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Enhancing The Worst

burger-on-trayIt’s bad enough when the junk in (or on) your food harms you—you know, the preservatives, the agricultural sprays, the stuff in there that you can’t begin to pronounce, the coloring agents, and whatever—but this is getting ridiculous.  It’s not necessarily the food you prepare at home from scratch that we’re talking about.  It’s not even the Boiled Water Helper that some “cooks” need to put something mostly edible in front of you.  It’s the wrapper, especially the one making cozy with your fast food burger.  And so we moan, “Now, what is it?”

If you’re ready, we’ll give you the list.  Even if you’re not, here it comes:  perfluoroalkyls, polyfluoroalkyl phosphate esters (PAP’s), polyfluorinated carboxylic acids (PFCA’s), and everyone’s favorite, perfluorooctanoic acid (PFOA).  You don’t have to remember these, but note that fluorine is a central player in the cast.  Yep, the same stuff in your toothpaste, the label of which tells you not to swallow too much.

Fluorine belongs to a group of chemical elements called halogens, along with chlorine, bromine, iodine, and astatine, the last of which is essentially unavailable in nature and is radioactive.   The halogens are the only group that contains elements in all three states of matter—fluorine and chlorine are gases, iodine is a solid, and bromine is a liquid.  All are non-metals.  Because they are highly reactive, they’re found in the environment only as compounds.  Iodine is the heaviest element needed by living creatures, and its appropriateness to thyroid health is well-known.  But it’s less reactive than its fellows, so it’s easily displaced.  That means that fluorine and bromine, which is used to bleach flour, can push it aside and take its place in your thyroid gland.   Hypothyroidism, anyone?

Fluorides are moderately toxic and, if conditions are right, can attack intracellular calcium.  It’s readily absorbed and forms an acid that binds with calcium and interferes with several enzymes.  Too much fluoride leads to skeletal fluorosis and mottled teeth.  (Reddy, 2009)  It might be all right to use on the teeth from the outside, but certainly not from inside the body.

What’s this got to do with food wrappers?  The compounds named in the second paragraph are stable synthetic chemicals that repel grease, oil, and water.  If you ever saw the television commercial that boasted of stain-repellent and water-repellent clothing, you’ve seen these chemicals at work.  Though still popular on carpets, they pretty much have been removed from materials that touch the skin.  Hmmm.  However, they are used to make paper and cardboard packaging.  These would be the PFCA’s, which break down into PAP’s, and they wrap your burger so you can eat it while you drive and stay relatively grease free.  Do you microwave popcorn?  Guess what coats the inside of the bag.

Human exposure to PFCA’s is worldwide.  These chemicals are environmentally persistent, as well, and have generated considerable scientific and regulatory interest on a global scale.  (Andersen, 2008)  Research at the University of Toronto found that the PAP in food contact applications does affect blood chemistry in humans, causing changes in sex hormones and cholesterol.  In laboratory animals, which are obviously smaller than people, premature death and developmental delay have been observed.  Some of the effects on rats—tumor growth, for example—may not be applicable to humans.  (D’eon, 2011)  But who knows?  We mentioned that these fluorinated substances are environmentally persistent.  They also persist in the blood stream.  Think of what happens to people who eat fast food every day.

PFOA has been detected in a high percentage of human blood samples and house dust taken from homes in Massachusetts, Maine, New York, Oregon, and California, and it has contaminated drinking water in West Virginia and Minnesota.  Two companies that manufacture the chemicals, DuPont and 3M, were allegedly aware of the potentially harmful effects on humans, but sequestered the data and never told the U.S. Environmental Protection Agency of the adverse effects information, as required under the Toxic Substances Control Act.  They got banged for a minimum of thirteen million dollars in fines, with the potential to reach three hundred million.  DuPont settled a class action suit with West Virginia in 2004.  The courts added that the ante will be upped if a definitive link is found between the chemicals and human misery.  This could exceed three hundred million dollars.  Ouch. (http://www.defendingscience.org/case_studies/perfluorooctanoic-acid.cfm)

The Office of Research and Development of the EPA issued a paper in March, 2009, that listed a hundred sixteen “articles of commerce” that contain perfluorocarboxylic acid (aka PFCA).  How come we never heard about any of this?  Of course, typical of many authorities, is the hedge that additional study is warranted before anything definite can be proposed.  The list covers commodities from household liquids to textiles, from Teflon cookware to food contact paper, and even…gets this…dental floss.  Dental floss???  You can check it out at www.oecd.org/dataoecd/47/50/48125746.pdf
Makes you proud, doesn’t it?

It appears that interest in this matter was contagious in the first decade of the new century.  The FDA learned that fluorochemical paper additives migrate into food, after it examined coconut and other oils, butter, water, vinegar, and alcohol.  Buttered microwave popcorn was a star.  (Begley, 2008)  The persistence of the fluorinated entities was supported by Canadian research the following year.  (Benskin, 2009)  Even the State of New Jersey got into the act and looked at drinking water in selected areas, finding detectable levels of PFOA in a variety of sources, but adding that levels are not regulated under State requirements.  That means everything is fine and dandy, right?  Of all the samples tested, 78% were positive for fluoride contamination.  This site http://www.nj.gov/dep/watersupply/pfoa.htm will give you the dope.

This stuff interferes with immunity in humans and wildlife (Dewitt, 2011), could possibly be associated with longer time to pregnancy (Vestergaard, 2012), and might affect your liver (Naile, 2012) and thyroid (Boas, 2011).  We need to call our favorite fast food emporiums and ask a few questions.  Does it matter to you?

References

Andersen ME, Butenhoff JL, Chang SC, Farrar DG, Kennedy GL Jr, Lau C, Olsen GW, Seed J, Wallace KB.
Perfluoroalkyl acids and related chemistries–toxicokinetics and modes of action.
Toxicol Sci. 2008 Mar;102(1):3-14.

Begley TH, Hsu W, Noonan G, Diachenko G.
Migration of fluorochemical paper additives from food-contact paper into foods and food simulants.
Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2008 Mar;25(3):384-90.

Benskin JP, De Silva AO, Martin LJ, Arsenault G, McCrindle R, Riddell N, Mabury SA, Martin JW.
Disposition of perfluorinated acid isomers in Sprague-Dawley rats; part 1: single dose.
Environ Toxicol Chem. 2009 Mar;28(3):542-54.

Boas M, Feldt-Rasmussen U, Main KM.
Thyroid effects of endocrine disrupting chemicals.
Mol Cell Endocrinol. 2011 Sep 10.

Cheng X, Klaassen CD.
Perfluorocarboxylic acids induce cytochrome P450 enzymes in mouse liver through activation of PPAR-alpha and CAR transcription factors.
Toxicol Sci. 2008 Nov;106(1):29-36.

Defending Science
Perfluorooctanoic Acid
http://www.defendingscience.org/case_studies/perfluorooctanoic-acid.cfm

D’Eon JC, Mabury SA.
Production of perfluorinated carboxylic acids (PFCAs) from the biotransformation of polyfluoroalkyl phosphate surfactants (PAPS): exploring routes of human contamination.
Environ Sci Technol. 2007 Jul 1;41(13):4799-805.

D’eon JC, Mabury SA.
Exploring indirect sources of human exposure to perfluoroalkyl carboxylates (PFCAs): evaluating uptake, elimination, and biotransformation of polyfluoroalkyl phosphate esters (PAPs) in the rat.
Environ Health Perspect. 2011 Mar;119(3):344-50. Epub 2010 Oct 29.

