Age-Related Nuclear Cataract
Age-related nuclear cataract is a common ocular condition characterized by the gradual clouding and yellowing of the central nucleus of the eye’s natural lens. This progressive opacity impairs vision, leading to symptoms such as blurred vision, increased glare sensitivity, and difficulty seeing in low light conditions. As a primary cause of visual impairment, its prevalence increases significantly with age, affecting a substantial portion of the elderly population[1].
Biologically, age-related nuclear cataracts result from complex processes involving oxidative stress, protein aggregation, and modifications to the lens proteins (crystallins) over time. These changes lead to a loss of the lens’s transparency, hindering light transmission to the retina. Genetic predisposition plays a notable role in the development and progression of cataracts, with research identifying several genetic loci linked to cataract susceptibility, including those potentially shared with childhood cataracts[1]. Continued exploration is needed to validate and replicate these associations and identify additional susceptibility loci for age-related forms [1].
Clinically, age-related nuclear cataract is the leading cause of vision loss in the United States and the primary cause of blindness globally[1]. Diagnosis typically involves a comprehensive eye examination. While initial symptoms can sometimes be managed with changes in eyeglass prescriptions, the definitive treatment for significant vision impairment is surgical removal of the clouded lens and its replacement with an artificial intraocular lens.
The social importance of age-related nuclear cataract is substantial. It accounts for approximately 60% of Medicare costs related to vision and is associated with increased risks of falls and higher mortality rates, possibly due to related systemic conditions[1]. Given rising life expectancies, the incidence of cataract cases and subsequent surgeries is projected to increase dramatically. This trend underscores the critical need for developing and implementing effective primary prevention strategies to mitigate the public health and economic burden of this condition[1].
Limitations
Section titled “Limitations”Research into the genetic basis of age-related nuclear cataract, while yielding valuable insights, is subject to several limitations that affect the interpretation and generalizability of findings. These constraints are common in complex disease genetics and highlight areas for future investigation.
Methodological and Statistical Constraints
Section titled “Methodological and Statistical Constraints”Current genetic studies on age-related nuclear cataract, including those utilizing electronic medical records and genomics (eMERGE) networks, often require further validation and replication of identified associations[1]. This necessity implies that initial findings may stem from cohorts that, while informative, might be limited in sample size or represent specific populations, potentially leading to an overestimation of effect sizes or the identification of associations that are not broadly reproducible. Robust replication in independent cohorts is therefore crucial to confirm the reliability of genetic signals and to differentiate true associations from statistical artifacts.
The reliance on specific study designs, such as those within the eMERGE network, can introduce inherent biases related to data collection from electronic health records, which might not capture all relevant clinical or demographic details comprehensively [1]. These design-specific characteristics mean that the observed genetic associations might be influenced by the structure and content of the available data, necessitating careful consideration when interpreting the general applicability of the results. Furthermore, the inherent complexity of age-related diseases means that detecting small genetic effects often requires very large sample sizes, and studies with insufficient power may miss genuine associations or struggle with consistent replication.
Phenotypic Definition and Population Heterogeneity
Section titled “Phenotypic Definition and Population Heterogeneity”A significant limitation in genetic studies for age-related nuclear cataract is the potential variability in phenotypic definition and measurement across different research settings. Inconsistent diagnostic criteria or diverse methods for cataract grading can introduce heterogeneity, which might obscure genuine genetic associations or lead to conflicting results when attempting to combine or compare findings from multiple studies[1]. Such challenges in precise phenotyping necessitate standardized approaches to ensure comparability and enhance the power to detect genetic influences.
Furthermore, the generalizability of genetic findings across diverse populations remains a key concern. While large-scale genome-wide association studies for related age-related eye diseases, such as macular degeneration, involve extensive international collaborations[2], specific research on age-related nuclear cataract may be predominantly focused on cohorts from certain ancestral backgrounds[1]. This can limit the direct applicability of findings to other ethnic groups, as genetic risk factors and their effect sizes can vary significantly across different ancestries, underscoring the need for broader investigations that encompass a wider range of global populations to fully understand the genetic architecture of the condition.
