The ketogenic diet (KD) is a high-fat, adequate-protein, low-carbohydrate diet established for treatment of therapy-resistant epilepsy. Was developed in the early 1920s to mirror the key metabolic effects of fasting. About half of the patients with epilepsy respond to the diet with at least 50% seizure reduction. Its efficacy in reducing seizures has been confirmed, but the mechanisms remain elusive. Several hypotheses have been proposed including changes in neurotransmitter systems, inhibitory action of polyunsaturated fatty acids, or enhancement of mitochondrial function. The diet has also shown certain positive effects in a wide range of other diseases, including Alzheimer’s, depression, autism, cancer, and type 2 diabetes.
A diet very high in fat and low in carbohydrates induces multiple changes in the intermediary metabolism and results in the use of ketones as the main energy substrate. Today, the classic KD is calculated with a ratio between 2:1 and 4:1 of fat to protein and carbohydrates combined. The ratio 4:1 contains 4 parts of fat and 1 part of proteins and carbohydrates together (in g). With a 4:1 ratio, 70–90% of energy intake is derived from fat. Different aspects of human metabolism may be implicated, but little is known about how KD influences our “second genome,” the microbiome.
Since 1860, and more recently, in 1972, low carbohydrate (low-carb) diets have been a strategy for weight loss. Today, there continues to be an interest in low-carb approaches. While all low carbohydrate approaches reduce the overall intake of carbohydrates, there is no clear consensus on what defines a low-carb diet.
Scientific studies have defined low carbohydrate as a percent of daily macronutrient intake or total daily carbohydrate load. It is defined as:
- Very low-carbohydrate (less than 10% carbohydrates) or 20-50 g/day
- Low-carbohydrate (less than 26% carbohydrates) or less than 130 g/day
Within the first 6-12 months of initiating KD, transient decreases in blood pressure, triglycerides, and glycosylated hemoglobin, as well as increases in HDL and weight loss may be observed. However, the aforementioned effects are generally not seen after 12 months of therapy, as the changes reported in the studies are not statistically significant.
Further research is warranted to evaluate the long-term implications of KD. Despite the diet's favorable effect on HDL-C, the concomitant increases in LDL-C and very-low-density lipoproteins (VLDL) may lead to increased cardiovascular risks. Additionally, the dietary restrictions required to sustain ketosis may actually lead to its low sustainability. Unfortunately, most available studies lack generalizability and validity due to their small sample sizes and short study durations.
Diet influences the composition of the human gut microbiome, so the fecal microbiome changes during KD. The compositional changes observed might not be favorable for gut or overall health based on the current understanding of the composition and role of a healthy gut microbiota. Taxa believed to be health promoting (bifidobacteria and E. rectale) decrease in relative abundance and with them their health-promoting metabolites. Reduction of carbohydrate intake - decrease of polysaccharide content associated with a decrease in beneficial gut microbiota bacteria such as Bifidobacteria.
Microbial increases such as Akkermansia or E.coli during KD express potential detrimental effect of HFD on the gut mucus barrier
Although KD has a positive impact on a wide range of diseases, there is a concern about the long term effects of KD on the gut microbiota composition and consequently mucus layer homeostasis and immunity functions - more specifically in healthy subjects adopting KD for weight loss. Further studies are warranted to understand the role of gut microbiota variations during KD and its therapeutic effect
Several studies have shown the important role of dietary fibers/NDCs (non-digestible carbohydrates) as energy sources for gut microbes in order to maintain gut health. Thus supplementing on KD with such fibers might seem advisable. The prebiotics inulin, lactulose, FOS, and galacto-oligosaccharides have been investigated in several human trials, and studies suggest that these carbohydrates preferentially increase bifidobacteria and decrease E. coli and enterococci.
If you are fan of long term keto diet and have problems with prebiotics intake and/or mentioned heath markers such as LDL or dysbiosis, you can try introducing fermented microdrinks regularly in your diet. Fermented foods/drinks are high in polyphenols that act as prebiotics, live bacterial cultures and their metabolites - postbiotics. New scientific studies will come and we will see clear impact on our health and in diminishing adverse effects of any restrictive diet pattern.