Orthomolecular Treatment Response: Author: Raymond J. Pataracchia, B.SC., N.D

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4 Case Reports Volume 25, Number 1, 2010 JOM

Orthomolecular Treatment Response

Author: Raymond J. Pataracchia, B.Sc., N.D.1


1
Naturopathic Medical Research Clinic, 20 Eglinton Avenue East, Suite#441
Toronto, ON, Canada, M4P 1A9.

Abstract The following six case studies illustrate assessment and treatment scenarios common to
orthomolecular psychiatry. These cases represent a sample of frequently seen mental health pathologies.
From case to case, we see not only a common overlap of symptoms but also, an overlap of biochem-
ical-nutrient imbalances. Imbalances depicted herein are widespread in an array of mental health
conditions. Targeted lab assessment techniques help to hone in on relevant biochemical-nutrient im-
balances. Consistent with treating these imbalances, we observe patients achieving greater mental
health and physical well-being.

Introduction Case Studies


Two years ago Dr. Abram Hoffer M.D., Case 1: Chronic Depression and Anxiety,
Ph.D., now deceased, suggested that I publish male, 46 years old
these cases with the addition of assessment Case 2: Chronic Anxiety and Depression,
and treatment stratagem. When Dr. Hoffer female, 47 years old
lectured he commented that “the cases are Case 3: Schizophrenia, male, 18 years old
what people want to hear.” So few articles ex- Case 4: Schizoaffective Disorder, male, 41
plain treatment strategy in a case series format years old
and I consider this essential in furthering the Case 5: ADHD/Dyslexia, male, 42 years old
development of the orthomolecular psychiatry Case 6: Chronic Depression, female, 56 years
knowledge-base. This article provides a viable old
treatment rationale for practitioners. The cases
are, in my opinion, a typical sample of com- Case 1: Chronic depression and anxiety,
monly seen mental health pathologies. From male, 46 years old
case to case, the histories reveal a commonly This patient was the mayor of a small town
seen overlap of symptoms and biochemical in Northern Ontario. He was struggling with
imbalances. My clinical strategy implements flat stoic depression for 10 years. Anti-depres-
the use of a targeted battery of tests that es- sants had become less effective with time and
tablish the biochemical profile at baseline. As he was considered treatment refractory (i.e. a
treatment progresses, I only assess salient lab non-responder). He had dominant negative
trends. I would expect to see consistent contin- thought rumination and occasional suicidal
ued improvement, and in many cases a com- propensity. His mother, sister, and brother had
plete change in symptoms after the biochemi- depression. He reacted badly to sweets and al-
cally influential imbalances are reversed. The cohol, and skipping meals caused headaches,
patients in these case studies have provided irritability, and fatigue (hypoglycemic trend).
consent to publish their stories and findings. He was dizzy 2 to 3 times a week (sluggish
Orthomolecular Treatment Response 5

adrenal), and he had insomnia 1 to 2 times Treatment


a week. He had prostatitis (inflamed prostate Copper toxicity was addressed initial-
gland) 12 years prior and several courses of an- ly with zinc 50 mg, sodium alginate, and
tibiotics had been taken. He had an Epstein chlorella. In these cases I typically raise the
Barr viral infection in 1972, a candidate trigger zinc dose as tolerated by 15 mg increments
for affective disorders,1 with report of visual il- monthly. Vitamin B6 was given in the active
lusions. He had significant fatigue and consti- pyridoxal-5-phosphate (P-5-P) form and I
pation. (Figure 1, below) often raise the dose until the patient experi-
ences significant dream recall, at least twice
Assessment weekly; memory acquisition is in part B6
• High tissue copper (toxicity) and a low dependant.2 Patients presenting with heavy
zinc/copper ratio. metals are suspect to having low thyroid me-
• High normal fasting blood homocysteine tabolisms. They often retain heavy metal tox-
(mild under-methylation) ins if a stressor is significant enough to slow
• Oral Glucose Tolerance Test (OGTT) the metabolism down and weaken the organs
blood glucose drops at the 2 and 3 hour that would normally eliminate it, i.e., the liv-
mark (hypoglycemia) er, kidney, and bowel.3-5 Common stress trig-
• ‘Normal’ blood thyroid levels with low body gers include not only exogenous sources but
temperature and clear hypothyroid symptom- also physical stressors such as viral infections
ology, i.e., Wilson’s Temperature Syndrome. or metal toxins. I treated the low thyroid

