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The Eyes Have It

fidoglassesDiet is vital to preservation of vision as we age. Some people have a higher risk of losing central vision than others—based partly on genetics—but that can be postponed or prevented by consuming sufficient levels of certain dietary nutrients. Clinicians are advised to provide dietary counsel especially to young persons who are susceptible to the vision-disabling consequences that accompany the genetic variations responsible for early onset of age-related macular degeneration (AMD). That gene is officially termed “complement factor H,” abbreviated to CFH. Researchers in the Netherlands tested more than two thousand individuals over age 55 for genetic susceptibility to AMD by way of the CFH gene. The subjects were followed for more than a decade, receiving eye exams every three years to learn who suffered from vision deterioration or loss. Careful, detailed dietary intake records were kept, and eating habits were monitored. The risk reduction ascribed to specific nutrients was associated with normal dietary intake.

Genetic variations can increase the risk of early age-related macular degeneration.  Using food frequency questionnaires and genetic testing, researchers at the Erasmus Medical Center in the Netherlands (Ho and van Leeuwen. 2011) evaluated biological interactions among risk factors for ARM, and found distinct relationships “…between CFH Y402H and zinc, beta-carotene, lutein/zeaxanthin, and eicosapentaenoic/docosahexaenoic acid (EPA/DHA)…”  Subjects with dietary intake of zinc in the highest third “…reduced their hazard ratio of early AMD…” by more than 40%.  Intakes of beta-carotene, lutein/zeaxanthin, and EPA/DHA reduced risk by more than a third.  Drs. Ho and van Leeuwen concluded their report with,”High dietary intake of nutrients with antioxidant properties reduces the risk of early AMD in those at high genetic risk.”

COMMENTARY
AMD is a disease that affects the macula, the most important part of the retina and an area that has a very high concentration of photoreceptors, responsible for central vision.  Nerve fibers in the macula coalesce with neighboring fibers to form the optic nerve, the “cable” that connects the eye to the brain.  The health of our eyes depends on the health of the cardiovascular and nervous systems.  The retina and surrounding structures are filled with blood vessels that depend on a healthy cardiovascular system.

The link between vision and diet has been recognized for a considerable time.  In 2006, a study funded by the Agricultural Research Service and reported in the American Journal of Clinical Nutrition  found a relationship between a high glycemic-index (GI) diet and AMD.  The glycemic index is a ranking of foods based on their elevation of blood glucose after ingestion, compared to a reference food such as white bread or glucose.  These scientists suggested a direct relationship of glycemic index to eye disease.  Study participants whose diets contained the highest GI foods also had the highest amount of macular pigment abnormalities, which is an early indicator of macular degeneration.  (Chiu. 2006)  It seems prudent, therefore, to limit or completely avoid foods that are high in starches and sugars, particularly sugars that are added, as found in processed foods, sweets, and the like.

Addressing the nutrients mentioned in the Ho and van Leeuwen study, zinc is already a necessary trace mineral, in that it is a component of several enzymes and brings vitamin A from the liver to the retina in order to produce melanin, a protective pigment of the eye.  Zinc is heavily concentrated in the eye, mostly in the retina and the choroid, the vascular tissue beneath the retina.  Food sources include red meats, beans, nuts (almonds), whole grains, shellfish (oysters), and fortified foods.

Lutein and zeaxanthin are nutrients found in green leafy vegetables and eggs, as well as in other foods.  There’s more reason to eat your spinach than merely to be like Popeye. These two compounds have identical chemical formulas, and are thus called isomers of each other. (The arrangement of atoms is slightly different.)  Many studies have related these substances to the prevention of AMD as well as cataracts.  Of all the carotenoids found in nature, these are in the greatest amounts in the eye, where they absorb the blue light that can cause oxidative damage.  They have to come from food, so we advise that you get the darkest greens you can find, including spinach, kale, collards, and turnip greens.  Squash, pumpkin, corn, Brussels sprouts, peas, carrots, and green beans are other vegetable sources.  The fruits include citrus.

Lack of vitamin A may cause might blindness, dry eyes, eye infections, skin problems and slowed growth.  Beta-carotene is a compound that can be converted by the body to vitamin A.  The need for vitamin A in vision was identified almost a hundred years ago.  Foods that contain beta-carotene or vitamin A include dark green leaves, and the yellow-orange groups, such as cantaloupe, pumpkin, yellow squashes, and others.  In the eye, beta-carotene becomes retinaldehyde, also called retinal, and is bound to a protein called opsin, which resides in the rods and cones.  This combination helps to carry electrical energy along the optic nerve to the brain.  Night blindness, by the way, is actually poor adaptation to low-light situations.

The essential fatty acids, in this case EPA and DHA, must come from the diet.  They maintain integrity of the nervous system, and help to prevent inflammation and arteriosclerosis, a noted enemy of vision.  One result of arteriosclerosis is a decrease in nutrients to the eye and a reduction in the removal of waste materials.  EPA and DHA also aid in the reduction of dry eyes.  It is well-known that oily fish are the best food sources of these essential fats, though supplements are available.

Oh, yeah.  You never see a rabbit wearing glasses.  Eat your carrots.

References

MAIN ABSTRACT
Arch Ophthalmol. June 2011;129(6):758-766.
Reducing the Genetic Risk of Age-Related Macular Degeneration With Dietary Antioxidants, Zinc, and {omega}-3 Fatty Acids
The Rotterdam Study
Lintje Ho, MD, MPH, MSc; Redmer van Leeuwen, MD, PhD; Jacqueline C. M. Witteman, PhD; Cornelia M. van Duijn, PhD; André G. Uitterlinden, PhD; Albert Hofman, MD, PhD; Paulus T. V. M. de Jong, MD, PhD, FRCOphth; Johannes R. Vingerling, MD, PhD; Caroline C. W. Klaver, MD, PhD

SUPPORTING ABSTRACTS
Semin Ophthalmol. 2011 May;26(3):192-7.
Inflammation and Age-Related Macular Degeneration (AMD).
Telander DG.

Department of Ophthalmology and Vision Science, University of California Davis Medical Center, Sacramento, CA, USA.

Arch Ophthalmol. 2007 Mar;125(3):300-5.
High-sensitivity C-reactive protein, other markers of inflammation, and the incidence of macular degeneration in women.
Schaumberg DA, Christen WG, Buring JE, Glynn RJ, Rifai N, Ridker PM.

