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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 We tend to look down on lard as being out of date.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.

Longevity And Stress

hand-squeezing-stress-ballJust as oxidation causes iron to rust and brass to tarnish, it causes our cells to rust and tarnish, only figuratively and not literally…unless the Tin Man is part of the gene pool.  When you get stressed out—and there’s a litany of reasons for that—your body makes oxidative chemicals that hasten aging, increase cardiovascular risk, and set the stage for myriad chronic and acute illnesses, including relatively benign things like colds.

Vanderbilt University discovered that accurate and uncomplicated assessment of oxidative stress inside the body could be accomplished by the measurement of chemicals called isoprostanes.  These substances are derived from the action of free radicals on fatty acids, and can be found in plasma and urine.  Primarily associated with risk of atherosclerosis, isoprostanes levels are elevated by “cigarette smoking, hypercholesterolemia, diabetes mellitus, and obesity,” among other factors.  Additionally, “Enhanced oxidant stress occurring either locally in the vessel or systemically is implicated…in atherosclerosis in humans.”  (Morrow. 2005)   In circumstances not cardiac-related, isoprostanes are inflammatory mediators that augment the perception of pain.

As long as there is oxygen there will be oxidation, but most species have developed ways to deal with it.  What separates humans from other life forms is that we do things on purpose to increase the oxidative process.  We eat the wrong foods, we smoke, we are sedentary, and we worry about things that never happen, while fretting about things we cannot change.  We even worry about getting diseases that are not likely to attack us by virtue of genetic exclusion, but sometimes do get a start because we worried about them needlessly.  The body’s response to oxidative stress, which can be prompted by both mental and physical assaults, is tied to aging and life span.  (Finkel. 2000)

There is increasing evidence that psychosocial stress can cause system-wide derangement of cellular homeostasis, accompanied by heightened oxidative stress and pro-inflammatory activity.  (Marotta. 2011)  Persons under stress have elevated levels of malondialdehyde (MDA), a product that stems from the oxidation of fatty acids and that degrades the integrity of the cell.  This, in turn, can cause mutations of DNA.  That can initiate a plethora of unwelcome events.

Mental stress can incite physical responses, some of which may appear as gastrointestinal conditions, tension headaches, hypertension, irritable bowel syndrome, sexual dysfunction, alcoholism, fatigue, and skin conditions that include psoriasis, lichen planus, itching and hives.  Some or all of these may be related to increased cortisol production by the adrenal glands.  Stress can affect other hormones, as well, and is implicated in depression and impaired immune function.

Because the brain has high fatty acid content, it seems logical that fatty acids are involved in brain chemistry, physiology, and function.  Therefore, it follows that cognitive health and neuropsychiatric well-being are intertwined.  Omega-3 fatty acids, such as those from fatty fish and fish oil supplements, appear effective in the prevention of stress (and manufacture of cortisol) and in the regulation of mood.  (Perica. 2011)  In fact, the first consistent demonstration of the effect of dietary ingredients on the structure and function of the brain involved omega-3 fats.  (Bourre. 2005)

At the ends of our chromosomes are telomeres, pieces of DNA that are the equivalent of shoelace aglets (those plastic sheaths that help to thread the laces).  When telomeres start to fray because of continual cell replication, cells become senescent—they grow old.  Oxidative stress shortens telomeres, thus hastening aging and the onset of age-related diseases, none of which started yesterday.  (Epel. 2004)  If cortisol is one of the major hormones related to telomere shortening, then it is to our benefit to diminish it.  Stressors coming from outside the body are not so easy to handle.  But this does not mean that internalized stressors are more manageable.  Maintaining proper weight and controlling glucose are important stressors to consider.

The employment of functional foods and certain supplements can help to ease stress, to lighten the cortisol load, and to bolster immune defenses.  Telomeres may be preserved by a diet that reduces added sugars.  Essential fatty acids can ease the mental burdens of the daily grind.  Green tea polyphenols have shown to be effective in addressing a variety of oxidative, pro-inflammatory processes (Yang. 1998), while having a beneficial effect on nucleic acid and protein synthesis (Beltz. 2006).  The vitamin B complex is collectively known as the stress vitamins, and their utility as such has been reported often over past decades (Kennedy. 2011)  (Stough. 2011)  Intense Chinese research has discovered that telomeres may be rescued from senescence by epigallocatechin gallate (ECGC) in green tea, and by quercitin from apples, onions, citrus, and dark berries. (Sheng. 2011)

Stress-fighting, mood-lifting foods include such simple ingredients as oatmeal, pistachios, avocadoes, and wine.  Turkey, eggs, water, and almonds can affect your affect.  Chocolate can calm things by releasing endorphins, and walnuts can get rid of the blues by increasing uridine, which boosts communication among neurons.  Spinach helps maintain normal levels of serotonin, a mood enhancer that also deals with the sleep-wake cycle and pain perception.  If, on the other hand, you care little about stress and what it does to your body, go ahead and eat half a dozen bacon-fried doughnuts.

References

Morrow JD.
Quantification of isoprostanes as indices of oxidant stress and the risk of atherosclerosis in humans.
Arterioscler Thromb Vasc Biol. 2005 Feb;25(2):279-86.

Finkel T, Holbrook NJ.
Oxidants, oxidative stress and the biology of ageing.
Nature. 2000 Nov 9;408(6809):239-47.

Marotta F, Naito Y, Padrini F, Xuewei X, Jain S, Soresi V, Zhou L, Catanzaro R, Zhong K, Polimeni A, Chui DH.
Redox balance signalling in occupational stress: modification by nutraceutical intervention.
J Biol Regul Homeost Agents. 2011 Apr-Jun;25(2):221-9.

Perica MM, Delas I.
Essential fatty acids and psychiatric disorders.
Nutr Clin Pract. 2011 Aug;26(4):409-25.

Bourre JM.
Dietary omega-3 Fatty acids and psychiatry: mood, behaviour, stress, depression, dementia and aging
J Nutr Health Aging. 2005;9(1):31-8.

Epel ES, Blackburn EH, Lin J, Dhabhar FS, Adler NE, Morrow JD, Cawthon RM.
Accelerated telomere shortening in response to life stress.
Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17312-5.

