What’s A Nice Bone Like You Doin’ In A Joint Like This? (Part 1)

joint-pain-manIt hurts. It hurts when I get out of bed. It hurts when I bend down to pick up the laundry basket. Ooh, my knees! Yow, my shoulder! What’s goin’ on?

Could it be arthritis, the affliction of the musculoskeletal system that attacks the joints and is the main cause of disability among people over fifty-five years of age? Maybe so. The word comes from the Greek arthron, meaning “joint,” and the Latin itis, meaning “inflammation.”  Aha! Inflammation. Drat! Where did that come from?

Arthritis is not a single disease, but one that covers almost a hundred conditions, the most common being osteoarthritis, which generally affects older folks. Some forms, though, can strike at any age—even very young.

Of course, you know what a joint is. It’s held together by ligaments, the elastic bands that keep bones in place when you move. The surface of each bone is covered with cartilage to keep the bones from rubbing directly against each other, allowing smooth, painless movement. At least that’s how it’s supposed to work. The joint is surrounded by a kind of capsule that contains synovial fluid, which is secreted by membranes inside joint cavities, tendon sheaths and bursae (always found at friction points) to provide lubrication. If you have arthritis something goes wrong with the machinery, and what goes wrong depends on the kind of arthritis you have. It could be that the cartilage is wearing thin, or that fluid is in short supply, or that there is an infection, or that the body is attacking itself in an autoimmune response. It might even be a combination of these factors.

Of the many types of arthritis, osteo- is probably the best known and most often treated. This is where we will focus—after a brief rundown of the other types. (Otherwise, this would take lots of room. Look for separate mention in future musings.) Osteoarthritis is characterized by cartilage that loses elasticity and shock absorption. As cartilage wears down, tendons and ligaments stretch, causing discomfort. Eventually, bone rubs against bone, causing considerable pain. Symptoms start slowly and develop over time, getting worse. Stiffness, especially in the A.M., might go away with use of the joint. Sometimes spurs appear around the joint; sometimes swelling, too. Hands, knees, hips and the spine are worst hit.

Rheumatoid arthritis is downright inflammatory. Here, the synovial membrane is attacked, resulting in swelling and agony. Untreated, it can cause deformity. More common in women than men, RA usually strikes between ages 40 and 60, but young children may also be afflicted. Here, the same joints in each side of the body are painfully swollen, inflamed and stiff. Fingers, arms, legs and wrists are the most common targets. Hands may be red and puffy, and tender when touched. The smaller joints are noticeably affected first.

The signs of infectious arthritis, another type, include fever, joint swelling and of course, inflammation. Tenderness or sharp pain is common. Often these symptoms are linked to an injury or another illness. Most often, only a single joint is affected. Bacterial or viral invasion of the synovial tissue might be at the root.

Juvenile rheumatoid arthritis (JRA) attacks children under sixteen and presents as one of three types: pauciarticular, which is mildest; polyarticular, which is more severe; and systemic, which is the least common, but the worst because it can affect organs. With this form, there will be intermittent fevers that spike at night and suddenly disappear. Appetite and weight will fall. Blotchy rashes may appear on the extremities, and joints will swell and remain larger than normal.

The medications used to treat arthritis vary according to the type of arthritis. Analgesics help to fight pain, but do not necessarily address inflammation. Tylenol is one, but prescription narcotics may be recommended in some cases. Nonsteroidal anti-inflammatory drugs (NSAIDS) reduce both pain and inflammation. Ibuprofen and naproxen are available over the counter, and some require a prescription. These can cause stomach upset. Rub-on creams and ointments containing capsaicin, the component that makes hot peppers hot, are called counterirritants. Sometimes they work; sometimes not. Biological medicines are genetically engineered to target specific proteins involved in an immune response. You see ads for these on TV. Each of these different kinds of medications can have unpleasant side effects, ranging from simple gastric distress to susceptibility to serious infections to cardiac involvement. To add insult to injury, you have to stay out of the sun. So much for trips to the beach. We can’t forget steroids, such as cortisone. They can reduce pain, but they also reduce vitamin and mineral levels in the body, especially calcium.

Are there alternatives to drugs? Yes. The one most often used is glucosamine, often accompanied by chondroitin. Glucosamine works by stimulating the metabolism of chondrocytes—the cartilage cells—and the cells that make synovial fluid. Chondroitin is found in cartilage tissue, where it serves as the substrate for the joint matrix and works to pull water into the joint. When money is available for research, integrative therapies may be tested against allopathic treatments and placebos. Some results are real eye-openers, while others are ho-hum. Not only is glucosamine alone, as well as combined with chondroitin, well-tolerated, but also as effective as commonly used pharmaceutical interventions, and faster acting than any placebo (Lopes, 1982). A characteristic of natural treatments for an ailment is that, since they come from plants or animals as opposed to chemicals, they take longer to evoke a positive response. In a head-to-head comparison with ibuprofen, glucosamine did a better job of ameliorating pain after eight weeks of treatment than did the drug (Lopes, 1982), and did so for a larger group of people (Pujalte, 1980). As the quality of most merchandise varies from maker to maker along the continuum, so does the quality of supplements, realizing that cost is not the best indicator of grade (McAlindon, 2000). But, in the long run, glucosamine seems to be an ally in modifying the course of osteoarthritis (Reginster, 2001) and in maintaining (and even improving) structural integrity of knee joints (Bruyere, 2004). Drugs come with caveats, but so, too, do alternatives. It is not a good idea to take a supplement without at least a little guidance from someone who knows the territory, such as an integrative dietitian, a holistic-oriented physician, or some other credentialed practitioner. People don’t generally know that glucosamine could increase eye pressure in those with glaucoma. That’s the last thing they need (Murphy, 2013). And if you take a blood thinner or an aspirin a day, be careful about taking chondroitin because its chemistry is close to that of heparin and that could increase bleeding risk (Rozenfeld, 2004).

SAM-e, S-Adenosyl Methionine, is a naturally-occurring molecule distributed throughout the body that diminishes as we get older. It plays a role in more than a hundred biochemical reactions involving methylation, where it contributes to hormones, neurotransmitters, nucleic acids, proteins and phospholipids. In an early study of SAM-e effectiveness in treating osteoarthritis of the knee, hip and spine, patients found relief from morning stiffness, pain at rest and pain at movement in the first few weeks of the trial, which lasted for twenty-four months. No adverse effects were reported and none of the subjects dropped out (Konig, 1987). Mild nausea may occur with SAM-e, but that inconvenience is more bearable than the effects of drugs like Indomethacin (Vetter, 1987). What’s more, SAM-e has virtues beyond arthritis treatment. Remember that we mentioned the slowness of natural substance results. In a test at the University of California, it was learned that SAM-e is equal to celecoxib (Celebrex®) in the management of knee osteoarthritis, but slower in onset of action (Najm, 2004). If there is a problem with SAM-e, it’s the cost. However, the result is worth the outlay.

Prostaglandins are chemicals in the body that regulate several functions, including inflammation and vascular permeability. Some can start the inflammation ball rolling, while others can interrupt it. The activity of these proteins can be modulated by essential fatty acids in the omega-3 family, notably EPA, a component of fish oil and the downstream product of the alpha linolenic acid common to flaxseed oil. We know that essential fatty acids are just that—essential, meaning they must come from food or supplements because the body cannot make them. Decades-long studies have pronounced the efficacy of omega-3 fats in the management of arthritis—and other inflammatory conditions—by virtue of their capacity to tone down the pro-inflammatory and to lift up the anti-inflammatory substances that alleviate pain (Hurst, 2010) (Zainal, 2009).  A Welsh study performed at the beginning of the century noticed that n-3 fats, in a dose-dependent manner, were able to abolish the expression of pro-inflammatory mediators via a mechanism different from that of other polyunsaturated fatty acids (Curtis, 2002). Later study, also in the British Isles, found that n-3 fats reduced arthritic disease in laboratory animals inclined to suffer it (Knott, 2011). When glucosamine and n-3 fats were combined, the positive results were declared superior (Gruenwald, 2009).

