OMEGA-3’S Effect On Aging

ageing-manHave you ever stopped to think there might be a difference between aging and getting old? Some ancient texts declare old age a virtue and a blessing, commanding the elderly to be respected for their wisdom, regardless of their scholarship. When your cheese gets old, it’s time to dump it; but when it ages, it reaches perfection, right?  When things get old, they might no longer be useful or in style. Aging is a managed process through which a thing gains value or desirability. Do we perceive ourselves the same way as cheese or steak? The way you live your life as you age just might dictate how others see you. Do you constantly complain about things outside your control, or do you roll with the punches and build on your strengths? You may balk at being reminded by your spouse to write things down. Make yourself look good; write them down. And try not to forget where you put the list.

Is there anything to be done to arrest the process of aging? There are scores of ads in magazines and on the web that proclaim the virtues of this or that herb or secret concoction to inhibit Mother Nature’s treacherous design. The only science that supports many of those claims is ringed by dollar bills. Really now, is there something, anything, that can take thirty years off my wrinkled brow, my flabby arms and other parts, my sagging skin, and shrinking self-concept? Instead of saying “No,” let’s take a look at science.

Inside the nucleus of a cell, our genes sit on double-twisted strands of molecules called chromosomes. At the ends of the chromosomes are protective caps called telomeres, which act just like the little plastic things at the end of your shoelaces (aglets) that keep them from raveling…or unraveling. Telomeres also keep the ends of the chromosomes from sticking to each other, which would not only make a big mess but could also scramble genetic information and cause diseases. But every time a cell divides, its telomeres shorten. After a while the telomeres get too short to duplicate and the cells kick out—they become old or they die. If enough of these die at the same time, so do we.

We’ll try not to get too complicated, but we need to explain that telomeres are sequences of DNA chemical codes that are made from the same stuff as the rest of the chromosomes and genes, called nucleic acid bases, that repeat. A neonatal telomere might have as many as eight thousand bases, about half that at middle age, and only fifteen hundred as an old timer. Each time a cell divides, we lose between 30 and 200 base pairs. Cells normally divide fewer than a hundred times before they die.  Now—pay attention here—there is an enzyme called telomerase that keeps the telomere from shrinking. Short telomeres set the stage for disease (Armanios, 2009) (Shen, 2007) (Serrano, 2004). Remember that. One thing science has yet to determine is whether telomeres start the aging process or are a sign that it has already begun. Still, the major cause of aging is believed to be oxidative stress, the state that results from simple things like breathing and from more complex activities that include infections, inflammation, smoking and booze, and the glycation that accompanies poor dietary choices (which is addressed in the AGE’s newsletter).

A very recent Ohio state study has discovered that omega-3 (n-3) fatty acids might slow aging. This work focused on overweight but healthy middle-aged and older adults who took n-3 supplements for four months and were later found to have altered the ratio of fatty acids in such a way as to preserve tiny segments of DNA in their white blood cells.  Guess what those tiny segments are…Yep, telomeres. Omega-3 supplementation also reduced signs of oxidative stress caused by excessive free radicals in the blood by almost fifteen percent compared to the controls (Kiecolt-Glaser, Sept 2012). The bottom line is that changing the omega-6 to omega-3 ratio from the common 15:1—up to 30:1 in some cases—to the tenable 4:1 is a prudent endeavor. However, don’t hurry to give the n-6’s short shrift. The American Heart Association announced in 2009 that a considerable body of research supports the use of omega-6 fatty acids as a means to reduce the incidence of coronary heart disease (Harris, 2009). Many of us have heard only negative things about omega-6 fats, never learning that they are precursors to many anti-inflammatory metabolites, including prostacyclins (vasodilators) and lipoxins (anti-inflammatory mediators). The findings of Harris and colleagues recommend that n-6 fatty acids make up 5% to 10% of daily energy intake. Given this, the 4:1 ratio of 6’s to 3’s is not so hard to handle (Simopoulos, 2002).

In a five-year study done at San Francisco General Hospital, patients with coronary heart disease, who also took omega-3 fatty acids as EPA and DHA, demonstrated prolonged survival by virtue of extended telomere length, in contrast to those whose telomeres were shortened by the absence or deficiency of omega-3 fatty acids (Farzaneh-Far, 2010). If maintaining telomere length is a positive step in deceleration of aging, we need to examine the elements that influence the opposite. Historical factors cannot be changed: genetics, early insults, prenatal conditions, and the like. But current factors can be altered and their results even reversed with behavioral interventions (Epel, 2012). One recommendation, then, is the faithful intake of n-3 fats, at least as a limiting agent for inflammation that relates to middle-aged torpid lifestyle and weight management (Kiecolt-Glaser, Aug 2010) and at most as an extender of telomere viability.

Telomeres maintain chromosome stability by repeating the sequence of the nucleic acid bases, TTAGGG on one strand of DNA bound to AATCCC on the other strand, where T is thymine, A is adenine, C is cytosine and G is guanine. In studies of human sisters with differing telomere lengths, investigators found that the women with shorter telomeres were at a moderately higher risk for breast cancer at premenopause than their siblings (Shen, 2007). Yes, short telomeres are acquired with aging, and yes, they need more study, and yes, they can mediate the degenerative effects of old age.

Inflammation is not a totally bad thing. Without it, wounds and infections wouldnot heal.  Pro-inflammatory chemicals start the attack against invaders,and then the real healing begins after the inflammation is shut off. The post-inflammatorysubstances clean up the dead and dying tissues and get rid of the inflammatorywaste products (Serhan, 2008) (Schwab, 2007) (Serhan, 2004). Those post-inflammatorymolecules—resolvins and protectins–are provided courtesy of n-3 fatty acids,and have proven themselves functional in telomere protection.


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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.

