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Orthomolecular Treatment of Mood and Behavior Disorders (PART TWO):  Under-Methylated Kids and Kids with Heavy Metals 

[Parts Three to Five of this series will cover Magnesium & Calcium Deficient Kids, Kids with Thyroid/Adrenal Imbalances, B6 and Zinc Deficient Kids, Hypoglycemic Kids, EFA Deficient Kids, Protein-Deficient Kids, Kids with Food Sensitivities, and Vitamin B3 and C Deficient adolescents (as seen in early-onset first-episode schizophrenia).]


Under-Methylated Kids

The brain requires efficient methylation status to form neurotransmitters on demand.  Methylation is a basic chemical reaction involving among other things, neurotransmitter manufacturing at the DNA promoter region.2  Poor methylation status is quite common in mood and behavior disorders.2-5  The under-methylated syndrome can be considered a neurotransmitter deficient syndrome.

In our clinic, we see a good portion of mood and behavior disorder kids with methylation compromise as indicated by elevated fasting homocysteine levels.  In mood and behavior disorders, researchers are aware that certain brain tracts are overstimulated while others are understimulated.  Every kid is different and some are low in serotonin versus the catecholamines (dopamine, norepinephrine, epinephrine), and vice versa.  If kids are methylating efficiently, they have the machinery to form neurotransmitters in brain areas that are underproducing and neurotransmitter deficient.

Orthomolecular treatment with B12, folic acid, and other methyl donor nutrients (TMG, etc.) can restore methylation status.5  Methyl donor treatment respects the brain’s innate ability to ‘decide’ what specific pathways need more neurotransmitter.  This “innate specificity” contrasts with conventional medication whose influence on given brain pathways is fixed and potentially off-target.  The off-target lack of specificity of medication can also cause side-effects.

In mood and behavior disorders, investigators have found genetic polymorphisms that disrupt folic acid pathways.6  These patients have a greater need for folic acid supplementation.  High homocysteine levels are an excellent indication of B12 and folic acid deficiency status.7  Depressed patients with low folic acid levels that do not respond well to anti-depressants often improve significantly with folic acid supplementation.  That being said, in clinical practice many practitioners including myself are observing greater dominancy of B12 versus folic acid deficient lab findings.  High B12 levels are associated with improved outcome in depression.  B12 and folic acid deficiencies can start early in childhood and significantly influence cognition.


Kids with Heavy Metals

It is not uncommon to see kid’s with mood or behavior disorders having mild to toxic levels of lead, mercury, aluminum, and copper.  Most heavy metals are free radicals that induce oxidative stress (lipid peroxidation) and have a direct affinity for brain tissue.9,10  Heavy metal free-radicals therefore have the ability to compromise brain tissue structure and metabolism.  Toxic metal imbalances are associated with mood and behavior disorders.11-13

Heavy metals make the body’s metal removing protein, metallothionein, work hard to excrete them.11,14,15  In the process of ridding heavy metals, this protein loses zinc which further compromises the ability to transcribe brain proteins (the initial manufacturing step), including neurotransmitters.  Zinc deficiency is a well know condition associated with central nervous system disorders and mental health compromise.

Although the exposure to external sources of a heavy metal may be similar for all siblings, those that have slower metabolic functions (which can be triggered life stress or viral illness, etc.) might retain ‘normal’ amounts of environmental metal that other siblings with faster more efficient metabolisms would readily eliminate.

If you are a city dweller, you have been exposed to lead.