Dewitt JC, Peden-Adams MM, Keller JM, Germolec DR.
Immunotoxicity of Perfluorinated Compounds: Recent Developments.
Toxicol Pathol. 2011 Nov 22. [Epub ahead of print]

Fromme H, Schlummer M, Möller A, Gruber L, Wolz G, Ungewiss J, Böhmer S, Dekant W, Mayer R, Liebl B, Twardella D.
Exposure of an adult population to perfluorinated substances using duplicate diet portions and biomonitoring data.
Environ Sci Technol. 2007 Nov 15;41(22):7928-33.

Naile JE, Wiseman S, Bachtold K, Jones PD, Giesy JP.
Transcriptional effects of perfluorinated compounds in rat hepatoma cells.
Chemosphere. 2012 Jan;86(3):270-7.

NJ Department of Environmental Protection
Determination of Perfluorooctanoic Acid (PFOA) in Aqueous Samples
January, 2007
http://www.nj.gov/dep/watersupply/pfoa.htm

J Ostertag SK, Chan HM, Moisey J, Dabeka R, Tittlemier SA.
Historic dietary exposure to perfluorooctane sulfonate, perfluorinated carboxylates, and fluorotelomer unsaturated carboxylates from the consumption of store-bought and restaurant foods for the Canadian population.
Agric Food Chem. 2009 Sep 23;57(18):8534-44.

Reddy DR.
Neurology of endemic skeletal fluorosis.
Neurol India. 2009 Jan-Feb;57(1):7-12.

U.S. EPA , March 2009
PERFLUOROCARBOXYLIC ACID CONTENT IN 116 ARTICLES OF COMMERCE
www.oecd.org/dataoecd/47/50/48125746.pdf

Vestergaard S, Nielsen F, Andersson AM, Hjøllund NH, Grandjean P, Andersen HR, Jensen TK.
Association between perfluorinated compounds and time to pregnancy in a prospective cohort of Danish couples attempting to conceive.
Hum Reprod. 2012 Jan 13. [Epub ahead of print]

 Yamashita N, Kannan K, Taniyasu S, Horii Y, Petrick G, Gamo T.
A global survey of perfluorinated acids in oceans.
Mar Pollut Bull. 2005;51(8-12):658-68.

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

Lead And Violent Behavior

police-lineWhat’s This?

Childhood exposure to lead dust has been associated with enduring physical and behavioral effects.  Recent exploration into this public health menace has revealed that leaded gasoline, used to reduce engine knocking and to modify octane levels from the 1920’s to the 1970’s, is no less involved in the damage than the lead from paint and water supply lines (either from solder or from lead pipes).  The city air that was contaminated by vehicle exhaust decades ago has been linked to increased violent crime.  You might wonder how lead would stay in the air for decades.  It usually doesn’t, but lead particles land on the lawn, the sidewalk, the playground, and waft into your front door, alighting on the carpet and furniture.

Recent research by Tulane toxicologist Howard W. Mielke and demographer Sammy Zahran, from Colorado State University’s Center for Disaster and Risk Analysis, compared the amount of lead released in six American cities:  Atlanta, Chicago, Indianapolis, Minneapolis, New Orleans, and San Diego, covering the span from 1950 to 1985.  The changes in lead values during those years were matched by parallel ups and downs of aggravated assaults, as garnered from FBI records.  The analysis of data revealed that for each one percent increase in airborne lead dust exposure there was a related increase in aggravated assault by a half percent (Mielke and Zahran, 2012).

Lead has been used for thousands of years, poisoning people along the way.  The complete picture of lead’s toxicity was barely realized until the second half of the 20th century, when it was finally admitted that there is no safe threshold for lead exposure—there is no known amount of lead too small to do damage.

Developing fetuses are susceptible to the lead contamination of their mothers, and are likely to be premature or of low birth weight, especially for first delivery (Torres-Sanchez, 1999) (Cleveland, 2008).  Because their bodies are smaller and in a constant state of growth and development, children are more at risk for lead poisoning.   They absorb it faster, suffering more physical harm than an adult, and because they spend time on the floor learning to crawl and walk, their exposure is pronounced.  It’s common to see slow development of expected childhood milestones, such as talking and combining words, in cases such as this, which often eventuate to loss of appetite, abdominal distress and vomiting, weight loss, constipation, anemia, kidney failure, irritability, lethargy, failure to thrive, learning disabilities and behavioral problems (Landrigan, 2002).  Early lead exposure is decidedly prophetic of later neurological abnormalities (Nie, 2011), reduced IQ among them.  Blood lead concentrations that peak at age two are thought to lower IQ scores at ages 4 to 6, when IQ becomes sufficiently stable to measure (Chen, 2005).

How Did It Get There?

By this time you might think this is more an urban concern than a suburban or rural one.  Depending on the age of the domicile, you’re partly right.  Regardless of location, many, if not most, homes built prior to 1978 were slathered with lead paint inside and out.  Because lead tastes sweet, flakes of it found their way into the mouths of toddlers, not only from walls and trim, but also from furniture and toys.  The rail of a crib often served as a teething ring.  Urban environs are more likely to house factories and industries that either produce lead-related goods, including batteries, wire and pipes, some medical equipment, ceramic glazes, ammunition, and circuit boards, or that recycle such commodities.  That would increase the odds of lead exposure by a substantial margin.  And the plumbing use of lead in solder and pipe joining was ubiquitous until the advent of plastics.  On the rural side of this coin sit lead-tainted pesticides and exhaust particles from agricultural equipment and contaminated ground water from airborne lead sources miles away.  Not many people eat game harvested with lead ammunition, so that source is not worth the mention.  Ingesting a bullet or a piece of lead shot is a remote probability.

Attitude Adjustment

Lead exposure is not limited to the United States, but is problematic wherever there is cultural and industrial development.  The birth-to-twenty cohort recently studied in South Africa, comprising more than a thousand adolescents, demonstrated a relationship of lead exposure to rule breaking and aggressive behavior (Naicker, 2012).  To explain this behavioral anomaly, scientists looked for a neuroanatomical commonality, discovering decreases in brain volume associated with childhood lead levels.  In this inquiry they found that total brain gray matter is inversely associated with blood lead concentration, particularly in the area of the brain responsible for relaying nerve signals between the right and left hemispheres, a spot that controls rational cognitive functions as well as autonomic functions such as the regulation of blood pressure, digestion and respiration (Cecil, 2008).  Gray matter volume loss was more obvious in males than in females.  The result is that lead affects the prefrontal cortex so dramatically that executive function and decision-making suffer, leading to persistent antisocial behavior (Tiihonen, 2008).

Society has associated underprivileged life with increased odds of criminal activity, but was heretofore unable to put a finger on causality.  Acceptable lead levels for children have been 10 micrograms per deciliter.  This was to have been lowered to 5 mcg/dL by 2012.  Adult levels have been established at 25 mcg/dL.  In children, an increase from 10 to 20 mcg is associated with almost a three point drop in IQ (Schwartz, 1994), affecting levels of GABA, which slows down the activity of nerve cells in the brain, and of NMDA, which is an amino acid derivative labeled as an excitotoxin that wires up neuronal circuits (Watkins, 2006).  Lead exposure crosses socio-economic lines and thus becomes an equal opportunity toxicant that is related even to ADD/ADHD disorders (Nigg, 2010).  A staggering declaration made by the National Center for Healthy Housing, after analyzing reports from The USA, Britain, Canada, Australia, France, Italy, West Germany, and New Zealand, suggests that murder could be associated with more severe cases of childhood lead poisoning, (Nevin, 2007).  The urban underprivileged may have been exposed to more lead residue (Cleveland, 2008) from gasoline, paint, and food can solder than their rural counterparts, so much so that traces of lead have been found in the enamel of their teeth (Cleymaet, 1991) (Uryu, 2003), levels of which tripled from 1930’s to the mid 60’s.

