Ocular health

Role in human eyes[edit]

Lutein was found to be concentrated in the macula, a small area of the retina responsible for central vision. The hypothesis for the natural concentration is that lutein helps keep the eyes safe from oxidative stress and the high-energy photons of blue light. Various research studies have shown that a direct relationship exists between lutein intake and pigmentation in the eye.[3][4][5][6][7][8][9]

Lutein may play a role in Haidinger's brush, an entoptic phenomenon that allows humans to detect polarized light.

Macular degeneration[edit]

Several studies show that an increase in macula pigmentation decreases the risk for eye diseases such as age-related macular degeneration (AMD).[10][11][12] The only randomized clinical trial to demonstrate a benefit for lutein in macular degeneration was a small study, in which the authors concluded that visual function is improved with lutein alone or lutein together with other nutrients and also that more study was needed.[11]

There is epidemiological evidence of a relationship between low plasma concentrations of lutein and zeaxanthin, and an increased risk of developing age-related macular degeneration (AMD). Some studies support the view that supplemental lutein and/or zeaxanthin help protect against AMD.[13]

In 2007, in a six-year study, John Paul SanGiovanni of the National Eye Institute, Maryland found that lutein and zeaxanthin (nutrients in eggs, spinach and other green vegetables) protect against blindness (macular degeneration), affecting 1.2 million Americans, mostly after age 65. Lutein and zeaxanthin reduce the risk of AMD.[13]

Cataracts[edit]

There is also epidemiological evidence that increasing lutein and zeaxanthin intake lowers the risk of cataract development.[13][14] Consumption of more than 2.4 mg of lutein/zeaxanthin daily from foods and supplements was significantly correlated with reduced incidence of nuclear lens opacities, as revealed from data collected during a 13- to 15-year period in the Nutrition and Vision Project (NVP).[15]

Photophobia (abnormal human optical light sensitivity)[edit]

A study by Stringham and Hammond, published in the January/February 2010 issue of Journal of Food Science, discusses the improvement in visual performance and decrease in light sensitivity (glare) in subjects taking 10 mg lutein and 2 mg zeaxanthin per day.[16]

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[Molecular mechanism of the protective effect of lutein against retinal damage induced by blue-light in rats].

[Article in Chinese]

Xu X, Lin X.

Source

Department of Nutrition and Food Hygiene, School of Public Health, Peking University, Beijing 100191, China. xuxianrong@bjmu.edu.cn

Abstract

OBJECTIVE:

To explore the possible mechanisms of the protective effect of lutein against retinal damage induced by blue-light.

METHODS:

Ninety six female SD rats (8 week-old, 200 g) were divided into six groups: normal control (NC), blue light injury (MC), blue light + solvent (SC), blue light + 0.5 mg/ml lutein (L0.5), blue light + 1.0 mg/ml lutein (L1.0) and blue light + 2.0 mg/ml lutein (L2.0). The content of malondialdehyde (MDA) and the activities of peroxide dismutase (SOD) and glutathione peroxidase (GSH-Px) of retina were measured as oxidative stress markers. Neuron nitricoxide synthase and the expression of c-fos protein in retina were analyzed by Western Blot.

RESULTS:

The content of MDA increased in the retina induced by photic injury, and the increase was protected significantly by lutein treatment (P < 0.05), but no dose-dependent response of lutein on the activities of SOD and GSH-Px was observed (P > 0.05). The expression of c-fos protein was significantly higher in the retina of MC and SC group than that in lutein-treated groups (P < 0.05), while the expression of nNOS was not significant different between groups.

CONCLUSION:

The mechanisms of lutein protecting retina from blue-light damage might be quenching singlet oxygen, inhibiting lipid peroxidation and c-fos gene expression.

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Macular pigments lutein and zeaxanthin as blue light filters studied in liposomes.

Junghans A, Sies H, Stahl W.

Source

Institut für Physiologische Chemie I and Biologisch-Medizinisches Forschungszentrum, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, D-40001, Germany.