Unaccounted Environmental Factors and Genetic Complexity
Section titled “Unaccounted Environmental Factors and Genetic Complexity”The genetic architecture of age-related nuclear cataract is undoubtedly complex, involving a multitude of genetic factors that interact with environmental influences. Studies on related conditions like age-related macular degeneration have highlighted the critical role of gene-environment interactions, such as the interplay between genetic predispositions and lifestyle factors like smoking[3]. For age-related nuclear cataract, a comprehensive understanding of these complex interactions is often challenging to capture in current study designs, potentially leading to an incomplete picture of disease etiology and contributing to the phenomenon of “missing heritability”[4], where known genetic variants explain only a fraction of the observed heritable risk.
Consequently, significant knowledge gaps persist regarding the full spectrum of genetic and non-genetic contributors to the development and progression of age-related nuclear cataract[1]. While new potential susceptibility loci are being identified, the precise mechanisms through which these variants exert their effects, their interactions with other genes, and their modulation by environmental factors often remain to be fully elucidated. Future research must therefore aim to integrate more sophisticated analytical approaches that can account for multifactorial etiology, ultimately advancing the understanding of this common age-related eye condition.
Variants
Section titled “Variants”Genetic variations play a crucial role in an individual’s susceptibility to age-related nuclear cataract, a condition characterized by the clouding of the central part of the eye’s lens. Research suggests that a significant number of genes may contribute to this complex trait, with evidence pointing to a major genetic component in nuclear cataract development[5]. The transparency of the eye lens is maintained by a delicate balance of structural proteins, cellular processes, and metabolic pathways, and disruptions caused by specific genetic variants can lead to opacification over time.
Variants in or near genes encoding crystallins, such as CRYAA(Alpha-crystallin A chain), are of particular interest due to their direct role in lens structure and function. For instance, the variantsrs7278468 near FRGCA - CRYAA and rs11911275 near CRYAA - LINC00322 are located in regions that can influence the CRYAA gene. Alpha-crystallins are primary structural proteins in the lens and also act as molecular chaperones, preventing other proteins from aggregating. Alterations in CRYAAcan compromise lens transparency, leading to cataract formation. The proximity ofrs11911275 to LINC00322, a long non-coding RNA, suggests potential regulatory interactions that could affect CRYAA expression or stability, further linking these variants to lens health. The familial aggregation of lens opacities underscores the genetic influence on this condition [6].
Other variants highlight the role of gene regulation and cellular maintenance in preventing age-related nuclear cataract. Thers9842371 variant is located in SOX2-OT (SOX2 Overlapping Transcript), a long non-coding RNA that can regulate the SOX2 gene, a critical transcription factor for eye development and stem cell maintenance. Similarly, rs16823886 in LINC01412 and rs1005911 in BICRA (BRD4 Interacting Chromatin Remodeling Complex Associated Protein) are associated with genes involved in non-coding RNA function and chromatin remodeling, respectively. These regulatory elements are essential for precise gene expression patterns required for lens cell differentiation and survival. Disruptions in these pathways can lead to cellular dysfunction and contribute to the degenerative processes observed in age-related cataracts.
Furthermore, variants affecting cellular homeostasis and stress responses are implicated in lens health. The rs4936279 variant in TMPRSS5(Transmembrane Serine Protease 5) could influence protein processing and degradation, whilers62149908 in COMMD1 (COMM Domain Containing 1) may impact copper metabolism and inflammatory signaling, both crucial for maintaining cellular integrity. Variants like rs11067211 near UBE3B (Ubiquitin Protein Ligase E3B) and MMAB (Methylmalonic Aciduria Type B), and rs61185326 near NDUFAF2P1 (NADH:Ubiquinone Oxidoreductase Complex Assembly Factor 2 Pseudogene 1) and HS1BP3(HS1 Binding Protein 3) point to the importance of protein quality control, vitamin B12 metabolism, and mitochondrial function. Lastly,rs7615568 in KCNAB1(Potassium Voltage-Gated Channel Subfamily A Regulatory Beta Subunit 1) suggests a role for ion channel regulation in maintaining the delicate osmotic balance within lens cells, all of which are vital mechanisms for protecting the lens against age-related damage and opacification.
