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ADHD and Magnesium

Magnesium deficiencyMagnesium deficiency has been reported in children with ADHD syndrome.  Signs of this malady include hyperactivity, hypermotivity with aggressiveness, and lack of attention, especially at school.  Biochemical and concurrent behavioral improvements have been realized by magnesium therapy in association with vitamin B6 supplementation.

An analysis of eighteen different study groups performed by Marianne Moussain-Bosc and her colleagues at a French institute for nervous system studies in 2006 indicated that ,”…B6/magnesium therapy benefits about half of autistic children,” but also noted that a related study showed benefits to those with ADHD, using the same doses of each supplement.  Children ranging from one to ten years of age “…received 0.6 milligrams per kilogram per day of vitamin B6 and 6 milligrams per kilogram per day of magnesium.  Treatment lasted an average of eight months.”  (Moussain-Bosc. 2006)   Both groups of children had significantly lower values of erythrocyte magnesium at the outset than the control group(s).  It was observed that after two months of the vitamin-mineral regimen there was a substantial change in clinical symptoms.

ADD and ADHD are on the upswing, and have been for some time.  Both conditions are hastily treated with drugs, often without a differential diagnosis, which is essentially a process of elimination.  Instead, the Diagnostic and Statistical Manual (DSM) of Mental Disorders criteria, and a series of observations and teacher questionnaires are employed.  (Pediatrics. 2000. No authors listed.)   Mineral and electrolyte imbalances are awfully hard to discover with that technique, don’t you think? Most parents wince at the thought of dosing their kids with “miracle” substances that have unknown long-term side effects. On the other hand, the clueless, self-centered, entitled faction applauds the quiet, calm, relatively immobile zombie of the house.

Although we live in plentiful times, where food, shelter, and clothing are accessible to all who earn them, there still exist children who are seriously shy of their required magnesium stores.  One reason is stress.  The number of stressors to which kids are exposed grows every year.  From sports practice, to violence in the streets and on television, to academic obligations, to peer pressure and self-image, and more, the kids are overloaded.  It’s the accompanying flood of adrenaline that siphons magnesium, since that hormone needs the mineral for its release.  Another reason is poor nutrition.  You know, processed foods, refined sugars, colorful and flavorful additives, artificial this and that…  This kind of diet is notoriously low in magnesium, which is calming to the nervous system.  The refined sugars and additives actually stress the body, especially the nervous system, as it tries to overcome the onslaught.  A double whammy.

In Poland, researchers studied ADHD children and assessed the value of magnesium supplementation on the DSM parameters, finding that six months of taking as little as 200 mg a day yielded a decrease in symptoms.  (Starobrat-Hermelin. 1997)  Later study performed by Moussain-Bosc saw a decrease in ADHD symptoms using a combined magnesium / B6 regimen in several dozens of children with low red blood cell magnesium stores.  (Moussain-Bosc. 2004)

Attention deficit hyperactivity disorder is a developmental perturbation characterized by attention problems and hyperactive behavior.  It’s the most commonly studied psychiatric disorder in children, affecting three to five percent of children worldwide.  Sadly, integrative therapies are spurned by traditional-minded doctors, so parents have taken it upon themselves to intervene, despite the lack of support from their physicians.

Bearing in mind that sugar has a nutrient-diluting effect might make a difference in ADHD management and magnesium stores in the body.  It’s normal to wonder where all the magnesium goes.  Doesn’t it stay still?  After all, it’s part of bone.  That’s true, but magnesium is also an electrolyte, helping to send calming electrical messages across the membrane of each cell, making it a natural calcium channel blocker.  It gets used up in the manufacture of more than three hundred enzymes the body needs, including those that make anti-inflammatory chemicals from fatty acids.  Situations and conditions within the body can push this mineral into the urine and then into the toilet.  Sugar intake, and even that of simple carbohydrates, increases the secretion of insulin by the pancreas.   Increased insulin, as might be found in insulin resistance, pushes magnesium out.  (Huerta. 2005)  The pancreas needs magnesium to make its other secretions, including those that break down proteins (trypsin and chymotripsin) and fats (lipase), as well as carbohydrates.  Carol Ballew and her colleagues found that carbonated beverages, namely soda, are negatively associated with magnesium levels This starts a vicious cycle because low magnesium is related to insulin resistance. (Ballew. 2000).

