eye health obesity electronics junk food liberal news media disinformation system

Many eye problems follow obesity
Macular Degeneration
not to mention other diseases – diabetes, dementia, cancer, stroke, heart attack, etc.

(junk food + sitting + electronics cause junk food eating and hormonal changes that cause both eye problems and obesity).

Rehab needed — change requires change
The first step in any cure is to normalize all readings in whatever can be easily measured.
weight, blood pressure, running speed, swimming distance, biking weight lifting strength, Insulin, Insulin resistance, glucose, cholesterol, BRCA genes etc.
Go to college and take biochemistry how to measure all that needs to be measured. Get DVM to practice on animals learn how to cure people and animals

Move to Hawaii, eat fruit, peer pressure to get outside and exercise.
Get energy from sun, not food, mitochondria ATP Adenosine Triphosphate signalling. learn Chinese Japanese vegetarian cooking.
No smog or smog test in Hawaii middle of ocean not many cars.
No snow in the populated areas, no heater needed, ocean is your cooler jump in. Don’t need electricity at all.
Best water quality possible.

Get rich on your photos and book on how you cured yourself and lived long healthy life. I will reduce down to 133 pounds high school weight, powerlifting class 132 1/4

Lots of footnotes in this large study but need to reduce obesity now before full dangers are documented


The prevalence of obesity has reached epidemic proportions in many countries.
While its impact on overall health is well documented, less is known about the ocular manifestations of obesity. Amongst different eye diseases, obesity has been linked with age-related cataract,
age-related maculopathy, and
diabetic retinopathy.

Numerous population-based and prospective studies support an association between obesity and risk of age-related cataract.

There is strong evidence that obesity is associated with elevated intraocular pressure

The medical consequences of obesity are numerous.
It is an established risk factor for many systemic diseases including coronary heart disease,
type 2 diabetes mellitus,
sleep apnea.
43, 69, 77, 123, 155

Obesity has also been associated with certain types of cancers.12, 20 One study estimated that obesity is responsible for approximately 40% of endometrial cancers,
25% of renal cancers, and
10% each of colonic and breast cancers. 12

Other obesity-associated co-morbidities include
polycystic ovary syndrome,
fatty liver as well as
secondary to social stigmatization and discrimination. 123

The impact of obesity on health is widespread, and the

deleterious effects of obesity on the cardiovascular and metabolic systems are well known. 77

Obesity has recently been reported to be negatively associated with visual acuity, 10

obesity has been associated with cataract,1, 21, 53, 63, 86, 94, 107, 108, 121, 129,168, 211, 222 age-related maculopathy,2, 28, 167, 173
diabetic retinopathy,8, 24, 83, 114, 171, 207 and
glaucoma.60, 127, 225

The purpose of this article is to review the potential ocular effects of obesity.

The relationship between obesity and cataract has been investigated in many epidemiological studies,10, 21, 22,53, 63, 74, 86, 94, 107, 108, 121, 126, 129, 144, 168, 197, 211, 222

The strongest evidence are based on prospective data from several large population-based studies demonstrating positive association between obesity and cataract.63, 73, 86,107, 168, 211

In 1995 63 and 2000, 168 the Physicians’ Health Study, a randomized trial of 22071 healthy male American physicians aged 40–84 years, reported both

overall obesity, measured as BMI, and

abdominal adiposity, measured as waist-to-hip ratio (WHR),

as independent risk factors for cataract.

It was found that at any given level of BMI, a 2-unit higher level predicted a 12% increase risk of cataract. 63

The Nurses’ Health Study, a large prospective study of female nurses in 1993, also found a higher rate of cataract surgery for women with BMI levels of 23 or greater compared to women with lower levels. 73

Subsequently, the Nurses’ Health and the Health Professionals Follow-up Study generated further results, reporting that obesity increases risk of cataract overall, but in particular, of posterior subcapsular (PSC) type, even after adjusting for variables such as smoking, age and diabetes. 211

Prospective data from the Framingham Eye Study also demonstrates an independent association between greater BMI and higher incident of cortical and PSC opacities. 86

Further support on the positive association between obesity and cataract is derived from cross-sectional data from other population-based,1, 21, 94, 121, 129, 222 and

hospital-based studies,126,197

, 10-year prospective data from this study showed an association between higher BMI and increased risk of PSC cataract in persons without diabetes. 107

There have also been inconsistencies regarding the types of cataract associated with obesity in these studies.

Cortical and PSC cataracts have been most consistently associated with obesity.1, 21, 121, 129, 222

Among these studies, the Barbados Eye Study in African Americans found higher WHR to be associated with cortical opacities. 129

The Blue Mountain Eye Study in white Australians suggested that obese persons (BMI of 30 kg/m 1 or greater) have about half- and twofold increase risk of having cortical and PSC cataracts respectively. 222

In the Age-Related Eye Disease Study (AREDS), both higher BMI and weight gain were found to have significant association with moderate cortical cataract, independent of age and gender. 1

Several plausible pathophysiological mechanisms have been proposed to explain the association of obesity and cataract.

One theory suggests that leptin, a 16-kDa pleiotropic cytokine expressed and secreted mainly by adipocytes, 227 is involved in the molecular mechanisms underlying cataract formation. 64

Studies have discovered that individuals with obesity likely exhibit hyperleptinemia and leptin resistance.59, 78, 79, 149

Leptin has also been found to increase accumulation of reactive oxygen species in various cellular models.14, 219

This link between obesity, hyperleptinemia and increased oxidative stress has been further reinforced by a subsequent study revealing a strong positive association between BMI and systemic oxidative stress as determined from creatinine-indexed urinary concentrations of 8-epi-prostaglandin F2α. 103

In addition, recent studies have proposed that oxidative stress may play an important pathogenic role in cataract formation.11, 58, 90,161, 187, 188, 189, 190

In view of these links, hyperleptinemia associated with obesity may promote cataract formation.

Apart from leptin, elevated levels of C-reactive protein and plasma fibrinogen were also found in obese individuals,32,52, 71, 209 and recently these markers of inflammation, such as fibrinogen, have been suggested to have association with cataract.65, 169

Furthermore, obesity has also been linked to cataract by its associated complications such as

diabetes,1,52, 115, 127, 130, 183

glucose intolerance,
insulin resistance, 69
hyperlipidemia and

They are all known risk factors for cataract,74, 96, 101, 129, 197, 211, 222

While the majority of data suggest that higher BMI is associated with cataract, there has been a body of literature that lower BMI may also be a risk factor for some forms of cataract,21, 22, 126 particularly in non-white populations.53,121, 144

Among Chinese people in the Shihpai Eye Study in Taiwan, for example, whereas higher BMI was associated with cortical opacity,121

In the Tanjong Pagar Survey in Chinese Singaporeans, lower BMI was an independent risk factor for cataract, particularly for cortical cataract. 53

lower BMI reflects poor nutritional status and malnutrition in developing countries is a potential risk factor for cataract. 198

Although several studies have proposed that weight loss and reduction of abdominal obesity would likely lessen incidence and costs of cataract,96, 168 the efficacy of obesity treatment in reducing risk of cataract has never been evaluated in clinical trials.

In summary, based on the current data, obesity is likely associated with cataract.

There are varying patterns and strengths of association for different cataract types, suggesting possible existence of distinct etiological pathways for the different types of cataracts. 212

The reason for the disparity of findings may also partly be due to racial/ethnic differences in population groups and use of different grading systems for cataract and lens opacities.


there have been several studies that have provided evidence in support of a positive association between obesity and intraocular pressure (IOP) (Table 2),

the strongest risk factor for glaucomatous optic neuropathy (GON).9, 66, 99, 127, 140,185

Table 2
Studies Investigating Relationship between Obesity and Glaucoma or Intraocular Pressure

Most epidemiological studies have been focusing on the association between obesity and IOP or ocular hypertension.

Population-based data from several studies have demonstrated independent cross-sectional association between obesity and ocular hypertension.17, 95, 109, 125, 148,175, 177, 218, 221

The Beaver Dam Eye Study reported a significantly positive association of IOP with several factors including BMI. 109

This was consistent with findings from a subsequent hospital-based study, indicating that ocular hypertension risk was significantly greater in persons with BMI of 30 or greater, independent of age and sex. 95

Studies of the Asian populations generated similar results.125, 146,175, 221

In a large population-based study of 25,216 Japanese aged 14–94 years, a positive association between obesity and ocular hypertension was evident in both longitudinal and cross-sectional analysis, even after controlling for age, gender and blood pressure. 146

This was further reinforced by another large population-based study of Koreans. 125

Some studies further suggest that the association between obesity and ocular hypertension may reflect underlying association between insulin resistance and ocular hypertension, as the association between obesity measures and IOP was not significant after adjustments for glucose and other confounders. 152

a hospital-based study, relying on review of medical records, reported that patients with higher BMI were more likely to have a clinical diagnosis of glaucoma on admission. 225

A clear pathophysiological explanation for the association of obesity with IOP and glaucoma Both the ‘mechanical’ and ‘vascular’ etiology theories of glaucoma may be related to obesity.

