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NEURO-TRANSMITTERS

ANXIETY & DEPRESSION

Addiction, attention deficit disorder, attention deficit hyperactivity disorder, anxiety, autism, depersonalisation disorder, depression, fibromyalgia, panic attacks, hyperactivity, insomnia, migraines, obsessive compulsive disorder, seasonal affective disorder, Tourette’s Syndrome are not diseases. They are terms that describe a group of symptoms that the patient experiences and that causes them distress. The actual disease, or diseases, are the underlying structural disorder/s and / or dysfunction/s in the body and / or its surrounding environment that causes these symptoms.

 

Often, one of the underlying causative diseases is an absolute or a relative imbalance in the neurotransmitters in part or all of the brain. An absolute neurotransmitter deficiency occurs when less than normal amounts of a neurotransmitter are made and released. A relative neurotransmitter deficiency occurs when the neurotransmitter requirement is increased to greater than can be manufactured and released whilst on an optimal diet.

 

Neurotransmitters are molecules made in neurons, that are released into the synapse connecting the pre and post-synaptic nerves. A membrane electrical signal travelling down the pre-synaptic (sending) nerve surface, triggers the release of neurotransmitters into the synapse. These neurotransmitters bind to their receptors on the surface of the post-synaptic (receiving) nerve at the synapse. Some neurotransmitter-receptor binding increases the likelihood of the post-synaptic nerve generating and continuing the electrical signal, and some neurotransmitter-receptor binding decreases the likelihood (depending upon the neurotransmitters). There can be over a thousand nerves inputting messages via their synapses onto a single nerve and influencing its likelihood of transmitting the electrical signal. In turn the single nerve can influence the firing of thousands of nerves that it connects to via its synapses.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

In conventional allopathic medicine, we often label the symptoms (with a name that we mistakenly believe is the disease) and act only to suppress the symptoms, often with medications or surgery. This is a worthy goal, as it affords the patient relief from their distressing symptoms. However if the underlying, causative structural and / or functional disorder/s are not addressed, the patient requires symptom relief for life, and the disorder is left free to continue and progress, leading to more symptoms, requiring more ‘treatments’.

 

In functional and integrative medicine, labelling the disorder and controlling the symptoms is the first step. Then we investigate the underlying root causes and modify or eliminate as many of them as possible. These causes include the many sources of neuro-inflammation that interfere with brain cell function. For instance, administering the pro-inflammatory cytokine (messenging molecules made by the body) Tumour Necrosis Factor alpha (for hepatitis) often causes depression. Administering lipo-poly-saccharide endotoxin (an inflammation stimulating molecule from the wall of particular bacteria in the gut) can cause depressive symptoms.

 

Sometimes this approach leads to cessation of the symptoms and ‘cure’ of the disease. Sometimes the previous damage / dysfunction can not be fully eliminated. In this case, symptom relief is required long term.

 

Many psychological symptoms are the result of an absolute or relative deficiency of some combination of neurotransmitters in parts of the brain.

 

Conventional allopathic medicine believes that it is usually an absolute deficiency of neurotransmitters ie there is a decrease in the amount of neurotransmitter being released into the synapse, so the post-synaptic neuron does not reach its firing threshold, does not transmit the electrical signal downstream, and this leads to the psychological symptoms. This is called the Central Monoamine Depletion Theory, as some of the important neurotransmitters in the Central Nervous System (the brain) are monoamines ie serotonin, dopamine, nor-epinephrine (nor-adrenaline), epinephrine (adrenaline). 

 

The most commonly used pharmaceutical medications to increase the amount of neurotransmitter in the synapse are called Re-Uptake Inhibitors (RUI). They block the pre-synaptic nerve's re-uptake transporter, preventing the neurotransmitter that was released into the synapse from being pumped back into the pre-synaptic neuron, ready to be used the next time that an electrical signal arrives. This increases the amount of neurotransmitter in the synapse (by redistributing it from within the pre-synaptic nerve to the synapse).

 

However, the neurotransmitter released into the synapse, as well as being pumped back into the pre-synaptic nerve, is also metabolised (broken down) by degradation enzymes in the synapse (ie monoamine oxidase A (MOA), catechol-O-methyl transferase (COMT)). When the RUI decreases the neurotransmitter transport back into the pre-synaptic neuron, it increases the time the neurotransmitter is ‘trapped’ in the synapse, allowing the degradation enzymes more time to breakdown the neurotransmitter. Now you have a reduction in the total amount of neurotransmitter in the system, leading to a loss of effect (referred to as tolerance or tachyphylaxis). This occurs in up to 60% of RUI users (see article). The standard response is to then either increase the dose of the RUI, add another RUI or swap to another RUI. Either way, the total amount of neurotransmitters in the system continues to decline by the continuing degradation in the synapse. If the RUI is ceased, due to the significantly reduced amount of neurotransmitter in the system, the symptoms may return at a higher intensity than before the RUI was commenced. This is referred to as addiction or Discontinuation Syndrome.