In tests done in the mid 90’s, it was discovered that elevated insulin levels result in increased magnesium excretion.  These researchers noted this as the explanation to the magnesium deficit that accompanies obesity, diabetes, and hypertension, as well as hyperinsulinemia.  (Djurhuus. 1995)  This same group later reported that high glucose levels, such as would come from a sugary breakfast or a plethora of sweet goodies, raise magnesium excretion by a factor greater than 2.0.  (Djurhuus. 2000)

The foods that once supplied dietary magnesium have become compromised by careless farming, harvesting, processing, storage, and handling practices.  We now get more calcium and less magnesium than ever in the history of mankind.  Sugar erases magnesium from the body’s slate. (Fuchs. 2002) (Tjaderhane. 1998) (Milne. 2000)  It’s time to put it back.  At 6.0 mg / kg / day, that equates to about 3.0 milligrams per pound of body weight…for all of us.

References

  • AUTISM RESEARCH REVIEW INTERNATIONAL Vol. 20, No.3, 2006
    Studies confirm benefits of vitamin B6/magnesium therapy for autism, PDD, and ADHD
    No Authors Cited

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  • Magnes Res. 1997 Jun;10(2):143-8.
    Assessment of magnesium levels in children with attention deficit hyperactivity disorder (ADHD).
    Kozielec T, Starobrat-Hermelin B.

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  • Pediatrics. 2000 May;105(5):1158-70
    Did not perform differentiated diagnosis
    Clinical practice guideline: diagnosis and evaluation of the child with attention-deficit/hyperactivity disorder. American Academy of Pediatrics.
    No authors listed

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  • Magnes Res. 2006 Mar;19(1):53-62.
    Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6. II. Pervasive developmental disorder-autism.
    Mousain-Bosc M, Roche M, Polge A, Pradal-Prat D, Rapin J, Bali JP.

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  • J Am Coll Nutr. 2004 Oct;23(5):545S-548S.
    Magnesium VitB6 intake reduces central nervous system hyperexcitability in children.
    Mousain-Bosc M, Roche M, Rapin J, Bali JP.

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  • J Clin Invest. 1970 July; 49(7): 1458–1465.
    A comparison of the effects of glucose ingestion and NH4Cl acidosis on urinary calcium
    and magnesium excretion in man

    Edward J. Lennon and Walter F. Piering

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  • J Abnorm Child Psychol. 1986 Dec;14(4):565-77.
    Behavioral effects of sucrose on preschool children.
    Goldman JA, Lerman RH, Contois JH, Udall JN Jr.

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  • Arch Pediatr Adolesc Med. 2000;154:1148-1152
    Beverage Choices Affect Adequacy of Children’s Nutrient Intakes
    Carol Ballew, PhD; Sarah Kuester, MS, RD; Cathleen Gillespie

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  • Diabetes Care. 2005 May;28(5):1175-81.
    Magnesium deficiency is associated with insulin resistance in obese children.
    Huerta MG, Roemmich JN, Kington ML, Bovbjerg VE, Weltman AL, Holmes VF, Patrie JT, Rogol AD, Nadler JL.
    SourceUniversity of Virginia, Department of Pediatrics, Box 800386, Charlottesville, VA 22908, USA. [email protected]

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  • Diabetic Medicine.  Volume 12, Issue 8, pages 664–669, August 1995
    Insulin Increases Renal Magnesium Excretion: A Possible Cause of Magnesium
    Depletion in Hyperinsulinaemic States

    Dr. M.S. Djurhuus, P. Skøtt, O. Hother-Nielsen, N.A.H. Klitgaard, H. Beck-Nielsen

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  • Scan Jou of Clin & Laboratory Investigation. 2000, Vol. 60, No. 5 , Pages 403-410
    Hyperglycaemia enhances renal magnesium excretion in Type 1 diabetic patients
    S. Djurhuus

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  • J. Nutr. October 1, 1998 vol. 128 no. 10 1807-1810
    A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats
    Leo Tjäderhane, and Markku Larmas
    Institute of Dentistry, University of Oulu, 90220 Oulu, Finland

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  • J Am Coll Nutr February 2000 vol. 19 no. 1 31-37
    The Interaction Between Dietary Fructose and Magnesium Adversely Affects
    Macromineral Homeostasis in Men

    David B. Milne, PhD and Forrest H. Nielsen, PhD

*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.

