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The Eyes Have It

fidoglassesDiet is vital to preservation of vision as we age. Some people have a higher risk of losing central vision than others—based partly on genetics—but that can be postponed or prevented by consuming sufficient levels of certain dietary nutrients. Clinicians are advised to provide dietary counsel especially to young persons who are susceptible to the vision-disabling consequences that accompany the genetic variations responsible for early onset of age-related macular degeneration (AMD). That gene is officially termed “complement factor H,” abbreviated to CFH. Researchers in the Netherlands tested more than two thousand individuals over age 55 for genetic susceptibility to AMD by way of the CFH gene. The subjects were followed for more than a decade, receiving eye exams every three years to learn who suffered from vision deterioration or loss. Careful, detailed dietary intake records were kept, and eating habits were monitored. The risk reduction ascribed to specific nutrients was associated with normal dietary intake.

Genetic variations can increase the risk of early age-related macular degeneration.  Using food frequency questionnaires and genetic testing, researchers at the Erasmus Medical Center in the Netherlands (Ho and van Leeuwen. 2011) evaluated biological interactions among risk factors for ARM, and found distinct relationships “…between CFH Y402H and zinc, beta-carotene, lutein/zeaxanthin, and eicosapentaenoic/docosahexaenoic acid (EPA/DHA)…”  Subjects with dietary intake of zinc in the highest third “…reduced their hazard ratio of early AMD…” by more than 40%.  Intakes of beta-carotene, lutein/zeaxanthin, and EPA/DHA reduced risk by more than a third.  Drs. Ho and van Leeuwen concluded their report with,”High dietary intake of nutrients with antioxidant properties reduces the risk of early AMD in those at high genetic risk.”

COMMENTARY
AMD is a disease that affects the macula, the most important part of the retina and an area that has a very high concentration of photoreceptors, responsible for central vision.  Nerve fibers in the macula coalesce with neighboring fibers to form the optic nerve, the “cable” that connects the eye to the brain.  The health of our eyes depends on the health of the cardiovascular and nervous systems.  The retina and surrounding structures are filled with blood vessels that depend on a healthy cardiovascular system.

The link between vision and diet has been recognized for a considerable time.  In 2006, a study funded by the Agricultural Research Service and reported in the American Journal of Clinical Nutrition  found a relationship between a high glycemic-index (GI) diet and AMD.  The glycemic index is a ranking of foods based on their elevation of blood glucose after ingestion, compared to a reference food such as white bread or glucose.  These scientists suggested a direct relationship of glycemic index to eye disease.  Study participants whose diets contained the highest GI foods also had the highest amount of macular pigment abnormalities, which is an early indicator of macular degeneration.  (Chiu. 2006)  It seems prudent, therefore, to limit or completely avoid foods that are high in starches and sugars, particularly sugars that are added, as found in processed foods, sweets, and the like.

Addressing the nutrients mentioned in the Ho and van Leeuwen study, zinc is already a necessary trace mineral, in that it is a component of several enzymes and brings vitamin A from the liver to the retina in order to produce melanin, a protective pigment of the eye.  Zinc is heavily concentrated in the eye, mostly in the retina and the choroid, the vascular tissue beneath the retina.  Food sources include red meats, beans, nuts (almonds), whole grains, shellfish (oysters), and fortified foods.

Lutein and zeaxanthin are nutrients found in green leafy vegetables and eggs, as well as in other foods.  There’s more reason to eat your spinach than merely to be like Popeye. These two compounds have identical chemical formulas, and are thus called isomers of each other. (The arrangement of atoms is slightly different.)  Many studies have related these substances to the prevention of AMD as well as cataracts.  Of all the carotenoids found in nature, these are in the greatest amounts in the eye, where they absorb the blue light that can cause oxidative damage.  They have to come from food, so we advise that you get the darkest greens you can find, including spinach, kale, collards, and turnip greens.  Squash, pumpkin, corn, Brussels sprouts, peas, carrots, and green beans are other vegetable sources.  The fruits include citrus.

Lack of vitamin A may cause might blindness, dry eyes, eye infections, skin problems and slowed growth.  Beta-carotene is a compound that can be converted by the body to vitamin A.  The need for vitamin A in vision was identified almost a hundred years ago.  Foods that contain beta-carotene or vitamin A include dark green leaves, and the yellow-orange groups, such as cantaloupe, pumpkin, yellow squashes, and others.  In the eye, beta-carotene becomes retinaldehyde, also called retinal, and is bound to a protein called opsin, which resides in the rods and cones.  This combination helps to carry electrical energy along the optic nerve to the brain.  Night blindness, by the way, is actually poor adaptation to low-light situations.

