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Orthomolecular Treatment of Mood and Behavior Disorders (PART THREE):  Magnesium & Calcium Deficient Kids and Kids with Thyroid/Adrenal Imbalances.

[Part Two covered Under-Methylated Kids and Kids with Heavy Metals.  Parts Four and Five of this series will cover 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).]

 

MAGNESIUM & CALCIUM DEFICIENT KIDS

For a full reference on Magnesium and Calcium Deficiency please refer to my desktop reference on ‘Minerals in Health & Disease’ (Wenzel K-G & Pataracchia RP, 2005; KOS Publishing; available via the International Schizophrenia Foundation, 416-733-2117).

Magnesium deficiency is quite useful in mood and behaviour disorders because it is important to central nervous system function and it is a natural relaxant.  Magnesium is calming and helpful for overstimulated states and anxiety.  Magnesium deficiency is associated with anxiety, sleep disturbance (problems staying asleep), clumsiness (dyspraxia), depression, muscle twitches, cramps/tension of skeletal muscles, blood pressure changes and bladder enuresis (bed wetting).  Your bone matrix is magnesium dependent so magnesium is important during development.  Magnesium is also indicated for headaches, migraines, impaired concentration, nervousness, and malaise.  When it comes to digestion, magnesium improves peristaltic bowel movement and helps draw water into the lower bowel.  Too much fiber (phytates) and too few vegetables (magnesium is the central mineral ion in chlorophyll) will deplete magnesium.  High salt fast foods can also deplete magnesium.

Calcium deficiency is common in kids with fast metabolisms.  Calcium has a natural sedating effect and can help especially in cases where kids have problems falling asleep.  Calcium is important for the development of bones, teeth, nerve, and muscle tissue.  Calcium uptake is hindered by foods/drinks containing phosphates (soft drinks, sausages, and processed cheese) and phytates (cereals and whole grains) and, by oxalic acid (in rhubarb) and excess fat intake.

 

KIDS WITH THYROID & ADRENAL IMBALANCES

Adults are not the only ones that can suffer from endocrine system imbalances.  The thyroid and adrenal gland (the main endocrine glands) can be compromised in kids with mental health conditions.  The low thyroid condition called cretinism occurs when you are born with (i.e. congenital) low thyroid metabolism.  There are however, less obvious low thyroid states that can occur during childhood or adolescence.

Both the thyroid and the adrenal gland are grouped together here because these influential endocrine system glands work together via negative feedback mechanisms.  Many symptoms common to adrenal dysfunction are seen in thyroid dysfunction, and vice versa.

The adrenal glands play a major role in stress response, sugar metabolism, electrolyte balance, blood pressure regulation, and sex hormone metabolism.  Hypothalamic-Pituitary-Adrenal axis dysregulation is integrally associated with anxiety and depression.23,24  The adrenal works in concert with the thyroid gland and often both glands need support.25,26  Low adrenal function symptoms include sluggishness on waking, stress intolerance, lack of enjoyment, post-traumatic stress, addiction, dizziness, low blood pressure, fluctuant body temperature, insomnia at 4am, multiple chemical sensitivity, hypoglycemia, skin conditions (eczema, etc.), PMS, and phobia.  Low blood pressure or significant drops in lying to standing (orthostatic) blood pressure are signs of sluggish adrenal function.

Researchers are beginning to recognize and observe sub-clinical thyroid lab results in children and adolescents with behavior and mood disorders.23,27-33

These subclinical metabolic changes are biochemical changes that occur before classic systemic low thyroid symptoms become obvious.  Before thyroid imbalances deepen and affect other body systems, clinicians need to assess the thyroid system then monitor and support it with nourishing and supportive approaches.

Fast and slow metabolic states are often related to thyroid (and adrenal) imbalance.  Kids and adolescents with hyperactivity and inattention can initially be in a fast metabolic state that burns out and reverts to a slow metabolic state.  Heavy metal overload is not uncommonly revealed in the slow metabolic phase; at this stage there is important to support the organs of elimination (liver, bowel, kidney).

The brain is highly dependent on thyroid hormone for the regulation of dopamine, norepinephrine, and serotonin pathways.28,34,35  Active thyroid hormone is responsible for enabling cells to maintain high metabolic rates.  Thyroid hormone maintains oxygen availability and with healthy thyroid hormone function, our cells produce energy which allows greater efficiency at a cellular/tissue level.  External stressors (life stress, viruses, environmental exposure) can influence thyroid metabolism; it is thought that the body shifts to conserve energy and shuts down active thyroid hormone production during times of stress.

The most common symptoms of low thyroid function for kids are fatigue, insomnia, depression, anxiety, impaired cognition, irritability, weak memory, pain, headache, indigestion, frequent infection, constipation, easy weight gain, hair loss, and PMS.23,29,36,37

In low thyroid conditions, the digestive tract has poor motility and slow stool transit which can cause constipation and inefficient nutrient absorption.38

In low thyroid conditions, core body temperatures are often so low that digestive enzymes do not reach the reaction thresholds needed to efficiently break food down and absorb nutrients.