Figure 1. Symptom changes during treatment of Case 1


6 Journal of Orthomolecular Medicine Vol 25, No. 1, 2010

state with a botanical protocol (blue flag, and improve compliance. His current custom
guggulipid, fucus, ashwaghanda) and desic- supplement dose is three pills, twice daily. His
cated thyroid (MD prescribed) while moni- current dose of ginkgo is three pills daily. He
toring temperatures daily three hours after is on thyroid medication and I aim to opti-
waking. I like to see temperatures rise into mize thyroid function further. I am currently
the upper end of the range to determine the assessing his blood and urinary mercury lev-
effectiveness of the thyroid protocol. I used els, both the ionic/inorganic and the methyl
high dose chromium 600-1,200 mcg and a species. [I now assess blood and urinary or-
40% lean protein diet to address glycemic ganic methyl and ionic/inorganic mercury
perturbations. The under-methylated aspect species early on in about 40% of mood dis-
in this case was mild and treatment with order cases. Hair tissue levels do not rule out
oral methylcobalamin (B12-methyl) 0.5-1 mercury toxicity alone. Hair measures help
mg, folic acid 0.5-1 mg, and betaine HCl in determining how efficient the body is at
500 mg daily was sufficient. B-complex used excreting organic mercury at a tissue level
here is a standard in most mental health when compared to the organic blood mer-
protocols. My essential fatty acid (EFA) cury load]. His ongoing treatment maintains
bias in adult cases with mood disorders is the “lowest” effective dose of medication; he
an eicosapentaenoic acid (EPA) to docosa- is off Tarazadone and currently weaning off
hexaenoic acid (DHA) ratio of 3:1. I do not Effexor from a low 75mg dose.
find EFA’s pivotal in reversing mental health
pathology but they have a stabilizing effect, Case 2: Chronic anxiety and depres-
and help keep neuron membrane structure sion– female, 47 years old
intact, which is important in clients who are This patient had been depressed for many
reducing medications. In these cases I often years. She had a family history of depression.
prescribe Ginkgo to help maintain neuronal She experienced a “nervous breakdown” in
receptor balance and electric signaling to 2003 where she lost 30 pounds. She had in-
prevent medication related receptor decom- somnia since a teenager with rousing at mid-
pensation effects. Magnesium glycinate is night and was unrefreshed on waking. She
an excellent bowel regulator and sleep aid had been on anti-depressants and sleeping
and the glycine component is a safe anti- pills for years. She had significant fibromyal-
anxiety amino acid. I usually maintain about gia (often a low thyroid state) related neck and
600 mg daily in adult mood cases. Magne- shoulder pain. [Musculoskeletal pain may be
sium is also useful in slow metabolizers to associated with the lack of adenosine triphos-
oppose high tissue calcium; tissue calcium (a phate (ATP) in muscle cells; ATP is required
sedative mineral) is high in low thyroid states. to allow muscle cells to relax.6 Inadequate
Vitamin C and niacin, 3 g of each were used thyroid function is related to inadequate ATP
initially and he now maintains 1,000 mg of production at the mitochondrial level].7 She
inositol hexanicotinate (B3-HEXA) and 750 had a non-malignant bowel tumor removed
mg of vitamin C. His current dose of zinc is two years prior. She was constipated with
under 60 mg a day. (Figure 1, p.5) only four bowel movements a week and only
four inches of stool per movement. She had
Summary a history of intractable headaches. She expe-
The root problem in this case was copper rienced blurry vision (which may be adrenal
toxicity and low thyroid metabolism. After related) all day worse in the morning and,
treating these factors he became much hap- she had cold hands and feet (often thyroid
pier, more in control, and had more energy. related). [Blurred vision is not always adre-
Within two years, he experienced almost nal related but adrenal physiology is linked to
complete reversal of depression and anxiety. the maintenance of blood pressure in times
I started him on a custom supplement mix of stress and retinal arterial supply fed via ce-
after six months to reduce the number of pills rebral blood flow can lag when blood pres-
Orthomolecular Treatment Response 7

