Relief for Dry Eyes
- Invented by a science team passionately determined to help those with dry eyes
- Biochemically balanced natural ingredients that enhance Omega fatty acid metabolism.
- Millions of doses safely used by satisfied repeat customers
- Manufactured to FDA Good Manufacturing Practice standards.
- 60-day full money back guarantee
- You have nothing to lose but your dry eyes.
BioTears First - the healthy tear film standard of care.
It's suggested in peer-reviewed literature that these specific nutrients support normal production of lubricants in other affected parts of the body, such as mucous membranes of the mouth and vagina, and interior body surfaces such as joints and synovial membranes.
A biochemically intact tear film is necessary for optimal visual acuity.
BioTears Oral GelCaps contain the optimal blend of Omega 3 and Omega 6 essentials fatty acids, plus all the nutrient co-factors suggested in peer-reviewed clinical studies to enhance the enzymatic metabolic conversion associated with the tear-specific series one anti-inflammatory prostaglandin, PGE1.
BioTears Oral GelCaps include nutrients that are suggested in peer-reviewed clinical studies to appropriately inhibit the essential fatty acid arachidonic acid production of the COX2 enzyme, the pro-inflammatory prostaglandin PGE2, and Interleukin Il-6.
BioTears Oral GelCaps also contain APO-Lactoferrin, which is suggested to inhibit the growth of both viral and bacterial pathogens and biofilms in the three-layer tear film, as well as Green Tea, which is suggested to modulate osmolarity and ocular surface tension, and curcumin to address ocular surface inflammation.
We recommend you scroll up and visit the BioTears Scientific
Rationale link for more information. The manufacturing link is at the
bottom of every page.
Recommended dosage: Four oral capsules per-day; two with each morning and evening meal.
Precautions: Coumadin patients should consult their primary care physician when taking this formulation. Pregnant or lactating women, or individuals with medical conditions should also consult a physician before using. These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, or treat any disease.
Dry Eye Overview
Was I in last night?
I remember a book
Pathology of the three-layer tear film:
The Mucus Layer - the closest layer to the corneal epithelium. It is 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. It is 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. It is 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 laye, 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 Disease:
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.
The typical symptoms of the dry eye syndrome include dryness, grittiness, irritation, difficulty reading for long periods of time, burning and even the apparent contradiction of excessive tearing or watering. In extreme cases of dry eye, patients may become unusually sensitive to light, experience severe eye pain, and start to notice diminished vision. Successful treatment may be needed to avoid permanent damage.
Blepharitis can often cause dry eye symptoms due to inflammation of the eyelid margins, which is caused by a bacterial infection (Staphylococci). This condition can compromise the quality of the tear film causing tears to evaporate more quickly. The bacteria produce waste material that can cause a mild toxic reaction leading to chronic red, irritated eyes.
Extended Contact Lens Wear can result in dry eye from corneal oxygen and nutrient deficiency. Protein build-up on contact lens can produce a breeding ground for bacterial growth and surface roughness, further contributing to inflammatory changes. Some contact lens solutions contain preservatives that can also cause chemical irritation of the corneal surface and result in dry eye symptoms.
LASIK Surgery temporarily disrupts the ocular surface/lacrimal gland unit. Also, during LASIK, roughly 60-70% of the superficial nerve fibers in the cornea are severed, which reduces sensation and affects aqueous tear production and delays wound healing. With compromised sensation, the blink rate can slow to the point that the tear film breaks up before the next blink can reconstitute. Though this condition usually clears up after a few months, it may result in mild to severe dry eye syndrome for several months after surgery.
Diseases that may be associated with dry eyes include Rheumatoid Arthritis, Sjogrens Syndrome, Diabetes, Asthma, Thyroid disease, Lupus, and possibly Glaucoma.
Age - Dry eye syndrome affects 75% of people over age 65. Tear volume decreases from age 18 as much as 60% by age 65.
Hormonal changes cause decreased tear production brought on by pregnancy, lactation, menstruation, and menopause.
Medications that can cause dry eyes are antibiotics, blood pressure medications, antidepressants, diuretics, over-the-counter vasoconstrictors such as Visine, antihistamines, birth control pills, appetite suppressants, and ulcer medications.