Flaxseed, Exercise and Your Heart

flax-seed-oilThe heart is a muscle, the most important one on the list. Legs that hurt from pedaling a bike all over the county or biceps that burn from curls are little more than an annoyance. A heart that hurts can mean something more. If you happen to be a cyclist, the odds are in your favor that your heart won’t hurt. If you think about cycling or other laborious exercise without actually doing it, well, that’s a different story. One of the more common bad habits we have is that we don’t pay attention to things until they make funny noises, smell like a bad catalytic converter, quit giving off light, or stop altogether. When the heart makes odd sounds or threatens to quit, “shoulda, woulda, coulda” enters the mind. Exercise undoubtedly has a profound effect on cardiac health… and the rest of the body, too, for that matter. Suppose you could boost the impact of regular exercise on cardiovascular wellness just by adding flaxseeds to your diet. This uncomplicated act offers a host of reward.

Most of us already know about flaxseed oil, a remarkable anti-inflammatory material in its own right, but with a different profile from the seeds. The oil contains the alpha-linolenic acid (ALA) component of flaxseeds without the fiber or lignan components. Therefore, the oil may demonstrate the lipid-lowering properties of the plant without the laxative or anti-cancer character. Oils high in essential fats are not good for cooking, by the way, mostly because they’ll oxidize and become degraded by the high heat. Flax oil that is extracted with heat shortchanges the consumer with a product that is virtually useless and mostly rancid. It can be added to foods after cooking, just before hitting the table. Back to the seeds…

Recent discovery using laboratory animals indicates that the constituents of flaxseeds—ALA, lignans and fiber—add a dramatic benefit to exercise when looking at cardiac markers, lipid profiles and markers of inflammation. With the first group of test animals serving as the control, the second having induced heart attack symptoms, the third having symptoms but provided with flaxseed supplementation, and the fourth like the third but with exercise included, forty lab rats were gathered for the study. Flaxseed supplementation combined with exercise produced a significant rise in HDL and an elevation of the enzyme called PON1, which is a major anti-atherosclerosis and anti-oxidant component of HDL. Simultaneously, measures of infarction—troponin and TNF-alpha—decreased, leading the scientists to infer the protective characteristic of flaxseed combined with muscular exercise against the harmful effects of ischemic heart disease (Nounou, 2012).

Canadian investigators explored the properties of flaxseed components and their influence on cardiovascular health, finding that flax lignans, especially one called secoisolariciresinol, play a significant protective role in cardiovascular disease, particularly against ischemic events (Prasad, 2009). In the last century, consideration was given to flaxseed’s influence on hypercholesterolemia and concomitant atherosclerosis, noting that flaxseeds containing 51%-55% alpha-linolenic acid (ALA—an omega-3 fatty acid) and plant lignans could reduce hypercholesterolemic atherosclerosis by as much as 46% without lowering serum lipids. But the more interesting notation was that flaxseed with a lower level of ALA—only 2%-3%–had the same effect (Prasad, 1998), leading these researchers to conclude that the lignans rather than the omega-3 fats were responsible for the result. Recall that no lignans are found in flaxseed oil unless they are replaced after extraction. Since the early 2000’s, flaxseed has earned the moniker “functional food” (Bloedon, 2004).

Ventricular fibrillation is a severely abnormal heart rhythm that can be life threatening if heartbeat is interrupted for only a few seconds. Though not entirely definitive, some evidence presents flaxseed as able to improve vascular relaxation and inhibit the incidence of ventricular fibrillation (Bassett, 2009), while working in the wings to reduce after-meal glucose absorption and to lower markers of inflammation (Bloedon, 2004). The mechanism behind flaxseed’s heroic reputation involves synergies that are under analysis, including the modulation of cardiac ion channels, attenuation of triglyceride levels, cell signaling, anti-thrombosis activity and anti-arrhythmic effect (Adkins, 2010). In rabbits, animals whose cardiovascular systems parallel humans’, ventricular fibrillation that occurred during induced ischemia was halted and reperfusion injury was attenuated (Ander, 2004).

Concern about plant lignans and hormone-related cancers may not be well-founded, as discovered in two cohort studies that examined the association (Pinder, 2002) (Keinan-Boker, 2004). Here it was intimated that no association of plant lignans to breast cancer exists in premenopausal women (Touillaud, 2006). In fact, high lignan intake may create a 15% decrease in breast cancer risk in postmenopausal women (Velentzis, 2009). Even with prostate disease there is no significant association of phytoestrogens with cancer (Strom, 1999) (Hedelin, 2006) (Travis, 2009). In fact, dietary lignans may lower risk for prostate cancer (Heald, 2007).

Since most of us have taken increased responsibility for our health, it’s likely that we participate in some kind of exercise. Walking counts, but not to the refrigerator to get a pint of Ben and Jerry’s. Adding flaxseeds to the diet isn’t that hard. You can use 3 tablespoons of flax meal to replace 1 tablespoon of fat in a recipe. You could replace one egg with 1 tblspn of flax plus 3 tblspn of water. (Don’t even think about doing this for breakfast. It just ain’t the same, bacon or not.) You could mix it into a meatloaf, stir it into soups or smoothies, throw it onto your oatmeal, or mix it with sugar and cinnamon as a substitute dessert topping. But it has to be ground to work. Whole flaxseeds will pass right through the digestive system, taking all the benefits along with it.


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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.

Methylation And Age: How Old Are You, Really?

innocence-and-experienceHave you noticed that medicine is called a practice? Maybe that’s because everybody isn’t the same. What works for you possibly won’t work for your neighbor, despite that the same doctor prescribes the same medicines for the same reason in the same doses for both of you. The age of individualized medicine is upon us, a time when what goes into your body, whether food or medication or supplement, will be geared toward your individuality. One size will not fit all. This makes sense—finally, as it becomes increasingly evident that our bodies don’t do things at the same rate…like age. Some of us age gracefully; others just get old. Aging can be managed. Getting old can strike out of nowhere, but some scientists think it’s controllable. Attitude matters.