Avoiding sugary foods and refined grains, and limiting red meats can do much to ease arthritic discomfort. Losing weight also helps by reducing stress on knees and hips, where the extra pounds squeeze cartilage into oblivion. Although moderate alcohol consumption is associated with decreased risk of arthritis, especially rheumatoid, it’s not recommended as a treatment. Nor is it a reason to start drinking (DiGiuseppe, 2012).


Bruyere O, Pavelka K, Rovati LC, Deroisy R, Olejarova M, Gatterova J, Giacovelli G, Reginster JY.
Glucosamine sulfate reduces osteoarthritis progression in postmenopausal women with knee osteoarthritis: evidence from two 3-year studies.
Menopause. 2004 Mar-Apr;11(2):138-43.

Curtis CL, Rees SG, Little CB, Flannery CR, Hughes CE, Wilson C, Dent CM, Otterness IG, Harwood JL, Caterson B.
Pathologic indicators of degradation and inflammation in human osteoarthritic cartilage are abrogated by exposure to n-3 fatty acids.
Arthritis Rheum. 2002 Jun;46(6):1544-53.

Daniela Di Giuseppe, Lars Alfredsson, Matteo Bottai, Johan Askling, Alicja Wolk
Long term alcohol intake and risk of rheumatoid arthritis in women: a population based cohort study
BMJ 2012;345:e4230

Delle Chiaie R, Pancheri P, Scapicchio P.
Efficacy and tolerability of oral and intramuscular S-adenosyl-L-methionine 1,4-butanedisulfonate (SAMe) in the treatment of major depression: comparison with imipramine in 2 multicenter studies.
Am J Clin Nutr. 2002 Nov;76(5):1172S-6S.

Gruenwald J, Petzold E, Busch R, Petzold HP, Graubaum HJ.
Effect of glucosamine sulfate with or without omega-3 fatty acids in patients with osteoarthritis.
Adv Ther. 2009 Sep;26(9):858-71.

Hedbom E, Häuselmann HJ.
Molecular aspects of pathogenesis in osteoarthritis: the role of inflammation.
Cell Mol Life Sci. 2002 Jan;59(1):45-53.

Hurst S, Zainal Z, Caterson B, Hughes CE, Harwood JL.
Dietary fatty acids and arthritis.
Prostaglandins Leukot Essent Fatty Acids. 2010 Apr-Jun;82(4-6):315-8.

Knott L, Avery NC, Hollander AP, Tarlton JF.
Regulation of osteoarthritis by omega-3 (n-3) polyunsaturated fatty acids in a naturally occurring model of disease
Osteoarthritis Cartilage. 2011 Sep;19(9):1150-7.

König B.
A long-term (two years) clinical trial with S-adenosylmethionine for the treatment of osteoarthritis.
Am J Med. 1987 Nov 20;83(5A):89-94.

Laudanno OM.
Cytoprotective effect of S-adenosylmethionine compared with that of misoprostol against ethanol-, aspirin-, and stress-induced gastric damage.
Am J Med. 1987 Nov 20;83(5A):43-7.

Lopes Vaz A.
Double-blind clinical evaluation of the relative efficacy of ibuprofen and glucosamine sulphate in the management of osteoarthrosis of the knee in out-patients.
Curr Med Res Opin. 1982;8(3):145-9.

Maccagno A, Di Giorgio EE, Caston OL, Sagasta CL.
Double-blind controlled clinical trial of oral S-adenosylmethionine versus piroxicam in knee osteoarthritis.
Am J Med. 1987 Nov 20;83(5A):72-7.

McAlindon TE, LaValley MP, Gulin JP, Felson DT.
Glucosamine and chondroitin for treatment of osteoarthritis: a systematic quality assessment and meta-analysis.
JAMA. 2000 Mar 15;283(11):1469-75.

Müller-Fassbender H.
Double-blind clinical trial of S-adenosylmethionine versus ibuprofen in the treatment of osteoarthritis.
Am J Med. 1987 Nov 20;83(5A):81-3.

Ryan K. Murphy, DO, MA; Lecea Ketzler, DO; Robert D. E. Rice, MD; Sandra M. Johnson, MD; Mona S. Doss, MA; Edward H. Jaccoma, MD
Oral Glucosamine Supplements as a Possible Ocular Hypertensive Agent
JAMA Ophthalmol. 2013; May 23:1-3.

Najm WI, Reinsch S, Hoehler F, Tobis JS, Harvey PW.
S-adenosyl methionine (SAMe) versus celecoxib for the treatment of osteoarthritis symptoms: a double-blind cross-over trial. [ISRCTN36233495].
BMC Musculoskelet Disord. 2004 Feb 26;5:6.

Pujalte JM, Llavore EP, Ylescupidez FR.
Double-blind clinical evaluation of oral glucosamine sulphate in the basic treatment of osteoarthrosis.
Curr Med Res Opin. 1980;7(2):110-14.

Reginster JY, Deroisy R, Rovati LC, Lee RL, Lejeune E, Bruyere O, Giacovelli G, Henrotin Y, Dacre JE, Gossett C.
Long-term effects of glucosamine sulphate on osteoarthritis progression: a randomised, placebo-controlled clinical trial.
Lancet. 2001 Jan 27;357(9252):251-6.

Roush JK, Cross AR, Renberg WC, Dodd CE, Sixby KA, Fritsch DA, Allen TA, Jewell DE, Richardson DC, Leventhal PS, Hahn KA.
Evaluation of the effects of dietary supplementation with fish oil omega-3 fatty acids on weight bearing in dogs with osteoarthritis
J Am Vet Med Assoc. 2010 Jan 1;236(1):67-73.

Soeken KL, Lee WL, Bausell RB, Agelli M, Berman BM.
Safety and efficacy of S-adenosylmethionine (SAMe) for osteoarthritis.
J Fam Pract. 2002 May;51(5):425-30.

Towheed TE, Anastassiades TP, Shea B, Houpt J, Welch V, Hochberg MC.
Glucosamine therapy for treating osteoarthritis.
Cochrane Database Syst Rev. 2001;(1):CD002946.

Towheed TE, Maxwell L, Anastassiades TP, Shea B, Houpt J, Robinson V, Hochberg MC, Wells G.
Glucosamine therapy for treating osteoarthritis.
Cochrane Database Syst Rev. 2005 Apr 18;(2):CD002946.

Vetter G.
Double-blind comparative clinical trial with S-adenosylmethionine and indomethacin in the treatment of osteoarthritis.
Am J Med. 1987 Nov 20;83(5A):78-80.

Zainal Z, Longman AJ, Hurst S, Duggan K, Caterson B, Hughes CE, Harwood JL.
Relative efficacies of omega-3 polyunsaturated fatty acids in reducing expression of key proteins in a model system for studying osteoarthritis.
Osteoarthritis Cartilage. 2009 Jul;17(7):896-905.

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

The Rumors on Rheumatoid Arthritis

hands-jarAunt Martha’s mother was the kindest, gentlest soul you’d ever meet. She went out of her way to make you feel at home. Food and drink were hallmarks of her cordial greeting. But she couldn’t open a package, twist open a jar or cut a cake. Her fingers were so badly gnarled that no two pointed in the same direction. Some of the joints formed the letter “Z.” Yet, despite the pain she must have borne, her loving smile prevailed. She was victimized by rheumatoid arthritis (RA) in an era when research was in its infancy, barely crawling.