Truth About Magnesium Stearate

mag-glassWe’ve all seen pitchmen, the medium-pressure peddlers who unashamedly try to lure us to their side of the street with great deals on auto insurance or oxygenated household cleaners. Forceful voices and rapid chatter are attention grabbers. But it needn’t be fast talk and loud volume that get our attention. It can be capital letters, bold print, fancy fonts, or any combination of these on the internet that tries to persuade or dissuade us from buying, doing, ingesting or using a tangible or intangible thing.

Recent internet talk, some by celebrity physicians, has focused on—and maligned—magnesium stearate, an innocuous substance used in the pharmaceutical and supplement industries as an excipient. Yes, it does have lubricative properties that prevent adhesion of a material to the tumbling and pressing surfaces of a tablet forming machine, but more importantly, it helps to ensure consistency and homogeneity of the finished product. It guarantees even distribution of the active ingredients in a tablet or capsule, so that each is identical to the last and the next. Acting as a flow agent, magnesium stearate lowers manufacturing costs, as well. Were this not the case, consumer dander would rise to greet the consequent price increase. If the active ingredient of a medication or supplement did cling to machine surfaces, dosages would be hit or miss. The average amount of magnesium stearate in a tablet or capsule is far less than 1.0% of the total weight, with many supplement makers using fractional amounts, down to thousandths of a percent.

Pharmaceutical and supplement companies are not deaf to consumers’ interests. They add only that amount of magnesium stearate necessary to the desired outcome, changing according to a specific blend. The variables involved in drug or nutrient manufacturing are numerous. Particle size of the main ingredient, moisture content, chemical nature, solubility, cohesive properties, mixing order of the components, electrostatic forces that cause factory explosions, mixing time, hydrophobicity, dissolution expectations, and factors herein unknown contribute to the complexity of the process. Each step is carefully monitored as part of a fail-safe system employed by responsible, accountable, cGMP-compliant companies. Sadly, there are those businesses that perpetrate fraud against consumers knowingly. It is these who market supplements for a buck ninety-nine. It is these whose cut-rate pharmaceuticals yield undesirable effects.

What started all the hoopla about magnesium sulfate is a 1990 report whose conclusions were never put to use. This was a preliminary cell study that sought an immunosuppressive drug for people with organ transplants and autoimmune diseases.  In the experiments, T cells and B cells were exposed to a concoction that mixed stearic acid with diatomaceous earth and bovine albumin—a little different from magnesium stearate. The intent of the study was to injure T cells with the brew after they were exposed to a toxic challenge, meaning that exposure to the cocktail had to be adequate to damage them. Any association with pharmaceuticals or supplement manufacture escapes even a casual reader.  What is particularly bothersome is the faulty conclusion that stearic acid destroys T cells and is, therefore, immune toxic. The study’s title is incriminating to stearic acid:  “Molecular basis for the immunosuppressive action of stearic acid on T cells,” having appeared in the journal Immunology in July, 1990. B cells in this test were unscathed, while T cells lost membrane integrity to stearic acid influx, which increased membrane rigidity. Only stearic acid, the 18.0 saturated fat common to chocolate and lean beef, was implicated. The roles of diatomaceous earth and bovine albumin remain a mystery. The former is an industrial filtering component and filler for paints and abrasives. The latter is a protein concentration standard used in cell cultures and immunohistochemistry because it has no effect on enzymes that do not need it for stabilization, and it takes part in very few biochemical reactions. Bovine albumin is inexpensive, too.

In the study, stearic acid was likened to the anti-rejection drug, cyclosporine, which suppresses the immune system following allograft. This drug is also selectively used to treat severe cases of psoriasis, rheumatoid arthritis, atopic dermatitis, and even dry eyes as an ophthalmic emulsion. But its adverse effects are numerous and intense, and it is suspected of carcinogenicity. If stearic acid, with zero side effects, could replace cyclosporine, it would be a welcome alternative. However, doses would have to exceed the no-effect level of magnesium stearate’s 2500 mg/kg of bodyweight/day (Søndergaard, 1980). That equates to 6 ounces of magnesium stearate for a 150-pound person each day.

Magnesium stearate is a compound of magnesium and solid organic acids, containing two equivalents of stearate and one of magnesium. The magnesium moiety is used to address conditions besides hypomagnesemia. Laxation aside, this mineral has been applied to respiratory and cardiovascular needs, aberrant lipid profiles, neuromuscular and neuroskeletal diseases, ADD/ADHD and other behavior disorders, restless leg syndrome, migraine headaches, and prevention of hearing loss, among others. Being the second most plentiful cation in the human body, magnesium is involved in more than three hundred enzyme systems and is divided almost equally between bone and soft tissue.  A fraction of magnesium sits on the surface of bone, acting as a reservoir to maintain the extracellular magnesium concentration.  Fifty-five percent of plasma magnesium is free; about thirty percent is bound to proteins.  The rest is complexed to anions.