Biologically, our clocks tick at a different rhythm. Once in a while a 70-year-old looks 50; often it’s the reverse. Science has tried to identify markers that quantify the actual rate of aging. First, it looked at telomeres, those aglet-like caps at the ends of chromosomes that shorten with age. (Aglets are the plastic sheaths at the ends of shoelaces that keep them from raveling.)  Telomeres might be part of the picture, but are not the sole influence on aging. DNA methylation is now a target of exploration, where researchers are examining the methylome, the whole set of methylation markers across the genome that almost predictably changes over time. This inquiry is expected to determine a person’s biological age from a single drop of blood. A methylation site gets fuzzier as people age, and the differences between the young and the old become more clearly defined.

Much of what extended life writers and websites would have us believe is bogus. If not backed by hard science, discount most of what you read.  On the other hand, the measurement of human age from recognized molecular profiles has merit, especially in preventing and treating disease and possibly even in the extension of human life. The process of methylation can be inhibited or hastened, depending on what we do and what we swallow.

What is methylation?

Methylation is a biological process in which a methyl group (CH3) is added to one of the amino acids in DNA. The result can suppress harmful activity and help to ensure proper DNA replication by replacing a single hydrogen atom with the whole group. Abnormalities in this process are linked to genetic defects. If it happens to a gene that controls cell division, for example, cell division may be uncontrolled and result in cancer. Methylation is typically brought about by vitamin B12-dependent enzymes, such as methionine synthase, which uses methylcobalamin as a co-factor to turn homocysteine back into methionine and to prevent some forms of anemia. Recently, researchers at the U of CA, San Diego School of Medicine measured more than 485,000 genome-wide markers of methylation in the blood of 656 people, aged from 19 to 101, noting that the process weakens with age, and that different organs within the same body methylate at different rates and efficacies (Hannum, 2012).  The hypomethylation of old age is far separated from the normal methylation of neonates and teenagers. This phenomenon can be seen in a parallel comparison of like sectors of the genome Heyna, 2012). The implications are that lifestyle modifications can prolong the methylation ability of the genome, thus promoting longevity and health.


This is the stuff that determines the makeup of all living cells. It consists of two long strands of compounds that are the building blocks of the nucleic acids that eventually control cellular function and heredity. The two strands coil around each other in what is called a double helix, which is a spiral that resembles that of a school notebook. Imagine a pencil inserted into the notebook’s spiral backbone. That pencil represents a material called histone, which forms a spool around which the DNA can wrap itself. It sort of helps to keep the spirals from getting kinked, like what happened to the old slinky you had to throw away. Histones are important because they keep the DNA under control by compacting it. Otherwise, the strand would be about six feet long. It’s tantamount to the modern telephone cords that coil to save space on the floor. Old-fashioned cords were straight, uncoiled wires that always got in the way of whatever you wanted to do. Methylation keeps histones in good shape. It is felt that histones influence the signaling pathways that may extend longevity (Han, 2012). If so, the inference is simple—keep histones well, live longer, or at least live healthier.

How Do I Do This?

The answer is too simple to ignore, but often is. For some obscure reason, humans look for the complicated way of doing things. Diet is an important element of genome methylation; maybe even paramount in the support of the process. Practically nothing is easier to implement, but keep in mind that all food is not created equal. Grass-fed meat, for example, is lower in total fat than grain-fed. A sirloin from a grass-fed steer has about half the fat of a grain-fed steer. It also contains conjugated linoleic acid, an omega-3 fat found in the chloroplasts of grass that may play a role in weight management (Whigham, 2007) and protect against some cancers (Ip, Aug, 1994) (Ip, Mar, 1994). Pastured hens lay eggs with goodly amounts of n-3 fats in contrast to factory-raised. Simply, the vitamin B12 from animal products supplies a methyl molecule.

Eating raw nuts and seeds gets you about 6 grams of protein an ounce, plus the polyunsaturated fats you need to fight inflammation and to prevent cardiovascular issues. Adding green leafy vegetables and legumes supplies additional folate, which is a noteworthy methyl donor. Supplementation with B12 and folinic acid or methyltetrahydrofolate is not out of place, and is a prudent move if one’s diet is less than wholesome. The promise of long-term health, well-being and extended life might be more real than we imagined. And it requires little effort.


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NIH Publication No. 07–0882
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Lyn Patrick, ND
Gastroesophageal Reflux Disease (GERD): A Review of Conventional and Alternative

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Quitadamo P, Buonavolontà R, Miele E, Masi P, Coccorullo P, Staiano A.
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Semeniuk J, Kaczmarski M.
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Adv Med Sci. 2006;51:321-6.

Sontag SJ.
The medical management of reflux esophagitis. Role of antacids and acid inhibition.
Gastroenterol Clin North Am. 1990 Sep;19(3):683-712.

van der Pol R, Smite M, Benninga MA, van Wijk MP.
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J Pediatr Gastroenterol Nutr. 2011 Dec;53 Suppl 2:S6-8.

van Marle J, Aarsen PN, Lind A, van Weeren-Kramer J.
Deglycyrrhizinised liquorice (DGL) and the renewal of rat stomach epithelium.
Eur J Pharmacol. 1981 Jun 19;72(2-3):219-25.

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Efficacy of the drinking magnesium-calcium sulfate mineral water in the combined treatment of duodenal ulcer comorbid with gastroesophageal reflux.      
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WebMD Health News. Dec. 22, 2011
Study: Acid Reflux on the Rise
Obesity Increase Likely to Blame, Researchers Say
Salynn Boyles;  Reviewed by Louise Chang, MD

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Dig Dis Sci. 1988 Sep;33(9):1127-33.

