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ORTHOMOLECULAR
TREATMENT FOR DEPRESSION,
ANXIETY & BEHAVIOR DISORDERS
Copyright
© 2008
Dr. Raymond J. Pataracchia B.Sc., N.D.
The
Naturopathic Medical Research Clinic
20 Eglinton Avenue East, Suite #441
Toronto, Ontario, M4P 1A9
(416)944-8824
(T); (647)439-1551 (F)
www.nmrc.ca
; info@nmrc.ca
Orthomolecular medicine can be helpful in
treating the biochemical imbalances of mood and behaviour disorders.
This broad grouping of disorders includes anxiety, severe depression,
bipolar disorder, postpartum
depression, hormonal depression, other endogenous depressions (cyclothymia,
seasonal affective disorder), OCD, ADHD, ODD and, addictive
behavior.
Mood and behavior disorders have similar
nutritional imbalance profiles and there is much overlapping of
diagnoses. Anxiety
for example, often coexists with depression. Depression often involves
negative thought rumination and sadness. Stoic depressives rarely
smile and are locked in despair often with suicidal thoughts. Suicidal
propensity is global in patients with depression, anxiety, and
behaviour disorders. Obsessive thinking is commonly found in anxiety
disorder but, is not diagnostic for obsessive compulsive disorder (OCD)
unless it is so severe that it profoundly interferes with thinking and
behaviour. People with addictive behaviour are often having
co-existing mood dysfunction, behavior disorders, or schizophrenia.
Addictive behaviour ranges from the realm of illicit substance use and
alcoholism to the compulsive behaviours of gambling and sexual
addiction. Anxiety is often an over-stimulated state and, in advanced
stages, becomes disruptive. Anxiety can be associated with phobic
disorders and schizophrenia. Over-stimulated states of anxiety are
typically not productive. Conversely, in bipolar/manic depression,
over-stimulated states (mania) are often productive and patients
report accomplishing tasks with immense intensity and creativity;
great artists for example, could paint a masterpiece overnight. In
bipolar disorder, patients cycle with a deep depressive burn out
phase. In depression and anxiety we often see inattention which can be
mild or, in severe cases, interfere with thought processing. Advanced
inattention can be seen as a pure component of ADHD (childhood or
adult). Inattention can be due to thought blocking which is an
interruption in the processing of thoughts for periods of time;
thought blocking is common in heavy metal toxicity. Irritability is
found globally in all mental illness categories. Anger and
irritability are often linked to the ‘stuckedness’ of depression
and hypoglycemia. Anger can extend into the realm of criminal
behaviour.
Neurotransmitter deficiency syndromes are common in mood and behaviour
disorders. Depression is used here as a classic example of a
neurotransmitter deficiency syndrome. Based on current research, mixed
neurotransmitter theory states that depression (including bipolar
depression) is caused by reduced numbers of brain neurotransmitters.
Serotonin and the catecholamines are master neurotransmitters. The
catecholamines include dopamine, norepinephrine, and epinephrine.
Conventional drug treatments attempt to increase synaptic availability
of one or both neurotransmitter pathways with SSRI’s, NRI’s, or
SNRI’s. However, these drugs depend on having enough
neurotransmitter to do the job.1 In clinical practice we
see many patients on medications that either are not working or have
been working less effectively with increased use and, in such cases,
there is often an increase in dosage, medication change or, another
medication added. Conventional medication does not act to increase the
total number of neurotransmitters and, in an attempt to increase
synaptic levels - by keeping neurotransmitters in the cleft - there is
further neurotransmitter depletion. As these medications increase the
synaptic concentration of neurotransmitters, there is an opposing
natural breakdown of neurotransmitters mediated by MAO and COMT
homeostatic regulation. The end result is a further depletion of
already low neurotransmitter levels. Many mood and behaviour disorder
patients are caught up in this neurotransmitter deficiency state.
Biochemical
syndromes of importance in mood and behaviour disorders are those that
ultimately influence neurotransmitter production, release, inhibition,
and signal transduction.1 Various
segments of the mood and behaviour disorder population fall into
subgroups of distinct biochemical imbalance. We often see subgroups of
essential fatty acid deficiency, inadequate nutriture, dysglycemia,
food intolerance, digestive compromise, malabsorption, under-methylation,
vitamin B3 deficiency, vitamin C deficiency, heavy metal toxicity, B6
deficiency, zinc deficiency, brain hypothyroidism, and hypoadrenia.