With regards to the mechanical theory, 72 obesity has been postulated to exert an effect on IOP by causing excessive intraorbital adipose tissue, increased blood viscosity, increased episcleral venous pressure, and impairment of aqueous outflow facility.17, 166,176, 177

Furthermore, ocular hypertension has been associated with obesity-related systemic diseases such as

hypertension,13, 37, 106, 128, 138, 200, 218

diabetes, 152

dyslipidemia, 95 and

insulin resistance.147, 152, 218

Increased blood pressure may lead to an increased filtration fraction of the aqueous humor through elevated ciliary artery pressure,17, 82, 177 while hyperglycemia may induce osmotic fluid shift into the intraocular space. 141

Both mechanisms can ultimately result in elevated IOP.

On the other hand, the vascular theory suggests that eyes with inherently poor vascular supply to the optic nerve head are more predisposed to damage by elevated or normal IOP.38, 134

Impaired vascular supply may be related to abnormal ocular blood flow and perfusion instability secondary to alternations in autonomic and endothelial function.16, 49, 68, 70, 75, 100

Obesity has been shown to cause both vascular endothelial dysfunction62, 223 and autonomic dysfunction, particularly in people with diabetes.132, 135

In addition, cellular factors, including neurotropin deprivation, release of excitatory amino acids, and oxidative stress, have also been suggested to contribute to GON on the molecular level.18, 46, 61, 93,145, 153, 154, 159, 165, 229

Among these, oxidative stress has recently gained intense interest.18, 46, 61, 93, 145, 153, 165, 229

Increased oxidative DNA damage was found in the trabecular meshwork of glaucoma patients, 93 and oxidative stress has been postulated to cause proteasome failure and induce human trabecular meshwork degeneration, leading to impairment of the ability of the tissue to modulate outflow resistance. 18

As discussed previously, hyperleptinemia, which is closely related to obesity, is associated with increased oxidative stress.14, 31, 59, 78, 79, 103, 149, 219

Therefore, theoretically, obesity-associated hyperleptinemia may cause an increase in systemic oxidative stress, priming the glaucoma pathogenetic cascade.165, 229
weight reduction, with adjuvant medical therapy, in obese patients with raised IOP may help preventing the development and progression of GON.

In summary, there is considerable evidence from clinical studies to support an association between obesity with higher IOP.


Age-related maculopathy (ARM) remains a major blinding condition in elderly people, despite the introduction of several new treatment modalities, including photodynamic therapy,27, 76, 136, 217 novel pharmacological approaches to inhibit angiogenesis34, 47, 67, 170 and the use of antioxidant supplement.27, 88

The relationship between obesity and ARM has been investigated in several studies (Table 3). Hirvela and colleagues 87 were the first to observe a positive association between obesity and ARM. This association was subsequently supported by epidemiological data from several large population-based studies.36, 108, 167, 184Prospective data from the Physicians’ Health Study demonstrated that the 15-year incidence for visually significant dry ARM was highest in obese men and lowest in men with normal BMI, even after controlling for age and cigarette smoking. 167 However, the study could not find any significant association between obesity and neovascular ARM, which was possibly due to small number of cases in the studied population. The AREDS has reported cross-sectional association between higher BMI and more advanced ARM, as documented from fundus photographs. 2A more recent report in 2005 among patients with baseline early or intermediate ARM showed that greater BMI was significantly associated with incident geographic atrophy and progression to advanced ARM with visual impairment, even after controlling for multiple factors including age, gender and treatment. 28 These findings are supported by cross-sectional data from the Blue Mountains Eye Study, although the Beaver Dam Eye Study only found this association in women, but not in men. 108 The Pathologies Oculaires Liées à l’Age (POLA) Study of large number of Europeans found that individuals with obesity have a two-fold increase in risk for developing late but not early ARM, 36 although adjustment for other variables such as smoking were not performed.

Table 3
Studies Investigating Relationship between Obesity and Age-Related Maculopathy
The pathophysiological mechanisms accountable for the probable association between obesity and ARM are unclear. ARM is a multifactorial disease with some common downstream pathophysiologic pathways leading to the spectrum of retinal signs seen clinically.89, 120, 164, 226Obesity has been hypothesized to be linked to some of these pathways. As discussed previously, obesity may increase systemic oxidative stress secondary to hyperleptinemia.14,31, 59, 78, 79, 103, 149, 219 There is compelling evidence that oxidative stress plays an important role in the pathogenesis of ARM.120, 164, 186, 226 Oxidative damage to lipids in Bruch membrane appears to be important in the etiology of choroidal neovascular ARM. 186 In response to excessive oxidative stress, the RPE cells may detach and migrate into the subretinal space or outer retina and secrete excessive vascular endothelial growth factor (VEGF), eliciting invasion of neovascularization in Bruch membrane. 186Given this, obesity may have a role in the development of ARM because of its associated hyperliptinemia-induced oxidative stress. Nevertheless, a study examining the association of plasma leptin with ARM found paradoxical results; plasma leptin was negatively correlated with severity of ARM, after controlling for age, sex and BMI. It was suggested by the authors that reduced leptin levels could result in loss of its lipidostatic function in cellular level, leading to an increased intracellular fatty acid accumulation within the lesions found in ARM patients. 44 Studies has also shown that plasma fibrinogen and other markers of inflammation (e.g., C-reactive protein) may be associated with late ARM, 184 suggesting that inflammation may play a role in ARM development. Plasma fibrinogen and C-reactive protein, for example, are elevated in both adults and children with obesity,6, 206 and may therefore be a potential link between obesity and ARM. Finally, other proposed risk factors for ARM, including hypertension2, 36, 91, 92, 116 and hyperlipidemia,112, 210 are also well-known conditions associated with obesity, raising the possibility that obesity may cause ARM by secondary effects from its associated complications.

Apart from an association between BMI and ARM, central obesity, as defined by the waist circumference or WHR, has also been found to increase risk of progression to advanced ARM in one study, 173 although not in another. 143 As with the association of BMI and cataract, there are also some conflicting data, based on a smaller number of studies, indicating that lean body mass may increase risk of ARM.115, 167, 183

In summary, there is considerable evidence that supports an association between obesity and ARM. The nature of this association with the different types of ARM and the role of weight loss in preventing the development or slowing the progression of ARM, however, remains to be determined.


The association between obesity and diabetic retinopathy has been investigated in several studies. Most,8, 35, 113, 203, 207,213, 228 but not all,23, 41, 114, 124, 150 studies have documented a relationship between higher BMI and increased risk of retinopathy (Table 4). Few of these studies, however, have prospective data.8, 24, 83, 114 A study in Sweden examined 582 young (aged 15–34) individuals with diabetes (79% type 1 diabetes) with 10 years follow-up, and found that individuals with higher BMI developed retinopathy at earlier stage. 83 The EURODIAB Prospective Complications Study of 764 individuals with type 1 diabetes after more than 7 years of follow-up reported WHR as an independent risk factor for diabetic retinopathy. 24 However, conflicting data were generated in the Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR).113,114 Although obesity (BMI >31.0 kg/m 1 for men and 32.1 kg/m 1 for women) was found to associate with progression and severity of retinopathy, these associations were not statistically significant and were limited to only individuals with older-onset insulin-independent diabetes. 113 On the other hand, for those who were underweight (BMI <20 kg/m 1), a 3-fold increase in risk of developing retinopathy was demonstrated. 114 Underweight has been suggested to be a marker of the more “severe” phase of diabetes, or an indicator of late-onset type 1 diabetes. 113

Table 4
Studies Investigating Relationship between Obesity and Diabetic Retinopathy
There are new data that show obesity is associated with retinopathy signs in the general population and non-diabetic persons. In the Hoorn Study in the Netherlands, WHR was also independently associated with a number of incident retinopathy signs, including retinal hemorrhages, microaneurysms, hard exudates and cotton-wool spots in the non-diabetic general population, although the association with BMI failed to achieve statistical significance. 208

The underlying pathophysiological mechanisms of the possible association between obesity and retinopathy are not understood. 40 Epidemiological data from various studies have identified hyperlipidemia25, 26, 29, 33, 48, 111, 117, 147,150, 193 and hypertension110, 119, 192, 196 as risk factors for diabetic retinopathy. Both conditions are common risk factors of obesity. In fact, metabolic syndrome, encompassing these conditions, has also been shown to be associated with retinopathy. 213

