It has been more than three decades since the first assay assessing circulating 25(OH)D in human subjects was performed. That publication as well as several that followed it defined 'normal' nutritional vitamin D status in human populations. Recently, the wisdom by which 'normal' circulating 25(OH)D levels in human subjects were assigned in the past has come under question. It appears that sampling human subjects, who appear to be free from disease, and assessing 'normal' circulating 25(OH)D levels by plotting a Gaussian distribution is grossly inaccurate. There are many reasons why this method is inaccurate, including race, lifestyle habits, sunscreen usage, age, latitude, and inappropriately low dietary recommendations for vitamin D. For instance, a 400IU/day. AI for vitamin D is insignificant when one considers that a 10-15 minute whole body exposure to peak summer sun will generate and release up to 20,000 IU vitamin $D_3$ into the circulation. Recent studies, which orally administered up to 10,000 IU/day vitamin $D_3$ to human subjects for several months, have successfully elevated circulating 25(OH)D levels to those observed in individuals from sun-rich environments. Further, we are now able to accurately assess sufficient circulating 25(OH)D levels utilizing specific biomarkers instead of guessing what an adequate level is. These biomarkers include intact parathyroid hormone (PTH), calcium absorption, bone mineral density (BMD), insulin resistance and pancreatic beta cell function. Using the data from these biomarkers, vitamin D deficiency should be defined as circulating levels of $25(OH)D{\leq}30ng/mL$. In certain cases, such as pregnancy and lactation, significantly higher circulating 25(OH)D levels would almost certainly be beneficial to both the mother and recipient fetus/infant.