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Aging and The Brain

coconut oil, fats oils, essential fatty acids

Our brains are 60% fat. In light of what we know of brain function and the essential fatty acids that are responsible, the term “fat-head” could now be a complement. Since our brains are in charge and require the right fats to run our thinking machinery, our first priority is to make sure we add the right ones into our diet, the omega 6s and omega 3s. They are essential and get the job done. First – let’s review some of the basics.

Fats and oils can be divided into two densities and two levels. The densities are not unlike the SAE oils, the Society of Automotive Engineers who organize the oils for our autos. But it is better to skip the details at the moment and divide them in two categories “thick” and “thin”. Fats are the thick ones and oils are thin, actually runny. It’s quite good to divide them in this simplistic way. The confusion about what we eventually eat is all over the lot and besides, our cells and membranes organize fats and oils as partners with each having a precise role. The membrane does not work without both, thick and thin, sluggish and active. We can begin with the ones we use in our kitchens because they wind up in our metabolism whether we like it or not.

You can think of the thick ones as butter or lard. We tend to look down on lard as being out of date. We regard it as a thing of the past. Our grandparents and great grandparents certainly didn’t think so. As cooking oil, lard has been with us for some time. It’s been a staple for centuries, probably hundreds of centuries, and we’ve survived and even flourished. It’s part of our evolutionary history. Those thick heavy oils were skimmed off the top of stews and saved, collected from roasts of pork, lamb, goose or turkey. It was regarded as valuable stuff. Before the light bulb, making candles was a basic part of life so the rendering of fat in the kitchen was universal. The plain fact is that lard is OK for cooking. However, just reminiscing, not pushing lard today.

Butter and olive oil are both excellent cooking oils, however, coconut is also marvelous for cooking. It’s not exactly a thick fat, for as you know, it quickly gets thin as the temperature rises. Castillo et al 1999, reports that “Supplementation of coconut oil produced a significant hypercholesterolemia after 7 days of treatment. However, supplementation of menhaden oil induced a significant decrease in total cholesterol after only 2 weeks of treatment”. The raising of cholesterol may sound sacrilegious; however, notwithstanding the loud din of media anti-cholesterol noise, there are those who have difficulty in doing just that – raising cholesterol. Cholesterol is an important fat for our cell membranes; it metabolizes up to our gonadal hormones — think sex. No necessity in elaborating on that subject. It’s also a precursor for our adrenal hormones, which produce our life saving impulses for fight or flight, and bile acids which shepherd the fats and oils around in the blood stream. Without further ado — cholesterol is necessary.

Castillo creates an interesting picture of coconut oil, or butter, as you prefer, and the essential oils that are part of our diet. By itself, coconut can raise cholesterol, but by introducing menhaden oil, it just as quickly reverses and lowers it. This feature of menhaden oil, basically an omega 3 essential fatty acid (EFAs), to lower cholesterol, is also duplicated with the omega 6 EFAs, and there is abundant research that corroborates it. We can regard all of the omega 6s and 3s as “thin oils” and cholesterol, when grouped together as a very “thick fat”.

The lesson here is more than casual. We need the thick ones and we desperately need the thin ones. The thin ones keep the thick ones from collecting to the degree where we tend to get into trouble that comes with aging, such as atherosclerosis, heart disease. In just these two words, thick and thin, we have covered half of all Fatty Acid biochemistry in human metabolism. But it may be just too simple to be looked at with the respect that it deserves. You may spend a third of your life getting a medical degree and half again practicing medicine, but if you do not see this simple relationship you will also retire as a failure from your chosen field of medicine.

Coconut used to be the preferred oil for making popcorn, but ADM and the other large oil producers chased it out of the movies over 30 years ago. It’s a shame we lost it. It was much healthier eating coconut oil than what is currently in use today. Most of the oils used for popcorn and fries are PUFAs, they are thin and should not be heated. They quickly degenerate and become partially hydrogenated and/or oxidize and become rancid.