Lead exposure in kids most often occurs by orally absorbing lead containing dust from old paint or dirt debris from city air or, from drinking water from water pipes that are lead lined or soldered.  Lead is found in paints, glass, batteries, rust protectants, alloys, and old bathtubs.  Lead can also be found in hobby materials including stained glass, paint, solder and fishing weights.  The extent for damage by lead for any child is unpredictable but lead toxicity in kids is associated with learning and behavior problems.  Lead levels can be toxic to patients with behavior dysfunction, mood disorder, insomnia, and immune compromise.16  Lead toxicity readily disrupts opiod neurotransmitter pathways and neurohormonal function.13  The opioid system has physiological role in the regulation of mood and stress responses, pain, locomotion, thermoregulation, respiration, diuresis, cardiovascular function, and digestion.  Lead has a negative effect on verbal memory and motor movement.17  Lead’s antagonism with calcium interferes with neurotransmitter release, second messenger systems, calcium channel transport, and mitochondrial uptake.15  Lead toxicity is more common in iron deficient kids and iron deficiency is not uncommon in young males and females.

Mercury can be toxic to kids with mood and behavior disorders, nervous irritability, and memory decline.16

Lab results occasionally confirm mercury toxicity in kids.  Mercury toxicity is associated with reduced neuronal uptake of dopamine and norepinephrine.18  Mercury is found in dental fillings, flourescents, vaccines, thermometers, fish, animals, and plants. Selenium is useful in combating mercury toxicity.15

Aluminum can be toxic in kids with mood and behavior disorders and, digestive pathologies.

Aluminum sources include aluminum cookware (especially when you heat and deglaze with an acid like vinegar or wine), drinking boxes, processed cheese, deoderants, and drinking water.16,19  Aluminum is more soluble in our acidic magnesium deficient drinking water.

Copper toxicity is prevalent in behavior disorders, depression, and anxiety.12,16,20,21

Copper toxicity is routinely found in kid’s lab results.  [That being said, copper deficiency is also quite common perhaps due to an emerging copper deficient food supply; this stresses the need for orthomolecular treatment balance; copper deficiency is commonly seen in poorly motivated kids.]  Copper’s role in the formation of oxidized serotonin intermediates might play a role in altering mood, behavior and sleep quality.12  It seems that serotonin’s opposing neurotransmitter system, the catecholamine system (dopamine, nor-epienephrine, epinephrine), is elevated in copper toxicity.  Copper excess causes dopamine levels to rise because copper is a cofactor of dopamine synthesis.  Copper can therefore over-stimulate the brain and paranoia is also associated with copper elevation.  

In ADHD and learning disability, we might see right brain copper dominance which is associated with visuo-spatial creativity; conversely, left brain dominance is associated with the verbal-analytical intellectual skills highly regarded in schools for evaluating academic performance.  

Blood estrogen levels rise when copper is in excess and may be associated with female hormonal depression.22  Copper toxic patients typically have adrenal and thyroid compromise which encourages copper retention.  Niacin, vitamin C, and zinc are important nutrients in copper toxic kids because they are physiologically antagonistic to copper.  Copper is abundant in food and water as it is found in soil, pesticides, and animal feed.  Since World War II we have been exposed to greater levels of copper due to copper piping implemented in modern homes and, due to widespread use of birth control pills (estrogen) which maintain high systemic copper levels that are thought to transfer via placenta, from generation to generation.  Other sources of copper include copper tea pots, copper sulphate treated jacuzzi’s or swimming pools, drinking water, and prenatal vitamins.  Drugs such as neuroleptics, antibiotics, antacids, cortisone, Tagamet®, Zantac®, and diuretics can exacerbate copper overload.

Orthomolecular medicine can be used to eliminate heavy metals.  In most cases, the elimination of metal toxins must be done gradually to avoid the excessive spill-over of toxins to the bloodstream; metals that are mobilized in the bloodstream need to be eliminated efficiently and this job falls on the liver, kidney, and bowel.  In clinical practice, we support the thyroid, adrenal, liver, kidney, and bowel to maximize the efficient removal of the metal via primary gastro-intestinal and biliary routes.  Kids with toxic metals need to avoid environmental exposures which include sources of metal ingested daily in our food supply.

Part Three of this Kid-Specific series on the orthomolecular treatment of mood and behavior disorders will cover Magnesium & Calcium Deficient Kids and Kids with Thyroid/Adrenal Imbalances. 