Orthomolecular medicine has a key role in the treatment of mood and
behaviour disorders. The goal of orthomolecular medicine is to correct
the causative factors that influence biochemistry.
Under-Methylated
Mood & Behavior Dysfunction
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 behaviour disorders.2-5
The under-methylated syndrome are a neurotransmitter
deficiency syndrome.
In our clinic, we see a good portion of mood and behaviour disorder
patients with methylation compromise as indicated by elevated fasting
homocysteine levels. In mood and behaviour disorders, researchers are
aware that certain brain tracts are overstimulated while others are
understimulated. Every patient is different and some are low in
serotonin versus the catecholamines (dopamine, norepinephrine,
epinephrine), and vice versa. If we can methylate efficiently, we have
the machinery to form neurotransmitters in brain areas that are
understimulated and neurotransmitter deficient.
Orthomolecular treatment with B12, folic acid, and other methyl donor
nutrients 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” is in direct contrast to conventional psychotropic
medication whose influence on given brain pathways is fixed,
non-flexible and, often with side-effects due to lack of specificity.
In mood and behaviour 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. High B12 levels are
similarly associated with improved outcome in depression.
Some evidence suggests that high circulating levels of homocysteine
increase the level of homocysteic acid and cysteine sulphinic acid,
both of which are NMDA receptor agonists that contribute to neuronal
excitotoxicity. This type of excitotoxicity with its corresponding
mood and cognitive deficits is associated with aging and dementia.8
Heavy
Metal Mood & Behavior Dysfunction
It
is not uncommon to see toxic levels of lead, mercury, aluminum, and
copper on lab test results of mood and behaviour disorder patients. 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 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 including neurotransmitters. Zinc
deficiency is a well know condition associated with central nervous
system disorders and mental health.
If
you are a city dweller, you have been exposed to lead. Lead is found
in paints, glass, baterries, rust protectants, alloys, water pipes,
and old bathtubs. Lead levels can be toxic to patients with behavior
dysfunction, mood disorder, insomnia, and immune compromise.16
Lead toxicity readily disrupts opiod
neurotransmitter 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
Mercury can be toxic
in patients with mood and behavior disorders, nervous irritability,
and memory decline.16 Lab results are often confirming the
mercury toxicity. 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 patients 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 behaviour disorders, depression, and
anxiety.12,16,20,21 Copper toxicity is routinely found on
lab results of this patient population. Copper’s role in the
formation of oxidized serotonin intermediates may play a role in
altering mood, behaviour, and sleep.12 It seems that serotonin’s opposing neurotransmitter system, the
catecholamine system, 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 see right brain copper dominance which is
associated with visuo-spatial creativity; conversely, left brain
dominance is associated with the verbal-analytical intellectual skills
that are 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 and
therefore retain copper. Niacin, vitamin C, and zinc are important
nutrients in copper toxic cases 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 include copper tea pots, copper sulphate treated jacuzzi’s
or swimming pools, drinking water, prenatal vitamins, and copper
IUD’s. 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 excessive
over-spill of toxins into the blood. Metals that are mobilized in the
bloodstream need to be eliminated efficiently and, this job falls on
the liver, kidneys, and bowel. In clinical practice, we support the
thyroid, adrenal, liver, kidneys, and bowel to maximize the efficient
removal of the metal via gastro-intestinal routes, biliary routes,
etc. Patients with toxic
metals need to avoid specific environmental exposures and food supply
sources.
‘Brain
Hypothyroidism’ and Hypoadrenic Mood & Behavior Dysfunction
The
thyroid and adrenal glands are compromised in the majority of mental
health cases. Both the thyroid and the adrenal gland are grouped
together here because they are influential endocrine glands that work
together by negative feedback mechanisms. Typically both glands are
sluggish and 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 Many people who are heavy coffee
drinkers have weak adrenals. 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, PMS, phobias, and poor sex
drive. Adrenal symptoms and orthostatic blood pressure are good
indicators of adrenal status and, in some cases, saliva testing is
useful.