Coconut oil is one of the most stable oils you can buy. It does not turn rancid easily. It does not attack your arteries. In fact, coconut oil was one of the foods Dr. Weston Price studied when he traveled the world searching for healthier people and their lifestyles. In his journeys he discovered that the coconut was considered a medicine food by the local populations. He found that those civilizations that consumed coconut regularly had no knowledge of cancer, heart disease, arthritis, or diabetes.

There are few other choices for cooking unless you think of the new GMO oils like high oleic soybean, sunflower or safflower oils, Canola also fits into that group because it was one of the first GMO oils to be converted. Canola contains erucic acid, a very long chain saturated fat. It is unhealthy for our membranes, it’s too long and slows the fluidity of the membrane. Think of erucic as a gawking fat blocking our healthy fats from doing what they want to do, running quickly in our membranes managing our cells. Please avoid canola. We simply do not like GMOs for anything we eat.

The thin oils, the PUFAs, come from seeds, nuts, and grains like olive, sunflower, corn, walnut, etc. They harbor the essential fatty acids which play a vital role when the time comes for them to reproduce new versions of themselves. Oils like olive are mostly Mono-Unsaturated Fatty Acids (MUFAs), and are OK, but do not stack up with the likes of the omega 6 and 3 PUFAs, the very healthy FAs. These Poly-Unsaturated Fatty Acids, with more than one double bond, are the stars in our choices of foods. They are predominantly made up of the essential oils, the omega 6s and the omega 3s and are exclusively made by plant seeds. They are important for life and especially the brain. When we use the term essential, we mean that the body cannot function without them. They are essential for life, our life. They hold the secret to Brain health, which we will delve into on Aging and the Brain: Part 2.

To learn more about one of the most important EFA discoveries of the last century, the ratio of 6s and 3s, which is 4: 1, 80% omega 6 (linoleic) to 20% omega 3 (linolenic), go tohttp://www.bodybio.com/BodyBio/docs/BodyBioBulletin-4to1Oil.pdf.

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

Diabetes and Omega-3’s

Diabetes, Omega-3 fatty acids Super FoodsReading, interpreting and understanding scientific literature can be tedious because the authors often find that their previous paper on the subject missed its mark or was completely wrong. Easy to do when you are blazing new trails; however, the caution they go through to cover their tracks oftentimes makes for difficult reading. Luc Djousse and his colleagues at the U of Washington reported in the May 18, 2011 edition of the American Journal of Clinical Nutrition that, “With the use of objective biomarkers, long-chain omega 3 Fatty Acids (FAs) and Alpha-Linolenic Acid (ALA) were not associated with a higher incidence of diabetes. Individuals with the highest concentrations of both types of FAs had lower risk of diabetes.”

Speed reading is absolutely out of place. Omega-3 fatty acids in the body help to control the inflammation process, which is a benefit because the start of the healing process—initiated by the omega-6 arachidonic acid—also involves the possibility of getting carried away with the exercise. Say you have a cut or abrasion. The key activity that ensues is to stop the loss of fluids – save the blood.  It is that process which tells the body to start the healing by sending white blood cells and platelets to the site of the wound and to agglomerate and close the exit door by swelling the tissues, which is also another way of looking at inflammation. To inflame can be life saving. The omega-3’s are then involved in the work of modulating the activity helping to ease the inflammation that comes with the correction process.

Fatty acids, especially those that are long and highly unsaturated, increase cell membrane fluidity and functionality. Fatty acids are essential to membrane activity at the location of hormone receptors. Insulin resistance in adult-onset diabetes is directly associated with fewer membrane enhancing long-chain fatty acids, largely due to impaired function of desaturase and elongase enzymes needed for a healthy membrane. Ruiz-Gutierrez 1993, “We have studied the fatty acid composition of erythrocyte membrane phospholipids in nine Type 1 (insulin-dependent) diabetic patients and nine healthy control subjects. Cell membranes from the diabetic patients showed a marked decrease in the total amount of polyunsaturated fatty acids mainly at the expense of docosahexaenoic acid, DHA, and arachidonic acid C20:4n6”.

