Natural Treatment of Chemical Imbalance of the Brain with Amino Acid Therapy

Fred M. Bogan, D.C.

Dr. Bogan is a private practitioner of chiropractic in Tulsa, Oklahoma. For 25 years he has enjoyed a holistic practice treating the usual spine related disorders. In addition he has been blessed with the privilege of treating thousands of patients with various metabolic disorders.

This experience coupled with various personal and family tragedies, or potential tragedies, resulted in a determined effort to find a real solution to depression and displaced anger disorder as well as migraine and other debilitating disorders.

It is hoped that what has been learned through these difficult situations can be used to help others resolve these extremely complex problems and thereby obtain peace for themselves and for the ones they love that may have otherwise never been attained.

Introduction

For 30 years I had heard the term “chemical imbalance of the brain” and never really knew what it meant. But as a physician trained in the art of natural healing I knew what it didn’t mean…I knew it didn’t mean a deficiency of Prozac, Zoloft, Valium, Ritalin or any other drug designed to affect brain function. What I did know was that if there really was such a thing as chemical imbalance of the brain it must be related to diet and nutrition. A real solution or healing would not, indeed could not come from drug therapy.

That is not to say that I believe no one should take prescription medication for symptoms related to chemical imbalance. Certainly there are situations that call for immediate treatment with medication. However I am certain that any one who is currently taking drugs for these conditions should also be (and usually are) searching for as many of the real answers as they can possibly find. This little booklet is dedicated to those who are seeking a real solution for themselves or a loved one.

My primary purpose in preparing this booklet is to shed the light of truth on the subject of depression. However, when one successfully treats depression they have inadvertently opened up a whole disease category that is correctable by the same treatment protocols. That’s because depression, as well as at least 60 other human ailments (many of them very serious), are the result of the same root cause: chemical imbalance of the brain.

If you or a loved one suffers with depression you’ll probably agree that depression seldom if ever occurs by itself. Look at this list of other conditions related to chemical imbalance of the brain. If you or a loved one suffers with depression you’ll probably agree that depression does not occur by itself but in combination with a number of other symptoms. Refer to the list of conditions on page 3 that are related to chemical imbalance of the brain. How many do you recognize as being a part of a “package” of conditions that goes along with depression?

How do we know that all of these conditions are related to the same underlying disorder? Because they all respond to the same treatment. That treatment is correcting for low levels of neurotransmitters.

Please indulge me to preach a little at this point. As always when assessing the nature and causes of human ailment one of the most important causative factors is our own lifestyle. My patients have often heard me say that if they want to know what is causing most of their problems all they need to do is look in the mirror.

Although chemical imbalance is dramatically affected by the subject of this booklet, it is also just as dramatically influenced by our own lifestyle. I am convinced that many people with chemical imbalance of the brain, and especially those suffering with depression and anxiety are often their own worst enemy. Any chemical imbalance of the brain is severely aggravated by poor decisions relating to the selection of our mate or “significant other”, or to poor financial decisions, our choice of work and our choices of friends, poor diet and bad habits, etc.

I am also convinced, both by observation and by my feeble attempt to live a Christian life that following the principles laid down in the Bible, and especially those found in Proverbs, is the best roadmap to a healthy mind and body. I encourage each of you, if you are not presently doing so to re-dedicate yourself to the study and practice of these timeless principles laid down in this great book; and to regularly attend a God-centered church where you can find and associate with positive people who can assist you in this journey through a difficult life.

Best of Luck, and if we can help each other, we’ll all be better for it!

Neurotransmitters: What they are & How they work

Neurotransmitters are naturally occurring chemicals in the body that carry a nerve impulse across a synapse, or the gap between one nerve and another nerve. There are four primary neurotransmitters in the brain: serotonin, norepinephrine, epinephrine and dopamine. At this time it is generally considered that serotonin and norepinephrine may be the most important for nerve transmission in the brain.

To understand the difference between drug and therapy and nutritional therapy, one must have a basic understanding of the anatomy of the synapse and how neurotransmitters function in that anatomy.