Low
thyroid symptoms are commonly seen in mood disorder cases and often in
psychosis.23,27-33 Stress influences thyroid metabolism and
we tend to conserve energy by shutting down active thyroid hormone
production. Active thyroid hormone is responsible for enabling our
cells to maintain high metabolic rates. Thyroid hormone also maintains
oxygen availability. With healthy thyroid hormone functioning, our
cells produce energy and complete their tasks efficiently. When cells
have energy, body systems work optimally. The brain is highly
dependent on thyroid hormone for the regulation of dopamine,
norepinephrine, and serotonin pathways.28,34,35
The
most common symptoms of low thyroid function are fatigue, insomnia,
depression, anxiety, impaired
cognition, irritability,
poor memory, easy weight gain, pain, headache, indigestion, hair loss, high
cholesterol, frequent infection,
constipation,
and in women, PMS. 23,29,36,37
Many patients with varied non-specific complaints have low thyroid
function. Chronic fatigue and fibromyalgia are not uncommon in mood
disorder patients. Muscle pain syndromes (such as fibromyalgia) are
also often associated with low thyroid function because muscle cells
require ATP (the energy molecule provided indirectly by peripheral
thyroid hormone metabolism) to relax. Chronic fatigue symptoms, at
least in part, are also often explained by low thyroid function.
The digestive system of a low thyroid patient has poor motility and slow
stool transit which cause constipation and inefficient nutrient
absorption.38 In low thyroid patients, core body
temperatures are often so low that digestive enzymes do not reach the
reaction threshold to enable efficient food breakdown. With optimal
thyroid treatment, mood and behaviour dysfunction patients do not
require as high a dose of nutrients because absorption improves.
Magnesium can be used to help improve peristaltic movement, draw water
into the lower bowel, and avert tenesmus.
Thyroid support is becoming accepted as an integral part of the
assessment and treatment of refractory depression.29,39
The brain is highly dependent on thyroid hormone for the
regulation of dopamine, norepinephrine, and serotonin pathways.28,34,40
“Brain hypothyroidism” has been described by Hatterer et al as a
state that occurs when systemic T4 does not readily cross into the
brain.40 Active thyroid
hormone T3 is synthesized in the brain by brain typeII 5’-deiodinase
conversion of T4 to T3.39,41 Brain
neurons therefore depend on a ready supply of T4. The choroid plexus
of the brain produces transthyretin (TTR), a transport protein that
binds T4 and transports it across the blood-cerebral spinal fluid
barrier to the brain.41 Reduced cerebral spinal fluid (CSF)
transthyretin is seen in depression and suicidal propensity.42,43
CSF Transthyretin is also downregulated in schizophrenia.44 Many
schizophrenics and depressives relapse when thyroid function drops.23
This suggests that mood and perceptual dysfunction are
associated with a lack of adequate T4 in the brain. Without adequate
T4, brain cells remain hypo-metabolic and this can, among other
things, reduce neurotransmitter synthesis and disrupt the regulation
of dopamine, norepinephrine, and serotonin.
Huang et al suggested that low CSF transthyretin could prove useful as a
biomarker for early diagnosis of bipolar disorder and psychotic depression.45
Also of interest is the fact that lead toxicity has been linked
to the reduction of CSF transthyretin in humans.46,47
Peripheral blood thyroid levels could be normal in the context of brain
hypothyroidism. 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 dysfunction,
especially during stress. Cortisol is a stress hormone and, during
stressful periods we tend to conserve energy by shutting down thyroid
hormone production.
