readily from saturated fats than from unsaturated ones. This could partly explain why dietary saturated fats are associated with poor health outcomes.
Saturated fats within our bodies originate in part from fats in our diet. The other important source of saturated fats is dietary carbohydrates (sugars). For example, someone who eats mostly candy can still put on weight. Is this person’s body filled with sugar? No! It’s filled with saturated fats produced by the liver when carbohydrates are abundant. This process is called “de novo lipogenesis” or “DNL”. About 80% of fats produced by the liver through DNL are saturated (Aarsland 1998), so lipids produced naturally by our bodies from carbohydrates are well suited for Malassezia.
Historically, DNL helped our ancestors make it through the winter: they ate ample carbohydrates during the summer and fall, excess calories were converted into fats and stored, and these fats were burned during the winter months when food was scarce. You might ask, “Why doesn’t the body just store sugar for the winter?” Sugar weighs 2.25 times more than fat for the same amount of energy stored. If we relied on sugar instead of fat to get through the winter, we would weigh 60 lbs (27 kg) more!
The surest way to avoid overfeeding Malassezia in the body is to lose weight—by any means. This will reduce the availability of all fats. Because of Malassezia’s preference for saturated fats, interventions which reduce saturated fats in the body might help more than those reducing unsaturated fats.
This is largely in line with the current USDA dietary guidelines: don’t eat too many carbohydrates (which our bodies naturally convert into saturated fats) and don’t eat too much saturated fats. Note that unsaturated fats and proteins are not efficiently converted into saturated fats by our bodies, but alcohol is (sadly).
* Δ3,2-enoyl-CoA isomerase
This post was largely based on Celis 2017.
Animated Malassezia and lipids video: https://youtu.be/u1pckKEkwF0
Further to my email regarding the anti-fungal itraconazole and PDAC (and CDKN2a mutation as well eczema in my family, I also have a family member with ulcerative colitis and one with Crohn's so I am very interested in following your research and contributing where I can.
Thank you for this information. Very helpful. I have lost 3 siblings to pancreatic ductal adenocarcinoma. There is a germline genetic mutation (CDKN2a) that these siblings had which pre-disposed them to this type of cancer. I read the research published in the Nature journal in October 2019 about the presence of malassezia in the pancreatic ducts causing lesions. I also read research that showed that in a clinical trial involving itraconazole as well as a chemotherapy combination in patients with PDAC a participant had a fungal lung infection so was taken off the chemo but kept on the antifungal and his pancreatic umour shrank significantly which his doctor credited to the impact of the itraconazole. My sister who recently …