Additional drugs found to be affected by grapefruit juice include, but are not limited to:

- Some statins, including atorvastatin (Lipitor), lovastatin (Mevacor) and simvastatin (Zocor, Simlup, Simcor, Simvacor)

- (In contrast, pravastatin (Pravachol), fluvastatin (Lescol) and rosuvastatin (Crestor) are unaffected by grapefruit.)

- Anti-arrhythmics including amiodarone (Cordarone), dronedarone (Multaq), quinidine (Quinidex, Cardioquin, Quinora), disopyramide (Norpace), propafenone (Rythmol) and carvedilol (Coreg)

- Amlodipine: Grapefruit increases the available amount of the drug in the blood stream, leading to an unpredictable increase in antihypertensive effects.

- Anti-migraine drugs ergotamine (Cafergot, Ergomar), amitriptyline (Elavil, Endep, Vanatrip) and nimodipine (Nimotop)

- Erectile dysfunction drugs sildenafil (Viagra), tadalafil (Cialis) and vardenafil (Levitra)

- Acetaminophen/paracetamol (Tylenol) concentrations were found to be increased in murinae blood by white and pink grapefruit juice, with the white juice acting faster. Interestingly, "the bioavailability of paracetamol was significantly reduced following multiple GFJ administration" in mice and rats. This suggests that repeated intake of grapefruit juice reduces the efficacy and bioavailability of acetaminophen/paracetamol in comparison to a single dose of grapefruit juice which conversely increases the efficacy and bioavailability of acetaminophen/paracetamol.

- Anthelmintics: Used for treating certain parasitic infections; includes praziquantel

- Apremilast (Otezla): Used to treat psoriasis.

- Buprenorphine: Metabolized into norbuprenorphine by CYP3A4

- Buspirone (Buspar): Grapefruit juice increased peak and AUC plasma concentrations of buspirone 4.3- and 9.2, respectively, in a randomized, 2-phase, ten-subject crossover study.

- Codeine is a prodrug that produces its analgesic properties following metabolism to morphine entirely by CYP2D6.

- Ciclosporin (cyclosporine, Neoral): Blood levels of ciclosporin are increased if taken with grapefruit juice, orange juice, or apple juice. A plausible mechanism involves the combined inhibition of enteric CYP3A4 and MDR1, which potentially leads to serious adverse events (e.g., nephrotoxicity). Blood levels of tacrolimus (Prograf) can also be equally affected for the same reason as ciclosporin, as both drugs are calcineurin inhibitors.

- Dihydropyridines including felodipine (Plendil), nicardipine (Cardene), nifedipine, nisoldipine (Sular) and nitrendipine (Bayotensin)

- Erlotinib (Tarceva)

- Exemestane, aromasin, and by extension all estrogen-like compounds and aromatase inhibitors which mimic estrogen in function will be increased in effect, causing increased estrogen retention and increased drug retention.

- Etoposide interferes with grapefruit, orange, and apple juices.

- Fexofenadine (Allegra)

- Fluvoxamine (Luvox, Faverin, Fevarin and Dumyrox)

- Imatinib (Gleevec): Although no formal studies with imatinib and grapefruit juice have been conducted, the fact that grapefruit juice is a known inhibitor of the CYP 3A4 suggests that co-administration may lead to increased imatinib plasma concentrations. Likewise, although no formal studies were conducted, co-administration of imatinib with another specific type of citrus juice called Seville orange juice (SOJ) may lead to increased imatinib plasma concentrations via inhibition of the CYP3A isoenzymes. Seville orange juice is not usually consumed as a juice because of its sour taste, but it is found in marmalade and other jams. Seville orange juice has been reported to be a possible inhibitor of CYP3A enzymes without affecting MDR1 when taken concomitantly with ciclosporin.

- Lamotrigine

- Levothyroxine (Eltroxin, Levoxyl, Synthroid): the absorption of levothyroxine is affected by grapefruit juice.

- Losartan (Cozaar)

- Methadone: Inhibits the metabolism of methadone and raises serum levels.

- Omeprazole (Losec, Prilosec)

- Oxycodone: grapefruit juice enhances the exposure to oral oxycodone. And a randomized, controlled trial 12 healthy volunteers ingested 200 mL of either grapefruit juice or water three times daily for five days. On the fourth day 10 mg of oxycodone hydrochloride were administered orally. Analgesic and behavioral effects were reported for 12 hours and plasma samples were analyzed for oxycodone metabolites for 48 hours. Grapefruit juice and increased the mean area under the oxycodone concentration-time curve (AUC(0-∞)) by 1.7 fold, the peak plasma concentration by 1.5-fold and the half-life of oxycodone by 1.2-fold as compared to water. The metabolite-to-parent ratios of noroxycodone and noroxymorphone decreased by 44% and 45% respectively. Oxymorphone AUC(0-∞) increased by 1.6-fold but the metabolite-to-parent ratio remained unchanged.