This nefarious disease causes pain, swelling, stiffness and loss of function in joints— mostly hands and fingers, though it can strike any. It hits women more often than men, starting between ages twenty-five and fifty-five, though some statisticians start at forty. Unlike osteoarthritis, RA is an autoimmune condition that can affect body parts besides joints, such as the eyes, mouth and lungs. Nobody knows the cause. It could be genes, maybe the environment, or maybe hormones that direct the immune system to attack the body’s own tissues. Whatever it is, RA afflicts more than a million Americans, a sizeable fraction being kids.

The inflammation of RA can reach to the tendons, ligaments and muscles in some patients. Its chronic nature causes degradation of cartilage, bone and the ligaments that bind bones, causing deformity. Active disease presents with fatigue, appetite loss, low-grade fever, muscle and joint aches, and stiffness, the last being most notable in the morning or following periods of inactivity. Because RA is a systemic ordeal, its malevolence can inflame the glands around the eyes and mouth, causing Sjögren’s syndrome. RA-induced pleuritis is the inflammation of lung lining that causes pain with a deep breath. Because the number of red blood cells is reduced, anemia occurs, while a drop in white cells can be associated with an enlarged spleen and increased risk of infection.

Following examination of inflammatory blood markers and other criteria, the doctor can make a proper diagnosis, at which time medications probably will be prescribed. Cortisone and aspirin have been first-line drugs for decades because they act quickly. The slower ones are called disease-modifying anti-rheumatic drugs—DMARD’s—and include some heavy duty chemistry, not all of which is anti-inflammatory, but most of which has truly nasty side effects, many you have learned from television ads. What may not be realized is that some drugs destroy the substances your body needs to work the right way. The package insert that comes with the drug doesn’t tell you this, so you’ll think the absence of pain has all the bases covered. This is sufficient reason to visit an integrative dietitian or holistic-minded physician, the rare one who knows about nutrition.

Keeping your physician in the loop, you may opt to explore integrative measures to deal with RA. The good news is that there are recognized mediators of inflammation-induced bone damage (Nanjundaiah, 2013). Because of space constraints, we’ll address those with a pretty reliable track record, starting with gamma linolenic acid (GLA), an omega-6 fatty acid found in borage and evening primrose oils. While it is true that borage contains almost twice the levels of GLA as evening primrose, it is also true that borage contains pyrrolizidine alkaloids that can tax the liver. Though possibly in non-toxic amounts, these alkaloids are nonetheless there.  For that reason, EPO is often a preferred source of GLA. On the other hand, borage oil is used in clinical and observational studies because of its higher GLA values, thus requiring a smaller dosage (that may influence subject participation) and reducing cost. A University of PA study done in the early 90’s found that patients who took borage oil capsules for three months experienced reductions in pro-inflammatory prostaglandins and leukotrienes, leading to noticeable clinical improvement in RA symptoms (Pullman-Mooar, 1990).

Supplementing GLA at 3.0 and 6.0 grams a day enhances its conversion to the anti-inflammatory dihommo-gamma-linolenic-acid (DGLA), causing neutrophils to synthesize less pro-inflammatory leukotriene and platelet-activating factor (PAF—a major trigger of thrombosis), thereby attenuating discomfort (Johnson, 1997).  Compared to placebo in a six-month trial in Philadelphia, GLA was found to reduce the number of tender joints by more than a third and swollen joint count by more than a fourth, in a study from which no one withdrew (Leventhal, 1993).

Not to be outdone by its omega-6 counterpart, omega-3 fish oil flexed its anti-inflammatory muscle in trials that included non-steroidal anti-inflammatory drugs (NSAIDS) as part of the treatment. Swelling index and duration of early morning stiffness were used as markers for RA severity, and were found to have improved in subjective assessment by virtue of a decrease in pro-inflammatory leukotrienes (van der Tempel, 1990). Patients who received fish oil in combination with naproxen fared better in similar assessments than those without the fish oil or with placebo oil in studies carried out in Norway (Kjeldsen-Kragh, 1992) and New York (Kremer, 2000). A Canadian meta-analysis of seventeen n-3 studies concluded that morning stiffness and number of tender joints were reduced in those who used n-3 PUFA’s (Goldberg, 2007). Those who supplemented their OTC medications with omega-3’s from cod liver oil were able to reduce their dependence on NSAIDS (Galarraga, 2008).

In early reports, Danish scientists found that RA patients were deficient in the only mineral with anti-oxidant properties—selenium. They noted that those with the most active disease had the lowest values, and that there is significant correlation of selenium status with the number of affected joints (Tarp, 1985). Almost a decade later, the same researchers confirmed their initial findings, but also found that some subjects lack the physiological wherewithal to convert selenium to functional anti-oxidant enzymes, a state that can be overcome by supplemental mineral (Tarp, 1994).

From frankincense through ginger, to the resveratrol of grapes, science is takinga deliberate look at additions to the arsenal of RA treatments.


Astorga G, Cubillos A, Masson L, Silva JJ.
Active rheumatoid arthritis: effect of dietary supplementation with omega-3 oils. A controlled double-blind trial.
Rev Med Chil. 1991 Mar;119(3):267-72.

Galarraga B, Ho M, Youssef HM, Hill A, McMahon H, Hall C, Ogston S, Nuki G, Belch JJ.
Cod liver oil (n-3 fatty acids) as an non-steroidal anti-inflammatory drug sparing agent in rheumatoid arthritis.
Rheumatology (Oxford). 2008 May;47(5):665-9.

Goel, F. J. Ahmad, R. M. Singh, and G. N. Singh
3-Acetyl-11-keto-β-boswellic acid loaded-polymeric nanomicelles for topical anti-inflammatory and anti-arthritic activity
Journal of Pharmacy and Pharmacology, vol. 62, no. 2, pp. 273–278, 2010.

Goldberg RJ, Katz J.
A meta-analysis of the analgesic effects of omega-3 polyunsaturated fatty acid supplementation for inflammatory joint pain.
Pain. 2007 May;129(1-2):210-23.

Johnson MM, Swan DD, Surette ME, Stegner J, Chilton T, Fonteh AN, Chilton FH.
Dietary supplementation with gamma-linolenic acid alters fatty acid content and eicosanoid production in healthy humans.
J Nutr. 1997 Aug;127(8):1435-44.

Kjeldsen-Kragh J, Lund JA, Riise T, Finnanger B, Haaland K, Finstad R, Mikkelsen K, Førre O.
Dietary omega-3 fatty acid supplementation and naproxen treatment in patients with rheumatoid arthritis.
J Rheumatol. 1992 Oct;19(10):1531-6.

Knekt P, Heliövaara M, Aho K, Alfthan G, Marniemi J, Aromaa A.
Serum selenium, serum alpha-tocopherol, and the risk of rheumatoid arthritis.
Epidemiology. 2000 Jul;11(4):402-5.

Kremer JM.
n-3 fatty acid supplements in rheumatoid arthritis.
Am J Clin Nutr. 2000 Jan;71(1 Suppl):349S-51S.

Lau CS, Morley KD, Belch JJ.
Effects of fish oil supplementation on non-steroidal anti-inflammatory drug requirement in patients with mild rheumatoid arthritis–a double-blind placebo controlled study.
Br J Rheumatol. 1993 Nov;32(11):982-9.

J. H. Lee, H. Jin, H. E. Shim, H. N. Kim, H. Ha, and Z. H. Lee
Epigallocatechin-3-gallate inhibits osteoclastogenesis by down-regulating c-Fos expression and suppressing the nuclear factor-κB signal
Molecular Pharmacology, vol. 77, no. 1, pp. 17–25, 2010.

M. Lei, S. Q. Liu, and Y. L. Liu
Resveratrol protects bone marrow mesenchymal stem cell derived chondrocytes cultured on chitosan-gelatin scaffolds from the inhibitory effect of interleukin-1β
Acta Pharmacologica Sinica, vol. 29, no. 11, pp. 1350–1356, 2008.