To begin let me compare a synapse to an electrical wire. Let’s assume you were to take any extension cord and cut it in the middle and then plug it into the wall. You could then take the bare ends of the cut wire and touch them to each other and, although sparks would fly, at least part if not all of the current would pass into the cut off piece just because the two wires touched. But nerves don’t work that way for several reasons. First, nerve endings don’t actually touch each other and secondly because a nerve impulse, though similar to electricity, is not exactly like electricity, and therefore requires more than contact between one nerve and another to transmit an impulse across the synapse.

That’s where neurotransmitters come in. Neurotransmitters (NT’s) carry the impulse across the gap, or synapse. But they don’t do it the way you would expect. They function by triggering receptors on the distal nerve ending. Once triggered, the nerve impulse will be re-generated in the distal nerve and continue on toward its destination in the body.

Let me explain, but before I do let’s review some terminology so we can have a more simplified discussion. The proximal nerve is the one carrying the impulse. The distal nerve is the one to which the impulse will be transmitted once the neurotransmitters have done their work. The proximal nerve is called an axon. The distal nerve ending is called a dendrite (see fig. 1)

[Alliance Brain Transmitter]

Now, if we magnify the synapse a few thousand times we will see several things. First we would see that the axon nerve ending has several vesicles that contain neurotransmitters. Some of these neurotransmitter vesicles are near the surface in what appears to be a ready position to release their NT’s. Other vesicles are situated further from the surface, more in a position of storage, so that as neurotransmitters are depleted they can move into position and release their cache of NT’s into the synapse. (fig. 2)

[Seratonin Alliance]

Once these neurotransmitters have been released by their vesicles they immediately lock onto a receptor site on the dendrite nerve ending (fig. 3). There are receptors for each type of NT: serotonin, dopamine, epinephrine and norepinephrine. As soon as all, or at least a minimal (threshold) number of receptor sites have been triggered by a NT molecule then the impulse is re-generated by the dendrite nerve ending either come to another synapse or stimulate an end organ, such as a muscle, gland or some other organ.

It is important to understand that once the impulse has been re-generated by the dendrite nerve ending that the NT molecules do not remain at the receptor sites. Nor do they even remain in the synapse. Instead, they return to the axon nerve endings through “gates” that allow them to ultimately return to the vesicles from which they came (see fig. 3). This process is called re-uptake and will be a very important concept to understand when we later discuss the difference between drug therapy and our own nutritional approach.

[Synapse Alliance]

The purpose of re-uptake is to preserve the neurotransmitters for future use when the nerves require them for another impulse re-generation at a later time. All of this activity, including the release of NT’s by the vesicles, receptor site stimulation and re-uptake of the NT’s back into the vesicles all occurs in a few milliseconds (millionths of a second).

Now, if there are insufficient levels of NT molecules released into the synapse to trigger the threshold level of receptors the dendrite will be unable to regenerate the impulse and thus the nerve impulse dies at the synapse.

You might say “what’s the big deal about one or two nerve impulses not getting through?” The fact is that if this happens at all it will happen billions or trillions of times. There are over a trillion neurons in the brain and spinal cord. Each of these neurons have 6,000 to 20,000 synapses (source) with other neurons. All of these synapses are critical to our ability to think and emote correctly. They act as filters to complete or smooth out the “edges” of our thoughts and emotions.

In other words, if a small percentage of our thought or emotion impulses fail to reach their destination due to low NT levels, then a thought that starts out as “I don’t like John very much so I’ll stay away from him” may come out as “I don’t like John so I think I’ll take my gun to work and shoot him”. Or maybe it just makes you want to cry all the time, or maybe it causes you to sleep too much or not enough, eat excessively-or not at all. Or maybe it causes migraine or displaced, inappropriate anger. Whatever the symptoms the cause comes down to incomplete or inappropriate thought processes resulting at least partially from inadequate NT levels to allow normal Neurologic function.

[Synapse Alliance]

What about Drug Therapy?

Let us now discuss the method of action of drugs such as Prozac or Zoloft as well as some other anti-anxiety or anti-depressant drugs.

This class of anti-depressant/anti-anxiety drugs is used to treat a whole class of disorders including depression, anxiety, obesity, psychoses, eating and sleeping disorders, ADHD, and dozens of other conditions.