Division of Preventive Medicine, 900 Commonwealth Ave E, Boston, MA 02215, USA. [email protected]

American Journal of Clinical Nutrition, Vol. 83, No. 4, 880-886, April 2006
Dietary glycemic index and carbohydrate in relation to early age-related macular degeneration
Chung-Jung Chiu, Larry D Hubbard, Jane Armstrong, Gail Rogers, Paul F Jacques, Leo T Chylack, Jr, Susan E Hankinson, Walter C Willett and Allen Taylor

Pol Merkur Lekarski. 2011 Apr;30(178):241-5.
[Vascular complications in patients with metabolic syndrome].      [Article in Polish]
Kowalski J, Sliwczyńska-Rodziewicz D, Ciećwierz J, Kowalczyk E, Pawlicki L, Irzmański R, Mejer A, Szadkowska I, Barylski M.

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

Hot Dog!

Processed MeatsAre we knowingly jeopardizing our collective lives? Common more to developed countries, colon cancer is the third most frequently diagnosed form of the disease. The risk in the United States is about 7%, but is based on certain factors: family history, colon polyps, and age among them. At the 2009 All-Star Game, the Physicians Committee for Responsible Medicine (PCRM) posted a 48-feet-wide billboard on the highway near Busch Stadium in St. Louis proclaiming the causative nature of the lowly hot dog in colorectal disease. Why? Because processed meats have been convincingly linked to colorectal cancer.

The physicians hoped to persuade the baseball commissioner, Bud Selig, to put a warning label on hot dogs, similar to that on cigarette packs.  In fact, the billboard portrayed a handful of franks posed inside a cigarette pack, which was labeled, “Unlucky Strike.”  Krista Haynes, a dietitian for the PCRM’s Cancer project, stated that, “Baseball stadiums need to be frank about the cancer risk posed by hot dogs and other processed meats,” adding that, “Like cigarettes, hot dogs should come with a warning label that helps baseball fans and other consumers understand the health risks.”
(http://www.pcrm.org/search/?cid=1686)

The National Hot Dog and Sausage Council projected that more than 21 million hot dogs would be sold at ball games that year.  Two years earlier, the American Institute for Cancer Research published a report showing that just one 2-ounce serving of processed meat ingested daily increased the risk of colorectal cancer by 21%.

To add salt to the wound—if not to the hot dog—the PCRM filed lawsuits in New Jersey against Nathan’s, Kraft/Oscar Meyer, Sara Lee and other processors for failing to warn consumers that hot dogs increase the risk of colon cancer.

Hot dogs were probably chosen because of their ubiquity.  Colorectal cancer is not the only disease linked to processed meats.  So, too, are pancreatic, breast, and prostate cancers.  In past years, conventional medicine blamed the saturated fat content of processed meats for risk of disease, but it ignored what are probably worse offenders:  toxins in the fats and, more importantly, additives.

Fats accumulate whatever toxins to which they have been exposed over the lifetime of an animal…or person.  Considering that a cow eats tons of grass in its lifetime, it collects and concentrates toxicants that fell in the rainfall, were sprayed on crops ten miles away (or farther), or that showed up in its man-made supplemental feed.  Heavy metals, pesticides, and even PCB’s have been found in meat, and not just from cattle.

The additives in processed meats include substances that are identified as being carcinogenic, especially the nitrites.  The stuff that meat packers put into sausages and hot dogs makes a list much too detailed to be addressed in this epistle, so attention will be put on what is most likely to cause colorectal cancer.  This does not necessarily apply to red meat—meat from four legs—that is unprocessed.

Nitrites and nitrates historically came into use as naturally occurring contaminants in salt.  People found that meats cured with these contaminants tasted better than meats without them.  After they were identified, nitrites and nitrates (synthetic, of course) were added on purpose.  Both can be toxic, and have to be used carefully.  Natural nitrites come from the breakdown of plant material, particularly from root crops and leaves.  Celery provides a natural source, and is deemed safer than the man-made material, which is cheaper.   Besides adding flavor, they act as antioxidants to prevent rancidity, and they stop bacteria from taking residence in your canned ham.  Think botulism.  Nitrates are not as effective as their cousins until they are broken down into nitrites by micro-organisms.  The problems surface when nitrites form nitrosamines in the digestive system and get into the bloodstream to raise havoc with internal organs.  The government tried to ban this ingredient in the 1970’s, but succumbed to the pressures of the meat industry, which cried that there was no alternative.

Proteins naturally break down into amines and they will mate with nitrites under the right conditions to make nitrosamines.  Such exists in the environs of human stomach acid.  The high cooking temperatures of frying can enhance the formation of nitrosamines.  Ascorbic acid, aka vitamin C, controls the production of this compound, and has been added to some processed meats for a few years.  Canadian cancer scientists discovered that adding salt to processed meats at the table further intensifies the carcinogenic nature of the initial product.  In this case, the list of affected organs expands to include the stomach, bladder, kidneys, and blood (leukemia).  (Hu. 2011)  The possibility of stroke and coronary heart disease are other additions.  (Micha. 2010)

Though it seems that simple red meat is blameless, its cooking process makes a difference.  High-temperature cooking and excessive charring, especially in well-done meats from the grill, add to the burden of cancer risk.  (Sinha. 1999)  This means that nitrite-laden hot dogs need to escape the charring that many people find alluring.

Hot dogs and most other sausage-type meats are normally gray, just like fresh kielbasa or Italian sausage.  People associate the color of their food with quality, red in the case of hot dogs. Nitrates are color fixers besides color enhancers.  Since the USDA and other agencies seem more interested in promoting the interests of industry than the health of the public, we are responsible for assuming our own safety strategies.  Taking vitamin C, and maybe even vitamin E, prior to a nitrite meal is a protective strategy that prevents the formation of nitrosamines.  (Tannenbaum. 1989)  (Tannenbaum and Wishnok. 1991)

References

http://www.pcrm.org/search/?cid=1686
Physicians Committee for Responsible Medicine.  Aug. 2009
Hot Dogs Strike Out at All-Star Game and in New Jersey

Eur J Cancer Prev. 2011 Mar;20(2):132-9.
Salt, processed meat and the risk of cancer.
Hu J, La Vecchia C, Morrison H, Negri E, Mery L;
Canadian Cancer Registries Epidemiology Research Group.
Collaborators (8)Paulse B, Dewar R, Dryer D, Kreiger N, Whittaker H, Robson D, Fincham S, Le N.

Int J Vitam Nutr Res Suppl. 1989;30:109-13.
Preventive action of vitamin C on nitrosamine formation.
Tannenbaum SR.

Am J Clin Nutr. 1991 Jan;53(1 Suppl):247S-250S.
Inhibition of nitrosamine formation by ascorbic acid.
Tannenbaum SR, Wishnok JS, Leaf CD.
SourceMassachusetts Institute of Technology, Cambridge 02139.