sure drops].8 She had a history of anemia, Treatment


menstrual disruption, premenstrual syndrome Initially I gave her a strong multi-mineral/
(PMS), and post-partum hormonal depres- vitamin, vitamin C 1,000 mg three times daily,
sion; she was currently peri-menopausal, with vitamin A 20,000 IU, a 3:1 EPA/DHA sup-
irregular menses. (Figure 2, below) plement, an adrenal botanical (eleutherococ-
cus, sarsaparilla, rose hip, hawthorne, alfalfa)
without licorice twice daily and magnesium
Assessment glycinate at bedtime. She did a gluten-free
• Low hair tissue and blood iron trial. Iron complex was added in November
• ‘Normal’ thyroid stimulating hormone 2008 and 5-hydroxy-tryptophan (5-HTP) 50-
(TSH) result despite low body temperature 100 mg at bedtime. A thyroid botanical proto-
• Low adrenal and thyroid hair tissue min- col (blue flag, guggulipid, fucus) was added in
eral trends indicative of a slow metabolizer March 2009. (Figure 2, below)
• No tissue heavy metals; inorganic mercury
not ruled out but given her quick response Summary
(below) she probably did not have signifi- The root cause of her condition was
cant blood mercury; the hair mercury ratios likely adrenal stress and inadequate vitamin-
showed no warring with important oppos- mineral nutriture leading to secondary thy-
ing minerals (iron, selenium, zinc). roid compromise. Note that some people
• High-normal fasting blood homocysteine have compromised thyroid function that re-

Figure 2. Symptom changes during treatment of Case 2


8 Journal of Orthomolecular Medicine Vol 25, No. 1, 2010

covers with adrenal treatment.3,9 By address- roid weakening secondary to post-viral stress)
ing these issues she experienced significant • Significant systolic blood pressure drop
improvement in anxiety and depression. Her from 108 lying to 94 on standing (sluggish
Hoffer-Osmond Diagnostic (HOD) depres- adrenal; typical in weakened thyroid metab-
sion score (DS) dropped from eight to three olisms) with a resting pulse of 60.
(normal range) and her husband noted she
was a “different person.” She had a 75% re- Treatment
duction in fibromyalgia-related pain symp- At intake I started this patient immedi-
toms within two months. She was better off ately on 3 g of B3-HEXA and 3 g of vitamin
gluten. Her maintenance treatment at last C. I also provided a potent multi-B com-
visit was minimal and ongoing. plex, multi-mineral, EFA with 2g of EPA,
an adrenal botanical twice daily, and a 40%
Case 3: Schizophrenia, male, 18 years protein diet. At the second visit I added a
old thyroid botanical protocol with iodine, B12/
This athletic 18 year old had experi- folic acid (1 mg of each) trans-dermal gel,
enced auditory hallucinations for six months. 2,000 mg of betaine HCl, and 30 mg of
This was a clear medically diagnosed case of zinc. A gluten-free trial was recommended
first-episode schizophrenia. The visual hallu- as well. (Figure 3, p.9)
cinations had recent high intensity suggest-
ing progression of schizophrenic pathology Summary
and associated neuronal degeneration. He The root cause of the biochemical im-
was withdrawing from society. His history balance in this case is foremost a vitamin B3
showed Epstein Barr Virus (EBV) infection dependency followed by under-methylation
two years prior; a potential trigger for schizo- syndrome, protein deficiency contributing
phrenia. [Viral infections from EBV and to glycemic imbalance, hypoadrenia, and low
other viruses have been implicated as poten- thyroid metabolism. This patient experienced
tial triggers of schizophrenia].10 His diet was a 69% reduction of symptoms in one month
carbohydrate dominant. He was constipated as was indicated by a HOD Total Score (TS)
with only one movement per day and low drop from 59 to 18. His HOD Perception
volume. The neuroleptic Risperdal was pro- Score (PerS), indicating hallucinatory in-
vided in hospital two weeks prior to the first tensity, dropped from 18 to 3. Within one
visit and discontinued. (Figure 3, p.9) month he only heard voices 1 to 2 times a day
versus constantly. His HOD DS dropped
Assessment by 100% and he was smiling! Niacin (the
• Vitamin B3 dependant trend – the default of B3-HEXA form in this case) addressed the
all schizophrenias due to unregulated spikes ‘negative’ symptoms, something rarely seen
in brain neurotransmitter with residual tran- in schizophrenics sedated on neuroleptics.
sient oxidized species similar to mescaline or The results seen here are not uncommon
LSD-25; the “Adrenochrome Hypothesis” in first-episode cases that are not exposed
was the first biochemical theory ever pre- to neuroleptics (i.e. neuroleptic-naïve) for
sented in the history of psychiatry.11 a significant period. We call these patients
• No tissue heavy metals; inorganic and organ- “good niacin responders.”
ic blood mercury toxicity was not ruled out Note that the response is more dramatic
• Poor sugar regulation early in the course of the disease when brain
• High liver enzymes, a transient issue that tissue structure is not as compromised. The
was present pre-treatment and probably due prognosis in such cases is good when treated
to medication with optimal niacin-therapy, and recovery ap-
• High fasting blood homocysteine (under- proaches 90% in the first year of treatment.12
methylated) Recovery here is defined as becoming free of
• Low body temperature (possibly due to thy- symptoms; being able to integrate well with
Orthomolecular Treatment Response 9