Cell membrane abnormalities in lipid content are found to be related to poor metabolic control, which is a characteristic of diabetes. Diet is a very important  factor, and interventions with dietary essential fatty acids (EFAs) in the correct ratio (found to be 4:1, omega-6:omega-3), can make a difference. Decsif  T., 2002, “Reduced availability of long-chain polyunsaturates in diabetic children suggests that an enhanced dietary supply of long-chain polyunsaturates may be beneficial”. Children with diabetes demonstrate a deficit of long-chain fatty acids, so incorporating them into a child’s diet is prudent. An unspoken benefit in the application of EFA’s to diabetes treatment is the decrease in triglyceride levels, themselves striking indicators of the potential for cardiovascular issues and very often appearing in persons with diabetes.

Herein resides the prolonged physiological support of the EFAs. For those who lack the efficient conversion of the omega-3 alpha linolenic acid from plant sources (notably flaxseeds and their oil) to EPA and DHA, fish oil may be a viable alternative. In fact the the FA conversion process with diabetes is almost non-existent, but also common with aging.

For quite some time the essential fatty acids have been misunderstood. Of the types of fatty acids, the omega-3’s have received the most publicity, having been applauded for positive health effects, principally, because over the last century the general population ate little fish and had little or no n-3s in the diet. Unless they were more or less health nuts, few did not have any exposure to omega 3s as in flax, and even if they did their ability to elevate up to EPA and DHA was minimal. Fish oil was the answer but the explosion that ensued caused over-consumption and still does.

Hence the comments of Djousse et al that n-3 FAs did not increase diabetes but if both the omega 6s and the 3 s were added together there was marked improvements. There is an inference that n-3s were of no benefit and needed the balance of both EFAs, which we applaud and so should you. Balance is paramount.

References

Djoussé L, Biggs ML, Lemaitre RN, King IB, Song X, Ix JH, Mukamal KJ, Siscovick DS, Mozaffarian D. Plasma omega-3 fatty acids and incident diabetes in older adults. Am J Clin Nutr. 2011 May 18.

Ruiz-Gutierrez V, Stiefel P, Villar J, García-Donas MA, Acosta D, Carneado J.  Cell membrane fatty acid composition in type 1 (insulin-dependent) diabetic patients: relationship with sodium transport abnormalities and metabolic control.  Diabetologia. 1993 Sep;36(9):850-6.

T. Decsif, H. Minda, R. Hermann, A. Kozári, É. Erhardt, I. Burus, Sz. Molnár and Gy. Soltész  Polyunsaturated fatty acids in plasma and erythrocyte membrane lipids of diabetic children  Prostaglandins, Leukotrienes and Essential Fatty Acids. 67(4); Oct 2002: 203-210

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

Atopic Dermatitis / Eczema

evening-primrose-oilSome unfortunate persons are not able to convert essential fatty acids (EFA’s) from their parent forms to their more active metabolites, such as converting linoleic acid, the primary omega-6, to gamma-linolenic acid (GLA). More than twenty years of research points to the inefficiency of this active conversion pathway as causative of inflammatory skin conditions. Wherever and whenever a metabolite cannot be made by the body on its own, administration of that substance may be in order.

At the start of the twenty-first century, research scientist David Horrobin described a positive relationship between evening primrose oil as a source of pre-formed GLA and the improvement in symptoms of atopic dermatitis, namely eczema.  He relates that, “In most but not all studies, administration of GLA has been found to improve the clinically assessed skin condition, the objectively assessed skin roughness, and the elevated blood catecholamine concentrations of patients with atopic eczema.”  Understandably, the condition may be ascribed a hereditary genesis.  (Horrobin. 2000)

When one of the crowd upsets the apple cart he becomes noticed because of the chaos he spawned.  David Horrobin is such a person.  He was responsible for opening the eyes of the research community to the potential of complementary and alternative medicine in the treatment of fatty acid deficiency conditions, including inflammatory skin conditions, schizophrenia, rheumatoid arthritis, and diabetes, to name but a few.  Horrobin—and others after him— discovered that metabolic inefficiency in the conversion of linoleic acid to gamma-linolenic acid (GLA) might be responsible for inflammatory skin responses that present as eczema, despite the presence of adequate linoleic acid in blood and adipose tissue.  (Dobryniewski. 2007. p. 100)