Abstract

Lutein and zeaxanthin are the predominant carotenoids in the human macula lutea. Epidemiological data suggest that an increased intake of a lutein-rich diet correlates with a diminished risk for age-related macular degeneration, a major cause of impaired vision in the elderly. Filtering of blue light has been proposed as a possible mechanism of protection. Here, the blue light filter efficacy of carotenoids was investigated in unilamellar liposomes loaded in the hydrophilic core space with a fluorescent dye, Lucifer yellow, excitable by blue light. Carotenoids were incorporated into the lipophilic membrane. Fluorescence emission in carotenoid-containing liposomes was lower than in carotenoid-free controls when exposed to blue light, indicating a filter effect. Filter efficacy was in the order lutein > zeaxanthin > beta-carotene > lycopene. Some of the difference in blue light filter efficacy of carotenoids is attributable to differences in extinction coefficients, and a major further contribution is suggested to be related to the orientation of the incorporated molecules in the liposomal membrane.

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RedFox said:

fwiw you may want to consider trying Lutein and Zeaxanthin

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Gertrudes said:

Mrs. Peel said:

KristinLynne said:

I tried to use this software from the above link and it worked great... for a minute. Somehow it must have had malware attached to it because my computer started acting weird after I installed it... so I had to delete the program and get some help removing the malware from McAfee. FWIW.

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I've used f.lux on several computers with no problem. Perhaps you did not download the current version, or downloaded it from a non-trustworthy site? You have to adjust the settings to your own time zone, etc., for it to work properly. I've always used free antivirus software so don't deal with McAfee.

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I had a similar experience to KristinLynne's one. I downloaded the program last year, it worked fine for that day, and after that my laptop nearly died. I removed lux but, in the end, I had to re install windows all over again through the recovery discs. I now have a functional computer, but which has never been quite the same since then. Well, mind you, my laptop is now 8 and a half years old, and it was already bought refurbished, so I suppose it is also getting "tired".

I would like to get a proper version of lux or any other similar software that wouldn't damage my computer, but I won't do it with this one. It is maybe too old for that and I'm afraid it will die for good.

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My PC's Anti-Virus program flagged f.lux as malware.
As long as you've downloaded f.lux from this site, you don't have any malware. Every once in a while we get flagged as a potential threat due to the nature of our installer and updater. If this happens to you, please post a comment with your anti-virus program and details and we will contact them for review.

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Chu said:

I notice that if I eat something inflammatory, I start having symptoms f blepharitis within 24hs.

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Oxajil said:

Gosh... My eye was doing so well with the diet and everything. Adjusting my sleeping patterns for the last few weeks had a great effect on it too. I was looking forward to go to the eyedoc next week for a picture, because I could clearly see in the mirror that things were clearing up. It wasn't perfect, but things did get better. In other areas of my life, things got better too. I'm spending more time and energy on my homework, which is quite a lot, but I'm managing pretty well so far and also on reading books before going to bed. Even started to read SHOTW yesterday evening. I can't spend too much time at the computer because I know that doesn't serve my eye very well, which is why I tried to change my schedules so it would be better for my eye. So things felt like they were going well.

Then I wake up this morning and my eye was all red, the virus grew a bit more which has made my sight more blurry. I think it could have been the magnesium oil that got into my eye and irritated it, but the thing is, I've always used it and it occassionally goes into my eye and it never really got bothered by it. So I really don't know what it is.

I did a full EE round, and amazingly, that got rid of most of the redness. The FAR infrared lamp I got helped as well.
I'll just continue with what I've been doing and be easy on myself. It does suck a little, but I guess that's how things go sometimes. I'll atleast stop with the magnesium oil and see how things go further.

Just needed to share this, thank you for reading.

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anka said:

RedFox said:

fwiw you may want to consider trying Lutein and Zeaxanthin

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Thanks very much RedFox. I also checked that at Mercola.com, where one can find some more info concerning the diet.

http://products.mercola.com/eye-support/

So green leafy veggies, black current, bilberry (haven't heard of it until now) and more. And/or supplements.

And thanks to Persej for keeping us informed about the LCD market. I have been gone from the scene for almost 3 months and things got moving quiet a lot so i need to remake my mind up:)

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The Age-Related Eye Disease Study (AREDS) is a major clinical trial sponsored by the National Eye Institute, one of the federal government's National Institutes of Health. {and since when has the government made any decisions in the interests of our health and well-being?!}

The AREDS was designed to learn more about the natural history and risk factors of age-related macular degeneration (AMD) and cataract and to evaluate the effect of high doses of vitamin C, vitamin E, beta-carotene and zinc on the progression of AMD and cataract.