Computer Use causes most people to blink less frequently (about 7 times per minute vs. a normal rate of around 22 times/minute). This leads to increased evaporation along with the fatigue and eye-strain associated with staring at a computer monitor. Any task requiring a great deal of concentration can result in decreased blink rate.
The conventional treatment for dry eyes is to treat the symptoms not the cause:
Artificial Tears: Some form of over-the-counter artificial tears is usually recommended. Although they may provide temporary relief, they merely palliate the symptoms. Worse, the preservatives can aggravate the condition, and can even kill corneal cells. Tears that promise 'get the red out'
Punctal Occlusion: Punctal occlusion is a procedure used to help dry eye patients by closing the tear drainage canals with silicone plugs, which keep most of the fluid from leaving the surface of the eye. This may provide long-term relief.
BioTears Scientific Rationale
Artificial tears flush out debris, dilute substances trapped in the tear film, and increase tear clearance. They do not, however, provide all the factors critical for the maintenance and repair of the ocular surface, nor do they optomize tear film structure and function, which is necessary for improved visual acuity.
- BioTears Oral Gel Caps has been clinically suggested to improve the tear chemistry and the health of the ocular surface on over 75% of the dry eye patients studied.
- BioTears Oral Gel Caps has been clinically suggested, through slit lamp observation, rose bengal staining, and lisemine green staining to improve the health of the ocular surface.
- BioTears Oral Gel Caps has been clinically suggested to extend tear break-up time (TBUT).
- BioTears Oral Gel Caps has been clinically suggested to increase aqueous output through the use of both ZoneQucik and Schrimers tests.
- BioTears Oral Gel Caps has been clinically suggested to increase tear lactoferrin levels with the Touch Tear MicroAssay System.
BioTears ingredients are proving to modulate tear film osmolarity levels with the Tear Lab test.
- BioTears has been clinically suggested to decrease tear film
inflammatory markers, IL-1 and IL-6.
- Thousands of satisfied BioTears customers strongly suggest, with every monthly repeat order, the very real subjective data that further proves product efficacy.
Clinical studies have suggested that the nutrient co-factors included in BioTears Oral Gel Caps may restore normal production of lubricants in the eyes and other affected parts of the body, such as mucous membranes of the mouth and vagina, and interior body surfaces such as joints and synovial membranes. (4)
In developing a tear-specific formula for oral administration, Biosyntrx included the nutrient co-factors suggested necessary to address dry eye syndrome by physiologic rather than pharmacological means. These ingredients are designed to work synergistically rather than individually, and are suggested in published scientific literature to effectively address the inflammatory process responsible for most dry eye syndrome, as well as enhancing and restoring function to the glands involved in all three layers of the tear film. (5-11)
Mechanism of Action:Omega 6 fatty acids are suggested to metabolize to the site-specific anti-inflammatory ecosinoid, prostaglandin E1 (PGE1). These particular prostaglandins are suggested in peer-reviewed published literature to reduce ocular surface inflammation, as well as reduce the inflammatory process associated with meibomitis and reduced lacrimal gland aqueous output.
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, we included the nutrient co-factors, vitamins A, C, B6, and magnesium. The delta-six-desaturase (D6D) enzyme necessary for this conversion is too easily disrupted by alcohol, aging, smoking, elevated cholesterol levels, and environmental factors without these additional nutrient co-factors, which are also suggested to modulate goblet cell production and neurotransmitter blink response.
Pharmaceutical grade cod liver oil, as a source of Omega 3 EPA/DHA is germane to the formulation. It serves as a metabolic gateway boost to the downstream conversion of the Omega 3 to the anti-inflammatory PGE3, while also preventing inappropriate Omega 6 arachidonic acid cleavage via the delta-5-destaurase enzyme (D5D). (12-13)
Vitamin E, specifically gamma tocopherols, is suggested in peer-reviewed literature to prevent oxidation by stabilizing the EFAs, and inhibiting COX2 enzyme activity that promotes inflammatory response. (14)
Curcumin is suggested in peer-reviewed literature to appropriately block Omega 6 and Omega 3 fatty acids from metabolizing to the pro-inflammatory PGE2 and IL1. (15)
Background: Curcumin is a natural COX2 inhibitor with similar chemical properties to ibuprofens Motrin and Advil (NSAIDS). The difference is Curcumin does not inhibit production of the COX1 enzyme that is necessary to protect the stomach lining. NASIDS can cause hemorrhage and have been responsible for a number of deaths. The first sign of an adverse response can be severe gastric bleeding.
