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.


    Studies confirm benefits of vitamin B6/magnesium therapy for autism, PDD, and ADHD
    No Authors Cited


  • 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.


  • 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


  • 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.


  • 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.


  • 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


  • 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.


  • 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


  • 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]


  • 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


  • 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


  • 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


  • 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.

Technology And Children: A Negative Effect On Health?

Technology & ChildrenOne of the vagaries of parenthood is that we think we know more than our kids, enough to maintain a watchful eye over all they do and the places they go.  That might have been true before the advent of wireless technology and electronic media, but that’s an iffy proposition today.  Of course, the connected parent is concerned about his child’s safety and does all he can to ensure it.  But that idea transcends the physical, for the motivational, psychological and emotional dangers are ubiquitous.

Anything that has benefits, whether subjectively perceived or real, could be laden with risks.  Dr. Gwenn Schurgin O’Keeffe, detailing her research from a recent issue of Pediatrics and reporting to WebMD, feels that, “Some young people find the lure of social media difficult to resist, which can interfere with homework, sleep, and physical activity,” adding that, “Parents need to understand how their child is using social media so they can set appropriate limits.”   The element of internet risk is recognized by about half the parents interviewed, but only a fourth deems internet sites safe.  (WebMD. 3/28/11)

Concerning the children’s point of view, half admitted not to have spoken with their parents about their internet and social media activities.  Only four percent of parents realize that their kids log-on more than ten times a day, and twelve percent don’t even know their kids have a social account.  “Nurturing friendships and community engagement” are named as positive reasons to connect online, but the downsides of bullying and sexual inappropriateness receive equal attention.  Dr. O’Keeffe suggests that age thirteen is suitable for social interaction via the internet, agreeing with federal privacy rules outlined on some of the more popular networking sites, such as Facebook.  (O’Keeffe. 2011)

For years, health care professionals, teachers (especially PE teachers) and too few parents have been concerned with the amount of time their kids spend in front of the TV, which for many households had been an electronic babysitter from the get-go. While the Journal of Adolescence tells us that kids’ TV time hasn’t increased appreciably in the last fifty years (Marshall. 2006), their video game and social networking time has. Electronic sexual solicitation of underage youth is not as widespread as one would think from the reports (Ybarra. 2008), but that does not eliminate or reduce the risk.  Such solicitation is more likely to come through text messaging and in chat rooms, and harassment of one kind or another through instant messaging than through social networking sites (Ibid).

Nonetheless, kids spend more than seven hours a day, on average, in front of a screen.  Recent evidence raises concerns about media’s effects on aggression, sexual behavior, substance use, disordered eating, and academic difficulties.  Intense and regular parental involvement can increase the benefits and reduce the harm that media can have for a developing child and for adolescents.  (Strasburger. 2010)  Such anxieties are not limited to this side of the Atlantic or Pacific, either.  Online “addictions” were found to be related not only to aggression, but also to narcissistic personality traits and self-control, in studies conducted in Korea using international parameters.  (KIM. 2008)

The same kids who have problems with their peers at school or in the mall are likely to be the ones at risk for manipulation and targeting on the internet or smart phone.  Picking up signs of aberrant behavior are important, but we have to be vigilant.  Changes in behavior that include depression or aggression, delinquency or truancy, and becoming a loner or hanging with the wrong crowd are signals.  From the biomedical position, sedentary habits at a young age might just be able to predict health problems in adulthood.   Now, that’s another issue.  This topic should not entertain role reversal, even if your child is more adept at using the computer than you are.

Social Networking May Affect Kids’ Health
Report Urges Parents to Communicate and Participate When Kids Socialize Online

Pediatrics Vol. 127 No. 4 April 1, 2011 pp. 800 -804
The Impact of Social Media on Children, Adolescents, and Families
Gwenn Schurgin O’Keeffe, MD, Kathleen Clarke-Pearson, MD,
Council on Communications and Media

J Adolesc. 2006 Jun;29(3):333-49. Epub 2005 Oct 21.
A descriptive epidemiology of screen-based media use in youth: a review and critique.
Marshall SJ, Gorely T, Biddle SJ.

Pediatrics Vol. 121 No. 2 February 1, 2008 pp. e350 -e357
How Risky Are Social Networking Sites? A Comparison of Places Online Where Youth Sexual Solicitation and Harassment Occurs
Michele L. Ybarra, MPH, PhD, Kimberly J. Mitchell, PhD

Pediatrics Vol. 125 No. 4 April 1, 2010 pp. 756 -767
Health Effects of Media on Children and Adolescents
Victor C. Strasburger, MDa, Amy B. Jordan, PhDb, Ed Donnerstein, PhDc

Eur Psychiatry. 2008 Apr;23(3):212-8. Epub 2007 Dec 31.
The relationship between online game addiction and aggression, self-control and narcissistic personality traits.
Kim EJ, Namkoong K, Ku T, Kim SJ.

Br J Sports Med. 2011 Sep;45(11):906-13.
Sedentary behaviour in youth.
Pate RR, Mitchell JA, Byun W, Dowda M.

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

Sleep and Kids

boy-watching-tv-with-remoteIt would be too easy if we put our kids to bed and they fell asleep in the average nine minutes it takes for an adult to drop into the arms of Morpheus. If your child struggles to fall asleep, know that this is not likely to resolve merely by moving from crib to bed. As he ages, there will fewer cries and screams, and more pleas and refusals. Could there be a reason behind this? Maybe television? Video games?

Each child is unique and has his own distinct needs for sleep.  Generally, a preschooler needs 10 to 12 hours a night, maybe with a nap during the day.  The surprise is that the school-age and preteen group benefit from the same, except for the nap.  But, “media use has been shown to negatively affect a child’s sleep,” according to researchers at Seattle’s Children’s Research Institute.  In their randomized controlled study of preschoolers, they found that the children had more than 70 minutes of screen time a day, with a fifth of that after 7 PM.  Almost 20% of the parents interviewed indicated at least one sleep problem with their preschooler.  Daytime TV showing violent behavior exacerbated problems.  (Garrison. 2011)  In a similar study a decade earlier, investigators at Brown University discovered that the sleep domains most affected by television were “bedtime resistance, sleep onset delay, and anxiety around sleep, followed by shortened sleep duration.”  (Owens. 1999)  In both studies—and in several between— it is agreed that a TV in the child’s bedroom compounds the matter and translates into less-than-stellar academic performance.

Recent assaults on Sponge Bob and his kin have raised the hackles of the entertainment industry.  But theirs is not righteous indignation, and transcends the humor of a “Who?  Me?” response.  It has been suspected for decades that the electronic babysitter would require a payback.  If a person believes that life is a series of trade-offs, here’s one of them, usually showing up during the school years, unknowingly invited earlier.

