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Health Protocols


Dietary and Lifestyle Management Strategies

By proactively managing identified risk factors for cataracts, one may be able to reduce their onset and/or progression. The following lifestyle management strategies center on avoiding oxidative damage and glycation reactions in the lens (National Eye Institute 2009):

  • Quitting smoking, since toxins from tobacco smoke damage proteins such as crystallins (Randerath 1992; Paik 2000)
  • Limiting or eliminating exposure to UV radiation from the sun
  • Avoiding work-related exposure to X-rays and gamma irradiation
  • Limiting or reducing the consumption of alcohol

In addition to these lifestyle changes, numerous studies revealed that food-based antioxidants are useful in the treatment of cataracts (Agte 2010). By increasing the consumption of foods rich in antioxidants and phytochemicals, such as vegetables and fruits, the human body may be able to more effectively scavenge and eliminate free radicals and reactive oxygen species. 

Other dietary considerations include avoiding meats high in cholesterol and saturated fats (eg, fatty cuts of beef, processed meats) and consuming more fish rich in omega-3-fatty acids (eg, salmon). Nuts and seeds, particularly walnuts and flaxseed oil, are additional sources of omega-3 fatty acids (Psota 2006). Omega-3 fatty acids were shown to protect against oxidative damage caused by UV radiation in other tissues, and since the development of cataracts was causally linked to oxidative damage in the lens, this action could represent another mechanism by which they protect against cataract formation or progression (Rhodes 2003; van der Pols 2011).

Controlling Blood Glucose Levels to Prevent Cataracts – Even in Non-Diabetics

Diabetes is a well-known risk factor for cataracts (Rowe 2000; Heydari 2012), but the link between elevated blood glucose levels and cataracts is less appreciated in non-diabetics.

Even in people without overt diabetes, elevated blood sugar causes significant damage throughout the body by increasing oxidative stress and promoting protein-destroying glycation reactions, leading to a number of chronic diseases (Paik 2012; McNeilly 2011; Nitenberg 2006; Miyazawa 2012; Lindsey 2009). The lens of the eye is particularly susceptible to damage associated with elevated glucose (Jain 2002; Pereira 1996; Franke 2003).

Researchers at Harvard University conducted a meticulous analysis on more than 87 000 individuals over a 16-year period and concluded that “[posterior subcapsular] cataract may be mediated in part by glucose intolerance and insulin resistance, even in the absence of clinical diabetes” (Weintraub 2002). Several subsequent studies corroborated these findings:

  • In an analysis of nearly 3600 people 49 or older, fasting glucose levels above 108 mg/dL were associated with a 79% greater risk of cortical cataract development over a 10-year period compared to concentrations below 108 mg/dL. Moreover, for each 18 mg/dL increase above this level, risk of progression of some types of cataracts increased by up to 25% (Kanthan 2011).
  • In a similarly designed study on more than 2300 people, fasting glucose levels above 108 mg/dL were associated with a 2.2-fold higher risk of cortical cataracts over a 5-year period (Saxena 2004).
  • Another analysis of 3654 elderly subjects in Australia showed that glucose concentrations between 108 and 126 mg/dL were predictive of doubled risk of cortical cataracts over a 10-year period (Tan 2008).

Interventions associated with improved glucose control have been shown to reduce cataract risk. For example, in an animal model of cataracts, caloric restriction, that is, the reduction of calorie intake to a level short of malnutrition, was associated with a 27% reduction in glucose levels, fewer incidence of cataracts, and less cataract progression (Taylor 1995). Other animal studies showed that use of the anti-diabetic drug acarbose, which inhibits carbohydrate absorption and suppresses glucose concentrations, both reduced incidence and lessened progression of cataracts (Madar 1993, 1994; Cohen-Melamed 1995).

The dangers posed by impaired fasting glucose concentrations are, sadly, often underappreciated by the medical establishment (Jessani 2009). Conventional physicians, in many cases, fail to take preventive action until clinical diabetes manifests, which is defined as fasting blood glucose levels of 126 mg/dL or higher (Aoki 2007; Drexler 2001). In order to avert unnecessary disease, Life Extension® suggests that most individuals strive for an optimal fasting blood glucose level of 70 - 85 mg/dL. More information about glucose control is available in the Weight Loss protocol.