family, friends, and society; and returning to etc. It is not remarkably difficult to diagnose
previous levels of functioning in terms of vo- schizophrenia and there should not be a cloud
cation or career.13 Ultimately these healthy of skepticism in doing so. We see so many
and often bright people will recover and con- schizophrenics presenting often too late on
tribute to society by paying taxes and sup- one or more psychotropics with minimal if any
porting our countries’ Gross Domestic Prod- improvement. In my experience, chronic pa-
uct. There is nothing better than helping one tients can recover up to 40-60% with targeted
of these patients and seeing changes unfold orthomolecular therapy after which further
first-hand with a gradual fading of family improvement is dependant on their ability to
turmoil. Very few people realize how much withdraw from medications as tolerated.14-17 If
the family suffers and yearns for that former they had been treated early on with appropri-
person to reveal themselves again. ate niacin therapy this would not be the case
Schizophrenia need not be a life sentence in the vast majority.18,19 I consider optimal or-
of relapses, “remissions” and drug side effects. thomolecular protocol as a first-line treatment
Poor conventional prognosis repeatedly delays in first-episode neuroleptic-naïve schizophre-
diagnosis as psychiatrists are often loath to nia. It can reverse over the next 70 years up-
make such conclusions without first exhaust- wards of 55 million cases; that is, 80-90% of
ing all other differential diagnoses–schizoaf- the approximate 70 million cases worldwide at
fective disorder, personality disorder, bipolar our current population size, which is now fast
disorder, mood disorder with psychotic break, approaching the 7 billion mark.

Figure 3. Symptom changes during treatment of Case 3


10 Journal of Orthomolecular Medicine Vol 25, No. 1, 2010

Is ‘Recovery’ Possible with Neuroleptic he was given a diagnosis of schizoaffective