As of 2002, more than a million housing units offered shelter to low-income families (earning < $30 K yearly) with children under age six.  Of those, 17% of government-subsidized units had hazards.  Thirty-five percent of all low-income families had hazards.  For families with modestly higher earnings, it’s 19%.  Understandably, the greatest risks appear in dwellings that are antiquated, often also having high lead concentrations in the soil.  Housing in the Northeast had twice the danger of the rest of the country.

What To Do?

Removal of heavy metals, notably lead, mercury and cadmium, is important to body function at the cellular level.  The traditional medical approach to chelation, the process whereby the chelator binds to the metal and carries it away from the body, might use succimer, which is an analogue of dimercaprol, a toxic substance with a small therapeutic range and many adverse side effects.  In a succimer trial sponsored by the National Institute of Environmental Health Sciences that enrolled almost eight hundred children with blood lead levels from 20-40 mcg/dL, the lead values of the study group decreased with succimer, but also did their IQ’s by a single point, which seems insignificant.  But what is significant is that their behavior worsened, as reported on a parent assessment scale, leading investigators to infer that this treatment may not be ideal for children with lead levels in the particular range, citing accompanying decline in tests of cognition and psychological function (Rogan, 2001).  Later study at the University of Cincinnati that followed a like protocol also noted a decrease in blood lead levels, but, too, a lack of benefit for cognitive, learning/memory, attention, and neuromotor skills, drawing researchers to the same conclusion (Dietrich, 2004).

As a chelator, chlorella vulgaris has been found to reduce damage by lead exposure and to maintain the integrity of bone marrow (Queiroz, 2003), while reducing lead levels in blood and tissues and restoring liver function (Queiroz, 2008).  Later study found chlorella to restore the activity of natural killer cells and to reverse the zinc loss caused by lead exposure (Queiroz, 2011).  Ascorbic acid, vitamin C, has been known to handle lead problems since the late 1930’s, when scientists found lead-exposed factory workers to respond to daily doses of vitamin C and to excrete lead in their urine (Holmes, 1939).  Sixty years later, investigators saw lead levels decline as ascorbic acid levels increased in the general population having baseline lead values of 15 mcg/dL or higher (Simon, 1999).  Though both these modalities were shown to reduce lead levels, no commentary about cognitive or behavioral character is retrieved from these studies.  Sadly, lead stored in bone can leach into the blood even after chelation is deemed successful.

Where lead levels are high, trace mineral levels may be low, and probably are.  The earnest and judicious use of minerals that belong in the body may be able to push out those that do not belong and, by virtue of their own properties, rescue the mental and physical domains transgressed upon by lead and other heavy metals.

References

Bakhireva LN, Rowland AS, Young BN, Cano S, Phelan ST, Artyushkova K, Rayburn WF, Lewis J.
Sources of Potential Lead Exposure Among Pregnant Women in New Mexico.
Matern Child Health J. 2012 Feb 24. [Epub ahead of print]

Bellinger DC.
Lead.
Pediatrics. 2004 Apr;113(4 Suppl):1016-22

Bouchard MF, Bellinger DC, Weuve J, Matthews-Bellinger J, Gilman SE, Wright RO, Schwartz J, Weisskopf MG.
Blood lead levels and major depressive disorder, panic disorder, and generalized anxiety disorder in US young adults.
Arch Gen Psychiatry. 2009 Dec;66(12):1313-9.

Carpenter DO, Nevin R.
Environmental causes of violence.
Physiol Behav. 2010 Feb 9;99(2):260-8. Epub 2009 Sep 14.

Cecil KM, Brubaker CJ, Adler CM, Dietrich KN, Altaye M, Egelhoff JC, Wessel S, Elangovan I, Hornung R, Jarvis K, Lanphear BP.
Decreased brain volume in adults with childhood lead exposure.
PLoS Med. 2008 May 27;5(5):e112.

Chen A, Dietrich KN, Ware JH, Radcliffe J, Rogan WJ.
IQ and blood lead from 2 to 7 years of age: are the effects in older children the residual of high blood lead concentrations in 2-year-olds?
Environ Health Perspect. 2005 May;113(5):597-601.

Aimin Chen, MD, PhD
Improving Behavior of Lead-Exposed Children: Micronutrient Supplementation, Chelation, or Prevention
The Journal of Pediatrics.  Volume 147, Issue 5 , Pages 570-571, November 2005

Chen A, Cai B, Dietrich KN, Radcliffe J, Rogan WJ.
Lead exposure, IQ, and behavior in urban 5- to 7-year-olds: does lead affect behavior only by lowering IQ?
Pediatrics. 2007 Mar;119(3):e650-8

Cleveland LM, Minter ML, Cobb KA, Scott AA, German VF.
Lead hazards for pregnant women and children: part 1: immigrants and the poor shoulder most of the burden of lead exposure in this country. Part 1 of a two-part article details how exposure happens, whom it affects, and the harm it can do.
Am J Nurs. 2008 Oct;108(10):40-9; quiz 50.

Cleymaet R, Collys K, Retief DH, Michotte Y, Slop D, Taghon E, Maex W, Coomans D.
Relation between lead in surface tooth enamel, blood, and saliva from children residing in the vicinity of a non-ferrous metal plant in Belgium.
Br J Ind Med. 1991 Oct;48(10):702-9.

Dietrich KN, Ware JH, Salganik M, Radcliffe J, Rogan WJ, Rhoads GG, Fay ME, Davoli CT, Denckla MB, Bornschein RL, Schwarz D, Dockery DW, Adubato S, Jones RL; Treatment of Lead-Exposed Children Clinical Trial Group.
Effect of chelation therapy on the neuropsychological and behavioral development of lead-exposed children after school entry.
Pediatrics. 2004 Jul;114(1):19-26.

Holmes HN, Amberg EJ, Campbell K.
VITAMIN C TREATMENT IN LEAD POISONING.
Science. 1939 Apr 7;89(2310):322-3.
http://www.seanet.com/~alexs/ascorbate/193x/holmes-hn-etal_j_lab_clin_med-1939-v23-n11-p1119.html

Houston DK, Johnson MA.
Does vitamin C intake protect against lead toxicity?
Nutr Rev. 2000 Mar;58(3 Pt 1):73-5.

Howard W. Mielke, Sammy Zahran
The urban rise and fall of air lead (Pb) and the latent surge and retreat of societal violence
Environment International. Volume 43, August 2012, Pages 48–55

Jacobs DE, Clickner RP, Zhou JY, Viet SM, Marker DA, Rogers JW, Zeldin DC, Broene P, Friedman W.
The prevalence of lead-based paint hazards in U.S. housing.
Environ Health Perspect. 2002 Oct;110(10):A599-606.

Koike S.
[Low-level lead exposure and children’s intelligence from recent epidemiological studies in the U.S.A. and other countries to progress in reducing lead exposure and screening in the U.S.A].
Nihon Eiseigaku Zasshi. 1997 Oct;52(3):552-61.

Kordas K, Stoltzfus RJ, López P, Rico JA, Rosado JL.
Iron and zinc supplementation does not improve parent or teacher ratings of behavior in first grade Mexican children exposed to lead.
J Pediatr. 2005 Nov;147(5):632-9.

Landrigan PJ, Schechter CB, Lipton JM, Fahs MC, Schwartz J.
Environmental pollutants and disease in American children: estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities.
Environ Health Perspect. 2002 Jul;110(7):721-8.

Naicker N, Richter L, Mathee A, Becker P, Norris SA.
Environmental lead exposure and socio-behavioural adjustment in the early teens: the birth to twenty cohort.
Sci Total Environ. 2012 Jan 1;414:120-5. Epub 2011 Dec 3.

Nevin R.
How lead exposure relates to temporal changes in IQ, violent crime, and unwed pregnancy.
Environ Res. 2000 May;83(1):1-22.