Children who watch fast-paced programs—even for as little as nine minutes — perform poorly in executive function tasks, those that control and regulate other behaviors and abilities, and are necessary for goal-directed activities.  These might include knowing when to start and stop behaviors and when to change them if the situation calls for it.  It also includes being able to plan ahead, to pay attention, and to fine tune memory and motor skills.  Although they are not easy to assess, their absence is noticeable.  (Lillard. 2011)  Teachers have lamented since the 1970’s that too many children start school with five-minute attention spans.

The U.S. is not the only nation facing this problem.  German researchers realized that 25% of their children do not get the ten hours of sleep they need.  They advise that parents and care givers limit TV time in order to prevent the negative consequences of sleep deprivation.  (Heins. 2007)  The Japanese learned that not only TV, but also after-school activities that last past 8 PM can interfere with sleep / wake patterns.  (Oka. 2008)

Other electronic entertainment, not only TV, plays a role in cerebral interference.  Electronics may induce the fight-or-flight state, increase blood pressure and pulse, and disrupt overall brain performance.  The unnatural brightness of the screen can interfere with production of melatonin, the signaling molecule that tells you to fall asleep.  Fast-moving and quick-changing scenes can interrupt the wiring of a young brain, possibly leading to bad dreams and restlessness.  Electromagnetic radiation is a by-product of anything electronic, affecting children more than adults, considering that their brain tissue is more conductive, radio frequency penetration is greater relative to head size, and children will have a longer lifetime exposure than adults.  (Kheifets. 2005)

Problems begin to manifest by age seven, the time when academic load may become a family affair.  When and if you help your child with his homework, you’re sure to notice what all this is about.  A two-hour delay between electronic stimulation and bedtime is not a bad idea.   Prior to that, naturally-paced shows, or even those seemingly in slow motion (Mr. Rogers), can offset, or even prevent, the surreal experiences that occur later. (Christakis. 2011)


Garrison MM, Liekweg K, Christakis DA.
Media use and child sleep: the impact of content, timing, and environment.
Pediatrics. 2011 Jul;128(1):29-35.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

Angeline S. Lillard, PhD,  Jennifer Peterson, BA
The Immediate Impact of Different Types of Television on Young Children’s Executive Function
Pediatrics. Published online September 12, 2011   (doi: 10.1542/peds.2010-1919)

Heins E, Seitz C, Schüz J, Toschke AM, Harth K, Letzel S, Böhler E.
Bedtime, television and computer habits of primary school children in Germany. [Article in German]
Gesundheitswesen. 2007 Mar;69(3):151-7.

Oka Y, Suzuki S, Inoue Y.
Bedtime activities, sleep environment, and sleep/wake patterns of Japanese elementary school children.
Behav Sleep Med. 2008;6(4):220-33.

Leeka Kheifets, PhD, Michael Repacholi, PhD, Rick Saunders, PhD, Emilie van Deventer, PhD
The Sensitivity of Children to Electromagnetic Fields
Pediatrics Vol. 116 No. 2 August 1, 2005 pp. e303 -e313

Dimitri A. Christakis
The effects of Fast-Paced cartoons
Pediatrics. 2011; peds. 2011-2071;  Published Online, 12 Sept., 2011

Gröer M, Howell M.
Autonomic and cardiovascular responses of preschool children to television programs.
J Child Adolesc Psychiatr Ment Health Nurs. 1990 Oct-Dec;3(4):134-8.

Christakis DA, Zimmerman FJ, DiGiuseppe DL, McCarty CA.
Early television exposure and subsequent attentional problems in children.
Pediatrics. 2004 Apr;113(4):708-13.

Al-Khlaiwi T, Meo SA.
Association of mobile phone radiation with fatigue, headache, dizziness, tension and sleep disturbance in Saudi population.
Saudi Med J. 2004 Jun;25(6):732-6.

Owens J, Maxim R, McGuinn M, Nobile C, Msall M, Alario A.
Television-viewing habits and sleep disturbance in school children.
Pediatrics. 1999 Sep;104(3):e27.

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

Lack Of Sleep Alters Hormones, Affects Weight

male-sleepySleep disorders are coming under closer scrutiny in a society plagued by their ubiquity, prompted by extraneous and self-induced pressures and obligations.  Discovery of the genetic basis for circadian rhythms has expanded our knowledge of the temporal role of behavior and physiology.  The relationship between sleep deprivation and hormone imbalance is publicized, but disregarded.  That part of the hypothalamus in charge of daily metabolic rhythm is called the suprachiasmatic nucleus, and it controls physical activity and hormone levels, as well as sleep, body temperature, immunity, and digestion.

Sleep deprivation, or even fragmentation, interrupts the machinery that controls energy expenditure and food intake.  A single night of sleep deprivation has been found to increase the risk of obesity by disturbing secretion and function of thyrotropin, cortisol and ghrelin (Benedict. 2011).  Thyrotropin is better known as TSH, the pituitary secretion that regulates the endocrine function of the thyroid gland.   Cortisol is excreted by the adrenal glands to address stress, affecting the metabolism of glucose, protein and fats. Ghrelin regulates appetite by telling you to eat, while its partner, leptin, tells you to stop.  Aberrations of these substances, aggravated by lack of sleep, reduce expenditure of energy during the waking hours.  Because fewer calories are burned, weight gain is almost certain.  Although the mechanisms behind it are not completely understood, “epidemiological evidence indicates that chronic sleep curtailment increases risk of developing obesity.” (Ibid.).

When we run low on energy from lack of sleep, many of us grab a coffee or three and a handful of junk to get a quick fix of comfort food.  That doesn’t last very long, though, does it?  Sleep affects one’s ability to maintain or to lose weight by regulating hormones and metabolism, which includes the way we handle food as part of the range of processes that occur within a living organism.  This entails anabolism (buildup) and catabolism (break down).  Deprivation of sleep is also tied to cardiovascular health and inflammation that is below the radar, called subclinical (Sharma. 2010).

We need about seven and a half hours of sleep each night.  An extra half hour, by the way, won’t help you to lose the last ten pounds.  But moving from five hours to eight might just be able to accomplish that.  It’s all in the hormones.  If you’re sleep-deprived, you have higher levels of ghrelin, telling you to eat.  That means that leptin is in short supply, and you’ll eat more than you need, ending up with more calories in and fewer calories out.  Oops, imbalance.

