Dietary Supplements and the Ophthalmologist

Stephen G. Schwartz, MD; Pamela S. Chavis, MD

Disclosures

Compr Ophthalmol Update. 2005;6(3):153-159. 

In This Article

Direct Ocular Effects

Dietary supplements that have demonstrated direct ocular effects, either beneficial or deleterious, are listed here in alphabetical order. Several preparations appear to demonstrate at least some therapeutic effect. However, with the exception of the vitamin combination from the Age-Related Eye Disease Study (AREDS) Group, none of these supplements has accumulated enough evidence in the peer-reviewed literature to be considered standard of care at this time.

Bilberry (Vaccinium myrtillus) has been used for a variety of purposes, including as an astringent to treat diarrhea, and to induce diuresis. It also stimulates the regeneration of rhodopsin, although its clinical effects on young, healthy volunteers appear negligible.[9]

Canthaxanthine is a carotenoid pigment used in the treatment of photosensitivity disorders and vitiligo; it is also marketed as an oral tanning agent (Orobronze; DeWitte, Greenville, SC). It may cause a characteristic retinopathy, with a ring of yellow-orange crystalline material in the macula.[10] Although the retinopathy is frequently asymptomatic, subnormal responses on electroretinography and dark adaptometry may be noted.[11] Although the long-term effects are unknown, the crystals typically resorb upon discontinuation of the agent.

Chamomile (Matricaria spp.), an anxiolytic, is occasionally used topically as a folk remedy for ocular infections. It may cause an IgE-mediated conjunctivitis with lid edema.[12] Treatment consists of discontinuation of the agent, as well as nonspecific supportive measures.

Echinacea (Echinacea spp.), used to treat viral upper respiratory tract infections, is also occasionally used topically. Similar to chamomile, it may cause a self-limited allergic conjunctivitis.[2,13]

The fish oils eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) appear to have myriad effects on the eye. Docosahexaenoic acid, when combined with vitamin A, has been claimed to slow progression of retinitis pigmentosa (RP) in certain patients: For example, in patients beginning treatment with 15,000 IU/day vitamin A (retinyl palmitate), adding 1,200 mg/day DHA slows progression of RP for 2 years.[14] A diet high in omega-3 fatty acids and fish and low in linoleic acid is associated with a relatively decreased risk of advanced AMD.[15]

Forskolin (Coleus forskohlii) is an aqueous human secretin suppressant and lowers IOP.[16]

Ginkgo (Ginkgo biloba) is mainly used to increase memory function. It appears to be neuroprotective through beneficial effects on blood flow, serum viscosity, and vasospasm. It has direct antiplatelet activity and has been linked to spontaneous hyphema, retinal hemorrhage, and orbital hemorrhage.[2] Ginkgo increases ocular blood flow, but does not affect IOP.[17] In one small placebo-controlled trial, patients with normal-tension glaucoma receiving 120 mg/day of ginkgo extract had short-term improvement of pre-existing visual field defects.[18]

Kava (Piper methysticum) has been used as an anxiolytic and as an antigonorrheal agent. It may cause impaired accommodation.[19]

Licorice (Glycyrrhiza glabra), used to treat gastric ulcer, may cause blood vessel spasm. It has been linked to one case of central retinal vein occlusion[20] and several cases of transient visual loss, presumably secondary to retinal and/or cortical vasospasm.[21]

Lily of the valley (Convallaria majalis), a cardioactive agent, is structurally similar to cardiac glycosides and may cause similar disturbances in color vision.[2]

Marijuana (Cannabis sativa), when inhaled, may lower IOP by as much as 25% for up to 4 hours,[22] although there is significant systemic toxicity.[23] A recent small, uncontrolled, nonrandomized trial suggested some efficacy, but both oral and inhaled preparations studied were not tolerated for more than a few months.[24]

Niacin (nicotinic acid, vitamin B3), used to lower serum lipids, has a well documented dose-related association with pseudocystoid macular edema (CME), usually at doses greater than 1.5 mg/day. Clinically, niacin maculopathy is similar to typical CME, but the two entities may be differentiated by fluorescein angiography. Niacin toxicity does not show leakage of fluorescein in the macula, which therefore represents intracellular fluid accumulation rather than true (extracellular) edema. Maculopathy typically resolves upon discontinuation of the agent.[25]

Valerian (Valeriana spp.), used as an anxiolytic, may cause mydriasis.[26]

Vitamins affect various ocular structures, particularly the retina. The Age-Related Eye Disease Study (AREDS) Group reported a beneficial effect for patients with at least intermediate AMD and without medical contraindications (e.g., smokers) with the following daily dose: 28,640 IU of beta-carotene, 452 mg of vitamin C (ascorbic acid), 400 IU of vitamin E (alphatocophorol), 69.6 mg of zinc oxide, and 1.6 mg of copper (cupric oxide).[27] Vitamin A (retinol), when combined with DHA, may have a positive effect on RP (see fish oils). One trial reported increased tear production in patients with Sjogren syndrome using essential fatty acid precursors of prostaglandin E1, vitamin C, and vitamin B6 (pyridoxine).[28] Potential adverse effects of vitamins include pseudotumor cerebri with vitamin A[29] and corneal pigmentation with beta-carotene.[30]

The various ocular effects, stratified by ocular structure, are summarized in Table 1 (beneficial effects) and Table 2 (deleterious effects).

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