However, there is also evidence that obesity may have a more direct role in the development of retinopathy. Several pathogenetic theories of diabetic retinopathy exist based on the potential roles of aldose reductase activity, vasoproliferative factors, oxidative stress, platelet function and blood viscosity. Of these, vasoproliferative factors, such as the vascular endothelial growth factor (VEGF), have recently gained intense interest. The concentration of VEGF has been found to be higher in the vitreous of eyes with proliferative diabetic retinopathy. 5 Serum angiogenic factors, including VEGF, have been observed to be elevated in obese human.142, 179 These findings provide a potential link between obesity and proliferative diabetic retinopathy. Moreover, oxidative stress has also been suggested to contribute in the pathogenesis of diabetic retinopathy,19, 156possibly by inducing over-expression of VEGF and cause features of diabetic retinopathy including retinal neovascularization and macular edema.19, 178 Finally, as discussed in previous sections, obesity may increase oxidative stress because of its associated hyperleptinemia.14,31, 59, 78, 79, 103, 149, 219 High levels of plasma leptin have been found to relate to both hypertensive4, 172, 194, 203 and diabetic retinopathy.57, 203 Detailed pathophysiological pathways leading to hypertensive retinopathy has been described elsewhere, 215 but leptin has been postulated to worsen hypertension by activation of the sympathetic nervous system, accelerating the development of hypertensive retinopathy. 80 Positive association between severity of hypertensive retinopathy and plasma leptin, independent of BMI, has been reported. 204 Apart from leptin, other adipocytokines have also been investigated, but the evidence to support their roles in the pathogenesis of retinopathy is currently weak.42, 45, 56, 137, 220

The impact of weight loss, particularly in obese individuals, on regression of retinopathy has been inadequately investigated.174, 195 Lifestyle changes, such as weight loss, has been advocated as a key factor in helping prevent diabetes and to delay diabetic complications including retinopathy in susceptible patients. 174 However, patients with type 1 diabetes and anorexia nervosa with weight loss have also been observed to have higher risk of developing early retinopathy. 195 In spite of the insufficient data, it is generally accepted that weight reduction should be advised in obese diabetic individuals to reduce the risk of cardiovascular disease118, 180, 181, 182, 191, 201, 202, 216 and possibly diabetic retinopathy. 224


Obesity has been recognized as a significant risk factor for retinal vein occlusion in a very limited number of studies.7,214 In the ARIC and Cardiovascular Health Studies (CHS), obese persons were found to have a nearly four-fold increased risk of having retinal vein occlusion, and there was a significant trend of increasing risk across all quartiles of BMI. 214 Moreover, retinal venous and arterial occlusions are known to be associated with hypertension, diabetes mellitus and hypercoagulability or hyperviscosity syndromes.122, 157, 162, 214 In addition to the known associations of obesity with hypertension and diabetes, several reviews have presented some evidence supporting the association of hypercoagulability disorders with obesity and metabolic syndrome.3, 151 This provides further support for the possible association between obesity and retinal vascular occlusive diseases.

Other ophthalmic conditions may also be associated with obesity. For example, it has been suggested that obesity may be related to oculomotor nerve palsy. 199 Obesity has also been associated with recurrent lower eyelid entropion. 160Obstructive sleep apnea syndrome, a common co-morbid condition related to obesity, has been associated with papilledema 158 and floppy eyelid syndrome. 139 Moreover, obesity is also a risk factor for benign intracranial hypertension (pseudotumor cerebri).15, 102, 163 It has been postulated that central obesity may increase intracranial pressure by increasing intra-abdominal, and subsequently pleural, pressure, with a resultant increase of cardiac filling pressure, impeding venous return from the brain. 15 This suggestion, however, is not agreed by all investigators. 131And finally, Prader-Willi syndrome, an obesity-associated condition, was found to be related with a number of ocular abnormalities including myopia, astigmatism, amblyopia, strabismus and exotropia. 84

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Future Research
This review suggests that further research is required to fully understand the relationship between obesity and eye diseases. Several lines of investigation are suggested. First, given the growing epidemic of childhood obesity, the lack of data on the ocular effects of obesity early in life needs to be addressed. Secondly, as this review shows, prospective studies are lacking for many of the associations identified from the cross-sectional data. For example, the associations between obesity and IOP, while consistent, are largely based on cross-sectional data, and there are no studies that show obesity is associated with an demonstrable increase in IOP over time. Third, because obesity is closely related to dietary habits, there is a need to study the effect of dietary risk factors on the association of obesity and eye diseases. Fourth, because the criteria for obesity and the dietary habits varies widely between racial/ethnic groups, further studies are needed to address the potential ocular effects of obesity in different racial/ethnic populations. The association between obesity and ARM is an example where studies have only been conducted in white populations. Fifth, the pathophysiological mechanisms underlying the reported associations identified in the epidemiological studies are unknown, and remain as speculations. Thus, additional experimental, cellular or molecular studies may broaden our understanding of the impact of obesity on eye health. Six, most studies have only provided information about how obesity, defined as BMI, weight or WHR, relates to the different eye diseases, and the impact of weight change (weight gain or loss) on eye diseases is less clear. Weight change is more clinically relevant and useful in terms of guiding management. Future epidemiological studies should therefore concentrate on the association of weight change and risk of eye diseases. Finally, in contrast to systemic diseases, there are no clinical trials to demonstrate the potential ocular benefits of weight loss. If weight loss is proven to be an effective method, either as a sole or adjuvant treatment, in delaying the onset or slowing the progression of eye diseases in obese individuals, both clinicians and patients will likely gain additional incentive to battle against this major public health problem.

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Obesity is a major public health problem and its impact on ocular health is increasing recognized. Associations of obesity with cataract, glaucoma, age-related maculopathy and retinopathy have been reported with varying degree of certainty. The inconsistency of results, combined with the deficiency of robust data, suggest that further investigations are required to clarify these associations. The efficacy of obesity treatment in reducing the risk of eye diseases is also unknown, but studies in this area may provide important insight for the potential use of weight loss strategies to reduce the burden of eye diseases in individuals with obesity.

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Method of Literature Search
A systematic MEDLINE search on National Institute of Health’s PubMed (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?DB=pubmed) with coverage up to 18 August 2005 was conducted initially using the following keywords: “obesity, body mass index, waist-to-hip ratio, weight, risk factor” in various combinations with “eye (368 citations), eye disease (725), ocular (225), cataract (66), lens opacity (48), glaucoma (37), intraocular pressure (32), maculopathy (13), diabetic retinopathy (24), hypertensive retinopathy (34), retinal arterial occlusion (8), retinal venous occlusion (10)”. After review of abstracts, relevant articles were retrieved and reviewed. All English articles were read, and for the relevant non-English articles, the English abstracts were reviewed. Bibliographies of these articles provided further references, including books and internet-based data.

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This article was partially funded by NIH grant R21-HL077166, the Science, Technology Innovation (STI) Grant and the Sylvia and Charles Viertel Clinical Investigator Award, Australia (TYW). The authors reported no proprietary or commercial interest in any product mentioned or cnocept discussed in this review.