The essential fatty acids, in this case EPA and DHA, must come from the diet.  They maintain integrity of the nervous system, and help to prevent inflammation and arteriosclerosis, a noted enemy of vision.  One result of arteriosclerosis is a decrease in nutrients to the eye and a reduction in the removal of waste materials.  EPA and DHA also aid in the reduction of dry eyes.  It is well-known that oily fish are the best food sources of these essential fats, though supplements are available.

Oh, yeah.  You never see a rabbit wearing glasses.  Eat your carrots.

References

MAIN ABSTRACT
Arch Ophthalmol. June 2011;129(6):758-766.
Reducing the Genetic Risk of Age-Related Macular Degeneration With Dietary Antioxidants, Zinc, and {omega}-3 Fatty Acids
The Rotterdam Study
Lintje Ho, MD, MPH, MSc; Redmer van Leeuwen, MD, PhD; Jacqueline C. M. Witteman, PhD; Cornelia M. van Duijn, PhD; André G. Uitterlinden, PhD; Albert Hofman, MD, PhD; Paulus T. V. M. de Jong, MD, PhD, FRCOphth; Johannes R. Vingerling, MD, PhD; Caroline C. W. Klaver, MD, PhD

SUPPORTING ABSTRACTS
Semin Ophthalmol. 2011 May;26(3):192-7.
Inflammation and Age-Related Macular Degeneration (AMD).
Telander DG.

Department of Ophthalmology and Vision Science, University of California Davis Medical Center, Sacramento, CA, USA.

Arch Ophthalmol. 2007 Mar;125(3):300-5.
High-sensitivity C-reactive protein, other markers of inflammation, and the incidence of macular degeneration in women.
Schaumberg DA, Christen WG, Buring JE, Glynn RJ, Rifai N, Ridker PM.

Division of Preventive Medicine, 900 Commonwealth Ave E, Boston, MA 02215, USA. [email protected]

American Journal of Clinical Nutrition, Vol. 83, No. 4, 880-886, April 2006
Dietary glycemic index and carbohydrate in relation to early age-related macular degeneration
Chung-Jung Chiu, Larry D Hubbard, Jane Armstrong, Gail Rogers, Paul F Jacques, Leo T Chylack, Jr, Susan E Hankinson, Walter C Willett and Allen Taylor

Pol Merkur Lekarski. 2011 Apr;30(178):241-5.
[Vascular complications in patients with metabolic syndrome].      [Article in Polish]
Kowalski J, Sliwczyńska-Rodziewicz D, Ciećwierz J, Kowalczyk E, Pawlicki L, Irzmański R, Mejer A, Szadkowska I, Barylski M.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

The Eyes Ought Not Have It

man-rub-eyesWe humans anticipate that certain things will happen at specific times of the year. Flowers are supposed to bloom in spring and summer; snow is supposed to fall in winter. Unfortunately, certain physical conditions follow a similar timeline. We might get athlete’s foot in the summer from walking unshod on the lawn, and might catch a cold in winter, usually from being cooped up in a stuffy building surrounded by contagious people. There’s no theory for the foot fungus, but the absence, or at least the dearth, of endogenous vitamin D and its salutary relationship to colds and flu can be blamed on the lack of enough sunshine to make it. Vitamin D, that is. It isn’t that the sun fails to show up for work every day; it’s that its angle is too shallow to hit the skin just right. Then there are those things that attack us by surprise, like pink eye, a.k.a.conjunctivitis.  Just because you hear about it in kids doesn’t mean adults are immune.

Conjunctivitis can strike any of us; there’s more than one kind. Symptoms can vary from one type and from one person to another.  It’s an inflammatory condition of the conjunctiva, which is the outermost layer of the eye and the inner lining of the eyelid. Bacterial or viral infections are the most common causes, but allergies and chemical reactions can sneak in, as well.  Redness is a giveaway, and tearing and itching in one or both eyes are common. Blurred vision, sensitivity to light, feeling of grittiness and discharge are other signs. Despite that conjunctivitis caused by infection is highly contagious, it doesn’t cause serious health problems if caught early. There’s no doubt that symptoms can be distressing, but complete recovery without after-effects can be expected.

Viral conjunctivitis, the most common, can be diagnosed from signs and symptoms…and from patient history, which should be an element of any medical diagnosis. If discharge from the eye is watery rather than thick, and if it accompanies a cold, it’s probably viral. Lab tests aren’t usually necessary unless there’s a glaring reason. This is something that kids catch from each other, and it doesn’t take much to travel—a shared tissue, swimming in contaminated pool water, sharing a contaminated towel, using the same eye makeup and touching. Thank goodness this is self-limiting (Jackson, 1993).