Vitamin C, as ascorbic acid and fat-soluble absorbyl palmitate, is suggested to best modulate prostaglandin (PGE1) synthesis due to the extended half-life of the fat-soluble vitamin C over water-soluble ascorbic acid. This Vitamin C combination is also suggested in peer-reviewed literature to enhance the production of IgE concentrates in tears, the first line of basophil and mast cell defense against invading pathogens and allergens that frequently cause dry eye symptoms. (16)
Lactoferrin is suggested in peer-reviewed literature to increase the level of iron binding proteins to better inhibit viral and bacterial infections and to balance other tear lipocalins (family of proteins that transport small hydrophobic molecules), which modulate the surface tension of the tear film and affect the comfort of the contact lens wearer. Lactoferrin taken orally appears to survive absorption in the stomach by converting to a very small molecule called lactoferricin which can easily find its way into secretory tissue including the eyes. (17-24)
Background: Lactoferrin is produced in the tear film by neutrophils that constitute the "first line of defense" against infection. Neutrophil apoptosis (programmed cell death) signals the macrophage to clean up debris from wound sites, including surgically induced wounds (LASIK).
Green Tea is included to modulate osmolarity, one of the causative factors in dry eye, resulting in inflammation and subsequent cell damage.
BioTears Oral GelCaps are designed to help inhibit the LASIK induced dry eye by supporting post-surgical wound healing response, enhancing lacrimal and meibomian gland output, as well as enhance the post-op acetylcholine neurotransmitter blink response. (25-28)
linoleic and gamma-linolenic acid therapy in dry eye syndrome with an
inflammatory component. Barabino S, Rolando M, Camicione P, Ravera G, Zanardi
S, Giuffrida S, Calabria G. Cornea.
2003 Mar;22(2):97-10 [abstract]
of dietary supplementation with black currant seed oil on the immune
response of healthy elderly subjects. Wu D, Meydani M, Leka LS, Nightingale Z,
Handelman GJ, Blumberg JB, Meydani SN. American
Journal of Clinical Nutr. 1999 Cot;70(4):536-43. [abstract]
supplementation with gamma-linolenic acid alters fatty acid content and
eicosanoid production in healthy humans. Johnson MM, Swan DD, Surette ME, Stegner
J, Chilton T, Fonteh AN, Chilton FH. J
Nutr. 1997 Aug;127(8):1435-44. [abstract]
Sjogren's syndrome and the sicca syndrome: the role of prostaglandin E1 deficiency. Treatment with essential fatty acids and vitamin C. Horrobin DF, Campbell A. Med Hypotheses 1980 Mar;6(3):225-32 [abstract]
The immunoregulatory role of vitamins A, D and E in patients with primary Sjogren's syndrome. Szodoray P, Hovath IF, et al. Rheumatology 2009 Nov 27 [abstract]
compositional based model for the tear film layer. McCulley JP, Shine W. Trans Am Ophthalmol Soc.
1997;95:79-88; discussion 88-93. [abstract]
of antiandrogen treatment on the fatty acid profile of neutral lipids
in human meibomian gland secretions. Sullivan BD, Evans JE, Krenzer KL, Reza Dana M,
Sullivan DA J Clin Endocrinol Metab.
2000 Dec;85(12):4866-73. [abstract]
by gas chromatography/mass spectrometry of long-chain fatty acids and
alcohols from hamster meibomian glands using picolinyl and nicotinate
DJ. Biomed Chromatogr. 1989
E prevents changes in the cornea and conjunctiva due to vitamin A
A, Gong H, Amemiya T. Graefes Arch
Clin Exp Ophthalmol. 2003 Apr;241(4):287-97. [abstract]
A deficiency alters the expression of mucin genes by the rat ocular
surface epithelium. Tei M, Spun-Michaid SJ, et al. Invest
Ophthalmol Vis Sci. 2000 Jan;41(1):82-8. [abstract]
gland uptake and metabolism of ascorbic acid. Dreyer R, Rose RC. Proc Soc Exp Biol Med. 1993
between goblet cell density and tear function tests. Yeo AC, Carkeet A, Carney
LG, Yap MK. Ophthalmic Physiol Opt.