Key Variants
Section titled “Key Variants”| RS ID | Gene | Related Traits |
|---|---|---|
| rs9842371 | SOX2-OT | Age-related nuclear cataract cataract age at onset, eye measurement |
| rs7278468 | FRGCA - CRYAA | Age-related nuclear cataract |
| rs4936279 | TMPRSS5 | Age-related nuclear cataract |
| rs16823886 | LINC01412 | Age-related nuclear cataract basophil count |
| rs62149908 | COMMD1 | Age-related nuclear cataract |
| rs1005911 | BICRA | Age-related nuclear cataract |
| rs11067211 | UBE3B - MMAB | Age-related nuclear cataract body height |
| rs61185326 | NDUFAF2P1 - HS1BP3 | Age-related nuclear cataract |
| rs11911275 | CRYAA - LINC00322 | Age-related nuclear cataract |
| rs7615568 | KCNAB1 | Age-related nuclear cataract |
Definition and Core Terminology
Section titled “Definition and Core Terminology”Age-related nuclear cataract refers to the opacification and hardening of the central nucleus of the eye’s crystalline lens, a common condition associated with advancing age. This progressive clouding interferes with light transmission to the retina, leading to impaired vision. As a form of age-related cataract, it is a significant public health concern, globally recognized as the leading cause of blindness and the primary cause of vision loss in the United States[1]. The term “cataract” itself denotes any opacity of the lens, with “nuclear” specifically referring to the central zone of the lens where this particular type of cataract develops.
Classification and Subtypes of Age-Related Cataract
Section titled “Classification and Subtypes of Age-Related Cataract”Age-related cataracts are broadly classified into several subtypes based on their location within the lens, primarily nuclear, cortical, and posterior subcapsular (PSC) cataracts. Nuclear cataract is distinguished by the yellowing and hardening of the central lens nucleus. While other subtypes like cortical and PSC cataracts have been associated with risk factors such as higher body mass index (BMI), nuclear cataract has shown distinct associations[1]. Research indicates significant familial aggregation for nuclear cataract in older populations, even after accounting for shared environmental factors[7]. Furthermore, specific genetic loci, such as the FTO obesity gene, have been associated with nuclear cataract in certain populations[8].
Diagnostic and Operational Measurement Criteria
Section titled “Diagnostic and Operational Measurement Criteria”The diagnosis of age-related nuclear cataract relies on clinical examination and specific operational criteria, particularly in research settings. In studies, cases may be identified as “surgical” if an individual has undergone cataract extraction in at least one eye, or “diagnosis-only” based on multiple diagnostic codes or a single diagnosis supported by natural language processing (NLP) and optical character recognition (OCR) of medical notes[1]. The specific type of cataract, such as nuclear, is often extracted from these clinical notes using NLP/OCR, with validation through manual chart abstraction to ensure accuracy[1]. Controls in such studies typically consist of individuals aged 50 years or older with recent eye exams showing no diagnostic codes for cataract or evidence of prior cataract surgery[1]. This structured approach ensures consistent identification and classification of cases for epidemiological and genetic research.
Age-related nuclear cataract, a common subtype of age-related cataract, significantly impacts visual health, contributing to global blindness and ranking as the leading cause of vision loss in the United States . Studies suggest that as many as 40 genes could be involved in age-related cataract, and evidence points to the existence of major genes contributing to both cortical and nuclear cataract types[1].
Nuclear cataract, in particular, demonstrates significant familial aggregation even after accounting for shared environmental factors, indicating a strong inherited component. This aggregation often stems from polygenic effects, where multiple genes collectively contribute to an individual’s overall susceptibility. These polygenic influences, sometimes in conjunction with lifestyle factors like cigarette smoking, help explain the observed patterns of familial inheritance[7].
Environmental and Lifestyle Risk Factors
Section titled “Environmental and Lifestyle Risk Factors”Environmental and lifestyle choices are crucial determinants of age-related nuclear cataract risk. Cigarette smoking, for instance, is a well-established risk factor that contributes to the familial clustering of the condition. Furthermore, genetic variations in detoxification pathways, such as the null genotype of glutathione S-transferase M1, have been associated with increased susceptibility to senile cataract, particularly in non-smoking females, highlighting how the body’s response to environmental toxins can influence disease development[9].
Beyond direct exposures, metabolic health and demographic characteristics also play a part. Obesity has been linked to an elevated risk of age-related cataract, underscoring the impact of systemic metabolic dysfunction on ocular health. Moreover, demographic analyses indicate that women face a slightly higher risk of developing cataracts compared to men. These diverse environmental and lifestyle elements collectively illustrate the multifaceted nature of cataract etiology[8].
