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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.

Neuro-Transmission In Overdrive?

neuro-transmittersIf ever there was a commonality among the senior crowd, lack of sound sleep is a top contender. An enigma of the twenty-first century—based on hustle and bustle, multiple job and social obligations, and harried family life—is that the definition of senior now includes fifty-year-olds. Some people contend that fifty is the new thirty; others hold that it’s the new seventy, largely based on inflammatory markers not visible from the outside. Looks like both ends are meeting in the middle, eh? Sleep, or rather the lack of it, seems not to have been much of an issue in the 50’s and 60’s. If getting there is half the fun of a journey, it’s doubly so with sleep. The problem is that it sometimes takes too long to reach the realm of Morpheus.

To encourage sleep there are things to do and not to do. Depending on your personal guru, some to-do’s might include getting comfortable, adjusting room temperature to the mid-sixties (Onen, 1994), picking the right position and wearing loose night clothes. If you happen to be one of those adults afraid of total darkness, use a night light if the moon has too few lumens, but keep it in the hallway. Go for the glow, not the glare. If you’re of the opposite persuasion, try a mask. In either case, be happy you don’t live in Alaska. If you need music, use it. White noise can be helpful, too. If your partner is bothered by your needs, move.

Tense muscles will keep you awake. So will pondering the exciting events of the day. Tensing and then relaxing muscles, working from bottom to top, while focusing on a muscle group, can help you to sink into the mattress until you feel ready to get into your desired position. The head and torso are somewhat stubborn, which explains why you start at the bottom. If it’s hard to get rid of the day’s stimuli, picture items and events as being black, considered the most tiresome color. A brand new black Porsche, on the other hand, might undo all this effort. You could try breathing exercises, guided imaginations, thinking of relaxing activities like fishing or woodworking, or even getting out of bed and watching a dull movie or reading.

Eating a carbohydrate snack or a protein that contains tryptophan might make you sleepy. Taking a magnesium supplement (Abassi, 2012) or an herbal such as valerian has been helpful in some instances (Salter, 2010). Chemicals are the last resort—after the lighting and temperature have been adjusted, after the aromatherapy has proven ineffective, and after everything else.

Some things you don’t want to do before bed include exercising, eating a sizeable feast, and drinking coffee or alcohol. Smoking also interrupts the drowse. And taking a fish oil supplement could amp your rpm’s past the red line. What’s that?? Is my high DHA fish oil keeping me awake?  Yes, it is because it’s out of balance with EPA. While it’s true that DHA is needed by the brain and retina to stay at optimal function, like the gas tank in your car, once filled, you can turn off the pump. It appears that DHA stimulates brain neurons by impinging on receptors that react to the presence of glutamic acid, the non-essential amino acid abundant in the human body, most prominently in the brain, where it is the prime excitatory neurotransmitter. Glutamate receptors are implicated in excitotoxicity, a state linked to neurodegenerative diseases (Lau, 2010) (Heath, 2002) (Hynd, 2004).

There is more than one kind of glutamate receptor, but the one called NMDA-receptor is the trouble maker that opens calcium channels. Besides being found in bone, calcium is an electrolyte that turns things on and makes things happen. When these channels are kept open, calcium rushes into a cell and causes muscle contractions, excitation of neurons, and the release of hormones and neurotransmitters. This kind of physiological activity is exactly what you don’t need when you’re trying to go to sleep. DHA substantially potentiates the peak electrical activity of NMDA/glutamate receptors (Nishikawa, 1994).

The advancement of science has relied on the question, “why?”  There comes a point where there is no answer because that’s just the way it is. Why do two hydrogens and one oxygen atom make water instead of something spendable?  Long-term potentiation is initiated by the influence of DHA on NMDA/glutamate receptors. That’s just the way it is. At this time, magnesium offers a feasible blockade to the opening of the calcium channels. But you’d need lots of it. In the mean time, DHA is responsible for learning and memory. You don’t want to turn that off. You just want to tone it down at night.