2003 Jan;23(1):87-94. [abstract]
and Anti-inflammatory Forms of Interleukin-1 in the Tear Fluid and
Conjunctiva of Patients with Dry-Eye Disease Abraham Solomon, Dilek Dursun, Zuguo
Liu, Yuhuan Xie, Angelo Macri and Stephen C. Pflugfelder. Invest Ophthalmol Vis Sci. 2001
of eicosapentaenoic acid to gamma-linolenic acid-supplemented diets
prevents serum arachidonic acid accumulation in humans Barham JB, Edens MB,
Fonteh AN, Johnson MM, Easter L, Chilton FH. J Nutr. 2000 Aug;130(8):1925-31. [abstract]
and its major metabolite, in contrast to alpha-tocopherol, inhibit
cyclooxygenase activity in macrophages and epithelial cells Jiang Q, Elson-Schwab,
Courtemanche C, Ames BN Proc Natl Acad
Sci U S A. 2000 Oct 10; 97(21):11494-9. [abstract]
and Anti-Inflammatory Activity of Curcumin: A Component of Turmeric
(Curcuma longa). Chainani-Wu N. Altern
Complement Med 2003 Feb;9 (1): 161-8 [abstract]
caused by rosacea. Dursun D, Piniella AM, Pflugfelder SC. Cornea 2001 Aug;20(6):668-9 [abstract]
lipocalins: potential lipid scavengers for the corneal surface. Glasgow BJ, Marshall G,
Gasymov OK, Abduragimov AR, Yusifov TN, Knobler CM Invest Ophthalmol Vis Sci 1999
inhibition of mast cell activation by neutrophil lactoferrin: uptake by
mast cells and interaction with tryptase, chymase and cathepsin G. HeS, McEven AR,
blewell SA. Biochem Pharmacol
2003 Mar 15; 65 (6): 1007-15 [abstract]
responsible for the surface tension of human tears. Nagyova B, Tiffany JM. Curr Eye Res 1999 Jul;19(1):4-11 [abstract]
down-regulates the LPS-induced cytokine production in monocytic cells
via NFkappa B. Haversend L, Ohlsson BG, Hahn-Sone M. et al. Cell Immunol. 2002 Dec; 220 (2);
lactoferrin stimulates the phagocytic activity of human neutrophils:
identification of its active domain. Miyacchi H, Hashimoto S, et al. Cell Immunol. 1998 Jul
is dry eye and what does it mean to the contact lens wearer? Foulks, GN. Eye Contact Lens. 2003 Jan;29(1
Suppl):S96-100; discussion S115-8, S192-4. [abstract]
multi-centre study of lapsed contact lens wearers. Ophthalmic Physiol Opt. 2002 Nov;22(6):516-27. [abstract]
lipase and lipocalin differences between tolerant and intolerant
contact lens wearers. Glassom M, Stapleton F. Willcox M Curr Eye Res. 2002 Oct; 25 (4);
of linoleic acid and gamma-linolenic acid on tear production, tear
clearance and on the ocular surface after photorefractive keratectomy.
Macri A, Giuffrida
S, et al. Graefes Arch Clin Exp
Ophthalmol. 2003 May 27 [epub ahead of print] [abstract]
- Anti-inflammatory and anti-oxidative effects of the green tea polyphenol epigallocatechin gallate in human corneal epithelial cells. Cavet M, Harrington K, et al. Molecular Vision 2011: 17:533-542 [abstract]
of corneal refractive surgery on the lacrymal film. Pisella PJ, Godon C,
Auzerie O, Baudouin C. Fr Ophtalmol
2002 Apr;25(4):416-22 [abstract]
and therapy of LASIK-induced neurotrophic epitheliopathy. Breil P, Frisch L, Dick
HB. Ophthalmologe 2002
eye after refractive surgery. Ang RT, Dartt DA, Tsubota K. Curr Opin Ophthalmol 2001 Aug;12(4):318-22 [abstract]