The bacterial type of conjunctivitis is similarly diagnosed, with the exception of describing discharge as thick instead of watery, possibly in the presence of an ear infection.  The physician might order a lab test to determine which bacterium is the culprit so the treatment plan can be more direct if one is deemed necessary. Some bacterial forms can be more severe than others, requiring drops or ointments. In any case, medications will hasten recovery regardless of bacterium strain. Adults are less likely than children to contract this form of conjunctivitis, the discharge of which can be so sticky that the eyelids glue shut.

Allergic conjunctivitis often is seasonal, particularly when pollen counts are elevated. Itching can be intense and is common in people who have other signs of allergic disease. Besides pollen, dust mites, animal dander, medications, cosmetics and other provoking substances, such as house and garden chemicals, can evoke misery. In this form, the entire eyelid can become swollen. We learned recently that overuse of contact lenses, prolonged exposure to UV from the sun, and vitamin deficiency can relate to allergic pink eye (Sankaridurg, 1999) (Lin, 2013) (Chan, 2007) (Malm, 2007) (Engel, 2009).

The doctor might request an allergen-specific immunoglobin-E (IgE) test to determine allergy to specific substances, but this is usually reserved for those with coexisting skin disease. Allergy shots and antihistamine eye drops can help with allergic conjunctivitis. Over-the-counter drops might do the trick, as well. Medications to address viral and bacterial modes are available. Cool compresses applied to the eyes can ease mild symptoms.

As with any health condition, the ounce of prevention is worth more than the pound of cure. Hygiene is cheap and effective, but relies on the common sense that kids haven’t yet developed, not that all adults have it. Rubbing one’s eyes after coughing into one’s hands can take a respiratory infection to higher places. Genital infections can likewise be transmitted to eyes. Viral conjunctivitis can spread through a community or institution, such as a school, like wildfire. In schools, especially in elementary grades, strict hygiene standards demand enforcement. We have to teach our kids the whys and whens of hand washing. Allergic conjunctivitis is virtually impossible to prevent without moving away from the offending environment or job unless it’s possible to identify the allergen and to remove it. You might not want to remove all the oak trees on your property, and the family’s attachments to the cat might preclude its ouster. But whatever you decide, it would be just your luck to move to Arizona and develop a reaction to clean air and sand.

References

Baudouin C.
Conditions bordering on allergy.
J Fr Ophtalmol. 2007 Mar;30(3):306-13.

Bielory L.
Differential diagnoses of conjunctivitis for clinical allergist-immunologists.
Ann Allergy Asthma Immunol. 2007 Feb;98(2):105-14; quiz 114-7, 152.

Chan Cheuk Ki V, Cheng Lu L, Lam Tsze Ho P.
Chronic conjunctivitis in a patient with folic acid deficiency.
Acta Ophthalmol Scand. 2007 Nov;85(7):802

Creuzot-Garcher C.
Different clinical forms of conjunctival allergy.
J Fr Ophtalmol. 2007 Mar;30(3):288-91.

Engel JM, Molinari A, Ostfeld B, Deen M, Croxatto O.
Actinic conjunctivitis in children: Clinical features, relation to sun exposure, and proposed staging and treatment.
J AAPOS. 2009 Apr;13(2):161-5.

Fauquert JL.
Childhood allergic conjunctivitis: the allergist’s point of view.
J Fr Ophtalmol. 2007 Mar;30(3):292-9.

Granet D.
Allergic rhinoconjunctivitis and differential diagnosis of the red eye.
Allergy Asthma Proc. 2008 Nov-Dec;29(6):565-74.

Jackson WB.
Differentiating conjunctivitis of diverse origins.
Surv Ophthalmol. 1993 Jul-Aug;38 Suppl:91-104.

Lin MC, Yeh TN.
Mechanical complications induced by silicone hydrogel contact lenses.
Eye Contact Lens. 2013 Jan;39(1):115-24.

Malm E, Ghosh F.
Chronic conjunctivitis in a patient with folic acid deficiency.
Acta Ophthalmol Scand. 2007 Mar;85(2):226.

Mantelli F, Lambiase A, Bonini S.
A simple and rapid diagnostic algorithm for the detection of ocular allergic diseases.
Curr Opin Allergy Clin Immunol. 2009 Oct;9(5):471-6.