Yang F, de Villiers WJ, McClain CJ, Varilek GW.
Green tea polyphenols block endotoxin-induced tumor necrosis factor-production and lethality in a murine model.
J Nutr. 1998 Dec;128(12):2334-40.

Beltz LA, Bayer DK, Moss AL, Simet IM
Mechanisms of cancer prevention by green and black tea polyphenols.
Anticancer Agents Med Chem. 2006 Sep;6(5):389-406.

Kennedy DO, Veasey RC, Watson AW, Dodd FL, Jones EK, Tiplady B, Haskell CF.
Vitamins and psychological functioning: a mobile phone assessment of the effects of a B vitamin complex, vitamin C and minerals on cognitive performance and subjective mood and energy.
Hum Psychopharmacol. 2011 Jul 12. doi: 10.1002/hup.1216.

Stough C, Scholey A, Lloyd J, Spong J, Myers S, Downey LA.
The effect of 90 day administration of a high dose vitamin B-complex on work stress.
Hum Psychopharmacol. 2011 Sep 8. doi: 10.1002/hup.1229.

Sheng R, Gu ZL, Xie ML
Epigallocatechin gallate, the major component of polyphenols in green tea, inhibits telomere attrition mediated cardiomyocyte apoptosis in cardiac hypertrophy.
Int J Cardiol. 2011 Oct 14.

Huk-Kolega H, Skibska B, Kleniewska P, Piechota A, Michalski Ł, Goraca A.
Role of lipoic acid in health and disease
Pol Merkur Lekarski. 2011 Sep;31(183):183-5.

Rios A, Delgado-Casado N, Cruz-Teno C, Yubero-Serrano EM, Tinahones F, Malagon MD, Perez-Jimenez F, Lopez-Miranda J.
Mediterranean diet reduces senescence-associated stress in endothelial cells.
Marin C, Delgado-Lista J, Ramirez R, Carracedo J, Caballero J, Perez-Martinez P, Gutierrez-Mariscal FM, Garcia-
Age (Dordr). 2011 Sep 6.

Lin J, Epel E, Blackburn E.
Telomeres and lifestyle factors: Roles in cellular aging.
Mutat Res. 2011 Aug 22.

Murillo-Ortiz B, Albarrán-Tamayo F, Arenas-Aranda D, Benítez-Bribiesca L, Malacara-Hernández J, Martínez-Garza S, Hernández-González M, Solorio S, Garay-Sevilla M, Mora-Villalpando C.
Telomere length and type 2 diabetes in males, a premature aging syndrome.
Aging Male. 2011 Aug 9.

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

Age-Related Macular Degeneration

eyeglasses-and-eye-chartWhat is AMD?

When given a checklist to rank their greatest health-related fears, most adults didn’t choose cancer or heart disease as number one. Of more than ten thousand people surveyed during an international study conducted by India’s Prasad Eye Institute, over ninety percent chose blindness (Giridhar, 2002). In a survey commissioned by Pfizer, twice as many respondents feared blindness as premature death (Pfizer, 2008).  But mere fear of something doesn’t make it go away. Taking action, though, could.

Age-related macular degeneration, or AMD, is a degenerative disease of the retina (the thin layer of nerve cells lining the back of the eyeball) that causes progressive loss of central vision, where the macula interprets details. Photoreceptor cells in the macula convert light into electrical messages that are transferred to the brain by the optic nerve.  If these cells degenerate, central vision does likewise. Risk for macular degeneration increases with age, and is the most common cause of vision loss in those over sixty.  It’s estimated that eight million people in the United States over age fifty-five have one or both eyes affected by intermediate AMD (Bressler, 2003). Because life expectancy has increased, the number of AMD cases is likely to rise to three million by 2020 (Friedman, 2004), thus becoming a major public health problem.

There are two types of AMD: dry and wet. The dry form accounts for more than 90% of all cases, and is characterized by yellowish-whitish deposits, called drusen, that accumulate behind the macula. Drusen are composed of the glycoprotein and glycolipid waste products of the photoreceptor cells, and they interfere with the blood supply to those cells.  In dry AMD, vision loss is gradual over the course of many years, often affecting only one eye. The wet form of AMD is identified by the appearance of newly created abnormal blood vessels growing under the macula. Unfortunately, these vessels leak, bleed and scar the macula, distorting or destroying central vision. Because the blood and fluid lift the macula out of position at the back of the eye, damage occurs rapidly. Wet AMD is the leading cause of irreversible legal blindness.

What Are The Risk Factors?

Age and race are common factors. As Caucasians age from their 60s to their late 70s, the risk changes from about 2% to almost 30%. No such increase is seen in other populations. Smoking reduces the amount of oxygen that reaches the eye—and other organs—and precludes the use of nutritional interventions that may prevent AMD in the first place. It’s been discovered that certain supplements related to vitamin A are causative of respiratory disease among smokers, including cancer. As with many diseases, family history plays a role, as well as a gene labeled CFH, compliment factor H, which is probably implicated in more than half the AMD cases in the United States (Chakravarthy, 2010) (Klein, 2005).

What Are The Symptoms?

The need for increasingly bright illumination (especially for close work), difficulty in adapting to lower levels of illumination (as when entering a dimly lit restaurant), increasing blurriness of printed material, reduced intensity of bright colors, and a blurred or blind spot combined with a loss of central visual sharpness are signs of dry AMD. Wet AMD may present as crookedness or waviness of lines known to be straight, a street sign that is out of focus, objects appearing farther away than they actually are, and a decrease in central vision, among others. Because a good eye can compensate for one affected by AMD, symptoms might not be noticed right away.

Pupil dilation by your eye doctor will enable him or her to see your retina through a tool called a slit lamp, which allows examination through a kind of microscope. The doctor will look for drusen and for other suspicious features. Because new blood vessels beneath the retina are hard to see, the doctor will look for other signs of wet AMD that may include bleeding, fluid behind the retina or elevation of the retina. Should these be identified, further evaluation is probably needed.

How About Treatment?

