AMD • Nutrition • Genetics

AMD • Age-Related Macular Degeneration

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  What is AMD?    



AMD is a common eye condition and a leading cause of vision loss among people age 50 and older. 

It causes damage to the macula, a small spot near the center of the retina and the part of the eye needed for sharp, central vision, which lets us see objects that are straight ahead.


In some people, AMD advances so slowly that vision loss does not occur for a long time. In others, the disease progresses faster and may lead to a loss of vision in one or both eyes. 

As AMD progresses, a blurred area near the center of vision is a common symptom. Over time, the blurred area may grow larger or you may develop blank spots in your central vision. Objects also may not appear to be as bright as they used to be.


AMD by itself does not lead to complete blindness, with no ability to see. However, the loss of central vision in AMD can interfere with simple everyday activities, such as the ability to see faces, drive, read, write, or do close work, such as cooking or fixing things around the house. 


Even more devastating is the lost of independence, personal self confidence, plus the continuous monthly 2-4 hour eye check-ups and never ending monthly or bi-monthly intra-ocular eye injections of anti-VEGF medication to prevent or reduce the damage of macular hemorrhage that causes blindness.



The Macula


The macula is made up of millions of light-sensing cells that provide sharp, central vision. It is the most sensitive part of the retina, which is located at the back of the eye. When the macula is damaged, the center of your field of view may appear blurry, distorted, or dark.


Types of AMD


In its early and intermediate forms, Dry AMD presents as small deposits on the retina comprised of cholesterol and complement (inflammatory) proteins called Drusen and pigmentation changes in the macula. 

The advanced form may be dry geographic atrophy (30% of advanced disease) or wet choroidal neovascularization (70% of advanced disease).


  • Non-exudative or Dry AMD
  • Exudative or Wet AMD


In Wet AMD, abnormal blood vessels grow under the retina to aid nutrient transport to the macula 

(choroidal neovascularization or CNV).



Reference: NEI, National Eye Institute, AMD Facts https://nei.nih.gov/health/maculardegen/armd_facts


National Eye Institute

symptoms and risk factors

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Symptoms and Risk Factors



As the leading cause of adult blindness in developed countries, age-related macular degeneration is three times more common than glaucoma and affects one in eight adults over age 60. Though common, it often goes undiagnosed until after significant, irreversible vision loss has occurred. Knowing the signs and symptoms of AMD is the first step toward preventing the dramatic consequences of untreated disease.


AMD Symptoms


Some symptoms of macular degeneration are detected early, yet not connected to the disease until after the condition is fairly advanced. Other symptoms seem more obtrusive and are likely to trigger a visit to 

the eye care professional:


  • Difficulty seeing or driving at night
  • Difficulty reading in dim light
  • Worsened visual acuity
  • Distorted vision
  • Central vision loss



Did You Know?

Up to 78% of AMD patients have substantial, irreversible vision loss at first treatment. This includes 37% who are legally blind in at least one eye.


  


Improve Ability to Diagnose AMD


A landmark study published recently in JAMA Ophthalmology shows at least 

25% of clinical AMD is going undiagnosed 

in primary eye care today. 


Moreover, 

30% of the undiagnosed patients had large drusen

a known risk factor for advanced AMD (wet AMD). 

Complementing structural exams with functional dark adaptation evaluation helps safeguard against failure to catch clinically-detectable AMD. Dark adaptation testing using AdaptDx provides a clear, objective measure that is easy to interpret. 


2017,  Neely, Bray , Prevalence of Undiagnosed Age-Related Macular Degeneration in Primary Eye Care. JAMA Ophthalmology 

  



JAMA Ophthalmology

the disease process

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What Happens in the Back of the Eye?


Cholesterol deposits accumulate in the macula years before drusen are visible, making drusen the tip of the iceberg in AMD pathology.