Cancer Prev Res (Phila). 2010 Jul;3(7):852-64. Epub 2010 Jun 8.
Meat processing and colon carcinogenesis: cooked, nitrite-treated, and oxidized high-heme cured meat promotes mucin-depleted foci in rats.
Santarelli RL, Vendeuvre JL, Naud N, Taché S, Guéraud F, Viau M, Genot C, Corpet DE, Pierre FH.
SourceUniversité de Toulouse, ENVT, INRA, UMR Xénobiotiques, France.

Circulation. 2010; 121: 2271-2283
Expand+Epidemiology and Prevention
Red and Processed Meat Consumption and Risk of Incident Coronary Heart Disease, Stroke, and Diabetes Mellitus  A Systematic Review and Meta-Analysis
Renata Micha, RD, PhD; Sarah K. Wallace, BA; Dariush Mozaffarian, MD, DrPH

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

MSG and Weight Gain

No MSGThe Body Mass Index (BMI) is a measure of the relative percentages of fat and muscle mass in the human body, based on a person’s weight and height, used to assess obesity. This barometer was used by researchers to determine the effect of the food additive, monosodium glutamate (MSG), on weight over a period of time. It was learned that those persons who consume MSG regularly experience changes in the part of the brain that controls appetite, thus having an influence on energy balance and consequent weight gain.

When researcher, Ka He, and his colleagues at the University of North Carolina began to look for a relationship between monosodium glutamate and weight gain, they hypothesized that it would be a positive one.  As a design element of the study, “…overweight was defined as a body mass index ≥ 25…based on World Health Organization recommendations for Asian populations.”  With an average MSG intake of 2.2 grams a day, and a five-year follow-up, the study population demonstrated that “MSG consumption was positively, longitudinally associated with overweight development…”

The better it tastes, the more we’ll eat.  That seems logical.  Most Americans eat so fast that their brains don’t have enough time to process the information that says they’re full.  Since that lag time is about twenty minutes, we should take at least that much time to eat.  But the school cafeteria, the incessant phone calls, the pressures of the job, and other lifestyle components disallow that.  Combine any of these facets of life with food additives that enhance flavor, and start looking for a longer belt.

Leptin is a hormone that plays an important role in energy intake and expenditure, and it tells us when to stop eating…if it works the right way.  It’s made by fat cells, oddly enough, but can also come from other parts of the body, such as the bones, stomach, and liver.  It acts on parts of the brain’s hypothalamus, where it inhibits appetite. If leptin is not appropriately received and taken up by the hypothalamus, appetite fails to shut off and food intake is uncontrolled.  Where does MSG fit into this picture?  It seems to be able to induce hypothalamic lesions and ensuing leptin resistance (He, et al. 2008).  The stage is now set for weight gain.

Glutamate is the major excitatory transmitter in the brain, meaning that it makes things happen, especially in cognition, memory and learning.  It also affects brain development, cellular survival and the manufacture of synapses.  Too much glutamate, though, can raise serious concerns because its excitatory nature becomes intensified by virtue of its accumulation, allowing excess calcium to enter a nerve cell and damage it beyond repair.  This is what happens in the hypothalamus.

Glutamate, sometimes as glutamic acid, is responsible for the tantalizing flavors of poultry, some fishes, and eggs, among other foods.  Its salt, MSG, was introduced to the United States after WW II as “Accent” flavor enhancer.  It can be made by the fermentation of beets, sugar cane, or molasses.  People began to experience adverse reactions to MSG after eating Chinese food prepared with it, thereby coining the expression “Chinese Restaurant Syndrome.”  Sensitivity to monosodium glutamate may present with headaches, asthmatic symptoms, hyperactivity (especially in children), and obesity.  Frequency of such responses is low, but if it happens in your family, it’s high enough to merit attention.

We all know that the world revolves around the dollar bill and the ball point pen, the latter often employed to guarantee the former.  As long as clandestine groups can get away with something, they’ll persist.  And so it is with MSG.  It has more disguises than Artemus Gordon and Sherlock Holmes combined.  Here are a couple handfuls of MSG aliases:  glutamic acid, monopotassium glutamate, magnesium, glutamate, monoammonium glutamate, yeast extract, hydrolyzed anything, calcium or sodium caseinate, yeast nutrient, gelatin, textured protein, soy protein isolate, soyprotein concentrate, whey protein, ajinomoto.

These ingredients often contain glutamic acid:  carrageenan, bouillon, stock, maltodextrin, barley malt, protease, malt extract, soy sauce, and any protein that is fortified or fermented.  Additionally, these work with MSG to further enhance flavor:  Disodium 5’-guanylate; Disodium 5’-inositate; and Disodium 5’-ribonucleotides.  Wherever these three abide, it’s almost guaranteed that MSG is a companion.

Individual amino acids are not generally listed on the ingredients labels of food or health care products.  Binders and fillers may or may not contain MSG.  Believe it or not, MSG may also appear in cosmetics, including shampoos, soaps and hair conditioners.  If the words “hydrolyzed,” “amino acids,” or “protein” appear on the label, MSG could be in it.  Live virus vaccines may also have it.  Even though reactions to MSG are dose-dependent, you could react to a very small amount all of a sudden, when you never did so before.  Yes, MSG is natural, but so is arsenic.  To most of us, MSG does not cause problems.  MSG might make you want to eat more.  It might affect the state of your hypothalamus.  On the other hand, it’s not likely to make you wash your hair more often.  Is it?

Referneces

Am J Clin Nutr. 2011 Jun;93(6):1328-36. Epub 2011 Apr 6.
Consumption of monosodium glutamate in relation to incidence of overweight in Chinese adults: China Health and Nutrition Survey (CHNS).
He K, Du S, Xun P, Sharma S, Wang H, Zhai F, Popkin B
Departments of Nutrition and Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC.

Acta Physiol Hung. 2011 Jun;98(2):177-88.
Monosodium glutamate versus diet induced obesity in pregnant rats and their offspring.
Afifi MM, Abbas AM.
Department of Biochemistry, Zagazig University, Zagazig, Egypt.
Abstract

Am J Clin Nutr. 2011 Jun;93(6):1328-36. Epub 2011 Apr 6.
Consumption of monosodium glutamate in relation to incidence of overweight in Chinese adults: China Health and Nutrition Survey (CHNS).
He K, Du S, Xun P, Sharma S, Wang H, Zhai F, Popkin B.

Nutrition. 2005 Jun;21(6):749-55.
Monosodium glutamate in standard and high-fiber diets: metabolic syndrome and oxidative stress in rats.
Diniz YS, Faine LA, Galhardi CM, Rodrigues HG, Ebaid GX, Burneiko RC, Cicogna AC, Novelli EL.
Department of Clinical Cardiology, Faculty of Medicine, University of São Paulo State, Botucatu, Brazil.