Lifestyle changes (and medications) can alter the progress of dry AMD. Antioxidant deficiencies, notably of zinc, and vitamins A, C, and E, have been noted in age-related macular degeneration (Age-Related Eye Disease Study [AREDS] Group, 2001). These substances prevent free radicals and unstable oxygen from damaging the retina, and are commonly found in leafy greens, colorful vegetables (oranges, yellows and purples), and fruits. A person diagnosed with AMD should look at diet anyway, so why not take the preventive route? Do it now. Lowering intake of animal fats and getting a little exercise to drop a few pounds is part of the regimen.

Early in this century the Dutch conducted a review of work that started in the 1990’s, examining an over-55 population of middle-class suburbanites who had at least one risk factor for AMD. Of almost six thousand at-risk subjects, all of whom had supplied a comprehensive dietary inventory, fewer than ten percent experienced incident AMD after an 8-year follow-up. It was noted that those with the highest intakes of all four antioxidant compounds (Zn, A, C, E) had a significant reduction in risk of disease (vanLeeuwen, 2005).

An earlier British study acknowledged the protective function of vitamins A, C, and E, concurrently citing the role of zinc in retinal metabolism and that of selenium as anti-oxidative. High serum levels of carotenoids, the yellow to red pigments in plants that are concentrated in the retina, are associated with reduced risk of AMD. A serendipitous discovery in this elderly group, though not directly related to its goal, found that the essential omega-6 fat, gamma-linolenic acid (GLA), helps in dry eye conditions. The value of the omega-3 fats in retinal development is reiterated (Brown, 1998).

Harvard investigations found that omega-3 fats from fish oil and fish consumption reduced risk for AMD, especially among smokers (Seddon, 2006), whose additional risks include uncontrolled cholesterol and diabetes (Tomany, 2004). Most recently, investigators at the University of Alberta found DHA, the omega-3 that partners with EPA in fish and fish oil, able to block the accumulation of toxic molecules behind the retina (Dornstauder, 2012). Keep in mind that DHA must be balanced with EPA, at a ratio of approximately 3:1, EPA:DHA. The reason? Alone, or in unbalanced supplementation, DHA can be excitatory, despite its known connection to eye and brain health.

A randomized trial recounted by Harvard Medical School says that markers of inflammation provide an environment conducive to AMD. Homocysteine and C-reactive protein are analytes that can be mitigated by the judicious use of vitamins B12, B6, and folic acid, all of which are related to the reduced incidence of coronary episodes. Together, these supplements proved effective in reducing incidence of AMD in a considerably large group enrolled in a women’s cardiovascular study (Christen, 2009).  That these markers are implicated in eye-related pathologies had been established earlier (Seddon, 2004).

Getting antioxidants from foods is held by traditional medicine to be the best route, but this may be a misguided stance. The general food supply has been denigrated by less-than-stellar corporate farming practices that use chemical soil enhancers and biocides that linger on food surfaces. Dousing stored seeds with pesticides that eventually appear in the stems, leaves, roots, and fruits of plants, followed by sloppy storage and shipping practices negate the veracity of obtaining all the nutrition we need from our food. It’s bad enough that much food lacks nutrition, but it’s an insult that our livers have to detoxify it, too. Add all this to what happens in a careless kitchen and we can establish the need for supplementation.

References

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

Age-Related Eye Disease Study Research Group.
A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E and beta carotene for age-related cataract and vision loss: AREDS report no. 9.
Arch Ophthalmol. 2001 Oct;119(10):1439-52.

Pia Allegri, Antonio Mastromarino, Piergiorgio Neri
Management of chronic anterior uveitis relapses: efficacy of oral phospholipidic curcumin treatment. Long-term follow-up
Clinical Ophthamology. October 2010 Volume 2010:4 Pages 1201 – 1206

Beatty S, Koh H, Phil M, Henson D, Boulton M.
The role of oxidative stress in the pathogenesis of age-related macular degeneration.
Surv Ophthalmol. 2000 Sep-Oct;45(2):115-34.

Bressler NM, Bressler SB, Congdon NG, Ferris FL 3rd, Friedman DS, Klein R, Lindblad AS, Milton RC, Seddon JM; Age-Related Eye Disease Study Research Group.
Potential public health impact of Age-Related Eye Disease Study results: AREDS report no. 11.
Arch Ophthalmol. 2003 Nov;121(11):1621-4.

Brown NA, Bron AJ, Harding JJ, Dewar HM.
Nutrition supplements and the eye.
Eye (Lond). 1998;12 ( Pt 1):127-33.

Chakravarthy U, Wong TY, Fletcher A, Piault E, Evans C, Zlateva G, Buggage R, Pleil A, Mitchell P.
Clinical risk factors for age-related macular degeneration: a systematic review and meta-analysis.
BMC Ophthalmol. 2010 Dec 13;10:31.

Cho E, Hung S, Willett WC, Spiegelman D, Rimm EB, Seddon JM, Colditz GA, Hankinson SE.
Prospective study of dietary fat and the risk of age-related macular degeneration.
Am J Clin Nutr. 2001 Feb;73(2):209-18.

Christen WG, Glynn RJ, Chew EY, Albert CM, Manson JE.
Folic acid, pyridoxine, and cyanocobalamin combination treatment and age-related macular degeneration in women: the Women’s Antioxidant and Folic Acid Cardiovascular Study.
Arch Intern Med. 2009 Feb 23;169(4):335-41.

Delcourt C, Carrière I, Cristol JP, Lacroux A, Gerber M.
Dietary fat and the risk of age-related maculopathy: the POLANUT study.
Eur J Clin Nutr. 2007 Nov;61(11):1341-4. Epub 2007 Feb 14.

Dornstauder B, Suh M, Kuny S, Gaillard F, Macdonald IM, Clandinin MT, Sauvé Y.
Dietary Docosahexaenoic Acid Supplementation Prevents Age-Related Functional Losses and A2E Accumulation in the Retina
Invest Ophthalmol Vis Sci. 2012 Apr 24;53(4):2256-65. Print 2012.

Edwards AO, Ritter R 3rd, Abel KJ, Manning A, Panhuysen C, Farrer LA.
Complement factor H polymorphism and age-related macular degeneration.
Science. 2005 Apr 15;308(5720):421-4. Epub 2005 Mar 10.