Results from the AREDS showed that high levels of antioxidants and zinc significantly reduce the risk of advanced AMD and its associated vision loss. These same nutrients had no significant effect on the development or progression of cataract.

Press Release-AREDS Results, October 12, 2001

In May 2013, the NEI completed the Age-Related Eye Disease Study 2, which tested several changes to the formulation. They tried adding omega-3 fatty acids, as well as the antioxidants lutein and zeaxanthin, which are in the same family of nutrients as beta-carotene. The researchers also tried substituting lutein and zeaxanthin for beta-carotene, which prior studies had associated with an increased risk of lung cancer in smokers. The study found that while omega-3 fatty acids had no effect on the formulation, lutein and zeaxanthin together appeared to be a safe and effective alternative to beta-carotene.

Late Updated: May 2013

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Mitochondrial DNA Damage as a Potential Mechanism for Age-Related Macular Degeneration
Pabalu P. Karunadharma, Curtis L. Nordgaard, [...], and Deborah A. Ferrington

Abstract
Purpose.
Increasing evidence suggests a central role for mitochondrial (mt) dysfunction in age-related macular degeneration (AMD). Previous proteomic data from the retinal pigment epithelium (RPE) revealed significant changes to mt proteins, suggesting potential functional defects and damage to mitochondrial DNA (mtDNA) with AMD progression. The present study tests the hypothesis that mtDNA damage increases with aging and AMD.

Conclusions.
Collectively, the data indicate that mtDNA is preferentially damaged with AMD progression. These results suggest a potential link between mt dysfunction due to increased mtDNA lesions and AMD.

Age-related macular degeneration (AMD) is a progressive eye condition that is the leading cause of legal blindness in individuals older than 65 in the developed world.1 By affecting the central (macular) region of the human retina, AMD degrades the central visual function that subserves reading, driving, writing, and face recognition. The loss of these abilities significantly affects daily function and quality of life.2 Currently approved treatment options for AMD are available to a limited number of patients with advanced wet-type AMD, in which the treatments limit vision loss by inhibition of vascular leakage3,4 but do not address disease pathogenesis. In addition, the inconvenience, cost, and quality of life that result from monthly injections increase the burden on patients as well as the health care system. Despite recent improvements, many patients still progress to the advanced stages of AMD. The next major steps in sight preservation include strategies centered on early detection, treatment of the early stages, and prevention. Importantly, studying the early disease process is the first step toward the development of new treatments.

Many investigators believe that the pathogenesis of AMD begins in the retinal pigment epithelium (RPE), a monolayer of cells between the neural retina and the retinal basement membrane (Bruch's membrane). The RPE maintains retinal health and homeostasis by photoreceptor phagocytosis, nutrient transport, and secretion of growth factors.5 Drusen, the earliest clinical sign of AMD, appear beneath the RPE as yellow, lipoproteinaceous deposits. Drusen features (e.g., size, character, quantity, and shape) provide the basis for the grading system used in this study (Minnesota Grading System, MGS6). This system replicates a widely used clinical research classification system7 by linking common definitions from clinics to eye bank tissue (ex vivo). Thus, the use of MGS provides a methodology to directly link biochemical changes in human donor eyes at distinct stages of AMD to clinical phenotypes in patients.6

Converging evidence from several recent studies implicate mitochondrial (mt) damage in the AMD disease process.8 Severe disruptions to mt cristae structure and a decreased number of mitochondria were reported in a morphologic analysis of AMD donor RPE.9 Our first proteomic analysis of the RPE identified altered mt proteins with AMD progression,10 thus prompting an in-depth investigation of the mt proteome. The second proteomic analysis suggested potential damage to mtDNA with AMD.11 Since aging is a strong risk factor for AMD, the present study evaluated the extent of mtDNA damage in human RPE with both aging and AMD progression. To our knowledge, this is the first study to distinguish damage associated with normal from pathologic aging (i.e., AMD). Our data revealed low mtDNA damage with normal aging compared with AMD and elevated damage preceding significant macular degeneration and vision loss. Collectively, these results suggest a role for mtDNA damage in AMD.