The Central Monoamine Depletion Theory of Depression has never been proven. It is a theoretical construct that partially explains what we see when we give medications that increase the amount of neurotransmitters in brain synapses (Re-Uptake Inhibitors). However, it doesn’t explain why:

    around 45% of patients with the same symptoms don’t improve

    of the 55% that improve, 45% will have improved by doing nothing (placebo). That is, medications that increase synapse neurotransmitter levels resolve depression symptoms at only 7-13% more than taking an inactive placebo (but are guaranteed to cost more and expose to the risk of side-effects).

    elderly people (65 year old plus) have no greater symptom improvement taking medication, than taking placebo ie the increase in synaptic neurotransmitter is not enough to overcome the relative or absolute deficiency that exists

    the incidence of depression is increasing world-wide, and especially in the industrialised countries

    a particular Re-Uptake Inhibitor can be used for multiple symptoms.

 

An alternative theory, is called the Nerve Bundle Damage Theory. We know that a nerve can connect to thousands of nerves via thousands of synapses and influence these post-synaptic nerve’s electrical firing threshold. For instance one serotonin releasing pre-synaptic nerve can connect in the brain to two thousand post-synaptic nerves. These post-synaptic nerves are referred to as a Nerve Bundle.

 

If nerves in a Nerve Bundle are damaged, the bundle will require a larger amount of neurotransmitter than can be produced to be released into the synapse, before the post-synaptic bundle nerves can be triggered. This is a relative deficiency of neurotransmitter. Nerves can be damaged by poor nutritional status, one or more of the 1,179 known neurotoxins and the unknown synergies between them, synergies between other environmental chemicals, physical trauma, hormone imbalances, infections, electromagnetic fields exposure, biological insults, poor inherited protection and the amount and length of these exposures.

 

This theory explains why :

    45% of subjects in RUI studies are non-responders (removing the 45% who improve by placebo) ie they don’t have enough systemic neurotransmitter to address the relative deficiency by merely blocking re-uptake of the deficient amount of neurotransmitter from the synapse

    elderly people and those living in more polluted areas have more toxic damage to the nerve bundles, and thus have a greater relative neurotransmitter deficiency.

 

 

A treatment for this state is to increase the amount of neurotransmitter in the system, by orally providing more of the amino acid precursor molecules from which the neurotransmitter is made. This approach requires the use of precursor molecules:

    that cross the blood brain barrier into the brain

    that don’t have negative feedback induced by increasing amounts of the neurotransmitter they are making, so that much higher levels of neurotransmitter can be manufactured

    that don’t lead to a competitive imbalance in other neurotransmitters that use the same pathways for synthesis, transport and metabolism.

 

Two major, interacting neurotransmitter systems are the serotonin and the catecholamine (dopamine, nor-epinephrine, epinephrine) systems. Their neurotransmitter levels can be modified by taking their amino acid precursors 5-hydroxy-tryptophan (5HTP) and L-Dopa respectively.

 

Because :

    too much of a neurotransmitter can cause the same symptoms as not enough

    adding one amino acid precursor changes the precursor and neurotransmitter levels of the associated systems

    increased neurotransmitter production requires more of the co-factor vitamins and minerals used in the production process

    changes in sulphur-based amino acids (thiols) used to metabolise (break-down) the increased levels of neurotransmitters needs to be controlled,

    every patient has their unique dose requirement for 5HTP and L-Dopa which can only be determined by slowly increasing the precursors until symptoms are optimally controlled in the competitive inhibition state.

 

As the increased neurotransmitters released by the electrical signal of the pre-synaptic nerve do not remain in the synapse (they can be transported back into the pre-synaptic nerve ready to be used again), they do not have an increased exposure to the synaptic degradation enzymes, and tolerance and addiction does not occur.

Rebalancing the serotonin and catecholamine neurotransmitters can provide safe, rapid symptom relief while the underlying causes of the neuron damage are investigated and modified, and the neurons regain function as much as possible.

 

There is a protocol that can optimise the CNS serotonin and dopamine levels, tailored to the individual, using the amino acid precursors 5HTP and L-dopa, with vitamin, mineral and thiol amino acid cofactors to avoid imbalance side effects. The protocol requires initial weekly 30 minute consults (can be done online) to assess progress and adjust the doses of the precursors and the cofactors. The standardised products come from a US website. It takes one to six months to find the perfect dose of the various precursors and cofactors for an individual. The final cost is around US$40-75 a week for the supplements.

 

Dr Hart is one of very few doctors in Australasia to have trained with the developer of this protocol, Dr Marty Hinz.

More information about the science behind this protocol can be found here.

 

Here is an introduction to the structure and function of the Nervous System.

 

The science behind this protocol can be examined by this video and via these published articles:

 

The dual-gate lumen model of renal monoamine transport

 

Both stimulatory and inhibitory effects of dietary 5-hydroxytryptophan  and tyrosine are found on urinary excretion of serotonin and dopamine in a large human population

 

Relative nutritional deficiencies associated with centrally acting monoamines

 

The discrediting of the monoamine hypothesis

 

Monoamine depletion by reuptake inhibitors

 

APRESS: apical regulatory super system, serotonin and dopamine interaction

Treatment of attention deficit hyperactivity disorder with monoamine amino acid precursors and organic cation transporter assay interpretation

 

Neurotransmitter testing of the urine: a comprehensive analysis

 

Validity of urinary monoamine assay sales under the “spot baseline urinary neurotransmitter testing marketing model”

 

Urinary neurotransmitter testing: considerations of spot baseline norepinephrine and epinephrine

 

5-HTP efficacy and contraindications

 

Management of L-Dopa overdose in the competitive inhibition state