Leventhal LJ, Boyce EG, Zurier RB.
Treatment of rheumatoid arthritis with gammalinolenic acid.
Ann Intern Med. 1993 Nov 1;119(9):867-73.

S. A. Levy, O. Simon, J. Shelly, and M. Gardener
6-Shogaol reduced chronic inflammatory response in the knees of rats treated with complete Freund’s adjuvant
BMC Pharmacology, vol. 6, article 12, 2006.

D. O. Moon, M. O. Kim, Y. H. Choi, Y. M. Park, and G. Y. Kim
Curcumin attenuates inflammatory response in IL-1β-induced human synovial fibroblasts and collagen-induced arthritis in mouse model
International Immunopharmacology, vol. 10, no. 5, pp. 605–610, 2010.

Morinobu, W. Biao, S. Tanaka et al.,
 (-)-Epigallocatechin-3-gallate suppresses osteoclast differentiation and ameliorates experimental arthritis in mice
Arthritis and Rheumatism, vol. 58, no. 7, pp. 2012–2018, 2008.

Nanjundaiah SM, Astry B, Moudgil KD.
Mediators of inflammation-induced bone damage in arthritis and their control by herbal products.
Evid Based Complement Alternat Med. 2013;2013:518094.

Pullman-Mooar S, Laposata M, Lem D, Holman RT, Leventhal LJ, DeMarco D, Zurier RB.
Alteration of the cellular fatty acid profile and the production of eicosanoids in human monocytes by gamma-linolenic acid.
Arthritis Rheum. 1990 Oct;33(10):1526-33.

M. L. Sharma, S. Bani, and G. B. Singh
Anti-arthritic activity of boswellic acids in bovine serum albumin (BSA)-induced arthritis
International Journal of Immunopharmacology, vol. 11, no. 6, pp. 647–652, 1989.

Tarp U, Overvad K, Hansen JC, Thorling EB.
Low selenium level in severe rheumatoid arthritis.
Scand J Rheumatol. 1985;14(2):97-101.
Tarp U.
Selenium and the selenium-dependent glutathione peroxidase in rheumatoid arthritis.
Dan Med Bull. 1994 Jun;41(3):264-74.

van der Tempel H, Tulleken JE, Limburg PC, Muskiet FA, van Rijswijk MH.
Effects of fish oil supplementation in rheumatoid arthritis.
Ann Rheum Dis. 1990 Feb;49(2):76-80.

G. Xuzhu, M. Komai-Koma, B. P. Leung, et al.
Resveratrol modulates murine collagen-induced arthritis by inhibiting Th17 and B-cell function
Annals of the Rheumatic Diseases, vol. 71, no. 1, pp. 129–135, 2012.

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

What Gets YOU Inflamed?

knee-inflammationAre you an adult? Would you prefer the pound(s) of cure to the ounce of prevention? One of the sad commentaries about adulthood is that we don’t take care of ourselves until something hurts, the detection of which relies on the nervous system. The nervous system is plastic, meaning that it exhibits a wide range of responses according to different conditions. The perception of pain depends on more than one factor, the environment included. With inflammation, however, there exists a hypersensitivity state that makes us aware of what’s going on. This realization is called nociception, involving a network that identifies a noxious condition that evokes responses ranging from mild to severe. Once the pain message is recognized by the nervous system it registers as an “ouch.” The greater the intensity of the stimulus, the greater is the perception of pain. In some cases, no external trigger is needed, such as one would experience with arthritis pain.

Inflammation is the body’s attempt at self-protection, the intention of which is to remove the harmful stimuli, including damaged cells, irritants or pathogens. If the stimulus comes from outside, it can be removed, although pain may linger. If it comes from inside, the body is left to its own devices. In either instance, tissue repair is the ultimate goal. To our dismay, inflammation may beget further inflammation in a self-perpetuating cascade. This occurs because of cellular alterations that cause mediator chemicals to be released and certain white cells, called macrophages, to become activated. The job of the macrophage is to swallow (-phage) the debris that comes from, or causes, tissue damage. Without inflammation, infections and wounds would never heal. In fact, too much anti-inflammatory medication, such as cortisone, slows wound healing (Goforth, 1980). The innate immunity with which we were born is always at the ready to start the inflammatory cascade and to bring healing.

Signs of overt inflammation include pain, redness, immobility (as in loss of function), swelling, and heat (more blood to the area makes it feel warm). Covert inflammation, occurring with internal organs, does not necessarily present with all these signs. Pain arises when swelling pushes on nerves, but sometimes the brain gets used to it and ignores the stimulus. The risk for inflammatory conditions rises with weight gain, as determined by an increase in white blood cells. Regardless of body mass index, C-reactive protein and homocysteine are markers for the presence of inflammatory state, which is at the center of many disorders, from arthritis, through Crohn’s disease, to various allergies and vitamin deficiencies.

Treatment for inflammation abounds in the world of allopathic medicine. Most of us know about NSAIDS, non-steroidal anti-inflammatory drugs, among which Tylenol is not, but aspirin, naproxen and ibuprofen are. Then, there are the corticosteroids—or just plain steroids—that are naturally made by the body in the adrenal glands. But these guys, given as drugs, prevent phospholipid release, and that undermines the activity of eosinophils, which are designed to fight back against allergy, for example, by releasing histamine.

Of the alternative modalities to address inflammation, ginger has accrued quite a following. For hundreds of years it’s been used to treat gastric distress, including dyspepsia and constipation. Recent research points to ginger’s role as an anti-inflammatory agent in the prevention of colon cancer, where inflammation has been identified as a precursor to the disease (Zick, 2011), the markers of which are pro-inflammatory prostaglandins—primarily PGE2—produced by cyclooxygenase (COX) as an early event in the course of the condition (Jiang, 2012).

In a British examination of pain studies, those suffering from osteoarthritis, dysmenorrhea, and acute muscle pain had been administered ginger as the sole treatment. Though additional rigorous trials are anticipated, these subjects reported a reduction in pain, as cited on subjective assessment tools (Terry, 2011). Even before interest in alternative medicine was accelerated to its present status, scientists scrutinized ginger’s reputation in the Ayurvedic community among people treated with the herb for rheumatic concerns, finding efficacy that paralleled traditional interventions (Srivastava, 1989). Applying oral powdered ginger to generalized musculoskeletal discomfort, Danish physicians realized that the safety factor of ginger far exceeded that of any known drugs, while presenting significant efficacy in the relief of pain and swelling via the inhibition of pro-inflammatory prostaglandins (Srivastava, 1992).

By sequestering these incendiary prostaglandins (PG’s), ginger proves itself to be on a par with NSAIDS, minus the concerns of adverse side effects. Similar to prostaglandins in promoting physical aberrations are leukotrienes, products of an enzyme called lipoxygenase (LOX), like COX an offspring of arachidonic acid metabolism. Leukotrienes generally work within the immune system, while PG’s almost always play a role in pure inflammation and pain. (There are beneficent PG’s, by the way.)  Leukotrienes are signaling molecules that call immune cells to the site of infiltration, as from airborne allergens. Bluntly, ginger suppresses the synthesis of leukotrienes (Grzanna, 2005), a property that separates it from NSAIDS. Other of ginger’s attributes point to an anti-oxidant character in the interruption of free radical generation (Ali, 2008), which is helpful in the fight against allergens and pain.

Nitric Oxide (NO) is one of the few signaling gases in the body. The smooth muscle that lines blood vessels is told by NO to relax, thus dilating the vessels and lowering blood pressure. In excessive concentrations, though, NO becomes a pro-oxidant as a naturally unstable free radical, especially when made by white cells (monocytes and macrophages)  during their battle against an infective agent. One logistician that maintains regulation of NO is ginger, where it was shown to control white cell activation as part of its job as an anti-inflammatory vehicle (Shimoda, 2010). Modulating inflammation is what ginger does, and not so gingerly, at that.