Before drusen are visible, an invisible layer of cholesterol builds up between the pigmented layer of the retina (RPE) and the elastic layer of Bruch’s membrane. These cholesterol depositsbasal laminar (BLamD) and basal linear (BLinD)—cause oxidative stress and inflammation, hindering nutrient transportation to photoreceptor cells.ii As photoreceptor cells die, it becomes harder for the eyes to adjust to darkness and night vision declines. 


This Dark Adaptation™ impairment is the first sign of AMD.


Prior to pivotal research conducted at the University of Alabama Birmingham, the Alabama Study on Age-Related Macular Degeneration (ALSTAR), AMD was  staged as early, intermediate, and advanced. Thanks to the groundbreaking findings of this investigation, we can identify a subclinical stage of AMD.

  

Reference: 2016, Owsley, McGwin, Clark, Delayed Rod-Mediated Dark Adaptation is a Functional Biomarker for Incident Early Age-Related Macular Degeneration (ALSTAR), Journal Ophthalmology.


Dark Adaptation


Also known as “night blindness,” impaired dark adaptation is the earliest symptom of AMD. Physical changes occurring in the early development of AMD compromise the eye’s ability to adjust to darkness. This can make it difficult to drive at night, read in dim light or adjust to dark places, like walking into a dark movie theater. More noticeable visual deficits become evident as the disease progresses, such as worsened visual acuity, distorted vision and central vision loss.


Dark Adaptation impartment will occur many years before any visible structural changes are detectable in your eye by your doctor.

Dark adaptation testing utilizing AdaptDx, provides a clear, objective measure that is easy to interpret.


  

Earlier, More Accurate Detection

Structural changes (the appearance of drusen) in the retina are not always easily discernible. They often become evident only after AMD has progressed from a subclinical state.

But AdaptDx® is 90% sensitive and 90% specific in identifying the earliest onset of AMD. This makes AdaptDx more accurate than current testing for glaucoma (as the accuracy of visual field is only 83%).

Being able to detect AMD with such accuracy will greatly improve your patients’ outcomes. It allows you to detect AMD at the earliest stage, at least three years before drusen are visible, when action can be taken to slow disease progression and prevent vision loss.

Dark Adaptation Testing

  

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AMD • Nutrition • AdaptDx Dark Adaptation Testing

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Stages of AMD

  

From subclinical to advanced AMD, all stages of the disease are the manifestation of the same underlying pathology 


Sublinical AMD

Diagnosing the earliest stages of AMD can present a challenge because these patients often have good corrected visual acuity and the retina appears normal upon clinical examination. Consequently, a routine vision test may not raise any suspicion of the disease.

Subtle yet progressive, night vision difficulty is the earliest symptom of AMD. Often presented as problems driving or reading at night, impaired Dark Adaptation function is the first biomarker of AMD—with impairment taking place at a subclinical level at least three years before drusen are visible. 

No pigmentary abnormalities are apparent upon examination at this stage, and if drusen is detected, these are <63 μm. 


Early AMD

Most people do not experience vision loss in the early stage of AMD, but night vision problems are often reported. Though no pigmentary abnormalities are apparent upon examination, medium-sized drusen (>63 μm and ≤125 μm) are present. 


Intermediate AMD

At this stage, some people may see a blurred spot in the center of their vision. In addition to night vision issues, these patients may also have issues with contrast sensitivity. Some pigmentary abnormalities may be observed and at least one druse >125 μm is present.


Advanced AMD


· Choroidal Neovascularization (CNV) or “Wet AMD” occurs in about 10-15% of patients as a result of abnormal blood vessels forming under the central retina. Vision distortion and/or vision loss begins when these blood vessels leak into the retina. Vision loss caused by Wet AMD typically occurs quite rapidly. However, if the wet form is caught early enough, treatment by a retinal specialist can stabilize vision.


· Geographic Atrophy (GA) or “Advanced Dry AMD” is an advanced form of AMD, during which cells within a region of the retina waste away and die (atrophy). These regions of cell atrophy result in a blind spot in the visual field that cannot be reversed.