Apnea, bruxism (teeth grinding), narcolepsy, and insomnia are only a few of the sleep disorders that plague us.  Overcoming these insults can prevent the health conditions that stem from their upswing in modern society.  Besides obesity, impaired glucose tolerance and insulin resistance are real threats.  Losing some sleep for only a single night can upset the apple cart of insulin sensitivity (Donga. 2010).  That may be of significant relevance to a person harboring Type 2 diabetes, and most assuredly will be with Type 1.  What’s interesting is that voluntary sleep deprivation is a characteristic of modern life, where people put more stock into their jobs than into themselves and their families (Bosy-Westphal. 2008).  Here, weight gain from increased energy intake is earned, even without conscious thought.  Once the inborn clock gets out of whack, don’t be surprised by physiological dysregulation of one kind or another (Huang. 2011).

Sleeping as little as possible is not admirable behavior.  High-schoolers and students cramming for college exams are not doing themselves any favors.  Neither is the mom or dad who works into the wee hours, a common activity in industrialized nations.  Since the 90’s, researchers have paralleled sleep deprivation with the rise of obesity, especially in kids (Leproult. 2010) (Knutson. 2008).  Since our hormones vary from day to night, it matters that we keep circadian rhythm aligned with the design of their function.  Shut off the TV and get rid of the computer games at bedtime.  Put the cell phone away while you’re at it.


Benedict C, Hallschmid M, Lassen A, Mahnke C, Schultes B, Schiöth HB, Born J, Lange T.
Acute sleep deprivation reduces energy expenditure in healthy men.
Am J Clin Nutr. 2011 Jun;93(6):1229-36.

Sunil Sharma and Mani Kavuru
Sleep and Metabolism: An Overview
International Journal of Endocrinology. Vol. 2010 (2010), Article ID 270832, 12 pages

Donga E, van Dijk M, van Dijk JG, Biermasz NR, Lammers GJ, van Kralingen KW, Corssmit EP, Romijn JA.
A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects.
J Clin Endocrinol Metab. 2010 Jun;95(6):2963-8.

Bosy-Westphal A, Hinrichs S, Jauch-Chara K, Hitze B, Later W, Wilms B, Settler U, Peters A, Kiosz D, Muller MJ.
Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women.
Obes Facts. 2008;1(5):266-73.

Wenyu Huang, Kathryn Moynihan Ramsey, Biliana Marcheva1,and Joseph Bass
Circadian rhythms, sleep, and metabolism
J Clin Invest. 2011;121(6):2133–2141.

Leproult R, Van Cauter E.
Role of sleep and sleep loss in hormonal release and metabolism.
Endocr Dev. 2010;17:11-21.

Knutson KL, Van Cauter E.
Associations between sleep loss and increased risk of obesity and diabetes.
Ann N Y Acad Sci. 2008;1129:287-304.

Spiegel K, Tasali E, Leproult R, Van Cauter E.
Effects of poor and short sleep on glucose metabolism and obesity risk.
Nat Rev Endocrinol. 2009 May;5(5):253-61.

Morris CJ, Aeschbach D, Scheer FA.
Circadian system, sleep and endocrinology.
Mol Cell Endocrinol. 2011 Sep 10. [Epub ahead of print]

Beccuti G, Pannain S.
Sleep and obesity.
Curr Opin Clin Nutr Metab Care. 2011 Jul;14(4):402-12.

Spiegel K, Leproult R, L’hermite-Balériaux M, Copinschi G, Penev PD, Van Cauter E
Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin.
J Clin Endocrinol Metab. 2004 Nov;89(11):5762-71.

Nedeltcheva AV, Kessler L, Imperial J, Penev PD.
Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance.
J Clin Endocrinol Metab. 2009 Sep;94(9):3242-50. Epub 2009 Jun 30.

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

Brain Fog

red-bow-on-fingerThere is a relationship between central nervous system missteps and markers of inflammation. Age doesn’t matter; it happens across the board. If the occasional bout of forgetfulness strikes you, you might recoil in fear of early-onset dementia, especially if the “occasions” are too close together. Is there anything you can do about this? Could it be something you ate? Maybe it’s something you didn’t eat.

Inflammation is a protective response to injury or destruction of tissue that tries to rid the body of the detrimental agent. The process elevates blood markers that are useful in predicting the onset of chronic conditions, such as diabetes or cardiovascular disease. One of these markers is called homocysteine, an amino acid made from methionine that degrades arterial architecture.  But what of mental lapses?  “Epidemiological studies show a positive, dose-dependent relationship between mild-to-moderate increases in plasma total homocysteine concentrations (Hcy) and the risk of neurodegenerative diseases, such as…cognitive impairment…”  (Herrmann.  2011)  Cognitive impairment is not necessarily a sign of impending dementia or Alzheimer’s disease, but elevated homocysteine is “…a surrogate marker for B vitamin deficiency (folate, B12, B6) and a neurotoxic agent.”  (Ibid.)

If you can provide details about your forgetfulness, you don’t have dementia. If you can recall what you read yesterday about the local political scene, you don’t have dementia. If you forgot where you put the car keys, join the crowd.  Nonetheless, you could have homocysteine levels that are too high for your own good.  It’s recognized that taking classes, doing word puzzles, playing chess, and generally challenging the mind can preserve memory.  But these activities won’t necessarily influence renegade body chemistry. Though conjectural, it has been suggested that inflammation disrupts the integrity of the blood-brain barrier, the highly selective membrane that protects the brain from pathogens in the blood, as well as regulates which molecules can pass between the blood and the cerebral spinal fluid. Inflammation compromises the function of the membrane, allowing large molecules access to the brain, resulting in neuronal damage.  (Stolp. 2009).

Herrmann and Obeid (2011) admit that the prospect of improving any degree of neurological distortion caused by homocysteine can be realized with B vitamins. Parallel independent investigation revealed that women with cognitive abasement had higher Hcy values than women without such a burden, and that the folate (a B vitamin also called B9) levels of the affected cohort were measurably lower.  (Faux. 2011)

Homocysteine can be changed back to methionine under the right conditions, namely in the presence of a methylation molecule, such as folic acid (called folate in food). Folate insufficiency, or outright inadequacy, can initiate mental lapses that could balloon into more serious conditions if deficit is prolonged. Therapeutically, folic acid is able to reduce Hcy and the occurrence of neural tube defects in neonates. A side benefit was observed to be the prevention of cervical dysplasia and protection against neoplasm formation in ulcerative colitis.  (Kelly.  1998) Geriatric scientists had indicted homocysteine as causative of neurobehavioral anomalies across a wide range of cognitive domains (Jyme. 2005), and later identified vitamin B12, vitamin B6, and folate (or folic acid) as ameliorative agents.  (Selhub. 2010)

Homocysteine levels do not always increase because of something we did or ate, but because of something we didn’t eat. That would be the foods providing ample supplies of B12, B6, and folic acid.  Certain chronic and contagious diseases that evoke an inflammatory response, even the flu or seasonal allergies, can bring on a foggy mind. Relieving the cause should bring physical relief, and changing the body chemistry should eliminate the fog. All you need is a cue to help you remember that your sunglasses are sitting above your eyebrows.


