Dietary modification and supplementation for the treatment of age-related macular degeneration

Broadhead, Geoffrey; Grigg, John; Chang, Andrew; McCluskey, Peter

doi:10.1093/nutrit/nuv005

Cited by 49 publications

(67 citation statements)

References 133 publications

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“…There are good rates of compliance with the dietary advice; that is, patients change their diet but patient education by health professionals can be improved [120]. …”

Section: The Genetic Risk Lifestyle and Amdmentioning

confidence: 99%

“…If the patients are unsure of their dietary lutein intake, they should be advised to use lutein/zeaxanthin AREDS-based supplements, given the lack of side effects found in most trials [120]. If they have a normal or high dietary lutein intake they can consume the modified beta-carotene free AREDS formulation [120].…”

Section: Conclusion: Nutritional Advice To Patients With Amdmentioning

confidence: 99%

“…If they have a normal or high dietary lutein intake they can consume the modified beta-carotene free AREDS formulation [120]. …”

Section: Conclusion: Nutritional Advice To Patients With Amdmentioning

confidence: 99%

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Nutritional and Lifestyle Interventions for Age‐Related Macular Degeneration: A Review

Carneiro

Andrade

2017

Oxidative Medicine and Cellular Longevity

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Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world. In this narrative review, we will summarize the nutritional interventions evaluated in numerous observational studies and a few randomized clinical trials. The AREDS and AREDS2 studies demonstrated that supplements including vitamins C and E, beta-carotene, and zinc may reduce the progression to advanced AMD, in some patients, by 25% in five years. This is one of the few nutritional supplements known to have beneficial effects in any eye disease. Lutein/zeaxanthin supplementation may have beneficial effects in some individuals whereas omega-3 fatty acids supplementation needs to be further investigated and supported by more evidence. Genetic factors may explain the different patterns of response and explain differences found among individuals. More importantly, a combination of lifestyle behaviors such as the avoidance of smoking, physical activity, and the adoption of a healthy dietary pattern like the Mediterranean diet was associated with a lower prevalence of AMD. The adoption of these lifestyles may reduce the prevalence of the early stages of AMD and decrease the number of individuals who develop advanced AMD and consequently the onerous and climbing costs associated with the treatment of this disease.

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“…There are good rates of compliance with the dietary advice; that is, patients change their diet but patient education by health professionals can be improved [120]. …”

Section: The Genetic Risk Lifestyle and Amdmentioning

confidence: 99%

Section: Conclusion: Nutritional Advice To Patients With Amdmentioning

confidence: 99%

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Nutritional and Lifestyle Interventions for Age‐Related Macular Degeneration: A Review

Carneiro

Andrade

2017

Oxidative Medicine and Cellular Longevity

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“…The results of the Age-Related Eye Disease Studies (AREDS) demonstrated that the disease process can be impacted by nutritional interventions 2–4 . It is important to note that AREDS supplements are useful in slowing the progression of existing disease but do not appear to prevent development of AMD 5 . Moreover, the benefits or safety of using such high-dose antioxidants for long periods, as might be needed in patients with AMD, has not been established 2, 6 .…”

Section: Introductionmentioning

confidence: 99%

Combined influence of poor health behaviours on the prevalence and 15-year incidence of age-related macular degeneration

Gopinath

Liew

Flood

et al. 2017

Sci Rep

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We aimed to establish the collective influence of four lifestyle practices (physical activity, diet, smoking and alcohol consumption) on the prevalence and incidence of AMD. At baseline, 2428 participants aged 49+ with complete lifestyle and AMD data were examined, and of these, 1903 participants were re-examined 15 years later. AMD was assessed from retinal photographs. A health behaviour score was calculated, allocating 1 point for each poor behaviour: current smoking; fruits and vegetables consumed <4 serves daily; <3 episodes of physical activity per week; and >2 alcoholic drinks per day. Cross-sectional analysis showed that participants who engaged in all 4 poor health behaviours (n = 29) versus those who did not engage in unhealthy behaviours (reference group; n = 677) had greater odds of any and late AMD: multivariable-adjusted OR, 5.14 (95% CI, 1.04–25.45) and OR 29.53 (95% CI 2.72–321.16), respectively. A marginally non-significant association was observed between increasing number of poor health behaviours and 15-year incidence of early AMD (multivariable-adjusted P-trend = 0.08). Our data suggests that motivating patients with AMD to eat better, exercise more, limit alcohol intake and avoid smoking seems advisable to decelerate the development or worsening of existing AMD.

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“…Animal models and the Age-Related Eye Disease Study (AREDS) trial strongly support a role for oxidative stress in the development of AMD. 4,5 Because of the importance of oxidative stress as a contributing factor in AMD, treatments that reduce the accumulation of reactive oxygen species (ROS) may be valuable as therapeutics, though antioxidant therapy has shown more benefit in preventing progression to wet AMD than to GA. 6–9 Our lab has developed a mouse model of GA in which the knockdown or deletion of Sod2 , the gene for manganese superoxide dismutase (MnSOD), in the RPE leads to elevated oxidative stress, causing some of the features of GA including damage to the RPE and Bruch's membrane and death of photoreceptors. 10,11 Depletion of MnSOD in the RPE in mice shows accumulation of lipofuscin-like fluorescent aggregates containing A2E and Iso-A2E.…”

mentioning

confidence: 99%

Timing of Antioxidant Gene Therapy: Implications for Treating Dry AMD

Biswal

Han

Zhu

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PurposeTo investigate whether antioxidant gene therapy protects the structure and function of retina in a murine model of RPE atrophy, and to determine whether antioxidant gene therapy can prevent degeneration once it has begun.MethodsWe induced mitochondrial oxidative stress in RPE by conditional deletion of Sod2, the gene for manganese superoxide dismutase (MnSOD). These mice exhibited localized atrophy of the RPE and overlying photoreceptors. We restored Sod2 to the RPE of one eye using adeno-associated virus (AAV) by subretinal injection at an early (6 weeks) and a late stage (6 months), injecting the other eye with an AAV vector expressing green fluorescent protein (GFP). Retinal degeneration was monitored over a period of 9 months by electroretinography (ERG) and spectral-domain optical coherence tomography (SD-OCT). Immunohistochemical and histologic analyses were conducted to measure oxidative stress markers and to visualize retinal structure.ResultsOne month after delivery, the AAV-Sod2 injection resulted in production of MnSod in the RPE and negligible expression in the neural retina. Electroretinography and OCT suggested no adverse effects due to increased expression of MnSOD or subretinal injection. Decrease in the ERG response and thinning retinal thickness was significantly delayed in eyes with early treatment with the Sod2 vector, but treatment at 6 months of age did not affect the ERG decline seen in these mice.ConclusionsWe conclude that antioxidant gene therapy may be effective in preventing the detrimental effects of oxidative stress, but may not be beneficial once substantial tissue damage has occurred.

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Dietary modification and supplementation for the treatment of age-related macular degeneration

Cited by 49 publications

References 133 publications

Nutritional and Lifestyle Interventions for Age‐Related Macular Degeneration: A Review

Nutritional and Lifestyle Interventions for Age‐Related Macular Degeneration: A Review

Combined influence of poor health behaviours on the prevalence and 15-year incidence of age-related macular degeneration

Timing of Antioxidant Gene Therapy: Implications for Treating Dry AMD

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