- Quetiapine (Seroquel)

- Repaglinide (Prandin)

- Tamoxifen (Nolvadex): Tamoxifen is metabolized by CYP2D6 into its active metabolite 4-hydroxytamoxifen. Grapefruit juice may potentially reduce the effectiveness of tamoxifen.

- Trazodone (Desyrel): Little or no interaction with grapefruit juice.

- Verapamil (Calan SR, Covera HS, Isoptin SR, Verelan)

- Warfarin (coumadin)

- Zolpidem (Ambien): Little or no interaction with grapefruit juice.

Several approaches have been taken to address tumor hypoxia. Some companies tried to develop drugs that are activated in hypoxic environments (Novacea, Inc. Proacta, Inc, and Threshold Pharmaceuticals, Inc), while others are currently seeking to reduce tumor hypoxia (Diffusion Pharmaceuticals, Inc. and NuvOx Pharma, LLC).

Several companies have tried to develop drugs that are activated in hypoxic environments. These drug candidates target levels of hypoxia that are common in tumors but are rare in normal tissues. The hypoxic zones of tumors generally evade traditional chemotherapeutic agents and ultimately contribute to relapse. In the literature, hypoxia has been demonstrated to be associated with a worse prognosis, making it a determinant of cancer progression and therapeutic response. Several review articles summarize the current status of hypoxic cytotoxins (hypoxia activated prodrugs). Companies that have tried drugs that are activated in hypoxic environments included Novacea, Inc. Proacta, and Threshold Pharmaceuticals. Novacea Inc discontinued development of its hypoxia activated drug. Proacta’s drug PR610 failed a Phase I clinical trial due to toxicity. Threshold Pharmaceuticals discontinued the hypxia activated prodrug, TH-302, after Phase III trials failed to show statistically significant overall survival.

Niacinamide, the active form of vitamin B, acts as a chemo- and radio-sensitizing agent by enhancing tumor blood flow, thereby reducing tumor hypoxia. Niacinamide also inhibits poly(ADP-ribose) polymerases (PARP-1), enzymes involved in the rejoining of DNA strand breaks induced by radiation or chemotherapy. As of August 2016, no clinical trials appear to be in progress for this indication.

Another approach to the treatment of tumor hypoxia is the use of an oxygen diffusion-enhancing compound to reoxygenate the hypoxic zones of tumors. The developer of oxygen diffusion-enhancing compounds, Diffusion Pharmaceuticals, tested its lead compound, trans sodium crocetinate (TSC), in a Phase II clinical trial in 59 patients newly diagnosed with glioblastoma multiforme. The results of the Phase II showed that 36% of the full-dose TSC patients were alive at 2 years, compared with historical survival values ranging from 27% to 30% for the standard of care. The main endpoint of the trial was survival at two years, not overall survival.

Another drug in development that is designed to reduce tumor hypoxia is NuvOx Pharma’s NVX-108. NVX-108 is a formulation of the perfluorocarbon, dodecafluoropentane (DDFPe). NVX-108 is injected intravenously, flows through the lungs and picks up oxygen, then flows through the arteries and releases oxygen in the precense of hypoxic tissue. A Phase Ib/II clinical trial is in progress for newly diagnosed glioblastoma multiforme. Early results have shown reversal of tumor hypoxia, and the trial continues to progress.

Some drugs, such as the prokinetic agents increase the speed with which a substance passes through the intestines. If a drug is present in the digestive tract's absorption zone for less time its blood concentration will decrease. The opposite will occur with drugs that decrease intestinal motility.

- pH: Drugs can be present in either ionised or non-ionised form, depending on their pKa (pH at which the drug reaches equilibrium between its ionised and non-ionised form). The non-ionized forms of drugs are usually easier to absorb, because they will not be repelled by the lipidic bylayer of the cell, most of them can be absorbed by passive diffusion, unless they are too big or too polarized (like glucose or vancomicyn), in which case they may have or not specific and non specific transporters distributed on the entire intestine internal surface, that carries drugs inside the body. Obviously increasing the absorption of a drug will increase its bioavailability, so, changing the drug's state between ionized or not, can be useful or not for certain drugs.

Certain drugs require an acid stomach pH for absorption. Others require the basic pH of the intestines. Any modification in the pH could change this absorption. In the case of the antacids, an increase in pH can inhibit the absorption of other drugs such as zalcitabine (absorption can be decreased by 25%), tipranavir (25%) and amprenavir (up to 35%). However, this occurs less often than an increase in pH causes an increase in absorption. Such as occurs when cimetidine is taken with didanosine. In this case a gap of two to four hours between taking the two drugs is usually sufficient to avoid the interaction.