Mol Pharmacol. 1989 Jul;36(1):106-12.
Delayed increase of Ca2+ influx elicited by glutamate: role in neuronal death.
Manev H, Favaron M, Guidotti A, Costa E.
Fidia-Georgetown Institute for the Neurosciences, Georgetown 4niversity, Washington, DC 20007.

Cell Calcium. 2003 Feb;33(2):69-81.
Calcium influx constitutes the ionic basis for the maintenance of glutamate-induced extended neuronal depolarization associated with hippocampal neuronal death.
Limbrick DD Jr, Sombati S, DeLorenzo RJ.

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

Child Athletes Nutrition

children-sportsA child is not a miniature adult. His or her nutrition and hydration needs are not exactly the same, especially in sports participation.  With the growth and availability of sports opportunities, you’d think that related nutrition needs would be a concern. To the contrary, sports nutrition for youngsters receives less attention than it deserves.

“Most children and adolescents who are strongly committed to sports are not concerned about nutrition as it relates to energy balance and obesity,” states a report from a 2004 issue of Nutrition.  The interactions among nutrition, growth, and development deserve attention if a participant expects to achieve optimal performance and to avoid the injuries and problems that stem from nutritional deficiencies.   Daily fluid turnover in adult athletes has received intense study, but that for children and adolescents hasn’t.  That of adults may be two to three liters a day, but in youngsters has only been estimated at half that—and that has been based on sedentary youth.  Although “sweating capacity is typically reported to be lower in children,” there is an increase in sweat rate when adjusted for body surface area.  Besides the energy needed for normal growth and development, children athletes need to accommodate the greater expenditure from physical activity.  That can vary from one sport to another.  (Petrie. 2004).

Besides the fun, kids participate in sports to hone their skills, to experience the excitement of competition, to be part of a team, and to stay in shape, among other reasons.  But they pay little or no attention to fuel and hydration needs.  Parents and coaches, on the other hand, do.  At least they should.  Hectic schedules, availability of foods, limited time and extended days interfere with choices and timing.

Even though the number of kids playing organized sports is on the rise, fitness levels are on the decline, and are much lower than in previous decades.  This partially explains the spate of sports-related injuries.  (Cordelia. 2011).  Targeted intervention strategies include ample hydration and nutrition.  Because of maturation differences, kids need more protein to support growth, more calcium to support bone, and more attention to the prevention of hypohydration.  (Bar-Or. 2001).

Sweat helps to cool the body, and what comes out has to be replaced, otherwise performance suffers and health is at risk.  To prevent the dizziness, fatigue, nausea, and cramps that characterize dehydration, the young athlete should drink one or two cups of water or electrolyte within four hours of an event.  If no urine has been passed, or if urine is bright yellow and minimal, another 1 ½ cups is suggested within two hours of the game.  During the event, try to replace fluids as they are lost to sweat, about a cup every fifteen or twenty minutes if possible.  Plain water will do, but if the event is longer than an hour, use an electrolyte replacement.  Recovery is just as important to a preteen or teen as it is to an adult.  The best way to determine post-exercise hydration needs is to weigh the child to compute weight loss, and to replace fluid at one and a half times the volume lost to sweat.  One ounce of water (sweat) weighs one ounce, so the math is simple.  A kid’s thirst mechanism is not well-developed, so you’ll almost have to force him to drink…but do it.

The nutrients in which young athletes are most deficient include carbohydrates, calcium, vitamin B6, folate and iron, the last being especially important to girls.  Carbohydrate inadequacy leads to shortened glycogen stores and premature fatigue, especially if the game is sixty minutes or longer.  Once glycogen is gone, fat gets mobilized and the child will “bonk.”  The last thing you want is for the young athlete to burn protein for fuel. An active child will need as many as 500 to 1500 more calories a day than his inert peers.

Two to three hours before an event, give your athlete a light, carb-rich meal:  carrot sticks and a piece of cheese; a little pasta; a small sandwich.  Have him exert himself on a slightly empty stomach to avoid cramping, even fatigue.  Chips, cakes or cookies, and candy are out.  The protein your child needs will not build bulk.  That comes with age.  Normal muscle development will require as much as one and a half grams of protein for each kilogram of body weight, but need not be much more than fifteen to twenty percent of daily calorie intake.  Reduce that during the off season. Thirty percent fat in the daily intake will help to supply needed calories.  Reduce that off-season, too, lest you greet Tweedledee one morning.

The matter of iron deficiency is a particular concern for girls, especially after the onset of menarche, which can be a couple of years late for an iron-fisted ball player.  Iron-deficiency anemia is a real threat for female athletes.  Besides affecting performance and recovery, low iron stores impair immune function and may initiate other physiological problems.  Supplementation is not intended to replace food as a source of nutrients, but in the case of iron deficit, it may be recommended.  (Beard. 2000).  There’s no need for your daughter to join the 50% of the world population who are deficient in iron.  (Ahmadi. 2010).  Raw meat probably won’t help, but getting 15 mg a day from supervised supplementation will.

Youngsters are often grossly misinformed about what they need and don’t need.  Their peers and the internet are not always reliable sources of information.  Some young athletes need only a minor tweak to their diets; others need a complete overhaul.  If you feel inadequate, don’t be embarrassed.  There are dietitians and sports nutritionists who can help.

References

Petrie HJ, Stover EA, Horswill CA.
Nutritional concerns for the child and adolescent competitor.
Nutrition. 2004 Jul-Aug;20(7-8):620-31.

Cordelia W Carter, Lyle J Micheli
Training the child athlete: physical fitness, health and injury
Br J Sports Med 2011;45:880-885

Bar-Or O.
Nutritional considerations for the child athlete
Can J Appl Physiol. 2001;26 Suppl:S186-91.

Beard J, Tobin B.
Iron status and exercise.
Am J Clin Nutr. 2000 Aug;72(2 Suppl):594S-7S.

Ahmadi A, Enayatizadeh N, Akbarzadeh M, Asadi S, Tabatabaee SH.
Iron status in female athletes participating in team ball-sports.
Pak J Biol Sci. 2010 Jan 15;13(2):93-6.

Koehler K, Braun H, Achtzehn S, Hildebrand U, Predel HG, Mester J, Schänzer W.
Eur J Appl Physiol. 2011 May 19. [Epub ahead of print]
Iron status in elite young athletes: gender-dependent influences of diet and exercise.

Committee on Sports Medicine and Fitness
AMERICAN ACADEMY OF PEDIATRICS
Intensive Training and Sports Specialization in Young Athletes
Pediatrics Vol. 106 No. 1 July 1, 2000 : pp. 154 -157

Martinez LR, Haymes EM.
Substrate utilization during treadmill running in prepubertal girls and women.
Med Sci Sports Exerc. 1992 Sep;24(9):975-83.