NMDA is N-Methyl-D-aspartic acid, an amino acid derivative used to stimulate a receptor by mimicking glutamate, which is the normal visitor to that receptor. NMDA differs from glutamate in that it stimulates only the NMDA receptor, having no bearing on other glutamate receptors involved in synaptic transmissions. Sequestering NMDA/glutamate by avoiding high-DHA supplements prevents the opening of the calcium gates and the consequent stampede that disrupts sleep. That’s just the way it is.

References

Abbasi B, Kimiagar M, Sadeghniiat K, Shirazi MM, Hedayati M, Rashidkhani B.
The effect of magnesium supplementation on primary insomnia in elderly: A double-blind placebo-controlled clinical trial.
J Res Med Sci. 2012 Dec;17(12):1161-9.

Bonin A, Khan NA.
Regulation of calcium signalling by docosahexaenoic acid in human T-cells. Implication of CRAC channels.
J Lipid Res. 2000 Feb;41(2):277-84.

Cao D, Kevala K, Kim J, Moon HS, Jun SB, Lovinger D, Kim HY.
Docosahexaenoic acid promotes hippocampal neuronal development and synaptic function.
J Neurochem. 2009 Oct;111(2):510-21.

Connor S, Tenorio G, Clandinin MT, Sauvé Y.
DHA supplementation enhances high-frequency, stimulation-induced synaptic transmission in mouse hippocampus.
Appl Physiol Nutr Metab. 2012 Oct;37(5):880-7.

Hamano H, Nabekura J, Nishikawa M, Ogawa T
Docosahexaenoic acid reduces GABA response in substantia nigra neuron of rat.
J Neurophysiol. 1996 Mar;75(3):1264-70.

Heath PR, Shaw PJ.
Update on the glutamatergic neurotransmitter system and the role of excitotoxicity in amyotrophic lateral sclerosis.
Muscle Nerve. 2002 Oct;26(4):438-58.

Hynd MR, Scott HL, Dodd PR.
Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer’s disease.
Neurochem Int. 2004 Oct;45(5):583-95.

Kathleen N. Kannass, John Colombo, and Susan E. Carlson
Maternal DHA levels and Toddler Free-Play Attention
Dev Neuropsychol. 2009; 34(2): 159–174.

Kauer JA, Malenka RC, Nicoll RA.
NMDA application potentiates synaptic transmission in the hippocampus.
Nature. 1988 Jul 21;334(6179):250-2.

Kim HY, Spector AA, Xiong ZM.
A synaptogenic amide N-docosahexaenoylethanolamide promotes hippocampal development.
Prostaglandins Other Lipid Mediat. 2011 Nov;96(1-4):114-20.

Lau A, Tymianski M.
Glutamate receptors, neurotoxicity and neurodegeneration.
Pflugers Arch. 2010 Jul;460(2):525-42.

Miller B, Sarantis M, Traynelis SF, Attwell D.
Potentiation of NMDA receptor currents by arachidonic acid.
Nature. 1992 Feb 20;355(6362):722-5.

Nabekura J, Noguchi K, Witt MR, Nielsen M, Akaike N.
Functional modulation of human recombinant gamma-aminobutyric acid type A receptor by docosahexaenoic acid.
J Biol Chem. 1998 May 1;273(18):11056-61.

Nishikawa M, Kimura S, Akaike N.
Facilitatory effect of docosahexaenoic acid on N-methyl-D-aspartate response in pyramidal neurones of rat cerebral cortex.
J Physiol. 1994 Feb 15;475(1):83-93.

Onen SH, Onen F, Bailly D, Parquet P.
Prevention and treatment of sleep disorders through regulation] of sleeping habits
Presse Med. 1994 Mar 12;23(10):485-9.

