05/18/2026
Ketogenic diets can be transformative for some neurological and metabolic conditions, but they are not metabolically neutral for everyone.
My own experience showed a dramatic rise in LDL-C and non-HDL cholesterol after starting a ketogenic diet, despite favorable triglycerides and HDL levels. Rather than abandoning the approach immediately, I adapted. I shifted toward olive oil, avocados, nuts, seeds, and fatty fish while reducing saturated fat and dietary cholesterol intake. I cut out half-and-half, whipping cream, and many cheeses. When I do have cheese, I enjoy high protein Parmesan as a flavorful treat with a zing. I stopped using MCT oil daily to maintain ketosis, and use it as a support for hypoglycemic periods on instead (rapidly converted to glycogen in liver). Over time, my lipid profile improved substantially, and will continue to normalize.
This phenomenon is real. Some individuals experience marked increases in LDL-C on ketogenic diets, potentially related to altered lipid trafficking and intestinal sterol hyperabsorption. Monitoring matters. Personalization matters. Physiology matters.
The goal is not ideology and a one size fits all approach. The goal is individual neurometabolic optimization and homeostasis.
Keto may help one system while stressing another. Understanding that balance, measuring biomarkers, and making individualized decisions with your healthcare team is how we move toward precision medicine instead of one-size-fits-all nutrition advice.
I am grateful my lipids improved with adaptation and prioritization of healthy fats, as my brain’s fuel system is much more stable on a ketogenic diet when compared to a standard American diet, which caused hypothalamic obesity and worsening hypoglycemic unawareness in the setting of my autosomal dominant MC4R deficiency.
Knowledge. Awareness. Action.
