NeuroResearch Clinics, Inc.

  AMA Category 1
  Continuing Medical Education
In the tube, Billabong World Championship of Surfing Bonsai Pipeline Oahu Hawaii taken by Marty Hinz, MD
 
The neurotransmitter approach used in over 900 medical clinics
Contact us or find a caregiver using this approach.
 
USE OF VICIA FABA
aka faba bean or fava bean
 AS A SOURCE OF L-DOPA

March 18, 2008

   We recently became aware of an alternate source of L-dopa that is available over the counter without prescription, “Vicia Faba Bean” aka faba bean or fava bean.

  Ingestion of “Vicia Faba Bean” aka faba bean or fava bean can cause, “Favism” in individuals with glucose-6- phosphate dehydrogenase deficiency (also known as, G6PD). Symptoms of Favism include hemolytic crisis, kidney failure, acute hemolytic anemia, and in severe cases death.

For the incidence of G6PD is outlined in the U.S. Army study of 20061 which states, “Data were available for 63,302 (54,874 males and 8,428 females) subjects; 2.5% of males and 1.6% of females were deficient, with most having only moderate enzyme deficiency. African American males (12.2%) and females (4.1%), along with Asian males (4.3%), had the highest rates of G6PD deficiency.”
  Use of “Vicia Faba Bean” aka faba bean or fava bean in the general population should be done with caution. It would appear that the prudent thing to do prior to administering “Vicia Faba Bean” aka faba bean or fava bean as a source of L-dopa would be to test all patients for glucose-6-phosphatase deficiency prior to starting in order to manage favism properly. There is no need for pre-treatment testing with Mucuna.
   “Vicia Faba Bean” aka faba bean or fava bean are not a safe alternative to Mucuna Pruriens as a source of L-dopa if proper pretesting is not done.
  1. Prevalence of glucose-6-phosphate dehydrogenase deficiency in U.S. Army personnel. Mil Med. 2006 Sep;171(9):905-7 Chinevere TD, Murray CK, Grant E Jr, Johnson GA, Duelm F, Hospenthal DR.
 
 
 
If you need a medical speaker for AMA Category I CME call NeuroResearch Clinics, Inc.
NeuroResearch Clinics, Inc. only deals with and provides information to licensed health care professionals.
 
NeuroResearch Clinics, Inc 
1150 88th Ave W 
Duluth, MN 55808 
Ph. 877-626-2220 
E-Mail: Info@NeuroAssist.com 
 

DISCLAIMER: NeuroResearch is a research company that provides speakers to programs for AMA category I continuing medical education (CME) for physicians, continuing education for psychologists approved by the American Psychological Association, and licenses intellectual property for use. The NeuroResearch formulas and theory of medicine is designed for the use of combining amino acid precursors of the serotonin and catecholamine systems. The formulas are intended to be used as nutritional supplements and not as a drug to treat, mitigate, treat, cure, or prevent disease.   This web site is intended to be educational purposes only. Constantly we receive e-mails from people who are not licensed health care providers. We wish we could answer them, but the new telemedicine laws that were recently legislated (and put in place) prohibit us from providing advice directly to people with no medical license or providing medical care over the Internet.

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

AMINO ACID
SIDE EFFECT PROFILE
 
No patient should have to stop amino acid therapy due to side effects, if the amino acids are used properly in the medical practice.
 
The follow represents over 50 patient-years of data from patients taking amino acids with no drugs.
 
THE GROUP ANALYZED:
  Regarding the following side effect profile:
Ø      It is the Incidence of side effects reported at patient visits.
Ø     A database grouping of 494 patients.
Ø       It represents 1,604 patient visits.
Ø      Patients were under treatment with amino acids only.
Ø     Patients taking prescription drugs that might have effect on neurotransmitters were excluded.
Ø     Patients were from practices that had mastered amino acid therapy.
Ø      The data represents 50 patient-years of treatment.
 