Reference: 2016, Owsley, McGwin, Clark, Delayed Rod-Mediated Dark Adaptation is a Functional Biomarker for Incident Early Age-Related Macular Degeneration (ALSTAR), Journal Ophthalmology.



Source:   https://www.maculogix.com/amd/biology-of-amd/

Macular Vitamins & Macular Pigment

Macular Pigment Supplementation: A Prescription for Vision & Cognitive Health - John Nolan, PhD

Macular Pigment Density

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The macula or macula lutea (“yellow spot” in Latin) is an oval yellow area near the center of the retina of the human eye.

At the center of the macula is the fovea: with the largest concentration of cone cells (responsible for detailed vision and colour vision) in the eye and is responsible for central vision. Within the macula is the fovea – a small depression in the macula – which contains a high density of cones (photoreceptors with high acuity).

The macula has an important and naturally occurring protective substance known as the macular pigment (MP). The MP is made up of several carotenoids (phytochemicals – found in plants) commonly found in certain fruits and vegetables that provide the red, orange and yellow colors of these foods. The MP is made of three known compounds:

Lutein, Zeaxanthin and Meso-Zeaxanthin

  

Lutein and Zeaxanthin are obtained through food and are found primarily in broccoli, corn, squash and dark green leafy vegetables like spinach and kale. Meso-Zeaxanthin is obtained by an enzyme conversion of Lutein to Meso-Zeaxanthin in the macula. A recent peer reviewed study published, August of 2014, in Journal of Food Processing & Technology has verified the presence of MZ in salmon skin, sardine skin, trout skin and trout flesh. This study confirmed the presence MZ in nature, and in the human food chain.

In a 1994 Journal of American Medical Association report, Dr. Johanna M. Seddon and her associates at Harvard University found that 6 mg per day of lutein lead to a 43 percent lower risk for Macular Degeneration.

“When we compared the amount of macular pigment, which is comprised of Lutein and Zeaxanthin, present in the eyes of people with age-related macular degeneration to people without the disease, those with the lowest levels of carotenoid accumulation in the outer retina were significantly more likely to suffer from age-related macular degeneration than those with higher pigment levels, ” said Dr. Landrum. “The difference in risk between those having the highest and lowest levels was 75 percent.”

2003, Vrabec, Tantri  et al. Autosomal dominant Stargardt-like macular dystrophy: identification of a new family with a mutation in the ELOVL4 gene. Am J Ophthalmology

What do Lutein and Zeaxanthin do?

  

Lutein and Zeaxanthin are dietary carotenoids (pigments) that filter damaging high energy blue wavelength light from the visible-light spectrum by as much as 90%. Lutein and Zeaxanthin are also antioxidants and therefore protect against the damage caused by harmful molecules that are produced through normal body processes, such as oxygen metabolism, these are called free radicals. Environmental sources of free radicals include cigarette smoke, air pollutants, radiation, certain drugs and environmental toxins.

Why is Meso-Zeaxanthin so vital?

  

Meso-Zeaxanthin, the most potent antioxidant of the three carotenoids, is only found in the center portion of the macula where vision is sharpest. Meso-Zeaxanthin is obtained converting ingested Lutein inside the retina and is not found in the diet. Most Macular Degeneration patients have 30% less Meso-Zeaxanthin in their macula* and show an inability to convert Lutein into Meso-Zeaxanthin. Supplementation with MacuHealth with LMZ3 will ensure that this crucial component of macular pigment accumulates in the target tissue (i.e. the central macula) in a way that is not dependent on an enzyme converting Lutein to Meso-Zeaxanthin.



Source:  https://www.macuhealth.com/learning-center/macular-pigment-density/

AMD Genetic Testing

Dr Jerome Sherman discusses the importance of genetic testing and the value customized AMD vitamin supplementation based on your genome type. 

Macula Risk & Vita Risk Genetic Testing