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1. Risk factors associated with age-related nuclear and cortical cataract : a case-control study in the Age-Related Eye Disease Study, AREDS Report No. 5. Ophthalmology. 2001;108:1400–8. [PMC free article] [PubMed]
2. Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3. Ophthalmology. 2000;107:2224–32.[PMC free article] [PubMed]
3. Abramson N, Abramson S. Hypercoagulability: clinical assessment and treatment. South Med J. 2001;94:1013–20.[PubMed]
4. Agata J, Masuda A, Takada M, et al. High plasma immunoreactive leptin level in essential hypertension. Am J Hypertens. 1997;10:1171–4. [PubMed]
5. Aiello LP, Avery RL, Arrigg PG, et al. Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders. N Engl J Med. 1994;331:1480–7. [PubMed]
6. Alam AA, Mitwalli AH, Al-Wakeel JS, et al. Plasma fibrinogen and its correlates in adult Saudi population. Saudi Med J. 2004;25:1593–602. [PubMed]
7. Backhouse O, Parapia L, Mahomed I, et al. Familial thrombophilia and retinal vein occlusion. Eye. 2000;14 ( Pt 1):13–7. [PubMed]
8. Ballard DJ, Melton LJ, Dwyer MS, et al. Risk factors for diabetic retinopathy: a population-based study in Rochester, Minnesota. Diabetes Care. 1986;9:334–42. [PubMed]
9. Bengtsson B, Heijl A. A long-term prospective study of risk factors for glaucomatous visual field loss in patients with ocular hypertension. J Glaucoma. 2005;14:135–8.[PubMed]
10. Bergman B, Nilsson-Ehle H, Sjöstrand J. Ocular changes, risk markers for eye disorders and effects of cataract surgery in elderly people: a study of an urban Swedish population followed from 70 to 97 years of age. Acta Ophthalmol Scand. 2004;82:166–74. [PubMed]
11. Bhuyan KC, Bhuyan DK, Podos SM. Lipid peroxidation in cataract of the human. Life Sci. 1986;38:1463–71.[PubMed]
12. Bianchini F, Kaaks R, Vainio H. Weight control and physical activity in cancer prevention. Obes Rev. 2002;3:5–8. [PubMed]
13. Bonomi L, Marchini G, Marraffa M, et al. Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study. Ophthalmology. 2000;107:1287–93.[PubMed]
14. Bouloumie A, Marumo T, Lafontan M, et al. Leptin induces oxidative stress in human endothelial cells. FASEB J. 1999;13:1231–8. [PubMed]
15. Brazis PW, Lee AG. Elevated intracranial pressure and pseudotumor cerebri. Curr Opin Ophthalmol. 1998;9:27–32.[PubMed]
16. Broadway DC, Drance SM. Glaucoma and vasospasm. Br J Ophthalmol. 1998;82:862–70. [PMC free article][PubMed]
17. Bulpitt CJ, Hodes C, Everitt MG. Intraocular pressure and systemic blood pressure in the elderly. Br J Ophthalmol. 1975;59:717–20. [PMC free article] [PubMed]
18. Caballero M, Liton PB, Epstein DL, et al. Proteasome inhibition by chronic oxidative stress in human trabecular meshwork cells. Biochem Biophys Res Commun. 2003;308:346–52. [PubMed]
19. Caldwell RB, Bartoli M, Behzadian MA, et al. Vascular endothelial growth factor and diabetic retinopathy: role of oxidative stress. Curr Drug Targets. 2005;6:511–24.[PubMed]
20. Calle EE, Rodriguez C, Walker-Thurmond K, et al. Overweight, obesity, and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003;348:1625–38. [PubMed]
21. Caulfield LE, West SK, Barrón Y, et al. Anthropometric status and cataract: the Salisbury Eye Evaluation project. Am J Clin Nutr. 1999;69:237–42. [PubMed]
22. Chatterjee A, Milton RC, Thyle S. Prevalence and aetiology of cataract in Punjab. Br J Ophthalmol. 1982;66:35–42. [PMC free article] [PubMed]
23. Chaturvedi N, Fuller JH. Mortality risk by body weight and weight change in people with NIDDM. The WHO Multinational Study of Vascular Disease in Diabetes. Diabetes Care. 1995;18:766–74. [PubMed]
24. Chaturvedi N, Sjoelie AK, Porta M, et al. Markers of insulin resistance are strong risk factors for retinopathy incidence in type 1 diabetes. Diabetes Care. 2001;24:284–9.[PubMed]
25. Chew EY. Diabetic retinopathy and lipid abnormalities. Curr Opin Ophthalmol. 1997;8:59–62. [PubMed]
26. Chew EY, Klein ML, Ferris FL, et al. Association of elevated serum lipid levels with retinal hard exudate in diabetic retinopathy. Early Treatment Diabetic Retinopathy Study (ETDRS) Report 22. Arch Ophthalmol. 1996;114:1079–84. [PubMed]
27. Chopdar A, Chakravarthy U, Verma D. Age related macular degeneration. BMJ. 2003;326:485–8.[PMC free article] [PubMed]
28. Clemons TE, Milton RC, Klein R, et al. Risk factors for the incidence of Advanced Age-Related Macular Degeneration in the Age-Related Eye Disease Study (AREDS) AREDS report no. 19. Ophthalmology. 2005;112:533–9. [PMC free article] [PubMed]
29. Cohen RA, Hennekens CH, Christen WG, et al. Determinants of retinopathy progression in type 1 diabetes mellitus. Am J Med. 1999;107:45–51. [PubMed]
30. Cole TJ, Bellizzi MC, Flegal KM, et al. Establishing a standard definition for child overweight and obesity worldwide: international survey. BMJ. 2000;320:1240–3.[PMC free article] [PubMed]
31. Considine RV, Sinha MK, Heiman ML, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334:292–5. [PubMed]
32. Cushman M, Yanez D, Psaty BM, et al. Association of fibrinogen and coagulation factors VII and VIII with cardiovascular risk factors in the elderly: the Cardiovascular Health Study. Cardiovascular Health Study Investigators. Am J Epidemiol. 1996;143:665–76. [PubMed]
33. Cusick M, Chew EY, Chan CC, et al. Histopathology and regression of retinal hard exudates in diabetic retinopathy after reduction of elevated serum lipid levels. Ophthalmology. 2003;110:2126–33. [PubMed]
34. D’Amico DJ, Goldberg MF, Hudson H, et al. Anecortave acetate as monotherapy for treatment of subfoveal neovascularization in age-related macular degeneration: twelve-month clinical outcomes. Ophthalmology. 2003;110:2372–83. discussin 2384–5. [PubMed]
35. De Block CE, De Leeuw IH, Van Gaal LF. Impact of overweight on chronic microvascular complications in type 1 diabetic patients. Diabetes Care. 2005;28:1649–55.[PubMed]
36. Delcourt C, Michel F, Colvez A, et al. Associations of cardiovascular disease and its risk factors with age-related macular degeneration: the POLA study. Ophthalmic Epidemiol. 2001;8:237–49. [PubMed]
37. Dielemans I, Vingerling JR, Algra D, et al. Primary open-angle glaucoma, intraocular pressure, and systemic blood pressure in the general elderly population. The Rotterdam Study. Ophthalmology. 1995;102:54–60.[PubMed]
38. Dielemans I, Vingerling JR, Wolfs RC, et al. The prevalence of primary open-angle glaucoma in a population-based study in The Netherlands. The Rotterdam Study. Ophthalmology. 1994;101:1851–5. [PubMed]
39. Dietz WH. Overweight in childhood and adolescence. N Engl J Med. 2004;350:855–7. [PubMed]
40. Dorchy H, Claes C, Verougstraete C. Risk factors of developing proliferative retinopathy in type 1 diabetic patients : role of BMI. Diabetes Care. 2002;25:798–9.[PubMed]
41. Dowse GK, Humphrey AR, Collins VR, et al. Prevalence and risk factors for diabetic retinopathy in the multiethnic population of Mauritius. Am J Epidemiol. 1998;147:448–57. [PubMed]
42. Duntas LH, Popovic V, Panotopoulos G. Adiponectin: novelties in metabolism and hormonal regulation. Nutr Neurosci. 2004;7:195–200. [PubMed]
43. Eckel RH, Krauss RM. American Heart Association call to action: obesity as a major risk factor for coronary heart disease. AHA Nutrition Committee. Circulation. 1998;97:2099–100. [PubMed]
44. Evereklioglu C, Doganay S, Er H, et al. Serum leptin concentrations are decreased and correlated with disease severity in age-related macular degeneration: a preliminary study. Eye. 2003;17:350–5. [PubMed]
