​Food safety regulation in the United States is the responsibility of two departments of the federal government. The United States Department of Agriculture (USDA) is responsible for overseeing the way that basic agricultural production such as meat, milk, eggs, vegetables, etc. are handled. And the Food and Drug Administration (FDA) is in charge of regulating manufactured foods that have undergone extensive processing and packaging — basically, everything that is not regulated by USDA.

​The United States Department of Agriculture (USDA) provides inspection services for meat and poultry processing plants. Specifically, the Food Safety and Inspection Service (FSIS), which is part of the USDA, is responsible for ensuring that meat, poultry, and egg products are safe, wholesome, and accurately labeled.

​We're all well aware of the fact that using certain medications, including nonsteroidal anti-inflammatory drugs, (NSAIDs), especially when used for long-term treatment, is associated with the development of microscopic colitis (MC). And after the disease develops, their use tends to trigger a flare. In a study of 155 adult subjects, researchers compared the respective drug use of those subjects for the prior 30 days, with a stool specimen that each of them submitted (Rogers, and Aronoff, 2016).[1] Interestingly, it was clear that certain drugs had established unique microbiome populations.

​for example, those who were using aspirin, showed gut bacteria populations that consisted primarily of Prevotella spp. (spp. is an abbreviation standing for the plural of species), Bacteroides spp., Family Reminococaceae, and Bamesiella spp.. Those using celecoxib or ibuprofen, showed higher population levels of Acidaminococcaceae and Enterobacteriaceae. Distinctive gut bacteria population patterns could be distinguished by the combination of medications that the subjects were using. So it's quite clear that using any drugs in this class alters our gut bacteria population to attain a specific profile, unique to that combination of medications.

​A normal stomach acid level is required for healthy digestion. The pH level in the stomach of healthy individuals typically ranges between 1.0 and 2.0. The pH scale ranges from zero on the low end (highly acidic), to 14.0 on the high-end (highly alkaline). The neutral level at which a substance is neither acidic nor alkaline, is 7.0. The medical term used to describe the condition of sub-normal production of stomach acid is hypochlorhydria. And the medical term used to describe the condition of above normal production of stomach acid is hyperchlorhydria.

​The term hypochlorhydria refers to compromised acid production, regardless of the pH level in the stomach at any given time. And accordingly, the term hyperchlorhydria refers to excess acid production, regardless of the actual pH levels in the stomach at any given time. In general, these two terms refer to the production of hydrochloric acid (HCL), relative to what's considered normal, and this association is reflected in the names chosen for these terms.

​A recent article published in the Journal Medicine describes a research project that involved the investigation of the association between inflammation levels (and disease severity), and serum vitamin D levels among IBD patients , compared with the vitamin D levels of healthy controls (Topalova-Dimitrova, Dimitrov, and Nikolov, 2023).[1] As most of us are already well aware, the researchers pointed out that vitamin D is a steroid hormone that plays a vital role in the performance of our immune system.​

​The researchers noted that IBD patients are commonly found to have low vitamin D levels due to issues associated with IBD [such as nutrient malabsorption, bile acid malabsorption (BAM), and medications such as immunosuppressants and corticosteroids]. Low vitamin D levels in IBD patients are associated with an increased risk of disease relapse, a slower response to biological therapy, and an increased risk of the need for surgical intervention. Naturally, as is typically the case, MC patients were excluded from this study. Only Crohn's and ulcerative colitis patients were qualified to participate in the study.