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OUTLINE FOR CATARACT SECTION- Stuart Richer, OD, PhD, FAAO
I PHYSIOLOGY & BIOCHEMISTRY OF CATARACTOGENESIS
Anterior Epithelial layer
Fiber cell crystalline proteins
Metabolism
Electrolyte Imbalance
II DISEASE ASSOCIATION - Ocular & Systemic
CONGENITAL CATARACTS
NON CONGENITAL / NON AGE RELATED CATARACTS
Capsular - Cortical - Nuclear - Posterior Subcapsular
Opacities
Reference: Richer SP, Yonatan E, Harper CK, McNelis M, Rudy DR,
Perdue A, A Clinical review of non-age related cataracts, Optometry,
2001; 72:767-78.
III CATARACT AS A WORLDWIDE PUBLIC HEALTH ISSUE
Prevalence
Sunlight
Malnutrition
AGING AMERICANS
Driving Safety Issues
Hip Fracture Risk
Quality of Life (QOL)
Airplane pilots
Astronauts
IV INSTRUMENTATATION TO MEASURE OPACIFICATION
Brightness Acuity Test (BAT)(r) & LOCSIII
Pentacam(r)
NASA Diffuse Light Scattering Probe(r)
Holometer(r)
V CATARACT PREVENTION EPIDEMIOLOGY
Caloric Restriction
Diet & Multivitamins
Vitamin C
Lutein and carotenoids
B Vitamins
Sulfur containing molecules
Bioflavanoids
Herbs-i.e. ECGC in green tea
VI HOMEOPATHIC REMEDIES
Cinaria Maritima (5x & 6x)
OTC vs. Rx
VII NON SURGICAL CATARACT MEDICAL EYE DROP TREATMENT
Pantetheine, Prof John Clark, University of Washington School of
Medicine
National Eye Institute collaboration
N-acetyl carnosine gtts BID, Dr Mark Babizhayev www.can-c.net
Animal data-new Veterinary Medicine Studies
In Vitro human lens data
Clinical Trial Data
Human data - Moscow
Commercial data - veterinary practice
Commercial data - human internet sales
FDA, LEGAL AND PROFESSIONAL CONSIDERATIONS
The Power of Nutrition as it effects AMD: Dennis Ruskin OD, FAAO
Discussion of AMD, review new testing protocols, and inform attendees the nutritional strategies
to deal with this disease:
Outline:

Introduction

Past nutritional studies related to AMD

Ongoing nutritional studies related to AMD

Current concepts

Biomarkers of AMD to aid in early identification of the disease

Genetics and AMD

Genetic testing and AMD

Neutragenomics and epigenetics of AMD

Nutritional recommendations and guidelines
Non-Pharmaceutical Recommendations for the Glaucoma Patients
Larry Alexander, O.D., F.A.A.O.
Course Description:
There is strong support in the medical literature regarding diet and nutritional support in the
management of glaucoma. The manipulation of this aspect of therapy may be particularly when
applied to vaso-regulative with neurodegenerative issues.
Outline:
 Summary and Introduction
 Diet and Behavior That Supports Anti-Inflammation and Neuroprotection
o Is There a Place for Bear Bile?
o Is There Any Science?
 The Science of Nutritional Supplements and Natural Sources
 Nutrition and Behavior with Mitochondrial Impact
Take Home Message and Excellent Natural Sources for the following nutrients:
 Vitamin A
 Vitamin C
 Vitamin E
 Lutein/Zeaxanthin
 Lycopene
 Selenium
 Glutathione
 Vitamin B 6
 Folic Acid
 Vitamin B-12
 Magnesium
 Omega 3 Fatty Acids
 Ginkgo Biloba
 Coenzyme Q10-Ubiqquinone
 Alpha-lipoic Acid
 Lycopene
 Melatonin
 Curcumin
 Acetyl-Carnitine
 Bilberry
 Quercitin
 Taurine
 N-acetyl cysteine
 Resveratrol
Exercise
Overall Take Home Message
Maintenance of health does not occur in a vacuum
====================================================================
Nutritional Influence on Tear Film Biochemistry
Ellen Troyer, MA, MT
Addressing the biochemical role micronutrients play in functionality of the three layers of
the tear film.
Pathology of the three-layer tear film:
The Mucus Layer - the closest layer to the corneal epithelium: produced by the conjunctival
goblet cells, and is absorbed by the corneal surface glycoproteins, creating a hydrophilic surface.
Mucin deficiency, or mucopolysaccharide abnormalities, can lead to poor wetting or glycation of
the corneal surface with subsequent desiccation and epithelial damage, even in the presence of
adequate aqueous tear production.
The Aqueous Layer - the layer between the mucous and lipid layers: secreted by the lacrimal
gland and incorporates all water-soluble components of the tear film. It also comprises 90% of
the tear thickness. The aqueous layer provides moisture and supplies oxygen and important
nutrients to the cornea.
The Lipid Layer - the most superficial layer: produced by the Meibomiam glands with
contributions from the glands of Zeis and Moll of the eye lids. The secretion is an oily material,
which is fluid at body temperature and retards evaporation of the aqueous layer and lowers
surface tension, thereby allowing the tear-film to adhere to the eye’s surface. Androgen receptors
are located in both the lacrimal and meibomian glands. A decrease in circulating androgen
hormones can result in loss of the oil layer, exacerbating the evaporative tear loss.
The Blink Reflex renews the tear film by delivering aqueous and lipid to the tear film and
sweeping away debris. The normal blink interval is about 5 seconds under normal conditions.
The tear film is typically stable for about 10 seconds. Tears are normally evaporated or forced
out through the nasolacrimal ducts in the inner corner of the eyes on blinking.
The Root Causes of Dry Eye Syndrome:
Many different things cause dry eye syndrome. The normal aging of tear glands, as well as
extended use of contact lens, environmental pollutants, prescription drugs, refractive surgery,
auto immune diseases, nutrient deficiencies and other disorders can cause disruption in the tear
production and retention process.
Essential Fatty Acids and the tear film
Adequate oral intake of Omega-6 essential fatty acids that contain sufficient amounts of gammalinolenic-acid (GLA) are suggested to stimulate the natural production of tear-specific antiinflammatory series one prostaglandins (PGE1).
Omega 6 fatty acids convert to PGE1 via the linoleic-acid (LA) to gamma-linolenic-acid (GLA)
to dihomo-gamma-linolenic-acid (DGLA) to the series one prostaglandins (PGE1). To help
ensure this conversion, the nutrient co-factors, vitamins A, C, B6, and magnesium or zinc must
be available. Without these nutrient co-factors, neuronal signaling necessary for aqueous tear
production is limited. The delta-six-desaturase (D6D) enzyme necessary for all EFA metabolic
conversion is easily disrupted by nutrient deficiencies, alcohol, aging, smoking, elevated
cholesterol levels, and environmental factors.
These micronutrient co-factors are also suggested to modulate goblet cell and mucin production
and neurotransmitter blink response.
Oral administration of long chair Omega-3 essential fatty acids are equally important.
Eicosapentaenoic acid (EPA) blocks the delta-5-desaturase and prevents development of proinflammatory ecosinoids. Docosahexaenoic acid (DHA) helps maintain cellular membranes,
which is particularly important for optimal production and release of neutral lipids in human
meibomian gland secretions.
An essential fatty acid metabolic chart will be included in the discussion.