There is little doubt about it: blockage of the Vitamin D Receptor severely impairs human health. Since the Th1 pathogens create substances that block the receptor, they are easily able to create an environment that is conducive to their survival but quite detrimental to the host. If a person acquires enough of the Th1 pathogens, their VDRs likely become blocked by so many bacterial substances that the activity of the receptor decreases to a point where it is essentially off.

Since having a Vitamin D Receptor with no activity is analogous to having no VDR at all, studies on VDR knockout mice can be extremely informative. VDR knockout mice are rodents that have been grown in the lab under conditions that cause them to develop without Vitamin D Receptors. Their receptors are missing, or have been “knocked out.”

This week, a team of researchers at the University of Chicago examined the effects of inducing colitis on VDR knockout mice. Their goal: to investigate the role of the VDR in mucosal barrier homeostasis. The mucosal barrier allows the intestines to retain the proper pH and structure. The team used a substance called dextran sulfate sodium (DSS) in order to create an environment in the rodents’ intestines that resembles that of people with bowel disease.

The team found that while healthy mice did not develop colitis after exposure to 2.5% DSS, mice without VDRs developed severe diarrhea, rectal bleeding, and marked body weight loss, leading to death in two weeks. Examination of the intestines of the dead mice also revealed extensive ulceration and impaired wound healing among cells that had been impacted by DSS. When the researchers examined the intestines of the VDR knockout mice under an electron microscope, they also found “severe disruption” of the junctions that keep the skins of the intestines connected.

The results reveal quite a difference between how healthy mice and VDR knockout mice are affected by DSS! While DSS didn’t even impact the mice with active VDRs it’s obvious how much havoc the substance was able to render on the rodents without the receptor. With the Chicago team’s data in mind, it’s easy to see how someone with a VDR blocked by bacterial substances and/or high levels of 25-D is primed to suffer greatly when the bacteria that cause IBS and colitis infect the tissues of the intestines. Whereas the intestines of a person without VDR blockage might remain stable enough to survive much of the inflammatory damage generated by the Th1 pathogens, the intestines of patients without VDRs are likely so weak that they are literally at the mercy of numerous chronic bacterial forms.

It follows that if patients with severe VDR blockage take a medication such as Olmesartan that is able to push bacterial substances and 25-D out of the VDR and activate the receptor, their intestines should gradually become more resilient to the effects of the Th1 pathogens. Indeed, the Chicago team found when cell cultures of damaged rodent bowel tissue were administered 1,25-D – the vitamin D metabolite that, like Olmesartan, also activates the VDR – subsequent activation of the VDR markedly enhanced the strength of the junctions in the intestines, and preserved their integrity in the presence of DSS. Patients on the Marshall Protocol also find that once on Olmesartan and the MP antibiotics, their intestines are gradually able to recover from the damage caused by the Th1 pathogens.