Marmouz F, Raffard M.
Allergic conjunctivitis: diagnosis and treatment.
Eur Ann Allergy Clin Immunol. 2004 Jan;36(1):25-9.

Messmer EM.
Ocular allergies
Ophthalmologe. 2005 May;102(5):527-43

Sankaridurg PR, Sweeney DF, Sharma S, Gora R, Naduvilath T, Ramachandran L, Holden BA, Rao GN.
Adverse events with extended wear of disposable hydrogels: results for the first 13 months of lens wear.
Ophthalmology. 1999 Sep;106(9):1671-80.

Sethuraman U, Kamat D.
The red eye: evaluation and management.
Clin Pediatr (Phila). 2009 Jul;48(6):588-600.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Seeing Eye To Eye?

shopping-decisionsThe world of conflicting information is still doing well, thanks. In the 1950’s, doctors who smoked, smoked Camels. By the 1990’s, many of those doctors had passed away. A few decades back, headlines announced that black pepper caused cancer. Then, miraculously, it didn’t. Conflicting stories about scientific findings abound, even today, and have been the subject of study in an effort to determine the public’s reaction to information that may be harmful or helpful, depending on context (Jensen, 2012). The association of statin drugs and cataracts is a hot topic of recent vintage. The bottom line is evasive because of…conflicting information. It takes only one contrary comment to upset the apple cart of certainty—just one.

The first FDA-approved HMG-CoA reductase inhibitor, or statin, was lovastatin, introduced in 1987. It was, however, found to cause cataracts in beagles if given at high doses, a term that defies definition.  Naturally produced by red yeast rice, certain Aspergillus fungi, and higher fungi such as oyster mushrooms, lovastatin, better known as Mevacor, removes a required building block for cholesterol biosynthesis. Because cholesterol has never been convicted of causing a heart attack (although often accused), there is much wonder these days why statins were ever invented in the first place, since the list of caveats is extensive. But that’s common to most pharmaceuticals, even over-the-counter. Maybe you’ve never noticed, but some brands of OTC meds are more effective than others at treating whatever malady you choose to control. Cough syrup is a good example. The same applies to statins. Some people respond better to some than to others (deVries, 1993).

To indict an inanimate object requires an absolute relation between two events, processes, objects, properties, facts, or states of affairs, where the second event is a consequence of the first. Does owning a swimming pool eventuate a drowning? Does having a throat mean you’ll choke some day? Will you get a ticket every time you speed? Will taking a statin cause you to get a cataract? If you search hard and long, you’re apt to find as many positive as negative correlations to address the last query. For that matter, the same could be said about any human activity or entailment. If you ponder the situation, you might realize that the longer a person lives, the higher the probability of enduring even a minor adversity, including cataracts. Surprisingly, colonoscopy at middle-age has a ten-time higher risk for adverse effect than other commonly used screening tools (Levin, 2006).

Things we learned yesterday differ from ten years ago because of improved measuring techniques and tools, greater understanding of the states of matter and of biological entities, more-user-friendly applications and state-of-the-art materials. In the early 90’s, there was no accurately measureable difference in cataract progression between users and non-users of statin drugs (Chylack, 1993). Almost two decades later, the sophistication of measuring devices has grown considerably enough to track any changes. Something that has been realized along that timeline is the fact that cholesterol is present in the lens of the eye, where its antioxidant effect contributes to lens transparency (Girao, 1999) (Duindam, 1995). There is reasonable speculation that, since statins lower cholesterol levels, there is an increased risk of lens clouding because statins will interfere with the cells responsible for the beneficial process (Leuschen, 2013). Some researchers think that the absence of cholesterol invites lens proteins to move in and take up cholesterol’s space.

The lens is the only part of the body that gets oxygen without blood vessels. It has neither nerves nor connective tissue. Its capsule is made from collagen; its largest mass, from fibers called laminae. Compared to other parts of the eye, the lens has a low energy demand. If they appear, cataracts make the lens opaque. Some opacities are small and require no attention, while others may be large enough to block vision.  For some of us, the proteins in the lens clump together and cloud a small area. This may be the group of statin users (Lai, 2013). Smoking and diabetes hasten this occurrence, although the environment is not totally excused.  Spreading the blame, however, some reports declare systemic drugs like antidepressants, amiodarone, Tamoxifen and nifedipine (a calcium channel blocker known as Procardia) as causative of cataract onset (Lei, 2013).

The number of available statins has grown since their introduction. Their adverse effects are shared, but some are more intense than others, where fluvastatin (Lescol), for example, causes the greatest liver and kidney dysfunction with chronic use (Hippisley, 2010). With this particular drug, its discontinuation returns the risk of cataract to normal within a year.

