Do you guys sell st johns wort extract?

Cataracts are when protein builds up in the lens of your eye. Let's see why hypericin might exacerbate that.

https://sci-hub.se/10.3109/02713680903144692

The human ocular lens is made up of two layers,epithelial cells (cortex) on the surface and protei fibers located on the inside or nucleus, which must be arranged in an organized manner to be translucent. Any damage to the epithelial cells on the outer layer or the structure of the crystalline proteins found on the inner layer will result in cataract formation. The major lens protein a-crystalline, found in both the external and internal layers of the ocular lens, can become photo-oxidized by ultraviolet (UV) and visible light (UVA and UVB on the epithelial cells and UVA and visible light on the nuclear layer), causing early catarogenesis. Drug compounds with multiple hydroxyl groups, such as hypericin, have been shown to bind with ocular tissues more easily before photo-oxidation occurs. The risk of cataracts associated with SJW use may be related to hypericin’s photosensitive property, which produces damaging reactive oxygen species and free radicals in the presence of UV and visible light. The phototoxic property of a drug depends on several factors: (1) the absorption spectrum of the drug; (2) the binding to ocular tissues and rate of clearance from the eye; (3) the transmission and absorption characteristics of ocular tissues; and (4) the properties of the light source. Hypericin, which can absorb in the UV and visible range (with longer wavelengths penetrating deeper), might therefore potentially be responsible for catarogenesis. Schey et al. reported that damage to the a-crystalline lens proteins in the presence of hypericin stimulated by light generated free oxygen radicals, specifically to the methionine, tryptophan, and histidine residues, which increased with irradiation time. This suggests that the damage caused to the a-crystalline may generate lens opacities directly by denaturing it and obliquely by interrupting its ability to act as a molecular chaperone.

Additionally, hypericin may contribute to cataract formation via its influence on the biogenic amine neurotransmitters that help with mental functioning and alleviate depression, including histamine, serotonin, and the three catecholamines (dopamine, norepinephrine/noradrenaline, and epinephrine/adrenaline). These biogenic amines have been demonstrated to affect the eye’s peripheral blood vessels and influence its blood viscosity, platelet aggregation, vasoconstriction/dilatation, and enhance capillary permeability. In rats, the ocular lens has shown to be very sensitive to one biogenic amine in particular, serotonin, in which its influence on the blood-retinal barrier and retinal and choroidal vasculature may cause cataracts by decreasing the production of aqueous humor that primarily protects the ocular lens surface from damage.

Super interesting! Still, there are confounding variables that need to be addressed.

The results of this study should be interpreted in light of several strengths and limitations. First, the cross-sectional nature of the study design prohibits demonstrating a temporal relationship between SJW and cataracts. Second, we were unable to evaluate whether the observed association was dose dependent as information on the duration of SJW use and dosage was not available. Third, all of the information in the NHIS data is self-reported. Self-report of cataract has been used in a number of large, prospective studies though its ability to identify age-related opacities with reductions in visual acuity is limited. However, there is little reason to believe that such misclassification would be differential with respect to SJW use. To our knowledge, there is no research regarding the validity of self-reported information on SJW. Finally, the role of residual confounding must also be acknowledged, particularly given that information on all known or suspected risk factors for cataracts (e.g., family history) is not available in the 2002 NHIS data.