There are several different types of neurotransmitter drugs and they work in different ways. Most of the newer drugs prevent re-uptake of selected neurotransmitters from the synapse. Remember when we described NT re-uptake earlier? Well, the way that NT drugs work is by preventing re-uptake of certain NT’s from the synapse. Thus the name “Selective Serotonin Re-uptake Inhibitor (SSRI)” or “Selective Norepinephrine Re-uptake Inhibitor (SNRI)”.

Examples of SSRI’s are:

  • Luvox
  • Zoloft
  • Prozac
  • Celexa/Lexapro

Examples of combination SSRI & SNRI’s are:

  • Effexor
  • Meridia
  • Remeron
  • Wellbutrin/Zyban(often used for smoking cessation)
  • Senequan/Doxepin

Other drugs that manipulate NT’s in various ways include:

  • Ritilin and other amphetamines
  • Tenuate
  • Remeron
  • Imitrex
  • Zomig

By inhibiting re-uptake of NT’s from the synapse a “cloud” of NT’s is maintained in the synapse. As subsequent impulses force more and more NT’s from the storage vesicles and into the synapse, the number of molecules in the neurotransmitter cloud increases until there is finally a sufficient number of NT molecules to trigger the threshold number of receptor sites. This generally works quite well to increase the NT levels in the synapse, at least to the point where the impulse can be re-generated. But the increase is in the synapse only. There is no real increase in body levels of neurotransmitters. And there is a price to be paid for this NT cloud and for tricking the body into thinking there are more NT’s than there really are. That price is depletion of NT stores throughout the body, and especially in the brain!

This depletion may occur slowly over a period of months or years, or it may occur rapidly over a period of a few weeks, depending on the individual. It occurs because there is no barrier around the synapse to prevent NT molecules from drifting out of the synapse and being lost in the tissues only to be carried to the kidneys where they are excreted through the urine.

Certainly this loss of NT molecules is not a good thing. A little linear thinking here and you will quickly realize that the patients who are taking these drugs are already low (sometimes dangerously low) on NT’s. For them to lose even a small percentage of their NT molecules from their brain and nervous system can have tragic consequences.

Examples of these consequences have already been experienced by many families, and society as a whole. Think of Columbine High School where Eric Harris who had been treated with the SSRI drug Luvox, along with Dylan Klebold killed twelve students and two teachers before turning their guns on themselves. Or think of Andrea Yates in Houston, Texas where the mother of five drowned her five children one at a time. She had been taking the anti-depressants Haldol, Effexor, and Wellbutrin for depression and psychotic behavior for months or years before her tragic decision. The list goes on and on: Kip Kinkel who graduated from Ritalin to Prozac and finally killed his classmates and his parents; Michael McDermott and Joseph Wesbecker, both of whom committed mass murders of co-workers while being treated with Prozac. (Wesbecker also killed himself.)

According to John Cornwell who wrote the book The Power to Harm: Mind, Medicine, and Murder on Trial, a little known secret is that the manufacturers of these drugs knew that 8% of patients taking an antidepressant like Prozac would already be obsessed with “suicidal ideation”. Suicidal ideation is associated not only with suicide but also with general acts of violence. These drug companies, especially Ely Lily who makes Prozac, went to great lengths to conceal this and other incriminating facts from the FDA during the approval process.

What we see far too often is that most patients respond well to the neurotransmitter drugs for 3 to 9 months. Following a period of what seems to be improvement, gradual depletion of neurotransmitters results in a return of the symptoms. As you might expect many of these patients are doing fine one day but wake up the next day with full-blown depression, anxiety or whatever other symptoms they were experiencing that resulted in the need for medication. This occurs because of the threshold effect. In other words, as long the threshold number of receptor sites are triggered everything works normally. But as soon as just a few molecules below threshold are lost then the system fails again. So the threshold effect is like an on-off switch. As long as there are sufficient neurotransmitters to trigger the threshold number of receptor sites everything seems to work fine. But as soon as the neurotransmitter levels drop below threshold stimulation the system no longer works. Marty Hinz, M.D., to whom I owe so much for sharing his knowledge with me and others puts it this way: “Drugs that work with neurotransmitters don’t work when there aren’t enough neurotransmitters to work with”.

