At the completion of this article, the reader should be able to…
• Explain how lifestyle factors like smoking, nutrition, exercise and weight can affect AMD risk
• Recognise environmental and behavioural contributors to AMD
• Discuss the role of physical activity in retinal health
• Explain potential ocular effects of GLP-1 receptor agonists (Ozempic)
Dr David Ng
MBBS MPH FRANZCO
Vision Eye Institute
Chatswood and Drummoyne, NSW
Dr DAVID NG shows how optometrists can apply the latest evidence on diet, exercise, supplementation, and weight management to support retinal health and help reduce the risk of progression from early to advanced AMD.
As a normal functioning macula and good central vision are essential for undertaking most basic activities of daily life, a diagnosis and the subsequent development of age-related macular degeneration (AMD), which may rob people of their independence and their enjoyment of life, can be devastating.1
Globally, an estimated 196 million people were diagnosed with AMD in 2020, a number expected to increase to 288 million by 2040, representing a significant health and economic issue.1
Although many patients with AMD retain functional vision, approximately six million have moderate-to-severe vision impairment and 1.85 million people are considered blind due to AMD.2
According to the 2017 Australian National Eye Health Survey, the weighted prevalence of early AMD was 14.8% in non-indigenous Australians, 10.5% for intermediate AMD and 0.96% for late AMD.3
The prevalence increases with age. Analysis of the European Eye Epidemiology Consortium indicated the prevalence of early AMD increased from 3.5% in those aged 55-59 to 17.6% in those aged 85 years and older. Similarly, for late AMD, these figures were 0.1% and 9.8% respectively.4
Although neovascular AMD responds well to anti-VEGF (anti vascular endothelial growth factor) intravitreal injections, the treatment pathway is indefinite and eventual progression considered likely.
Lifestyle factors and AMD
AMD is a multifactorial disease. As it is better to prevent, or at least reduce the risk of progression of AMD to the late stages, consideration of contributing variables can play a key role in preserving vision and quality of life.
Multiple lifestyle factors have been shown to have significant effects suggesting that a revision of these variables may have a positive impact on AMD progression. Smoking, Body Mass Index (BMI) and general health, daily caloric intake, sleep and diet are modifiable risk factors.
Positively, the EYE-RISK consortium concluded that adherence to a healthy lifestyle was associated with reduced prevalence of AMD across all genetic risk strata.
The strongest effect, however, was seen in the highest genetic risk group.5 In this cohort, modifiable lifestyle factors may contribute up to 60% of progression from early or intermediate AMD to advanced AMD.
In other words, patients with a high genetic risk of AMD can reduce their risk by up to 50% through healthy lifestyle choices.
Notably, having two or more relatives with AMD did not automatically place one in the highest genetic risk group – approximately half (51%) of people with two or more relatives with AMD were placed in the highest genetic risk group.6
An in-depth discussion about lifestyle factors is an important part of the counselling process for a newly diagnosed patient with AMD.
It has been my experience that many patients are interested in a holistic approach to their health, and many ask about what they should or shouldn’t eat.
Modifiable lifestyle factors
Smoking
Smoking remains the single most important modifiable risk factor.
Smokers are more likely to develop a clinical diagnosis earlier (mean 5.5 years earlier compared to never-smokers and mean 4.4 years earlier compared to past smokers).7
Further, current smokers when compared to never-smokers have a 2.5-fold increased risk of developing atrophic AMD and 4.5-fold increased risk of developing neovascular AMD. 8,9
As may be expected, smoking cessation is associated with decreasing risk of developing geographic atrophy and choroidal neovascularization.10 After smoking cessation for 20 years, risks are comparable to never-smokers.10
Studies have identified that most clinicians routinely discuss the impact of smoking on health, however barriers such as time constraint and patient reluctance to change have been noted to impact the conversation.11
Adherence to smoking cessation remains low; one telephone questionnaire reported 0% adherence, despite strong uptake of diet and weight reduction recommendations (81% and 76% respectively).12
Cigarette smoke contains numerous pro-oxidant compounds such as tar. These can cause oxidative injury to the retinal pigment epithelium resulting in thickening of Bruch’s membrane and formation of sub-RPE deposits.9
Notably, nicotine replacement therapy (NRT) has been linked to a short-term reduction in AMD risk, although this benefit was not sustained over the long term.13
Obesity and associated biomarkers
A Body Mass Index (BMI) ≥ 25 is classified as ‘overweight’ and is associated with an increased risk of progression to advanced AMD.6
Additional measures, such as body roundness index (BRI) have also shown a positive association in patients over 40 years across large datasets.14
Variability across cohorts likely reflects differences in weight-related metrics and classification methods, but also underscores the multifactorial nature of the condition; however, evidence suggests that dietary modification and weight reduction may positively influence AMD progression.