45. Fasshauer M, Paschke R, Stumvoll M. Adiponectin, obesity, and cardiovascular disease. Biochimie. 2004;86:779–84. [PubMed]
46. Ferreira SM, Lerner SF, Brunzini R, et al. Oxidative stress markers in aqueous humor of glaucoma patients. Am J Ophthalmol. 2004;137:62–9. [PubMed]
47. Ferris FL. A new treatment for ocular neovascularization. N Engl J Med. 2004;351:2863–5.[PubMed]
48. Ferris FL, Chew EY, Hoogwerf BJ. Serum lipids and diabetic retinopathy. Early Treatment Diabetic Retinopathy Study Research Group. Diabetes Care. 1996;19:1291–3.[PubMed]
49. Flammer F, Orgul S, Costa VP, et al. The impact of ocular blood flow in glaucoma. Prog Retinal Eye Res. 2002;21:359–93. [PubMed]
50. Flegal KM, Carroll MD, Kuczmarski RJ, et al. Overweight and obesity in the United States: prevalence and trends, 1960–1994. Int J Obes Relat Metab Disord. 1998;22:39–47. [PubMed]
51. Flegal KM, Carroll MD, Ogden CL, et al. Prevalence and trends in obesity among US adults, 1999–2000. JAMA. 2002;288:1723–7. [PubMed]
52. Ford ES. Body mass index, diabetes, and C-reactive protein among U.S. adults. Diabetes Care. 1999;22:1971–7.[PubMed]
53. Foster PJ, Wong TY, Machin D, et al. Risk factors for nuclear, cortical and posterior subcapsular cataracts in the Chinese population of Singapore: the Tanjong Pagar Survey. Br J Ophthalmol. 2003;87:1112–20. [PMC free article][PubMed]
54. Friedman N, Fanning EL. Overweight and obesity: an overview of prevalence, clinical impact, and economic impact. Dis Manag. 2004;7 Suppl 1:S1–6. [PubMed]
55. Friedrich MJ. Epidemic of obesity expands its spread to developing countries. JAMA. 2002;287:1382–6. [PubMed]
56. Frystyk J, Tarnow L, Hansen TK, et al. Increased serum adiponectin levels in type 1 diabetic patients with microvascular complications. Diabetologia. 2005;48:1911–8.[PubMed]
57. Gariano RF, Nath AK, D’Amico DJ, et al. Elevation of vitreous leptin in diabetic retinopathy and retinal detachment. Invest Ophthalmol Vis Sci. 2000;41:3576–81.[PubMed]
58. Garner MH, Spector A. Selective oxidation of cysteine and methionine in normal and senile cataractous lenses. Proc Natl Acad Sci U S A. 1980;77:1274–7. [PMC free article][PubMed]
59. Garofalo C, Surmacz E. Leptin and cancer. J Cell Physiol. 2006;207:12–22. [PubMed]
60. Gasser P, Stümpfig D, Schötzau A, et al. Body mass index in glaucoma. J Glaucoma. 1999;8:8–11. [PubMed]
61. Gherghel D, Griffiths HR, Hilton EJ, et al. Systemic reduction in glutathione levels occurs in patients with primary open-angle glaucoma. Invest Ophthalmol Vis Sci. 2005;46:877–83. [PubMed]
62. Głowińska B, Urban M, Hryniewicz A, et al. Endothelin-1 plasma concentration in children and adolescents with atherogenic risk factors. Kardiol Pol. 2004;61:329–38.[PubMed]
63. Glynn RJ, Christen WG, Manson JE, et al. Body mass index. An independent predictor of cataract. Arch Ophthalmol. 1995;113:1131–7. [PubMed]
64. Gómez-Ambrosi J, Salvador J, Frühbeck G. Is hyperleptinemia involved in the development of age-related lens opacities? Am J Clin Nutr. 2004;79:888–9. author reply 889. [PubMed]
65. Goodrich ME, Cumming RG, Mitchell P, et al. Plasma fibrinogen and other cardiovascular disease risk factors and cataract. Ophthalmic Epidemiol. 1999;6:279–90. [PubMed]
66. Gordon MO, Beiser JA, Brandt JD, et al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002;120:714–20. discussion 829–30.[PubMed]
67. Gragoudas ES, Adamis AP, Cunningham ET, et al. Pegaptanib for neovascular age-related macular degeneration. N Engl J Med. 2004;351:2805–16. [PubMed]
68. Grieshaber MC, Flammer J. Blood flow in glaucoma. Curr Opin Ophthalmol. 2005;16:79–83. [PubMed]
69. Grundy SM. Metabolic complications of obesity. Endocrine. 2000;13:155–65. [PubMed]
70. Grunwald JE, Piltz J, Hariprasad SM, et al. Optic nerve and choroidal circulation in glaucoma. Invest Ophthalmol Vis Sci. 1998;39:2329–36. [PubMed]
71. Hak AE, Stehouwer CD, Bots ML, et al. Associations of C-reactive protein with measures of obesity, insulin resistance, and subclinical atherosclerosis in healthy, middle-aged women. Arterioscler Thromb Vasc Biol. 1999;19:1986–91. [PubMed]
72. Halpern DL, Grosskreutz CL. Glaucomatous optic neuropathy: mechanisms of disease. Ophthalmol Clin North Am. 2002;15:61–8. [PubMed]
73. Hankinson SE, Seddon JM, Colditz GA, et al. A prospective study of aspirin use and cataract extraction in women. Arch Ophthalmol. 1993;111:503–8. [PubMed]
74. Harding JJ. Recent studies of risk factors and protective factors for cataract. Curr Opin Ophthalmol. 1997;8:46–9.[PubMed]
75. Harris A, Zarfati D, Zalish M, et al. Reduced cerebrovascular blood flow velocities and vasoreactivity in open-angle glaucoma. Am J Ophthalmol. 2003;135:144–7.[PubMed]
76. Hart PM, Chakravarthy U, Mackenzie G, et al. Visual outcomes in the subfoveal radiotherapy study: a randomized controlled trial of teletherapy for age-related macular degeneration. Arch Ophthalmol. 2002;120:1029–38.[PubMed] 77. Haslam DW, James WP. Obesity. Lancet. 2005;366:1197–209. [PubMed]
78. Hassink SG, Sheslow DV, de Lancey E, et al. Serum leptin in children with obesity: relationship to gender and development. Pediatrics. 1996;98:201–3. [PubMed]
79. Haynes WG. Role of leptin in obesity-related hypertension. Exp Physiol. 2005;90:683–8. [PubMed]
80. Haynes WG, Sivitz WI, Morgan DA, et al. Sympathetic and cardiorenal actions of leptin. Hypertension. 1997;30:619–23. [PubMed]
81. Hedley AA, Ogden CL, Johnson CL, et al. Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002. JAMA. 2004;291:2847–50. [PubMed]
82. Hennis A, Wu SY, Nemesure B, et al. Hypertension, diabetes, and longitudinal changes in intraocular pressure. Ophthalmology. 2003;110:908–14. [PubMed]
83. Henricsson M, Nyström L, Blohmé G, et al. The incidence of retinopathy 10 years after diagnosis in young adult people with diabetes: results from the nationwide population-based Diabetes Incidence Study in Sweden (DISS) Diabetes Care. 2003;26:349–54. [PubMed]
84. Hered RW, Rogers S, Zang YF, et al. Ophthalmologic features of Prader-Willi syndrome. J Pediatr Ophthalmol Strabismus. 1988;25:145–50. [PubMed]
85. Hill JO, Catenacci V, Wyatt HR. Obesity: overview of an epidemic. Psychiatr Clin North Am. 2005;28:1–23. vii.[PubMed]
86. Hiller R, Podgor MJ, Sperduto RD, et al. A longitudinal study of body mass index and lens opacities. The Framingham Studies. Ophthalmology. 1998;105:1244–50.[PubMed]
87. Hirvelä H, Luukinen H, Läärä E, et al. Risk factors of age-related maculopathy in a population 70 years of age or older. Ophthalmology. 1996;103:871–7. [PubMed]
88. Hogg R, Chakravarthy U. AMD and micronutrient antioxidants. Curr Eye Res. 2004;29:387–401. [PubMed]
89. Holz FG, Pauleikhoff D, Klein R, et al. Pathogenesis of lesions in late age-related macular disease. Am J Ophthalmol. 2004;137:504–10. [PubMed]
90. Horwitz J. Anatomy and embryology. In: Podos SM, Yanoff M, editors. Textbook of Ophthalmology 3, Lens and Cataract. Gower Medical Publishing; New York: 1992.
91. Hyman L, Neborsky R. Risk factors for age-related macular degeneration: an update. Curr Opin Ophthalmol. 2002;13:171–5. [PubMed]
92. Hyman L, Schachat AP, He Q, et al. Hypertension, cardiovascular disease, and age-related macular degeneration. Age-Related Macular Degeneration Risk Factors Study Group. Arch Ophthalmol. 2000;118:351–8.[PubMed]
93. Izzotti A, Saccà SC, Cartiglia C, et al. Oxidative deoxyribonucleic acid damage in the eyes of glaucoma patients. Am J Med. 2003;114:638–46. [PubMed]
94. Jacques PF, Moeller SM, Hankinson SE, et al. Weight status, abdominal adiposity, diabetes, and early age-related lens opacities. Am J Clin Nutr. 2003;78:400–5. [PubMed]