Ali BH, Blunden G, Tanira MO, Nemmar A.
Some phytochemical, pharmacological and toxicological properties of ginger (Zingiber officinale Roscoe): a review of recent research.
Food Chem Toxicol. 2008 Feb;46(2):409-20. Epub 2007 Sep 18.

ltman RD, Marcussen KC.
Effects of a ginger extract on knee pain in patients with osteoarthritis.
A Arthritis Rheum. 2001 Nov;44(11):2531-8.

Drozdov VN, Kim VA, Tkachenko EV, Varvanina GG.
Influence of a specific ginger combination on gastropathy conditions in patients with osteoarthritis of the knee or hip.
J Altern Complement Med. 2012 Jun;18(6):583-8. doi: 10.1089/acm.2011.0202.

Frondoza CG, Sohrabi A, Polotsky A, Phan PV, Hungerford DS, Lindmark L.
An in vitro screening assay for inhibitors of proinflammatory mediators in herbal extracts using human synoviocyte cultures.
In Vitro Cell Dev Biol Anim. 2004 Mar-Apr;40(3-4):95-101.

Goforth P, Gudas CJ.
Effects of steroids on wound healing: a review of the literature.
J Foot Surg. 1980 Spring;19(1):22-8.

Grzanna R, Lindmark L, Frondoza CG
Ginger–an herbal medicinal product with broad anti-inflammatory actions.
J Med Food. 2005 Summer;8(2):125-32.

Jiang Y, Turgeon DK, Wright BD, Sidahmed E, Ruffin MT, Brenner DE, Sen A, Zick SM.
Effect of ginger root on cyclooxygenase-1 and 15-hydroxyprostaglandin dehydrogenase expression in colonic mucosa of humans at normal and increased risk for colorectal cancer.
Eur J Cancer Prev. 2012 Dec 6.

Levy AS, Simon O, Shelly J, Gardener M.
6-Shogaol reduced chronic inflammatory response in the knees of rats treated with complete Freund’s adjuvant.
BMC Pharmacol. 2006 Oct 1;6:12.

Lu H, Huang D, Saederup N, Charo IF, Ransohoff RM, Zhou L.
Macrophages recruited via CCR2 produce insulin-like growth factor-1 to repair acute skeletal muscle injury.
FASEB J. 2011 Jan;25(1):358-69.

Ramji, Divya; ho, chi; Huang, Qingron; Rafi, Mohamed; Huang, Mou
Isolation of gingerols and shogaols from ginger and evaluation of their chemopreventive activity on prostate cancer cells and anti-inflammatory effect on 12-O-tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear inflammation
RUcore – Rutgers University Community Repository. 2007

Shen CL, Hong KJ, Kim SW.
Effects of ginger (Zingiber officinale Rosc.) on decreasing the production of inflammatory mediators in sow osteoarthrotic cartilage explants.
J Med Food. 2003 Winter;6(4):323-8.

Sehwan Shima, Sokho Kima, Dea-Seung Choia, Young-Bae Kwonb, Jungkee Kwona
Anti-inflammatory effects of [6]-shogaol: Potential roles of HDAC inhibition and HSP70 induction
Food and Chemical Toxicology. Volume 49, Issue 11, November 2011, Pages 2734–2740

Shimoda H, Shan SJ, Tanaka J, Seki A, Seo JW, Kasajima N, Tamura S, Ke Y, Murakami N.
Anti-inflammatory properties of red ginger (Zingiber officinale var. Rubra) extract and suppression of nitric oxide production by its constituents.
J Med Food. 2010 Feb;13(1):156-62.

Srivastava KC, Mustafa T.
Ginger (Zingiber officinale) and rheumatic disorders.
Med Hypotheses. 1989 May;29(1):25-8.

Srivastava KC, Mustafa T.
Ginger (Zingiber officinale) in rheumatism and musculoskeletal disorders.
Med Hypotheses. 1992 Dec;39(4):342-8.

Terry R, Posadzki P, Watson LK, Ernst E.
The use of ginger (Zingiber officinale) for the treatment of pain: a systematic review of clinical trials.
Pain Med. 2011 Dec;12(12):1808-18.

Tripathi S, Maier KG, Bruch D, Kittur DS.
Effect of 6-gingerol on pro-inflammatory cytokine production and costimulatory molecule expression in murine peritoneal macrophages.
J Surg Res. 2007 Apr;138(2):209-13. Epub 2007 Feb 8.

Tripathi S, Bruch D, Kittur DS.
Ginger extract inhibits LPS induced macrophage activation and function.
BMC Complement Altern Med. 2008 Jan 3;8:1. doi: 10.1186/1472-6882-8-1.

Zick SM, Turgeon DK, Vareed SK, Ruffin MT, Litzinger AJ, Wright BD, Alrawi S, Normolle DP, Djuric Z, Brenner DE.
Phase II study of the effects of ginger root extract on eicosanoids in colon mucosa in people at normal risk for colorectal cancer.
Cancer Prev Res (Phila). 2011 Nov;4(11):1929-37.

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

Fat Facts on Omega 3 and Omega 6 Fatty Acids

Omega-3 fatty acids —EPA and DHA— are the BIG news in nutritional m medicine today — and for some very good reasons. The scientific evidence is now irrefutable that EPA and DHA are essential for good health and long life. They are such important nutrients that agencies and institutions historically hostile to nutrition have gone on record to support their use. The American Medical Association, the American Heart Association, the United States Department of Agriculture (USDA), even the good ol’ “Food and Drug Administration (FDA),” are all praising EPA and DHA.

While all of this is certainly a positive development, the rise in sales of omega 3 (n-3) fatty acid is in direct response to the high press coverage. It’s like everybody on the globe is jumping on the omega 3 fish oil bandwagon. The result of this excessive reporting in the media with relatively little knowledge of fatty acid chemistry, has lead to overindulgence (prescribing and taking too much). TThis overzealous use of omega-3 fish oils has occurred worldwide at a disturbing rate.

At BodyBio we have been observing these results through the in-depth examination of thousands of individual fatty acid tests, year after year. Analyzing red blood cell fatty acids (RBCFAs) is a principal part of what we do at BodyBio. The bioactive ingredients of fish oil, EPA and DHA, are generally found in a ratio of 3 to 2 (180 mg of EPA and 120 of DHA). They are both dynamic and powerful nutrients, with a wide range of functions that influence the brain, the sensory organs, synaptic and cardiac activity, and the modulation of arachidonic acid effects in inflammation. All membrane fatty acids are intimately involved in regulating all aspects of the body’s chemistry, including control of each others’ families, the 6s and the 3s. However, excess omega 3s will easily suppress the omega 6s, whereas the reverse does not seem to occur; 6s do not suppress the 3s.

If we follow the popular media mantra, we are led to believe that adding fish oil to the diet will improve our wellbeing by raising the omega 3s and avoiding / lowering the omega 6s. This should be a good thing, since any suppression of omega 6 arachidonic acid would tend to reduce inflammation and lead to a healthier state. However, based on our research and the testing of red cell lipids over the years, we have found the opposite to be true. Dr. Patricia Kane’s own findings concur.

To understand the fatty acid disturbance we see requires a shift in thinking about omega 6 fatty acids and inflammation. While inflammation can be disturbing, in itself it should not be regarded as bad. Aside from the correction that the body undertakes to alleviate the stress that results in inflamed tissues, it is predominantly sending a signal, a message that something is wrong. We certainly want to suppress the disturbance, but the last thing we should be doing is killing the messenger, which is exactly what fish oil does.

