USAAA 2011 Presentation
All about LDA
Written by Rick Neubrander
History of LDA.
The origin and roots of Low Dose Antigen (LDA) therapy are found in Dr. Leonard McEwen’s creation of Enzyme Potentiated Desensitization (EPD) in the 1960s. EPD attempts to eliminate a patients’ allergic reactions by injecting minute doses of numerous allergens in combination with an enzyme called beta-glucuronidase.
EPD was an allergy treatment which was allowed in the United States between 1992 and 2001 through the IRB process. It was shown to be highly successful for a wide variety of allergic as well as non-allergic immune system illnesses. In April of 2001, the FDA intervened, and no longer allowed the 50 or so U.S. physicians who were using EPD to import the materials from the U.K. The reason that the FDA gave the physicians was that they now must apply for an IND (investigational new drug). Such an endeavor costs drug companies hundreds of millions of dollars and years of research studies, something that the fewer than 100 U.S. EPD-providers could do. This was an unnecessary move by the FDA because EPD fell under the grandfather clause due to the fact that it had been safely and effectively used since the mid ‘60s. However, the FDA held firm to their position. Because of their actions, thousands of patients who had been benefiting from EPD shots were now stranded without appropriate medical assistance as there was no other treatment that effectively provided them with the same level of relief that they had been receiving from EPD.
Fortunately for the patients and physicians alike, Dr. William Shrader from Santa Fe, New Mexico, principle investigator for the EPD IRB, Director of the U.S. EPD Society, and the physician who first brought EPD to the States in the early ’90s worked diligently to create an American version of EPD. (To those on this blog who are patients of Dr. Neubrander, it may be of interest to know that Dr. Neubrander, always an innovative thinker for his patients, hosted the first EPD Physician Training Seminar at his clinic in Princeton, N.J. in 1992.)
In 2002, Dr. Shrader began to offer his version of this allergy treatment, something he called low dose allergen therapy or LDA. This therapy has many similarities to EPD. For example, like as with EPD, Dr. Shrader’s LDA therapy injects minute doses of various allergens in combination with the enzyme, beta glucuronidase. Also, as with EPD, LDA is administered to patients about once every sixty days at first, then less often as the patient improves clinically.
What is LDA and how does it work?
LDA consists of 4 different cocktails of numerous antigens in fixed combinations enhanced by including a minute dose of chondroitin sulfate as well as the enzyme beta glucuronidase. It does not contain any foreign proteins, adjuvants, or preservative as found in vaccines and other types of injections. The LDA shots are produced once each month by one specific compounding pharmacy that Dr. Shrader has trained to produce the shots exactly the same month-after-month. In addition, the shots are always fresh because they are only produced and distributed once a month, therefore they are never close to expiring when one receives his or her shot. However, though the FDA “allows” LDA to be used under regulations that apply to compounding pharmacies, it is not an “FDA approved” allergy treatment and therefore not suitable for billing to insurance. (To clear a FAQ: thousands of devices, therapies, and treatments are not “FDA-approved” but safely and effectively are used by millions of Americans every day.) The reason you most likely have never heard of LDA is because the single compounding pharmacy that makes it for the limited number of U.S. physicians and their patients who use it are not allowed to produce it as a retail product, something that the FDA does frown upon and will therefore shut the operation down. With that being the case, the only way you will hear about LDA is by word of mouth from other patients who have experienced it or by one of the few physicians utilizing it in their practice.
The mixture is injected just under the skin, usually in the forearm. The volume of the injection is extremely small, only 0.05 mL. What occurs next is the “immune system ‘sentry’ cells” migrate to the scene to investigate. Once they investigate, LDA seems to work by stimulating the production of T-suppressor cells, ultimately shutting down overactive allergic responses. Thus, LDA activity appears to be primarily cell-mediated, which creates a much longer lasting desensitization than conventional immunotherapy. Typical LDA therapy is repeated initially every two months for several injections (how soon a person can move from more frequent to less frequent shots varies greatly, based primarily on their personal condition) and then less often with time as the patient experiences fewer symptoms that last for shorter amounts of time
LDA immunotherapy is used to treat all types of allergies and immune/autoimmune system problems. This includes, but is not limited to sensitivity and intolerance to foods, allergies to airborne and environmental allergens (pollens, dust, mites, dander, and molds), and even various chemicals problematic in patients who have “multiple chemical sensitivities.” In addition, it has also been useful for many chronic diseases and auto-immune problems that are beyond the scope of this blog to discuss.
What are the benefits of LDA?
What are the drawbacks?
For more information you should contact a doctor who uses this treatment and discuss in more depth the details of this treatment.
Written by Rick Neubrander
I admit it. I love videos. My kids find me a bit weird as I am always finding some new video that is “Awesome”! It pains me to think they start running from me when I charge into a room and say “Have you seen…” My problem is that I keep forgetting where I saw a video to show someone else. So I created a playlist of my favorite documentaries and inspirational videos about autism. This page is not about treatment. It is about knowledge and hope.