Absorption of supplemental magnesium, probably occurring in distal duodenum, is inversely proportional to the amount ingested.  Even dietary (from foods) mineral enjoys only about one-third absorption, depending on body stores and physiological/metabolic needs.  In supplements, magnesium oxide is the least bioavailable; citrate and glycinate among the more available.  Enteric coating reduces absorption.

Magnesium deficit is associated with cardiac arrhythmia, cessation of bone growth (activity of osteoclasts and osteoblasts), muscle spasticity, anorexia, seizures, confusion, muscle cramping and hypertension, among other disorders.  Such deficiency is common in diabetes, malabsorption syndromes, alcohol abuse, and in extended use of thiazide and loop diuretics.  Magnesium is intimately linked to calcium in the manufacture of adenosine triphosphate (ATP).  On the other hand, they antagonize each other in the synthesis of nucleic acids and proteins.  In some ways, magnesium is nature’s calcium channel blocker because it regulates the intracellular flow of calcium ions.  The virtues of magnesium extend beyond the scope of this newsletter, but it is worth noting that foods high in fiber are usually good sources of magnesium.

Stearic acid is one of the most common long-chain fatty acids, found in both animal and vegetable fats, appearing in foods in amounts far greater than in any supplement.  This fatty acid is the immediate precursor to oleic acid, an important fatty acid in olive oil.  Studies in humans have determined that stearic acid, desaturated to oleic acid by the liver, is less apt to elevate cholesterol than other saturated fatty acids, possibly due to absorption vagaries.  Nonetheless, the rapid conversion of stearic to oleic acid suggests that stearic acid is as effective as oleic acid in lowering plasma cholesterol when it replaces palmitic acid in the diet (Bonanome, 1988).  But more dramatic is the finding that stearic acid may be toxic to cancer cells.  Decreased cell membrane rigidity is a characteristic of malignant cells, partly because of the desaturation of stearic acid.  British tests that examined a chemically-induced murine mammary carcinoma line discovered that subcutaneous administration of stearic acid at weekly intervals prevented tumor development (Habib, 1987).  Later study found that stearic acid inhibited colony forming abilities of several human cancer cell lines (Fermor, 1992).  The innocuous nature of stearic acid had been established well before it was maligned as being part of a “persona non grata” molecule.

The street vendors have declared magnesium stearate as causative of intestinal biofilms that interfere with absorption of nutrients and foods.  Yet, no proof is offered.  To the contrary, the molecules used by micro-organisms to make biofilms are inhibited by stearic and several other saturated fatty acids (Soni, 2008).  Since most people have never heard of biofilms, mentioning them as ominous factors is an effective marketing tool.  The bacteria that form biofilms to protect themselves use polyunsaturated fats to flourish by injecting a fat with an oxygen molecule in order to form an oxylipin, which is a pro-inflammatory eicosanoid.  It is not likely that a saturated fat has room to accept another atom, much less a molecule.

Even though FDA credibility has raised a few eyebrows in recent years, it is generally accepted that its revised 2006 Code of Federal Regulations is reliable. Title 21, Volume 3 of that tome allows that stearic acid is a GRAS substance that can be used according to Good Manufacturing Practices (GMP’s).

The science agrees that magnesium stearate is a safe analog of stearic acid.   Red meats, chocolate products and Brazil nuts are ordinary sources of stearic acid.  Despite its fat content, chocolate does not have any adverse effect on plasma lipids, not even milk chocolate.  Stearic acid deserves not to be spoken in the same sentence with other saturated fats (Kris-Etherton, 1994).  In fact, stearic acid has shown itself to increase excretion of endogenous cholesterol (Schneider, 2000) and even to lower LDL’s compared with other fatty acids (Mensink, 2005).  If at fault, the worst that magnesium stearate does is to prolong dissolution of the main ingredient.  Does it matter whether it comes from animal or vegetable sources?  Concerning dissolution and safety, no.  Concerning the force needed to eject a tablet from its mold, the animal-derived product has stronger adhesion properties (Hamad, 2008).  Paracelsus, the Renaissance physician held to be the father of toxicology, pointed out that the dose makes the poison.  In that matter, water can be a lethal substance.  Beware of misleading and inaccurate information.