Friedman DS, O’Colmain BJ, Muñoz B, Tomany SC, McCarty C, de Jong PT, Nemesure B, Mitchell P, Kempen J; Eye Diseases Prevalence Research Group.
Prevalence of age-related macular degeneration in the United States.
Arch Ophthalmol. 2004 Apr;122(4):564-72.

Giridhar P, Dandona R, Prasad MN, Kovai V, Dandona L.
Fear of blindness and perceptions about blind people. The Andhra Pradesh Eye Disease Study.
Indian J Ophthalmol. 2002 Sep;50(3):239-46.

Hageman GS, Anderson DH, Johnson LV, Hancox LS, Taiber AJ, Hardisty LI, Hageman JL, Stockman HA, Borchardt JD, Gehrs KM, Smith RJ, Silvestri G, Russell SR, Klaver CC, Barbazetto I, Chang S, Yannuzzi LA, Barile GR, Merriam JC, Smith RT, Olsh AK, Bergeron J, Zernant J, Merriam JE, Gold B, Dean M, Allikmets R.
A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration.
Proc Natl Acad Sci U S A. 2005 May 17;102(20):7227-32. Epub 2005 May 3.

Hodge WG, Schachter HM, Barnes D, Pan Y, Lowcock EC, Zhang L, Sampson M, Morrison A, Tran K, Miguelez M, Lewin G.
Efficacy of omega-3 fatty acids in preventing age-related macular degeneration: a systematic review.
Ophthalmology. 2006 Jul;113(7):1165-72; quiz 1172-3, 1178.

Johnson EJ, Schaefer EJ.
Potential role of dietary n-3 fatty acids in the prevention of dementia and macular degeneration.
Am J Clin Nutr. 2006 Jun;83(6 Suppl):1494S-1498S.

Klein RJ, Zeiss C, Chew EY, Tsai JY, Sackler RS, Haynes C, Henning AK, SanGiovanni JP, Mane SM, Mayne ST, Bracken MB, Ferris FL, Ott J, Barnstable C, Hoh J.
Complement factor H polymorphism in age-related macular degeneration.
Science. 2005 Apr 15;308(5720):385-9. Epub 2005 Mar 10.

Pfizer
Twice as many people fear blindness more than premature death
Friday, 7 March, 2008
http://www.ncbi.ie/news/press-releases/2008-03-07_twice-as-many-people-fear-blindness-more-than-premature-death

Pratt S.
Dietary prevention of age-related macular degeneration.
J Am Optom Assoc. 1999 Jan;70(1):39-47.

Seddon JM, Ajani UA, Sperduto RD, Hiller R, Blair N, Burton TC, Farber MD, Gragoudas ES, Haller J, Miller DT, et al.
Dietary carotenoids, vitamins A, C, and E, and advanced age-related macular degeneration. Eye Disease Case-Control Study Group.
JAMA. 1994 Nov 9;272(18):1413-20.

Seddon JM, Gensler G, Milton RC, Klein ML, Rifai N.
Association between C-reactive protein and age-related macular degeneration.
JAMA. 2004 Feb 11;291(6):704-10.

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

Anxious About Anxiety?

mid-adult-male-portraitYou’re not anxious about going on vacation or performing a pleasant task. You’re enthusiastic (but not enthused). You could be anxious about going to the dentist or to defend your last income tax return. Here, you’re entertaining a feeling of dread or apprehension, probably lacking clear justification.  Anxiety results from a subjective way of looking at a situation in the absence of a clear and actual danger. Of course, the sweating, increased pulse, and tension coupled with self-doubt about being able to handle the matter tell a different story. Sometimes respirations increase, the mouth gets dry and the intestines gurgle. All this is part of a defense mechanism. Anxiety can be particular, such as a panic attack in a crowd of people, in which case the stimulus can be identified. Or it may be generalized, being a long-term experience with no explanation of its cause. Obsessive-compulsory disorder (OCD) is an anxious state characterized by quandaries of uncertainty and compulsions to act. If the act is frustrated, the uncertainty remains and anxiety is intensified. Anxiety is considered a normal, but transient, response to stress, encouraging a person to take action in order to deal with what is perceived to be a difficult situation.

What’s The Risk?

Women are twice as likely as men to become anxious, mostly because of hormones and the archaic expectations that women are supposed to take care of everybody else before themselves. Age plays a minor role, in that OCD, separation anxiety and social phobias that include panic disorder show up in childhood and the teenage years. Early identification and treatment can forestall later problems. Certain environmental factors, such as poverty, separation from family, overly strict parents, family conflicts, anxious family members and lack of support can induce anxiety disorders. That anxiety runs in families is accepted, but it’s not known if the onset is genetic or learned, or both.

Physiologically, anxiety may be prompted by faulty brain chemistry, where an imbalance of serotonin, for instance, may result in irregular moods and emotions. There may be a structural fault, too.  The amygdala is the part of the brain in charge of processing emotional reactions and memory consolidation, including the recollection of fear.  If it’s overactive, this structure will heighten the fear response and increase anxiety in social situations.   Non-structural physical concerns, such as health problems, can cause anxiety.  Diabetes, alcoholism, heart disease, odd sensations that have no apparent cause, and thyroid disease are a few.

How Do I Handle Anxiety?

Besides the traditional psychotherapy practices and anti-anxiety medications, there are a few things you can do to take charge. First, you need to know that withdrawal from a psychoactive drug can cause anxiety. So, weaning from benzodiazepines causes the thing for which you took the drug in the first place. But beta-blockers, typically used for blood pressure control, have no such effect. They’re used off label to control rapid heartbeat, nervousness, trembling voice and shaky hands that accompany anxiety attacks. Alcohol withdrawal causes anxiety in many people.

Alternative approaches to anxiety treatment include things you can do and things you can swallow. Some modalities that require active participation include music therapy, art therapy, aromatherapy and meditation. With these you have to turn the music on, wield a paintbrush, light a candle, or think about pleasant things. But many people are unwilling or unable to be so engaged because of time constraints, family and job obligations, or simple faineance. Deglutition is the answer.