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Age-Related Eye Disease Study--Results


The Age-Related Eye Disease Study (AREDS) is a major clinical trial sponsored by the National Eye Institute, one of the federal government's National Institutes of Health.

The AREDS was designed to learn more about the natural history and risk factors of age-related macular degeneration (AMD) and cataract and to evaluate the effect of high doses of vitamin C, vitamin E, beta-carotene and zinc on the progression of AMD and cataract.

Results from the AREDS showed that high levels of antioxidants and zinc significantly reduce the risk of advanced AMD and its associated vision loss. These same nutrients had no significant effect on the development or progression of cataract.

Press Release-AREDS Results, October 12, 2001

In May 2013, the NEI completed the Age-Related Eye Disease Study 2, which tested several changes to the formulation. They tried adding omega-3 fatty acids, as well as the antioxidants lutein and zeaxanthin, which are in the same family of nutrients as beta-carotene. The researchers also tried substituting lutein and zeaxanthin for beta-carotene, which prior studies had associated with an increased risk of lung cancer in smokers. The study found that while omega-3 fatty acids had no effect on the formulation, lutein and zeaxanthin together appeared to be a safe and effective alternative to beta-carotene.

Late Updated: May 2013

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Mitochondrial DNA Damage as a Potential Mechanism for Age-Related Macular Degeneration
Pabalu P. Karunadharma, Curtis L. Nordgaard, [...], and Deborah A. Ferrington

Abstract
Purpose.
Increasing evidence suggests a central role for mitochondrial (mt) dysfunction in age-related macular degeneration (AMD). Previous proteomic data from the retinal pigment epithelium (RPE) revealed significant changes to mt proteins, suggesting potential functional defects and damage to mitochondrial DNA (mtDNA) with AMD progression. The present study tests the hypothesis that mtDNA damage increases with aging and AMD.

Conclusions.
Collectively, the data indicate that mtDNA is preferentially damaged with AMD progression. These results suggest a potential link between mt dysfunction due to increased mtDNA lesions and AMD.

Age-related macular degeneration (AMD) is a progressive eye condition that is the leading cause of legal blindness in individuals older than 65 in the developed world.1 By affecting the central (macular) region of the human retina, AMD degrades the central visual function that subserves reading, driving, writing, and face recognition. The loss of these abilities significantly affects daily function and quality of life.2 Currently approved treatment options for AMD are available to a limited number of patients with advanced wet-type AMD, in which the treatments limit vision loss by inhibition of vascular leakage3,4 but do not address disease pathogenesis. In addition, the inconvenience, cost, and quality of life that result from monthly injections increase the burden on patients as well as the health care system. Despite recent improvements, many patients still progress to the advanced stages of AMD. The next major steps in sight preservation include strategies centered on early detection, treatment of the early stages, and prevention. Importantly, studying the early disease process is the first step toward the development of new treatments.

Many investigators believe that the pathogenesis of AMD begins in the retinal pigment epithelium (RPE), a monolayer of cells between the neural retina and the retinal basement membrane (Bruch's membrane). The RPE maintains retinal health and homeostasis by photoreceptor phagocytosis, nutrient transport, and secretion of growth factors.5 Drusen, the earliest clinical sign of AMD, appear beneath the RPE as yellow, lipoproteinaceous deposits. Drusen features (e.g., size, character, quantity, and shape) provide the basis for the grading system used in this study (Minnesota Grading System, MGS6). This system replicates a widely used clinical research classification system7 by linking common definitions from clinics to eye bank tissue (ex vivo). Thus, the use of MGS provides a methodology to directly link biochemical changes in human donor eyes at distinct stages of AMD to clinical phenotypes in patients.6

Converging evidence from several recent studies implicate mitochondrial (mt) damage in the AMD disease process.8 Severe disruptions to mt cristae structure and a decreased number of mitochondria were reported in a morphologic analysis of AMD donor RPE.9 Our first proteomic analysis of the RPE identified altered mt proteins with AMD progression,10 thus prompting an in-depth investigation of the mt proteome. The second proteomic analysis suggested potential damage to mtDNA with AMD.11 Since aging is a strong risk factor for AMD, the present study evaluated the extent of mtDNA damage in human RPE with both aging and AMD progression. To our knowledge, this is the first study to distinguish damage associated with normal from pathologic aging (i.e., AMD). Our data revealed low mtDNA damage with normal aging compared with AMD and elevated damage preceding significant macular degeneration and vision loss. Collectively, these results suggest a role for mtDNA damage in AMD.