References

Baer DJ, Judd JT, Kris-Etherton PM, Zhao G, Emken EA.
Stearic acid absorption and its metabolizable energy value are minimally lower than those of other fatty acids in healthy men fed mixed diets.
J Nutr. 2003 Dec;133(12):4129-34.

Bonanome A, Grundy SM.
Effect of dietary stearic acid on plasma cholesterol and lipoprotein levels.
N Engl J Med. 1988 May 12;318(19):1244-8.

Buttke TM, Cuchens MA.
Inhibition of lymphocyte proliferation by free fatty acids. II. Toxicity of stearic acid towards phytohaemagglutinin-activated T cells.
Immunology. 1984 Nov;53(3):507-14.

Denke MA.
Effects of cocoa butter on serum lipids in humans: historical highlights.
Am J Clin Nutr. 1994 Dec;60(6 Suppl):1014S-1016S.

Denke MA.
Role of beef and beef tallow, an enriched source of stearic acid, in a cholesterol-lowering diet.
Am J Clin Nutr. 1994 Dec;60(6 Suppl):1044S-1049S.

Eddington ND, Ashraf M, Augsburger LL, Leslie JL, Fossler MJ, Lesko LJ, Shah VP, Rekhi GS.
Identification of formulation and manufacturing variables that influence in vitro dissolution and in vivo bioavailability of propranolol hydrochloride tablets.
Pharm Dev Technol. 1998 Nov;3(4):535-47.

Fermor BF, Masters JR, Wood CB, Miller J, Apostolov K, Habib NA.
Fatty acid composition of normal and malignant cells and cytotoxicity of stearic, oleic and sterculic acids in vitro.
Eur J Cancer. 1992;28A(6-7):1143-7.

Firoz M, Graber M.
Bioavailability of US commercial magnesium preparations.
Magnes Res. 2001 Dec;14(4):257-62.

GRAS Substances (SCOGS) Database
Select Committee on GRAS Substances (SCOGS) Opinion: Stearic acid (packaging)
Stearic acid (packaging)
SCOGS-Report Number: 54*
Type Of Conclusion: 1
ID Code: 57-11-4
Year: 1975
21 CFR Section: 184.1090

Habib NA, Hershman MJ, Salem R, Barker W, Apostolov K, Wood CB.
Increased erythrocyte stearic acid desaturation in rats with chemically induced colorectal carcinomas.
Int J Colorectal Dis. 1987 Feb;2(1):12-4.

N. A. Habib, C. B. Wood, K. Apostolov, W. Barker, M. J. Hershman, M. Aslam, D. Heinemann, B. Fermor, R. C. Williamson, W. E. Jenkins
Stearic acid and carcinogenesis.
Br J Cancer. 1987 October; 56(4): 455–458.

Hamad ML, Gupta A, Shah RB, Lyon RC, Sayeed VA, Khan MA.
Functionality of magnesium stearate derived from bovine and vegetable sources: dry granulated tablets.
J Pharm Sci. 2008 Dec;97(12):5328-40.

M.S.H. Hussain, P. York, P. Timmins
Effect of commercial and high purity magnesiumstearates on in-vitro dissolution of paracetamol DC tablets
International Journal of Pharmaceutics.  Vol 78, Iss 1–3, 1 Jan 1992, Pp 203–207

Khalil MH, Marcelletti JF, Katz LR, Katz DH, Pope LE.
Topical application of docosanol- or stearic acid-containing creams reduces severity of phenol burn wounds in mice.
Contact Dermatitis. 2000 Aug;43(2):79-81.

Kris-Etherton PM, Mustad VA.
Chocolate feeding studies: a novel approach for evaluating the plasma lipid effects of stearic acid.
Am J Clin Nutr. 1994 Dec;60(6 Suppl):1029S-1036S.

Li S, Lin S, Chien YW, Daggy BP, Mirchandani HL.
Statistical optimization of gastric floating system for oral controlled delivery of calcium.
AAPS PharmSciTech. 2001 Jan 13;2(1):E1.

Mensink RP.
Effects of stearic acid on plasma lipid and lipoproteins in humans.
Lipids. 2005 Dec;40(12):1201-5.