More than 80% of the BodyBio red cell fatty acid tests performed yearly* register high omega 3s and low omega 6s. There is a direct correlation with the amount of fish oil consumed and the elevation of EPA and DHA. Associated with the distorted fatty acid analysis is a wide array of disorders, such as fatigue, irritable bowel syndrome, nausea, eczema, headaches, visual disturbance, memory loss, etc.

While we are told that omega 6s are “bad guys,” there is really no such thing. If it is essential, as omega 6s are, and the body spends precious energy to create and maintain it, it is wrong to assume that the metabolic effort is misdirected. Maybe too little or too much — but certainly not bad. Currently, there is no way for humans to survive without omega 6 fatty acids. This includes arachidonic acid (AA), containing 4 double bonds and occupying as much as 14% of the red cell membrane.  Arachidonic acid also boasts the highest concentration of energy in the membrane as the lead regulator of all cellular signaling, and quite possibly of all regulation in the body. As we have recently seen and hereby report the suppression of AA in a large number of individuals by the over-consumption of fish oil has been directly responsible for an unusual increase in physical and mental distress.

Our approach is to remove fish oil from the diet for a time and to encourage a nutrient-dense diet that is low in carbohydrates and rich in omega 6 fats from foods that include egg yolks, evening primrose oil and a blend of cold-pressed safflower and flaxseed oils (BodyBio Balance Oil delivers a 4:1 ratio of linoleic acid to alpha-linolenic acid.).  Together with essential vitamins and minerals, these dietary inclusions help to elevate lower-order EFA saturation levels. The patients, after shifting their diet and supplementation, consistently report that they all improve. In the world of medicine one should never say all, however, we repeat, all patients tend to reverse their negative symptoms by bringing their omega 6s and their omega 3s back in balance.

It is, after all, about balance. Is fish oil bad for you?? Of course not! The error, either by self-medication or by being over prescribed, is an excessive expression of omega 3s which can occur with any drug or nutrient. Also required, and in part because the medical reliance on fatty acid nutrition is quite new, is a new-found respect for the metabolic power of the omega 3s, especially EPA. Without the valuable analysis from the world’s premier fatty acid laboratory, we would never have been able to make this analysis and relay to you how to readjust your patient’s essential fatty acid balance. We would have no reference to do so.

*The vast majority of BodyBio Red Cell tests were performed on individuals who had been seeking medical help for a period of time before consenting to do an Fatty Acid Analysis. Fish oils were commonly employed in their effort to find relief. The 80% referred to above is unusually high but is the result of 1) that narrow select group and 2) the individuals personal reporting of the use of fish oils often over several years. Would this have been the case 20 years ago? Probably not.

Annette was determined that she would not follow in her family’s footsteps in regard to her health. To hold off aging and ill health she used 10 capsules daily of fish oil, restricted all meat, eggs and dairy in her diet and limited her intake of all oil except olive oil that she used in her salad and to cook with. After two years of high fish oil intake, Annette noticed that she was developing eczema. Her allergies got much worse and she felt tired all the time. Her moodiness was irritating to others but worst of all she had developed severe difficulties with her ability to think and perform at work. Annette visited a physician specializing in fatty acid therapy and longevity who tested her red cell lipids and found them to be alarmingly unbalanced. Her omega 3 EPA was 1500% high while her omega 6 Arachidonic Acid was 156 % low and her omega 6 Gamma Linolenic Acid was 94% low. Her doctor explained the importance of balance of her fatty acids and set up a targeted nutritional protocol for her. After two weeks of getting on the correct balance of fatty acids Annette felt much better. Her eczema started to clear, her mood stabilized, her energy and alertness returned and she found her work performance normalized. After 6 months of re-balancing Annette’s physician allowed her to begin fish oil with one capsule of Kirunal daily along with wild salmon and sardines, evening primrose, 4:1 omega 6 to omega 3 balanced oil, and eggs / butter in her diet.

Jordan is a 3 year old boy with autism. His mother was told by his natural practitioner to give him 4 capsules of fi sh oil daily. After 4 months on fish oil Jordan’s behavior and attention had deteriorated. Testing Jordan’s red cell lipids revealed that he had a gross overdose of omega 3 as EPA and DHA with a deep suppression of the omega 6s. Jordan was then given primrose oil, eggs, butter and safflower oil for a few months and his behavior and attention improved dramatically. In keeping with balance, Jordan was then given 4:1 omega 6 to omega 3 balanced oil, primrose, eggs / butter and one capsule of Kirunal three times weekly to maintain a balance of his essential fatty acids.

Adam is an 8 year old boy with Muscular Dystrophy. A health care practitioner prescribed 6 tablespoons of fish oil which he took over an 18 month period. Adam’s parents were deeply concerned with his deteriorating condition and a red cell lipid test was drawn June 2005. Adam’s EPA was grossly elevated (H) at 3888 %, his DHA was also (H) at 312 % and his Arachidonic was deeply suppressed (L) at 356 %. Adam’s EPA was the highest on record with Arachidonic Acid the lowest ever recorded. Adam presented with symptoms of nausea, poor appetite, hypotonia (low muscle tone), poor coordination, severely abnormal gait (walking), with stiff and very slow movement. Interesting to note that Adam’s brain function was good, even elevated, however he could not perform physically. As soon as the fi sh oil was stopped Adam’s appetite increased and his nausea disappeared. He was started on 10 capsules of high potency evening primrose oil daily along with 4 tablespoons of 4 to 1 omega 6 to omega 3 oil. Because of the severe distortion of Adam’s essential fatty acids it will be necessary to retest in 3 months to track the changes. Fatty Acids are normally tested yearly.

Adam’s hypotonia provides a clearer picture of the modulating effect of EPA on Arachidonic. the term modulate is insuffcient to describe the power of EPA considering excess intake. It takes an exaggerated overdose such as Adam’s to paint a vivid picture of the power of fatty acid function. Elevation of EPA can literally block function, not just modulate, thereby impacting all thought and motion. EPA’s effect is similar to the action of NSAIDS blocking Cox I and II, and could be an alternative therapy to those common drugs. A concept anathema to the drug world since the occasional use of EPA would have few negative concerns, however, deep over-expression could be — as with the above case histories. the mode of action of NSAIDS is to specifically block Arachidonic, which it effectively does. EPA accomplishes the same effect, which opens a new focus on EFA metabolism. It also brings the omega 3 fatty acids into sharper focus in relation to drugs and homeostasis, all of which is little understood or appreciated in today’s rush to endorse too much fish oil. A smaller fish oil capsule with a higher EPA content such as Kirunal could be a much better choice to fight inflammation. It’s natural (NSAIDs are drugs) and we all need fish oil, they’re essential – however, as stated above, use carefully.

Note: There is an innate ability to re-acquire a balanced state given a change in lifestyle. The variation in age, gender, and general health are so varied that to make an estimate as to time difficult. Physicians can order a BodyBio Fatty Acid Profile for accurate assessment to determine the right balance of fatty acids needed. (Information on the BodyBio Red Blood Cell FA test for Health Care Providers – please call BodyBio at 888 320 8338 or go to our website at

The literature is replete with information on the value of omega 3, with little on the value of omega 6. It is much too deep and complicated a subject to address in brief; however, the omega 6 family is by far the predominant fatty acid family, having vast number of management functions throughout the body. The power of EPA, at ~ 0.46% of the red cell compared to ~14% of arachidonic acid, is relegated to modulate and down-regulate arachidonate, thereby refining function and raising performance to a higher level, which it effectively does. A look inside the retina provides an excellent example of the specialization of the two fatty acid families.

There are 100 million photoreceptor cells responsible for sight in each retina. To perform at a high level they require the optimal lipid energy available in the membranes of the outer segment of the cell. Predators such as cats, bears, birds of prey, all carnivorous life in the oceans, and especially primates have a high concentration of DHA, a 22 lipid carbon chain. DHA has the highest number of double bonds [6] within that chain. The more double bonds, the higher the energy value.