Nevin R.
Understanding international crime trends: the legacy of preschool lead exposure.
Environ Res. 2007 Jul;104(3):315-36. Epub 2007 Apr 23.

Nie LH, Wright RO, Bellinger DC, Hussain J, Amarasiriwardena C, Chettle DR, Pejović-Milić A, Woolf A, Shannon M.
Blood lead levels and cumulative blood lead index (CBLI) as predictors of late neurodevelopment in lead poisoned children.
Biomarkers. 2011 Sep;16(6):517-24. doi: 10.3109/1354750X.2011.604133. Epub 2011 Aug 9.

Nigg JT, Nikolas M, Mark Knottnerus G, Cavanagh K, Friderici K.
Confirmation and extension of association of blood lead with attention-deficit/hyperactivity disorder (ADHD) and ADHD symptom domains at population-typical exposure levels.
J Child Psychol Psychiatry. 2010 Jan;51(1):58-65. Epub 2009 Nov 23.

Queiroz ML, Rodrigues AP, Bincoletto C, Figueirêdo CA, Malacrida S.
Protective effects of Chlorella vulgaris in lead-exposed mice infected with Listeria monocytogenes.
Int Immunopharmacol. 2003 Jun;3(6):889-900.

Queiroz ML, Torello CO, Perhs SM, Rocha MC, Bechara EJ, Morgano MA, Valadares MC, Rodrigues AP, Ramos AL, Soares CO.
Chlorella vulgaris up-modulation of myelossupression induced by lead: the role of stromal cells.
Food Chem Toxicol. 2008 Sep;46(9):3147-54. Epub 2008 Jul 19.

Queiroz ML, da Rocha MC, Torello CO, de Souza Queiroz J, Bincoletto C, Morgano MA, Romano MR, Paredes-Gamero EJ, Barbosa CM, Calgarotto AK.
Chlorella vulgaris restores bone marrow cellularity and cytokine production in lead-exposed mice.
Food Chem Toxicol. 2011 Nov;49(11):2934-41. Epub 2011 Jul 26.

Rogan WJ, Dietrich KN, Ware JH, Dockery DW, Salganik M, Radcliffe J, Jones RL, Ragan NB, Chisolm JJ Jr, Rhoads GG; Treatment of Lead-Exposed Children Trial Group.
The effect of chelation therapy with succimer on neuropsychological development in children exposed to lead.
N Engl J Med. 2001 May 10;344(19):1421-6.

Schwartz J.
Low-level lead exposure and children’s IQ: a meta-analysis and search for a threshold.
Environ Res. 1994 Apr;65(1):42-55.

Simon JA, Hudes ES.
Relationship of ascorbic acid to blood lead levels.
JAMA. 1999 Jun 23-30;281(24):2289-93.

Tiihonen J, Rossi R, Laakso MP, Hodgins S, Testa C, Perez J, Repo-Tiihonen E, Vaurio O, Soininen H, Aronen HJ, Könönen M, Thompson PM, Frisoni GB.
Brain anatomy of persistent violent offenders: more rather than less.
Psychiatry Res. 2008 Aug 30;163(3):201-12. Epub 2008 Jul 26.

Luisa E. Torres-Sánchez, Gertrud Berkowitz, Lizbeth López-Carrillo, Laura Torres-Arreola, et al
Intrauterine LeadExposure and Preterm Birth
Environmental Research. Volume 81, Issue 4, November 1999, Pages 297–301

Uryu T, Yoshinaga J, Yanagisawa Y, Endo M, Takahashi J.
Analysis of lead in tooth enamel by laser ablation-inductively coupled plasma-mass spectrometry
Anal Sci. 2003 Oct;19(10):1413-6.

Watkins JC, Jane DE.
The glutamate story.
Br J Pharmacol. 2006 Jan;147 Suppl 1:S100-8.

Wright JP, Dietrich KN, Ris MD, Hornung RW, Wessel SD, Lanphear BP, Ho M, Rae MN.
Association of prenatal and childhood blood lead concentrations with criminal arrests in early adulthood.
PLoS Med. 2008 May 27;5(5):e101.

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

Growing Old With Zinc

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

What Is This Stuff?

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

Do I Have Enough?

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

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

What About Aging?

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

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

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

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

References

Bin QH, Garfinkel D.
The cadmium toxicity hypothesis of aging: a possible explanation for the zinc deficiency hypothesis of aging.
Med Hypotheses. 1994 Jun;42(6):380-4.

Daaboul D, Rosenkranz E, Uciechowski P, Rink L.
Repletion of zinc in zinc-deficient cells strongly up-regulates IL-1β-induced IL-2 production in T-cells.
Metallomics. 2012 Oct 1;4(10):1088-97. Epub 2012 Sep 14.

Fabris N, Mocchegiani E.
Zinc, human diseases and aging.
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Franceschi C, Capri M, Monti D, Giunta S, Olivieri F, Sevini F, Panourgia MP, Invidia L, Celani L, Scurti M, Cevenini E, Castellani GC, Salvioli S.
Inflammaging and anti-inflammaging: a systemic perspective on aging and longevity emerged from studies in humans.
Mech Ageing Dev. 2007 Jan;128(1):92-105. Epub 2006 Nov 20.

Garfinkel D.
Is aging inevitable? The intracellular zinc deficiency hypothesis of aging.
Med Hypotheses. 1986 Feb;19(2):117-37.

GPN–General Practice Notebook–a UK Medical reference
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Emily Ho
Zinc deficiency, DNA damage and cancer risk
The Journal of Nutritional Biochemistry. Vol 15, Iss 10 , PP 572-578, Oct 2004

Andrea Hönscheid, Svenja Dubben, Lothar Rink, Hajo Haas
Zinc differentially regulates mitogen-activated protein kinases in human T cells
The Journal of Nutritional Biochemistry. Vol 23, Iss 1 , Pp 18-26, Jan 2012

Hunt JR.
Bioavailability of iron, zinc, and other trace minerals from vegetarian diets.
Am J Clin Nutr. 2003 Sep;78(3 Suppl):633S-639S.
Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2001.
http://ods.od.nih.gov/factsheets/Zinc-HealthProfessional/#en2

Mahoney MG, Brennan D, Starcher B, Faryniarz J, Ramirez J, Parr L, Uitto J.
Extracellular matrix in cutaneous ageing: the effects of 0.1% copper-zinc malonate-containing cream on elastin biosynthesis.
Exp Dermatol. 2009 Mar;18(3):205-11.

Maret W, Sandstead HH.
Zinc requirements and the risks and benefits of zinc supplementation.
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Messner B, Knoflach M, Seubert A, Ritsch A, Pfaller K, Henderson B, Shen YH, Zeller I, Willeit J, Laufer G, Wick G, Kiechl S, Bernhard D.
Cadmium is a novel and independent risk factor for early atherosclerosis mechanisms and in vivo relevance.
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Mocchegiani E, Malavolta M, Marcellini F, Pawelec G.
Zinc, oxidative stress, genetic background and immunosenescence: implications for healthy ageing.
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Mocchegiani E.
Zinc and ageing: third Zincage conference.
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O’Dell BL.
Role of zinc in plasma membrane function.
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Prasad AS, Fitzgerald JT, Hess JW, Kaplan J, Pelen F, Dardenne M.
Zinc deficiency in elderly patients.
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Prasad AS.
Zinc deficiency.
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Sandström B.
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Truong-Tran AQ, Ho LH, Chai F, Zalewski PD.
Cellular zinc fluxes and the regulation of apoptosis/gene-directed cell death.
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Vasto S, Mocchegiani E, Malavolta M, Cuppari I, Listì F, Nuzzo D, Ditta V, Candore G, Caruso C.
Zinc and inflammatory/immune response in aging.
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Wise A.
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Carmen P. Wong, Kathy R. Magnusson, Emily Ho
Increased inflammatory response in aged mice is associated with age-related zinc deficiency and zinc transporter dysregulation
The J of Nutr Biochem.  Article in Press–published online 17 September 2012.