Complex Gene-Environment Interactions and Systemic Influences
Section titled “Complex Gene-Environment Interactions and Systemic Influences”The progression of age-related nuclear cataract is not solely dictated by either genetic makeup or environmental exposures, but rather by their complex and dynamic interactions. Genetic predispositions, such as polygenic effects, can significantly interact with environmental triggers like cigarette smoking, collectively modulating an individual’s overall risk. Similarly, the presence of specific “obesity genes” can modify the influence of obesity on cataract formation, demonstrating how an individual’s genetic background can alter their susceptibility to environmental factors[9].
Furthermore, age-related nuclear cataract is frequently associated with broader systemic health conditions, which can lead to increased risks such as falls and higher mortality rates. The fundamental process of aging itself is the most prominent overarching factor, as the global increase in life expectancy directly correlates with a dramatic rise in cataract incidence. While the specific effects of various medications are not detailed in current research, the interplay among different health comorbidities and the cumulative physiological changes associated with aging substantially contribute to the pathogenesis of age-related nuclear cataract[1].
Biological Background
Section titled “Biological Background”Age-related nuclear cataract is a prevalent ocular condition characterized by the progressive clouding of the eye’s natural lens, specifically affecting its central nucleus. This condition is a major global health challenge, representing the leading cause of blindness worldwide and the primary cause of vision loss in the United States. With increasing life expectancy, the number of individuals affected by age-related cataract is projected to rise significantly, highlighting the importance of understanding its biological underpinnings[1]. The opacification process disrupts the lens’s ability to focus light clearly onto the retina, leading to blurred vision, reduced visual acuity, and, if untreated, severe visual impairment.
The Lens and Cataract Formation
Section titled “The Lens and Cataract Formation”The human lens is a unique, avascular, and transparent tissue essential for focusing light onto the retina. Its transparency is maintained by a highly ordered arrangement of specialized lens fiber cells and a precise balance of proteins and water. Age-related nuclear cataract develops when the proteins within the lens nucleus undergo changes that cause them to aggregate and scatter light, leading to the characteristic clouding[1]. This progressive opacification is a hallmark of the aging process, reflecting the cumulative effects of cellular damage and impaired maintenance mechanisms over decades.
The formation of cataracts is a complex pathophysiological process that disrupts the delicate homeostasis of the lens. Unlike other tissues, lens cells persist throughout life, accumulating damage without the ability to shed old cells. This makes the lens particularly vulnerable to long-term stressors that compromise protein stability and cellular integrity, ultimately leading to lens opacification and impaired vision.
Genetic Influences on Cataract Development
Section titled “Genetic Influences on Cataract Development”Genetic mechanisms play a substantial role in determining an individual’s susceptibility to age-related nuclear cataract, with evidence demonstrating significant familial aggregation even after accounting for shared environmental factors[7]. Research into childhood cataract has identified numerous genetic loci, and it is hypothesized that many of these same genes may also contribute to the development of age-related forms[10]. It is estimated that as many as 40 different genes may be involved in the complex etiology of age-related cataract, suggesting a polygenic inheritance pattern[11].
Specific genetic variations, including major genes, have been linked to both cortical and nuclear cataract types, indicating that inherited factors can significantly influence disease risk[5]. These genes are thought to encode critical proteins involved in maintaining lens structure, regulating cellular pathways, and protecting against oxidative stress. The intricate interplay between these genetic predispositions and various environmental factors ultimately dictates an individual’s lifetime risk of developing age-related nuclear cataract.
Cellular Homeostasis and Oxidative Stress
Section titled “Cellular Homeostasis and Oxidative Stress”The maintenance of cellular homeostasis and metabolic processes within the lens is crucial for preserving its transparency. Disruptions in these molecular and cellular pathways, particularly those involving oxidative stress, are key contributors to the development of age-related lens opacification. The lens possesses an elaborate antioxidant defense system, comprising various enzymes and molecules, designed to protect its proteins and cellular components from damage caused by reactive oxygen species.
Among the key biomolecules involved in these protective mechanisms is glutathione S-transferase M1 (GSTM1), an enzyme vital for detoxification. Studies have shown that individuals with a null genotype for GSTM1, meaning they lack a functional copy of the gene, exhibit an increased susceptibility to senile cataract, particularly in non-smoking females[12]. This highlights how genetic variations impacting critical enzymes and their regulatory networks can compromise the lens’s ability to combat oxidative damage, leading to protein aggregation and the characteristic clouding of nuclear cataract.
