One of the greatest ongoing food fights in eye care concerns the role of antioxidants and zinc in age-related macular degeneration (AMD) prevention and the movement of genetic testing from the theoretical research lab to applied science.1 Two principals, Dr. Carl Awh and Dr. Emily Chew have done a great service in moving forward this debate. However, amidst battles among dueling statisticians, commercial interests, and NEI recommendations much has been lost in this conversation concerning zinc.
Age-Related Eye Disease Study (AREDS) 1 nutrients are not synonymous with AREDS 2 nutrients because the latter have lutein and zeaxanthin—which dampen the potential for “the high-dose hyper-immune zinc effect” in specific genetic groups by reducing alternate compliment factor D.2 Lampalizumab, one of the most promising Phase 3 drugs for the future intravitreal treatment of geographic atrophic AMD, inhibits factor D.3
Previously from Dr. Richer: Examining poster themes at ARVO 2017
There is “sickness” in evidence-based medicine as described by UK pharmacologists Hickey and Roberts.4 There is no such thing as an average patient, and populations are not people.5 Genetic testing is therefore appropriate and reasonable, especially if one eye is wet, and if only to optimally protect the remaining eye, or in the unfortunate case of monocular AMD—protect the only eye.
The AREDS 1 formula with high-dose zinc has saved lives. As reported in May 2004, AMD patients taking 80 mg zinc per day for high-risk AMD experienced a 27 percent decline in mortality.6
In 2006, Eby and Holcomb wrote about high-dose zinc to resolve angina pectoris. They based the report on other concurring reports from the 1960s and 1970s, and they hypothesized that high-dose zinc (50 to 300 mg per day) decreases high-density lipoprotein (HDL) and increases circulating low-density lipoprotein (LDL) cholesterol.7 The increased LDL blood concentration with mega-dose zinc is believed to be due to the disposal of LDL as it exits the body.
Eby and Holcomb also emphasized that zinc prevented oxidation (hardening) of LDL cholesterol in the aorta and halted the main mechanism of atherosclerosis. Calcium and iron, in contradistinction, interfere with zinc absorption and zinc activated enzymes—exacerbating atherosclerosis.8