INCIDENCE OF SIDE EFFECTS REPORTED AT > 0.2% OF VISITS.
Ø      Dry mouth ---- 34 (2.1%)
Ø      Insomnia ------ 14 (0.9%)
Ø      Headache ----- 12 (0.7%)
Ø      Nausea -------- 10 (0.6%)
Ø      Dizziness ------- 6 (0.4%)
Ø      Constipation --- 6 (0.4%)
 

INCIDENCE OF SIDE EFFECTS REPORTED AT < 0.2% OF VISITS.

Moodiness, cold extremities, cravings, diarrhea, drowsy, irritability, fingers tingle, sweats, jittery, fatigue, flatulence, palpitations, flush face, hypoglycemia, light headed, sore tongue (glossitis), depression, thirst, abdominal pain, abdominal burning, spots before eyes, non-specific dermatitis.

 
 
 
 

GI UPSET ON START UP

 

 
 

 
 
 
 

  GI upset (98% of start up problems) and other problems that occur on starting the amino acids can be managed properly and easily. With GI upset the typical scenario is that the patient experiences GI upset with the first dose of amino acids. The GI upset then builds until day 3 at which point the patient quits the amino acids.

  From our work we know that start up GI upset occurs in the patients that are most depleted of neurotransmitters, the patients who need amino acid therapy the most. Patients who have recently (in the last 18 to 24 months) been on certain drugs that deplete neurotransmitters can experience this problem at an increased rate. A nutrient poor diet can also contribute to this problem as well as other mechanisms of action.

  So how do you manage this? FIRST you need to tell all patients starting amino acid therapy, “If you have problems with upset stomach as you start the pills, quit the pills until you can get back into the office for instructions on how to manage the problem. Simply doing this will keep new patients from dropping out of treatment if problems with GI upset are encountered.

  When a patient returns complaining of GI upset or other start up problems the proper management is to simply cut back the dosing to one pill at bed time. Bedtime is when the patient is ready to go to sleep not ready get in bed and read a book. If patients with start up problems can take the one pill and fall asleep within 15 to 20 minutes the problems do not crop up. Patients who have experienced GI upset on start up have reported that eating one or two “soda crackers” before taking the pills at bed time also helps the problem, but we have no studies on this. After the patient has had no symptoms for 3 to 4 days, add an additional pill at bedtime and continue to increase dosing in a similar manner until the patient is on 4 pills at bed time then start adding one pill in the AM in a similar manner until the patient is at the starting dose of 8 pills a day. Once the patient is on 8 pills a day the amino acid dosing can be titrated upward as per usual with the NeuroResearch treatment protocols until therapeutic neurotransmitter levels are established as verified by lab testing and clinical observations. It generally takes 3 to 4 weeks to get depleted patients up to the starting dose of amino acids (8 pills a day).

  From the database where the incidence of GI upset on start up is 0.5%, although we have seen practices where the incidence is much higher, such as the practice of an addictionologist or practices that were using large amounts of drugs that had a propensity for depleting neurotransmitters.

 
 
 
 

  In 1999 as we pushed the dosing of amino acids higher and got rid of prescription drugs from the picture in treatment we began to get reports of patients who were experiencing GI upset several weeks or months into treatment. Initially we thought this was from neurotransmitter depletion, but it did not make sense. How could patients under treatment for several weeks or months now be experiencing depletion problems? It took us seven months of intensive patient care to find the answer. These patients all were fully adjusted out on their amino acids to obtain the desired clinical response and the answer was that they were experiencing problems with “carbohydrate intolerance”. These were primarily medical weight loss patients who need higher levels of neurotransmitters and amino acids to obtain the desired response. In weight loss as patients are placed in appetite suppression with prescription drugs or amino acids, in many patients the physical response is to food changes. In this case it was their response to carbohydrates. We found that it was not all carbohydrates but highly selective and usually involved just one carbohydrate. Typically the GI upset occurred in the morning about 2 to 3 hours after breakfast, although the problem could be seen anytime during the day. Most common foods were breads, noodles, and cereals, although rare cases were seen such as the woman who ate fried chicken almost every day and the problem was tracked down to the breading on the chicken. The treatment is to simply remove or change the food involved. For example, I had a 54 year old male present for a clinic visit at 10 AM who was complaining of GI upset at the clinic visit. I asked him, “What did you ear for breakfast?” He said, “Two eggs and two pieces of white bread”. I immediately said, “It is your bread.” He changed from white bread to whole wheat bread and never had another problem until a month later when he ate a piece of white bread.