Treatment? disorder. He reported he had been unable
In my discussions with psychiatrists, I to work since 2006 while on Olanzapine;
have never heard them say that conventional Olanzapine interfered with his memory and
neuroleptic treatment will enable more than executive processes including problem solv-
10-25% of patients to ‘recover’. Sixty-six per- ing.16,17 He had Olanzapine-induced diabe-
cent of schizophrenic cases do not achieve a tes and was overweight. His insomnia was
full remission of symptoms with neuroleptic destabilizing. He felt better taking niacin
treatment.20 Thirty-three percent of cases three weeks prior to the first visit. His HOD
suffer “persistent cognitive disturbance and Ratio Score (RS) revealed greater domi-
associated deficits of mood, motivation, and nance in perceptual (receipt of sensory in-
behavioural responses.”21 After a psychotic formation) versus mood dysfunction which
episode, 30-40+% of compliant neuroleptic- is a typical niacin dependant trend. He had
treated schizophrenics who have had a “posi- glucose-6-phosphate dehydrogenase defi-
tive” response will relapse within 1 year.22,23 ciency. (Figure 4, p.11)
The highest suicide risk occurs in the first 5
yrs – the “critical period.”24 Fifteen percent Assessment
of cases will successfully complete suicide.25 • I consider this patient vitamin B3 depen-
The best case scenario is first episode early dant until proven otherwise (i.e. if niacin
intervention with the lowest effective neu- treatment does not produce a profound re-
roleptic dose and adjunct psycho-education, sponse with sequentially higher doses)
relapse prevention, and psycho-social in- • High fasting glucose, iatrogenic dysglyce-
tervention.26 These “patients are more likely mia
to be taking medication at the end of three • High cholesterol and triglycerides
years… more compliant… more likely to be • Gluten-intolerant symptoms
prescribed atypical medication… more likely • Copper deficient trend from hair and blood
to have returned to work or education… more assessment
likely to remain living with their families… • Protein catabolism trend from hair and
less likely to suffer depression to the extent blood assessment
of requiring anti-depressants… commit less • No tissue heavy metals; blood inorganic
suicide attempts… less likely to suffer relapse and methyl mercury had not been ruled out
and re-hospitalisation… less likely to have • Normal body temperature
involuntary admission to hospital.” A double
blind study in the USA (the PRIME study) Treatment
allocated prodromal schizophrenic patients Pure niacin was provided at 2 g, three
to olanzapine versus placebo groups. After 1 times daily at the outset along with a B-
year of treatment, researchers found olanzap- complex and a multi-mineral, a botanical
ine to be of no advantage over placebo; both complex for glucose regulation (syzygium,
groups experienced similar progressions and oplopanax, sylibum, nopal), an EFA with 2
worsening of psychotic symptoms.27 Patients g of EPA, magnesium 400 mg, and a 40%
commonly have poor quality of life and the lean protein diet. In the second visit I raised
majority remain dependent on parents and the B3 dose to 4 g three times a day (pill then
few have skilled or paying jobs.28 later powder form). [Sometimes clients need
and want to be maintained at high B3 dose
Case 4: Schizoaffective disorder, male, levels]. Blood copper-zinc status, liver en-
41 years old zymes, and uric acid levels are checked an-
This patient experienced three nervous nually in these cases. He had no liver enzyme
breakdowns with paranoia (1982) and men- elevations on high dose B3 and his uric acid
tal confusion (1985, 1987). He was on and off (which competes with niacin for urinary ex-
neuroleptics and anti-depressants. In 1988, cretion) levels remained normal.29 I see liver
Orthomolecular Treatment Response 11

enzyme elevations in less than 5% of niacin him to intramuscular B12 and folic acid,
treated schizophrenics and in all cases, levels added iron and increased manganese. Also,
normalized after a proper 1 to 2 week wash- I started a custom supplement series to im-
out; this confirms what other researchers have prove compliance and the average dose was
found, that vitamin B3 does not cause struc- seven pills twice daily. I included vitamin D
tural damage but merely speeds liver function 2,000 IU, betaine (TMG) 1.8g, chromium
and sometimes in that process spills excess 1,200 mcg, 6 mg copper, a multi-mineral base,
microsomal liver enzymes. In contrast, medi- and R-lipoic acid 150 mg daily. In the forth
cation-related enzyme elevations can linger at visit I added 1g vitamin C twice daily. I added
high levels for months. Lecithin and betaine a thyroid botanical protocol (blue flag, gug-
are excellent at addressing liver enzyme eleva- gulipid, fucus, ashwaghanda) in the fifth visit.
tions when and if that occurs.29 In the sixth visit I upped the vanadium dose.
I added P-5-P 50 mg and pyridoxine I recently recommended gymnema for sugar
hydrochloride (B6-HCl) 200 mg, vitamin E regulation and he is maintained well on the
400 IU, methyl-B12 1.5 mg and folic acid 2.4 custom supplement. (Figure 4, below)
mg daily. His dream recall returned within a
month of B6-HCl and P-5-P dosing; dream Summary
recall had been absent for a decade. He felt This is a vitamin B3 dependant case. The
better off gluten and I recommended he RS score dropped from a high seven to five be-
maintain this. In the third visit I switched tween August and June of 2007 which shows