The
faster the metabolic rate, the higher the temperature and therefore,
one of the best methods for assessing thyroid function is measuring
body temperature.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 body temperature remains low. Intolerance to cold is a typical
complaint in cases of low thyroid.23 It is not uncommon to
have male patients reporting that they feel warm when, in fact, their
body temperature measures are clearly low. Some people may have
fluctuant temperatures where they feel warm at times yet are cold at
other times; this inability to adapt to temperature (decreased heat
tolerance) is indicative of low adrenal function which, is typically
associated with low thyroid function.50
Note that ‘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. However, low thyroid function cases
may have normal blood test measures, low body temperature, and obvious
low thyroid symptomology. It is not uncommon to see hypothyroid
patients on thyroid hormone treatment with normal test measures and
low thyroid symptoms. This can happen if adequate levels of
circulating thyroid hormone (T4) are not readily converted
peripherally into active thyroid hormone (T3).29,30,51
Currently, there is no conventionally accepted diagnostic agreement on
physiological states that account for normal test measures and poor
peripheral conversion. Wilson’s Temperature Syndrome however has
emerged as a syndrome that fits that criterion. Orthomolecular
interventions can help support the thyroid gland directly and also
help support peripheral conversion. Orthomolecular thyroid treatment
can be done safely as an adjunct to thyroid hormone medication. Blood
testing can help rule out immune involvement typical of Hashimoto’s
thyroiditis. Hashimoto’s is seen in 80% of hypothyroid cases and it
responds well to low thyroid treatment. Blood testing can also help to
rule out the thyroid hyper-functioning state typical in Grave’s
Disease. Grave’s, in its active phase, is a state of thyroid
hyperfunction and requires orthomolecular treatment to calm thyroid
function. In mood and behaviour disorders, thyroid support has global
benefits because it improves the cellular physiology of the brain,
liver, gastrointestinal tract, kidney, immune system, and
musculoskeletal system.
B6 and Zinc Deficient Mood
& Behavior Dysfunction
Zinc
and B6 are involved at a basic biochemical level in the manufacture of
protein complexes, including neurotransmitters, out of simple amino
acid building blocks.52,53 B6 and zinc deficiency
are clearly associated with mood and behaviour disorders and optimal doses of B6 and zinc are required to treat this condition.54,55
Zinc is important to several biochemical pathways as over 200 enzymes
are zinc dependant. Zinc and iron are the most concentrated metals in
the human brain. Insufficient levels of zinc are associated with
depression, dementia, mental retardation, learning disabilities,
lethargy, and apathy.56 Zinc is essential for the synthesis
of serotonin and melatonin.57 It is crucial to brain
development as it plays a major role in protein synthesis.56,57
In the brain, zinc lowers excitability by moderating NMDA
receptor release of excitatory glutamate. Zinc is involved in the
synthesis of inhibitory GABA by the modulation of glutamate
decarboxylase activity. Among the zinc-dependant proteins are
metallothionein which is essential for heavy metal regulation and zinc
bioavailability. The synthesis of Zn-thionein and CuZnSOD are
essential in averting oxidative damage.57 Zinc protects
against fatty acid peroxidation which destroys neuron structure and
function. Zinc is involved in neuronal plasma membrane structure and
functioning and may play a key role in blood-brain-barrier integrity.58
Zinc has a role in biogenic amine storage in synaptic vesicles and in
axonal transport. The biogenic amine histamine regulates nucleus
accumbens activity which is responsible for filtering sensory
information and communicating with the amygdala, ventral tegmentum,
and hypothalamus. Zinc is involved in limbic system metabolism which
regulates emotions. Hormonal metabolism of the hypophysis and
hypothalamus are dependant on zinc as well.
B6 is involved in the decarboxylation of tyrosine, tryptophan, and
histadine into the neurotransmitters nor-epinephrine, serotonin, and
histamine.55 It is a cofactor in homocysteine
re-methylation.59 B6 has been found useful in memory
acquisition, with just a 20mg dose.60 B6 is essential for
the synthesis of antioxidants such as metallothionein, glutathione,
and CoQ10 which help to prevent neuronal oxidative stress. B6 (and
zinc) are involved in the synthesis of glutamic acid decarboxylase
(GAD) which blocks excitotoxicity which causes secondary oxidative
damage. B6 is essential for glutathione peroxidase and glutathione
reductase which help prevent mitochondrial decay.
It is interesting to note here that zinc and vitamin B6 together are
needed by the body as cofactors for neurotransmitter synthesis; zinc
is needed for transcription and B6 is needed for transamination.