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

Protein Zaps Belly Fat

abdomenIn a sedentary, over-fed, yet undernourished society, the dissolution of abdominal fat with a magic bullet is an incessant quest.  First, we cut out the junk food.  Then we try to eat a balanced diet, the definition of which seems elusive.  After that, we add the foods we think are good for us.  Still, we can’t burn the belly.  Next, we look closer at the ads for products guaranteed to get rid of excess adiposity.  Only after these promises fail do we notice the small print that says the results you see are not typical, and that it must be accompanied by diet and exercise.  Oh, no, I have to work at it.  What happened to the magic bullet?

To be realistic about losing fat, we have to do something actively, not passively.  But that might be as simple as upping the ante on protein.  However, it just isn’t plain, old protein, but the quality of the protein that makes the difference.  Actually it’s the amino acids, the protein building blocks whose chemical properties determine the biological activity of the proteins of which they are a constituent.   Proteins catalyze many of the reactions in living cells—enzymes, hormones, antibodies.  The folding of proteins into three dimensional structures depends upon the information in the amino acid sequences.  Although several hundred kinds of amino acids have been found in nature, only twenty or so apply to human peptides (two or more aminos joined together) and proteins.  Low levels of certain amino acids telegraph as specific problems that include hormone imbalances, lack of concentration, irritability, and even depression.

Based on their individual characteristics, amino acids may be classified as essential, non-essential, or conditionally essential.  Essentiality does not bespeak importance, but acquisition.  The essential ones need to be acquired from diet because they can’t be made by the body.  Here’s a quick rundown of the essential amino acids, with some of their features:

Leucine — a BCAA (branched chain amino), is used for tissue repair after surgery, to build muscle mass, to balance blood sugar, to de-stress, to manufacture HGH (human growth hormone), and for protein synthesis.  It helps to maintain healthy bone, skin, and hemoglobin.

Isoleucine — a BCAA (branched chain amino), addresses mental disorders, tissue rebuild after surgery, energy, muscle, endurance, and blood hemoglobin.

Valine — a BCAA (branched chain amino), is used for mental and emotional disorders, for glycogen production, and in alcohol and drug recovery.  It’s used in muscle metabolism, where it contributes to the structure of proteins.

Lysine — absorbs and conserves calcium and maintains nitrogen balance.  It helps to make collagen, to manage cholesterol and triglycerides, and bolsters the immune system.  (People use this for fever blisters.)

Methionine — has been used to address schizophrenia, and the muscle weakness of Parkinson’s.  It helps to detoxify heavy metals, to form collagen, to prevent brittle hair and nails, to protect against radiation toxicity, and to control histamine levels that may affect cognitions.  Additionally, methionine is a strong antioxidant.

Phenylalanine — addresses chronic pain, helps to make endorphins, assists the manufacture of norepinephrine to direct nerve signals in the brain, promotes alertness and elevates mood, and has been used to treat arthritis, depression, migraines, and Parkinson’s disease.

Threonine — helps to maintain proper protein balance, is important to collagen, elastin, and tooth enamel, aids wound healing, may prevent fatty liver, and assists assimilation.

Tryptophan — is a natural relaxant that helps to alleviate insomnia.  It stabilizes mood, fights migraines and fibromyalgia, and may aid in weight control by reducing appetite.

Histidine — is conditional in adults, but deemed essential to infants and children, and is the immediate precursor to histamine (and carnosine).  Histidine is abundant in hemoglobin, and has been used in the treatment of arthritis, gastric disorders, and the maintenance of the myelin sheath.  It protects against heavy metals and radiation, and aids in the manufacture of red and white blood cells.

The remaining amino acids are non-essential, and are produced from the breakdown of proteins or from the essential ones.  They and a few of their jobs are:

Alanine — (the other component of carnosine) transfers nitrogen from peripheral tissue to the liver in glucose metabolism and guards against the buildup of toxins when muscle tissue is broken down to meet energy needs, as occurs in serious aerobic exercise.

Arginine — is considered the natural Viagra, relaxes blood vessels, supports thymus immunity activity, helps to neutralize ammonia, assists the release of growth hormones, and stimulates the pancreas to release insulin.

Aspartic Acid — from asparagine, is used to treat chronic fatigue and depression, aids the elimination of ammonia, rejuvenates cell activity, and helps to move minerals across the intestinal lining into the bloodstream.

Cysteine — (and cysteine) works as a potent antioxidant and protects against radiation and the toxins of tobacco smoke.  It promotes recovery from burns and promotes the burning of fats. Cystine is formed from the oxidation of two cysteines, but has the same character and activity.

Glutamic Acid — is an excitatory neurotransmitter that is called glutamine after coupling with ammonia, which is carried to the liver for disposal.  Free glutamic acid is important to the metabolism of fats and sugars, and helps to carry potassium into spinal fluid.

Glutamine — is structurally akin to glutamic acid.  It’s the most abundant amino found in muscles, which it helps to build and maintain, where it is useful for those confined to bed for long periods.  It helps to maintain acid-alkaline balance, and might be able to reduce cravings for sugar and alcohol.

Glycine — participates in the biosynthesis of hemoglobin, improves glycogen storage, and is part of the purine component of genetic material.

Ornithine — could be classed with “other” amino acids, helps to release growth hormones, which promotes the metabolism of excess body fat.  It detoxifies ammonia and may help insulin to function as an anabolic agent.  It’s formed from arginine.

Proline — improves skin texture via formation and salvation of collagen.  It works with vitamin C to promote healthy connective tissues.

Serine — is needed for the metabolism of fats and fatty acids, and for participation in the biosynthesis of genetic compounds important to RNA and DNA.

Taurine — is also among the “others.”  It boosts the heart muscle and vision, where it helps to deal with macular degeneration.  Taurine is a key component of bile, and may prevent cardiac arrhythmia.

Tyrosine — is important to overall metabolism, and is a precursor to norepinephrine and dopamine, which regulate mood.  It may suppress appetite and helps to reduce body fat.  Tyrosine affects thyroid hormones.

In a weight management study described in the January, 2012, issue of Nutrition and Metabolism, researchers were able to determine a relationship between the amount of quality protein ingested and central abdominal fat.  They especially paid attention to the number of times that approximately ten grams of essential amino acids (EAA) were consumed in a meal.  Noting that the dietary reference intake (DRI) has no specific recommendations for the types of dietary protein consumed or the distribution of protein throughout the day (Layman, 2009) (Drewnowski, 2001), these scientists drew their conclusion based on maximal stimulation of muscle protein synthesis, thereby arriving at the ~10 gram level, adding that greater amounts do not improve the outcome. (Loenneke, 2012)

Calculating the amount of essential amino acids (EAA) in a meal requires more labor than many of us are able or willing to perform, mostly because we lack the immediate resources needed to find out the base levels of each food in the meal.  There are books and websites that can help with this venture if you are so inclined.  However, eating a quality protein at each meal should do the job.  That usually includes meat, fish, eggs, and dairy, which are complete proteins, meaning that they have all the essential amino acids.   (Egg whites are excellent protein foods.)  Because grains and nuts lack lysine, and legumes lack methionine, it’s a good idea to combine them, as in rice and beans.  Combining essential aminos is not necessary at every meal, but it is in the course of the day.