I sincerely hope that your reactions to my videos will not be the same as my children’s. Also, if there are videos that you like added make a comment and typing in the link to your favorite video and if I think it fits the theme of this playlist then I will add it.
Click on the photo to see the playlist.
As written by Rick Neubrander.
As many of those who have seen Dr. Neubrander know, he really knows powerpoint and is famous for his presentations as well as his treatment protocols. Recently he created a simple presentation on methylation. It is short and to the point in that the methylation issues so many ASD kids have is very treatable. I like it for another reason. I often get so many people saying “where is your science for what you do?” I think when that question comes up in the future I will use this presentation as just another quiver in my arsenal of biomedical evidence for autism treatments.
This is just a presentation. No sound in the video.
This is the 2nd post in the “Pretty Pictures” series. To review the first post, see Pretty pictures from qEEGs and what they show.
The last article about pretty pictures that showed qEEG information of patients using biomed treatments was admittedly a teaser to whet your appetite to learn more about qEEGs as a means to validate a treatment by showing the improvements in the electrical patterns of the brain. Before I continue with this post I will reiterate what we learned in the previous post that “GREEN IS GOOD — LINES ARE BAD.” That rule will apply for all the images that follow. Also remember that the bump at the front of each head map is the nose; the two bumps on the sides are the ears and your vantage point is from above as if you are looking down on the child’s head facing forward.
Speech and language centers—receptive, expressive, and integrative–are often impaired in children on the autism spectrum. For the majority of children, speech is something that is predominantly a left brain function. Because this post is focusing on speech and the improvements that can be seen from the types of therapy we do at our clinic using our specific protocols, the next set of images I will present will highlight changes that occurred in the left side of the brain. Changes that are necessary for improved speech and language are predominantly functions of the left temporal lobe, posterior-inferior frontal lobe, and portions of the anterior-inferior parietal lobe. As you look at the picture above, the areas involved in speech and language are represented by a region that is several centimeters in size and lies adjacent to where the red (frontal lobe), green (temporal lobe), and gold (parietal lobe) come together and touch each other. Unfortunately the brain is not so simple as to just use these areas for effective speech and language. Therefore, for many children to effectively understand language and effectively speak, the brain often calls upon anatomically similar regions on the right side of the brain to help it out.
In the “BEFORE” image, you see VERY LITTLE GREEN on the left side of the brain. Instead you see yellow, orange and red brain wave activity that represents overactivity. This overactivity causes interference in the child’s ability to understand spoken language, process it appropriately, and then speak effectively. The following analogy should help you understand this concept better. If a child’s teacher is in a quiet room and asks, “Tell me what you did last night,” the child first hears the question (receptive language), processes what the teacher wants to be done (integrative language), and then tells the teacher the answer to what was asked (expressive language). However, if the radio or TV is blaring away (analogous to excess brain activity depicted as yellow, orange, or red on a QEEG), depending on how loud it is and how close the child is to the teacher will determine how much the child hears the question, can process what to do, and then give the teacher the correct answer. The reason is obvious why language did not occur at the desired moment in time, that being because there was too much activity and interference (analogous to “colors” other than green and interference “lines”).
The pictures below show young five and a half year old boy who came to our office naïve to biomedical treatments. Dr. Neubrander started him on two distinct protocols he has developed that combine methyl-B12 and soft chamber HBOT in very specific ways.
After implementing our protocols over the course of 30 days, a different pattern emerged. In the “AFTER” image, you now see A LOT OF GREEN on the left side of the brain. These green areas are the areas that correspond to the speech and language centers and demonstrate that within 30 days of intense therapy, following very specific protocols, we had made substantial”electrical improvements” in the speech and language regions of the brain. This corresponded to major “clinical improvements” documented by significant gains in language as well as cognition. Though I have not discussed it previously, the area of the brain that is responsible for executive functions–how we think and act–is located in the frontal lobes of the brain (the red area in the picture at the beginning of this post). As you compare the before and after pictures above, and additional before and after pictures of this child that will follow immediately below, not only do you see substantial improvements in the language zones, but you also see significant positive changes in both the left and right frontal areas of the brain responsible for executive functions. This is the reason that the child’s parents were amazed at how much his awareness had improved, how he was now “present” to the things going on all around him, and how he was (according to their own words), “now in our world!” As you study the before and after images below, you will see that they demonstrate quite nicely that many areas of the brain were improving, not just his speech and language centers. Though probably unnecessary, it is important to point out the obvious, that being that we cannot fix the brain in 30 days. Therefore you will see that though the “after” picture is much better than the “before” picture, we still have more work to do to “finish the job”.
Before I move on to the next case, I believe that it is important to point out that treatments need to be continued for the best results. Fortunately this boy’s family continued following Dr. Neubrander’s treatment protocols and by their 12 month follow-up, their child had continued to make significant progress and was well on his way to full or almost full recovery, something that typically requires two to three years of combined types of treatments to achieve.