Systemic Factors and Disease Associations
Section titled “Systemic Factors and Disease Associations”Age-related nuclear cataract is not merely an isolated ocular condition but can be intertwined with broader systemic health issues and consequences. Impaired vision due to cataract has been associated with an increased risk of falls and, potentially, higher mortality rates, suggesting links to underlying systemic conditions[1]. These systemic connections underscore the importance of considering cataract within the context of overall health and aging.
Homeostatic disruptions and systemic factors, such as obesity, have also been explored for their potential association with age-related cataract, particularly in certain populations[8]. Additionally, epidemiological data indicate that women have a slightly higher risk of developing cataract than men[13]. These observations suggest that a combination of metabolic, environmental, and potentially hormonal or sex-linked biological factors contribute to the complex etiology and progression of age-related nuclear cataract.
Pathways and Mechanisms
Section titled “Pathways and Mechanisms”Genetic Basis of Cataract Susceptibility
Section titled “Genetic Basis of Cataract Susceptibility”Research into age-related cataract has identified several potential susceptibility loci, suggesting a genetic predisposition to the condition[1]. These genomic regions are hypothesized to influence the risk of developing age-related nuclear cataract primarily through mechanisms of gene regulation. Variations within these loci may impact the expression levels, functional integrity, or stability of proteins essential for maintaining the transparency and structural integrity of the ocular lens. While specific molecular pathways and their detailed interactions remain subject to further elucidation, the identification of these genetic markers points towards an underlying regulatory dysregulation contributing to the pathogenesis of cataract. Continued exploration, including validation and replication of these associations, is crucial for understanding the complex interplay of genetic and environmental factors in cataract development[1].
Frequently Asked Questions About Age Related Nuclear Cataract
Section titled “Frequently Asked Questions About Age Related Nuclear Cataract”These questions address the most important and specific aspects of age related nuclear cataract based on current genetic research.
1. My parents both had cataracts; will I definitely get them too?
Section titled “1. My parents both had cataracts; will I definitely get them too?”While genetic predisposition plays a notable role in developing cataracts, it’s not a guarantee. You might have a higher susceptibility due to family history, but environmental factors also interact with your genes. Regular eye check-ups are key to monitor your eye health.
2. Is it true that everyone eventually gets cataracts as they get really old?
Section titled “2. Is it true that everyone eventually gets cataracts as they get really old?”Age-related nuclear cataract is very common and its prevalence significantly increases with age, affecting a substantial portion of the elderly. However, not everyone will develop it. Some individuals may be more genetically predisposed, while others might experience different age-related eye changes.
3. Can my diet or lifestyle prevent me from getting cataracts?
Section titled “3. Can my diet or lifestyle prevent me from getting cataracts?”While genetic factors are important, lifestyle choices like diet and avoiding oxidative stress may play a role in prevention. Research is ongoing into effective primary prevention strategies, as the condition is complex and involves many genetic and environmental interactions.
4. Why am I suddenly struggling to see when I drive at night?
Section titled “4. Why am I suddenly struggling to see when I drive at night?”Difficulty seeing in low light conditions and increased glare sensitivity are common symptoms of age-related nuclear cataract. The clouding of your eye’s lens can scatter light, making night driving particularly challenging. It’s a good idea to get your eyes checked.
5. My vision feels blurry sometimes; when should I worry about it?
Section titled “5. My vision feels blurry sometimes; when should I worry about it?”Blurred vision is a primary symptom of age-related nuclear cataract. If you’re experiencing persistent blurriness, increased glare sensitivity, or difficulty seeing in low light, it’s time for a comprehensive eye examination. Early diagnosis can help manage symptoms or plan treatment.
6. Why did my friend get cataracts earlier than I did, even though we’re the same age?
Section titled “6. Why did my friend get cataracts earlier than I did, even though we’re the same age?”Individual differences in cataract development can be due to a combination of genetic factors and environmental influences. Some people are simply more genetically predisposed to developing cataracts at an earlier age, while others might have different lifestyle exposures.