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

Hypertension and The Kidneys

HypertensionFor their size, the kidneys do an awful lot of work. Besides filtering the blood of potentially harmful substances, they secrete hormones that influence the manufacture of red blood cells and the absorption and metabolism of calcium. Another job is to monitor blood pressure and to take corrective action if it drops. The kidney does this by secreting a proteolytic enzyme called renin (not to be confused with rennin, the bovine enzyme that curdles milk and is used to make cheeses and junkets), whose function is to control another hormone, angiotensin, the polypeptide that constricts blood vessels. Angiotensin, especially angiotensin 2, is occasionally the target of blood pressure medications. This compound constricts the walls of arterioles and closes capillary beds, causing the kidney to reabsorb sodium while stimulating the adrenal cortex to release aldosterone, itself encouraging the kidney to reclaim still more sodium and, therefore, water. To add to this complicated cycle, angiotensin 2 prompts the pituitary to secrete vasopressin, yet another hormone that constricts blood vessels and elevates blood pressure, but also reduces excretion of urine by causing the kidney to reabsorb water. Because of this activity, vasopressin is also known as antidiuretic hormone, which conserves water stores in times of dehydration. All this spirited activity is directed by the brain.

We all realize that blood pressure (BP) involves the heart. In response to elevated BP, the heart releases two natriuretic peptides, type A and type B. (natri from ‘sodium’ and uretic from urine). These hormones relax the arterioles, inhibit the secretion of renin and aldosterone, and constrain the reabsorption of sodium ions by the kidney. This reduces reabsorption of water, so the volume of urine increases along with the volume of sodium in it. The net effect is to lower BP by reducing the volume of blood in the circulatory system. Whew! If ever you have heard the expression from Psalm 139:14 that mentions man being fearfully and wonderfully made, you now know what it means.

High blood pressure, usually anything above 140/90, can be caused by a number of things, including overweight, race, age, diet and exercise, family history, smoking, alcohol and stress levels. Healthy lifestyle can help. If there is such a thing as a worldwide hypertension epidemic, it may now be addressed by tackling a newfound cellular source in the brain, the targeting of which can reverse the condition. It has been found that angiotensin 2 is causative of hypertension because of the dysregulation of certain brain mechanisms involving the endoplasmic reticulum (Young, 2012).

The Endo What?
The endoplasmic reticulum is common to all eukaryotic cells—those that have a membrane-bound nucleus, genetic material organized within chromosomes, and organelles, such as mitochondria, chloroplasts…and endoplasmic reticula (ER). The ER is a network of membranes important to protein synthesis and folding, and it helps in the transport of cellular materials. The actual job of the ER varies from cell type to cell type, and occasionally within the same cell, depending on whether it is smooth or rough. The smooth ER is shaped like a tube and synthesizes phospholipids, which are the chief constituents of cell membranes. It also breaks down toxins in the liver, helps to regulate calcium concentrations, and controls the metabolism of carbohydrates. The rough ER is a line of flattened sacs with little bumps called ribosomes on the outside. This is where serum proteins, such as albumin, are synthesized.

Back To BP
Researchers have recently found that a water-soluble (hydrophilic) bile acid called tauroursodeoxycholic acid (TUDCA) reduces stress to the endoplasmic reticulum, which acts as a stress manager for every cell. If something goes wrong in a cell, the ER starts processes that help adapt to the stressors, angiotensin 2 among them. Because different ER’s do different jobs, only those that orchestrate the cascade of events causing hypertension are influenced by TUDCA. These are located outside the blood-brain barrier, near the bottom, allowing them to be affected by substances that are too large to cross the barrier, such as certain medications. Nonetheless, these ER’s are able to communicate with the brain’s inner chambers. TUDCA may then be able to treat the stress on hypertension-related endoplasmic reticula that control the release of angiotensin 2 (Young, 2012).

Chronic metabolic disorders, such as obesity, diabetes and insulin resistance are also mediated by the ER’s failure or success in launching an adequate stress defense.  Insulin resistance associated with the production of inflammatory factors, both related to fat cells, can activate the ER stress pathway. Research at the Hallet Diabetes Center of Brown University discovered that TUDCA reduces inflammatory signaling and thus may attenuate the ER stressors that trigger blood pressure elevation (Jiao, 2011). Additional study of intracellular regulatory proteins found that regular treatment with TUDCA lowers systolic blood pressure while lessening glucose intolerance (Ceylan-Isik, 2011).

Overactivity of the renin-angiotensin system, for which the kidneys are partly responsible, leads to the vasoconstriction that characterizes hypertension. It is easier to control angiotensin than renin, so angiotensin-related drugs are used, such as ACE inhibitors or angiotensin-receptor blockers (ARBs). It is renin that converts angiotensin. Renin blockers demonstrate poor bioavailability, so are rarely used. To avoid the side effects that accompany drugs, sodium reduction is the first step of a natural protocol in giving the kidneys a break and reducing BP. Following the DASH diet (Dietary Approaches to Stop Hypertension) is not a difficult strategy (Sacks, 2001) (Svetkey, 1999). Water will clear wastes from the kidneys, acidulation being recommended. Increase vegetable intake while reducing meat, especially red. Fill half the plate or more with produce. To bless the kidneys and to control BP add omega-3 fatty acids to the daily regimen (Friedman, 2010) (Cabo 2012) (Mori, 2010). If urine is any darker than a manila folder, drink more water.


Amin A, Choi SK, Galan M, Kassan M, Partyka M, Kadowitz P, Henrion D, Trebak M, Belmadani S, Matrougui K.
Chronic inhibition of endoplasmic reticulum stress and inflammation prevents ischaemia-induced vascular pathology in type II diabetic mice.
J Pathol. 2012 Jun;227(2):165-74.

