VITAMIN D DEFICIENCY IN OBESE PEOPLE
Vitamin D insufficiency from 30% to 50% in Europe and USA
Vitamin D is synthesized by our bodies through absorption of the sun’s rays. Vitamin D is our regulator of calcium metabolism, useful for bone calcification and helps maintain phosphorus levels in the blood. Vitamin D has been studied in the prevention of leukemia and breast cancer, while its usefulness in the prevention of prostate and colon cancer has not been demonstrated.
Vitamin D comes not only from the sun’s rays, but also from our healthy diet. The foods where it is found most are only cereals, fatty fish such as salmon, mackerel, herring, egg yolk and liver.
Vitamin D is not only used to fix calcium in bones, but it also has a function in preventing rickets in children and osteoporosis in the elderly.
Excess vitamin D can cause widespread calcification in various organs, resulting in vomiting and muscle spasms.
Most vitamin D is taken up by humans through sunlight.
Vitamin D is also lost due to unhealthy behaviors such as alcohol abuse and drug use, as well as medication use.
Vitamin D deficiency has often been observed in obese people. One of the suggested mechanisms for low vitamin D levels in obesity was reduced vitamin D bioavailability (VD) due to sequestration in adipose tissue. However, only a few studies have investigated this mechanism by quantifying vitamin D levels from the tissues of the obese.
Vitamin D (VD) insufficiency (serum 25-hydroxyvitamin D (25(OH)D) levels below 30 ng/mL) is widespread worldwide and it has been estimated that over 30-50% of populations in Europe and the United States and over 50% in East Asia are insufficient or deficient in VD. Low serum levels of 25(OH) D have been observed in obese persons and circulating levels of 25(OH) D correlate inversely with body mass index and fat mass.
It was reported that the prevalence of VD deficiency was 35% higher in obese persons and 24% higher in overweight persons than in non-obese persons. Although several mechanisms such as low ultraviolet B (UVB) exposure of obese people and VD sequestration or dilution in adipose tissue have been proposed for the higher prevalence of VD deficiency among obese people, the causes of their low 25(OH)D levels are still inconclusive.
Early adipose tissue studies with animals or humans supplemented with radiolabeled 14C cholecalciferol (VD3), followed by radioactivity measurement, showed that VD and its metabolites are stored in adipose tissue. Scientific studies have observed that serum 25(OH)D levels increased more in a non-obese group than in an obese group when they were exposed to UVB exposure or when they were given VD supplements. Therefore, it was suggested that adiposity might lead to the reduction of VD bioavailability because of VD sequestration in body fat.
VD is fat-soluble and is usually absorbed from dietary fat by passive diffusion into the proximal jejunum and distal ileum. Dietary VD is packed into chylomicrons with triglycerides, cholesterol, and other lipids within the intestinal wall, and this process is dependent on microsomal triglyceride transfer protein (MTP). The VD contained in chylomicron is secreted into the lymphatic system, and some of it is absorbed into adipose tissue and the liver during hydrolysis of chylomicron by lipoprotein lipase (LPL). Fat intake could influence the absorption of dietary VD in the small intestine, and the impact of the amount of fat in a meal on serum VD status has been investigated in several studies, although the results remain inconclusive. Raimundo et al  reported that a single oral intake of 50,000 IU of VD3 with a high-fat meal containing 25.6 g fat/meal resulted in a significant increase in serum 25(OH)D levels after 14 days, whereas there were no significant changes in 25(OH)D levels when VD was taken with a low-fat meal (1.7 g fat/meal).
In addition to adiposity, the amount of dietary fat and the expression of transporter proteins involved in VD uptake need to be considered for the circulatory 25(OH)D response to VD intake.