Ketogenic Diet-Induced Weight Loss is Associated with an Increase in Vitamin D Levels in Obese Adults

Abstract

Vitamin D is an important micronutrient involved in several processes. Evidence has shown a strong association between hypovitaminosis D and cardio-metabolic diseases, including obesity. A ketogenic diet has proven to be very effective for weight loss, especially in reducing fat mass while preserving fat-free mass. The aim of this study was to investigate the effect of a ketogenic diet-induced weight loss on vitamin D status in a population of obese adults. We enrolled 56 obese outpatients, prescribed with either traditional standard hypocaloric Mediterranean diet (SHMD) or very low-calorie ketogenic diet (VLCKD). Serum 25(OH)D concentrations were measured by chemiluminescence. The mean value of serum 25-hydroxyvitamin D (25(OH)D) concentrations in the whole population at baseline was 17.8 ± 5.6 ng/mL, without differences between groups. After 12 months of dietetic treatment, in VLCKD patients serum 25(OH)D concentrations increased from 18.4 ± 5.9 to 29.3 ± 6.8 ng/mL (p < 0.0001), vs 17.5 ± 6.1 to 21.3 ± 7.6 ng/mL (p = 0.067) in the SHMD group (for each kilogram of weight loss, 25(OH)D concentration increased 0.39 and 0.13 ng/mL in the VLCKD and in the SHMD groups, respectively). In the VLCKD group, the increase in serum 25(OH)D concentrations was strongly associated with body mass index, waist circumference, and fatty mass variation. In a multiple regression analysis, fatty mass was the strongest independent predictor of serum 25(OH)D concentration, explaining 15.6%, 3.3%, and 9.4% of its variation in the whole population, in SHMD, and VLCKD groups, respectively. We also observed a greater reduction of inflammation (evaluated by high-sensitivity C reactive protein (hsCRP) values) and a greater improvement in glucose homeostasis, confirmed by a reduction of HOMA values, in the VLCKD versus the SHMD group. Taken together, all these data suggest that a dietetic regimen, which implies a great reduction of fat mass, can improve vitamin D status in the obese.

Effectiveness of a Very Low Calorie Ketogenic Diet on Testicular Function in Overweight/Obese Men

“…Notably, these results are in line with previous studies. A 2013 meta-analysis of 13 studies showed that body weight decreased significantly after VLCKD [ 15 ]. Similarly, Merra et al studied the effects of three types of VLCKD (all with carbohydrates intake <50 g/day) in 54 overweight/obese patients, observing a significant reduction in BMI, waist circumference, and total body fat after three weeks of VLCKD [ 16 ].…”

“…A very interesting aspect to consider is the relationship between VLCKD and vitamin D. It is known that vitamin D levels are lower in obese people than in normal-weight subjects, possibly given volumetric dilution effects, but also due to other obesity-related factors, such as poor dietary intake, lack of exposure to sunlight, and lower skin synthesis [ 1 , 15 ]. Although the 2020 European Society of Endocrinology (ESE) guidelines about the work-up in obesity do not suggest the routine measurement of vitamin D levels in obese patients, its evaluation in patients undergoing VLCKD is of great interest since suboptimal levels seem to be associated with impaired glucose homeostasis, insulin resistance, and DM2 [ 15 ]. In our experience, we found that vitamin D levels become significantly increased after VLCKD.…”

“…Obesity and low vitamin D levels (and other comorbidities that are obesity-related, such as metabolic syndrome and DM2) are also associated with a functional “dysmetabolic” hypogonadism [ 1 , 15 , 21 ]. In men with obesity, the prevalence of hypogonadism ranges between 22.9% and 78.8% [ 6 ].…”

Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management

“…However, the VLCKD group had a greater significant increase relative to the SHMD, from 18.4 to 29.3 ng/mL, p<0.0001 versus 17.5 to 21.3 ng/mL, p=0.067, as well as decreases in C reactive protein. 48 These results indicate the role of dietary macronutrient distribution on insulin secretion stimulus and its consequential effect on mitochondrial vitamin D hydroxylation activity and possible inflammation mediated depletion (usage) of vitamin D.…”

Skeletal Muscle and the Maintenance of Vitamin D Status

“…The second difference with vitamins A, E and K, is that there is no apparent storage organ or tissue for vitamin D or 25(OH)D. Although vitamin D is found in adipose tissue, suggesting that this is a storage site [5,6], it can only be released when stored fatty acids are mobilized to supply energy [7,8,9]. Thus, sequestered vitamin D in adipocytes cannot be a functional store, ready to be transported to the liver and converted to 25(OH)D, when circulating levels of this metabolite decline.…”