Herrmann W, Obeid R.
Homocysteine: a biomarker in neurodegenerative diseases.
Clin Chem Lab Med. 2011 Mar;49(3):435-41.

Stolp HB, Dziegielewska KM.
Review: Role of developmental inflammation and blood-brain barrier dysfunction in neurodevelopmental and neurodegenerative diseases.
Neuropathol Appl Neurobiol. 2009 Apr;35(2):132-46.

Faux NG, Ellis KA, Porter L, Fowler CJ, Laws SM, Martins RN, Pertile KK, Rembach A, et al
Homocysteine, Vitamin B12, and Folic Acid Levels in Alzheimer’s Disease, Mild Cognitive Impairment, and Healthy Elderly: Baseline Characteristics in Subjects of the Australian Imaging Biomarker Lifestyle Study.
J Alzheimers Dis. 2011 Sep 2.

Kelly GS
Folates: supplemental forms and therapeutic applications.
Altern Med Rev. 1998 Jun;3(3):208-20.

Jyme H. Schafer, MD, MPH; Thomas A. Glass, PhD; Karen I. Bolla, PhD; Margaret Mintz, MS; Anne E. Jedlicka, MS; Brian S. Schwartz, MD, MS
Homocysteine and Cognitive Function in a Population-based Study of Older Adults
J Am Geriatr Soc. 2005;53(3):381-388

Selhub J, Troen A, Rosenberg IH.
B vitamins and the aging brain.
Nutr Rev. 2010 Dec;68 Suppl 2:S112-8.

Schulz RJ.
Homocysteine as a biomarker for cognitive dysfunction in the elderly
Curr Opin Clin Nutr Metab Care. 2007 Nov;10(6):718-23.

Aron M. Troen, Melissa Shea-Budgell, Barbara Shukitt-Hale, Donald E. Smith, Jacob Selhub, and Irwin H. Rosenberg
B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice
PNAS August 26, 2008 vol. 105 no. 34 12474-12479

Roberts RO, Geda YE, Knopman DS, Boeve BF, Christianson TJ, Pankratz VS, Kullo IJ, Tangalos EG, Ivnik RJ, Petersen RC.
Association of C-reactive protein with mild cognitive impairment.
Alzheimers Dement. 2009 Sep;5(5):398-405.

Mancinella A, Mancinella M, Carpinteri G, Bellomo A, Fossati C, Gianturco V, Iori A, Ettorre E, Troisi G, Marigliano V.
Is there a relationship between high C-reactive protein (CRP) levels and dementia?
Arch Gerontol Geriatr. 2009;49 Suppl 1:185-94.

Herrmann W
Significance of hyperhomocysteinemia.
Clin Lab. 2006;52(7-8):367-74.

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

Electromagnetic Fields (EMF)

young-businesswomanHave you ever had the feeling that your body, mind and spirit were in three separate places, and that you needed the better part of the day to call them to a serious get-together? How about the nondescript notion that something is amiss, but you can’t quite put your finger on it, and it’s not sufficiently debilitating to see the doctor? You might be living with—or through—electromagnetic sensitivity (ES). What makes this hard to understand is that some scientists and physicians recognize this state as a legitimate concern, while others treat it disdainfully. (Genuis. 2011) Often it is connected to multiple chemical sensitivity (MCS), which is also a controversial diagnosis, despite being recognized by the Social Security Administration and the U.S. Department of Housing and Urban Development as a disabling condition. Too many medical professionals have tried to convince patients that their incapacitation is “in their heads,” or is the manifestation of a “poor attitude.” The sufferers of ES / MCS can conclude that their physicians’ training and education stopped at the medical school portals…narrow door, narrow mind. What worked for medicos a decade ago may not be part of today’s tool kit.

ES is an environmentally-triggered illness that produces symptoms in those exposed to common levels of electromagnetic fields (EMF) from electrical sources in the environment: power lines, motors, computers, trains, stereos, kitchen appliances, electric blankets, cell phones, and more, including the microwave oven. The nervous system is the primary site affected by electromagnetic fields, and those with nervous system damage from prior insult seem predisposed to ES. (Rea. 1991) Persons with chronic fatigue and mercury toxicity (from dental amalgams) are among the more susceptible. Although possibly begotten from other causes, symptoms include fatigue, nausea, headaches, loss of memory and concentration, buzzing ears (tinnitus), skin problems, insomnia, seizures, dizziness, and vague feelings of illness. Because the etiology is evasive, patients may be dismissed as psychosomatic.

One’s exposure to electromagnetic fields (EMF) varies according to occupation, venue, and routine. The general population is likely to see EMF as more invasive than those in occupations that employ electromagnetism regularly, such as radiographers or certain security personnel who work around metal detectors. (van Dongen. 2011) This attitude may be a matter of education, or what some may term selective indoctrination (brainwashing). Perceived health risks, therefore, are subjective. For people suffering ES, a trip to the doctor is akin to jumping from the pan into the fire, since the office is loaded with EMF’s from computers and their monitors, fluorescent lights, and testing equipment. It’s even worse in a hospital. MRI machines and ultrasound sources are especially bothersome. Regular cell phone use, and even wearing one, can contribute to misery. No medicine is available to bring relief…only avoidance, which is practically impossible.

Studies on the effects of EMF on pregnant women have returned mixed results. Group sizes have been too small to be significant; the combined expertise in EMF physics, engineering and reproductive biology has been absent; and the properties of the electromagnetic waves themselves are listed as confounding factors. To some scientists, this sounds more like excuses than truth. But it’s been determined that exposure to “normal” levels of EMF are not harmful to the developing fetus. (Brent. 1993) (Brent. 1999) In this context, “normal” levels of exposure relate to video display terminals. All common EMF sources were reviewed in Italian research, where video display terminals again were exculpated. However, electric blankets, power lines, heated waterbeds, and other sources that directly contact the body or that emit high intensity pulses have been weakly associated with congenital defects and growth retardation. (Luchini. 1992)

Microwave exposure, regardless of source, has been seen to reduce levels of glutathione in the human (and lab animal) body. Glutathione occurs widely in plant and animal tissue, where it plays a role in cellular respiration and serves as a cofactor for several enzymes. It’s best known as the prime protector against oxidative stress where, for example, it protects red blood cells against the toxic hydrogen peroxide that results from certain metabolic activities. Furthermore, such exposure leads to the overproduction of reactive oxygen species and the inhibition of protective enzymes and hormones (Kesari. December, 2011), such as melatonin, the hormone that regulates sleep, mood, and even ovarian cycles, and may be protective against cancer. (Kesari. November, 2011) These studies focused on 2.45 GHz microwave radiation, that which comes from microwave ovens, radio-controlled toys, and some phone systems. The EMF’s found in parts of the house where FM radios, blue tooth and television sets are common are often very low, sometimes not measurable. (Breckenkamp. 2011)