Nina L. Salazar-Weber and Jeffrey P. Smith
Copper Inhibits NMDA Receptor-Independent LTP and Modulates the Paired-Pulse Ratio after LTP in Mouse Hippocampal Slices
International Journal of Alzheimer’s Disease Volume 2011 (2011), Article ID 864753, 10 pages.

Salter S, Brownie S.
Treating primary insomnia – the efficacy of valerian and hops.
Aust Fam Physician. 2010 Jun;39(6):433-7.

Saugstad LF.
A “new-old” way of thinking about brain disorder, cerebral excitability–the fundamental property of nervous tissue.
Med Hypotheses. 2005;64(1):142-50.

Michelle L. Schlief, Ann Marie Craig, Jonathan D. Gitlin
NMDA Receptor Activation Mediates Copper Homeostasis in Hippocampal Neurons
The Journal of Neuroscience, January 5, 2005. 25(1):239–246-239

Schlief ML, Gitlin JD.
Copper homeostasis in the CNS: a novel link between the NMDA receptor and copper homeostasis in the hippocampus.
Mol Neurobiol. 2006 Apr;33(2):81-90.

Vlachová V, Zemková H, Vyklický L Jr.
Copper modulation of NMDA responses in mouse and rat cultured hippocampal neurons.
Eur J Neurosci. 1996 Nov;8(11):2257-64.

Wurtman RJ, Cansev M, Ulus IH.
Synapse formation is enhanced by oral administration of uridine and DHA, the circulating precursors of brain phosphatides.
J Nutr Health Aging. 2009 Mar;13(3):189-97.

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

Blood Pressure and…

bloodpressure-cuffThere is no naturally normal value for blood pressure (BP), but if yours is higher than that level deemed risky, you need to do something about it or face the possibility of some nasty consequences, such as stroke or cardiac episode, both of which can kill you—and are preventable. During each beat of the heart, pressure varies between a maximum, called systolic, and a minimum, called diastolic. The systolic pressure is the force that pushes blood out of the left ventricle; diastolic pressure refers to the heart at rest. The word diastole means dilation.

High blood pressure can cause arteries to become harder and thicker. Sometimes that can cause a bulge, an aneurysm, a weak spot in the artery that is subject to rupture, resulting in hemorrhage and probably death. Aneurysms don’t disappear by themselves, so some kind of invasive procedure might follow, depending on size and location. Copper deficiency is associated with aneurysm risk, so you might want to look at your diet, particularly if it’s high in zinc, the element some believe will improve male health and performance. But assuring copper sufficiency won’t necessarily prevent an aneurysm caused by elevated BP.

If the heart has to work harder to pump blood against the elevated pressures in the vessels, the heart muscle can get thicker, which makes it even more difficult to pump blood. This is the onset of heart failure, which may or may not be easily treated. In fortunate instances, a thickened heart can revert to normal size. Effects of continued high BP may involve the kidneys, brain and eyes. In polls, most people would rather die than face blindness (Giridhar, 2002) (Pfizer, 2008), which can result from hypertensive retinopathy.

There is no known cause of essential hypertension, but risks have been identified to include salt intake, obesity, race, physical activity, stress, heredity and diet. Secondary hypertension may be related to kidney, endocrine or neurological dysfunction. Medications, such as amphetamines and decongestants, can elevate blood pressure, as can alcohol. What is termed “normal” BP is a systolic pressure less than 120 mmHg and a diastolic pressure less than 80 mmHg (120/80). It takes a visit with your physician to determine your personal baseline and to work out a protocol if one is deemed necessary. That might include a medication besides a dietary intervention to address overweight.