95. Jaén Díaz J, Sanz Alcolea I, López De Castro F, et al. [Glaucoma and ocular hypertension in primary care] Aten Primaria. 2001;28:23–30. [PubMed]
96. Jahn CE, Janke M, Winowski H, et al. Identification of metabolic risk factors for posterior subcapsular cataract. Ophthalmic Res. 1986;18:112–6. [PubMed]
97. James PT. Obesity: the worldwide epidemic. Clin Dermatol. 2004;22:276–80. [PubMed]
98. James PT, Leach R, Kalamara E, et al. The worldwide obesity epidemic. Obes Res. 2001;9 Suppl 4:228S–233S.[PubMed]
99. Jonas JB, Grundler AE, Gonzales-Cortes J, et al. Pressure-dependent neuroretinal rim loss in normal-pressure glaucoma. Am J Ophthalmol. 1988;125:137–44. [PubMed]
100. Kaiser HJ, Flammer J, Wenk M, et al. Endothelin-1 plasma levels in normal-tension glaucoma: abnormal response to postural changes. Graefes Arch Clin Exp Ophthalmol. 1995;233:484–8. [PubMed]
101. Karasik A, Modan M, Halkin H, et al. Senile cataract and glucose intolerance: the Israel Study of glucose Intolerance Obesity and Hypertension (The Israel GOH Study) Diabetes Care. 1984;7:52–6. [PubMed]
102. Kaur H, Hyder ML, Poston WS. Childhood overweight: an expanding problem. Treat Endocrinol. 2003;2:375–88.[PubMed]
103. Keaney JF, Larson MG, Vasan RS, et al. Obesity and systemic oxidative stress: clinical correlates of oxidative stress in the Framingham Study. Arterioscler Thromb Vasc Biol. 2003;23:434–9. [PubMed]
104. Kennedy RL, Chokkalingham K, Srinivasan R. Obesity in the elderly: who should we be treating, and why, and how? Curr Opin Clin Nutr Metab Care. 2004;7:3–9.[PubMed]
105. Kitazawa Y, Horie T, Aoki S, et al. Untreated ocular hypertension. A long-term prospective study. Arch Ophthalmol. 1977;95:1180–4. [PubMed]
106. Klein BE, Klein R. Intraocular pressure and cardiovascular risk variables. Arch Ophthalmol. 1981;99:837–9. [PubMed]
107. Klein BE, Klein R, Lee KE. Diabetes, cardiovascular disease, selected cardiovascular disease risk factors, and the 5-year incidence of age-related cataract and progression of lens opacities: the Beaver Dam Eye Study. Am J Ophthalmol. 1998;126:782–90. [PubMed]
108. Klein BE, Klein R, Lee KE, et al. Measures of obesity and age-related eye diseases. Ophthalmic Epidemiol. 2001;8:251–62. [PubMed]
109. Klein BE, Klein R, Linton KL. Intraocular pressure in an American community. The Beaver Dam Eye Study. Invest Ophthalmol Vis Sci. 1992;33:2224–8. [PubMed]
110. Klein BE, Klein R, Moss SE. Incident cataract surgery: the Beaver Dam eye study. Ophthalmology. 1997;104:573–80. [PubMed]
111. Klein BE, Moss SE, Klein R, et al. The Wisconsin Epidemiologic Study of Diabetic Retinopathy. XIII. Relationship of serum cholesterol to retinopathy and hard exudate. Ophthalmology. 1991;98:1261–5. [PubMed]
112. Klein R, Klein BE, Franke T. The relationship of cardiovascular disease and its risk factors to age-related maculopathy. The Beaver Dam Eye Study. Ophthalmology. 1993;100:406–14. [PubMed]
113. Klein R, Klein BE, Moss SE. Is obesity related to microvascular and macrovascular complications in diabetes? The Wisconsin Epidemiologic Study of Diabetic Retinopathy. Arch Intern Med. 1997;157:650–6. [PubMed]
114. Klein R, Klein BE, Moss SE, et al. The Wisconsin epidemiologic study of diabetic retinopathy. III. Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. Arch Ophthalmol. 1984;102:527–32.[PubMed]
115. Klein R, Klein BE, Tomany SC, et al. The association of cardiovascular disease with the long-term incidence of age-related maculopathy: the Beaver Dam eye study. Ophthalmology. 2003;110:636–43. [PubMed]
116. Klein R, Peto T, Bird A, et al. The epidemiology of age-related macular degeneration. Am J Ophthalmol. 2004;137:486–95. [PubMed]
117. Klein R, Sharrett AR, Klein BE, et al. The association of atherosclerosis, vascular risk factors, and retinopathy in adults with diabetes : the atherosclerosis risk in communities study. Ophthalmology. 2002;109:1225–34. [PubMed]
118. Knowler WC, Barrett-Connor E, Fowler SE, et al. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med. 2002;346:393–403. [PMC free article] [PubMed]
119. Kohner EM, Aldington SJ, Stratton IM, et al. United Kingdom Prospective Diabetes Study, 30: diabetic retinopathy at diagnosis of non-insulin-dependent diabetes mellitus and associated risk factors. Arch Ophthalmol. 1998;116:297–303. [PubMed]
120. Kopitz J, Holz FG, Kaemmerer E, et al. Lipids and lipid peroxidation products in the pathogenesis of age-related macular degeneration. Biochimie. 2004;86:825–31.[PubMed]
121. Kuang TM, Tsai SY, Hsu WM, et al. Body mass index and age-related cataract: the Shihpai Eye Study. Arch Ophthalmol. 2005;123:1109–14. [PubMed]
122. Lahey JM, Kearney JJ, Tunc M. Hypercoagulable states and central retinal vein occlusion. Curr Opin Pulm Med. 2003;9:385–92. [PubMed]
123. Lawrence VJ, Kopelman PG. Medical consequences of obesity. Clin Dermatol. 2004;22:296–302. [PubMed]
124. Lee ET, Lee VS, Lu M, et al. Development of proliferative retinopathy in NIDDM. A follow-up study of American Indians in Oklahoma. Diabetes. 1992;41:359–67.[PubMed]
125. Lee JS, Lee SH, Oum BS, et al. Relationship between intraocular pressure and systemic health parameters in a Korean population. Clin Experiment Ophthalmol. 2002;30:237–41. [PubMed]
126. Leske MC, Chylack LT, Wu SY. The Lens Opacities Case-Control Study. Risk factors for cataract. Arch Ophthalmol. 1991;109:244–51. [PubMed]
127. Leske MC, Connell AM, Wu SY, et al. Risk factors for open-angle glaucoma. The Barbados Eye Study. Arch Ophthalmol. 1995;113:918–24. [PubMed]
128. Leske MC, Podgor MJ. Intraocular pressure, cardiovascular risk variables, and visual field defects. Am J Epidemiol. 1983;118:280–7. [PubMed]
129. Leske MC, Wu SY, Hennis A, et al. Diabetes, hypertension, and central obesity as cataract risk factors in a black population. The Barbados Eye Study. Ophthalmology. 1999;106:35–41. [PubMed]
130. Leske MC, Wu SY, Hyman L, et al. Biochemical factors in the lens opacities. Case-control study. The Lens Opacities Case-Control Study Group. Arch Ophthalmol. 1995;113:1113–9. [PubMed]
131. Lessell S. Pediatric pseudotumor cerebri (idiopathic intracranial hypertension) Surv Ophthalmol. 1992;37:155–66. [PubMed]
132. Lim HS, MacFadyen RJ, Lip GY. Diabetes mellitus, the renin-angiotensin-aldosterone system, and the heart. Arch Intern Med. 2004;164:1737–48. [PubMed]
133. Lobstein T, Baur L, Uauy R, et al. Obesity in children and young people: a crisis in public health. Obes Rev. 2004;5 Suppl 1:4–104. [PubMed]
134. Maier PC, Funk J, Schwarzer G, et al. Treatment of ocular hypertension and open angle glaucoma: meta-analysis of randomised controlled trials. BMJ. 2005;331:134.[PMC free article] [PubMed]
135. Mapstone R, Clark CV. Prevalence of diabetes in glaucoma. Br Med J (Clin Res Ed) 1985;291:93–5.[PMC free article] [PubMed]
136. Marcus DM, Sheils W, Johnson MH, et al. External beam irradiation of subfoveal choroidal neovascularization complicating age-related macular degeneration: one-year results of a prospective, double-masked, randomized clinical trial. Arch Ophthalmol. 2001;119:171–80. [PubMed]
137. Matsuda M, Kawasaki F, Yamada K, et al. Impact of adiposity and plasma adipocytokines on diabetic angiopathies in Japanese Type 2 diabetic subjects. Diabet Med. 2004;21:881–8. [PubMed]
138. McLeod SD, West SK, Quigley HA, et al. A longitudinal study of the relationship between intraocular and blood pressures. Invest Ophthalmol Vis Sci. 1990;31:2361–6. [PubMed]