For the patient and doctor who does not understand this principle (and that’s almost every doctor, including psychiatrists—especially psychiatrists) this can be a very frustrating thing. Most doctors will respond with one of four approaches:

1. They will initially increase the dosage assuming the patient is becoming resistant to the medication.
2. They will change the medication in hopes that working another part of the system will again trigger the receptor sites. They often switch from an SSRI to a SNRI, or a combination drug.
3. They will keep the patient on the primary drug and add a second or even third drug in fear that the patient will get even worse if they discontinue any medication. Now the patient is getting a double whammy!
4. They may do all the above.

Unfortunately for the patient none of these approaches is a real solution to the problem. If these drugs cause neurotransmitter levels to fall below the minimal number required to trigger the threshold number of receptor sites not even powerful drugs can trick the body into thinking it has more neurotransmitters than it does. That’s why 8% of patients who take NT medications never experience any benefit at all from the very beginning. They just don’t have enough neurotransmitters to make the drug work. This also explains why increasing the dosage to any level or even adding meds does not work once the NT levels have dropped below threshold.

The Solution

If the solution seems obvious it’s only because it is. If the problem is low neurotransmitter levels at the synapse and if drugs only trick the body (synapse) into thinking that there are more NT’s than there are, while simultaneously causing a NT deficiency, then why can’t we just do something to actually increase neurotransmitter levels. In other words, why can’t we stimulate the body to produce more NT’s, instead of just tricking the body into thinking there are more.

The fact is we can! We now know that those vesicles wherein lie the “neurotransmitters in waiting” are not just storage vesicles. They are also little neurotransmitter factories that can manufacture NT’s on demand. However they do require certain nutrient building blocks for construction of NT molecules.

The building blocks required are primarily the amino acids L-Tryptophan and Tyrosine. Amino acids are naturally occurring molecules that our body assimilates to make proteins. There are also some co-factors such as vitamin C, B6, folate and calcium. L-Lysine is not essential but experience has taught that it is helpful in maintaining balance between the other amino acids. I also like to see my patients taking a high quality multivitamin comparable to our multicaps and a high quality trace mineral comparable to Standard Process Min Tran as well as one or two Standard Process Protefood capsules daily.

Some of you will remember back in the mid 80’s the FDA removed L-Tryptophan from the market because there was an epidemic of eosinophilia myalgia syndrome associated with its use. L-Tryptophan never was the cause of the disease. Eosinophilia myalgia syndrome was caused by a contaminant in a few batches of product manufactured in Japan. But the FDA under pressure from the pharmaceutical industry removed L-Tryptophan from the market. A curious side note is that within three months Prozac hit the market and was prescribed for many of the same conditions for which people had been using L-Tryptophan. But interestingly the FDA never prevented the use of L-Tryptophan in baby foods and formulas, so if you want a good source of Tryptophan just eat some baby food or turkey.

So, instead of using L-Tryptophan in our formula we use the L-Tryptophan derivative 5-Hydroxytryptophan (5-HTP). 5HTP is what L-Tryptophan is converted to just before it becomes serotonin (see fig. 4a). Once the 5-HTP is converted to L-Tryptophan it is then converted to serotonin, one of the master neurotransmitters. Tyrosine is only one step away from dopamine. Dopamine is converted to norepinephrine, the other inter-synaptic neurotransmitter. Finally, if not utilized in the synapse as norepinephrine it will end up as epinephrine, otherwise known as adrenalin (see fig. 4b).

[Synapse Alliance]
[Synapse Alliance]

The important thing to remember here is that once these nutrients are provided to the body that it will indeed increase NT levels. This is something that you can count on. This is not a maybe thing. It will happen. Just as you can count on your body converting sucrose, or table sugar to glucose, you can count on it converting 5-HTP and Tyrosine to serotonin and norepinephrine respectively.