- Drug solubility: The absorption of some drugs can be drastically reduced if they are administered together with food with a high fat content. This is the case for oral anticoagulants and avocado.

- Formation of non-absorbable complexes:

- Chelation: The presence of di- or trivalent cations can cause the chelation of certain drugs, making them harder to absorb. This interaction frequently occurs between drugs such as tetracycline or the fluoroquinolones and dairy products (due to the presence of Ca).

- Binding with proteins. Some drugs such as sucralfate binds to proteins, especially if they have a high bioavailability. For this reason its administration is contraindicated in enteral feeding.

- Finally, another possibility is that the drug is retained in the intestinal lumen forming large complexes that impede its absorption. This can occur with cholestyramine if it is associated with sulfamethoxazol, thyroxine, warfarin or digoxin.

- Acting on the P-glycoprotein of the enterocytes: This appears to be one of the mechanisms promoted by the consumption of grapefruit juice in increasing the bioavailability of various drugs, regardless of its demonstrated inhibitory activity on first pass metabolism.

The primary treatment method for fatty-acid metabolism disorders is dietary modification. It is essential that the blood-glucose levels remain at adequate levels to prevent the body from moving fat to the liver for energy. This involves snacking on low-fat, high-carbohydrate nutrients every 2–6 hours. However, some adults and children can sleep for 8–10 hours through the night without snacking.

Apple juice, especially commercially produced products, interferes with the action of OATPs. This interference can decrease the absorption of a variety of commonly used medications, including beta blockers like atenolol, antibiotics like ciprofloxacin, and antihistamines like montelukast.

Apple juice has been implicated in interfering with etoposide, a chemotherapy drug, and cyclosporine, taken by transplant patients to prevent rejection of their new organs.

The treatment is some form of Vitamin E supplementation.

Aggressive vitamin E replacement therapy has been shown to either prevent, halt or improve visual abnormalities.

Carnitor - an L-carnitine supplement that has shown to improve the body's metabolism in individuals with low L-carnitine levels. It is only useful for Specific fatty-acid metabolism disease.

Metabolic disorders can be treatable by nutrition management, especially if detected early. It is important for dieticians to have knowledge of the genotype to therefore create a treatment that will be more effective for the individual.

It has been suggested that a possible method of treatment for histidinemia is through the adoption of a diet that is low in histidine intake. However, the requirement for such dietary restrictions is typically unnecessary for 99% of all cases of histidinemia.

Bioreductive prodrugs play a significant part in dealing with these kinds of cells: they can kill the oxygen-deficient tumor cells selectively as hypoxia-activated prodrugs. Example drugs include Tirapazamine and Evofosfamide. The study of tumors in such conditions was pioneered by Dr L. H. Gray.

There is no cure for GALT deficiency, in the most severely affected patients, treatment involves a galactose free diet for life. Early identification and implementation of a modified diet greatly improves the outcome for patients. The extent of residual GALT enzyme activity determines the degree of dietary restriction. Patients with higher levels of residual enzyme activity can typically tolerate higher levels of galactose in their diets. As patients get older, dietary restriction is often relaxed. With the increased identification of patients and their improving outcomes, the management of patients with galactosemia in adulthood is still being understood.

After diagnosis, patients are often supplemented with calcium and vitamin D3. Long-term manifestations of the disease including ovarian failure in females, ataxia. and growth delays are not fully understood. Routine monitoring of patients with GALT deficiency includes determining metabolite levels (galactose 1-phosphate in red blood cells and galactitol in urine) to measure the effectiveness of and adherence to dietary therapy, ophthalmologic examination for the detection of cataracts and assessment of speech, with the possibility of speech therapy if developmental verbal dyspraxia is evident.

Among US adults older than 55, 4% are taking medication and or supplements that put them at risk of a major drug interaction. Potential drug-drug interactions have increased over time and are more common in the low educated elderly even after controlling for age, sex, place of residence, and comorbidity.

In the middle of the 20th century the principal treatment for some of the amino acid disorders was restriction of dietary protein and all other care was simply management of complications. In the past twenty years, enzyme replacement, gene therapy, and organ transplantation have become available and beneficial for many previously untreatable disorders. Some of the more common or promising therapies are listed:

Treatment is depended on the type of glycogen storage disease. E.g. GSD I is typically treated with frequent small meals of carbohydrates and cornstarch to prevent low blood sugar, while other treatments may include allopurinol and human granulocyte colony stimulating factor.

Individuals presenting with Type III galactosemia must consume a lactose- and galactose-restricted diet devoid of dairy products and mucilaginous plants. Dietary restriction is the only current treatment available for GALE deficiency. As glycoprotein and glycolipid metabolism generate endogenous galactose, however, Type III galactosemia may not be resolved solely through dietary restriction.