There are no objective tests to diagnose ES, but there have been enough subjective reports to warrant a closer look. Some people are bothered only when devices are put through on-off cycles; others all the time, reporting constant headaches, muscle twitches and even skipped heartbeats. (McCarthy. 2011) As luck would have it, it’s hard to duplicate most symptoms in a blinded laboratory setting, leading investigators to question biophysical hypersensitivy without completely denying its existence. (Rubin. 2005) One symptom that appears often is tinnitus—ringing in the ears. More than half the subjects with self-reported EMS experience this, adding that it disrupts sleep and work. Individual use of a cell phone has been excused from tinnitus causation in at least one report. (Landgrebe. 2009)

But that does not excuse cell phones from all purported debilitations. Memory function was impaired in laboratory animals exposed to cell phone radiation for as little as two hours a week for almost a year. But these creatures are considerably smaller than an adult human, so interpretation of the results calls for a light touch. (Nittby. 2008) Pulsed EMF, which results from storage and sudden release of energy, may have adverse effects on neuronal function, as determined by German studies on subjects whose auditory discrimination tasks suffered following exposure. The ensuing recommendation of these investigators is to remove cell phones from children, the elderly, and the sick. (Maier. 2004)

As research gains momentum and relates EMF’s to a multitude of ills, including Alzheimer’s disease, impaired red blood cell flow and conditions of lesser chronicity, we may come to realize that progress has more take than give. People react to some frequencies more than to others, but not all people respond the same way. Altering an environment to accommodate all comers is neither feasible nor likely. That means taking matters into one’s own hands. There is little room to get into the physics of EMF, but suffice it to say that 2.5 mG (milligauss) is close to the tolerable limit of exposure, though no RDA has been set. Most states in the U.S. have adopted a 3.0 mG cutoff, though some researchers prefer 1.0. The EPA says 1.0 mG, which agrees with Sweden. The Russians view .001 mG as enough. Protecting yourself is as simple as turning off the electric blanket before getting into bed, shutting off the TV and computer monitor when not using them, stepping away from the microwave while it’s on, eschewing fluorescent lamps where possible, testing appliances with a handheld meter before purchasing, and fighting the power company that wants to put high tension wires in your neighborhood. If you own a gauss meter, look for a level of 0.5 mG in your home. That’s where you put your pillow. Of course, you may not be a victim of electromagnetic sensitivity. You might be interested in, where Dr. David Carpenter, noted EMF researcher, looks at high-voltage power lines.


Aalto S, Haarala C, Brück A, Sipilä H, Hämäläinen H, Rinne JO.
Mobile phone affects cerebral blood flow in humans.
J Cereb Blood Flow Metab. 2006 Jul;26(7):885-90.

Breckenkamp J, Blettner M, Schüz J, Bornkessel C, Schmiedel S, Schlehofer B, Berg-Beckhoff G.
Residential characteristics and radiofrequency electromagnetic field exposures from bedroom measurements in Germany.
Radiat Environ Biophys. 2011 Oct 1.

Brent RL, Gordon WE, Bennett WR, Beckman DA.
Reproductive and teratologic effects of electromagnetic fields.
Reprod Toxicol. 1993 Nov-Dec;7(6):535-80.

Brent RL
Reproductive and teratologic effects of low-frequency electromagnetic fields: a review of in vivo and in vitro studies using animal models.
Teratology. 1999 Apr;59(4):261-86.

Cao Z, Liu J, Li S, Zhao X.
Effects of electromagnetic radiation from handsets of cellular telephone on neurobehavioral function.
Wei Sheng Yan Jiu. 2000 Mar 30;29(2):102-3.

Eulitz C, Ullsperger P, Freude G, Elbert T.
Mobile phones modulate response patterns of human brain activity.
Neuroreport. 1998 Oct 5;9(14):3229-32.

Feychting M, Jonsson F, Pedersen NL, Ahlbom A.
Occupational magnetic field exposure and neurodegenerative disease.
Epidemiology. 2003 Jul;14(4):413-9; discussion 427-8.

Genuis SJ, Lipp CT.
Electromagnetic hypersensitivity: Fact or fiction?
Sci Total Environ. 2011 Dec 5.

International Commission on Non-Ionizing Radiation Protection
Health Physics. 97(3):257-258, September 2009.
doi: 10.1097/HP.0b013e3181aff9db

Kesari KK, Behari J, Kumar S.
Mutagenic response of 2.45 GHz radiation exposure on rat brain.
Int J Radiat Biol. 2010 Apr;86(4):334-43.

Kesari KK, Kumar S, Behari J.
Pathophysiology of Microwave Radiation: Effect on Rat Brain.
Appl Biochem Biotechnol. 2011 Nov 29.

Kesari KK, Kumar S, Behari J.
900-MHz microwave radiation promotes oxidation in rat brain.
Electromagn Biol Med. 2011 Dec;30(4):219-34.

Michael Landgrebe, Ulrich Frick, Simone Hauser, Goeran Hajak, Berthold Langguth
Association of Tinnitus and Electromagnetic Hypersensitivity: Hints for a Shared Pathophysiology?
PLoS ONE 4(3): e5026. March 27, 2009

Levallois P, Neutra R, Lee G, Hristova L.
Study of self-reported hypersensitivity to electromagnetic fields in California.
Environ Health Perspect. 2002 Aug;110 Suppl 4:619-23.

Luchini L, Parazzini F.
Exposure to low-frequency electromagnetic fields and pregnancy outcome: a review of the literature with particular attention to exposure to video terminals.
Ann Ostet Ginecol Med Perinat. 1992 Mar-Apr;113(2):102-13.

Maier R, Greter SE, Maier N.
Effects of pulsed electromagnetic fields on cognitive processes – a pilot study on pulsed field interference with cognitive regeneration.
Acta Neurol Scand. 2004 Jul;110(1):46-52.

McCarty DE, Carrubba S, Chesson AL, Frilot C, Gonzalez-Toledo E, Marino AA.
Electromagnetic hypersensitivity: evidence for a novel neurological syndrome.
Int J Neurosci. 2011 Dec;121(12):670-6.

Nittby H, Grafström G, Tian DP, Malmgren L, Brun A, Persson BR, Salford LG, Eberhardt J.
Cognitive impairment in rats after long-term exposure to GSM-900 mobile phone radiation.
Bioelectromagnetics. 2008 Apr;29(3):219-32.

William J. Rea, MD, FACS, Yaqin Pan, MD, et al
Electromagnetic Field Sensitivity
Journal of Bioelectricity, 1991; 10(1&2), 241-256.