Thyroid support is becoming more accepted as an integral part of the assessment and treatment of refractory depression (depression that is not responding to treatment).29,39  The biochemistry of thyroid metabolism is becoming more and more complex but research (much of it unfortunately is based on adult populations) is showing clear pathways of thyroid compromise that affect the whole population.  The brain is highly dependent on thyroid hormone for the regulation of dopamine, norepinephrine, and serotonin pathways.28,34,40

Peripheral blood thyroid levels could be normal in the context of ‘brain hypothyroidism’, a condition where systemic T4 does not readily cross into the brain; this is associated with depression, bipolar and psychotic illnesses in adults.39-47  Although research is not focused on ‘brain hypothyroidism’ in children or adolescent populations, we can glean that healthy brain function would be dependent on an adequate supply of active thyroid hormone in the brain.

T4 to T3 conversion by brain typeII 5’-deiodinase can be inhibited by cortisol.38,48  This is important because cortisol levels are commonly elevated in mood and behaviour disorders, especially during stress.  Cortisol is the dominant stress response hormone and, during stressful periods we tend to conserve energy by shutting down thyroid hormone production.  Conversely, in line with orthomolecular balance, it is also important to recognize that low cortisol levels influence thyroid function as cortisol is needed to transfer active T3 hormone from the blood into the cell and also to raise cellular glucose (which provides the energy to produce neurotransmitters, etc.).

The faster the metabolic rate, the higher the temperature; measuring body temperature therefore provides a means of assessing thyroid function.49

When the body temperature is adequate, the enzymes in our body, including the digestive enzymes, form chemical reactions with greater ease.  If cells are working slowly and producing minimal energy, they don’t give off a large amount of heat and the average body temperature can remain low.  Intolerance to cold is a typical complaint in low thyroid cases, but this inability to adapt to temperature (decreased heat or cold tolerance) is indicative of low adrenal function which, as is explained above, is associated with low thyroid function.23,50

You don’t have to have a classic diagnosis of hypothyroidism to have a ‘low thyroid metabolism’.

Classic hypothyroidism is a problem with the gland itself and more specifically, with its inability to produce adequate thyroid hormone.  In classic hypothyroidism, blood tests reveal that there is low output of thyroid hormone (T4 or T3) and/or elevated thyroid stimulating hormone (TSH) levels.  By contrast, low thyroid function cases commonly have normal blood test measures, low body temperatures, and obvious low thyroid symptoms.  This can happen if adequate levels of circulating thyroid hormone (T4) are not readily converted into T3, the active thyroid hormone (this is called poor peripheral thyroid hormone conversion).29,30,51  Wilson’s Temperature Syndrome has emerged as a syndrome that fits that criterion.  Other conventional diagnostic considerations (Euthyroid Sick Syndrome, etc.) are also becoming recognized.  Orthomolecular interventions can help support thyroid metabolism both at the gland and peripheral hormone level.

Autoimmune involvement is typical of Hashimoto’s thyroiditis.  Blood thyroid autoimmune markers can help determine Hashimoto’s but about 80% of classic hypothyroid cases (i.e. with elevated TSH) have autoimmune involvement.  Blood tests can also help rule out the thyroid hyper-functioning state of Grave’s Disease.  Grave’s, in its active phase, is a state of thyroid hyperfunction that often requires botanical, orthomolecular, and conventional medication treatment.  Kids with first degree relatives with autoimmune thyroid conditions may be predisposed to thyroid metabolism compromise.

In mood and behaviour disorders, thyroid and adrenal support have global benefits.

Thyroid metabolism improves the cellular physiology of all body systems including the brain, liver, gastrointestinal tract, kidney, immune system, and musculoskeletal system.  Based on the research and rationale provided here, it is apparent that children and adolescents need to have an efficient thyroid and adrenal metabolism to maintain and/or achieve general well-being and mental health.

Part Four of this Kid-Specific series on the orthomolecular treatment of mood and behavior disorders will cover B6 and Zinc Deficient Kids, Hypoglycemic Kids, EFA Deficient Kids, and Protein-Deficient Kids.

 

References

23. Heinrich TW, Grahm G: Hypothyroidism Presenting as Psychosis: Myxedema Madness Revisited. Prim Care Companion J Clin Psychiatry, 2003 Dec; 5(6): 260-266.

24. Mello AA, Mello MF, Carpenter LL, et al: Update on stress and depression: the role of the hypothalamic-pituitary-adrenal (HPA) axis. Rev Bras Psiquiatr, 2003 Oct; 25(4): 231-238.

25. Abdullatif HD, Ashraf AP: Reversible subclinical hypothyroidism in the presence of adrenal insufficiency. Endocr Pract, 2006 Sep-Oct; 12(5): 572.

26. Candrina R, Giustina G: Addison’s disease and corticosteroid-reversible hypothyroidism. J Endocrinol Invest, 1987 Oct; 10(5): 523-526.