 
CARBOHYDRATE INTOLERANCE
 

Patient Information Sheet GI Upset Carbohydrate Intolerance

 
 
 

 
 
 
 
 
 
 
 

 

GI UPSET FROM CYSTEINE

 

  All patients taking a combination of amino acid precursors of the serotonin and catecholamine (dopamine, norepinephrine and epinephrine) systems need to take proper amounts of cysteine two pills three times a day) each day to prevent depletion of the sulfur amino acid system. It has been observed in clinics that 20% of patients taking cysteine in the early morning experience GI upset. The mechanism of action of this problem is unknown but the treatment is to instruct patients at the start of treatment to take the cysteine at noon, 4 or 5 PM, and bed time. From time to time you will run into a patient who did not understand the instructions and is taking cysteine in the AM with no problems, this is fine.

   
 
 
 

  Drugs that work with neurotransmitters do not work if there are not enough neurotransmitters to work with. Drugs that work by redistributing neurotransmitter from one place to another in the brain such as reuptake inhibitors and execrators deplete neurotransmitters in the long run in most patients. When this happens drugs quit working and symptoms return.

  The recommendation for treatment is to simply leave the patient on any prescription drugs they may be on at initiation of amino acid therapy until the patient is stabilized on the amino acids. Another consideration exists here. As the patient with diminished effects of prescription drugs is started on amino acid therapy, not only the effects of the drugs once again become fully evident, the side effects of the drugs also become evident. This occurs in approximately 5% to 10% of patients and is more prominent in patients taking a dosing of drugs that is higher than the starting dose. If patients early on in treatment experience symptoms not list above under side effect profile and are on prescription drugs, the work with neurotransmitters, review the side effects of the drugs involved in the PDR. Odds are that the patient is experiencing a drug side effect and the treatment is to lower the daily dosing of the drug instead of cut back on the amino acid dosing.

 

PRESCRIPTION DRUG SIDE EFFECTS

 
 
 
 

 
 
 
 
 

REFORMULATION OF AMINO ACIDS

 

The amino acid formulas and protocols of NeuroResearch were formulated for optimal group results AND to minimize side effects. Use of amino acids outside of there NeuroResearch guidelines is associated as an increase in side effects above those listed at the top of this web page. Also of confusion is the fact that there are amino acid formulas out there for treatment of neurotransmitter disease that were not scrutinized properly in order to minimize side effects in clinical applications.

   
 
 
 

PARADOXICAL REACTIONS

 
  I received a call from a physician who reported that a weight patient started the level 1 amino acid dosing and experienced a profound exacerbation of depression. In responding, the physician had changed the amino acid dosing by significantly lowering the dopamine precursor, while increasing the serotonin precursor with no relief.
  The real problem was the patient was experiencing a “paradoxical reaction” - an exacerbation of depression. When starting amino acid therapy with weight patients or other patients, it is not uncommon for a paradoxical reaction to occur in approximately 2 to 4% of patients. The proper approach to manage paradoxical reactions is to increase the amino acid dosing of both the serotonin and dopamine precursors to the next level, then paradoxical symptoms will resolve in 1 to 2 days. Unless guided by a laboratory test, it is best to use the recommended level changes and not lower the precursor dosing of one system and raise the dosing of the other.