W.F. Ng, M.H. Wong, F.T. Cheng
Stearic acid coating on magnesium for enhancing corrosion resistance in Hanks’ solution
Surface and Coatings Technology. Vol 204, Iss 11, 25 Febr 2010, Pp 1823–1830

John T.H Ong, Zak T Chowhan, Glenn J Samuels
Drug-excipient interactions resulting from powder mixing. VI. Role of various surfactants
International Journal of Pharmaceutics. Vol 96, Issues 1–3, 31 July 1993, Pp 231–242

Pereira CS, Thompson JA, Xavier KB.
AI-2-mediated signalling in bacteria.
FEMS Microbiol Rev. 2012 Jun 19. doi: 10.1111/j.1574-6976.2012.00345.x. [Epub ahead of print]

Schneider CL, Cowles RL, Stuefer-Powell CL, Carr TP.
Dietary stearic acid reduces cholesterol absorption and increases endogenous cholesterol excretion in hamsters fed cereal-based diets.
J Nutr. 2000 May;130(5):1232-8.

Søndergaard D, Meyer O, Würtzen G.
Magnesium stearate given perorally to rats. A short term study.
Toxicology. 1980;17(1):51-5.

Soni KA, Jesudhasan P, Cepeda M, Widmer K, Jayaprakasha GK, Patil BS, Hume ME, Pillai SD.
Identification of ground beef-derived fatty acid inhibitors of autoinducer-2-based cell signaling.
J Food Prot. 2008 Jan;71(1):134-8.

Tebbey PW, Buttke TM.
Molecular basis for the immunosuppressive action of stearic acid on T cells.
Immunology. 1990 Jul;70(3):379-84.

Tholstrup T.
Influence of stearic acid on hemostatic risk factors in humans.
Lipids. 2005 Dec;40(12):1229-35.

Uzunović A, Vranić E.
Effect of magnesium stearate concentration on dissolution properties of ranitidine hydrochloride coated tablets.
Bosn J Basic Med Sci. 2007 Aug;7(3):279-83.

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

Tuning In Your ADD/ADHD Child

tv-head-childAll of us know children who have a hard time staying still, who find it difficult to listen, who can’t follow directions no matter how many times you present them, and who occasionally blurt out comments at the most inopportune times. Often the criticism is poorly aimed. Are they just being kids, or could they be suffering from attention deficit disorder or attention deficit hyperactivity disorder?  ADD/ADHD can make it difficult for a person to inhibit his spontaneity. The diagnosis is not a simple one, and too often relies on nothing but subjective reports from school personnel and parents, leading to a prescription pad resolution. A complete examination is required for diagnosis. Have there been any sudden life changes, such as divorce, moving, death in the family, or entering a new school? Have thyroid and sleep problems been considered? How about anxiety or depression? Could there be heavy metal toxicity or other toxic exposure?

Some kids with ADD are hyperactive, but not all. Some have a physiological reason, some don’t. Many are able to pay close attention to things they like, while others get bored quickly. Some are impulsive or quick-tempered. Those who seem disobedient may not be so intentionally. Whether they outgrow this or not is anyone’s guess; there are plenty of adults with ADD/ADHD.  As often as drugs are prescribed, they might not be the best option for you or your child. At one end of the spectrum, there are the hyperactive kids; at the other end are the quiet dreamers who stare off into space. Bad parenting is not an issue, but effective parenting strategies can go a long way to correct problems.

One theory of ADD/ADHD has to do with a person’s executive function, which involves the cognitive processes needed to organize thoughts and actions, to prioritize tasks, to manage time efficiently, and to make decisions. Looking at this list, we might know more people with executive dysfunction than we thought, especially when it comes to situations that require the control of habitual responses or of resisting temptations. Occasionally a parent hears that his child is a joy in the classroom, making the parent wonder why that doesn’t hold true at home. More often, however, the parent hears the opposite. In school, the teacher’s strategies to manage executive function problems might include inhibition, organization of materials, peer tutoring and other student-friendly approaches. Parent strategies often stop at inhibition, others being clouded by frustration. Weakness in executive function may not be characteristic of all cases of ADD/ADHD, but appear to be one important component of the disorder (Willcutt, 2005).  Adults with frontal lobe damage exhibit similar behaviors as children suspected of having the ADD/ADHD spectrum, leading some researchers to associate the physiological dysfunction while implicating the catecholamine neurotransmitters that respond to the stressors that arouse fight or flight (Faraonea, 1998).

