Potent CYP3A4 inhibitors such as clarithromycin, erythromycin, fluvoxamine, grapefruit juice, ketoconazole, and ritonavir may lead to increased concentrations of trazodone and decreased concentrations of mCPP, while CYP3A4 inducers like carbamazepine, enzalutamide, phenytoin, phenobarbital, and St. Johns wort may result in decreased trazodone concentrations and increased mCPP concentrations. CYP2D6 inhibitors may result in increased concentrations of both trazodone and mCPP while CYP2D6 inducers may decrease their concentrations. Examples of potent CYP2D6 inhibitors include bupropion, cannabidiol, duloxetine, fluoxetine, paroxetine, quinidine, and ritonavir, while CYP2D6 inducers include dexamethasone, glutethimide, and haloperidol. CYP1A2 inhibitors may increase trazodone concentrations while CYP1A2 inducers may decrease trazodone concentrations. Examples of potent CYP1A2 inhibitors include ethinylestradiol (found in hormonal birth control), fluoroquinolones (e.g., ciprofloxacin), fluvoxamine, and St. Johns wort, while potent CYP1A2 inducers include phenytoin, rifampin, ritonavir, and tobacco. A study found that ritonavir, a strong CYP3A4 and CYP2D6 inhibitor and moderate CYP1A2 inducer, increased trazodone peak levels by 1.34-fold, increased area-under-the-curve levels by 2.4-fold, and decreased the clearance of trazodone by 50%. This was associated with adverse effects such as nausea, hypotension, and syncope. Another study found that the strong CYP3A4 inducer carbamazepine reduced concentrations of trazodone by 60 to 74%. The strong CYP2D6 inhibitor thioridazine has been reported to increase concentrations of trazodone by 1.36-fold and concentrations of mCPP by 1.54-fold.
Hypervitaminosis is a condition of abnormally high storage levels of vitamins, which can lead to various symptoms as over excitement, irritability, or even toxicity. Specific medical names of the different conditions are derived from the given vitamin involved: an excess of vitamin A, for example, is called hypervitaminosis A. Hypervitaminoses are primarily caused by fat-soluble vitamins  (D and A), as these are stored by the body for longer than the water-soluble vitamins.Generally, toxic levels of vitamins stem from high supplement intake and not always from natural sources but rather the mix of natural, derived vitamins and enhancers (vitamin boosters). Toxicities of fat-soluble vitamins can also be caused by a large intake of highly fortified foods, but natural food in modest levels rarely deliver extreme or dangerous levels of fat-soluble vitamins. The Dietary Reference Intake recommendations from the United States Department of Agriculture define a "tolerable upper intake level" for most vitamins. For those who are entirely healthy and do not experience long periods of avitaminosis, vitamin overdose can be avoided by not taking more than the normal or recommended amount of multi-vitamin supplement shown on the bottle and not ingesting multiple vitamin-containing supplements concurrently. Signs and symptoms
A few described symptoms:

Causes
With few exceptions, like some vitamins from B-complex, hypervitaminosis usually occurs with the fat-soluble vitamins A and D, which are stored, respectively, in the liver and fatty tissues of the body. These vitamins build up and remain for a longer time in the body than water-soluble vitamins.