2. Shelton RC: The molecular neurobiology of depression. Psychiatr Clin North Am. 2007 Mar; 30(1): 1-11.

3. Herrmann W, Lorenzl S, Obeid R: [Review of the role of hyperhomocysteinemia and B-vitamin deficiency in neurological and psychiatric disorders–current evidence and preliminary recommendations]. Fortschr Neurol Psychiatr. 2007 Sep; 75(9): 515-27. (abstract only)

4. Herrmann W, Obeid R. Review: Biomarkers of folate and vitamin B(12) status in cerebrospinal fluid. Clin Chem Lab Med. 2007 Sep 24. (abstract only)

5. Bottiglieri T: Homocysteine and folate metabolism in depression. Prog Neuropsychopharmacol Biol Psychiatry. 2005 Sep; 29(7): 1103-12.

6. Gilbody S, Lewis S, Lightfoot T: Methylenetetrahydrofolate reductase (MTHFR) genetic polymorphisms and psychiatric disorders: a HuGE review. Am J Epidemiol. 2007 Jan 1; 165(1): 1-13.

7. Coppen A, Bolander-Gouaille C: Treatment of depression: time to consider folic acid and vitamin B12. J Psychopharmacol. 2005 Jan; 19(1): 59-65.

8. Strand et. al.: Cobalamin and folate status predicts mental development scores in North Indian children 12-18 mo. of age.

Am J Clin Nutr, 2013; 97(2): 310-317.

9. Kelly G: Peripheral Metabolism of Thyroid Hormones: A Review. Alternative Medicine Review, 2000; 5(4): 306-333.

10. Aschner M, Cherian MG, Klaassen CD, et al: Metallothioneins in brain–the role in physiology and pathology. Toxicol Appl Pharmacol, 1997; 142(2): 229-242.

11. Stanley PC, Wakwe VC: Toxic trace metals in the mentally ill patients. Niger Postgrad Med J. 2002 Dec; 9(4): 199-204.

12. Jones CE, Underwood CK, Coulson EJ, et al: Copper induced oxidation of serotonin: analysis of products and toxicity. J Neurochem, 2007 Aug; 102(4): 1035-1043.

13. Kitchen I: Lead toxicity and alterations in opioid systems. Neurotoxicology, 1993 Summer-Fall; 14(2-3): 115-124.

14. Cai L, Li XK, Song Y, Cherian MG: Essentiality, toxicology and chelation therapy of zinc and copper. Curr Med Chem, 2005; 12(23): 2753-2763.

15. Goyer RA: Nutrition and metal toxicity. Am J Clin Nutr, 1995 Mar; 61(3 Suppl): 646S-650S.

16. Wenzel KG, Pataracchia RJ: The earth’s gift to Medicine: Minerals in health and Disease. Alton, Ontario. KOS Publishing. 2005.

17. Pasternak G, Becker CE, Lash A, et al: Cross-sectional neurotoxicology study of lead-exposed cohort. J Toxicol Clin Toxicol, 1989; 27(1-2): 37-51.

18. Rajanna B; Hobson M: Influence of mercury on uptake of [3H]dopamine and [3H]norepinephrine by rat brain synaptosomes. Toxicol Lett, 1985 Sep; 27(1-3): 7-14.

19. Foster HD: What really causes Alzheimer’s Disease? 2004. (A pdf of the book is available at

20. Pfeiffer CC: Excess copper as a factor in human diseases. J Ortho Med, 1987; 2(3): 171-182.

21. Pfeiffer CC, Iliev V: Pyrroluria, urinary mauve factor, causes double deficiency of B6 and zinc in schizophrenics. Fed Proc, 1973; 32: 276.

22. Gittleman AL: Why am I always so tired? New York, NY. HarperSanFrancisco. 1999.

MindCheck is the Weekly Wednesday Kids Mental Health series with Dr. Ray Pataracchia, N.D.   MindCheck provides in depth information on the orthomolecular approach to coping with mood and/or behavior disorders. The MindCheck Health Series is endorsed by the Mindful Network – ‘A Better Future for Children’s Mental Health’.