Options to psychological interventions for anxiety were sought in order to overcome limitations on time and resources. Because of adverse side-effects, alternatives to anxiolytic drugs also were explored. There is a shrub from the South Pacific islands that’s been used for centuries to calm the nerves, Piper methysticum, commonly known as kava kava. In a meta-analysis performed by the Cochrane Database at England’s Exeter University, researchers found that anxious subjects who took kava extract as a sole constituent in their treatment experienced a substantial reduction in symptoms compared to those taking a placebo (Pittler, 2000, 2003). One of the differences between a natural substance and a synthetic one is the time it takes to demonstrate effectiveness.  With a natural substance—in this example, herbal—you get the active ingredient and all the supportive components of the plant. Many enjoy an unexplainable synergy.  With a synthetic one—a drug—you get an isolated chemical that is not toned down by collaborative elements. Although earlier study found kava to be effective at taming anxious moments, it took eight weeks for kava’s superiority to placebo to be displayed (Volz, 1997).

Benzodiazepines are the drugs commonly used to treat anxiety. Their side effects, besides excessive drowsiness and decreased alertness, include paradoxical consequences, such as aggression, impulsivity, and irritability. Cognitive impairment and tolerance can result, as well. Tapering off these medications requires deliberation and a watchful eye. Using kava kava during such an ordeal, patients who were weaned from the drugs while being introduced to the herbal showed good tolerance and improved symptoms over a period of two weeks in a five-week trial in Germany (Malsch, 2001).

Generalized anxiety disorder has responded well to another folk remedy, passion flower. In a study comprising three dozen individuals, half received passion flower plus placebo and half received a benzodiazepine plus placebo in a one-month trial. The outcome showed both the herb and the drug to be effective in controlling anxiety symptoms. The drug, with rapid onset of action, impaired job performance (Akhondzadeh, 2001). The herb did not. Pharmacologically, extracts of the upper parts of the passion flower plant are most dynamic (Dhawan, 2001).

If you’ve taken fish oil for heart and brain health, that’s good. It’s been discovered that low levels of omega-3 fatty acids play a significant role in a number of mental irregularities (Buydens-Branchley, 2008) and that mood disorders respond especially well to omega-3 supplementation, with EPA getting better press than its companion, DHA (Ross, 2007). With a ratio of 3 to I, EPA to DHA, a fish oil product called Kirunal appears more than adequate to satisfy the mono- or adjunctive therapy approach in treating mood anomalies. For decades it’s been given that omega-3 fats are effective in the treatment of major depressive disorders, so it is reasonable to submit that they be likewise in anxiety disorders (Ross, 2009). If the presence of a substance yields a specific result, then the absence of that substance should yield the opposite. A deficit of n-3 fats has been identified in the red cell membranes of anxious persons (Greena, 2006), specifically those with social anxieties. Overall, it’s been proposed that human foods be supplemented with omega-3 fats as a strategy to improve behaviors and cognitive functions (Vinot, 2011). This makes one wonder if the education community needs to sit up and take notice. If that’s an inflammatory statement, n-3 supplementation can ameliorate that while reducing self-induced anxiety (Kiecolt-Glaser, 2011).

A relative newcomer on the anti-anxiety supplement stage is curcumin, the active ingredient of the turmeric spice common to Southern Asian and Middle Eastern cuisine.  Known predominantly as an anti-inflammatory agent, curcumin was found to have antidepressant like activity similar to tricyclic antidepressants, such as fluoxetine and imipramine (Sanmukhani, 2011). Because it is a natural substance, doses of curcumin used in an Indian trial were extraordinarily high, at 100 mg per kilogram of body weight, which equates to about 6,800 mg (6.8 grams) for a 150-pound person. Lesser dosages, from 10 to 80 mg/kg, demonstrated a positive effect on serotonin and dopamine activity, acting similarly to commonly prescribed drugs (Kulkami, 2008).

If you maintain a healthy diet, making sure to get the full array of macro and micro minerals, especially magnesium and zinc, as well as sufficient B vitamins, focusing on B 12, you’ll be able to avoid at least one cause of anxiety. Cutting back on alcohol and caffeine, and getting ample sleep are others. A caveat: before embarking on a supplement regimen to address anxiety, check with a healthcare professional to look for interactions with medicines and foods.

References

Andreatini R, Sartori VA, Seabra ML, Leite JR.
Effect of valepotriates (valerian extract) in generalized anxiety disorder: a randomized placebo-controlled pilot study.
Phytother Res. 2002 Nov;16(7):650-4.

Akhondzadeh S, Naghavi HR, Vazirian M, Shayeganpour A, Rashidi H, Khani M.
Passionflower in the treatment of generalized anxiety: a pilot double-blind randomized controlled trial with oxazepam.
J Clin Pharm Ther. 2001 Oct;26(5):363-7.

Buydens-Branchey L, Branchey M.
n-3 polyunsaturated fatty acids decrease anxiety feelings in a population of substance abusers.
J Clin Psychopharmacol. 2006 Dec;26(6):661-5.

Buydens-Branchey L, Branchey M, Hibbeln JR.
Associations between increases in plasma n-3 polyunsaturated fatty acids following supplementation and decreases in anger and anxiety in substance abusers.
Prog Neuropsychopharmacol Biol Psychiatry. 2008 Feb 15;32(2):568-75. Epub 2007 Nov 1.

Dhawan K, Kumar S, Sharma A.
Anti-anxiety studies on extracts of Passiflora incarnata Linneaus.
J Ethnopharmacol. 2001 Dec;78(2-3):165-70.

Dhawan K, Kumar S, Sharma A.
Anxiolytic activity of aerial and underground parts of Passiflora incarnata.
Fitoterapia. 2001 Dec;72(8):922-6.

Ernst E.
The risk-benefit profile of commonly used herbal therapies: Ginkgo, St. John’s Wort, Ginseng, Echinacea, Saw Palmetto, and Kava.
Ann Intern Med. 2002 Jan 1;136(1):42-53.

Ernst E.
Herbal remedies for anxiety – a systematic review of controlled clinical trials.
Phytomedicine. 2006 Feb;13(3):205-8. Epub 2005 Aug 15.