Aneja A, El-Atat F, McFarlane SI, Sowers JR.
Hypertension and obesity.
Recent Prog Horm Res. 2004;59:169-205.

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

Ceylan-Isik AF, Sreejayan N, Ren J.
Endoplasmic reticulum chaperon tauroursodeoxycholic acid alleviates obesity-induced myocardial contractile dysfunction.
J Mol Cell Cardiol. 2011 Jan;50(1):107-16.

Colin N. Young, Xian Cao, Mallikarjuna R. Guruju, Joseph P. Pierce, Donald A. Morgan, Gang Wang, Costantino Iadecola, Allyn L. Mark, Robin L. Davisson
ER stress in the brain subfornical organ mediates angiotensin-dependent hypertension
J Clin Inv. November 1, 2012; Volume 122, issue 11: 3960

Esler M, Jennings G, Biviano B, Lambert G, Hasking G.
Mechanism of elevated plasma noradrenaline in the course of essential hypertension.
J Cardiovasc Pharmacol. 1986;8 Suppl 5:S39-43.

Esler M.
High blood pressure management: potential benefits of I1 agents.
J Hypertens Suppl. 1998 Aug;16(3):S19-24.

Esler M, Kaye D.
Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease.
J Cardiovasc Pharmacol. 2000;35(7 Suppl 4):S1-7.

Friedman AN.
Omega-3 fatty acid supplementation in advanced kidney disease.
Semin Dial. 2010 Jul-Aug;23(4):396-400.

Hall JE, Brands MW, Henegar JR.
Mechanisms of hypertension and kidney disease in obesity.
Ann N Y Acad Sci. 1999 Nov 18;892:91-107.

Hall JE.
The kidney, hypertension, and obesity.
Hypertension. 2003 Mar;41(3 Pt 2):625-33.

Hotamisligil GS.
Endoplasmic reticulum stress and the inflammatory basis of metabolic disease.
Cell. 2010 Mar 19;140(6):900-17. doi: 10.1016/j.cell.2010.02.034.

Jiao P, Ma J, Feng B, Zhang H, Diehl JA, Chin YE, Yan W, Xu H.
FFA-induced adipocyte inflammation and insulin resistance: involvement of ER stress and IKKβ pathways.
Obesity (Silver Spring). 2011 Mar;19(3):483-91.

Koji Sakai, Khristofor Agassandian, Satoshi Morimoto, Puspha Sinnayah, Martin D. Cassell, Robin L. Davisson, and Curt D. Sigmund
Local production of angiotensin II in the subfornical organ causes elevated drinking
J Clin Invest. 2007 April 2; 117(4): 1088–1095.

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

Ozcan L, Ergin AS, Lu A, Chung J, Sarkar S, Nie D, Myers MG Jr, Ozcan U.
Endoplasmic reticulum stress plays a central role in development of leptin resistance.
Cell Metab. 2009 Jan 7;9(1):35-51.

Purkayastha S, Zhang H, Zhang G, Ahmed Z, Wang Y, Cai D.
Neural dysregulation of peripheral insulin action and blood pressure by brain endoplasmic reticulum stress.
Proc Natl Acad Sci U S A. 2011 Feb 15;108(7):2939-44.
Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER 3rd, Simons-Morton DG, Karanja N, Lin PH; DASH-Sodium Collaborative Research Group.

Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group.
N Engl J Med. 2001 Jan 4;344(1):3-10.

Schulman IH, Zhou MS, Raij L.
Interaction between nitric oxide and angiotensin II in the endothelium: role in atherosclerosis and hypertension.
J Hypertens Suppl. 2006 Mar;24(1):S45-50.

Svetkey LP, Simons-Morton D, Vollmer WM, Appel LJ, Conlin PR, Ryan DH, Ard J, Kennedy BM.
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Wilcox CS.
Oxidative stress and nitric oxide deficiency in the kidney: a critical link to hypertension?
Am J Physiol Regul Integr Comp Physiol. 2005 Oct;289(4):R913-35.

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

You Expect Me To Believe That?

fishoil-hookSome things just belong together. Not too many of us eat only the meringue from the lemon pie. Sauerkraut on a bun without the sausage isn’t quite the same gustatory delight. And sometimes the aunt is more fun when in the company of the uncle. Such is the case with essential fatty acids. The omega-3’s can do their job without the omega-6’s, but the outcome will eventually be out of whack. It’s this imbalance that wrought the nefarious genius of a twisted, fear-huckstering fish oil report, so carefully crafted that the typical reader comes to believe that black is white.

The study reported in the Journal of the National Cancer Institute determined a positive relationship of non-vegetable sourced omega-3 fatty acids to prostate cancer. If non-vegetable, that leaves fish oil, known better for its downstream n-3 fats, EPA and DHA, than for the mother n-3, alpha-linolenic acid. The concern with this proposition is that the authors seem to have gone from home plate to home plate, in a 360-foot path without ever touching any of the bases. Healthy incredulity befits the reading of a ‘scientific’ paper. That leaves questions that most of us don’t ponder, including these:  Why would anyone take n-3 fats without also taking n-6 complements? Did any of the subjects bear a pre-existing pathology? Were the supplements, if used, of sufficiently high quality, as you would expect from a cGMP-obligated company? (The term “pharmaceutical grade” means only that toxins have been removed, and is otherwise unregulated, since many products that call themselves fish oil are not oils but ethyl esters instead of triglycerides.) Is it possible that individuals were removed from the study because they got healthy all of a sudden? Not to be too picky, but what were the capsules themselves made from, if supplements are to blame? Could the supplements have been combined with active pharmaceuticals or with contraindicated other supplements? Not finally, but at least additionally, why is it so that countries whose cuisine is dominated by fish—Scandinavia or Japan—do not also present a high level of prostate cancer? Funny thing:  this study failed to tell us where the men in this investigation got their omega-3 fats. The dollar store? Canned tuna? Maybe from the fish they ate an hour prior to the blood draw?