Röösli M, Moser M, Baldinini Y, Meier M, Braun-Fahrländer C.
Symptoms of ill health ascribed to electromagnetic field exposure–a questionnaire survey.
Int J Hyg Environ Health. 2004 Feb;207(2):141-50.

Rubin GJ, Das Munshi J, Wessely S.
Electromagnetic hypersensitivity: a systematic review of provocation studies.
Psychosom Med. 2005 Mar-Apr;67(2):224-32.

Tynes T, Klaeboe L, Haldorsen T.
Residential and occupational exposure to 50 Hz magnetic fields and malignant melanoma: a population based study.
Occup Environ Med. 2003 May;60(5):343-7.

van Dongen D, Smid T, Timmermans DR.
Perception of health risks of electromagnetic fields by MRI radiographers and airport security officers compared to the general Dutch working population: a cross sectional analysis.
Environ Health. 2011 Nov 9;10(1):95.

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

Cell Phone Radio Frequency And Child Behavior

Radiation-Cell-phoneUntil we’ve mastered the art of telepathy as a means of universal communication, we’re stuck with the cell phone and all that it brings to the table, some of which can be anticipated, like the bill at the end of the month, and some that can’t be expected, like the radio frequency radiation that is alleged to change your unborn child from Mother Teresa to Attila the Hun. Funny thing about science, there’s a study for everything, except for why the eye of a needle is not at the other end.

It has been assumed that using a cell phone in front of your unborn child will render cerebral changes in him/her that will eventuate into attention deficit and hyperactivity. Such is the conclusion of a group of Yale School of Medicine researchers who worked with mice. The authors of this study noted an increase of neurobehavioral disorders in children and decided to look for a cause. To be fair to researchers, mice are used in the laboratory because some of their metabolic characteristics parallel those of humans, and because they mature quickly enough to track their development in a reasonable time span. They also share 99% of their genes with humans.

In this experiment, pregnant mice were exposed to an activated, but muted, cell phone suspended above their cage, while a pregnant control group was exposed to a deactivated phone. As adults, those mice subjected to cell phone radiation as fetuses tended to be more hyperactive and had reduced memory capacity compared to the controls. The outcome was attributed to dose-responsive impaired glutamatergic synaptic transmission onto layer V pyramidal neurons of the prefrontal cortex. Got it?  Not exactly a topic at your next cocktail party, this scientific crooning means that the neurological wires in the front part of the brain don’t develop the right way. This is the section of the brain in charge of complex cognitive behaviors, personality expression, decision making and social behavior.  Like other pronouncements in the research world, “further experiments are needed…to determine the risk of exposure during pregnancy.”  (Aldad, 2012)

Rodent pregnancies typically last fewer than three weeks, and the brains of newborn mice are far less developed than those of human babies. Despite the findings, potential risks in humans might not be similar. However, in human studies done in Germany, scientists found that about 6% of children who were exposed to radio-frequency electromagnetic fields at any time in their existence exhibited “abnormal mental behavior.”  Here, too, “more studies…are warranted…”  (Thomas, 2010)

If a definitive case can be made for the hazard of cell phone radiation, it’ll certainly be a major public health concern. But a trend in this direction might have been established in a Danish study that recruited the cell-phone-using mothers of more than 13,000 children. The mothers were enrolled early in their pregnancies, and seven years later were asked to submit a subjective questionnaire regarding the current health and behavior status of their school-aged children. Those children who had prenatal or postnatal exposure to cell phone use demonstrated greater association with behavioral difficulties and hyperactivity. (Divan, 2008)  Other, confounding, factors may have come into play, though, including diet, lifestyle and permissiveness, exposure to environmental contaminants such as heavy metals, and genetics. Cognitive and language development seem not to be affected by cell phones, as evidenced in a subsequent study by the same research team. (Divan, 2011)

Repeatability is characteristic of a well-constructed study. To ascertain the results of their 2008 report, Divan and colleagues duplicated that work, but with more than twice the number of subjects and the consideration of the confounders. The findings were the same:  prenatal and postnatal cell phone use is associated with behavior problems in school-aged children. (Divan, 2010)  To confuse the issue, Spanish researchers found little evidence of abnormal neurodevelopment in a prenatal group exposed to cell phone radiation when tested at 14-months of age and compared to a group of nonusers. (Vrijheid, 2010)  What seems to be needed is a longitudinal study, one that tracks the development of, and tests, the same group of users and nonusers over a period of time, maybe ten or more years.

If the results of a ten-year study were absolutely definitive of cell phone culpability, it’s unlikely that patterns of cell phone use would change, despite a risk of uncomfortable child behavior. Returning to the dark ages of landlines is unthinkable. Besides, in a few years the problem will belong to somebody else. What self-respecting parent would sacrifice immediate convenience for the future?


Divan HA, Kheifets L, Obel C, Olsen J.
Prenatal and postnatal exposure to cell phone use and behavioral problems in children.
Epidemiology. 2008 Jul;19(4):523-9.

Divan HA, Kheifets L, Obel C, Olsen J.
Cell phone use and behavioural problems in young children.
J Epidemiol Community Health. 2010 Dec 7. [Epub ahead of print]

Divan HA, Kheifets L, Olsen J.
Prenatal cell phone use and developmental milestone delays among infants.
Scand J Work Environ Health. 2011 Jul;37(4):341-8. doi: 10.5271/sjweh.3157. Epub 2011 Mar 14.

Tamir S. Aldad, Geliang Gan, Xiao-Bing Gao, & Hugh S. Taylor
Fetal Radiofrequency Radiation Exposure From 800-1900 Mhz-Rated Cellular Telephones Affects Neurodevelopment and Behavior in Mice
Scientific Reports. Volume:2 ,Article number:312  doi:10.1038/srep00312  15 March 2012

Thomas S, Heinrich S, von Kries R, Radon K.
Exposure to radio-frequency electromagnetic fields and behavioural problems in Bavarian children and adolescents.
Eur J Epidemiol. 2010 Feb;25(2):135-41. Epub 2009 Dec 4.

Vrijheid M, Martinez D, Forns J, Guxens M, Julvez J, Ferrer M, Sunyer J.
Prenatal exposure to cell phone use and neurodevelopment at 14 months.
Epidemiology. 2010 Mar;21(2):259-62.

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

Low Cholesterol And Mental Health

sad-eggsIf mental health is defined as a state of emotional and psychological well-being in which an individual is able to use his or her cognitive and emotional capabilities, function in society, and meet the ordinary demands of everyday life, then we need to take care of the garage in which this vehicle is kept.  Measures of depression and anxiety assess things such as self-disparagement, pessimism, lack of drive, apprehension, inability to relax, and irritability, to name a few.  Interestingly, these evaluations have demonstrated a relationship to low lipid and lipoprotein concentrations.