In primates, particularly humans, the membrane of the eye contains ~50-55% DHA (the highest in the body, the brain has ~17- 22%). Grazing animals have ample access to the lowest order of omega 3, alpha linolenic (ALA), which begins the n-3 family with 3 double bonds. ALA is high in green leafy vegetation, although the fatty acid content is low. However, grazing animals cannot efficiently metabolize ALA up to DHA. We are also inefficient in this process, however, we are a predator – we can eat fish and get all the DHA we need. Small mammals, such rats are 100% efficient in fatty acid metabolism. The big grass eaters use instead a 22 carbon omega 6, which they metabolize up to 5 double bonds, the maximum number for the n-6s.

There is a dramatic difference in the energy value of a 22 carbon n-6 with 5 double bonds contrasted to a 22 carbon n-3 DHA with 6 double bonds. That difference registers with a significant improvement in eyesight, which gives all predators a leg up in survival. The big cats can watch the herd close u,p whereas the antelopes have to raise their noses high in the air and sniff, hoping to get a sense of what’s out there. That’s a huge advantage. In addition, the higher concentration of DHA in our predator brains translates to higher intelligence since DHA is directly involved with synaptic activity and brain function. However, it does not correlate that an over-expression of DHA will increase brain power in adults, but if the mother does not take in sufficient omega 3 HUFAs (highly unsaturated fatty acids with DHA) during pregnancy or when nursing, the baby’s intellect may not fully develop. The pregnant mother needs generous intakes to nurture her fetus throughout pregnancy. Postpartum depression has in fact, been linked to omega-3 deficiency. The newborn needs it to build and mature all the organs. Older children need the omega-3s to help them function in school and avoid behavioral problems. Parents need them also, perhaps even more so.

The Right Stuff

Getting these vital fatty acids into the body has presented a challenge of purity, itself a concept that encompasses more than a single idea. Acquiring oil from fish is not as simple as getting juice from an orange, where a single earnest squeeze yields results. In juice, there is nothing that needs to be separated, unless pulp is an issue. With fish bodies, there are concerns with removing proteins, environmental insults like heavy metals and micro-organisms, and even ancillary fats that might impede EFA/DHA uptake.

Practically endless discussion has pitted the triglyceride (TG) form of fish oil against the ethyl-ester (EE) form in terms of bioavailability, safety and efficacy. Looking at myriad scientific reviews, we conclude that the differences are minor and inconsequential, unable to be judged as physiologically or clinically significant. So far, it seems that once a steady state of supplementation has been achieved, the biological outcomes are alike. In fact, most CVD-related trials have used the EE form and the National Eye Institute uses it in its AREDS 2 trials (West, 2016) (Ackman, 1992). Clouding the matter is that humans absorb these fats through different routes:  preduodenal, lymphatic via chylomicrons, and the route that uses the portal vein to the liver. Thus, it is difficult to compare results. It is the EE form that has been recommended for standardization (and has been used to manufacture a pharmaceutical fish oil).

BodyBio Kirunal is derived from fish bodies by a process that uses supercritical fluid extraction based on the very low temperatures of solid carbon dioxide. This process provides an oxygen-free media, therein preventing the oxidation and eventual rancidity common to most fish oil products on the market. It further allows extracting selectively low polar lipid compounds, thus avoiding the co-extraction of polar impurities that include inorganic substances, such as heavy metals.

If there be a limitation to supercritical CO2 extraction, it is the increased cost, not only because of the high-pressure equipment, but also because the raw material needs to be freeze dried in order to reduce moisture below 20% and to keep the n-3 fats, the delicate PUFA’s, unaltered. The high level of n-3 fats in supercritical CO2 extraction surpasses all other processes, largely due to low temperatures and a non-oxidant atmosphere. Rarely does the temperature reach 104° F (40 ° C).

There is no detriment to appearance of the oil liberated in this manner, since color, neutral lipid composition and fatty acids profiles are similar. Important are oil acidity, total oxidation value, inclusion of volatile compounds, sensory properties and heavy metals, all of these characters favoring the supercritical CO2 method. Here, fishy off-flavors are eliminated and the potential for a trimethylamine miasma removed.

To BodyBio’s delight, in spite of the high initial investment, refinement costs and downstream processing eventually make the process competitive in that it may likewise be used to make specialty oils, such as nut oils and seed oils.

EPA and DHA are large and spacious n-3 fats, unable to sit next to each other on a single glycerol molecule. Therefore, most fish oils do not contain more than about 30% EPA and DHA. To increase concentration, these fatty acids can be removed by converting them to ethyl esters. Once they are freed, their concentrations are enriched. Supercritical extraction is able to reduce or eliminate cholesterol and contaminants that include the typical environmental insults, such as dioxins, PCB’s, and heavy metals, offering an EPA/DHA content in excess of 60%. Extending the process to feature supercritical fluid chromatography, 90%+ concentrations may be realized.

Molecular distillation, long the darling of the fish oil trade, suffers as much as 350% higher thermal stress than supercritical fluid extraction, and a much lower capability to selectively extract the essential fats desired. Attaining 95% EPA and DHA gives BodyBio Kirunal a triple value in a single capsule.

Fat Facts: Separating Fat From Fiction

Our life blood is in the sources of fatty acids we ingest to nourish our bodies. The media circus makes it difficult to separate the factoidal wheat from the chaff. The internet would have us believe that fish oil is the answer to all of life’s aches, pains and decrepitudes, and that omega-6 (n-6) fatty acids, especially the linoleic acid that is common to seed oils, is the scourge of our well-being. Nothing could be further from the truth.

Here Are The Facts In A Nutshell:

All essential fatty acids are just that – essential. Removing an essential fatty acid from the diet will likely lead to serious medical conditions. The omega-6 fats in the food supply include linoleic, gamma-linolenic and arachidonic acids. Although health enthusiasts now agree that pasture-raised butter and free-range eggs are healthy, they draw the line at seed oils, labeling linoleic acid as especially detrimental to health. However, these purveyors of misinformation have no qualms about pushing the consumption of nuts, which are heavy in monounsaturated fats and shallow in the polyunsaturated omega-6s. The judgment that n-6 fats are unhealthy arose from their capacity to drive inflammation by converting to arachidonic acid (AA), a physiological process actually lacking in efficiency and reliable outcome. Nonetheless, indisputable is that Linoleic acid (LA) is a primary essential fatty acid vital to the mitochondria. Do you see the problem? No one checked the medical facts. Linoleic acid is crucial to health. To settle the dispute, not one medical paper, not even from the most respected lipid researchers, has found LA to be a threat to health at all.

So What Is Bad For The Body?

Toxic fatty acids from heated, overheated and continuously-heated oils are harmful. The greater is their unsaturation, the greater is their toxicity. While there is no doubt that trans-fats are vile, toxic fatty acids are worse. What they exact upon the brain and body is frightening.

Have you ever noticed a health food store chains with prepared food cook in canola oil? They actually fry chicken in canola oil! Canola is a genetically-modified, polyunsaturated oil that creates dangerous aldehydes when heated to cooking temperatures. These formaldehyde cousins eventually embed themselves into our lipid membranes, causing inflammatory responses and a menagerie of diverse problems. Is olive oil any better? A monounsaturated omega-9, it contains oleic acid, a fatty acid whose health benefits are heralded, but whose associated polyphenols display more salubrity by modulating the oxidation of blood lipids, this according to a 2011 report by the European Food Safety Authority. A monumental concern, made public recently, is that olive oil is being diluted as much as 70% with sunflower, canola, walnut and other polyunsaturated fatty acids (PUFAs).  These relatively tasteless adulterants contribute to aldehyde toxicity when heated. Even at two dollars an ounce, first-cold-pressed extra virgin olive oil may be a contaminated fraud. At its finest, (extra virgin) olive oil serves better as an enhancement than as a cooking oil, unless its temperature is carefully monitored, lest its phenolic promises be compromised. It is prudent to avoid cooking with any monounsaturated (avocado, olive) and especially with polyunsaturated oils (grape seed, sesame, canola, safflower, sunflower, corn) due to their PUFA content. It is advisable to cook at moderate temperatures, using coconut oil, animal fats, or butter/ghee. Get back to basics; guess what our grandmothers used?