Have you ever heard static on your radio or seen a snowy picture on the TV? That kind of interference in a child’s brain can jostle the connections. You might be able to tune out extraneous input and focus on what has your interest, like Sunday’s football game, but kids can’t always do that because, first of all, their brains are far from being completely wired and, second of all, they might have a few aberrant neurons. Multiple, simultaneous stimuli compete for neural attention, whether visual or auditory in the case of formal education. It requires purposive attention to separate stimuli and to focus on an assigned task. Therefore, goals need to be announced prior to a task and motivation needs to be stirred. The first part is easy; the second, not. Even in the presence of imminent reward, children may be hard to motivate. Negative feedback or punishment is futile (Stevens, 2012) (Crone, 2003). In some instances there is a need for family counseling, especially where cognitive disorders appear to have a heritable nature.  Attendant conduct disorders (Toupin, 2000) can amplify and become legitimate societal concerns. Socioeconomic status may or may not be involved, although attention disorders may interfere with economic wherewithal, present and future. This may co-occur with food insecurity, in which case nutritional deficit plays a role in ADD/ADHD, where even subtle nutritional irregularities can affect attention and motor behavior (Conners, 1982).

It has been suggested that children of lower socioeconomic status who are academically and behaviorally challenged be supplemented with micronutrients and essential fatty acids to learn if positive changes in cognition, learning and behavior occur, for such effect has been seen in developed and developing societies (Frensham, 2012). No reason was given for targeting this population. Since many educators have had remarkable social and academic interactions with this group, this is curious. Although the cause of ADD/ADHD has not been absolutely identified, its link to vitamin/mineral/fatty acid deficiencies has been proposed. Zinc, iron, magnesium and iodine, and the long-chain polyunsaturated fats may have a profound impact on the development and aggravation of ADD/ADHD symptoms (Konikowska, 2012). The fact is that all of us should keep an eye on levels of these nutrients (Milne, 2000) (Fuchs, 2002).

It has been established that zinc is a co-factor in more than a hundred enzymes, including those that metabolize carbohydrates, prostaglandins and nucleic acids. It has a striking effect on neurotransmission, as well, and may be factored in hyperkinetic disorders, especially noting that children diagnosed with ADD/ADHD suffer from low levels. Low zinc values may point to other nutrient deficits, such as outright malnutrition.  Feasting on bags of snacks and sweets may fill an empty belly, but doesn’t answer physiological needs despite the low cost. Maternal habits that increase exposure to additives, alcohol and smoking during pregnancy are other factors to consider (Dodig-Curkovic, 2009). Magnesium is part of more than three enzymes, and its shortfall is conspicuous in ADD/ADHD individuals. That many youngsters avoid a wide range of vegetables, limiting themselves to corn and French fries, helps to explain this.  Supplementation with these minerals has brought positive outcomes (Starobrat-Hermelin, 1997, 1998) (Kozielec, 1997).

Whether ADD/ADHD will pervade a child’s life or not is undetermined. Many have outgrown the disorder, or at least have matured to the point of controlling the outward signs. Because mature gustatory sense admits a variety of plants into the diet, this alone might make a difference. Being proactive matters and introducing a child to one concept, task or image at a time can make a considerable difference in forming concepts from percepts.

References

Arnold LE, Bozzolo H, Hollway J, Cook A, DiSilvestro RA, Bozzolo DR, Crowl L, Ramadan Y, Williams C.
Serum zinc correlates with parent- and teacher- rated inattention in children with attention-deficit/hyperactivity disorder.
J Child Adolesc Psychopharmacol. 2005 Aug;15(4):628-36.

Carol Ballew, PhD; Sarah Kuester, MS, RD; Cathleen Gillespie
Beverage Choices Affect Adequacy of Children’s Nutrient Intakes
Arch Pediatr Adolesc Med. 2000;154:1148-1152

C.Keith Conners, Arthur G. Blouin
Nutritional effects on behavior of children
Journal of Psychiatric Research. Vol 17, Iss 2, 1982–1983, Pp 193–201

Eveline A. Crone, J. Richard Jennings, Maurits W. Van Der Molen
Sensitivity to interference and response contingencies in Attention-Deficit/Hyperactivity Disorder
Journal of Child Psychology and Psychiatry.  Vol 44, Iss 2, pp 214–226, Feb 2003

Dodig-Curković K, Dovhanj J, Curković M, Dodig-Radić J, Degmecić D.
The role of zinc in the treatment of hyperactivity disorder in children.
Acta Med Croatica. 2009 Oct;63(4):307-13.

