Most Common Adverse Effects
The effects of drugs on the nutrients found in food are of three phases. The first one is the absorption of nutrients. The second one is the breakdown of complex food into simpler forms, and the third one is the excretion of nutrients. The absorption process of the drug can make changes in the amounts of minerals in the gut. Sometimes it can reduce the bioavailability and sometimes may create toxicity. Drugs can also influence the breakdown of food and its assimilation. The excretion phase adversely affects the gut’s lining by causing the accumulation of water-insoluble medications. It negatively affects the organs like the heart, liver, and kidneys and leads to its malfunctioning. Several drugs can affect nutrient absorption adversely. Some other problems due to drug interaction with minerals are as follows:
Inducing adverse metabolic effects: Drug interactions severely affect the glucose and lipids levels in the body. It reduces the efficacy of insulin to reduce the glucose level and leads to diabetes mellitus. Some drugs interact with lipids and may lead to cholesterol.
Damaging vital organs: The body allows the drugs to different organs via blood. Blood reaches the kidney for filtration. Therefore, it increases the possibility of accumulating drug content in the kidneys. It severely affects the functioning of nephrons.
Effect on appetite and gastrointestinal (GI) tract: The absorption and digestion process occurs in the GI tract. Continuous and excessive consumption of drugs for a long time will lead to several nutrient deficiency problems.
Significance of Sodium in Several Drug Interactions
Both low and high-sodium diets possess different pharmacokinetics and pharmacodynamics. Several researchers believe that a low sodium diet can reduce the risk of cardiovascular diseases. Renin-Angiotensin System (RAS) blockers halt RAS activation and increase the blood pressure-lowering effect. Therefore, it lowers blood pressure and thereby reduces the risk for heart diseases. A low sodium diet serves as a stimulating factor of RAS. Hence, RAS activation increases blood pressure and, this is how both the low and high sodium diet balance the blood pressure.
High sodium intake reduces the oral bioavailability of cardiovascular drugs such as verapamil, atenolol, and quinidine. P-glycoprotein (p-sp) transporter and cytochrome p4503A (CYP3A) are the two substrates of these cardiovascular drugs. A high sodium diet creates hypotonic stress and triggers the intestinal mucosal cells to increase the release of p-sp and CYP3A. The modifications in p-sp and CYP3A decrease the bioavailability (20 to 60%) of verapamil, atenolol, and quinidine.
Candesartan (an angiotensin receptor blocker) contains P-GP but not CYP3A as substrate exhibits low bioavailability (approximately 30\%30%) at high sodium diets. However, drugs such as valsartan and ramipril do not affect the sodium diet. Alteration of the CYP3A enzyme (due to sodium intake) is not the exact reason for the low bioavailability of fimasartan drugs. It depends on the baseline level of RAS activation that depends on the high sodium intake.