G. Fontani, F. Corradeschi, A. Felici, F. Alfatti, S. Migliorini, L. Lodi
Cognitive and physiological effects of Omega-3 polyunsaturated fatty acid supplementation in healthy subjects
European Journal of Clinical Investigation. Vol 35, Iss 11, pages 691–699, Nov 2005

Pnina Greena, Haggai Hermeshb, Assaf Monselisec, Sofi Marom, Gadi Presburger, Abraham Weizman
Red cell membrane omega-3 fatty acids are decreased in nondepressed patients with social anxiety disorder
European Neuropsychopharmacology. Feb 2006; 16(2): 107-113

Harauma A, Moriguchi T.
Dietary n-3 fatty acid deficiency in mice enhances anxiety induced by chronic mild stress.
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Jadoon A, Chiu CC, McDermott L, Cunningham P, Frangou S, Chang CJ, Sun IW, Liu SI, Lu ML, Su KP, Huang SY, Stewart R.
Associations of polyunsaturated fatty acids with residual depression or anxiety in older people with major depression.
J Affect Disord. 2012 Feb;136(3):918-25. Epub 2011 Nov 21.

Kiecolt-Glaser JK, Belury MA, Andridge R, Malarkey WB, Glaser R.
Omega-3 supplementation lowers inflammation and anxiety in medical students: a randomized controlled trial.
Brain Behav Immun. 2011 Nov;25(8):1725-34. Epub 2011 Jul 19.

Kinrys G, Coleman E, Rothstein E
Natural remedies for anxiety disorders: potential use and clinical applications.
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Kulkarni SK, Bhutani MK, Bishnoi M.
Antidepressant activity of curcumin: involvement of serotonin and dopamine system.
Psychopharmacology (Berl). 2008 Dec;201(3):435-42. Epub 2008 Sep 3.

Lakhan SE, Vieira KF.
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Malsch U, Kieser M.
Efficacy of kava-kava in the treatment of non-psychotic anxiety, following pretreatment with benzodiazepines.
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McBride S, Graydon J, Sidani S, Hall L.
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Pittler MH, Ernst E.
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Pittler MH, Ernst E.
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Ross BM, Seguin J, Sieswerda LE.
Omega-3 fatty acids as treatments for mental illness: which disorder and which fatty acid?
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Brian M. Ross
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Saeed SA, Bloch RM, Antonacci DJ.
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Sanmukhani J, Anovadiya A, Tripathi CB.
Evaluation of antidepressant like activity of curcumin and its combination with fluoxetine and imipramine: an acute and chronic study.
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Song C, Li X, Leonard BE, Horrobin DF
Effects of dietary n-3 or n-6 fatty acids on interleukin-1beta-induced anxiety, stress, and inflammatory responses in rats.
J Lipid Res. 2003 Oct;44(10):1984-91. Epub 2003 Jul 1.

Vinot N, Jouin M, Lhomme-Duchadeuil A, Guesnet P, Alessandri JM, Aujard F, Pifferi F.
Omega-3 fatty acids from fish oil lower anxiety, improve cognitive functions and reduce spontaneous locomotor activity in a non-human primate.
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Volz HP, Kieser M.
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tYehuda S, Rabinovitz S, Mostofsky DI.
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Growing Old With Zinc

zinc-supplementsIf you read—and were enlightened by—the newsletter about aging and omega-3 fatty acids, you’ll likely be interested in this one about zinc and its relationship to aging and disease. For a long time, zinc has been associated with a strong immune system, but its connection to aging is a relatively new exploration. Whether zinc deficiency promotes aging or results from it matters little to those who endure its aftermath in their “golden” years.

What Is This Stuff?

Zinc is a mineral essential to all life. In humans, it plays a functional role in immunity, in growth and development, in neurological mechanisms, and in reproduction, as well as in several avenues of cellular metabolism. It performs a structural role in some proteins as a stabilizer and in cell membranes as a guard against oxidative insults and functional impairment (O’Dell, 2000). Additionally, zinc is a component of “zinc fingers,” which are structural domains that are wrapped around a zinc ion and regulate gene expression by acting as transcription factors by cleaving to DNA. Zinc has been found to be integral to programmed cell death, called apoptosis (Truong-Tran, 2000).

Do I Have Enough?

Possibly not. The World Health Organization (WHO) suggests that zinc deficiency is widespread and affects the health and well-being of populations worldwide. The International Zinc Nutrition Consultative group (IZiNCG) has determined that zinc intake is inadequate based on the presence and bioavailability of this micro-nutrient in each country’s food supply. Deficiency in children, especially, raises the risk for diarrheal diseases, pneumonia and malaria, the latter a defined danger for populations so exposed (WHO, 2008). Conservative estimates posit that one-fourth of the world’s population is deficient in zinc (Maret, 2006).

Although zinc deficiency is typically diet-related, it can spring from malabsorption, chronic liver and kidney disease, sickle-cell disease, diabetes, malignancy, and as a result of bariatric surgery, heavy metal exposure and possibly the ingestion of FD&C Yellow #5, known as tartrazine (GPN, 2012). The problem of zinc deficiency has been known for decades, but has received scant attention because it was believed that it could never occur in humans (Prasad, 2003). Yet its burden is outstanding and simply resolved with supplementation. The bioavailability of zinc from vegetarian diets is lower than from non-vegetarian diets because meat is not part of the vegan regimen. The legumes and plants common to vegetarian diets contain phytates that bind zinc and inhibit its absorption (Hunt, 2003) (Sandstrom, 1997) (Wise, 1995). Considering that poor agricultural, storage, shipping and kitchen practices can take a toll on any food’s nutritional profile, it can readily be seen that deficit is not the impossibility it once was thought to be. Eleven milligrams a day for an adult male and nine for a female is enough to meet nutritional requirements. Doses for children and pregnant women may be retrieved from the Office of Dietary Supplements at the National Institute of Health website (IOM, 2001).

What About Aging?

As we age, our DNA replication may become increasingly undependable because of shortened telomeres, possibly setting the stage for chronic, debilitating diseases, including cancer. There is a substantial body of evidence suggesting that a significant percentage of cancer deaths could be avoided by paying attention to proper nutrition.  Only in this century has zinc been tagged as a vital element in host defense against the initiation and progression of this disease, based partly on zinc’s character as supporting more than three hundred mammalian proteins (Ho, 2004). Because cancer is a disease mostly of the middle and older years, it is fitting to maintain a healthy nutritional intake, including supplementation if needed, noting that the elder population is vulnerable to zinc deficiency.