  When faced with a paradoxical reaction, if you decrease the amino acid dosing, you will not resolve the paradoxical reaction, you will simply leave your patient suffering needlessly and never get to where you need to go. Proper management of a paradoxical reaction is to increase the amino acid dosing of both the dopamine and serotonin systems.

 
 
 
 

MORE ON PARADOXICAL SIDE EFFECTS

 
 

When an amino acid dosing is started or increased, some patients experience an increase in their neurotransmitter disease symptoms. This is known as a “Paradoxical Reaction.” Some common examples of paradoxical reactions are:

Ø      Depression becomes worse.
Ø      Sleep becomes worse
Ø      The weight loss patient’s appetite increases.
Ø        Anxiety becomes worse.
Ø      Migraine headaches become worse.
  Any neurotransmitter dysfunction disease can display a paradoxical reaction during treatment.

  If you encounter a paradoxical reaction in your patients, treat by increasing the amino acid dosing to the next level of treatment. Physicians are trained to decrease or stop prescription drugs if a problem is encountered. This is exactly the opposite of what needs to be done with amino acid associated   paradoxical reactions.  When treating with amino acids, decreasing the dose and then bringing it up slowly will greatly prolong the time that patients experience an exacerbation of symptoms, which is unethical.

  In general, paradoxical reactions occur in the first week or two of treatment. However, in Parkinson patients, it is not uncommon to see paradoxical reactions occur after the patient has been treated for several weeks and dopamine is ready to inflect into the therapeutic range. While this primarily happens with Parkinson patients, it can happen later in treatment in other patients as well.

  Paradoxical reactions indicate a need to increase the amino acid dosing. When obtaining urinary neurotransmitter testing on a patient, if you spot a paradoxical reaction, simply increase the amino acid dosing. Do not wait for the results of another test to be returned.

 
 
 
 

   A “Paradoxical reaction” is where symptoms of neurotransmitter disease exacerbate or get worse in the early phases of treatment as the amino acids are started or being adjusted. For example, a weight loss patient complains of increased hunger, a patient with migraine headaches complains of increased headaches, or a patient with depression complains of increased depression. Examples are numerous. All related to increased symptoms of neurotransmitter disease. The knee jerk response of physicians is to lower the dose of amino acids. This is exactly the opposite of what needs to be done. If you have a patient who experiences increased symptoms of neurotransmitter disease early on in treatment the proper treatment is to increase the amino acid dosing to the next step of the treatment protocol NOT decrease the dose. In decreasing the dose and working up slowly you will subject the patient to a situation where they will experience the exacerbation of symptoms for a prolonged period of time and in all probability quit treatment.

 

PARADOXICAL REACTIONS

 
 

 
 
 
 

HEARTBURN

  If a patient complains of heart burn 10 to 15 minutes after taking the pills the problem is easily managed. The amino acid pills are larger capsules and in some patients if they simply throw the pills in their mouth and gulp them down the pills can get stuck in the esophagus producing irritation leading to symptoms of heart burn. Management of this problem is to tell the patients to hold the pills in their mouth for 10 to 15 second with a small amount of water until the surface of the pills start to liquefy at which point the pill will slide down the esophagus into the stomach and not get stuck on the way down.
   
 
 
 
 

DIZZINESS

  If a patient complains of dizziness, the first thing to do is take a history and ask the patient, “What happened before we started treating you if you missed a meal? Did you get dizzy?” Odds are the patient will say, “Yes.” We firmly believe the problem is carbohydrate addiction. Treatment is to increase the patient to the next step of the dosing protocol. The mechanism of action here is complex. Discussion could easily fill more than one newsletter.

   
 
 
 
 

HYPERSOMNOLENCE

 

  If the patient complains of extreme tiredness on starting amino acids, take a sleep history. Odds are that the patient had poor sleep prior to treatment and will have to pay back the acquired “sleep debt” prior to sleeping normal. In extreme cases have the patient start amino acids on Friday if they have the weekend off and tell the patient, “Plan on sleeping all weekend to catch up.