The Public Library of Science has a journal called PLoS One. It covers primary research in science and medicine, submissions of which are subjected to intense scrutiny and peer review. However, the Journal does invite post-publication discussion and critique. In its April, 2013 issue, it printed an Icelandic study on consumption of fish products and the risk of prostate cancer. There were almost 2300 men, aged 67 and up, in this four-year project. Except for processed fish that was salted or smoked, fish oil or very high fish consumption was determined not to be associated with early or midlife prostate cancer risk (Torfadottir, 2013). Hmm. Go figure. Earlier Canadian meta-analysis discovered a 63% reduction in prostate-cancer-specific mortality among fish eaters, but no incipient protective effect by fish ingestion (Szymanski, 2010). That means eating fish did not prevent disease. There are other causes, such as too much conventionally raised red meat.

There is a strong suggestion in a Harvard study that total fat and certain saturated fatty acids may be implicated in prostate disease incidence, but that, “Among all men, those with the highest omega-3 docosahexaenoic acid and total marine fatty acid intakes were 40% less likely to die from prostate cancer,” adding that “…high marine omega-3 fatty acid intake may improve disease-specific survival for all men” (Epstein, 2012). Although the source of DHA is not identified in the study in question, an Italian work cited the 22:6 n-3 as protective against physiological activities involved in the progression of prostate cancer cells (Bianchini, 2012).  Marshall University mice that were fed a high n-3 diet containing fish oil concentrate presented with a decreased expression of genes expected to increase proliferation of prostate cancer cells by virtue of lowering estradiol values (Akinsete, 2012).

What about the n-6 to n-3 ratio we mentioned earlier?  Glad you asked. In no particular order, try reading these authors  to get the picture that n-3 fats need the accompaniment of the n-6 fats: (vanJaarsveld, 1997) (Ramirez0Silve, 2011) (Caramia, 2008) (Wijendran, 2004) (Simopoulos, 2002, 2008) (Gomez, 2011) (Yehuda, 1993, 1996). The additional info you need to find these is at the end of this piece. The ideal omega-6 to omega-3 ratio is generally agreed to be 4 to 1. That’s four times the omega-6 as omega-3. How come?  The enzymes that desaturate and elongate fatty acids prefer to work along the n-3 pathway, and by the time they get to the n-6 fats, part of the n-6’s have been burned for energy. Also, the enzyme pathway could be interrupted by age, booze, trans-fats, disease and overdose of dietary cholesterol (which is a good thing that can be overdone).

If fish oil is held culpable, which form?  The ethyl ester form (EE) is made when the glycerol backbone of fish body oil is removed during molecular distillation and replaced by an ethanol, allowing the process to be completed at a lower temperature. It isn’t a fat any more, and really shouldn’t be allowed to be called an oil. This is now an ester that is not digested and absorbed by the body in the same manner as the original triglyceride. Once distilled, true fish oil has its triglyceride put back in a process called re-esterification, or re-concentration, a procedure that adds about 40% to the cost of the finished product. But this replacement of the glycerol—fish oil is a triglyceride—returns the substance to its natural state. Fish oil that has an alcohol head is metabolized just like an alcohol from liquor, and that’s not what we expect from a supplement that’s supposed to be a boon to health. Bioavailability of re-esterified triglycerides is superior to all other forms of fish oil (Dyerberg, 2010).

The study in question (Brasky, 2013) is of an observational nature, not experimental, such as a randomized, controlled, double-blinded trial would be.  Observational studies are not used as reliable sources, though they can help to formulate hypotheses to be used in subsequent experiments (Nahin, 2012). Additionally, cause-effect has not been established. The paper was quick to point the finger at a dietary supplement. True, many supplements are misused for lack of direction by a qualified health care practitioner, such as a dietitian or clinical nutritionist. But that can be resolved with a phone call and an appointment. Mega-doses of fish oil do not mix well with drugs or supplements that thin the blood. If a person doesn’t know that, he needs to. Though there is no established upper limit for fish oil, six grams might be too much, while two or three grams might just be on the mark for most adults. Actual dosage depends on the fish species and the levels of EPA and DHA in the product.

To balance the omega-3 fatty acids, evening primrose oil (EPO) is a good source of omega-6 fats, particularly of gamma-linolenic acid (GLA), which is the preferred launching point for conversion to the longer derivatives. Yes, borage oil has more GLA than EPO, but also contains alkaloids that can tax the liver.

An interesting comment from the University of Guelph in Ontario, Canada is, “I have no idea how this paper got accepted for publication.”  (Professor Gopinadhan Paliyath)



Akinsete JA, Ion G, Witte TR, Hardman WE.
Consumption of high ω-3 fatty acid diet suppressed prostate tumorigenesis in C3(1) Tag mice.
Carcinogenesis. 2012 Jan;33(1):140-8.

Astorg P.
Dietary N-6 and N-3 polyunsaturated fatty acids and prostate cancer risk: a review of epidemiological and experimental evidence.
Cancer Causes Control. 2004 May;15(4):367-86.

Beckermann B, Beneke M, Seitz I.
Comparative bioavailability of eicosapentaenoic acid and docasahexaenoic acid from triglycerides, free fatty acids and ethyl esters in volunteers.
Arzneimittelforschung. 1990 Jun;40(6):700-4.

Bianchini F, Giannoni E, Serni S, Chiarugi P, Calorini L.
22 : 6n-3 DHA inhibits differentiation of prostate fibroblasts into myofibroblasts and tumorigenesis.
Br J Nutr. 2012 Dec 28;108(12):2129-37

Brasky TM, Crowe FL, Kristal AR.
n-3 Fatty acids and prostate cancer risk.
Br J Nutr. 2012 Nov 14;108(9):1721.