Previous investigators have described B6 and zinc depletion in the
context of pyrolluria. In this metabolic syndrome, B6 and zinc
interact with 2,4-dimethyl-3-ethylpyrrole which is readily excreted.61-65
Hypoglycemic
Mood
& Behavior Dysfunction
Hypoglycemia
is the term that describes low sugar in the blood. The brain’s
demand for glucose is so immense that about 20% of the total blood
volume circulates to the brain, an organ that represents only 2% of
body weight. The brain demands a substantial amount of glucose to
maintain its high metabolic rate. Gluco-sensing neurons regulate
glucose availability in the brain as a fail-safe mechanism to ensure
the homeostasis of brain glucose.66 The brain has a great
demand for sugar and doesn’t like to be starved for long. Neurons
function poorly in sugar deficient states. The
hypoglycemic state involves a sharp rise of simple sugars in the blood
followed by a sharp decline which robs the neurons of their main
energy source; the sharper the decline, the greater the effect on
brain cells. Irritability,
poor memory, “late afternoon blues”, poor concentration,
tiredness, cold hands, muscle cramping, and “feeling better when
fighting” are typical hypoglycemic symptoms.61
Mono-croping of grains and resultant ‘saccharine diseases’ have lead
to serious problems in society today including depression and
carbohydrate neuroses.67
Diabetic or pre-diabetic cases also exhibit hypoglycemic symptoms. Mood
and behaviour disorder patients with hyperglycemia, much like
diabetics, present with hypoglycemic mental symptoms because glucose
doesn’t get into the brain neurons. Brain neurons starved for energy
behave differently resulting in mood and cognitive dysfunction.68,69
It is not clear if dysglycemia has a causative role in mood and
behaviour dysfunction but it can be deemed an aggravating factor.
It
is said that hypoglycemia is 100% treatable in compliant patients.
This emphasizes the need to address diet. The dysglycemic mood and
behaviour disorder patient requires three solid meals (of 40% protein)
a day and sometimes additional protein-containing snacks. Many
patients need to be educated about ‘complex’ versus ‘fast’
carbohydrates (e.g. avoiding junk food and sugar). When they increase
protein intake, they release glucose to the brain at a steady rate and
sugar cravings lessen. Chromium and zinc are useful for sugar balance
and botanical medicine is useful in advanced hypoglycemia.
Essential Fatty Acid
Deficient Mood & Behavior Dysfunction
Depression,
anxiety, bipolar disorder, ADHD, and behavior disorders are benefited
by EFA supplementation.70 EFA’s, including omega-3 (DHA
& EPA) and omega-6, are good fats, not saturated with hydrogen,
and unfortunately not readily provided in the American diet. 60% of the dry weight of the brain is fat. EFA’s are important
components of nerve cell walls and are involved in neurotransmitter
electrical activity and post-receptor phospholipid mediated signal
transduction. DHA
and EPA have proven the most useful in the clinical treatment
of mood and behavior disorders.71-73
Inadequate
Nutriture, Digestive Compromise, and Mal-absorption in Mood & Behavior
Dysfunction
Neurotransmitter production is dependant on amino acid protein building
blocks (phenylalanine, tyrosine, tryptophan, etc.) supplied from the
diet. The catecholamines dopamine, norepinephrine, and epinephrine are
derived from phenylalanine and tyrosine. Catecholamines are involved
in executive functions and motivation. Serotonin, the ‘feel good’
neurotransmitter, is derived from the amino acid tryptophan. Protein
nutriture is very important for mood and behaviour disorder and,
general mental well-being. I have seen many mood and behaviour
disorder patients respond when they start increasing their protein
intake with each meal. A diet that has 40% protein, 40% carbohydrate,
and 20% fat is ideal for many patients.
Many mood and behaviour disorder patients do not eat three meals a day
and their diet is invariably carbohydrate dominant. Carbohydrate
dominant North American diets release glucose to the bloodstream
quickly. Such patients do well to avoid high glycemic load foods
including junk food, white sugar, white rice, and white bread. If they
have poor appetite, this can lead to inadequate nutriture. Poor
appetite may be associated with zinc or iron loss.
Fat nutriture is important in mood and behaviour disorders. Cold water
fish with teeth have a fat profile suitable for these patients.
Salmon, tuna, mackerel, herring, cod, and trout provide the highest
omega-3 profile. Other high EFA sources include scallops, shrimp,
flaxseeds, walnuts, winter squash, and kidney beans.