Length of time required for recovery depends on how low your neurotransmitter levels are when you start the program, as well as the dosage and your body’s ability to assimilate the nutrients. At full dosage most people can feel a noticeable difference in about 2 to 4 weeks, and generally within 2 to 6 months neurotransmitter levels are high enough to obtain complete or near complete recovery. At that time it may be possible to reduce the dosage to a maintenance level. It is essential that sufficient dosage is ingested, but because these nutrients can be difficult for some people to digest it is also important not to overload. A typical dose for most conditions including depression and ADHD is 150 mg of 5-HTP, 1,500 mg of Tyrosine and 250 mg of L-Lysine twice daily. This dosage may need to be adjusted up or down depending on the patient and the condition. Considerably more may be needed to successfully treat obesity. One should never take more than their body can handle. To do so will almost certainly cause a person to abandon the only therapy that will actually treat their condition at its source.

After some experience I now begin my patients at a 1/3 to 1/4 dose and build them up to tolerance. If at any time they feel stomach irritation they are instructed to discontinue the nutrients completely for 3 days and then after notifying me they can once again build back up to the level that did not cause stomach distress. Naturally this results in an extra few weeks of recovery time but prevents about 15% of patients from dropping out of the program.

Dr. Hinz, who has tested thousands of patients, states emphatically that those who have gastric symptoms early in the program are those who are most deficient in neurotransmitters. He has also discovered another group who has stomach pain later in the program, say 4 to 6 weeks or more. These people are eating too many carbohydrates and have to reduce the starches and sugars they consume. Often dramatically reducing bread consumption helps, or maybe switching from white to whole wheat might help. Other factors may be liver dysfunction, insufficient stomach acid or pancreatic enzymes, or a past history of ulcer(s).

When lecturing on the subject I am always asked if there is a way to test the NT levels. NT levels can actually be tested three different ways: urine, saliva and blood. We use the urine method because urine levels do not fluctuate hour to hour as blood levels do and it is less expensive than the saliva method. Currently, the testing costs $135 at our office.

It is not necessary to test every patient before beginning therapy. However there are certain groups of patients that should be tested prior to therapy. One group that should be tested are those who are currently taking prescription anti-depressant drugs, especially those under the care of a psychiatrist. This gives the holistic practitioner a baseline value to know the patient’s status (NT levels) at initiation of amino acid therapy. If low, they can be re-tested later to determine if dosage can safely be lowered or if the medication can safely be reduced or eliminated. And psychiatrists are notorious for being very reluctant to allow, much less encourage their patients to reduce or eliminate medication. The testing helps all parties to know the status of the patient and can be very good data to give that same patient the knowledge required to stand up to an adamant medical doctor who does not understand the information provided in this booklet.

The Downside

The downside of amino acid therapy seems to be non-existent. As in almost every metabolic problem treated with nutrition one sees more benevolent side effects than malevolent. As stated earlier I have yet to see a patient who suffers with any one of the conditions listed, it is a package of illnesses, if you will. As neurotransmitter levels improve you will see the whole package of symptoms improve, not just one or two.

Currently, the primary side effect is the aforementioned gastric irritation. This can generally be minimized simply by taking the supplements immediately before eating. Putting food on top of these and any other supplements nearly always minimizes gastric irritation and enhances absorption and assimilation of nutrients.

So it seems there is little or nothing to lose and a normal life to gain. It is my hope that the information provided here will assist you in your decision to take a brave, new, scientifically validated approach to your or your loved one’s future.

Drugs Known to Cause Neurotransmitter Depletion

  • Luvox
  • Zoloft
  • Prozac
  • Celexa/Lexapro
  • Paxil
  • Trazadone (Deseryl)
  • Sinequan (Doxepin)
  • Serzone
  • Effexor
  • Meridia
  • Ephedra
  • Alcohol
  • Nicotine
  • Imitrex
  • Zomig
  • Maxalt
  • Phendimetrazin (Bontril)
  • Phentermine (Adipex)
  • Phenylpropanolamine (Dexatrim)
  • Tenuate
  • Mazindol
  • Fenfluramine (Pondimin)
  • D-Fenfluramine
  • Amphetamines (includes Ritalin)
  • Amerge
  • Amitriptyline (Elavil)
  • Nortryptyline (Norpramin)
  • Remeron
  • Wellbutrin (Zyban)
  • Thioridazine (Mylan)