To our disappointment, a majority of polyunsaturated fats have become hybridized without our knowledge, leaving us with altered products that fail to deliver the health benefits we once enjoyed. What is now high-oleic sunflower or safflower oil is not the same healthful fat we used to know. To compound matters, the food supply has become a nationwide, uncontrolled experiment in culinary and dietary manipulation, offering the spoils to the victorious industry and the spoiled results to the victims. Salad dressings, mayonnaises and assorted fat-related condiments have suffered a similar fate.

If people are destroyed for lack of knowledge, it is doubly so in the realm of fatty acids. To render false information is lying, but to hide information is also a lie. In this regard, we have been deprived of knowing the details of omega-6 pathways, having been told only that omega-6s present with inflammatory compounds as end-products. First, let’s be aware that pre-formed AA, provided by meat and its fat, and by butter and cream leads to the essential series 2 prostaglandins. Albeit pro-inflammatory, these prostaglandins are the lead eicosanoids in the body and are crucial to maintenance of our health. For example, without them there would be no healing of a cut, since white blood cells and platelets would not be beckoned to the scene. Linoleic acid, the mother n-6 fatty acid, is the premier support of cardiolipin and the mitochondria. LA is converted by enzyme activity to gamma-linolenic acid (GLA), dihomo-gamma linolenic acid (DGLA) and eventually to the anti-inflammatory series 1 prostaglandins. 

The second tidbit to which we need attend is the potentially virulent, toxic and inflammatory character of oils exposed to elevated temperatures. The problem does not come from linoleic acid or any other n-6 fat! We have seen microscope images of cell membranes that have been assaulted and battered by these debased and corrupted lipid entities, particularly in the membranes of individuals suffering autoimmune and neurological diseases, where aberrant, renegade lipids have become attached to their DNA, effectively altering gene expression from epigenetic insult. Removal of aldehyde-ridden supermarket oils from the diet is mandatory if optimal health is our goal. Though not top heavy with PUFAs, olive oil is likewise categorized.

Third in the list we find that essential fatty acids (EFAs) appear in echelons of physiological activity. The lower-echelon fats include linoleic acid (from sunflower seeds, high-linoleic safflower oil and high-linoleic acid sunflower oil) along the n-6 branch, and alpha-linolenic acid (from flaxseed oil, chia seeds and walnuts) along the n-3 branch. The higher-order fatty acids include arachidonic acid (from cream, egg yolks, cheeses and meat) along the n-6 branch, and EPA / DHA (from marine sources) along the n-3 branch.

The fourth item of interest tells us that monounsaturated fatty acids (MUFAs) and saturated fatty acids (SFAs) are not essential, meaning that the body can make them from the diet. These fats offer us only calories and gustatory satiety; they are not bioactive lipids. Avocados, olive oil and tree nuts provide MUFAs, while coconut oil and coconut butter, cocoa butter, meat fats, and dairy butter give us SFAs.

The quality of our Life is riveted in the lipids we ingest as they pivotal in the health of the cell membrane and as we have come to understand… the membrane is everything in optimizing our state of health.

Most Important To Avoid To Regain And Stabilize Health:

  • All fried food including French fries unless cooked at home in coconut oil
  • Fast foods, almost all contain heated, toxic oil
  • Commercial foods organic or not, almost all contain heated, toxic oil
  • Hydrogenated vegetable oil, margarine, processed oils
  • Canola oil -often in processed foods / dressing, contains very long chain fatty acids
  • Peanut butter, peanuts, peanut oil, contains very long chain fatty acids
  • Mustard- contains very long chain fatty acids
  • Commercial mayo or salad dressing, use homemade with high linoleic safflower instead
  • Most Olive oil, limited availability of the pure oil, difficult to tell which one is pure
  • Commercial oils, high-oleic hybrid oils, including those labeled organic

Lipids, Oils And Fats You May Be Included In The Diet, But Don’t Contain Bioactive Lipids:

  • Organic coconut oil, useful in cooking
  • Olive oil, caution – limited availability of the pure oil, does not contain bioactive lipids

Lipids, Oils And Fats That Contain EFAs To Include To Optimize Health:

  • Concentrated phospholipids as PC and PE from BodyBio
  • 4:1 omega-6 to omega-3 oil, SR-3, as BodyBio Balance oil
  • High Linoleic, organic, cold pressed Safflower oil (this is imported)
  • Nutiva® Organic Hempseed oil
  • Evening primrose oil, pure cold pressed (not sourced from China)
  • Wild caught, cold water fish
  • Caviar, Anchovies, Sardines from clean waters, not farmed
  • Free range, organic egg yolks
  • Raw, organic seeds-hemp, chia, sunflower, pumpkin, fenugreek, sesame
  • Homemade kefir (cow, goat, sheep, camel)
  • Limited amounts of grass-fed, free-range sources of dairy (cow, goat, sheep, camel) butter, ghee, cream

Alterations to the food supply explain the fifth entry. Where sunflower, safflower and soybean oils once were high in linoleic acid, they now are high in oleic acid, ostensibly making them candidates for the sauté pan, a place where they will still be denigrated and debased, yet a bad thing, although at a slower rate. The damage done to an oil that has been heated and reheated in a fast-food restaurant or local diner is mind-boggling. It’s little wonder that these oils are reclaimed to be used as biofuels in diesel engines. Using them in salad dressing or atop steamed vegetables is one thing, but cooking with them is quite another. No matter the molecular nature, a heated MUFA / PUFA oil is ultimately toxic.

Sixth in our hit parade is the contraindication of marine oils in the treatment of childhood seizure disorders, where administration of such has only exacerbated the condition. Here, the DHA fraction impinges upon the NMDA receptors and stimulates excitation, while the EPA moiety suppresses beta hydroxybutyrate, the primary ketone. Aggravating the matter is that most commercial fish oils are processed using elevated temperatures for extraction, leading to aldehyde formation and degradation of the fatty acids. Thus-damaged fish oils are toxic. On the other hand, wild fish, the ultimate source of marine oils, are not. Salmon, anchovies, sardines and caviar are preferred.

To realize that coconut oil, olive oil, and avocado oil, among a few others, are not essential fatty acids makes number seven in our list. Coconut oil and MCT oil produce ketones quickly, not needing bile to be digested and absorbed. Since coconut does not contain EFAs or MUFAs, it may be used for cooking.

Number eight is worthy of fanfare and flourish. Oils that carry very-long-chain fatty acids are a considerable challenge to the liver and the brain. Because of their size, they dangle outside the mitochondrial membrane, so need peroxisomes to be metabolized, to be burned or beta oxidized. Mustard oil, canola oil, peanut oil and peanut butter are sources.

Knowing the ninth entry introduces us to the bioactive oils that display EFAs and phospholipids crucial to optimal health. In this camp we find Specific-Ratio 3 or SR-3 oil as a prime source of a balanced 4:1 omega-6 / omega-3 ratio, featuring organic, cold-pressed, non-GMO safflower and flaxseed oils as the mother fatty acids. Related bioactive oils are high-linoleic safflower oil, raw organic seeds (sunflower, hemp, pumpkin, chia) and seed creams (soak overnight, blend), Canadian evening primrose oil, wild cold-water fish (especially caviar, anchovies, sardines), free-range eggs (the yolks).