On the flip side of the coin, an anti-inflammatory portrait of statins has appeared on the scene. Because the cholesterol model of CVD is increasingly viewed with a jaundiced eye in favor of the inflammation model, statins are being touted as the stars of the anti-inflammatory cavalcade. (Truth be told, some culinary/gustatory compounds are better.)  If inflammation increases the risk of cataracts and if statins are anti-inflammatory, then it may be inferred that statins can help to protect against cataract genesis (Gavin, 2000) (Alexios, 2012) (Chodick, 2010)… unless the statins are inhibited by an antibiotic (Schlienger, 2001).

With all this uncertainty, it might pay to take a closer look at statin therapy and to find an alternative.  The naturally-appearing statin in red yeast rice and the other fungi is surrounded by food factors that prevent adverse effects. After all, a statin drug is a chemical isolated from the synergies of foods. Taking a drug provides no excuse to continue behaviors that prompted the drug in the first place, so lifestyle changes might be considered. Cholesterol levels are believed to be minor considerations in cardiovascular health. Besides, who said levels should be lower than 200? Thirty years ago, it was 250. Be careful of what you eat, dump tobacco, take it easy on the ethanol, wear your shades, get enough antioxidants, and listen to your mother.

References

Alexios S Antonopoulos, Marios Margaritis, Regent Lee, Keith Channon, and Charalambos Antoniades
Statins as Anti-Inflammatory Agents in Atherogenesis: Molecular Mechanisms and Lessons from the Recent Clinical Trials
Curr Pharm Des. 2012 April; 18(11): 1519–153

Babizhayev MA, Deyev AI, Yermakova VN, Brikman IV, Bours J.
Lipid peroxidation and cataracts: N-acetylcarnosine as a therapeutic tool to manage age-related cataracts in human and in canine eyes.
Drugs R D. 2004;5(3):125-39.

Chodick G, Heymann AD, Flash S, Kokia E, Shalev V.
Persistence with statins and incident cataract: a population-based historical cohort study.
Ann Epidemiol. 2010 Feb;20(2):136-42.

Chylack LT Jr, Mantell G, Wolfe JK, Friend J, Rosner B.
Lovastatin and the human lens; results of a two year study. The MSDRL Study Group.
Optom Vis Sci. 1993 Nov;70(11):937-43.

de Vries AC, Vermeer MA, Bloemendal H, Cohen LH.
Pravastatin and simvastatin differently inhibit cholesterol biosynthesis in human lens.
Invest Ophthalmol Vis Sci. 1993 Feb;34(2):377-84.

Duindam HJ, Vrensen GF, Otto C, Puppels GJ, Greve J.
New approach to assess the cholesterol distribution in the eye lens: confocal Raman microspectroscopy and filipin cytochemistry.
J Lipid Res. 1995 May;36(5):1139-46.

Gavin J Blake and Paul M R
Are statins anti-inflammatory?
Curr Control Trials Cardiovasc Med. 2000; 1(3): 161–165.

Girao H, Mota C, Pereira
Cholesterol may act as an antioxidant in lens membranes.
Curr Eye Res. 1999 Jun;18(6):448-54.

Hippisley-Cox J, Coupland C.
Unintended effects of statins in men and women in England and Wales: population based cohort study using the QResearch database.
BMJ. 2010 May 20;340:c2197. doi: 10.1136/bmj.c2197.

Jensen JD, Hurley RJ.
Conflicting stories about public scientific controversies: Effects of news convergence and divergence on scientists’ credibility.
Public Underst Sci. 2012 Aug;21(6):689-704.

Lai CL, Shau WY, Chang CH, Chen MF, Lai MS.
Statin Use and Cataract Surgery: A Nationwide Retrospective Cohort Study in Elderly Ethnic Chinese Patients.
Drug Saf. 2013 Jun 15.

Lei JY, Yao K.
Research relating the use of systematic drug and cataracts.
Zhonghua Yan Ke Za Zhi. 2013 May;49(5):468-71.

Leuschen J, Mortensen EM, Frei CR, Mansi EA, Panday V, Mansi I.
Association of Statin Use With Cataracts: A Propensity Score-Matched Analysis.
JAMA Ophthalmol. 2013 Sep 19.

Levin TR, Zhao W, Conell C, Seeff LC, Manninen DL, Shapiro JA, Schulman J.
Complications of colonoscopy in an integrated health care delivery system.
Ann Intern Med. 2006 Dec 19;145(12):880-6.