Figure 4. Symptom changes during treatment of Case 4


12 Journal of Orthomolecular Medicine Vol 25, No. 1, 2010

the progression of reversal of perceptual dys- firing of the follower neuron which results
function as the dominant symptom. Within in classic denervation super-sensitivity and
seven months his paranoia totally dissipated, sometimes neuronal death; two excellent pa-
his mood improved substantially, and he pers by Gur et al and Chakos et al discuss
was no longer as stoic. He was able to work the finding of brain tissue loss.36,37 More re-
and became a functional member of society searchers need to do studies like this to ex-
within one year of treatment. His physical plore further the potential for neuroleptics
improvements were also consistent with or- to cause iatrogenic brain damage and psy-
thomolecular treatment which addresses all chosis secondary to withdrawal. Neuroleptic
body systems. Medication side effects were rebound potential should be part of the pre-
much reduced and the patient continued to treatment discussion between the psychia-
improve. A maintenance protocol is in effect. trist, patient and family members.
He continues to do well and is active in the With prolonged neuroleptic administra-
work force. tion tardive dyskinesia can appear. This is not
uncommon. Symptoms involve tongue dart-
Risks of Neuroleptic Sedation ing, mouth smacking and extremity jerk-
Neuroleptics sedate brain areas in need ing or writhing. This can be permanent if
of correction and dilute effect of nutrients by cholinergic interneurons of the striatum are
reducing the amount of viable tissue avail- damaged. This is thought to be concurrent
able to be acted upon. In my experience, or- with episodes of SSP.38
thomolecular treated patients who have been Neuroleptics are associated with meta-
on neuroleptics longer than six to twelve bolic syndrome and premature mortality.
months plateau at the landmark 40-60% Several reviews describe neuroleptics (es-
improvement level. Further improvement pecially atypicals) causing metabolic syn-
is dependant on maintaining lower effec- dromes including diabetes, weight gain, hy-
tive doses of medication.30,31 Many of these perglycemia, dyslipidemia and hypertension.
patients have difficulty remaining stabile on In discussions on neuroleptic outcome some
lower neuroleptic doses due to symptom re- researchers mention “[p]ersons with major
emergence. mental disorders lose 25 to 30 years of po-
Olanzapine and other neuroleptics are tential life in comparison with the general
associated with rebound psychosis or su- population, primarily due to premature car-
per sensitivity psychosis (SSP) which is a diovascular mortality.”39,40
receptor decompensating effect secondary
to neuroleptic withdrawal.32-35 Many psy- Case 5: ADD/dyslexia, male, 42 years
chiatrists argue that symptom reemergence old
after withdrawal of neuroleptics is due to The patient was a scattered unfocused
dropping the dose of a drug that is stabi- adult. He had moderate to severe adult atten-
lizing. That being said, you cannot rule out tion deficit disorder (ADD) with a high HOD
the addictive hold secondary to altered fol- TS of 60, a high DS of 10, and a high PerS of
lower neuron receptor numbers. That is, with 13. He was an idea person, good at business
neuroleptic follower neuron blockade there strategy. He was dyslexic with sequential in-
is a natural compensation to upregulate fol- formation tasks as required for following legal
lower neuron receptors and produce greater contracts. He had good visuo-spatial memory
numbers of receptors that are also blocked and math skills (common in right-brained
by the neurolpetic if provided in sufficient dominant ADD, children and adult), but poor
amounts. When the neuroleptic drug dose is short term memory and critical reasoning. He
later dropped the receptor blockade is lifted had restless legs with sleeplessness that was
and neurotransmitter in the cleft is left free worse with ADD medication. He was using
to bind to the follower neuron with greater a proton pump inhibitor for the gastric reflux
receptor numbers. The end result is excess of a hiatal hernia. (Figure 5, p.13)
Orthomolecular Treatment Response 13

Assessment tion by omitting the B-complex, zinc, B6 HCl,


• Normal fasting blood homocysteine betaine HCl and vitamin C, and implement-
• Low blood iron with low normal saturation ing a custom multi-mineral-vitamin (five pills
• No tissue heavy metals; inorganic and or- a day) for fast metabolizers with a B-complex
ganic blood mercury not ruled out weighted in B12-methyl 2 mg (no folic acid),
• Hypoglycemic trend copper 2 mg, chromium polynicotinate 600 µg,
and calcium hydroxyappatite 200 mg. On the
Treatment fifth visit after a lengthy trip overseas I pro-
I placed this patient on a 40% lean pro- vided him with a potent probiotic to normalize
tein diet and a daily regimen of B-complex digestion. On the sixth visit I added a botanical
100’s, B3-HEXA 1.5 g, vitamin C 3 g, P-5-P for glucose regulation (Syzygium, Oplopanax,
50 mg, B6-HCl 200 mg, zinc 30 mg, chro- Sylibum, Nopal). (Figure 5)
mium 800 µg, magnesium 800 mg and an
EFA with 3:1 EPA/DHA. On the second Symptom Changes Summary
visit I added an adrenal glandular and be- This ADD adult experienced significant
taine HCl. On the third visit I added vitamin improvement in thinking and mood. The
E 400 IU, a low dose iron complex and had over-stimulated ADD symptoms includ-
him maintain a gluten-free diet which he felt ing his dyslexia were no longer present. Or-
better on. By the fourth visit his metabolism thomolecular treatment allowed him greater
picked up and I tailored back his supplementa- work performance and greater overall well-