World health Organization. Published Online: 17 January 2008
Comparative Quantification of Health Risks
Childhood and maternal undernutrition
Chapter 5: Zinc deficiency

Laura E. Caulfield and Robert E. Black
http://www.who.int/publications/cra/chapters/volume1/part2/en/index.html

Zatta P, Lucchini R, van Rensburg SJ, Taylor A.
The role of metals in neurodegenerative processes: aluminum, manganese, and zinc.
Brain Res Bull. 2003 Nov 15;62(1):15-28.

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

Keeping Your Electrolytes in Balance

Gym girlWithout electrolytes, physiological stability—called homeostasis—goes haywire and nerve and muscle function are disturbed, body fluid balance is upset, and other critical body workings are interrupted. These tiny particles of metals carry electrical charges and are present in all body fluids, including urine, blood and plasma. Without the proper timing and intensity of electrical impulses, nerve, heart and muscle function suffer, and might even stop in severe instances. If electrolytes are lost, as would happen in extreme exercise or sickness, replenishment is necessary, but in appropriate amounts. Imbalances can have terrible effects, and they can be caused by a deficiency or an excess. In the chemistry jargon, the prefix hypo- means “too little,” and the prefix hyper- means “too much.”

There is a laundry list of conditions that can lead to electrolyte imbalances, including dehydration and over-hydration, diabetic ketoacidosis, cancer, and head injuries like concussions. Kidney disease, though, is at the top of the list because the kidney’s job is to control fluid, electrolyte, and acid-base balance (Claure, 2012). The surest way to deal with electrolytes is through diet or supplementation, using an electrolyte replacement if necessary, as you might when exercising in the hot weather or when participating in endurance events.

We’ll start with sodium, since it’s the most abundant cation (positive ion) in the extracellular fluid (outside the cell). We need sodium to maintain normal blood pressure in addition to sending electrical messages to initiate a muscle contraction. Water will follow salt into the body. Too much salt will increase blood osmolality, meaning, in a way, that blood has more stuff floating in it because there is too little liquid. If that happens you get thirsty, and anti-diuretic hormone tells the kidneys not to let go of water. Opposite that, low osmolality means that the blood is more watery. If too much water is lost from sweat, respiration, urination, or the weather, or if too much salt is taken in, you have hypernatremia and may suffer symptoms such as disorientation, nausea without vomiting, rapid heartbeat, sunken eyes, or trembling. Your cells are drying out and the kidneys are conserving water, so you don’t urinate.

Losing sodium—hyponatremia—can happen when you drink volumes of plain water during a bout of intense exercise, especially in hot weather. Add lethargy and confusion to the hypernatremia symptoms. If sodium falls too low, permanent neurological damage can occur.  People who have been forced to drink water to take a work-related urine drug test have fainted from hyponatremia, and have experienced hypertension and difficulty breathing.

Potassium is the primary cation inside the cell, where its major physiological role is the regulation of muscle and nerve excitability as the director of relaxation immediately following a muscular contraction initiated by sodium. Potassium imbalance is particularly monitored because of its relationship to coronary health and the heart’s ability to change electrical potential. Imbalance may cause arrhythmia. Excess (hyperkalemia) will cause cardiac arrest; deficit (hypokalemia) will irritate cardiac muscle and increase the chance of premature atrial or ventricular contractions, possibly leading to death. Potassium balance leaves little room for error (van der Meer, 1986) (Lindinger, 1995).

Magnesium, like potassium, is also found inside the cell, where it affects muscle function, energy production and carbohydrate and protein metabolism. Kidney disease is a major cause of hypermagnesemia, although taking too many magnesium-bearing antacids can contribute. Too much magnesium will cause lethargy, which is understandable because magnesium is a relaxant (Gold, 1990) (Spivey, 1990). Too little magnesium is common in the critically ill (Dacey, 2001), among whom mortality is high. Similar to hypokalemia, hypomagnesemia may induce cardiac arrhythmia, although milder signs occur before that happens. Muscle weakness, tremors, anorexia and dizziness are the more common. Can’t sleep?  Got leg cramps?  Magnesium may help (Young, 2002, 2009) (Geurrera, 2009) (Allen, 2012).

Although calcium is electrolytic, it seldom appears in electrolyte replacement drinks because most Americans, especially women, supplement at the behest of their doctors. Calcium works with phosphorus in an inverse relationship. When the value of one is high, the other is generally low. Calcium is involved in contraction of cardiac and smooth muscle, but also enhances the clotting mechanism, maintains cell membrane permeability and helps to transmit nerve impulses. You already know about the bones and teeth. Phosphorus also plays a role in bone formation, but is also needed for energy production and for macronutrient metabolism. By buffering hydrogen ions, it helps to maintain acid-base balance, as well. Like calcium, phosphorus needs are easily met without an electrolyte beverage. Deficiency is rare and occurs secondary to other conditions rather than as a result of low dietary intake. High doses of antacids may deplete phosphorus.

If your exercise regimen lasts more than an hour, especially in warm weather, you’re a candidate for electrolyte replacement. Hard games like tennis, cycling and marathon running, and assiduous resistance training call for such a beverage. During these times, you might need to drink a cup of electrolyte replacement every fifteen or twenty minutes to keep a steady pace and to avoid cramps. Thirst is not always the best barometer for gauging electrolyte needs. A beverage with sugar will compromise the bioavailability of minerals. Since sodium is the first electrolyte lost to heavy sweating, it’s a major consideration in repletion, so don’t be alarmed if you see high levels of sodium in your drink. If you’re interested in balancing electrolytes for yourself and the family, which is especially important when the kids get sick, take a look here:
http://crampnomore.com/sportshealth/electrolytes-101.html. There’s an informative bulletin explaining the how and why of electrolytes, the balance of which is no laughing matter.

References

Allen RE, Kirby KA.
Nocturnal leg cramps.
Am Fam Physician. 2012 Aug 15;86(4):350-5.

Chiasson JL, Aris-Jilwan N, Bélanger R, Bertrand S, Beauregard H, Ekoé JM, Fournier H, Havrankova J.
Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state.
CMAJ. 2003 Apr 1;168(7):859-66.

Claure R, Bouchard J.
Acid-base and electrolyte abnormalities during renal support for acute kidney injury: recognition and management.
Blood Purif. 2012;34(2):186-9

Dacey MJ.
Hypomagnesemic disorders.
Crit Care Clin. 2001 Jan;17(1):155-73, viii.

Gold ME, Buga GM, Wood KS, Byrns RE, Chaudhuri G, Ignarro LJ.
Antagonistic modulatory roles of magnesium and calcium on release of endothelium-derived relaxing factor and smooth muscle tone.
Circ Res. 1990 Feb;66(2):355-66.

Guerrera MP, Volpe SL, Mao JJ.
Therapeutic uses of magnesium.
Am Fam Physician. 2009 Jul 15;80(2):157-62.

Heinrich S, Wagner A, Gross P.
Hyponatremia.
Med Klin Intensivmed Notfmed. 2012 Sep 6.

Lindinger MI.
Potassium regulation during exercise and recovery in humans: implications for skeletal and cardiac muscle.
J Mol Cell Cardiol. 1995 Apr;27(4):1011-22.

Nakao I, Ito T, Kasai N.
Electrolyte metabolism and emergency.
Gan To Kagaku Ryoho. 1983 Feb;10(2 Pt):198-203.