In work done at the end of the last century, an inverse association between mental challenges and total cholesterol and lipids was found.  That means when one goes up, the other goes down.  Testing young adult females, Duke University Medical Center discovered that women “…with low total cholesterol concentrations (<4.14 mmol/liter) relative to those with moderate to high cholesterol levels, were more likely to have higher scores on the NEO depression subscale…and anxiety subscale…” after adjustments were made for age, body mass index, oral contraceptive use and physical activity.  (Suarez.  1999)

Before we got too involved, it pays to know that 4.14 mmol/liter is equal to a cholesterol level of 160 mg/dL, or just plain 160.  Cholesterol is a steroid substance necessary to human life.  It forms the cell membranes in all organs and tissues of the body, is essential to the production of the hormones we need for growth, development, and reproduction, and it makes the bile acids necessary for absorption of nutrients.  Very little, if any, dietary cholesterol becomes serum cholesterol.

Back in the 1990’s it was noted that cholesterol levels below 160 were tied to excess mortality from all causes, primarily from a variety of cancers, respiratory and digestive diseases, and violent deaths from suicide and trauma.  Reasons behind low cholesterol have been ascribed to genetics, resistance to dietary sources, acute infections, and alcohol use/abuse.  (Meilahn.  1995)  If suicide is tied to depression, then it may be a legitimate effect.  Depression is twice as common among women as men, with about one in four suffering at some point in her lifetime.  The greatest vulnerability appears during the childbearing years, the time when its diagnosis is often overlooked.  The turbulence of hormones flooding a woman’s system at different times and in differing amounts can surely be a potent stressor.

Scientists in Barcelona, Spain, realized the connection of cholesterol to neuropsychiatric disease in a review of related literature that preceded their interest.  They found a link to early death, suicide and aggression, and personality disorders and dementia. (Martinez-Carpio.  2009). It appears that the good intentions of reducing what was thought to be the cause of cardiac mortality opened a different can of worms.  The Japanese explored the intrigue that was sparked when total mortality was not reduced despite reduction of mortality due to coronary heart disease, and found an increase in death rates due to suicide and accidents, many of which were tied to risky behaviors in persons with low cholesterol levels.  (Kunugi.  2001)  Does low cholesterol compromise judgment?  The U. of California conducted trials in the early 90’s to determine the cause behind the rise in suicides in men older than fifty years, and found that depression was three times more prevalent in those whose cholesterol was lower than 160.  Health status, number of chronic diseases, number of medications, and exercise seemed not to have had an adverse effect on depressive signs and symptoms. This led to the suggestion that the intentional lowering of cholesterol be more deliberate.  (Morgan. 1993)

Cedars-Sinai Medical Center, in Los Angeles, reported that serotonin, a neurotransmitter that controls impulsive behaviors, is tied to cholesterol levels at the synapses.  Low membrane cholesterol decreases the number of serotonin receptors, thereby reducing suppression of aggressive and destructive behaviors.  (Engelberg. 1992)  That magic number, 160, once again made headlines in the Netherlands, where epidemiologists discovered a higher prevalence of depression in males whose cholesterol was below that level.  (Steegmans. 2000)  Low cholesterol was cited as causative to rises in criminal violence in Sweden, following the association of reduced cholesterol values to low serotonin activity. (Golomb. 2000)  Reduced levels of total cholesterol, LDL, and HDL resulted in minimized serotonin values in personality disordered cocaine users, as reported by addiction researchers in their journal. (Buydens-Branchey. 2000)  In school-aged children, those with cholesterol values lower than 145 were three times more likely to have been suspended or expelled from school.  This is an absolute consideration, and has nothing to do with socio-economic status or ethnic background, nor with nutrition status or academic achievement.  (Zhang. 2005)

Life is supposed to be a balancing act.  Lots of us overdo something.  The balance between total cholesterol and HDL can allay fears of cardiovascular disease, despite cholesterol in the 200 range.  Cholesterol levels below 170 can make us irritable…and irritating.


Suarez EC.
Relations of trait depression and anxiety to low lipid and lipoprotein concentrations in healthy young adult women.
Psychosom Med. 1999 May-Jun;61(3):273-9.

Elaine N. Meilahn, MD
Low Serum Cholesterol  Hazardous to Health?
Circulation. 1995;92:2365-2366

Martínez-Carpio PA, Barba J, Bedoya-Del Campillo A.
[Relation between cholesterol levels and neuropsychiatric disorders].  [Article in Spanish]
Rev Neurol. 2009 Mar 1-15;48(5):261-4.

Kunugi H.
[Low serum cholesterol and suicidal behavior].  [Article in Japanese]
Nihon Rinsho. 2001 Aug;59(8):1599-604.

Morgan RE, Palinkas LA, Barrett-Connor EL, Wingard DL.
Plasma cholesterol and depressive symptoms in older men.
Lancet. 1993 Jan 9;341(8837):75-9.

Engelberg H.
Low serum cholesterol and suicide.
Lancet. 1992 Mar 21;339(8795):727-9.

Paul H. A. Steegmans, MD, Arno W. Hoes, MD, PhD, Annette A. A. Bak, MD, PhD, Emiel van der Does, MD, PhD and Diederick E. Grobbee, MD, PhD
Higher Prevalence of Depressive Symptoms in Middle-Aged Men With Low Serum Cholesterol Levels
Psychosomatic Medicine 62:205-211 (2000)

Beatrice A Golomb, Håkan Stattin, Sarnoff Mednick
Low cholesterol and violent crime
Journal of Psychiatric Research. Volume 34, Issue 4 , Pages 301-309, July 2000

Laure Buydens-Branchey, Marc Branchey, Jeffrey Hudson, Paul Fergeson
Low HDL cholesterol, aggression and altered central serotonergic activity
Psychiatry Research. Volume 93, Issue 2 , Pages 93-102, 6 March 2000

Zhang J, Muldoon MF, McKeown RE, Cuffe SP
Association of serum cholesterol and history of school suspension among school-age children and adolescents in the United States.
Am J Epidemiol 2005; 161:691-9.

Scanlon SM, Williams DC, Schloss P.
Membrane cholesterol modulates serotonin transporter activity
Biochemistry. 2001 Sep 4;40(35):10507-13.

Laure Buydens-Branchey,a Marc Branchey,a and Joseph R. Hibbelnb
Prog Neuropsychopharmacol Biol Psychiatry. 2008 February 15; 32(2): 568–575.

Essential fatty acids and mental health
The British Journal of Psychiatry (2005) 186: 275-277

Hillbrand M, Waite BM, Miller DS, Spitz RT, Lingswiler VM
Serum cholesterol concentrations and mood states in violent psychiatric patients: an experience sampling study.
J Behav Med 2000; 23:519-29.

