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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.

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.

Microwave Safety

microwave-ovenIn the United States, food grade containers are known not to leach harmful substances into the foods they hold, whether for storage or for microwave cooking. In most homes in the country, you’ll find a range of containers in the refrigerator, from plastics of known and unknown origin to paper to glass to metals to ceramics. Although many of us probably don’t, maybe we should care whether or not a container is safe for microwave use.

How does a microwave work?  

The oscillating waves produced by a microwave oven are similar to radio waves but much faster. They act mainly by energizing the water molecules present in a food, causing them to vibrate and to make heat. Because of the speed involved, food cooks faster than with conventional means, where heat is transferred from an external source to the material, working from the outside in by way of thermal conduction. Only substances that absorb microwaves can be heated by a microwave oven, with the food itself becoming the heat source for cooking. Heating metals in a microwave produces different, and sometimes unexpected, results. Low penetration depth results in reflection of the waves, setting up high voltage between the metal and the magnetron that is the heart of the system. When this voltage surpasses a threshold, sparks fly. Powdered metal probably would react differently. But we suggest you refrain from trying this unless you work in a science laboratory.

I heard that microwaves destroy the nutrient value of food.

Yeah, we heard that, too. The fact is that any cooking method destroys some character of a food. Using too much water in a pot to cook frozen vegetables, for example, will render water-soluble nutrients to the water, which often goes down the drain. Several studies have shown that microwave cooking, if used the right way, has no more adverse effect on food nutrition than conventional heating methods. In fact, probably because of shorter cooking time, there might even be a tendency for greater nutrient retention (Lassen, 1995). If there be a fault, it would be uneven heating. Moisture loss is more noticeable (Cross, 1982) (Quan, 1985), though, and that makes sense, since all those water molecules bumping against each other create friction, and friction creates heat.

Some studies examined the effects of microwaves on human milk. Besides the usual nutrients a baby needs, breast milk contains immunity factors, such as IgA. Microwaving to temperatures between 161°F and 208°F caused a marked decrease in anti-infective factors (Quan, 1992). We have questions about this. Who heats jarred or bottled baby food or formula hotter than the human wrist can tolerate, which is far lower than the temperature of your water heater? Doesn’t milk come from mom at about 98.6°? At temperatures up to 149°F, fatty acids, most vitamins and immunoglobin are safe (Ovesen, 1996). The hydroxo- form of Vitamin B12, which predominates in foods, appears to be degraded by microwave heating as evidenced in tests on B12-dependent organisms fed a microwaved diet (Watanabe, 1998). But this is only one such test. And most of us don’t put all our eggs into one basket. Because adults cannot metabolize the vitamin B12 from food sources anyway (we lack the gastric intrinsic factor required), we mention this study as a courtesy to the young readers. To overcome poor absorption, sublingual or injectable forms of B12 are available.

So, what should not go into the microwave?

There are some things to keep in mind when using the microwave. Most containers from the takeout place, water bottles, plastic tubs from margarine, yogurt, cream cheese, mustard and mayonnaise, and whipped toppings are not safe for microwave use. Some microwavable trays, such as those from frozen dinners, are designed for one-time use. It should say that on the package. Plastic bags of any kind belong in the trash. If the plastic containers you just bought at the dollar store do not say “Microwave Safe,” don’t use them. Choosing to microwave with a plastic lacking such a declaration doesn’t necessarily mean it’s unsafe, but it is missing the assurance of safety. The symbol on the bottom of the container means nothing in this case.

Plastic wrap—saran—helps to retain moisture but it should not touch the food. The wrap itself is not heated by microwaves, but it will conduct heat from warmed food, and it could melt. The result would have to be an acquired taste that may present toxicity issues. The box of wrap will tell you if it’s microwave safe. Don’t even think about Styrofoam cups and dishware unless it says otherwise.

How about paper?

Paper coffee cups are occasionally lined with wax, and sometimes plastic. Overheating is the worry here. Learn to control the microwave. Many papers are manufactured with chemicals you don’t want in your mouth. You have to read the label. The dyes from printed paper towels can contain toxins. White paper towels are usually safe, but reading that affirmation on the package lets you know for sure. Paper grocery bags—or paper bags of any kind, for that matter—may contain unwanted metals or be recycled from who knows what. Waxed paper and parchment are safe in the microwave. Except for those coated with wax or a plastic film, paper plates should not be a problem. The wrapping will tell you. But plain paper plates are flimsy. The big-name companies have microwavable dinnerware. There is always a bottom line, right? Here it is: the preferred options are glass and ceramic. Still, the best habit to cultivate is to become a label reader. We said that already, didn’t we?

References

Anna Angela Barba, Antonella Calabretti, Matteo d’Amore, Anna Lisa Piccinelli, Luca Rastrelli
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Anne Lassen, Lars Ovesen
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*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Methylation And Age: How Old Are You, Really?

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

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

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

What is methylation?

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

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