Sawka MN, Burke LM, Eichner ER, Maughan RJ, Montain SJ, Stachenfeld NS.
American College of Sports Medicine position stand. Exercise and fluid replacement.
Med Sci Sports Exerc. 2007 Feb;39(2):377-90.

Shibata H.
Cancer and electrolytes imbalance.
Gan To Kagaku Ryoho. 2010 Jun;37(6):1006-10.

Spivey WH, Skobeloff EM, Levin RM.
Effect of magnesium chloride on rabbit bronchial smooth muscle.
Ann Emerg Med. 1990 Oct;19(10):1107-12.

van der Meer C, Valkenburg PW, Snijders PM.
Studies on hyperkalemia as a cause of death in intestinal ischemia shock in rats.
Circ Shock. 1986;19(3):329-45.

Young GL, Jewell D.
Interventions for leg cramps in pregnancy.
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Young G.
Leg cramps.
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Zümrütdal A.
Basic principles in liquid electrolyte treatment
Anadolu Kardiyol Derg. 2012 Dec 17. doi: 10.5152/akd.2013.043.

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

Mineral Balance: Copper-Zinc

copper-zinc-scaleThe last mineral topic we covered dealt with sodium and potassium. Important stuff, this mineral balance. Recall that the amounts of minerals needed by the body are not an indication of their importance, and that we probably can’t get all that we need from our foods because of untrustworthy practices from seed to table. Remember, too, that kids, especially, need to eat the plants to get the minerals. The recommended number of servings of fruits and vegetables is now nine to thirteen, up from five to nine. Either way, how many people do you know who eat that much?

Copper and zinc are antagonists, and the balance between them is an example of biological dualism. This does that, and that does this, and they often fight with each other. Kind of a simple explanation, but maybe you get it. Yes, it’s possible for there to be zinc toxicity and copper toxicity. In the past, it’s been copper toxicity and zinc deficiency. Today it might be just the reverse, considering that people take supplements without the faithful reading of labels. Both minerals play important roles in the body.

Copper is necessary for blood vessel formation, a strong heart and for stabilizing collagen. You know what collagen is…the glue that holds us together. We need copper for brain development and for communication between nerve cells in the brain. Copper is essential to a number of enzymes involved in energy production by the mitochondria.  It helps to make superoxide dismutase to get rid of reactive oxygen species (free radicals). Because it’s found in a number of foods, copper deficiency is not common. Meats, shellfish, nuts, and seeds are premier sources, followed by mushrooms, lentils, shredded wheat and chocolate. Daily intake by adults normally is a little more than a milligram, which is only a bit higher than the RDA of 0.9 mg. The tolerable upper limit for adults is 10 mg, while most supplements contain 2 mg. Infants fed a cow’s milk diet are the ones most likely deficient because milk has little copper, but people with malabsorption disorders are close behind. Anemia and low white blood cell count are signs of deficit. Take care to note that very high doses of vitamin C might interfere with copper-related enzyme efficiency (Finley, 1983). But that’s not written in stone. Zinc overdose, however, might be a legitimate cause of copper deprivation.

Now, here’s the rub with zinc. Concerns arise when you take several supplements that each contain zinc. The tolerable upper limit, the dose above which there may be adverse reactions, is 40 milligrams for an adult. Let’s see, Hmm, prostate formula contains 15 mg; cold/flu formula contains 15 mg; daily multi-vitamin contains 15 mg; nasal spray contains 5 mg; other zinc complexes aimed at myriad conditions contain more…  Can you see where we’re going?  Copper deficiency now becomes a possibility. The need for zinc hovers around 11 mg for a guy, about 8 mg for a non-pregnant female.

Zinc is needed for steroid hormone synthesis, being a well-known catalyst for testosterone manufacture as well as luteinizing hormone, the one that stimulates ovulation. Of all the body parts, the prostate contains the highest concentrations. More than a hundred different enzymes rely on zinc for their ability to catalyze chemical reactions in the body. It plays a structural role in the superoxide dismutase mentioned in the earlier paragraph and in the integrity of the cell membrane. In fact, the loss of zinc from biological membranes increases their susceptibility to oxidative damage (O’Dell, 2000). Then, we have these nifty little things called zinc fingers, which are transcription factors that bind to DNA and influence specific genes, which are stabilized by the presence of zinc. Taking too much zinc over a period of a few weeks will upset copper bioavailability, possibly resulting in hematology issues down the line. Meanwhile, the bioavailability of folate/folic acid/folinic acid is enhanced by zinc.

Zinc deficiency usually follows genetic disorders and is identified as such. Immune deficiencies, impaired healing, diminished sense of taste (and perhaps smell), night blindness, opacity of the cornea, behavioral disturbances, and delayed maturation are common signs of low zinc values. Deficiency in children is dramatic in that neuropsychological development is impeded and susceptibility to life-threatening infections is increased (Hambidge, 2000).

Do those zinc lozenges advertisements have any immune system merit? We know that zinc deficiency causes immune dysfunction, but there is mixed commentary on the efficacy of zinc mega-doses for colds and other viral infections in people with ample zinc stores (Baum, 2000) (Salqueiro, 2000) (Fraker, 2000). The immune system relies on more than just zinc for its competence. Essential amino and fatty acids, selenium and iron, folic acid and vitamins B6 and B12, and vitamins E, A and C have a say in the immune system’s function. Consider, too, that a deficiency in one of these is likely to follow a deficiency in one or more of the others. Intakes of nutrients in excess of the recommendations do not necessarily translate to a boost in all immune activity unless a deficiency has been identified. Even then, despite the disparity in research conclusions, mega-doses of one mineral can knock another one out of the ring. On the other hand, using zinc lozenges as soon as cold symptoms appear seems to reduce severity and duration, depending on the formulation (Singh, 2011).

Balancing copper and zinc, though vitally important, may not be as easy as expected. Exposure to other metals, especially to lead that may originate from ancient water pipes, contaminated ground water, the shooting sports, some toys and paints,and fishing sinkers, can push zinc out. Iron, particularly from a supplement, may inhibit intestinal absorption of both zinc and copper through competition for transport molecules located in the gut. Wilson’s disease, the inability to metabolize copper out of the body, requires a dietary change that precludes mushrooms, nuts, chocolate, shellfish and dried fruits, and includes zinc therapy (Chasapis, 2012). The testing for zinc and copper values is not completely established because reference ranges are based on statistical averages, not on optimum functional levels. As with other nutrients, availability from foods is too often questionable, but supplementation should to be considered under the guidance of a knowledgeablenutrition professional, such as a credentialed nutritionist or dietitian. A caveat: Don’t even think about drinking water from a galvanized container. There are reports of a family that had collected its drinking water from a brand new refuse container and suffered from zinc overdose. Some denture adhesives contain zinc. Be careful. Read labels.

References

Baum MK, Shor-Posner G, Campa A.
Zinc status in human immunodeficiency virus infection.
J Nutr. 2000 May;130(5S Suppl):1421S-3S.

Brewer GJ, Yuzbasiyan-Gurkan V, Lee DY.
Use of zinc-copper metabolic interactions in the treatment of Wilson’s disease.
J Am Coll Nutr. 1990 Oct;9(5):487-91.

Calder PC, Kew S.
The immune system: a target for functional foods?
Br J Nutr. 2002 Nov;88 Suppl 2:S165-77.

Chan S, Gerson B, Subramaniam S.
The role of copper, molybdenum, selenium, and zinc in nutrition and health.
Clin Lab Med. 1998 Dec;18(4):673-85.

Chasapis CT, Loutsidou AC, Spiliopoulou CA, Stefanidou ME.
Zinc and human health: an update.
Arch Toxicol. 2012 Apr;86(4):521-34.

Finley EB, Cerklewski FL.
Influence of ascorbic acid supplementation on copper status in young adult men.
Am J Clin Nutr. 1983 Apr;37(4):553-6.