Theodore M. Brasky, Amy K. Darke, Xiaoling Song, Catherine M. Tangen, Phyllis J. Goodman, et al
Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial
JNCI J Natl Cancer Inst (2013) doi: 10.1093/jnci/djt174 First published online: July 10, 2013

Caramia G.
The essential fatty acids omega-6 and omega-3: from their discovery to their use in therapy
Minerva Pediatr. 2008 Apr;60(2):219-33.

Chua ME, Sio MC, Sorongon MC, Morales ML Jr.
The relevance of serum levels of long chain omega-3 polyunsaturated fatty acids and prostate cancer risk: A meta-analysis.
Can Urol Assoc J. 2013 May;7(5-6):E333-43.

Dyerberg J, Madsen P, Møller JM, Aardestrup I, Schmidt EB.
Bioavailability of marine n-3 fatty acid formulations.
Prostaglandins Leukot Essent Fatty Acids. 2010 Sep;83(3):137-41.

Epstein MM, Kasperzyk JL, Mucci LA, Giovannucci E, Price A, Wolk A, Håkansson N, Fall K, Andersson SO, Andrén O
Dietary fatty acid intake and prostate cancer survival in Örebro County, Sweden.
Am J Epidemiol. 2012 Aug 1;176(3):240-52.

Fradet V, Cheng I, Casey G, Witte JS.
Dietary omega-3 fatty acids, cyclooxygenase-2 genetic variation, and aggressive prostate cancer risk.
Clin Cancer Res. 2009 Apr 1;15(7):2559-66.

Edward Giovannucci, Eric B. Rimm, Graham A. Colditz, Meir J. Stampfer, Alberto Ascherio,
Chris C. Chute and Walter C. Willett
A Prospective Study of Dietary Fat and Risk of Prostate Cancer
JNCI J Natl Cancer Inst. Volume 85, Issue 19; Pp. 1571-1579.

C. Gómez Candela, L. M.ª Bermejo López and V. Loria Kohen
Importance of a balanced omega 6/omega 3 ratio for the maintenance
of health. Nutritional recommendations

Nutr Hosp. 2011;26(2):323-329.

Richard Nahin, PhD, MPH
Observational Studies and Secondary Data Analyses to Assess Outcomes in Complementary and Integrative Health Care
NCCAM Research Blog. 25 June, 2012

Neubronner J, Schuchardt JP, Kressel G, Merkel M, von Schacky C, Hahn A.
Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters.
Eur J Clin Nutr. 2011 Feb;65(2):247-54.

Pettersson A, Kasperzyk JL, Kenfield SA, Richman EL, Chan JM, Willett WC, Stampfer MJ, Mucci LA, Giovannucci EL.
Milk and dairy consumption among men with prostate cancer and risk of metastases and prostate cancer death.
Cancer Epidemiol Biomarkers Prev. 2012 Mar;21(3):428-36.

Ivonne Ramírez-Silva, Salvador Villalpando, Jessica E Moreno-Saracho and Daniel Bernal-Medina
Fatty acids intake in the Mexican population. Results of the National Nutrition Survey 2006
Nutrition & Metabolism 2011, 8:33

Reese AC, Fradet V, Witte JS.
Omega-3 fatty acids, genetic variants in COX-2 and prostate cancer.
J Nutrigenet Nutrigenomics. 2009;2(3):149-58.

Schuchardt JP, Neubronner J, Kressel G, Merkel M, von Schacky C, Hahn A.
Moderate doses of EPA and DHA from re-esterified triacylglycerols but not from ethyl-esters lower fasting serum triacylglycerols in statin-treated dyslipidemic subjects: Results from a six month randomized controlled trial.
Prostaglandins Leukot Essent Fatty Acids. 2011 Dec;85(6):381-6.

Simopoulos AP.
The importance of the ratio of omega-6/omega-3 essential fatty acids.
Biomed Pharmacother. 2002 Oct;56(8):365-79.

Artemis P. Simopoulos
The Importance of the Omega-6/Omega-3 Fatty Acid Ratio in Cardiovascular Disease and Other Chronic Diseases
Experimental Biology and Medicine  233:674-688 (2008)

Sorongon-Legaspi MK, Chua M, Sio MC, Morales M Jr.
Blood level omega-3 Fatty acids as risk determinant molecular biomarker for prostate cancer.
Prostate Cancer. 2013;2013:875615.

Szymanski KM, Wheeler DC, Mucci LA.
Fish consumption and prostate cancer risk: a review and meta-analysis.
Am J Clin Nutr. 2010 Nov;92(5):1223-33.

Torfadottir JE, Steingrimsdottir L, Mucci L, Aspelund T, Kasperzyk JL, Olafsson O, Fall K, et al
Milk intake in early life and risk of advanced prostate cancer.
Am J Epidemiol. 2012 Jan 15;175(2):144-53. .

Torfadottir JE, Valdimarsdottir UA, Mucci L, Stampfer M, Kasperzyk JL, Fall K, Tryggvadottir L et al
Rye bread consumption in early life and reduced risk of advanced prostate cancer.
Cancer Causes Control. 2012 Jun;23(6):941-50.

Torfadottir JE, Valdimarsdottir UA, Mucci LA, Kasperzyk JL, Fall K, Tryggvadottir L, et al
Consumption of fish products across the lifespan and prostate cancer risk.
PLoS One. 2013 Apr 17;8(4):e59799.