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Mitochondrial and nuclear DNA damage and repair in age-related macular degeneration.


Abstract
Aging and oxidative stress seem to be the most important factors in the pathogenesis of age-related macular degeneration (AMD), a condition affecting many elderly people in the developed world. However, aging is associated with the accumulation of oxidative damage in many biomolecules, including DNA. Furthermore, mitochondria may be especially important in this process because the reactive oxygen species produced in their electron transport chain can damage cellular components. Therefore, the cellular response to DNA damage, expressed mainly through DNA repair, may play an important role in AMD etiology. In several studies the increase in mitochondrial DNA (mtDNA) damage and mutations, and the decrease in the efficacy of DNA repair have been correlated with the occurrence and the stage of AMD. It has also been shown that mitochondrial DNA accumulates more DNA lesions than nuclear DNA in AMD. However, the DNA damage response in mitochondria is executed by nucleus-encoded proteins, and thus mutagenesis in nuclear DNA (nDNA) may affect the ability to respond to mutagenesis in its mitochondrial counterpart. We reported that lymphocytes from AMD patients displayed a higher amount of total endogenous basal and oxidative DNA damage, exhibited a higher sensitivity to hydrogen peroxide and UV radiation, and repaired the lesions induced by these factors less effectively than did cells from control individuals. We postulate that poor efficacy of DNA repair (i.e., is impaired above average for a particular age) when combined with the enhanced sensitivity of retinal pigment epithelium cells to environmental stress factors, contributes to the pathogenesis of AMD. Collectively, these data suggest that the cellular response to both mitochondrial and nuclear DNA damage may play an important role in AMD pathogenesis.

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Oxidative stress-induced mitochondrial DNA damage in human retinal pigment epithelial cells: a possible mechanism for RPE aging and age-related macular degeneration

Abstract
Oxidative stress is believed to contribute to the pathogenesis of many diseases, including age-related macular degeneration (AMD). Although the vision loss of AMD results from photoreceptor damage in the central retina, the initial pathogenesis involves degeneration of RPE cells. Evidence from a variety of studies suggests that RPE cells are susceptible to oxidative damage. Mitochondrial DNA (mtDNA) is particularly prone to oxidative damage compared to nuclear DNA (nDNA). Using the quantitative PCR assay, a powerful tool to measure oxidative DNA damage and repair, we have shown that human RPE cells treated with H(2)O(2) or rod outer segments resulted in preferential damage to mtDNA, but not nDNA; and damaged mtDNA is not efficiently repaired, leading to compromised mitochondrial redox function as indicated by the MTT assay. Thus, the susceptibility of mtDNA to oxidative damage in human RPE cells, together with the age-related decrease of cellular anti-oxidant system, provides the rationale for a mitochondria-based model of AMD.

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Mitochondrial DNA damage and its potential role in retinal degeneration.

Abstract
Mitochondria are central to retinal cell function and survival. There is increasing evidence to support an association between mitochondrial dysfunction and a number of retinal pathologies including age-related macular degeneration (AMD), diabetic retinopathy and glaucoma. The past decade has highlighted mitochondrial genomic instability as an important factor in mitochondrial impairment culminating in age-related changes and age-related pathology. This represents a combination of the susceptibility of mitochondrial DNA (mtDNA) to oxidative damage and a limited base excision repair pathway. This random cumulative mtDNA damage leads to cellular heteroplasmy and, if the damage affects a sufficient proportion of mitochondria within a given cell, results in loss of cell function and greater susceptibility to stress. mtDNA damage is increased in the neural retina and RPE with ageing and appears to be greatest in AMD. It thus appears that the mitochondrial genome is a weak link in the antioxidant defenses of retinal cells and that deficits in mitochondrial DNA (mtDNA) repair pathways are important contributors to the pathogenesis of retinal degeneration. Specifically targeting mitochondria with pharmacological agents {Big Pharma always on the lookout to make a buck! We know from the work done here that keto diets regenerate wild mitochondria}able to protect against oxidative stress or promote repair of mtDNA damage may offer potential alternatives for the treatment of retinal degenerations such as AMD.