Fraker PJ, King LE, Laakko T, Vollmer TL.
The dynamic link between the integrity of the immune system and zinc status.
J Nutr. 2000 May;130(5S Suppl):1399S-406S.

Hambidge M.
Human zinc deficiency.
J Nutr. 2000 May;130(5S Suppl):1344S-9S.

Hulisz D.
Efficacy of zinc against common cold viruses: an overview.
J Am Pharm Assoc (2003). 2004 Sep-Oct;44(5):594-603.

Jackson JL, Lesho E, Peterson C.
Zinc and the common cold: a meta-analysis revisited.
J Nutr. 2000 May;130(5S Suppl):1512S-5S.

McElroy BH, Miller SP.
Effectiveness of zinc gluconate glycine lozenges (Cold-Eeze) against the common cold in school-aged subjects: a retrospective chart review.
Am J Ther. 2002 Nov-Dec;9(6):472-5.

Milne DB, Davis CD, Nielsen F
Low dietary zinc alters indices of copper function and status in postmenopausal women.
Nutrition. 2001 Sep;17(9):701-8.

O’Dell BL.
Role of zinc in plasma membrane function.
J Nutr. 2000 May;130(5S Suppl):1432S-6S.

Perrone L, Di Palma L, Di Toro R, Gialanella G, Moro R.
Interaction of trace elements in a longitudinal study of human milk from full-term and preterm mothers.
Biol Trace Elem Res. 1994 Jun;41(3):321-30.

Salgueiro MJ, Zubillaga M, Lysionek A, Cremaschi G, Goldman CG, Caro R, De Paoli T, Hager A, Weill R, Boccio J.
Zinc status and immune system relationship: a review.
Biol Trace Elem Res. 2000 Sep;76(3):193-205.

Singh M, Das RR.
Zinc for the common cold.
Cochrane Database Syst Rev. 2011 Feb 16;(2):CD001364.

Turnlund J, Costa F, Margen S.
Zinc, copper, and iron balance in elderly men.
Am J Clin Nutr. 1981 Dec;34(12):2641-7.

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

Iodine Deficiency

iodinebookBeyond its role in antisepsis and breast health, iodine is perhaps best known for its regulatory function in the thyroid gland. Educators at the Linus Pauling Institute reiterate the mineral’s essentiality to the thyroid hormones, commonly listed as T3 and T4 on a blood test. T3 is the physiologically active form, while T4 is the more abundant circulating form. In targeted tissues, T4 is converted to T3 by enzymes that depend on selenium for their activity. In this manner, the thyroid comes to control growth and development, metabolism, and reproductive function. Can you see the need for selenium? In the absence of sufficient iodine, the pituitary gland will secrete thyroid-stimulating hormone (TSH) in an attempt to set things straight by increasing iodine trapping mechanisms. If TSH levels are persistently elevated, the thyroid gland may enlarge and form what is known as a goiter.

The World Health Organization (WHO) estimates that about a third of the world’s population is deficient in iodine, a deficit that is the most common cause of preventable brain damage in the world. The Food and Nutrition Board of the Institute of Medicine declares that iodine is responsible for myelination of the developing central nervous system, and that deficiency is associated with mental retardation, and in extreme cases, cretinism. More than thirty percent of children under twelve has insufficient iodine intake. Although iodized salt was intended to prevent iodine deficiency, the modern diet has put it away in favor of salts whose iodine values are inconsistent and perhaps even absent, as might be the case with the kosher salts that took over the culinary arts. The American Journal of Hypertension and its Polish counterpart report that those adults who choose to avoid salt in any form to control their sodium-sensitive high blood pressure may be realizing small benefit in the long run unless they fortify their diets with iodine from other sources.

Just as we are barraged with loud TV commercials for products in which we have little or no interest, we are likewise assaulted with chemicals and synthetic agents about which we know nothing and whose ubiquitous presence is hidden. Manufacturers of consumer goods apparently feel the need to add things to their products for our own good when, in truth, it’s for their bottom line. Among these ruinous substances is bromine, a member of the chemical family called halides, a group that includes fluorine, chlorine, iodine and astatine, the last having no biological value whatsoever to humans.  Bromine hides in a few forms—as methyl bromide and ethylene dibromide, used as fumigants. In the produce business, they relieve fresh fruits and vegetables of their B vitamins. Bromide is found in cleaners, dyes, water sanitation processes, pharmaceuticals, flame retardants in our kids’ PJs, and in our foods as brominated flour, brominated vegetable oil (BVO) and who knows what else.  BVO is used to make citrus-flavored soft drinks cloudy-looking by emulsifying ingredients to keep the flavoring suspended in the liquid.  Bromine, which has zero use by the body, pushes iodine out of the thyroid gland. Because it acts like iodine and chlorine, the body accepts it. Puzzlement is that bromine is listed in the Hazardous Substances Data Bank of the National Library of Medicine, yet is allowed as a food additive in the Federal Code. In one of his blog postings, Dr. David Brownstein, a celebrated holistic physician, explains that it is vital to maintain optimal iodine levels. Our constant exposure to chemicals like bromine requires daily iodine supplementation because bromine will either prevent iodine absorption or push out that which is already there. At 150 micrograms a day, the RDA for iodine is woefully inadequate to address our physiological needs.  Knowing that bromine is present in some psychotropic drugs helps us to understand why some patients never get well. They are iodine depleted.

There is little doubt among researchers that iodine deficiency is epidemic. Dr. Mark Sircus acknowledges the toxicity of another halogen—fluoride.  He points out that all the halogens use the same receptors in the body, and that the toxic ones will displace iodine at the first opportunity, but also that the intake of supplemental iodine can increase the excretion of the other halides, and even of heavy metals. Note that the toothpaste tube admonishes us not to let a child swallow his fluoridated dentifrice. Adults, likewise, are warned not to swallow more than used on the brush.  Hailed as one of the greatest health achievements of the 20th century, fluoridation of water is now limited, being cited as harmful to the liver and kidneys.

If you or a loved one is concerned about thyroid function, know that fluoride is used in Europe to treat hyperthyroidism because it reduces thyroid activity. If you have symptoms of hypothyroid—fatigue, sensitivity to cold, constipation, dry skin, puffiness, muscle weakness, thinning hair, slowed heart rate and mental fog—look at your toothpaste, your municipal or well water supply, black tea, pesticides, Teflon, moisture barriers, some drugs, refrigerants, certain medical scanning procedures, and your dentist.

An oddity of halogens is that their clinical activity is in inverse proportion to their atomic weights. A lighter one will displace a heavier one. The opposite does not hold. Of those in the body, iodine is the heaviest. Regular use of iodine will mitigate the damage from the others. Knowing that liquid iodine preparations work more efficiently than the solid forms can help you to make the right supplement choice.

References

Victoria J. Drake, Ph.D.
Iodine
Linus Pauling Institute Micronutrient Information Center. Mar 2010. Update
http://lpi.oregonstate.edu/infocenter/minerals/iodine/

Dunn JT.
What’s happening to our iodine?
J Clin Endocrinol Metab. 1998;83(10):3398-3400.
Fluoride history
http://www.fluoride-history.de/p-insecticides.htm

Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press, 2002. Available at: www.nap.edu/books/0309072794/html/.
http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~6PSNGt:1

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Dr. Mark Sircus blogs
http://www.greenmedinfo.com/gmi-blogs/[email protected]

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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.