Whey protein has been shown to stimulate a considerable rise in muscle protein synthesis and results in greater muscle cross-sectional area, especially if combined with a little resistance training—and it enhances recovery after exercise.  (Hulmi, 2010)  Older people show a decreased anabolic sensitivity to essential amino acids, probably because of declining intramuscular expression and receptor activation that are associated with slower anabolic signaling.  (Cuthbertson, 2005)   Among the countermeasures under investigation is regular resistance exercise, regardless of intensity or duration.  In physiological studies at the U. of TX, it was found that the only difference between young and old is the rapidity of the positive response to EAA’s.  (Drummond, 2008)  Timing of EAA ingestion for exercisers makes a difference.  Consume them afterwards.

Stimulating muscle protein synthesis is important to body composition.  If you multiply your body weight in kilograms (2.2 pounds) by 0.8, you’ll arrive at the number of grams of protein you need every day.  (You could also multiply pounds by 0.37.  Why didn’t we say that in the first place?)  More than 30 grams of protein in a single meal does not enhance protein synthesis.  This translates that 113 grams (about 4 oz.) of beef is enough, at 220 calories and 30 grams of protein.  (Symons, 2009)  Therefore, that 12-ounce steak from your favorite eatery isn’t doing much more than filling you up.  While you’re at that restaurant, skip the simple carbs if you’re looking to lose a few inches.  There’s a positive association between girth and consumption of potatoes, refined grains (including alcohol) and simple sugars, but a negative association with protein.  (Halkjaer, 2006)

Protein intake has added benefit—satiety.  If you feel full longer, you’ll eat less and, therefore, consume fewer calories.  Protein increases satiety to a greater degree than fats or carbohydrates (although fats beat carbs), and higher-protein diets result in thermogenesis, which augments energy expenditure.  And, if you have high triglycerides (from eating too many refined and starchy carbohydrates), complete protein is able to attenuate that while you change body composition to something more desirable.  (Clifton, 2009)  (Clifton, 2008)  Don’t forget to choose lean protein, to remove visible fat from your steaks and the skin from poultry, and to add legumes to your regimen.

References

Clifton PM, Keogh JB, Noakes M.
Long-term effects of a high-protein weight-loss diet.
Am J Clin Nutr. 2008 Jan;87(1):23-9.

Clifton PM, Bastiaans K, Keogh JB.
High protein diets decrease total and abdominal fat and improve CVD risk profile in overweight and obese men and women with elevated triacylglycerol.
Nutr Metab Cardiovasc Dis. 2009 Oct;19(8):548-54.

Cuthbertson D, Smith K, Babraj J, Leese G, Waddell T, Atherton P, Wackerhage H, Taylor PM, Rennie MJ.
Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle.
FASEB J. 2005 Mar;19(3):422-4.

Drewnowski A, Warren-Mears VA.
Does aging change nutrition requirements?
J Nutr Health Aging. 2001;5(2):70-4.

Drummond MJ, Dreyer HC, Pennings B, Fry CS, Dhanani S, Dillon EL, Sheffield-Moore M, Volpi E, Rasmussen BB.
Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging.
J Appl Physiol. 2008 May;104(5):1452-61.

Fujita S, Dreyer HC, Drummond MJ, Glynn EL, Volpi E, Rasmussen BB.
Essential amino acid and carbohydrate ingestion before resistance exercise does not enhance postexercise muscle protein synthesis.
J Appl Physiol. 2009 May;106(5):1730-9.

Halkjaer J, Tjønneland A, Thomsen BL, Overvad K, Sørensen TI.
Intake of macronutrients as predictors of 5-y changes in waist circumference.
Am J Clin Nutr. 2006 Oct;84(4):789-97.

Hulmi JJ, Lockwood CM, Stout JR.
Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein.
Nutr Metab (Lond). 2010 Jun 17;7:51.

Layman DK.
Dietary Guidelines should reflect new understandings about adult protein needs.
Nutr Metab (Lond). 2009 Mar 13;6:12.

Loenneke JP, Balapur A, Thrower AD, Syler G, Timlin M, Pujol TJ.
Short report: Relationship between quality protein, lean mass and bone health.
Ann Nutr Metab. 2010;57(3-4):219-20.

Loenneke JP, Wilson JM, Manninen AH, Wray ME, Barnes JT and Pujol TJ
Quality protein intake is inversely associated with abdominal fat
Nutrition and Metabolism.  Jan, 2012; 9:5

Paddon-Jones D, Westman E, Mattes RD, Wolfe RR, Astrup A, Westerterp-Plantenga M.
Protein, weight management, and satiety.
Am J Clin Nutr. 2008 May;87(5):1558S-1561S.

Sites CK, Cooper BC, Toth MJ, Gastaldelli A, Arabshahi A, Barnes S.
Effect of a daily supplement of soy protein on body composition and insulin secretion in postmenopausal women.
Fertil Steril. 2007 Dec;88(6):1609-17.

Symons TB, Sheffield-Moore M, Wolfe RR, Paddon-Jones D.
A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects.
J Am Diet Assoc. 2009 Sep;109(9):1582-6.

Tipton KD, Gurkin BE, Matin S, Wolfe RR.
Nonessential amino acids are not necessary to stimulate net muscle protein synthesis in healthy volunteers.
J Nutr Biochem. 1999 Feb;10(2):89-95.

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

Milk – It Does A Body Something, For Sure

milk-carton-glassMost advertisements try to float the reader / viewer to the side of the river that hosts the heralded product. You’ll unlikely see a car salesman tell you there’s a better deal across the street.  If you know someone who tells the doctor what medications to Rx based on TV blurbs, you know the story.  It’s all in the power of the ad, truth or not.  You probably don’t know that the dairy industry has a champion called the International Dairy Journal, a highly-respected periodical that doesn’t exactly promote good old dihydrogen oxide, the most abundant molecule on the planet.  In January of 2012 there appeared in this publication a piece that addressed dairy foods and cognitive decline, commonly known as dementia, declaring that study participants who consumed dairy products at least once a day performed better on measures of cognitive function than those who rarely or never consumed dairy.  (Crichton, 2012)  What?  Did you expect something less stellar?  At least, the study candidly admits that the causal mechanisms “are still to be determined.”  Maybe there’s more to dairy than we know about if something needs to be determined.