Mansi IA, Mortensen EM, Pugh MJ, Wegner M, Frei CR.
Incidence of musculoskeletal and neoplastic diseases in patients on statin therapy: results of a retrospective cohort analysis.
Am J Med Sci. 2013 May;345(5):343-8.

Mansi I, Frei CR, Pugh MJ, Makris U, Mortensen EM.
Statins and musculoskeletal conditions, arthropathies, and injuries.
JAMA Intern Med. 2013 Jul 22;173(14):1-10.

Jeanne Mitchell, MS; Richard J. Cenedella, PhD
Human Lens Cholesterol Concentrations in Patients Who Used Lovastatin or Simvastatin
Arch Ophthalmol. 1999;117(5):653-657.

Schlienger RG, Haefeli WE, Jick H, Meier CR.
Risk of cataract in patients treated with statins.
Arch Intern Med. 2001 Sep 10;161(16):2021-6.

Andrew M. Seaman
Statin use tied to cataract development: study
NEW YORK | Thu Sep 19, 2013 4:03pm EDT
http://www.reuters.com/article/2013/09/19/us-statin-cataract-idUSBRE98I11820130919

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Phosphatidylcholine and Vision: Will The Real PC Please Stand Up?

pc-vision-testA disquieting commentary about a globally progressive mentality is that even the most highly educated among us can be misled into believing a falsehood, a misrepresentation often based on linguistic nuance. It’s all in the spin enunciated by those with a systematic plan to pull the undereducated into their fold. The point in this case is the semantic concerning phosphatidylcholine (PC), the phospholipid purposely and ignorantly confused with lecithin, a material that contains PC as its main constituent, but itself is not PC.

Lecithin is an extracted and purified product made from soybeans, eggs, sunflower, or canola seeds, the last being genetically modified to make it what it is from rapeseeds. Lecithin is a natural emulsifier, keeping mayonnaise from separating, for example, but it contains triglycerides, sterols, fatty acids and carbohydrates that cause it to be digested in the gut before the phospholipid fraction can do its work in the cell membrane. True PC, the actual phospholipid, is an amphiphilic molecule, meaning that is has a polar, water-soluble group attached to a non-polar water insoluble hydrocarbon chain. It’s the primary component of the cell membrane and acts as a reservoir of choline for the obligatory manufacture of acetylcholine, the neurotransmitter in charge of nerve impulse transmission that enables muscle contraction, vasodilation, peristalsis and mood changes. Convention has permitted triple strength lecithin, which now is thirty-six percent phosphatidylcholine, to be called PC because of the chief constituent, adding to the confusion. Phosphatidylcholine is the largest fraction of the phospholipids that make the cell membrane. It’s accompanied by three others, however, including phosphatidylethanolamine (PE), phosphatidylserine (PS), and phosphatidylinositol (PI). Each of these fractions has its own character.

PC is a famous molecule in its own right but, as an ancillary agent to the function of fat-soluble nutrients, it displays the loyalty of a favorite sidekick. Lutein is one of the major players in eye health and has been the focus of considerable study as a therapeutic and preventative agent in the treatment of the retinal diseases. Found in green leafy vegetables such as spinach and kale, lutein is a yellow carotenoid pigment that modulates light energy to serve as a photoprotector by absorbing blue light and inhibiting the consequent free radicals from exposure to it. The increases in pigmentation of the retina afforded by lutein protect the eye against macular degeneration and the formation of cataracts (Richer, 1999, 2004) (AREDS Study Group, 2001, 2007) (Barker, 2010). Should the retina be scourged by inflammation, lutein can serve as a rescue molecule (Sasaki, 2009) and help to prevent damage to the functional proteins rhodopsin and synaptophysin (Ozawa, 2012). Some pharmaceuticals and nutraceuticals need a supporting cast to enhance their performances. Such is phosphatidylcholine, an adjuvant that increases the bioavailability and efficacy of more than only a few therapeutic materials.

Curcumin, the active ingredient of turmeric, is an anti-inflammatory agent with a substantial fan club. Combined with PC, curcumin enjoys increased respect in the clinical world, particularly in the treatment of uveitis, which is inflammation of the uvea, the part of the eye that includes the choroid, the ciliary body and the iris. Dry eye, maculopathy, glaucoma and diabetic retinopathy are other conditions addressed by using PC-enriched curcumin (Allegri, 2010).