Get Something Free… Radicals The Saga of Vitamins A, C and E

vitamins-foodThe same oxygen you need to stay alive and to burn food for energy makes you oxidize just as fast as a rusty fender on the old jalopy in the back yard…or maybe in the driveway if your surname is Clampett at 90210. If your apples turn brown and your fish or butter becomes rancid, blame it on oxygen. Lungs, eyes, skin, fruits, vegetables, herbs, you name it. If it has cells, it’ll oxidize and those cells will change. But it’s a normal part of living. Fret not. The Creator gave us a way to intercept the free radicals and undo their dastardly deeds. These molecules are “free” because they have parts missing, and they scour the neighborhood looking for replacements, sort of like the original equipment manufacturer you look for when rebuilding your ’57 Chevy. Being on a mission, these molecules will rampage to hook up with another molecule and steal electrons. Frankly, it would be simpler if free radicals just killed a cell and left it at that. But nope, it has to start the dominoes falling. If a cell were bumped off, the body would make a new one. Instead, the cell’s DNA gets damaged enough to set the stage for disaster.

Broken DNA can make a cell mutate and set up a chain reaction for other cells to do the same thing. Not good. Free radicals damage a bunch of cells. Overexposure to the sun, cigarette smoke (either first-hand or second-hand), vehicle exhaust (diesel is the worst), comestibles that are called food but really are not, booze, heavy metals and a few other hazards can work over time to create chronic sickness, including cancer, heart disease, Alzheimer’s disease and Parkinson’s. How do we fix things? Maybe it’s easier to put the brakes on oxidation in the first place. Waddya think?

Antioxidants are molecules that work to prevent damage due to both normal body processes and exposure to some chemicals and environmental perils. One of the benefits of antioxidants is their ability to slow oxidation in the smallest parts of the body—proteins and DNA. There are antioxidants made by the body and those that come from food or supplements. The water-soluble ones react with oxidants in the blood and in the free spaces inside cells. The fat-soluble protect cell membranes from a process known as lipid peroxidation. Some body tissues might have more of one antioxidant than another. For example, one may be plentiful in the kidney, but almost absent from the heart, while the opposite might apply to a different antioxidant. Some may appear at the same concentration in every part of the body.

The body has its own antioxidant defense system, one that relies partly on minerals for proper functioning. Superoxide dismutase (SOD) needs copper, zinc and manganese; glutathione peroxidase needs selenium; and catalase depends on iron. Except for selenium, minerals are not defined as antioxidants, but as cofactors in their manufacture. Although this endogenous system demands respect, we’re going to focus on the most commonly used exogenous antioxidants—vitamins A, C, and E. In most activities, biochemical as well as psycho-social, the buck stops somewhere. With antioxidants, the buck stops at glutathione, so we’ll give that molecule the respect it merits, particularly for the work it does in the lungs (Rahman, 2006) (Nadeem, 2008).

Vitamin A is a general term for a group of related fat-soluble substances, including retinal and retinol, cited as preformed vitamin A. Retinal is converted to retinoic acid, the form that influences gene transcription. Beta-carotene and other carotenoids are referred to as provitamin A compounds. Beta-carotene, the carotenoid that comes from yellow and orange foods, is converted by the liver to retinol. Some forms of this vitamin are occasionally used in pharmacological doses to treat a few conditions, including retinitis pigmentosa (Berson, 1993), acute promyelocytic leukemia (Thurnam, 1999) (Ross, 1999), and various skin conditions (Ross, 1999). However, it’s important to realize that high doses of retinoids, especially if synthetic, can override the body’s own control mechanisms and present toxicities.

Preformed vitamin A is available as retinyl palmitate or acetate, overdose of which is easy to happen because people don’t read labels and often get the vitamin from more than one source, such as from a multi-vitamin or fortified food and later from a separate supplement.  The chief concern is that vitamin A is rapidly taken up, but slowly cleared from the body. Alcohol depletes vitamin A stores from the liver, but taking vitamin A while drinking is an accident waiting to happen. Keeping intake from a supplement at 2500 IU (750 mcg) should do the trick, while avoiding adverse effects on bone in the geriatric crowd. Getting vitamin A from foods is not normally a problem of overdose unless the food is fortified with it (Promislow, 2002). Beta-carotene, by the way, has about half the potency of preformed A, where 2 mcg of supplemental beta-carotene can be converted to 1 mcg of retinol. With foods, though, it takes 12 mcg to make 1 mcg of retinol. Can you see why it’s hard to overdose on cantaloupe?  Pumpkin, carrots, sweet potatoes, mangoes and collards are decent sources.

Water-soluble vitamin C is ascorbic acid, not citric acid, the latter made commercially by the fermentation of molasses. Even though citric acid can be found in oranges, there aren’t enough oranges on the planet to meet a fraction of the demand from the food industry.  Besides being an antioxidant, vitamin C is required for the synthesis of collagen, the structural element that holds us together. Additionally, it helps to make the neurotransmitter norepinephrine. Most animals can make the vitamin C they need; humans and guinea pigs cannot (Linster, 2007). Like all reducing agents, vitamin C itself becomes oxidized. Such an entity donates one or more electrons to a substance that already has become oxidized and is a free radical. In this instance, an antioxidant can become a damaging molecule, running around, looking for an electron to replace the one it just donated. But there is a rescue molecule, where the buck stops, as mentioned earlier. Too much ascorbic acid may cause kidney stones, since oxalates are metabolites of vitamin C, but doses up to 2000 mg a day shouldn’t be a concern for healthy people (Taylor, 2004) (Auer, 1998). The original RDA was barely enough to prevent scurvy, the reason for the RDA in the first place. Citrus, bell peppers, broccoli, potatoes, tomatoes, and strawberries are good sources.

Vitamin E is a fat-soluble family of eight antioxidants—four tocopherols and four tocotrienols. Any adverse publicity you read about vitamin E is based only on alpha-tocopherol, synthetically produced at that and administered to people with pre-existing conditions. The alpha- form of tocopherol is the one most often encountered because it’s actively maintained in the body and has the greatest nutritional significance, although the beat-, delta-, and gamma- forms have merit. It is an antioxidant that prevents the oxidation of fats (rancidity). This is especially important to the cell membrane. After vitamin E gives up an electron, it becomes a free radical itself, but vitamin C and A sacrifice themselves for its salvation. Besides being antioxidant, vitamin E appears to modulate some genes, to inhibit cell proliferation, and to control platelet aggregation and monocyte adhesion. It might even interact with enzymes, structural proteins and lipids (Zingg, 2004) (Ricciarelli, 2002), and regulate cell signaling (Rimbach, 2002). The body recognizes synthetic forms of vitamin E as sham, so it pays to find the d- form, not the dl-form. Oils, avocados and nuts are good sources. If there be a caveat, it is that too much can interfere with blood clotting. Therefore, if taking an anti-coagulant medication, check with the doctor before supplementing. If a tooth extraction or more serious surgery is in the offing, stop supplementation days ahead of time.

Once an antioxidant gives up an electron it can act like the thugs it’s trying to sequester. It needs its own savior. Here comes glutathione to the rescue. This is the body’s master antioxidant, made from amino acids.  As long as sulfur-containing amino acid stores are adequate and are regularly refilled through diet or supplementation (N-acetyl cysteine is such a source), glutathione is able to spare an electron here and there to replace the ones lost by vitamins A, C and E. The dysregulation of glutathione is known to be a prime factor in pathology, from diabetes to pulmonary fibrosis (Lu, 2009), so it pays to consume enough sulfur foods to get the methionine, taurine and cysteine that glutathione needs to keep itself in perfect form. The crucifers, onions and garlic, and animal products, including egg yolks, are substantial sources.

Having the best home run hitter in the league doesn’t guarantee a championship season. You need defense, too; you need a team. The same applies to antioxidants. The overall collection rather than the heavily advertised super antioxidant is what it takes because different antioxidants counteract damage by different types of free radicals within different cellular compartments. Natural and balanced is the rule.

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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.