P.J. van Jaarsveld, C.M. Smuts, H.Y. Tichelaar, M. Kruger, C.J. Lombard, A.J.S. Benadé
The influence of different ratios and dosages of an ω6:ω3 fatty acid supplement on the lipoprotein cholesterol and fatty acid profile in nonhuman primates on a western atherogenic diet
Nutrition Research. 17(11-12); Nov-Dec 1997: 1733-1747

Vasuki Wijendran and K.C. Hayes
Annual Review of Nutrition. July 2004; 24: 597-615

Yehuda S, Carasso RL.
Modulation of learning, pain thresholds, and thermoregulation in the rat by preparations of free purified alpha-linolenic and linoleic acids: determination of the optimal omega 3-to-omega 6 ratio.
Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10345-9.

Yehuda S, Brandys Y, Blumenfeld A, Mostofsky DI.
Essential fatty acid preparation reduces cholesterol and fatty acids in rat cortex.
Int J Neurosci. 1996 Sep;86(3-4):249-56.

Yehuda S, Rabinovtz S, Carasso RL, Mostofsky DI.
Essential fatty acids preparation (SR-3) improves Alzheimer’s patients quality of life.
Int J Neurosci. 1996 Nov;87(3-4):141-9.

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

Phosphatidylcholine And Memory: Aw, Forget It. Oh, You Already Did.

Forgetful-manIn his 1932 inaugural address, FDR told the world that we have nothing to fear but fear itself. If you ask people today what they fear, the list will likely include more specific things, like public speaking, ostracism, blindness, death, poverty, failure, memory loss, disease and a host of other states, conditions or activities. Some fears can be overcome with counseling, such as acrophobia; some can be prevented by being active instead of passive, such as poverty and failure; and some might require nutritional or medical intervention, such as certain diseases. Getting and using education, which doesn’t necessarily entail sitting in a classroom, might possibly attend to these needs. A modern-day fear is that of Alzheimer’s disease (AD), one that people associate with memory dysfunction, disorientation, and eventual loss of function. It’s a matter of not knowing that you don’t know. And it’s frightening.

The loss of cognitive ability takes a while to manifest, maybe ten to fifteen years, and is associated with the development of abnormal tissues and protein deposits in the brain’s cerebral cortex, which is the outermost layer of gray matter responsible for higher brain functions, such as sensation, voluntary muscle movement, thought, reasoning and memory. The primary neurotransmitter involved with the latter three of these cerebral obligations is acetylcholine, which is released at the ends of nerve fibers to send nerve impulses from one cell to another. Other jobs of this neurotransmitter involve decreasing heart rate and contraction strength, dilating blood vessels, increasing peristalsis, and raising elimination pressure during urination.

The dementia we fear results in deterioration of mental faculties, causing apathy, confusion and occasional stupor. A couple centuries ago it was synonymous with insanity, and was termed dementia praecox, now known as schizophrenia. Of its several forms, senile dementia is the one most commonly recognized, usually occurring after age 65, though it can happen earlier.

Natural deficits of acetylcholine accompany the aging process, causing those sporadic lapses in short-term memory that many individuals experience from time to time. Called benign forgetfulness, this non-debilitating memory decline is not to be confused with Alzheimer’s disease. It’s the degeneration of neurons in the cerebral cortex that leads to difficulties with language and judgment in AD. From the cortex, degeneration proceeds to the hippocampus, which is the part of the limbic system that deals with memory and spatial navigation. The hippocampus helps us to retain facts that pertain to specific events so they can be regurgitated if needed, but it also helps to order the chronology of one’s lifetime events. All this is what we typically call recollection. Memory tasks usually excite considerable hippocampus engagement, but that response is substantially weakened by advancing age, particularly in the absence of nutrients that feed the process. In transient global amnesia, a state induced by statin drugs’ cholesterol reduction and subsequent interference with the body’s manufacture and use of co-enzyme Q10, hippocampus activity is seriously constrained, though reversible by judicious supplementation of the enzyme.

Late in the last century, scientists demonstrated interest in the enhancement of memory in lab animals by introducing the phospholipid called phosphatidylcholine (PC) to their diets. “Demented” mice showed very low levels of choline and acetylcholine. After adding PC to the rations of the experimental group, the examiners saw an expected reversal in choline and acetylcholine levels, and an improvement in memory (Chung, 1995). Yes, mice are not the same as people, but they share a commonality in cerebral function, providing a good model for this scrutiny of memory acquisition and retention (Moriyama, 1996).

PC not only increases neurotransmitter efficiency, but also improves the supportive nature of polyunsaturated fatty acids (PUFA’s) in the revival of cell membrane fluidity. Since PC is the major structural and functional component of the cell membrane, this is not small news. Its reinstatement to a place of high stature in membrane architecture helps to sequester renegade substances that inhibit the membrane’s full capabilities in directing the machinery of life (Hiratsuke, 2009) (Gong, 2004).

After it was found that Alzheimer’s disease is related to abnormal metabolism of membrane phospholipids, researchers began to examine faulty homeostasis for discovery of diagnostic biomarkers. Alterations in phosphatidylcholine and phosphatidylethanolamine values were seen as indicative of membrane breakdown that could lead to fatty acid and phospholipid-related disorders that include dementias (Gonzalez-Dominguez, 2014). This is of particular interest because the pathophysiological changes associated with AD begin decades before clinical symptoms appear (Trushina,2013) (Whiley, 2014).

Since the brain is about sixty percent fat, it seems logical to ensure its repletion. Fatty acids and phospholipids (PL’s) are the most crucial molecules to occupy the space. It’s not very likely that seniors can get sufficient phospholipids from their diets because of diminished sense of taste for food, living and eating alone, being food insecure, and being broke. We realize this doesn’t describe all people in the group, but it probably covers someone you know. Egg yolks, liver, wheat germ and peanuts have some of the precursors to PL’s, but frequency of ingestion and concentration are often insufficient. Neither are many older folks amply hydrated to allow the PL’s to become organized into carriers of helpful molecules. The administration of PL’s, notably PC, can do much to restore function—and structure—of the membranes that make life more enjoyably livable.


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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.

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.


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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.