Sleep
Like other risk factors, obstructive sleep apnoea (OSA) appears to share pathophysiological mechanisms involving oxidative stress and inflammation.
Although studies remain limited, a recent meta-analysis reported a modest increase in the risk for AMD progression in patients with OSA (OR 1.19).
However, no association was found between AMD and sleep duration or insomnia.15 Given investigators have identified a link between CPAP therapy for OSA in AMD patients and improved retinal anatomy, these findings appear to confirm the pathophysiological impact of OSA on AMD.16 Further large-scale, prospective studies are required.
Pollution
The association between ambient air pollution and AMD incidence is gaining increasing attention.
In contrasting population investigations in France, urban individuals exposed to the highest quartile of pollution (>2.33 10-5/m) had an 88% increased risk of AMD compared with those exposed at the level of the first quartile, suggesting a potential new insight into AMD incidence.17
Findings from the UK Biobank support these findings and suggest that the increased risk may be amplified by genetic susceptibility.18
Relocating due to pollution and AMD risk is unlikely to represent an option for most of us, however.
UV Exposure
Exposure to excessive irradiation can lead to oxidative stress.
Although historical review of UV exposure is limited by recall, a history of significant exposure (> 8 hours externally per day) has been associated with early AMD, though no link was found for current sunlight exposure.19
More recently, artificial blue light exposure is a potential concern; laboratory rat exposure experiments have found prolonged exposure to blue and white light can lead to irreversible retinal damage, but the relevance to humans remains unclear.20
Promoting the use of approved sunglasses remains a simple, low-risk strategy for general ocular health.
Modifiable lifestyle recommendations
Although many prognostic factors are not readily modifiable, reviewing lifestyle factors including diet which influence AMD progression remains beneficial for the whole of the patient’s health.
Caloric intake
In the Age-Related Eye Diseases Study (AREDS) study, daily caloric intakes greater than 1701 kcal/day for men and 1261 kcal/day for women were associated with an increased risk of progression to advanced AMD.6
These figures represent the median intakes reported by participants in a 90-item questionnaire, and are much lower than the recommended minimum for sedentary adults, reflecting a cautious interpretation.
As such, I do not routinely discuss this with patients.
Exercise and weight loss
International guidelines recommend at least 150 minutes of moderate-to-vigorous physical activity a week. Large-scale UK Biobank data show that both regular and ‘weekend warrior’ activity patterns are linked to lower risk of age-related eye disease. 21
Although exercise is likely to further impact weight and general health, it has also been associated with possible mediators of retinal neuroprotection.
Conversely, it has been suggested that AMD progression and vision loss could increase inactivity, which could, in turn, accelerate disease advancement.22
GLP-1 receptor agonists (GLP-1RAs), including Ozempic (semaglutide), are widely used for type 2 diabetes and obesity.
Preclinical studies show that this class of drugs can reduce oxidative and inflammatory stress, suggesting a potential effect in AMD.23
Compared with other weight-loss therapies, GLP-1RAs were associated with lower incidence of AMD diagnosis in a large retrospective cohort analysis.24
However, the absence of prospective, well-designed clinical trials limits our ability to confirm their role in AMD prevention or treatment.