It is such that omega-6 and omega-3 fatty acids compete for the enzymes that transform them into super hero molecules known to control the inflammation activities that promote health. The omega-3 fatty acids prevail at the expense of the omega-6s, leading to a deficit of omega-6 metabolites and their benefits.  Therefore, it makes sense to overcome deficiencies by administering these metabolites directly, as in the oral and/or topical use of evening primrose oil (EPO), an omega-6 fatty acid accepted for its GLA content.  Horrobin’s desire to herald the attributes of GLA spread to the European continent, where scientists from Poland agreed that GLA is one of the most frequently deficient fatty acids, and that supplementation brings hopeful effects in the treatment of eczema and other conditions.  (Horrobin. 1993)  (Dobryniewski. 2007. p. 91)

There are predisposing factors in acute or chronic skin disease, including family history of allergic disorders and sensitivity to contact allergens or to certain foods.  Chronic disease is difficult to treat.  Itching causes scratching, which increases inflammation, which causes itching … The cycle is hard to break.  But evening primrose oil (EPO), with a history of efficacy that predates Dr. Horribin’s interest, has produced “…significant clinical improvement on atopic eczema.” (Ebden. 1989)  In meta analyses conducted in the late 1980’s, the British Journal of Dermatology recounted significant improvement in eczema symptoms using a commercial EPO product called Epogam (the name seemingly gleaned from EPO and GLA), after which use, “ The effects on itch were particularly striking.” (Morse.1989).

BodyBio evening Primrose Oil contains ten percent GLA and a sufficient amount of its precursor, linoleic acid, to help the body make the molecules that inhibit the pro-inflammatory series 2 prostaglandins and series 4 leukotrienes.  There is a distinct correlation between improvements in clinical scoring devices and an elevation of fatty acid levels.  Compared to placebo, children treated with EPO significantly improved the symptoms of atopic eczema.  (Bordoni. 1988)

References

Horrobin DF.
Essential fatty acid metabolism and its modification in atopic eczema.
Am J Clin Nutr. 2000 Jan;71(1 Suppl):367S-72S.

Dobryniewski J, Szajda SD, Waszkiewicz N, Zwierz K.
The gamma-linolenic acid (GLA)–the therapeutic value.  [Article in Polish]
Przegl Lek. 2007;64(2):100-2.

Horrobin DF.
Fatty acid metabolism in health and disease: the role of delta-6-desaturase.
Am J Clin Nutr. 1993 May;57(5 Suppl):732S-736S; discussion 736S-737S.

Dobryniewski J, Szajda SD, Waszkiewicz N, Zwierz K.
Biology of essential fatty acids (EFA). [Article in Polish]
Przegl Lek. 2007;64(2):91-9.

Ebden P, Bevan C, Banks J, Fennerty A, Walters EH.
A study of evening primrose seed oil in atopic asthma.
Prostaglandins Leukot Essent Fatty Acids. 1989 Feb;35(2):69-72.

P.F. MORSE, D.F. HORROBIN,, M.S. MANKU, J.C.M. STEWART, R. ALLEN, et al
Meta-analysis of placebo-controlled studies of the efficacy of Epogam in the treatment of atopic eczema. Relationship between plasma essential fatty acid changes and clinical response
British Journal of Dermatology. Volume 121, Issue 1, pages 75–90, July 1989

Bordoni A, Biagi PL, Masi M, Ricci G, Fanelli C, Patrizi A, Ceccolini E.
Evening primrose oil (Efamol) in the treatment of children with atopic eczema.
Drugs Exp Clin Res. 1988;14(4):291-7.

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

Essential Fats Explained

fattyacid-sourceThe essential fatty acids (EFA’s) are just that—essential, meaning they have to come from the diet because the body can’t manufacture them. They might be used as fuel, but they are absolute components of the biological processes that make us work. Only two fatty acid families are vital to humans, omega-6’s and omega-3’s. It’s been shown that their ratio is more important than their volume. The parent fatty acid (FA) in the omega-6 (n-6) line is linoleic acid, abundant in many vegetable oils and ultimately responsible for the biosynthesis of arachidonic acid and related prostaglandins, which are compounds that regulate physiological activities. Alpha-linolenic acid (ALA) is the mother omega-3 (n-3) fatty acid, commonly extracted from seed oils such as flaxseed and hemp, but also found in walnuts. Nearly every aspect of human physiology is affected by essential fats, receptors for which are located in practically every cell.