Because cardiovascular disease is a leading cause of mortality in the economically developed world, much attention has been given to it. Diet and lifestyle are significant influences on cardiac risk, and may instigate abnormal lipid profiles, insulin resistance, diabetes and other pathologies suggestive of their impact. Of interest in the management of CVD risk factors are omega-3 fatty acids. Both omega-3 and omega-6 fats are considered essential; the body is unable to synthesize them. The conversion of the mother omega-3 and omega-6 fats, alpha-linolenic acid and linoleic acid, to longer-chain fatty acids, EPA/DHA and arachidonic acid, is terribly inefficient. Because omega-6 fats are held to be a dietary excess by virtue of a regimen high in processed foods and cheap supermarket oils, omega-3 fats, as fish oil, have received considerable interest. Fish oil is rich in EPA and DHA, the former having cardiovascular attributes and the latter having cerebral and retinal activity. Together, these fatty acids have induced moderate reductions in blood pressure at doses approximating 3 grams a day in both treated and untreated persons with elevated BP (Abeywardena, 2011). The mechanism explaining the activity is uncertain, but appears related to improvement in vascular endothelial function, one of these being reduction in stiffness. To address concerns about fish oil’s effect on LDL cholesterol, it is noted that the change in LDL particle size from small to large is a benefit (Ibid.).

One characteristic of hypertension is thickening of the arterial wall. In an animal model of hypertension, arterial thickening was attenuated with DHA treatment and the blood pressure decrease was compared to that induced by a beta blocker. Though only conjectural, other mechanisms by which fish oil lowers BP may involve activation of potassium channels (Toshinori, 2013). It is also possible that the anti-inflammatory compounds encouraged by fish oils ameliorate BP through a hormone-like effect that works in conjunction with the fatty acids’ blood-thinning character. Doses here approach 3 grams a day (Cabo, 2012).

In a twelve-week comparison/contrast trial pitting the omega-6 safflower oil against fish oil, the latter was found to offer significant benefit in reducing blood pressure in subjects with mild hypertension (Radack, 1991), while introducing no adverse changes in plasma lipid values. Including this with sixty-nine other random trials, researchers agree that available evidence indicates that inclusion of EPA/DHA in one’s diet reduces both systolic and diastolic BP at doses of at least 2 grams a day (Miller, 2014). Joining a fish oil protocol with a weight loss program, where applicable, wrought a 13 point drop in systolic and a 9 point drop in diastolic numbers in a cohort having a body mass index in excess of 31.0, the point at which obesity is defined (Bao, 1998).

If you take a prescription medication to keep your blood pressure controlled, don’t just stop it in favor of the fatty acids in fish oil. Doing so risks damage from BP rebound, which can cause serious damage to an artery. If you experience unwelcome side effects from your meds, talk with the doctor and look for an alternative drug. There certainly are enough of them on the market. Integrating fish oil with a BP drug is not generally a hazard, and may even be a boon. On the other hand, if BP falls too low, you can get dizzy, especially after standing from a sitting position. Essential fatty acids exist in the realm of complementary medicine, which is meant to complement, not necessarily to replace, conventional modalities in treating a variety of physical maladies. Hypertension is one that is relatively easy to manage.

References

Abeywardena MY, Patten GS.
Role of ω3 long-chain polyunsaturated fatty acids in reducing cardio-metabolic risk factors.
Endocr Metab Immune Disord Drug Targets. 2011 Sep 1;11(3):232-46.

Bao DQ, Mori TA, Burke V, Puddey IB, Beilin LJ.
Effects of dietary fish and weight reduction on ambulatory blood pressure in overweight hypertensives.
Hypertension. 1998 Oct;32(4):710-7.

Biermann J, Herrmann W.
Modification of selected lipoproteins and blood pressure by different dosages of n-3-fatty acids.
Z Gesamte Inn Med. 1990 Sep 15;45(18):540-4.

Borghi C, Cicero AF.
Omega-3 polyunsaturated fatty acids: Their potential role in blood pressure prevention and management.
Heart Int. 2006;2(2):98.

Cabo J, Alonso R, Mata P.
Omega-3 fatty acids and blood pressure.
Br J Nutr. 2012 Jun;107 Suppl 2:S195-200.

Cicero AF, Ertek S, Borghi C.
Omega-3 polyunsaturated fatty acids: their potential role in blood pressure prevention and management.
Curr Vasc Pharmacol. 2009 Jul;7(3):330-7.