These treatments have been used to help treat or manage toxicity in animals. Although not considered part of standard treatment, they might be of some benefit to humans.

- Vitamin E appears to be an effective treatment in rabbits, prevents side effects in chicks

- Taurine significantly reduces toxic effects in rats. Retinoids can be conjugated by taurine and other substances. Significant amounts of retinotaurine are excreted in the bile, and this retinol conjugate is thought to be an excretory form, as it has little biological activity.

- Cholestin - significantly reduces toxic effects in rats.

- Vitamin K prevents hypoprothrombinemia in rats and can sometimes control the increase in plasma/cell ratios of vitamin A.

Response to treatment is variable and the long-term and functional outcome is unknown. To provide a basis for improving the understanding of the epidemiology, genotype/phenotype correlation and outcome of these diseases their impact on the quality of life of patients, and for evaluating diagnostic and therapeutic strategies a patient registry was established by the noncommercial International Working Group on Neurotransmitter Related Disorders (iNTD).

Intolerance to analgesics, particularly NSAIDs, is relatively common. It is thought that a variation in the metabolism of arachidonic acid is responsible for the intolerance. Symptoms include chronic rhinosinusitis with nasal polyps, asthma, gastrointestinal ulcers, angioedema, and urticaria.

Clinical signs of PEM are variable depending on the area of the cerebral cortex affected and may include head pressing, dullness, opisthotonos, central blindness, anorexia, muscle tremors, teeth grinding, trismus, salivation, drooling, convulsions, nystagmus, clonic convulsions, and recumbency. Early administration of thiamine may be curative, but if the lesion is more advanced, then surviving animals may remain partially blind and mentally dull.

If liver damage has progressed into fibrosis, synthesizing capacity is compromised and supplementation can replenish PC. However, recovery is dependent on removing the causative agent; stopping high Vitamin A intake.

There are some preliminary studies that seem to indicate that treatment with hydrogen sulfide (HS) can have a protective effect against reperfusion injury.

Treatment or management of organic acidemias vary; eg see methylmalonic acidemia, propionic acidemia, isovaleric acidemia, and maple syrup urine disease.

As of 1984 there were no effective treatments for all of the conditions, though treatment for some included a limited protein/high carbohydrate diet, intravenous fluids, amino acid substitution, vitamin supplementation, carnitine, induced anabolism, and in some cases, tube-feeding.

As of 1993 ketothiolase deficiency and other OAs were managed by trying to restore biochemical and physiologic homeostasis; common therapies included restricting diet to avoid the precursor amino acids and use of compounds to either dispose of toxic metabolites or increase enzyme activity.

In light of recent research, high concentrations of sulfur intake has also been deemed responsible for PEM. Sulfur is necessary for the synthesis of important sulfur-containing amino acids and their contribution to the synthesis of different hormones, enzymes, and structural proteins. The ruminant diet, especially that of cattle, can be overly concentrated with sulfur. In ruminants, the same rumen microbes that generate thiamine molecules reduce sulfur into toxic sulfides. Among the sulfide toxins is hydrogen sulfide, a gas compound that will compete with oxygen to bind with red blood cells and eventually enter the brain to disrupt neural activity.

Pentosuria is a condition where the sugar xylitol, a pentose, presents in the urine in unusually high concentrations. It was characterized as an inborn error of carbohydrate metabolism in 1908. It is associated with a deficiency of L-xylulose reductase, necessary for xylitol metabolism. L-Xylulose is a reducing sugar, so it may give false diagnosis of diabetes, as it is found in high concentrations in urine. However glucose metabolism is normal in people with pentosuria, and they are not diabetic. Patients of pentosuria have a low concentration of the sugar d-xyloketose. Using, Phenyl pentosazone crystals, phloroglucin reaction, and absorption spectrum, pentose can be traced back as the reducing substance in urine, with those that have pentosuria.

Research has shown that pentosuria appears in 3 forms. The most widely studied is essential pentosuria, where a couple of grams of L-xylusol are released into a person’s system daily. L-xylulose reductase, contained in red blood cells, is composed of both a major and minor isozyme. For those diagnosed with essential pentosuria, the major isozyme appears to be the same as the minor one. Alimentary pentosuria can be acquired through fruits high in pentose. Finally, drug-induced pentosuria can be developed by those exposed to morphine, fevers, allergies, and some hormones.

Those diagnosed with Pentosuria are predominantly of Jewish root. However, it is a harmless defect, and no cure is needed.

The following therapeutic drugs were withdrawn from the market primarily because of hepatotoxicity: Troglitazone, bromfenac, trovafloxacin, ebrotidine, nimesulide, nefazodone, ximelagatran and pemoline.