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

Food Coloring And Behavior

food-coloringListen to a lie long enough and you’ll start to accept it as the truth. Didn’t the tobacco industry use images of physicians and athletes to sell cigarettes back in the last century? Babe Ruth hawked White Owl cigars and Raleigh cigarettes. William Bendix sold Chesterfield. The highly-trusted and unquestionably credible FDA had a meeting last March to discuss the properties of artificial food colorings and evaluate their relationship to hyperactivity in children. Based on their review of the published data, “FDA concludes that a causal relationship between exposure to color additives and hyperactivity in children in the general population has not been established.” For certain susceptible children, however, they admit their condition “may be exacerbated by exposure to a number of substances in food, including, but not limited to, synthetic color additives.”

The toxicity potential of synthetic food additives is hard to pin down. Just because a single substance demonstrates no harmful effects doesn’t explain what happens when it’s combined with another “harmless” substance.  Many foods contain more than one colorant. An example of single-substance safety is ammonia. Used with adequate ventilation it’s a relatively harmless cleaner unless abused.  The same for chlorine bleach.  But mix the two and you get a toxic gas, hydrazine, used to make rocket fuel.  That’ll clean the scum off the shower walls!   With the amount of adverse publicity about artificial colorings, you’d think the makers would look for something more natural, like beets.

Companies use artificial colors to make their products look pretty.  Foods with vibrant, saturated colors are more appealing than those without.  Hot dogs are naturally gray.  When’s the last time you saw one?  The color of a food tells us that it has value.  Red apples are more valued than green ones.  The natural medicines in foods are colorful.  Beta-carotene is associated with yellow and orange; anthocyanins with red and purple.  Even purple cabbage has its fans.  Some oranges don’t turn that color unless growing conditions are perfect: cool nights, warm days.  Many folks won’t buy green oranges from Florida, so what’s the broker to do?  Spray ‘em orange.  Now the mind is fooled into thinking this orange is healthier than the blotchy one next to it.

Most studies on food additives last for too short a time to render meaningful results.  A comet assay is a sensitive but uncomplicated testing procedure that detects DNA damage at the level of the cell.  Using this procedure, scientists at Japan’s Laboratory of Genotoxicity at Hachinohe National College found that, of the types of food additives, dyes are most genotoxic.  Dose-related DNA damage from commonly-used food dyes was found in the stomach, colon, and bladder of test animals, with colon damage appearing at doses close to the acceptable daily intake.  (Sasaki. 2002) (Tsuda. 2001)

Coal tar and petrochemicals are the main sources of the artificial colors that go into our foods, and these are ultimately dangerous to our health.  It makes little sense to put these into our food supply if we’re not designed to ingest them in the first place.  But selling products and making money are the bottom line.  Without at least a little prior knowledge, the unsuspecting consumer would never know that yellow #5 is cleverly disguised by its chemical name, tartrazine, sometimes called E102.  If mixed with blue #1, called E133, it makes green. Blue #1 may contain aluminum, although potassium and calcium salts are more common.  Most of E133 ends up in the feces, which could be green.  Tartrazine has provoked allergic reactions in sensitive persons, but you never know who that is until it happens, and most of us never make a connection.  (Kashanian. 2011)  To its credit, the FDA will seize products that do not declare the presence of tartrazine, which also is alleged to exacerbate asthma symptoms.  There is a blue #2, but it’s seldom used in foods because it fades at alkali pH.  Its use in snacks and candies may evoke a hyperactivity reaction.

Red #40 is an azo dye, meaning that it contains two nitrogens.  It’s also known as allura red or E129.  Originally made from coal tar, red #40 is now made from petroleum.  Isn’t that a comfort?  Contrary to popular misconception, it is not made from insects.  Carmine is, made from the female cochineal insect, whose body is dried and pulverized or otherwise processed.  From intensive European studies it was concluded that behavioral anomalies in children arise especially when the blues and the reds are combined with benzoate preservatives.  (McCann. 2007)  Red #3 is called erythrosine, E127, and is not that common in the U.S., having been replaced by #40.  Number 3 was found to be a potent inhibitor of a substance that blocks and destroys cancer cells, named tumor necrosis factor.  So, while some research says it may not directly cause cancer, red #3 interferes with the body’s protection against it, while simultaneously showing cytotoxicity, particularly to breast tissue.  (Ganesan. 2011) (Dees. 1997)

Why take the chance when there are natural colorants?  Read the labels.  Sweets and sports drinks, blueberry muffins and cereals with “fruits,” yogurt and canned icing could give you more than you bargained for.  Caramel coloring from sugar, annatto red-orange from achiote, chlorophyll green, turmeric yellow, paprika red, elderberry purple, butterfly pea blue, beet red, and blue from red cabbage are real.

Olsson Frank Weeda Terman Bode Matz PC;  Attorneys at Law;  Suite 400; 1400 Sixteenth Street, NW; Washington, D.C. 20036

Sasaki YF, Kawaguchi S, Kamaya A, Ohshita M, Kabasawa K, Iwama K, Taniguchi K, Tsuda S
The comet assay with 8 mouse organs: results with 39 currently used food additives.
Mutat Res. 2002 Aug 26;519(1-2):103-19.

Tsuda S, Murakami M, Matsusaka N, Kano K, Taniguchi K, Sasaki YF.
DNA damage induced by red food dyes orally administered to pregnant and male mice.
Toxicol Sci. 2001 May;61(1):92-9.

Kashanian S, Zeidali SH.
DNA binding studies of tartrazine food additive.
DNA Cell Biol. 2011 Jul;30(7):499-505.

McCann D, Barrett A, Cooper A, Crumpler D, Dalen L, Grimshaw K, Kitchin E, Lok K, Porteous L, Prince E, Sonuga-Barke E, Warner JO, Stevenson J.
Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomised, double-blinded, placebo-controlled trial.
Lancet. 2007 Nov 3;370(9598):1560-7.

Ganesan L, Margolles-Clark E, Song Y, Buchwald P.
The food colorant erythrosine is a promiscuous protein-protein interaction inhibitor.
Biochem Pharmacol. 2011 Mar 15;81(6):810-8.

Dees C, Askari M, Garrett S, Gehrs K, Henley D, Ardies CM.
Estrogenic and DNA-damaging activity of Red No. 3 in human breast cancer cells.
Environ Health Perspect. 1997 Apr;105 Suppl 3:625-32.

Shimada C, Kano K, Sasaki YF, Sato I, Tsudua S.
Differential colon DNA damage induced by azo food additives between rats and mice.
J Toxicol Sci. 2010 Aug;35(4):547-54.

Shaw DW.
Allergic contact dermatitis from carmine.
Dermatitis. 2009 Oct;20(5):292-5.

*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.


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.
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.
Science. 1939 Apr 7;89(2310):322-3.

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.