Figure 5. Symptom changes during treatment of Case 5


14 Journal of Orthomolecular Medicine Vol 25, No. 1, 2010

being. His gastric reflux improved quickly suggest potential estrogen progesterone imbal-
and was reversed within six months. The ance. She was stoic with suppressed emotions
root imbalance in this case was likely adrenal and irritability. She had a long-standing lack
and glycemic imbalance with gluten intol- of appetite history which I determined, with
erance.4 He was doing well enough at the laboratory results, was due to zinc and iron de-
last visit to continue on a maintenance regi- ficiency. She was light-headed without break-
men. Many ADD cases present with copper fast. She had gestational iron deficiency unre-
toxicity which in the initial stages forces a mitting and post-partum changes including
metabolism to shift from fast to slow. Fast anxiety, negative thoughts, inability to tolerate
metabolizing ADD cases tolerate Ritalin or stress, weeping, screaming, depression, fatigue,
Concerta but eventually become refractory apathy (worse winter, worse premenstrual), and
to, and aggravated by these stimulants. sweet cravings. In her mid-40’s she developed
osteoarthritis of the fingers and knees and se-
Case 6: Chronic depression, female, vere insomnia with less than four hours of sleep
56 years old a night. She had occasional suicidal propensity
This client had struggled with depression and significant despair. (Figure 6, below)
since her teens. She had negative thought rumi-
nation at age 17. Since age 10 she noted having Assessment
PMS mood swings as well as headaches and • Severe high hair tissue copper with low
migraines. She had menstrual disruptions that zinc/copper ratio and iron/copper ratio.

Figure 6. Symptom changes during treatment of Case 6


Orthomolecular Treatment Response 15

[Note that copper dominance is linked to Discussion on Orthomolecular Treat-


estrogen dominance and consequent relative ment Response
progesterone deficiency trends.41,42] Realigning specific biochemical-nutri-
• High normal fasting blood homocysteine ent imbalances is a foundational tenant of
• Low thyroid and adrenal slow metabolizer orthomolecular treatment. Herein we see
trend as indicated by hair tissue ratios the use of targeted lab tests and other eclec-
• Low normal body temperature despite tic naturopathic assessment techniques. This
‘normal’ TSH of 1.7 approach is advanced and helps us define
• Hypoglycemic hair tissue trend with nor- biochemical-nutrient imbalances that are
mal fasting blood sugar in dire need of being corrected. By revers-
• Protein catabolism confirmed in the blood ing targeted biochemical-nutrient imbal-
with elevated protein waste ratios ances we see a direct positive correlation
• Low ferritin iron levels with patient improvement. These imbalances
are widespread in mental health pathology.
Treatment Medication effects have important ramifica-
I treated this patient with daily supple- tions on outcome as discussed herein.
mental B-complex 100’s, sequentially higher
doses of zinc (up to 120 mg daily), manganese References
30 mg, chromium 1,200 mcg, an adrenal glan- 1. Gotlieb-Stematsky T, Zonis J, Arlazoroff A, et al:
dular, magnesium 600 mg, iron 25 mg, vitamin Antibodies to Epstein-Barr virus, herpes simplex
C 1,500 mg, potassium 300 mg (to oppose cal- type 1, cytomegalovirus and measles virus in psy-
chiatric patients. Arch Virol, 1981; 67(4): 333-339.
cium), betaine HCl 1,500 mg and vitamin E 2. Deijen JB, van der Beek EJ, Orlebeke JF, et al: Vi-
400 IU. I also recommended a 40% lean pro- tamin B6 supplementation in elderly men: effects
tein diet. In the third visit I added a thyroid on mood, memory, performance and mental effort.
botanical protocol (blue flag, guggulipid, fucus, Psychopharmacology (Berl), 1992; 109(4): 489-496.
ashwaghanda). Her metabolism had sped up 3. Heinrich TW, Grahm G: Hypothyroidism Pre-
senting as Psychosis: Myxedema Madness Revis-
nicely and we cut back to a maintenance sup- ited. Prim Care Companion J Clin Psychiatry, 2003;
plement regimen. I recommended she stay off 5(6): 260-266.
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