139. McNab AA. The eye and sleep. Clin Experiment Ophthalmol. 2005;33:117–25. [PubMed]
140. Mitchell P, Smith W, Attebo K, et al. Prevalence of open-angle glaucoma in Australia. The Blue Mountains Eye Study. Ophthalmology. 1996;103:1661–9. [PubMed]
141. Mitchell P, Smith W, Chey T, et al. Open-angle glaucoma and diabetes: the Blue Mountains eye study, Australia. Ophthalmology. 1997;104:712–8. [PubMed]
142. Miyazawa-Hoshimoto S, Takahashi K, Bujo H, et al. Elevated serum vascular endothelial growth factor is associated with visceral fat accumulation in human obese subjects. Diabetologia. 2003;46:1483–8. [PubMed]
143. Moeini HA, Masoudpour H, Ghanbari H. A study of the relation between body mass index and the incidence of age related macular degeneration. Br J Ophthalmol. 2005;89:964–6. [PMC free article] [PubMed]
144. Mohan M, Sperduto RD, Angra SK, et al. India-US case-control study of age-related cataracts. India-US Case-Control Study Group. Arch Ophthalmol. 1989;107:670–6.[PubMed]
145. Moreno MC, Campanelli J, Sande P, et al. Retinal oxidative stress induced by high intraocular pressure. Free Radic Biol Med. 2004;37:803–12. [PubMed]
146. Mori K, Ando F, Nomura H, et al. Relationship between intraocular pressure and obesity in Japan. Int J Epidemiol. 2000;29:661–6. [PubMed]
147. Nakamura M, Ishimitsu T, Matsuoka H, et al. [Implications of obesity for target organ injuries and cardiovascular risk factors in hypertensive subjects] Nippon Jinzo Gakkai Shi. 1997;39:746–52. [PubMed]
148. Nakamura M, Kanamori A, Negi A. Diabetes mellitus as a risk factor for glaucomatous optic neuropathy. Ophthalmologica. 2005;219:1–10. [PubMed]
149. Narin F, Atabek ME, Karakukcu M, et al. The association of plasma homocysteine levels with serum leptin and apolipoprotein B levels in childhood obesity. Ann Saudi Med. 2005;25:209–14. [PubMed]
150. Nelson RG, Wolfe JA, Horton MB, et al. Proliferative retinopathy in NIDDM. Incidence and risk factors in Pima Indians. Diabetes. 1989;38:435–40. [PubMed]
151. Nieuwdorp M, Stroes ES, Meijers JC, et al. Hypercoagulability in the metabolic syndrome. Curr Opin Pharmacol. 2005;5:155–9. [PubMed]
152. Oh SW, Lee S, Park C, et al. Elevated intraocular pressure is associated with insulin resistance and metabolic syndrome. Diabetes Metab Res Rev. 2005;21:434–40.[PubMed]
153. Ohia SE, Opere CA, Leday AM. Pharmacological consequences of oxidative stress in ocular tissues. Mutat Res. 2005;579:22–36. [PubMed]
154. Olney JW. Inciting excitotoxic cytocide among central neurons. Adv Exp Med Biol. 1986;203:631–45. [PubMed]
155. Pi-Sunyer FX. Medical hazards of obesity. Ann Intern Med. 1993;119:655–60. [PubMed]
156. Polak M, Zagórski Z. Lipid peroxidation in diabetic retinopathy. Ann Univ Mariae Curie Sklodowska [Med] 2004;59:434–7. [PubMed]
157. Prisco D, Marcucci R. Retinal vein thrombosis: risk factors, pathogenesis and therapeutic approach. Pathophysiol Haemost Thromb. 2002;32:308–11. [PubMed]
158. Purvin VA, Kawasaki A, Yee RD. Papilledema and obstructive sleep apnea syndrome. Arch Ophthalmol. 2000;118:1626–30. [PubMed]
159. Quigley HA, Nickells RW, Kerrigan LA, et al. Retinal ganglion cell death in experimental glaucoma and after axotomy occurs by apoptosis. Invest Ophthalmol Vis Sci. 1995;36:774–86. [PubMed]
160. Raina J, Foster JA. Obesity as a cause of mechanical entropion. Am J Ophthalmol. 1996;122:123–5. [PubMed]
161. Ramachandran S, Morris SM, Devamanoharan P, et al. Radio-isotopic determination of hydrogen peroxide in aqueous humor and urine. Exp Eye Res. 1991;53:503–6.[PubMed]
162. Robinson MK, Halpern JI. Retinal vein occlusion. Am Fam Physician. 1992;45:2661–6. [PubMed]
163. Rodríguez de Rivera FJ, Martínez-Sanchez P, Ojeda-Ruiz de Luna J, et al. Benign intracranial hypertension. History, clinical features and treatment in a series of 41 patients. Rev Neurol. 3115;37:801–5. [PubMed]
164. Roth F, Bindewald A, Holz FG. Keypathophysiologic pathways in age-related macular disease. Graefes Arch Clin Exp Ophthalmol. 2004;242:710–6. [PubMed]
165. Saccà SC, Pascotto A, Camicione P, et al. Oxidative DNA damage in the human trabecular meshwork: clinical correlation in patients with primary open-angle glaucoma. Arch Ophthalmol. 2005;123:458–63. [PubMed]
166. Savinova OV, Sugiyama F, Martin JE, et al. Intraocular pressure in genetically distinct mice: an update and strain survey. BMC Genet. 2001;2:12. [PMC free article][PubMed]
167. Schaumberg DA, Christen WG, Hankinson SE, et al. Body mass index and the incidence of visually significant age-related maculopathy in men. Arch Ophthalmol. 2001;119:1259–65. [PMC free article] [PubMed]
168. Schaumberg DA, Glynn RJ, Christen WG, et al. Relations of body fat distribution and height with cataract in men. Am J Clin Nutr. 2000;72:1495–502. [PubMed]
169. Schaumberg DA, Ridker PM, Glynn RJ, et al. High levels of plasma C-reactive protein and future risk of age-related cataract. Ann Epidemiol. 1999;9:166–71. [PubMed]
170. Schmidt-Erfurth U, Mi chels S, Michels R, et al. Anecortave acetate for the treatment of subfoveal choroidal neovascularization secondary to age-related macular degeneration. Eur J Ophthalmol. 2005;15:482–5. [PubMed]
171. Schoenfeld ER, Leske MC, Wu SY. Recent epidemiologic studies on nutrition and cataract in India, Italy and the United States. J Am Coll Nutr. 1993;12:521–6.[PubMed]
172. Schorr U, Blaschke K, Turan S, et al. Relationship between angiotensinogen, leptin and blood pressure levels in young normotensive men. J Hypertens. 1998;16:1475–80.[PubMed]
173. Seddon JM, Cote J, Davis N, et al. Progression of age-related macular degeneration: association with body mass index, waist circumference, and waist-hip ratio. Arch Ophthalmol. 2003;121:785–92. [PubMed]
174. Sheard NF. Moderate changes in weight and physical activity can prevent or delay the development of type 2 diabetes mellitus in susceptible individuals. Nutr Rev. 2003;61:76–9. [PubMed]
175. Shiose Y. Intraocular pressure: new perspectives. Surv Ophthalmol. 1990;34:413–35. [PubMed]
176. Shiose Y. The aging effect on intraocular pressure in an apparently normal population. Arch Ophthalmol. 1984;102:883–7. [PubMed]
177. Shiose Y, Kawase Y. A new approach to stratified normal intraocular pressure in a general population. Am J Ophthalmol. 1986;101:714–21. [PubMed]
178. Sierra-Honigmann MR, Nath AK, Murakami C, et al. Biological action of leptin as an angiogenic factor. Science. 1998;281:1683–6. [PubMed]
179. Silha JV, Krsek M, Sucharda P, et al. Angiogenic factors are elevated in overweight and obese individuals. Int J Obes (Lond) 2005;29:1308–14. [PubMed]
180. Sjöström CD, Lissner L, Sjöström L. Relationships between changes in body composition and changes in cardiovascular risk factors: the SOS Intervention Study. Swedish Obese Subjects. Obes Res. 1997;5:519–30.[PubMed]
181. Sjöström CD, Lissner L, Wedel H, et al. Reduction in incidence of diabetes, hypertension and lipid disturbances after intentional weight loss induced by bariatric surgery: the SOS Intervention Study. Obes Res. 1999;7:477–84.[PubMed]
182. Sjöström L, Lindroos AK, Peltonen M, et al. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med. 2004;351:2683–93.[PubMed]
183. Smith W, Assink J, Klein R, et al. Risk factors for age-related macular degeneration: Pooled findings from three continents. Ophthalmology. 2001;108:697–704. [PubMed]
184. Smith W, Mitchell P, Leeder SR, et al. Plasma fibrinogen levels, other cardiovascular risk factors, and age-related maculopathy: the Blue Mountains Eye Study. Arch Ophthalmol. 1998;116:583–7. [PubMed]