Two years prior to this study, the same authors told us that drinking low-fat milk improves social functioning, stress and memory.  Maybe this proclamation means that low-fat milk can make you a better dancer and that you won’t worry about it if you think you are, but really aren’t, whether you forget or not.  Funny thing, whole milk has no such benefit.  (Crichton, 2010)  Yet, there’s the admission that the jury is still out.  Neither report had a definitive conclusion.  Both of these studies took place in Australia, but that shouldn’t make any difference because Australian and American cows speak the same language, except the Aussies add “mate” after “moo.”

Not to pop the milk drinkers’ balloon, despite the pleasure it might bring, but an in-between 2011 investigation performed by the Agricultural Research Service section of the USDA found that milk was less effective than meat for improving cognitive function and physical activity, but this time in a child population.  (Allen, 2011)  What this boils down to is that the stuff in meat is the same as the stuff in milk, but there’s more of it.  That would be iron, zinc, riboflavin, vitamin B12, and the rest of the nutrients for which animal products are hailed.

There is, however, another side to this coin. (Maybe “dodecahedron” would be a better metaphor because there are a few sides.)  That milk contains about four hundred different fatty acids makes it the most complex of all natural fats.  These fats come from one of two sources—the feed or the microbial happenings in the cow’s rumen.  In the olden days, back in the 1940s and early 50s, these fats floated on top of the milk because homogenization either wasn’t used or didn’t work as planned.  The kid who was the first to rise in the morning could retrieve the glass container from the front steps and eat the cream from the top of the bottle, leaving the low-fat remainder for the rest of the family.  Little did he or she realize that the goodness of butyric acid, a salutary short-chain fatty acid, was accompanied by the not-so-goodness of saturated fat and a little trans fat.  A small fraction of the beneficent essential fatty acids is in the mix, but hardly enough to make much difference.  However, there are other things in milk.  Among them are somatic cells, which some people equate with pus.  Aww, they wouldn’t allow that, would they?  Note that the job of the USDA is to promote agricultural interests, not yours.  In fact, clever inventors have devised ways to measure the somatic cells in your milk bottle with amazing precision (Tsenkova, 2001), with each state in the nation setting its own allowable levels based on regional variables.  (http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5089395.) and
(http://aipl.arsusda.gov/publish/dhi/dhi11/sccrpt.htm)

Where does this stuff come from? The milking machine.  A cow’s udder is treated with iodine prior to being sucked dry, and both the iodine and a few of the cow’s body cells end up in the milk.  Doesn’t pasteurization kill germs?  Some.  But the dead cells are still in the milk, and besides, pasteurization is not sterilization.  The latter is intended to kill everything.  The former is intended to achieve a reduction in the number of viable organisms, reducing their number so they are unlikely to cause disease.  Milk can be pasteurized by heating to 145° F for half an hour or to 163° F for fifteen seconds.  The thermoduric bacteria that survive are held in check by refrigeration. To add insult to injury, the iodine may induce thyroid or dermatological issues over time.  That’s another story, though.

The casein in milk protein yields peptides called casomorphins, with different breeds of cattle offering different peptides, totaling about thirteen variants, each of which is divided into categories known as A1 and A2.  A1 caseins contain the amino acid histidine, essential for the growth and repair of tissue, but also responsible for manufacturing histamine, the stuff that makes your nose runny in an allergic reaction or that makes you itch after a mosquito attack. Although concentration-dependent, this state of affairs is uncomfortable at best, and is blamed specifically on beta-casomorphine-7, “…a naturally occurring product of cow’s milk with opiate-like activity…” (Kurek, 1992).  A2 caseins contain proline, a non-essential amino acid that is a component of cartilage.  That casomorphins have opioid activity matters little in light of the discovery that particular A1 casein can become glycated and promote adverse immune effects (Elliott, 2006), among them diabetes.

So, what is glycation?  It’s the result of a sugar bonding to a protein or a fat without the watchful eye of an enzyme, such as might happen in a frying pan or even in the body after ingesting a sugar, resulting in a haphazard process that impairs cellular function.  This is not to be confused with glycosylation, an enzyme-controlled process aimed at a specific molecule to enable its particular function.  Glycation forms advanced-glycation-end products, or AGE’s that are implicated in neurodegenerative diseases (Li, 2012) and mitochondrial dysfunction (Hashimoto, 2003).

About 8% of infants under age one are allergic to cow’s milk (Constantinide, 2011).  This might account for the crankiness of the child who is unable to define the earache or the gastric distress that cause discomfort and pain.  Yes, a child may outgrow milk allergy, only to be bombarded with symptoms decades later, most of which arise from reactions to the foreign protein that is casein, a material once used to make paint.  Casomorphin from type A1 is believed to play a role in ischemic heart disease, while that from type A2 encourages neither heart disease nor diabetes (Kaminski, 2007).  Are you expected to test your milk to find whether it’s higher in one or the other variant?  Type A1 Beta-casomorphin-7 is implicated in several human miseries, and is especially hazardous to those with leaky gut syndrome, to this day a questionable diagnosis to the traditional medical community.  Nonetheless, BCM-7 affects GI motility and mucosal immune function (Elitsur & Luk, 1991).  Now that it’s been established that type A1 is the bad casein, here’s the list of cattle ranked according to A1 casein content, from bad to good:  Holstein (much more A1 than A2); Jersey, Ayrshire and Milking Shorthorn (these three have almost equal levels);  Brown Swiss (more A2 than A1), and Guernsey (almost a 100 x A2 than A1).  The next time you get milk from the supermarket, the neighborhood convenience store or the gas station around the corner, be sure to ask the dairy manager/clerk from which breed of cow the milk was pumped.

There is much more to deny a cow its center stage, ranging from mineral imbalances to disease promotion via shared hormones with humans, items to be addressed another time.  But if there’s cognitive benefit to be derived from milk, it comes from phospholipids (Schubert, 2011) (Lopez, 2008), the structural and functional cellular components that are better obtained, without unwanted tag-a-longs, from non-dairy sources.  Milk phospholipid and fat content depends on what the cow is fed.  Cattle feed high in flaxseed, for example, will produce milk higher in polyunsaturated fats and lower in saturated ones (Lopez, 2008).  Regardless, only about 1% of milk lipids are phospholipids.  Even if there were a higher percentage, the heat of pasteurization that destroys enzymes (It takes only 120° F to deactivate an enzyme.) also would oxidize the phospholipids to uselessness.