Margolin G, Huster G, Glueck CJ, Speirs J, Vandegrift J, Illig E, Wu J, Streicher P, Tracy T.
Blood pressure lowering in elderly subjects: a double-blind crossover study of omega-3 and omega-6 fatty acids.
Am J Clin Nutr. 1991 Feb;53(2):562-72.

Miller PE, Van Elswyk M2, Alexander DD3.
Long-chain omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid and blood pressure: a meta-analysis of randomized controlled trials.
Am J Hypertens. 2014 Jul;27(7):885-96.

Mori TA.
Omega-3 fatty acids and blood pressure.
Cell Mol Biol (Noisy-le-grand). 2010 Feb 25;56(1):83-92.

Morris MC, Taylor JO, Stampfer MJ, Rosner B, Sacks FM.
The effect of fish oil on blood pressure in mild hypertensive subjects: a randomized crossover trial.
Am J Clin Nutr. 1993 Jan;57(1):59-64.

Radack K, Deck C, Huster G.
Arch Intern Med. 1991 Jun;151(6):1173-80.
The effects of low doses of n-3 fatty acid supplementation on blood pressure in hypertensive subjects. A randomized controlled trial.

Toshinori Hoshia, Bianka Wissuwab, Yutao Tiana, Nobuyoshi Tajimaa, Rong Xua, Michael Bauerb, Stefan H. Heinemannc, and Shangwei Houd
Omega-3 fatty acids lower blood pressure by directly activating large-conductance Ca2+-dependent K+ channels
PNAS March 4, 2013. Published online before print March 4, 2013

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

Understanding the Highs and Lows of Triglycerides

Triglycerides-choiceYou have triglycerides. So do we. Sometimes a lot, sometimes not, sometimes too many. They’re formed by combining glycerol with three molecules of fatty acid, which can be the same or different. Glycerol is a sugar alcohol that provides the backbone of many lipids. It’s an important intermediate in carbohydrate and fat metabolism. High levels of triglycerides have been linked to atherosclerosis and heart disease. They’re the natural molecular form that makes up virtually all fats and oils in both plants and animals. Most of us know our cholesterol levels, and we even know about the differences between HDL and LDL. But managing triglycerides (TG’s) is just as important to cardiac health. About a third of U.S. adults have borderline TG levels, between 150 and 199 milligrams per deciliter. Many of those with high TG’s are older whites who smoke, are overweight, and who get less than 150 minutes of exercise a week. Women have a lower risk than men, and blacks and Mexican Americans have even lower risks (Ford, 2009).

The body makes TG’s from carbohydrates and sends them to fat cells where they’re stored for energy. High TG levels often accompany low HDL, in a kind of lipid profile that may run in families. HDL cholesterol between 40 and 60 milligrams per deciliter, and LDL less than 100 are reasonable goals. Where TG’s store unused calories and provide energy, cholesterol is used to build cells and to make some hormones. Really high TG’s can be a sign that something else is amiss, like high blood pressure or high blood glucose. Low thyroid hormones, liver or kidney conditions, and some genetic missteps can affect how the body converts fat to energy, so TG readings will be elevated. But beta blockers taken for high blood pressure, some diuretics, steroids and birth control pills can raise TG levels, too.

Lifestyle changes are the first line of defense against high TG’s. Losing weight, cutting calories and avoiding excess sugars and refined foods are simple steps, although weight loss may initially be a challenge. It takes only a few pounds to make a difference, and light exercise and alcohol avoidance can help. But there is a supplement that can rescue high TG’s—fish oil. Of course, when Big Pharma realized this, they had to make a prescription form—Lovaza, Glaxo Smith-Kline’s omega-3 prescription. What makes it different from plain fish oil is the FDA’s blessing, which states that Lovaza is the only omega-3 medication so approved. No other fish oil product may be called a medication. The same effect, though, can be realized by taking multiple capsules of OTC product. But because one’s prescription plan pays for Lovaza, it’s cheaper for the patient…and GSK makes a ton of money.