27. Contreras F, Menchon JM, Urretavizcaya M, et al: Hormonal differences between psychotic and non-psychotic melancholic depression. J Affect Disord, 2007 Jun; 100(1-3): 65-73.

28. Bauer M, London ED, Silverman DH, et al: Thyroid, brain and mood modulation in affective disorder: insights from molecular research and functional brain imaging. Pharmacopsychiatry, 2003 Nov; 36 Suppl 3: S215-S221.

29. Jackson IM: The thyroid axis and depression. Thyroid, 1998 Oct; 8(10): 951-956.

30. Haggerty JJ, Stern RA, Mason GA, et al: Subclinical hypothyroidism: a modifiable risk factor for depression? American Journal of Psychiatry, 1993; 150: 508-510.

31. Monzani F, Del Guerra P, Caraccio N, et al: Subclinical hypothyroidism: neurobehavioral features and beneficial effect of l-thyroxine treatment. Clinical Investigator, 1993; 71: 367-371.

32. Holtmann et. al.  Severe affective and behavioral dysregulation in youth is associated with increased serum TSH.  J Affect Disord, 2010 Feb; 121(1-2): 184-8.

33. McGaffee J, Barnes MA, Lippmann S: Psychiatric presentations of hypothyroidism. Am Fam Physician, 1981 May; 23(5): 129-133.

34. Haddow JE, Palomaki GE, Allan WC, et al: Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med, 1999 Aug 19; 341(8): 549-555.

35. Brouwer A, Morse DC, Lans MC, et al: Interactions of persistent environmental organohalogens with the thyroid hormone system: mechanisms and possible consequences for animal and human health. Toxicol Ind Health, 1998 Jan-Apr; 14(1-2): 59-84.

36. Westphal SA: Unusual presentations of hypothyroidism. Am J Med Sci, 1997 Nov; 314(5): 333-337.

37. Heitman B, Irizarry A: Hypothyroidism: common complaints, perplexing diagnosis. Nurse Pract, 1995 Mar; 20(3): 54-60.

38. Shafer RB, Prentiss RA, Bond JH: Gastrointestinal transit in thyroid disease. Gastroenterology, 1984 May; 86(5 Pt 1): 852-855.

39. Oppenheimer JH, Braverman LE, Toft A, et al: A therapeutic controversy. Thyroid hormone treatment: when and what? J Clin Endocrinol Metab, 1995; 80(10): 2873-2883.

40. Hatterer JA, Herbert J, Hidaka C, et al: CSF transthyretin in patients with depression. Am J Psychiatry, 1993; 150(5): 813-815.

41. Schreiber G: The evolutionary and integrative roles of transthyretin in thyroid hormone homeostasis. J Endocrinol, 2002; 175(1): 61-73.

42. Sullivan GM, Mann JJ, Oquendo MA, et al: Low cerebrospinal fluid transthyretin levels in depression: correlations with suicidal ideation and low serotonin function. Biol Psychiatry, 2006; 60(5): 500-506.

43. Sullivan GM, Hatterer JA, Herbert J, et al: Low levels of transthyretin in the CSF of depressed patients. Am J Psychiatry, 1999; 156(5): 710-715.

44. Wan C, Yang Y, Li H, et al: Dysregulation of retinoid transporters expression in body fluids of schizophrenia patients. J Proteome Res, 2006; 5(11): 3213-3216.

45. Huang JT, Leweke FM, Oxley D, et al: Disease biomarkers in cerebrospinal fluid of patients with first-onset psychosis. PLoS Med, 2006; 3(11): e428.

46. Zheng W, Lu YM, Lu GY, et al: Transthyretin, thyroxine, and retinol-binding protein in human cerebrospinal fluid: effect of lead exposure. Toxicol Sci, 2001; 61(1): 107-114.

47. Zheng W, Blaner WS, Zhao Q: Inhibition by lead of production and secretion of transthyretin in the choroid plexus: its relation to thyroxine transport at blood-CSF barrier. Toxicol Appl Pharmacol, 1999; 155(1): 24-31.

48. Visser TJ, Leonard JL, Kaplan MM, et al: Kinetic evidence suggesting two mechanisms for iodothyronine 5′-deiodination in rat cerebral cortex. Proc Natl Acad Sci USA, 1982; 79(16): 5080-5084.

49. Barnes BO, Galton L: Hypothyroidism: The Unsuspected Illness. New York, NY. Harper & Row. 1976.

50. Michel V, Peinnequin A, Alonso A, et al: Decreased heat tolerance is associated with hypothalamo-pituitary-adrenocortical axis impairment. Neuroscience, 2007 Jun 29; 147(2): 522-531.

51. Lum SM, Nicoloff JT, Spencer CA, et al: Peripheral tissue mechanism for maintenance of serum triiodothyronine values in a thyroxine-deficient state in man. J Clin Invest, 1984 Feb; 73(2): 570-575.

 

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’.