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How low stomach acid levels ruin your health

_http://wrightnewsletter.com/2011/04/07/low-stomach-acid-levels/

Too little of a good thing

Q: I’ve been having stomach problems, and my doctor wants to put me on a prescription to suppress acid production. But don’t our bodies need stomach acid? I mean, it’s there for a reason, right?

Dr. Wright: You’re absolutely right. The main causes of poor digestion and assimilation are age-related gastric hypochlorhydria (more commonly referred to as low stomach acid) and age-related gastric achlorhydria (which is no stomach acid at all). Like it or not, the older you get, the more likely you are to develop these problems. Unfortunately, doctors rarely recognize the seriousness of this problem and treat the underlying cause. Instead, many doctors today are only making the problem worse by putting people on patent medications specifically designed to suppress stomach acid production.

Low stomach acid levels lead to alterations in your intestinal microflora. Friendly intestinal microorganisms are dependent on the natural intestinal pH balance that results when all digestive organs are working well. When the major source of intestinal acidity (the stomach) fails or when it’s suppressed by patent medications, intestinal contents become too alkaline, allowing unfriendly microorganisms to enter the scene, including Candida albicans (yeast) and many others.

Low stomach acid has been linked to hip fractures, pneumonia, macular degeneration, and more.

The increased risk of infection that goes along with low gastric acidity isn’t limited to the intestinal tract, though. Other studies have shown that when patent medications suppress stomach acid, many seemingly unrelated parts of the body are affected. And it makes sense when you think about it since individual nutrients are vital for maintaining all sorts of body functions.

You should work with your doctor to monitor your stomach acid. If you do have age-related gastric hypochlorhydria or achlorhydria — and we all develop one or the other sooner or later — the problem is fairly easy to treat. Talk to your doctor about taking hydrochloric acid and pepsin capsules to improve your digestion and balance the pH of your gastrointestinal system.[...]

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_http://www.royalrife.com/macular.html

MACULAR DEGENERATION

Macular degeneration is the leading cause of blindness in
those past the age of 70. As with so many chronic degenerative
conditions, there is currently no effective medical treatment.

There is, however, an effective nutritional program that
reverses the condition. A Yakima Washington physician reported
that he cured his own macular degeneration using selenium and
vitamin E. (Washington State soils are so low in selenium that
farm animals have died of "white muscle disease" which is a
selenium deficiency.)

Jonathan Wright, M.D. read of this and also found that these
supplements helped his patients improve. The program was even
more effective with added zinc, taurine, and gingko biloba. Dr.
Wright also found that more than 90% of those with macular
degeneration are low in stomach acid and digestive enzymes. This
makes absorption of minerals difficult or impossible. Some
people also have food allergies that damage the digestive tract
and may have to avoid foods like wheat, milk, and corn to be able
to absorb minerals.

Dr. Wright suggests a supplement program that includes 1000
mg. of taurine twice a day between meals, 800 IU of Vitamin E per
day, 60 mg. of zinc per day, and 200-300 mcg. of selenium per
day. Two 60 mg. capsules of gingko biloba (50:1 extract) can be
taken daily. A balanced multivitamin-mineral (like Oxygenic B)
that supplies copper should also be used. Digestive enzymes
are taken just before each meal. Stomach acid supplements (in
the form of betaine hydrochloride) are used with each meal to aid
digestion and absorption. This program will benefit about 95% of
those with this condition.

The other 5% have major absorption problems and may need IV
injections of zinc and selenium. Dr. Wright has had the vision
of a patient improve during the first IV. Others are adding zinc
and selenium to 70% DMSO and rubbing it on the skin. This also
works well, but requires expert help.

Some people cannot tolerate large amounts of vitamin E. If
you would like to try this program yourself, first ask your
doctor if there is any reason you should not do it.

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