The pertinence of zinc to the entire immune system is well-documented. The presence of chronic inflammation, whether from physical illness, oxidative stress or the mental challenges of daily asperities, may induce sub-optimal zinc levels for most of us. From this was born the recommendation that zinc be supplemented to at-risk populations, notably the aged (Mocchegiani, 2006). It has been proposed that genetic screening for response to zinc intake be considered in order to maintain a healthy immune system, to ensure the activity of anti-oxidant proteins, and to avoid the frailty and degeneration that often accompany old age (Mocchegiani, 2007).

Among the environmental bombardments suffered by the immune system is cadmium exposure, largely from fossil fuels combustion, but also from some fertilizers, metal refining, and tobacco use. Smokers have four times the cadmium levels as non-smokers, and this may be causative of early atherosclerosis and hypertension, both being risk factors for CVD, but also attenuated by high zinc concentrations (Messner, 2009). The long biological half-life of cadmium only compounds the concerns by presenting a cumulative effect, resulting in sterilizing, teratogenic and carcinogenic ramifications (Bin, 1994). The physical attack from cadmium and cohort environmental insults may lead to a state termed immunosenescence, the gradual deterioration of the immune system brought on by natural age advancement. As soon as you agree that, “Hey, this is just the way it is,” you have already decided to lose the race by a considerable margin. A large part of the aging drama can be explained by an imbalance between pro- and anti-inflammatory complexes, most often resulting in low-grade chronic inflammation. This condition is a driving force behind the frailty and the more common conditions associated with aging (Franceschi, 2007).  The Third Zinc Age Meeting in Madrid offered that zinc supplementation presents a strong case in the management of healthy aging (Mocchegiani, 2006), since  zinc deficiency is constantly observed in the chronic inflammation of old age (Vasto, 2007) (Fabris, 1995).

The absolute requirement for zinc is not known to be higher in the elderly, buttheir intake tends to be low. There are social factors that can interfere withsound dietary habits, loneliness being paramount. Insufficient intake of zinc(from food or supplements) may lead to loss of taste sensation, which leads tounwillingness to eat, which continues the vicious cycle. Drugs that promote zincexcretion (including some diuretics), poor absorption and chronic diseases contributeto the deficit. Although it might not turn back the clock, zinc may be able toslow its forward progression.

References

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Prasad AS, Fitzgerald JT, Hess JW, Kaplan J, Pelen F, Dardenne M.
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Nutrition. 1993 May-Jun;9(3):218-24.

Prasad AS.
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Sandström B.
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Truong-Tran AQ, Ho LH, Chai F, Zalewski PD.
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J Nutr. 2000 May;130(5S Suppl):1459S-66S.

Vasto S, Mocchegiani E, Malavolta M, Cuppari I, Listì F, Nuzzo D, Ditta V, Candore G, Caruso C.
Zinc and inflammatory/immune response in aging.
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Wise A.
Phytate and zinc bioavailability.
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Carmen P. Wong, Kathy R. Magnusson, Emily Ho
Increased inflammatory response in aged mice is associated with age-related zinc deficiency and zinc transporter dysregulation
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World health Organization. Published Online: 17 January 2008
Comparative Quantification of Health Risks
Childhood and maternal undernutrition
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Laura E. Caulfield and Robert E. Black
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Zatta P, Lucchini R, van Rensburg SJ, Taylor A.
The role of metals in neurodegenerative processes: aluminum, manganese, and zinc.
Brain Res Bull. 2003 Nov 15;62(1):15-28.

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

OMEGA-3’S Effect On Aging

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

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

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

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

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

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

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

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

References

Adler N, Pantell M, O’Donovan A, Blackburn E, Cawthon R, Koster A, Opresko P, Newman A, Harris TB, Epel E.
Educational attainment and late life telomere length in the Health, Aging and Body Composition Study.
Brain Behav Immun. 2012 Sep 5. pii: S08810.1016/j.bbi.2012.08.014. [Epub ahead of print]

Armanios M, Alder JK, Parry EM, Karim B, Strong MA, Greider CW.
Short telomeres are sufficient to cause the degenerative defects associated with aging.
Am J Hum Genet. 2009 Dec;85(6):823-32.

Burghardt PR, Kemmerer ES, Buck BJ, Osetek AJ, Yan C, Koch LG, Britton SL, Evans SJ.
Dietary n-3:n-6 fatty acid ratios differentially influence hormonal signature in a rodent model of metabolic syndrome relative to healthy controls.
Nutr Metab (Lond). 2010 Jun 28;7:53.

Epel E.
How “reversible” is telomeric aging?
Cancer Prev Res (Phila). 2012 Oct;5(10):1163-8. doi: 10.1158/1940-6207.CAPR-12-0370.

Farzaneh-Far R, Lin J, Epel ES, Harris WS, Blackburn EH, Whooley MA.
Association of marine omega-3 fatty acid levels with telomeric aging in patients with coronary heart disease.
JAMA. 2010 Jan 20;303(3):250-7.

Harris WS, Mozaffarian D, Rimm E, Kris-Etherton P, Rudel LL, Appel LJ, Engler MM, Engler MB, Sacks F.
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 Feb 17;119(6):902-7. Epub 2009 Jan 26.

Kay-Tee Khaw, Marlin D. Friesen, Elio Riboli, Robert Luben, Nicholas Wareham
The EPIC-Norfolk Prospective Study
Plasma Phospholipid Fatty Acid Concentration and Incident Coronary Heart Disease in Men and Women:

Kiecolt-Glaser JK, Belury MA, Andridge R, Malarkey WB, Hwang BS, Glaser R.
Omega-3 supplementation lowers inflammation in healthy middle-aged and older adults: a randomized controlled trial.
Brain Behav Immun. 2012 Aug;26(6):988-95. Epub 2012 May 26.

Kiecolt-Glaser JK, Epel ES, Belury MA, Andridge R, Lin J, Glaser R, Malarkey WB, Hwang BS, Blackburn E.
Omega-3 fatty acids, oxidative stress, and leukocyte telomere length: A randomized controlled trial.
Brain Behav Immun. 2012 Sep 23. pii: S0889-1591(12)00431-X. doi: 10.1016/j.bbi.2012.09.004.