Fish oil contains EPA and DHA, fatty acids that benefit the cardiovascular system and the eyes and brain, respectively. The fatty acids from fish oils are anti-inflammatory and anti-thrombotic; they compete successfully with substances that cause platelet aggregation and vasoconstriction. In hypertriglyceridemia, fish oil decreases the secretion of very low density lipoproteins (VLDL), increases VLDL clearance and reduces TG transport (Nestel, 2000) (Stark, 2000). It is held that fish oil can influence CVD risk factors to such an extent as to reduce risk of coronary heart disease by as much as twenty-seven percent (Stark, 2000).

Some products labeled as fish oil are not really oils at all, but rather alternate lipids known as fatty acid ethyl esters, differing from authentic fish oil triglycerides. Because free fatty acids are rapidly oxidized, the TG structure offers greater stability to the fatty acids and prevents breakdown and oxidation (Segura, 1988). Ethyl esters are derived from the reaction of free fatty acids with ethanol. Here, the glycerol backbone of the TG is removed and substituted with alcohol (Mogelson, 1984). The resulting ester allows for fractional distillation of the long-chain fatty acids at lower temperatures. At this point, the EPA and DHA can be manipulated to levels greater than those found in the fish (Saghir, 1997). Ethyl esters (EE’s) are uncommon in nature, so are not properly digested and absorbed by the body. The process can be reversed by using food grade enzymes, restoring the product to its rightful TG form with the glycerol backbone. Doing this is not common to the industry because of the cost. The fatty acid-ethanol bond is about fifty times more resistant to digestive enzymes (pancreatic lipase) as compared to the triglyceride form (Yang, 1990) (Yang, 1990). TG fish oil yields fifty percent more plasma EPA/DHA after absorption than the EE form (Beckerman, 1990) (Dyerberg, 2010). Over the long term, however, EE absorption seems to equal out after a few months’ intake (Sadovsky, 2009). It is conjectured that the slower activity of EE fish oil results in sustained inhibition of sodium and calcium channels, helping to prevent arrhythmia (Leaf, 2003) (Lavie, 2009).

There is no discernible health risk to EE fish oil, not even for a person sensitiveto alcohol. There are stories about EE being able to melt polystyrene. Alcoholand water are polar substances, having different electrical charges at oppositeends. They do not react with non-polar materials, such as Styrofoam. So, if you’veever heard that EE fish oil will dissolve a Styrofoam cup, dismiss the thought.When it comes to oxidation, though, EE will oxidize faster than the TG fish oil,making it less reliable (Song, 1997). The TG fish oil is naturally occurringand less likely to go rancid. Doubtless there are myriad studies to support andnegate the efficacy of each form, but if either one lowers your triglyceridelevels, there’s no debate.

References

Ackman RG.
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Bays HE, et al.
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Bays H:
Rationale for prescription omega-3-acid ethyl ester therapy for hypertriglyceridemia: a primer for clinicians.
Drugs Today (Barc). 2008;  44:205-246

Breslow, JL.
Review: n-3 Fatty acids and cardiovascular disease.
Am J Clin Nutr. 2006;  83(s):1477s-82s

Beckermann B, Beneke M, Seitz I.
Comparative bioavailability of eicosapentaenoic acid and docasahexaenoic acid from triglycerides, free fatty acids and ethyl esters in volunteers.
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Best CA, Laposata M.
Fatty acid ethyl esters: toxic non-oxidative metabolites of ethanol and markers of ethanol intake.
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Breslow JL.
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Carlier H., Bernard A, Caseli A.
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J Dyerberg , P Madsen , JM Moller ,I Aardestrup ,EB Schmidt.
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El Boustani S, Colette C, Monnier L, Descomps B, Crastes de Paulet A, Mendy F.
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