The n-6 fatty acids have been denigrated in recent years because their excess has been linked to several metabolic upsets. Unbalanced diets are harmful to health, and the n-6’s that overpopulate processed foods and rancid supermarket oils have contributed to myriad health woes. What possibly started out as a 1 to 1 or 2 to 1 ratio of n-6 fatty acids to n-3 fatty acids in the human diet eons ago has become a physiological disaster of imbalance, where the ratio exceeds 10 to 1 in the typical Western diet, and may even approach 20 to 1, or worse, in personal food intake. All fatty acids go through a process of desaturation and elongation to become eminently bioactive compounds. The ultimate products of the process are beneficial to human health, especially if they are made step-by-step by the body and not forced upon it through manufactured meals, unnaturally finished meat products, stale/oxidized vegetable oils, and fossilized eggs, not to mention horrific snack foods. In a healthy body, linoleic acid is converted to gamma-linolenic acid (GLA), which becomes arachidonic acid, from which come the chemicals that control inflammation. After adulthood, the body’s ability to make those conversions is uncertain, so starting with GLA gives us a head start. However, mother linoleic acid is anti-inflammatory in its own right and even a marginal conversion to GLA has been held effective in the management of conditions as diverse as rheumatoid arthritis, eczema and ADD/ADHD.

The n-3 parent, ALA, also must come from diet because humans lack the enzymes necessary to convert it from other fats. But it’s the downstream omega-3’s that get the publicity:  EPA and DHA. Like the n-6’s, the conversion of ALA to EPA and later to DHA is an uncertain proposition in adulthood, which is why most adults use fish oil, a source of pre-made fatty acids. Even in the absence of the requisite conversion co-factors (vitamin B6, Mg, biotin, vitamin B3, vitamin C and Zn), ALA is anti-inflammatory and cardiac friendly (Pan, 2012) (Vedtofte, 2012), with recent scrutiny heralding its potential to inhibit progression of atherosclerosis (Bassett, 2011). The most readily available source of ALA is flaxseed, although chia, the newest kid on the block, is entering the marketplace.

Signs of fatty acid deficiency include a dry scaly rash, impoverished growth in youngsters, increased susceptibility to infections and poor wound healing, but are uncommon. The enzymes that convert the parent fatty acids act preferentially toward the n-3’s. By the time these enzymes deal with the omega-3 fats, some of the omega-6’s have been used for energy, hence the need to get more 6’s than 3’s, in a ratio of about 4 to 1, as evidenced by intensive research done in the 1990’s and early-mid 2000’s (Yahuda, 1993, 1996) (Simopoulos, 2002, 2008). But this ratio is based on the body’s own manufacture of the downstream fatty acids, GLA and arachidonic acid (ARA) along the n-6 line (the latter now included in products designed for infants to insure proper brain development) and EPA/DHA down the n-3 line. Deficiency of essential fatty acids sometimes strikes those suffering from cystic fibrosis or fat malabsorption issues. If patients receive total parenteral nutrition without the inclusion of EFA’s, deficit will appear in about a week or two.

The dry weight of the brain is about 80% lipids, the highest of any organ. The long-chain polyunsaturated fats, especially the n-6 and n-3, are crucial in modulating neural function. They occupy as much as 30% of the brain’s dry weight, making their influence on neural membrane dynamics profound. The shift away from EFA’s in the Western—typically American—diet parallels a rise in mental disorders. The need to address EFA supplementation is real and current, with the inclusion of omega-6 fats a necessity, since GLA, the downstream scion of linoleic acid, has held its own in mental health studies (Vaddadi, 2006). Together, the n-6’s and n-3’s cooperate in a number of cellular functions that affect membrane fluidity, allowing the passage of food and energy into the cell and wastes out. Arachidonic acid is a precursor to signaling molecules in the brain and is a key inflammatory intermediate, while EPA and DHA work to support the cardiovascular system, and the brain and retina.