Stephen V Faraonea,  Joseph Biederman
Neurobiology of attention-deficit hyperactivity disorder
Biological Psychiatry. Volume 44, Issue 10, 15 November 1998, Pages 951–958

Mariellen Fischer, Russell A. Barkley, Lori Smallish, Kenneth Fletcher
Executive Functioning in Hyperactive Children as Young Adults: Attention,
Inhibition, Response Perseveration, and the Impact of Comorbidity

DEVELOPMENTAL NEUROPSYCHOLOGY, 2005; 27(1): 107–133

Frensham LJ, Bryan J, Parletta N.
Influences of micronutrient and omega-3 fatty acid supplementation on cognition, learning, and behavior: methodological considerations and implications for children and adolescents in developed societies.
Nutr Rev. 2012 Oct;70(10):594-610. doi: 10.1111/j.1753-4887.2012.00516.x.

Nan Kathryn Fuchs, Ph.D.
Magnesium: A Key to Calcium Absorption
http://www.mgwater.com/calmagab.shtml

Koller, Harold P.
Visual processing and learning disorders
Current Opinion in Ophthalmology. September 2012 – Volume 23 – Issue 5 – p 377–383

Konikowska K, Regulska-Ilow B, Rózańska D.
The influence of components of diet on the symptoms of ADHD in children.
Rocz Panstw Zakl Hig. 2012;63(2):127-34.

Kozielec T, Starobrat-Hermelin B
Assessment of magnesium levels in children with attention deficit hyperactivity disorder (ADHD).
Magnes Res. 1997 Jun;10(2):143-8.

Mares D, McLuckie A, Schwartz M, Saini M.
Executive function impairments in children with attention-deficit hyperactivity disorder: do they differ between school and home environments?
Can J Psychiatry. 2007 Aug;52(8):527-34.

McMains S, Kastner S.
Interactions of top-down and bottom-up mechanisms in human visual cortex.
J Neurosci. 2011 Jan 12;31(2):587-97.

Millichap JG, Yee MM.
The diet factor in attention-deficit/hyperactivity disorder.
Pediatrics. 2012 Feb;129(2):330-7.

David B. Milne, PhD and Forrest H. Nielsen, PhD
The Interaction Between Dietary Fructose and Magnesium Adversely Affects Macromineral Homeostasis in Men
J Am Coll Nutr February 2000 vol. 19 no. 1 31-37

Sonuga-Barke EJ, Sergeant JA, Nigg J, Willcutt E.
Executive dysfunction and delay aversion in attention deficit hyperactivity disorder: nosologic and diagnostic implications.
Child Adolesc Psychiatr Clin N Am. 2008 Apr;17(2):367-84, ix.

Starobrat-Hermelin B, Kozielec T.
The effects of magnesium physiological supplementation on hyperactivity in children with attention deficit hyperactivity disorder (ADHD). Positive response to magnesium oral loading test.
Magnes Res. 1997 Jun;10(2):149-56.

Starobrat-Hermelin B.
The effect of deficiency of selected bioelements on hyperactivity in children with certain specified mental disorders.
Ann Acad Med Stetin. 1998;44:297-314.

Alexander A. Stevens, Leeza Maron, Joel T. Nigg, Desmond Cheung, Edward F. Ester,
Edward Awh
Increased Sensitivity to Perceptual Interference in Adults with Attention Deficit Hyperactivity Disorder
Journal of the International Neuropsychological Society (2012), 18, 1–10.

Jean Toupin, Michèle Déry, Robert Pauzé, Henri Mercier, Laurier Fortin
Cognitive and Familial Contributions to Conduct Disorder in Children
Journal of Child Psychology and Psychiatry. Vol 41, Iss 3, pp 333–344, March 2000

Willcutt EG, Doyle AE, Nigg JT, Faraone SV, Pennington BF.
Validity of the executive function theory of attention-deficit/hyperactivity disorder: a meta-analytic review.
Biol Psychiatry. 2005 Jun 1;57(11):1336-46

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

Essential Fats Explained

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

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

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

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

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

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

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

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

References

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

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

Caramia G.
The essential fatty acids omega-6 and omega-3: from their discovery to their use in therapy.
Minerva Pediatr. 2008 Apr;60(2):219-33.

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

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