The retina is one of the vertebrate tissues with the greatest concentrations of polyunsaturated fats. Unlike most organs, though, the lens is another story, having a lipid composition that varies from species to species and with age. The sphingolipids and PC concentrations of the lens have been used to predict life span in some species, where humans have so adapted that their lens membranes have greater sphingolipids content to confer protection against oxidation, allowing the lens to remain clear longer than in other species (Borchman, 2004). Since the fibers of the human lens rely on phospholipids for their integrity, reductions in phospholipids may be predictive of cataracts, while simultaneously implying to clinicians that phospholipid intake will prevent, or at least slow, their progression (Siddique, 2010) (Deeley, 2010). As much as contemporary science would like to deem this a modern position on the architecture of the eye, the idea of ocular phospholipid degradation over time has been studied since the 1960’s, and perhaps earlier, when it was found that PC and PE do not exhibit phosphate turnover as readily as the other phospholipids, phosphatidic acid and PI, once more indicating a position of respect for PC (Broekhuyse, 1969).

Behind the cornea and before the lens is the aqueous humor, the transparent gelatinous fluid made mostly of water plus a little bit of amino acid, electrolytes and vitamin C. It helps to maintain intraocular pressure, to protect the cornea against the environment and to refract light. In a normal eye, all four phospholipid fractions are present, but not in a glaucomatous one. Supplemental PC, then, has the potential to resolve such an issue, while maintaining the structure and function of the framework that scaffolds the anterior members of the eyeball (Edwards, 2014) (Abindi, 2013).

There are mechanisms in the body that can make PC either from the methylation of PE or through the enlistment of a substance called citicoline, which directs the manufacture of PC from choline. Decreases in members of this cascade can change the phospholipid makeup of every cell, affecting every neuron of the central nervous system, of which vision is vital. To address this concern, PC is a desirable option, and both citicoline and exogenous PC have produced favorable results (Grieb, 2002) (Zigman, 1984).

Whether we look for enhanced lutein (Lakshminarayana, 2006), a sophisticated phospholipid complex (Baskaran, 2003), or supercharged curcumin (Belcaro, 2010), we can rely on phosphatidylcholine to vitalize the cell membrane and all that it does for the eyes… and for all our other parts.

References

Acar N, Berdeaux O, Grégoire S, Cabaret S, Martine L, Gain P, Thuret G, Creuzot-Garcher CP, Bron AM, Bretillon L.
Lipid composition of the human eye: are red blood cells a good mirror of retinal and optic nerve fatty acids?
PLoS One. 2012;7(4):e35102.

Age-Related Eye Disease Study Research Group.
A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8.
Arch Ophthalmol. 2001 Oct;119(10):1417-36.

Age-Related Eye Disease Study Research Group, SanGiovanni JP, Chew EY, Clemons TE, Ferris FL 3rd, Gensler G, Lindblad AS, Milton RC, Seddon JM, Sperduto RD.
The relationship of dietary carotenoid and vitamin A, E, and C intake with age-related macular degeneration in a case-control study: AREDS Report No. 22.
Arch Ophthalmol. 2007 Sep;125(9):1225-32.

Allegri P, Mastromarino A, Neri P.
Management of chronic anterior uveitis relapses: efficacy of oral phospholipidic curcumin treatment. Long-term follow-up.
Clin Ophthalmol. 2010 Oct 21;4:1201-6.

Anderson RE, Maude MB, Kelleher PA, Maida TM, Basinger SF.
Metabolism of phosphatidylcholine in the frog retina.
Biochim Biophys Acta. 1980 Nov 7;620(2):212-26.

Aribindi K, Guerra Y, Lee RK, Bhattacharya SK.
Comparative phospholipid profiles of control and glaucomatous human trabecular meshwork.
Invest Ophthalmol Vis Sci. 2013 Apr 30;54(4):3037-44.

Barker FM 2nd.
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Seasonal Allergies – Autumn In New York

seasonal-allergiesAutumn in New York might be a great song, but that’s about as far as it goes for allergy sufferers. In a city made from concrete and glass, you’d think it was easy to escape an attack by natural allergens, like pollen and mold. Ragweed is the chief culprit that arouses immune cells to churn out antibodies to its pollen. The subsequent biochemical reactions flood the bloodstream with histamine, the chemical that gives rise to the familiar allergy symptoms. One ragweed plant can produce a billion grains of pollen in a season, and the grains are so light that they can travel hundreds of miles on the gentlest waft of air. That is why a city made of concrete and glass is not immune to a covert pollen attack. To make matters worse, you can’t just move to the mountains. The ragweed will follow you.

What used to be an allergy season running from mid-August to September is now on the calendar from the first of August to the middle of October. Rising temperatures and elevated carbon dioxide levels extend the season. Trees, grasses and molds are not dismissed as causes of seasonal misery. Damp leaves harbor molds that are kicked up when hit by the rake. In school, kids are assaulted by dust mites that have waited all summer for company.