It is arachidonic acid that supports membrane fluidity in the hippocampus, the part of the brain that directs memory, spatial relations and inhibition (Fukaya, 2007). It is arachidonic acid that protects the brain against oxidative stress and activates proteins in charge of the growth and repair of neurons (Darios, 2006). There is conjecture that ARA supplementation during the early stages of Alzheimer’s disease may slow its progress and stave off symptoms (Schaeffer, 2009). That’s a pretty good promise for something that’s been spurned…for lack of knowledge. Of the n-3’s, EPA may be effective in addressing depressive conditions and behavioral anomalies, besides being able to reduce inflammation (Brind, 2001) (Song, 2007). There had been some concern that EPA adversely affects clotting factors and fibrinogen concentrations, increasing the likelihood of bleeding. That is not so (Finnegan, 2003). It does, however, improve blood viscosity and red blood cell deformity, which allows red cells to adjust their shape to squeeze through narrow blood vessels, like capillaries. Downstream from EPA is DHA, a major fatty acid in sperm, brain phospholipids and the retina of the eye, and found to lower triglycerides. But its claim to fame is its rapid accrual in the developing brain during the third trimester of pregnancy and early postnatal period (Auestad, 2003) (Wainwright, 2000).

You can safely bet the farm that endogenous (made by the body itself) substances are more tightly regulated than exogenous. For example, the arachidonic acid your body makes from linoleic acid is more respectable than that from a haphazardly slaughtered steer, which may or may not be completely lifeless before the abattoir starts to dress it. In fear and pain, the animal releases a torrent of adrenal hormones throughout its flesh, confounding the integrity of its innate fatty acids. Endogenous fatty acids are, therefore, more wholesome.

How do we acquire the parent fatty acids?  You could buy oils that boast omega-6 and omega-3 fatty acid content from the supermarket, but it’s almost guaranteed that the balance will be too far out of whack to deliver a benefit, and the purity of the oils is possibly iffy. In fact, they might upset the apple cart. An overabundance of n-3’s can shut the immune system down for lack of guidance by the n-6 inflammation directors. On the other hand, BodyBio Balance Oil is a blend of organic, cold-pressed sunflower and flaxseed oils that are purposely geared to supply a 4 to 1 ratio of fatty acids that the body needs to initiate the cascade to longer chain fats that present vibrant physiological activity. Just the anti-inflammatory properties of the mother fatty acids, linoleic from sunflower and alpha-linolenic from flax, are enough to warrant using the oils to bolster the body’s well-being and to work out some metabolic kinks. Used to make salad dressings or to dress vegetables in place of butter, Balance Oil has the potential to set straight that which is awry, and the essential fatty acid metabolites can help to clear the brain fog on a hazy day. Cerebral lipids, especially the long-chain fatty acids, have significant direct and indirect activity on cerebral function. Not only do they affect the membranes, but also many are converted to neurally active substances. There is good evidence that mental challenges are related to EFA depletion, the supplementation of which can ameliorate the most defiant state of affairs.

References

Auestad N, Scott DT, Janowsky JS, Jacobsen C, Carroll RE, Montalto MB, Halter R, Qiu W, et al
Visual, cognitive, and language assessments at 39 months: a follow-up study of children fed formulas containing long-chain polyunsaturated fatty acids to 1 year of age.
Pediatrics. 2003 Sep;112(3 Pt 1):e177-83.

Bassett CM, McCullough RS, Edel AL, Patenaude A, LaVallee RK, Pierce GN.
The α-linolenic acid content of flaxseed can prevent the atherogenic effects of dietary trans fat.
Am J Physiol Heart Circ Physiol. 2011 Dec;301(6):H2220-6. doi: 10.1152/ajpheart.00958.2010. Epub 2011 Sep 30.

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.

Chang CS, Sun HL, Lii CK, Chen HW, Chen PY, Liu KL.
Gamma-Linolenic Acid Inhibits Inflammatory Responses by Regulating NF-kappaB and AP-1 Activation in Lipopolysaccharide-Induced RAW 264.7 Macrophages.
Inflammation. 2009 Oct 20.