Cow’s milk does a body good if you’re a calf.  The ideal for humans is, well, breast milk.  If breast feeding is out of the question, there are alternatives that supply the fats an infant needs for development.  Hemp milk is one of these, but it’s expensive.  It’s loaded with omega-3 fatty acids and potassium, and enough vitamins to meet the need.  Omega-6 fats can be fortified with sunflower, safflower or evening primrose oils, and phospholipid needs can be more than satisfied with real, honest-to-goodness phosphatidylcholine.  After age four, a tot can switch to alternative milk, but the supplementary essential fats and phosphatidylcholine should stay because they definitely do a body good…all the way into old age.  It is not common for animals to drink the milk of another species.  Who chose cattle to be the source of beverage,  cavemen?  “Hey, Charlie, let’s yank on that thing hangin’ down under that animal and drink what comes out.”  One more thing:  what milk does to a prostate gland shouldn’t happen to anyone (Schmitz-Dräger, 2011)  (Tate, 2011)  (Torfadottir, 2012).

References

Allen LH, Dror DK.
Effects of animal source foods, with emphasis on milk, in the diet of children in low-income countries.
Nestle Nutr Workshop Ser Pediatr Program. 2011;67:113-30

Cie Li Ska A, Kostyra EB, Kostyra H, Ole Ski K, Fiedorowicz E, Kami Ski SA.
Milk from cows of different ?-casein genotypes as a source of ?-casomorphin-7.
Int J Food Sci Nutr. 2011 Nov 14.

Clemens RA.
Milk A1 and A2 peptides and diabetes.
Nestle Nutr Workshop Ser Pediatr Program. 2011;67:187-95. Epub 2011 Feb 16.

Constantinide P, Trandafir LM, Burlea M.
The role of specific IgE to evolution and prognosis of cow’s milk protein allergies in child. 
Rev Med Chir Soc Med Nat Iasi. 2011 Oct-Dec;115(4):1012-7.

Crichton GE, Murphy KJ, Bryan J.
Dairy intake and cognitive health in middle-aged South Australians.
Asia Pac J Clin Nutr. 2010;19(2):161-71

Crichton GE,  M.F. Eliasb, G.A. Dore, M.A. Robbins
Relation between dairy food intake and cognitive function: The Maine-Syracuse Longitudinal Study
International Dairy Journal. Volume 22, Issue 1, January 2012, Pages 15–23

Elitsur Y, Luk GD.
Beta-casomorphin (BCM) and human colonic lamina propria lymphocyte proliferation.
Clin Exp Immunol. 1991 Sep;85(3):493-7.

Elliott RB, Harris DP, Hill JP, Bibby NJ, Wasmuth HE.
Type I (insulin-dependent) diabetes mellitus and cow milk: casein variant consumption.
Diabetologia. 1999 Mar;42(3):292-6.

Elliott RB.
Diabetes–a man made disease.
Med Hypotheses. 2006;67(2):388-91.

Federal Milk Order Marketing Area, 2011
Somatic cell count of producer milk
http://www.ams.usda.gov/AMSv1.0/getfile?dDocName=STELPRDC5089395

Hashimoto M, Rockenstein E, Crews L, Masliah E.
Role of protein aggregation in mitochondrial dysfunction and neurodegeneration in Alzheimer’s and Parkinson’s diseases.
Neuromolecular Med. 2003;4(1-2):21-36.

Høst A, Halken S, Jacobsen HP, Christensen AE, Herskind AM, Plesner K.
Clinical course of cow’s milk protein allergy/intolerance and atopic diseases in childhood.
Pediatr Allergy Immunol. 2002;13 Suppl 15:23-8.

Kamiński S, Cieslińska A, Kostyra E.
Polymorphism of bovine beta-casein and its potential effect on human health.
J Appl Genet. 2007;48(3):189-98.

Kurek M, Przybilla B, Hermann K, Ring J.
A naturally occurring opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man.
Int Arch Allergy Immunol. 1992;97(2):115-20.

Kurek M, Czerwionka-Szaflarska M, Doroszewska G.
Pseudoallergic skin reactions to opiate sequences of bovine casein in healthy children.
Rocz Akad Med Bialymst. 1995;40(3):480-5.

Li J, Liu D, Sun L, Lu Y, Zhang Z.
Advanced glycation end products and neurodegenerative diseases: Mechanisms and perspective.
J Neurol Sci. 2012 Mar 11.

Christelle Lopez, Valerie Briard-Bion, Olivia Menard, Florence Rousseau, Philippe Pradel and Jean-Michel Besle
Phospholipid, Sphingolipid, and Fatty Acid Compositions of the Milk Fat Globule Membrane are Modified by Diet
J. Agric. Food Chem., 2008, 56 (13), pp 5226–5236

Månsson, Helena Lindmark
Fatty acids in bovine milk fat
Food Nutr Res. 2008; 52: 10

H.D. Norman, T.A. Cooper, and F.A. Ross, Jr.
Somatic cell counts of milk from Dairy Herd Improvement herds during 2010
Animal Improvement Programs Laboratory, Agricultural Research Service, USDA, Beltsville, Md
20705   http://aipl.arsusda.gov/publish/dhi/dhi11/sccrpt.htm

Schubert M, Contreras C, Franz N, Hellhammer J.
Milk-based phospholipids increase morning cortisol availability and improve memory in chronically stressed men.
Nutr Res. 2011 Jun;31(6):413-20.

Schmitz-Dräger BJ, Lümmen G, Bismarck E, Fischer C; Mitglieder des Arbeitskreises Prävention, Umwelt und Komplementärmedizin.
Primary prevention of urologic tumors: prostate cancer.
Urologe A. 2011 Oct;50(10):1271-2, 1274-5.

Tate PL, Bibb R, Larcom LL.
Milk stimulates growth of prostate cancer cells in culture.
Nutr Cancer. 2011 Nov;63(8):1361-6. Epub 2011 Nov 1.

Torfadottir JE, Steingrimsdottir L, Mucci L, Aspelund T, Kasperzyk JL, Olafsson O, Fall K, Tryggvadottir L, Harris TB, Launer L, Jonsson E, Tulinius H, Stampfer M, Adami HO, Gudnason V, Valdimarsdottir UA.
Milk intake in early life and risk of advanced prostate cancer.
Am J Epidemiol. 2012 Jan 15;175(2):144-53. Epub 2011 Dec 20.

Tsenkova R, Atanassova S, Kawano S, Toyoda K
Somatic cell count determination in cow’s milk by near infra-red spectroscopy: a new diagnostic tool
J Anim Sci. 2001; 79: 2550-2557

University at Buffalo.
Acne, Milk And The Iodine Connection.
ScienceDaily, 7 Dec. 2005.
http://www.sciencedaily.com/releases/2005/12/051207181144.htm

*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.

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*These statements have not been evaluated by the FDA.
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