It’s generally accepted that allergies are triggered by a protein. When a cruising lymphocyte identifies a threat it launches a countermeasure against it. In this complicated biochemical process antibodies are made. The particular antibody for allergic reactions is called immunoglobin E, or IgE, which attaches itself to mast cells and basophils, the cells that activate and release histamine. Histamine opens the flood gates of response, and blood vessels dilate, causing blood pressure to drop. The spaces surrounding cells fill with fluid and the symptoms begin—itching, hives, sneezing, wheezing, and more. In severe cases, anaphylactic shock may occur, a reaction that can be fatal if not handled immediately. The Epi-Pen addresses anaphylaxis. It contains epinephrine, a natural hormone that counteracts dangerous physiological changes that appear during allergic response.

Conventional treatments for allergies include steroid nasal sprays, antihistamines, decongestants, eye drops and shots. They’re used before, during and after symptoms occur. Rhinitis, characterized by irritated mucous membranes of the nose, is a common sign of seasonal allergy that responds to alternative measures, notably to butterbur. Butterbur rhizome extracts that are free of pyrrolizidine alkaloid hepatotoxic constituents have been found safe to use for up to four months (Schapowal, 2005), though many people use them longer. Pyrrolizidine alkaloids are produced by plants to protect them against insect herbivores, but are a danger to the liver, occluding small blood vessels and causing the organ to swell. Petasin, the active ingredient in butterbur, is an anti-inflammatory compound with relaxant properties (Ko, 2001), able also to inhibit histamine and leukotrienes, the latter being white blood cell components responsible for allergic and inflammatory reactions (Thomet, 2002).

Cetirizine is Zyrtec, the antihistamine that addresses the symptoms of allergic rhinitis. A quickened heartbeat, weakness or tremors, problems with urination, insomnia and dizziness are among its side effects. Butterbur, on the other hand, is generally well tolerated, although belching may occur, and those who are sensitive to some plant compounds may experience itching and mild rash. The fatigue and drowsiness common to cetirizine are absent. In a randomized study conducted in Switzerland, seasonal rhinitis patients receiving butterbur fared as well as those receiving cetirizine, without any of the sedative effects (Schapowal, 2002).

Nasal irrigation is the practice of using a fluid-filled vessel to flush excess mucus and debris from the nose and sinuses. Advocates insist that it promotes nasal and sinus health. The saline solution that is commonly employed may act as an antibacterial agent, as well. Being inexpensive and simple, the practice has gained considerable acceptance among Canadian and American medical practitioners, who agree that it could reduce reliance on antibiotics (Papsin, 2003) and antihistamines (Garavello, 2003). If it relieves symptoms, it’s a welcome ritual.

There is a plant chemical that acts simultaneously as a bronchodilator and an inhibitor of histamine and other allergic or pro-inflammatory chemicals in the body—quercetin, a compound common to apples, onions, dill, Hungarian peppers, capers and radishes. How’s that for diversity? Quercetin is a flavonoid, one of several substances known years ago as vitamin P, a designation that has fallen from favor. Flavonoids are noted for the coloration of many flowers designed to attract pollinators. In the higher plants, they act as chemical messengers, cell cycle inhibitors and directors of the total physiological machinery. Good for us is that these properties translate to humans, although they are slow to be recognized by the FDA and its European counterparts, primarily because absorption is an issue and clinical studies are few.

Where funding was available, outside the realm of pharmaceutical giants, quercetin and its comrades were found to demonstrate several pharmacological effects, including anti-viral, anti-microbial, anti-inflammatory and anti-allergic potential. These properties demonstrate a capability to down-regulate and to suppress certain of the many inflammatory pathways, including those involved in allergic inflammation and basophil enlistment (Chirumbolo, 2010). Of the flavonoids, quercetin is the most abundant, but has received the most attention because its effects on basophils are seen at billionth of mole concentrations, where studies in Italy learned that quercetin was able to sequester histamine release in activated cells (Chirumbolo, Marzotto, et al, 2010). Using mast cells sensitized with IgE, Japanese scientists learned that flavonoid varieties akin to quercetin display similar activity by inhibition of the calcium influx that signals the release of histamine and pro-inflammatory mediators (Kimata, 2000) (Kawai, 2007).

A regimen consisting of herbal interventions and dietary flavonoids (there are many to pick from) presents a complementary / alternative approach to the management of allergic misery with considerable effectiveness. Maybe it’s worth a try and you’ll save money on tissues.

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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.