Darios F, Davletov B.
Omega-3 and omega-6 fatty acids stimulate cell membrane expansion by acting on syntaxin 3.
Nature. 2006 Apr 6;440(7085):813-7.

da Rocha CM, Kac G.
High dietary ratio of omega-6 to omega-3 polyunsaturated acids during pregnancy and prevalence of post-partum depression.
Matern Child Nutr. 2012 Jan;8(1):36-48. doi: 10.1111/j.1740-8709.2010.00256.x. Epub 2010 Jun 21.

Dupasquier CM, Dibrov E, Kneesh AL, Cheung PK, Lee KG, Alexander HK, Yeganeh BK, Moghadasian MH, Pierce GN.
Dietary flaxseed inhibits atherosclerosis in the LDL receptor-deficient mouse in part through antiproliferative and anti-inflammatory actions.
Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2394-402. Epub 2007 Jul 6.

Fernandes FS, de Souza AS, do Carmo Md, Boaventura GT.
Maternal intake of flaxseed-based diet (Linum usitatissimum) on hippocampus fatty acid profile: implications for growth, locomotor activity and spatial memory.
Nutrition. 2011 Oct;27(10):1040-7.

Finnegan YE, Howarth D, Minihane AM, Kew S, Miller GJ, Calder PC, Williams CM.
Plant and marine derived (n-3) polyunsaturated fatty acids do not affect blood coagulation and fibrinolytic factors in moderately hyperlipidemic humans.
J Nutr. 2003 Jul;133(7):2210-3.

Fukaya T, Gondaira T, Kashiyae Y, Kotani S, Ishikura Y, Fujikawa S, Kiso Y, Sakakibara M.
Arachidonic acid preserves hippocampal neuron membrane fluidity in senescent rats.
Neurobiol Aging. 2007 Aug;28(8):1179-86. Epub 2006 Jun 21.

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.

Ángeles Guinda, M. Carmen Dobarganes, M. Victoria Ruiz-Mendez, Manuel Mancha
Chemical and physical properties of a sunflower oil with high levels of oleic and palmitic acids
European Journal of Lipid Science and Technology. 105(3-4); Apr 2003: 130-137

BRIAN HALLAHAN, MRCPsych and MALCOLM R. GARLAND, MRCPsych
Essential fatty acids and mental health
The British Journal of Psychiatry (2005); 186: 275-277

William S. Harris, PhD, FAHA, Chair;  Dariush Mozaffarian, MD, DrPH, FAHA;  et al
Omega-6 Fatty Acids and Risk for Cardiovascular Disease
A Science Advisory From the American Heart Association Nutrition Subcommittee of the Council on Nutrition, Physical Activity, and Metabolism; Council on Cardiovascular Nursing; and Council on Epidemiology and Prevention
Circulation. 2009; 119: 902-907

Kakutani S, Ishikura Y, Tateishi N, Horikawa C, Tokuda H, Kontani M, Kawashima H, Sakakibara Y, Kiso Y, Shibata H, Morita I.
Supplementation of arachidonic acid-enriched oil increases arachidonic acid contents in plasma phospholipids, but does not increase their metabolites and clinical parameters in Japanese healthy elderly individuals: a randomized controlled study.
Lipids Health Dis. 2011 Dec 22;10:241.

Lands B.
Consequences of essential Fatty acids.
Nutrients. 2012 Sep;4(9):1338-57.

Eric L. LIEN, Kurt STEINER and John C. WALLINGFORD
The Proper Balance of Essential Fatty Acids for Life
Journal of Oleo Science. Vol. 50 (2001) , No. 5 399-405

Maekawa M, Takashima N, Matsumata M, Ikegami S, Kontani M, Hara Y, Kawashima H, Owada Y, Kiso Y, Yoshikawa T, Inokuchi K, Osumi N.
Arachidonic acid drives postnatal neurogenesis and elicits a beneficial effect on prepulse inhibition, a biological trait of psychiatric illnesses.
PLoS One. 2009;4(4):e5085. doi: 10.1371/journal.pone.0005085. Epub 2009 Apr 8.