Inadequate nutriture can also occur with gastrointestinal compromise,
mal-absorption and, low thyroid function. I constantly see
gastrointestinal problems in mood and behaviour disorders; symptoms
include constipation, spastic obstipation, bloating, cramping,
abdominal discomfort, IBS, and GERD. Compromised gastrointestinal
function leads to malabsorption of nutrients. These patients often
require higher doses of nutrients and medication. Lack of stomach acid
can reduce intrinsic factor and diminish B12 utilization essential for
methylation and neurotransmitter formation. Poor bowel transit locks
in toxins and the build-up taxes the immune system and reduces the
absorptive surface area. Poor bowel transit may be due to the lack of
peristalsis, low thyroid function, and/or magnesium deficiency.
Adequate water intake for the average adult is about two litres per
day. This is essential to keep toxins moving out and bowel contents
hydrated. Orthomolecular treatment for digestive dysfunction and low
thyroid function helps to alleviate digestive symptomology and also
reduces the need for high nutrient dosing. Intact gastrointestinal
health is a prerequisite for improved outcome in mood and behaviour
dysfunction.
Food Intolerant Mood
& Behavior Dysfunction
Mood
and behaviour disorder patients have the potential to exhibit mild to
severe food intolerance symptoms and we see this commonly in the
general population.74-77 The digestive tract reacts to food
allergens by eliciting an immune response. Undigested food by-products
can be toxic (e.g. opioid peptide exorphins), pass through the gut
wall, enter the bloodstream, and reach the brain with subsequent brain
function compromise.78,79 I have several clients who have
an increased severity and frequency of depression, anxiety,
irritability, and insomnia when they eat intolerant foods. We see mood
and behaviour disorder patients that experience a wide range of food
related physical symptoms such as headaches, skin eruptions,
palpitations, weakness, painful digestion, constipation, diarrhea, and
arthralgia. Common food intolerances include gluten, dairy, eggs, tree
nuts, citrus, soy, fish, legumes and crustaceans (high in copper). It
is helpful to survey patient responses with a seven-day diet diary.
Often mood and behaviour disorder patients are tired, weak, irritated,
and moody after eating intolerant foods. Typically they either hate
the intolerant food or crave it and this may be due to the toxic
effects of opioid exorphin peptides. It is not uncommon to see
patients that have fasted in the past and reported feeling better.
This is a good indication that they have a food intolerance. An
elimination diet followed by provocation is helpful to assess cases
clinically. Elaborate lab testing may not be needed but, IgG Elisa
testing can be quite useful to assess food intolerances that are less
obvious.74,80 IgG responses are provoked when there is a
delayed response. IgG tests report the severity of the delayed
reaction and also provide a rotation diet guideline. Many
investigators have noted improvements with dietary restriction of food
intolerants. In our clinic, a small but significant portion of mood
and behaviour disorder patients experience profound improvements after
removing intolerant foods.
Vitamin
B3 and C Deficient Mood & Behavior Dysfunction
B3
and C are anti-stress vitamins and optimal dosing is indicated for
these two nutrients.67,81 A good portion of mood and
behaviour dysfunction patients do better with moderate orthomolecular
doses of vitamin B3 and C.
Copper
is involved in dopamine production and vitamin B3 and C are
physiologically antagonistic to copper and as such, can help to
moderate the overstimulation of dopamine pathways typical in mood and
behaviour dysfunction. When dopamine pathways are overstimulated,
serotonin (the opposing ‘feel good’ master neurotransmitter
system) can become depleted.
Vitamin
B3 and vitamin C (ascorbic acid) are centrally active in the brain as
“niacinamide in the brain acts on the diazepine receptors, while
ascorbic acid acts on the dopamine receptors”.67 Vitamin
B3 has an anti-anxiety effect.82
Mood
disorder and perhaps more specifically, psychotic depression, may have
a sub-clinical pellagra associated vitamin B3 deficiency component as
classic pellagra symptoms include depression, anxiety, confusion,
memory loss, fatigue, and psychosis.82-84
Overview
Figure
1 is a schematic of the key causative factors of mood and behaviour
disorders. Modern research continually confirms that these factors are
important to mood and behaviour disorder pathophysiology. The list of
assessments and treatments described herein are not exhaustive but,
represent the core considerations of optimal complementary treatment
for mood and behaviour disorders. Orthomolecular treatment can
be implemented safely as an adjunct to conventional psychiatric
therapy.
Figure 1. Mood and Behaviour Disorders: Summary of
Causative Factors
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