Quote from Dr. Garrett Smith on March 5, 2019, 7:43 pm

Put simply, Poison/"Vitamin A" is antagonistic to Vitamin D (Hormone D is more like it) function in the body, and is likely what is causing your so-called "low Vitamin D levels".  Just so you are aware, the lowest mortality rates (risk of death) has been shown to be between 20-40 ng/mL (50-100 micromol/L), and if your doctor--or your internet health guru of choice--has you shooting for levels WAY higher than this, then they are likely putting you in an early grave.  The only way those excessively high levels are reached is through supplementation, and Hormone D supplementation's real-world results only look worse and worse as more research comes out.  I've been advocating strongly against ANY Vitamin D by mouth (or injection insanity) since 2013.

Vitamin A and Osteoporosis - Experimental and Clinical Studies

An interaction between vitamin A and D in humans was also demonstrated, where the calcium response elicited by vitamin D was antagonized by simultaneous intake of vitamin A. In the rats with subclinical hypervitaminosis A, the serum levels of other fat-soluble vitamins were reduced, suggesting a general antagonistic effect on fat-soluble vitamins. These findings are consistent with previous literature and argue in favor of indirect effects in development of vitamin A toxicity.

Did you know I have other article on this blog-forum further confirming the above, demonstrating that Poison/"Vitamin A" depletes Vitamin E and Vitamin K (really the only two fat-soluble vitamins I recognize, due to Vitamin D really being a hormone, and Vitamin A really being a poison).

All-trans retinoic acid antagonizes the action of calciferol and its active metabolite, 1,25-dihydroxycholecalciferol, in rats.

An antagonistic interaction between retinol and calciferol has been established.
[...]
Therefore, both retinyl acetate and ATRA are able to antagonize the action of ergocalciferol [Vitamin D2] and cholecalciferol [Vitamin D3] in vivo. Additionally, ATRA antagonizes the in vivo action of 1,25(OH)2D3 [calcitriol] and an analog, 24-F2-1,25(OH)2D3, that cannot be 24-hydroxylated.

Vitamin A antagonizes calcium response to vitamin D in man.

In conclusion, an intake of vitamin A corresponding to about one serving of liver antagonizes the rapid intestinal calcium response to physiological levels of vitamin D in man.

Vitamin A antagonizes the action of vitamin D in rats.

Interactions between vitamin A and vitamin D have been suggested for several decades but have not been established. In particular, vitamin A has been proposed to intensify the severity of the bone mineralization disease, rickets and inhibit the ability of vitamin D to cure this disease. To investigate this hypothesis, weanling Holtzman rats were fed a 1.2% calcium, 0.1% phosphorus diet and 15.5 ng ergocalciferol (vitamin D(2)) every 3 d for 21 d in the presence of increasing amounts of retinyl acetate (0 microg to 8621 microg/d). The increasing amounts of retinyl acetate produced a progressive and significant decrease in total bone ash (P < 0.001) and an increase in epiphyseal plate width (P < 0.001). The same experiment conducted with increasing amounts of vitamin D(2) (0 to 645 ng/d) indicated that the antagonism by retinyl acetate could be demonstrated at all vitamin D(2) dosages. To further investigate this antagonistic relationship, weanling Holtzman rats were fed a 0. 47% calcium, 0.3% phosphorus diet and 15.5 ng vitamin D(2) every 3 d for 33 d in the presence of increasing retinyl acetate (0 to 3448 microg/d). In the absence of retinyl acetate, these rats maintained a normal serum calcium level (2.34 mmol/L). Increasing retinyl acetate, however, eliminated the ability of vitamin D(2) to elevate the level of serum calcium (1.35 mmol/L). These results illustrated in vivo antagonism of vitamin D(2) action on intestine and bone by retinyl acetate.

In my opinion, a Vitamin D level lower than 20 ng/mL should first be suspected to be caused by Poison/"Vitamin A" toxicity until proven otherwise.