Osumi N.
Fatty acid signal, neurogenesis, and psychiatric disorders
Nihon Shinkei Seishin Yakurigaku Zasshi. 2010 Jun;30(3):141-8.

Pan A, Chen M, Chowdhury R, Wu JH, Sun Q, Campos H, Mozaffarian D, Hu FB.
α-Linolenic acid and risk of cardiovascular disease: a systematic review and meta-analysis.
Am J Clin Nutr. 2012 Dec;96(6):1262-73. doi: 10.3945/ajcn.112.044040. Epub 2012 Oct 17.

Pawels EK, Volterrani D.
Fatty acid facts, Part I. Essential fatty acids as treatment for depression, or food for mood?
Drug News Perspect. 2008 Oct;21(8):446-51. doi: 10.1358/dnp.2008.21.8.1272136.

Peet M, Brind J, Ramchand CN, Shah S, Vankar GK.
Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia.
Schizophr Res. 2001 Apr 30;49(3):243-51.

Sakayori N, Maekawa M, Numayama-Tsuruta K, Katura T, Moriya T, Osumi N.
Distinctive effects of arachidonic acid and docosahexaenoic acid on neural stem /progenitor cells.
Genes Cells. 2011 Jul;16(7):778-90. doi: 10.1111/j.1365-2443.2011.01527.x. Epub 2011 Jun 13.

Sanders TA, Rana SK.
Comparison of the metabolism of linoleic and linolenic acids in the fetal rat.
Ann Nutr Metab. 1987;31(6):349-53.

Schaeffer EL, Forlenza OV, Gattaz WF.
Phospholipase A2 activation as a therapeutic approach for cognitive enhancement in early-stage Alzheimer disease.
Psychopharmacology (Berl). 2009 Jan;202(1-3):37-51.

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)

Meharban Singh
Essential fatty acids, DHA and human brain
Indian Journal of Pediatrics. Volume 72, Number 3 / March, 2005: 239-242

Song C, Zhao S.
Omega-3 fatty acid eicosapentaenoic acid. A new treatment for psychiatric and neurodegenerative diseases: a review of clinical investigations.
Expert Opin Investig Drugs. 2007 Oct;16(10):1627-38.

Uauy R, Hoffman DR, Peirano P, Birch DG, Birch EE.
Essential fatty acids in visual and brain development.
Lipids. 2001 Sep;36(9):885-95.

Vaddadi K.
Essential fatty acids and mental illness.
Int Rev Psychiatry. 2006 Apr;18(2):81-4.

Vedtofte MS, Jakobsen MU, Lauritzen L, Heitmann BL
The role of essential fatty acids in the control of coronary heart disease.
Curr Opin Clin Nutr Metab Care. 2012 Nov;15(6):592-6.

Wainwright P.
Nutrition and behaviour: the role of n-3 fatty acids in cognitive function.
Br J Nutr. 2000 Apr;83(4):337-9.

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.

Yehuda S, Rabinovitz S, Mostofsky DI.
Essential fatty acids are mediators of brain biochemistry and cognitive functions
J Neurosci Res. 1999 Jun 15;56(6):565-70.

Yehuda S, Rabinovitz S, Carasso RL, Mostofsky DI.
The role of polyunsaturated fatty acids in restoring the aging neuronal membrane.
Neurobiol Aging. 2002 Sep-Oct;23(5):843-53.

Young G, Conquer J.
Omega-3 fatty acids and neuropsychiatric disorders.
Reprod Nutr Dev. 2005 Jan-Feb;45(1):1-28.

*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)

Refere

References

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
DIETARY n-6 AND n-3 FATTY ACID BALANCE AND CARDIOVASCULAR HEALTH
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.

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.

References

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.

Blood Pressure and…

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

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

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

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

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

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

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

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

References

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Role of ω3 long-chain polyunsaturated fatty acids in reducing cardio-metabolic risk factors.
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Bao DQ, Mori TA, Burke V, Puddey IB, Beilin LJ.
Effects of dietary fish and weight reduction on ambulatory blood pressure in overweight hypertensives.
Hypertension. 1998 Oct;32(4):710-7.

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

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

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

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

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

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

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

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

*These statements have not been evaluated by the FDA.
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