Sanders TA, Lewis F, Slaughter S, Griffin BA, Griffin M, Davies I, Millward DJ, Cooper JA, Miller GJ.
Effect of varying the ratio of n-6 to n-3 fatty acids by increasing the dietary intake of alpha-linolenic acid, eicosapentaenoic and docosahexaenoic acid, or both on fibrinogen and clotting factors VII and XII in persons aged 45-70 y: the OPTILIP study.
Am J Clin Nutr. 2006 Sep;84(3):513-22.

Schwab JM, Chiang N, Arita M, Serhan CN.
Resolvin E1 and protectin D1 activate inflammation-resolution programmes.
Nature. 2007 Jun 14;447(7146):869-74.

Serhan CN, Chiang N.
Novel endogenous small molecules as the checkpoint controllers in inflammation and resolution: entrée for resoleomics.
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Serhan CN, Chiang N, Van Dyke TE.
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Antonio L. Serrano, Vicente Andrés
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Shen J, Terry MB, Gurvich I, Liao Y, Senie RT, Santella RM.
Short telomere length and breast cancer risk: a study in sister sets.
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Simopoulos AP.
The importance of the ratio of omega-6/omega-3 essential fatty acids.
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Simopoulos AP.
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Xia SH, Wang J, Kang JX.
Decreased n-6/n-3 fatty acid ratio reduces the invasive potential of human lung cancer cells by downregulation of cell adhesion/invasion-related genes.
Carcinogenesis. 2005 Apr;26(4):779-84. Epub 2005 Jan 20.

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

Flaxseed, Exercise and Your Heart

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

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

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

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

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

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

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

References

Adkins Y, Kelley DS.
Mechanisms underlying the cardioprotective effects of omega-3 polyunsaturated fatty acids.
J Nutr Biochem. 2010 Sep;21(9):781-92.

Ander BP, Weber AR, Rampersad PP, Gilchrist JS, Pierce GN, Lukas A.
Dietary flaxseed protects against ventricular fibrillation induced by ischemia-reperfusion in normal and hypercholesterolemic Rabbits.
J Nutr. 2004 Dec;134(12):3250-6.

Bassett CM, Rodriguez-Leyva D, Pierce GN.
Experimental and clinical research findings on the cardiovascular benefits of consuming flaxseed.
Appl Physiol Nutr Metab. 2009 Oct;34(5):965-74.

Bloedon LT, Szapary PO.
Flaxseed and cardiovascular risk.
Nutr Rev. 2004 Jan;62(1):18-27.

Heald CL, Ritchie MR, Bolton-Smith C, Morton MS, Alexander FE.
Phyto-oestrogens and risk of prostate cancer in Scottish men.
Br J Nutr. 2007 Aug;98(2):388-96. Epub 2007 Apr 3.

Hedelin M, Klint A, Chang ET, Bellocco R, Johansson JE, Andersson SO, Heinonen SM, Adlercreutz H, Adami HO, Grönberg H, Bälter KA.
Dietary phytoestrogen, serum enterolactone and risk of prostate cancer: the cancer prostate Sweden study (Sweden).
Cancer Causes Control. 2006 Mar;17(2):169-80.

Horn-Ross PL, Hoggatt KJ, West DW, Krone MR, Stewart SL, Anton H, Bernstei CL, Deapen D, Peel D, Pinder R, Reynolds P, Ross RK, Wright W, Ziogas A.
Recent diet and breast cancer risk: the California Teachers Study (USA).
Cancer Causes Control. 2002 Jun;13(5):407-15.

Keinan-Boker L, van Der Schouw YT, Grobbee DE, Peeters PH.
Dietary phytoestrogens and breast cancer risk.
Am J Clin Nutr. 2004 Feb;79(2):282-8.

National Council on Strength and Fitness
Flaxseed and Exercise
Date:  Oct. 29, 2012

Nounou HA, Deif MM, Shalaby MA.
Effect of flaxseed supplementation and exercise training on lipid profile, oxidative stress and inflammation in rats with myocardial ischemia.
Lipids Health Dis. 2012 Oct 5;11(1):129.

Prasad K, Mantha SV, Muir AD, Westcott ND.
Reduction of hypercholesterolemic atherosclerosis by CDC-flaxseed with very low alpha-linolenic acid.
Atherosclerosis. 1998 Feb;136(2):367-75.

Prasad K.
Flaxseed and cardiovascular health
J Cardiovasc Pharmacol. 2009 Nov;54(5):369-77.

Strom SS, Yamamura Y, Duphorne CM, Spitz MR, Babaian RJ, Pillow PC, Hursting SD.
Phytoestrogen intake and prostate cancer: a case-control study using a new database.
Nutr Cancer. 1999;33(1):20-5.

Touillaud MS, Thiébaut AC, Niravong M, Boutron-Ruault MC, Clavel-Chapelon F.
No association between dietary phytoestrogens and risk of premenopausal breast cancer in a French cohort study.
Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2574-6.

Travis RC, Spencer EA, Allen NE, Appleby PN, Roddam AW, Overvad K, Johnsen NF, Olsen A, et al
Plasma phyto-oestrogens and prostate cancer in the European Prospective Investigation into Cancer and Nutrition.
Br J Cancer. 2009 Jun 2;100(11):1817-23. Epub 2009 May 12.

Velentzis LS, Cantwell MM, Cardwell C, Keshtgar MR, Leathem AJ, Woodside JV.
Lignans and breast cancer risk in pre- and post-menopausal women: meta-analyses of observational studies.
Br J Cancer. 2009 May 5;100(9):1492-8.

Ward H, Chapelais G, Kuhnle GG, Luben R, Khaw KT, Bingham S.
Lack of prospective associations between plasma and urinary phytoestrogens and risk of prostate or colorectal cancer in the European Prospective into Cancer-Norfolk study.
Cancer Epidemiol Biomarkers Prev. 2008 Oct;17(10):2891-4.

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

Methylation And Age: How Old Are You, Really?

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

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

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

What is methylation?

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

DNA?

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

How Do I Do This?

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

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

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