Effects of an Eight Week Very Low-Calorie Ketogenic Diet (VLCKD) on White Blood Cell and Platelet Counts in Relation to Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in Subjects with Overweight and Obesity.

Obesity and metabolic dysfunction-associated steatotic liver disease (MASLD) are frequently associated conditions characterized by low-grade inflammation. Very low-calorie ketogenic diet (VLCKD) strategies are commonly used to simultaneously obtain weight loss and an improvement of liver steatosis. We evaluated the efficacy of 8 weeks' VLCKD in decreasing the white blood cell (WBC) and platelet (PLT) counts, as well as liver steatosis and fibrosis, diagnosed using transient elastography (FibroScan). Metabolic and anthropometric parameters commonly associated with MASLD were also evaluated. This study included 87 participants; 58 women and 29 men aged between 18 and 64 years with overweight (18%) or obesity (82%), but not taking any medication. Anthropometric measurements, bioimpedance analysis, and biochemical assays were performed before and after the dietary intervention. BMI (kg/m 2 ) ( p -value < 0.001), waist circumference (cm) ( p -value < 0.001), and fat mass (kg) ( p -value < 0.001) were significantly decreased following VLCKD. After VLCKD, the FibroScan parameter CAP (db/m), which measures the accumulation of fatty liver, significantly decreased ( p -value < 0.001), as did liver stiffness (kPA), the FibroScan parameter quantifying liver fibrosis ( p -value < 0.05). Seemingly, WBC ( p -value < 0.001) and PLT ( p -value < 0.001) counts were lowered by VLCKD in the whole group; however, the decrease in WBC and platelet counts were significant only in patients with steatosis (CAP ≥ 215 dB/m). Fasting blood glucose ( p -value < 0.001), insulin ( p -value < 0.001), HbA1c ( p -value < 0.001), triglycerides ( p -value < 0.001), total cholesterol ( p -value < 0.001), LDL-cholesterol ( p -value < 0.001), HDL-cholesterol ( p -value < 0.001); γGT ( p -value < 0.001) blood levels and insulin resistance (as measured by HOMAIR) ( p -value < 0.001); and systolic ( p -value < 0.001), and diastolic ( p -value < 0.001) blood pressure levels, were all significantly lower after VLCKD. In contrast, blood levels of vitamin D were higher following the diet ( p -value < 0.001). We conclude that treating subjects with overweight and obesity with VLCKD is followed by a simultaneous reduction in WBCs and platelets, the expression of low-grade inflammation, and of liver steatosis and fibrosis. Therefore, we can hypothesize that VLCKD decreases general and liver low-grade inflammation, thus improving liver health.