Diet and alcohol intake
The intake of green leafy vegetables such as spinach, greens, or collards is important for eye health.
These vegetables are rich in lutein and zeaxanthin, xanthophyll carotenoids that absorb high-energy blue light (peak absorption of zeaxanthin is 450nm and lutein is 445nm), mop up free radicals and reduce oxidative stress and inflammation in the retina.
Consuming ≥2.7 portions per week (half a cup per portion) has been associated with a lower risk of progression to advanced AMD.6
The retina is one of the most lipid-rich tissues in the body, with polyunsaturated fatty acids (PUFAs) making up 45% of retinal phospholipids, primarily sourced from the diet.
Omega 3 PUFAs help resist oxidative stress and reduce free radicals production, which, in turn, reduces the degradation of the RPE.25
In wet-AMD, they inhibit Interleukin-6 and VEGF, key mediators in neovascularisation.
Eating fish, which are rich in omega 3 fatty acids, merely once a week has been shown to reduce the development of early AMD.25 Two or more servings consisting of at least 4oz (113g) of oily fish such as tuna, salmon, mackerel or trout per week decreased risk of progression to advanced AMD.6
More broadly, adherence to dietary patterns such as the Mediterranean diet (rich in vegetables, whole grains and fruit, and lower in red meat and processed fats) may confer protective effects against AMD development and progression, likely through antioxidant and anti-inflammatory mechanisms, although findings remain variable across studies.
Recent meta-analysis indicated that following the Mediterranean diet may reduce the odds of progression by 23-34%.26
Elsewhere, higher intake of ultra-processed foods has been associated with an increased risk of AMD, suggesting a potentially modifiable target for risk reduction; however, this relationship should be interpreted within the context of socioeconomic factors that influence food access, affordability, and dietary choice.27
Traditional Chinese Medicine (TCM) represents a popular alternative and/or supportive pathway for many patients.
Multiple randomised controlled trials have attempted to determine a role for increased clinical efficacy with respect to retinal changes and visual acuity.
Although TCM appears to be safe, the impact on visual acuity remains variable and discussion of a collaborative approach remains sound.28
The association between alcohol intake and AMD progression is complex and likely influenced by multiple confounding factors. Recently, a subset of the large AREDS-2 study found that moderate alcohol consumption was associated with decreased progression to late AMD in men whereas higher consumption was associated with faster progression.29
Regardless, moderation would appear to represent the most appropriate advice.
Oral supplementation with vitamins and minerals
There is good evidence that high dose vitamins and minerals can help. It is important to discuss this with your AMD patients, particularly as many will have heard from their friends.
The AREDS research showed that oral supplementation of antioxidant vitamins with zinc and copper reduced the risk of progression from intermediate AMD to advanced AMD by 25%.30
The original AREDS formula also reduced risk of central vision loss by 19%. This formula contained 500mg of vitamin C, 400 IU of vitamin E, 15mg beta-carotene, 80mg of Zinc and 2mg of copper.
Unfortunately, an increase in the incidence of lung cancer in smokers was found. For smokers the risk of developing lung cancer was double if the supplements contained beta carotene.30
The AREDS2 formula replaced beta carotene with the carotenoids zeaxanthin and lutein, which are found in high concentration in the retina. Importantly, no benefit was found in preventing the development of AMD.
An important consideration for discussion is the review of current supplements.
Many supplements purported to support eye health do not contain the correct doses as specified by AREDS2.
If patients are already taking multivitamins, explain to them that the AREDS2 formulation contains much higher doses than would be contained in their multivitamin preparations.
Further, there is no contraindication to taking multivitamins along with the AREDS2 formulation.
Final thoughts
Although vision may remain largely unaffected for many years, a diagnosis of AMD is often unsettling for patients.
The primary goal is therefore to reduce the risk of progression to advanced disease. In most cases, early and intermediate AMD can be effectively managed by an engaged optometrist, particularly where OCT imaging is available.
Ongoing discussion and reinforcement of modifiable behaviours are central to optimising both general and retinal health and should be actively supported within the clinic.
References:
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