Among the seemingly constant changes in dietary advice—Low fat? Low-carb? Plant-based?—eating a wide variety of brightly colored vegetables and fruits is one of the general recommendations that has stood the test of time. Researchers continually discover new properties for individual components of these foods, which add up to it simply making good sense to include them in the diet, whatever the overarching nutritional philosophy is. Be it the lycopene in tomatoes and watermelon, or the anthocyanins in raspberries, we know that various phytochemicals impart impressive benefits upon human health.

Citrus fruit, in particular, is a category of edible plants that provides a host of helpful phytochemicals. Hesperidin is one; naringin is another. The name naringin is believed to be derived from the Sanskrit narangi, for orange, which clearly emphasizes its presence in citrus fruits. Naringin is also found in cherries, tomatoes, and oregano, but grapefruit, grapefruit juice, pummelo and other grapefruit hybrids are the most significant sources of naringin among commonly consumed foods. Naringin is a flavonoid that lends grapefruit its bitter taste. In fact, upon digestion, naringin is metabolized to naringenin, and it is naringenin that is theorized to be responsible for the well-known interaction between grapefruit juice and several pharmaceutical drugs. This is orchestrated primarily by naringenin’s effects on inhibiting the cytochrome P450 3A4 enzymes responsible for the first-pass metabolism or “detoxification” of many medications. However, individual variability regarding naringin metabolism and excretion of naringenin vary widely, which may account for significant differences in the effects of grapefruit and other citrus fruits on the potency and degradation of pharmaceuticals.

Moving on from the grapefruit-and-medication issue, naringin has quite a few interesting properties. It has been demonstrated to have antioxidant, anti-inflammatory and chemoprotective effects, which suggests that this compound could be helpful for any number of conditions associated with chronic inflammation and oxidative stress. The conditions for which naringin and naringenin supplementation has shown promise in animal models read like a who’s who of modern chronic illnesses: metabolic syndrome, obesity, dyslipidemia, hypertension and endothelial dysfunction, liver disease, and free radical-induced oxidative stress. This might sound too good to be true, but naringin and naringenin do affect mechanisms at the cellular level, which explains why these compounds seem so promising.

Naringin has been shown to have strong superoxide scavenging ability in vitro, and to inhibit lipid peroxidation and DNA damage induced by UVA radiation and heavy metals (specifically, cadmium and nickel). In vitro and in vivo studies have shown naringin to suppress the production of inflammatory cytokines, as well as inhibit the COX-1 and COX-2 enzymes implicated in pain and inflammation. As for its effects on hypertension and cardiovascular health, naringin is a natural vasodilator and increases the bioavailability of nitric oxide. It also may act as a kind of natural calcium channel blocker, similar to magnesium.

Regarding diabetes, metabolic syndrome and their long list of downstream complications, mouse models demonstrate that naringin may prevent the progression of hyperglycemia by increasing hepatic glycolysis and glycogen concentration, and lowering gluconeogenesis. In vitro studies employing naringin have shown that this flavonoid compound inhibits dipeptidyl peptidase-4 (DPP-4) more strongly than sitagliptin, the first DPP-4 inhibiting oral pharmaceutical drug to enter the market for diabetes treatment.

Naringin may also have therapeutic potential for conditions related to cognitive decline and neuronal injury. In vivo mouse studies have shown that naringin inhibits GSK-3β, an enzyme implicated in the hyperphosphorylation of tau proteins that result in the neurofibrillary tangles that are one of the hallmarks of Alzheimer’s disease. Naringin also exhibited acetylcholinesterase inhibiting activity, which helped enhance memory and alleviate cognitive deficits in experimental animals. Moreover, regarding neuronal injury, naringin supplementation started one day after spinal cord injury in rats facilitated recovery by decreasing apoptosis and enhancing brain derived neurotrophic factor (BDNF). This humble citrus compound might be a helpful adjunct to treatment immediately after traumatic brain injury and other neurological trauma.

The potential effects of grapefruit compounds on the hepatic metabolism of pharmaceutical drugs should not automatically relegate naringin to the graveyard of nutraceutical also-rans. For the appropriate patient populations, this flavonoid has wide-ranging applications across a host of the most common modern chronic illnesses encountered in everyday medical practice.