7. Will my vision just keep getting worse and worse if I don’t get surgery?
Section titled “7. Will my vision just keep getting worse and worse if I don’t get surgery?”Age-related nuclear cataract is characterized by progressive opacity, meaning the clouding of the lens typically worsens over time. While initial symptoms can sometimes be managed with eyeglass changes, significant vision impairment usually requires surgical intervention.
8. Does my ethnic background affect my risk of getting cataracts?
Section titled “8. Does my ethnic background affect my risk of getting cataracts?”Yes, genetic findings for age-related eye diseases can vary significantly across different ancestral backgrounds. While research is ongoing, certain genetic risk factors might be more prevalent or have different effects in specific ethnic groups, underscoring the need for diverse studies.
9. Can having other health problems make my cataracts worse or more likely?
Section titled “9. Can having other health problems make my cataracts worse or more likely?”Age-related nuclear cataract is associated with increased risks of falls and higher mortality rates, possibly due to related systemic conditions. The complex interplay between your overall health, genetic predispositions, and environmental factors can influence the development and progression of cataracts.
10. Are there any new treatments coming out that aren’t surgery?
Section titled “10. Are there any new treatments coming out that aren’t surgery?”The definitive treatment for significant vision impairment from cataracts is currently surgical removal of the clouded lens. However, there’s a critical need for developing and implementing effective primary prevention strategies, suggesting ongoing research into non-surgical options and early interventions.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Ritchie, M. D. “Electronic Medical Records and Genomics (eMERGE) Network Exploration in Cataract: Several New Potential Susceptibility Loci.”Mol Vis, Oct. 2014, 20: 1530-1540.
[2] Fritsche, L. G., et al. “A Large Genome-Wide Association Study of Age-Related Macular Degeneration Highlights Contributions of Rare and Common Variants.”Nat Genet, Feb. 2016, 48(2): 134-143.
[3] Naj, A. C., et al. “Genetic Factors in Nonsmokers with Age-Related Macular Degeneration Revealed through Genome-Wide Gene-Environment Interaction Analysis.”Ann Hum Genet, July 2013, 77(4): 277-285.
[4] Sobrin, L., et al. “Heritability and Genome-Wide Association Study to Assess Genetic Differences between Advanced Age-Related Macular Degeneration Subtypes.”Ophthalmology, Aug. 2012, 119(8): 1629-1635.
[5] Heiba, I. M., et al. “Genetic etiology of nuclear cataract: evidence for a major gene.”American Journal of Medical Genetics, vol. 71, no. 3, 1997, pp. 263-270.
[6] The Framingham Offspring Eye Study Group. “Familial aggregation of lens opacities: the Framingham Eye Study and the Framingham Offspring Eye Study.” American Journal of Epidemiology, vol. 149, no. 5, 1999, pp. 463-470.
[7] Congdon, N, et al. “Nuclear cataract shows significant familial aggregation in an older population after adjustment for possible shared environmental factors.”Invest Ophthalmol Vis Sci, vol. 46, 2005, pp. 1608-1612.
[8] Lim, L. S., et al. “Relation of age-related cataract with obesity and obesity genes in an Asian population.”American Journal of Epidemiology, vol. 169, no. 1, 2009, pp. 106-114. [PMID: 19001155].
[9] Klein, A. P., et al. “Polygenic effects and cigarette smoking account for a portion of the familial aggregation of.” Investigative Ophthalmology & Visual Science, vol. 46, no. 9, 2005, pp. 3131-3137. [PMID: 15800262].
[10] Moore, Anthony T. “Understanding the molecular genetics of congenital cataract may have wider implications for age related cataract.”British Journal of Ophthalmology, vol. 88, no. 10, 2004, pp. 1221-1222.
[11] Hejtmancik, J. F., and M. Kantorow. “Molecular genetics of age-related cataract.”Experimental Eye Research, vol. 88, no. 2, 2009, pp. 178-188.
[12] Saadat, M., et al. “Null genotype of glutathione S-transferase M1 is associated with senile cataract susceptibility in non-smoker females.”Molecular Vision, vol. 15, 2009, pp. 2088-2094. [PMID: 19893817].
[13] Kempen, John H., et al. “Prevalence of cataract and pseudophakia/aphakia among adults in the United States: data from the National Health and Nutrition Examination Survey 1999-2000.”Ophthalmology, vol. 111, no. 12, 2004, pp. 2193-2199.