185. Sommer A. Intraocular pressure and glaucoma. Am J Ophthalmol. 1989;107:186–8. [PubMed]
186. Spaide RF, Armstrong D, Browne R. Continuing medical education review: choroidal neovascularization in age-related macular degeneration–what is the cause? Retina. 2003;23:595–614. [PubMed]
187. Spector A. Oxidative stress-induced cataract: mechanism of action. FASEB J. 1995;9:1173–82. [PubMed]
188. Spector A, Garner WH. Hydrogen peroxide and human cataract. Exp Eye Res. 1981;33:673–81. [PubMed]
189. Spector A, Wang GM, Wang RR. The prevention of cataract caused by oxidative stress in cultured rat lenses. II. Early effects of photochemical stress and recovery. Exp Eye Res. 1993;57:659–67. [PubMed]
190. Spector A, Wang GM, Wang RR, et al. A brief photochemically induced oxidative insult causes irreversible lens damage and cataract. II. Mechanism of action. Exp Eye Res. 1995;60:483–93. [PubMed]
191. Stevens VJ, Obarzanek E, Cook NR, et al. Long-term weight loss and changes in blood pressure: results of the Trials of Hypertension Prevention, phase II. Ann Intern Med. 2001;134:1–11. [PubMed]
192. Stratton IM, Kohner EM, Aldington SJ, et al. UKPDS 50: risk factors for incidence and progression of retinopathy in Type II diabetes over 6 years from diagnosis. Diabetologia. 2001;44:156–63. [PubMed]
193. Su DH, Yeo KT. Diabetic retinopathy and serum lipids. Singapore Med J. 2000;41:295–7. [PubMed]
194. Suter PM, Locher R, Hasler E, et al. Is there a role for the ob gene product leptin in essential hypertension? Am J Hypertens. 1998;11:1305–11. [PubMed]
195. Tamburrino MB, McGinnis RA. Anorexia nervosa. A review. Panminerva Med. 2002;44:301–11. [PubMed]
196. Tapp RJ, Shaw JE, Harper CA, et al. The prevalence of and factors associated with diabetic retinopathy in the Australian population. Diabetes Care. 2003;26:1731–7.[PubMed]
197. Tavani A, Negri E, La Vecchia C. Selected diseases and risk of cataract in women. A case-control study from northern Italy. Ann Epidemiol. 1995;5:234–8. [PubMed]
198. Taylor A. Nutritional influences on risk for cataract. Int Ophthalmol Clin. 2000;40:17–49. [PubMed]
199. Teuscher AU, Meienberg O. Ischaemic oculomotor nerve palsy. Clinical features and vascular risk factors in 23 patients. J Neurol. 1985;232:144–9. [PubMed]
200. Tielsch JM, Katz J, Sommer A, et al. Hypertension, perfusion pressure, and primary open-angle glaucoma. A population-based assessment. Arch Ophthalmol. 1995;113:216–21. [PubMed]
201. Torgerson JS, Hauptman J, Boldrin MN, et al. XENical in the prevention of diabetes in obese subjects (XENDOS) study: a randomized study of orlistat as an adjunct to lifestyle changes for the prevention of type 2 diabetes in obese patients. Diabetes Care. 2004;27:155–61. [PubMed]
202. Tuomilehto J, Lindström J, Eriksson JG, et al. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance. N Engl J Med. 2001;344:1343–50. [PubMed]
203. Uckaya G, Ozata M, Bayraktar Z, et al. Diabetes Care. 2000;23:371–6. [PubMed]
204. Uckaya G, Ozata M, Sonmez A, et al. Is leptin associated with hypertensive retinopathy? J Clin Endocrinol Metab. 2000;85:683–7. [PubMed]
205. Ughade SN, Zodpey SP, Khanolkar VA. Risk factors for cataract: a case control study. Indian J Ophthalmol. 1998;46:221–7. [PubMed]
206. Valle V, Martos R, Gascon F, et al. Low-grade systemic inflammation, hypoadiponectinemia and a high concentration of leptin are present in very young obese children, and correlate with metabolic syndrome. Diabetes Metab. 2005;31:55–62. [PubMed]
207. van Leiden HA, Dekker JM, Moll AC, et al. Blood pressure, lipids, and obesity are associated with retinopathy: the hoorn study. Diabetes Care. 2002;25:1320–5. [PubMed]
208. van Leiden HA, Dekker JM, Moll AC, et al. Risk factors for incident retinopathy in a diabetic and nondiabetic population: the Hoorn study. Arch Ophthalmol. 2003;121:245–51. [PubMed]
209. Visser M, Bouter LM, McQuillan GM, et al. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999;282:2131–5. [PubMed]
210. Wachter A, Sun Y, Dasch B, et al. Münster age- and retina study (MARS). Association between risk factors for arteriosclerosis and age-related macular degeneration. Ophthalmologe. 2004;101:50–3. [PubMed]
211. Weintraub JM, Willett WC, Rosner B, et al. A prospective study of the relationship between body mass index and cataract extraction among US women and men. Int J Obes Relat Metab Disord. 2002;26:1588–95. [PubMed]
212. West SK, Valmadrid CT. Epidemiology of risk factors for age-related cataract. Surv Ophthalmol. 1995;39:323–34.[PubMed]
213. Wong TY, Duncan BB, Golden SH, et al. Associations between the metabolic syndrome and retinal microvascular signs: the Atherosclerosis Risk In Communities study. Invest Ophthalmol Vis Sci. 2004;45:2949–54. [PubMed]
214. Wong TY, Larsen EK, Klein R, et al. Cardiovascular risk factors for retinal vein occlusion and arteriolar emboli: the Atherosclerosis Risk in Communities & Cardiovascular Health studies. Ophthalmology. 2005;112:540–7. [PubMed]
215. Wong TY, Mitchell P. Hypertensive retinopathy. N Engl J Med. 2004;351:2310–7. [PubMed]
216. Wood PD, Stefanick ML, Dreon DM, et al. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med. 1988;319:1173–9. [PubMed]
217. Wormald R, Evans J, Smeeth L, et al. Photodynamic therapy for neovascular age-related macular degeneration. Cochrane Database Syst Rev. 2005;4:CD002030. [PubMed]
218. Wu SY, Leske MC. Associations with intraocular pressure in the Barbados Eye Study. Archives of Ophthalmology. 1997;115:1572–6. [PubMed]
219. Yamagishi S, Amano S, Inagaki Y, et al. Pigment epithelium-derived factor inhibits leptin-induced angiogenesis by suppressing vascular endothelial growth factor gene expression through anti-oxidative properties. Microvasc Res. 2003;65:186–90. [PubMed]
220. Yilmaz MI, Sonmez A, Acikel C, et al. Adiponectin may play a part in the pathogenesis of diabetic retinopathy. Eur J Endocrinol. 2004;151:135–40. [PubMed]
221. Yoshida M, Ishikawa M, Kokaze A, et al. Association of life-style with intraocular pressure in middle-aged and older Japanese residents. Jpn J Ophthalmol. 2003;47:191–8.[PubMed]
222. Younan C, Mitchell P, Cumming R, et al. Cardiovascular disease, vascular risk factors and the incidence of cataract and cataract surgery: the Blue Mountains Eye Study. Ophthalmic Epidemiol. 2003;10:227–40. [PubMed]
223. Yudkin JS, Eringa E, Stehouwer CD. “Vasocrine” signalling from perivascular fat: a mechanism linking insulin resistance to vascular disease. Lancet. 2127;365:1817–20.[PubMed]
224. Zanella MT, Kohlmann O, Ribeiro AB. Treatment of obesity hypertension and diabetes syndrome. Hypertension. 2001;38:705–8. [PubMed]
225. Zang EA, Wynder EL. The association between body mass index and the relative frequencies of diseases in a sample of hospitalized patients. Nutr Cancer. 1994;21:247–61. [PubMed]
226. Zarbin MA. Current concepts in the pathogenesis of age-related macular degeneration. Arch Ophthalmol. 2004;122:598–614. [PubMed]
227. Zhang F, Chen Y, Heiman M, et al. Leptin: structure, function and biology. Vitam Horm. 2005;71:345–72.[PubMed]
228. Zhang L, Krzentowski G, Albert A, et al. Risk of developing retinopathy in Diabetes Control and Complications Trial type 1 diabetic patients with good or poor metabolic control. Diabetes Care. 2001;24:1275–9.[PubMed]
229. Zhou L, Li Y, Yue BY. Oxidative stress affects cytoskeletal structure and cell-matrix interactions in cells from an ocular tissue: the trabecular meshwork. J Cell Physiol. 1999;180:182–9. [PubMed] Formats:

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