In the prior blog post we showed before and after “Qs” using our MB12 protocol. You should go back and review the “Case 2: MB12 only” images now that you have a better understanding of what information the “Q” shows in relation to the improvements seen in the areas of the brain that controls our speech and language and cognitive functions. Notice the red on the left side, as well as the red in the front and on the right side is also gone and the tremendous number of red lines is also greatly reduced.
To end this post I am going to introduce a set of “Qs” using another one of our protocols, HBOT at 1.5 atmospheres of pressure. Below the “pretty pictures” I will be quoting the doctor’s notes after 30 days of treatment. Pay close attention to the left side of the brain and read the doctor’s notes below.
From the doctor’s notes:
- A severely autistic 7 year old male from a foreign country presented to me totally naïve to biomedical treatments
- He was started on methyl-B12 shots once every three days, basic antioxidants, and my 1.5 atmosphere HBOT “Diagnostic Protocol”
- My speech pathologist evaluated him at baseline and again after 30 days of therapy
- At the end of the 30 days, the parents and speech pathologist reported the following:
- Per the parents: “Mild improvements in speech and language, cognitive abilities, socialization, and emotional responses.”
- Per the speech pathologist: “From my evaluation there is an 8 month improvement in receptive language and a 16 month improvement in expressive language.”
So ends this post. I hope that you are able to see the value in how a qEEG can be used to document the progress a treatment makes in a patient. Most people do not need a “Q” to see the progress of a treatment as they can observe the patient’s positive or negative gains by the behaviors expressed. But for those who have had a “before” and “after” qEEG performed, the documentation it provides will let parents and the doctor see how effective a treatment is for the patient. In addition, if no “immediate gains” were noted, or if gains were not as strong or as intense as the parents wanted to see, the “Q” will help everyone see that the treatment is a valuable one for the child and therefore a treatment that needs to be continued long enough for the hoped-for benefits to be realized by all.
Stay tuned as next week we shall investigate the X spot in autism.
Face it, we all like pretty pictures. Nice even colors. Symmetry. No jagged lines. The beauty of a grassy hill. Well, this post is going to be all about pretty pictures.
Many parents come to me and ask, “How do I know if a treatment works? What proof do you have other than an anecdotal story?” This is where we can show them some of the information we have gathered using qEEG scans.
A qEEG is an EEG which is compared against a database of “normal” EEGs and a graph (pretty pictures) is made showing standard deviations from normal. A normal qEEG would be colored green. Those sections of the brain having too much activity would move towards red. Areas of under-activity would move towards blue. Areas of the brain that do not connect properly are graphed as lines. The thicker the line, the more severe the problem. Therefore, for this first blog all you need to know to be certified as an expert in QEEG interpretation is that GREEN IS GOOD – LINES ARE BAD!
The pictures you will see are drawn over the image of a head. As you look at each “head map”, remember that you are looking down from above. Because the pictures are so small to see clearly, note that the little bump at the top of each picture is the nose and the bumps on the sides represent the ears. As you look at the pictures, you will see that there are five rows and five columns. The meaning of each of these rows and columns is something that we will discuss in more detail in future posts. For now, all you have to know is that a “Q” is looking for several different types of abnormalities in each of these five rows and five columns. These abnormalities will be represented by colors other than green and lines that are either red or blue.
Remember that green is good and lines are bad. Therefore, the qEEG shown below is that of a fairly “normal” brain. A peaceful picture.
The next picture is a common qEEG pattern seen in children with autism. The picture is filled with ragged reds and blasé blues. It is a picture filled with many angry red and blue lines.
I will, over several blog entries, show some qEEGs in a Before and After Format. To start, I will post a before and after picture of a child doing our 6 week “trial” of MB12. The left side of the picture is the “before” image and the right is the “after” image. This “Q” is of a child using our MB12 every 3 day protocol during which absolutely no other changes were allowed other than the addition of methyl-B12. Improvements were evident in the areas of language, cognition, and socialization. Notice the reduction of the reds and the greening of the blues. Finally look at the loss of the problematic lines.
Aaahhh, we all like pretty pictures, especially pictures of success stories. In the picture that follows, you will see a before picture that demonstrates the blank stare so many children on the autism spectrum share. We call this look “Autism Eyes”. Then, for many kids, after they are treated for medical issues by the biomedical methods we use, we get a different look that we call “Autism Byes”.
Hopefully these articles will let you see that biomed is not voodoo science but has actual reproducible scientific evidence of benefit. Stay tuned. More pretty pictures to come!
[The following comment is to help you understand the complexities of choosing one diet over another, combining them, or interpreting lab results correctly. Because of the complexity of the problem, the comment is given for educational purposes. However, you will need to discuss the specific application(s) with your clinician.]
Frequently Dr. Neubrander is asked what diet is the best or in what order the diets should be added. Please note that diets are an individualized thing and there is no simple answer. A few general rules that will apply to most patients the majority of the time (with major exceptions, of course!) are as follows: Begin with the GFCF diet first and observe for clinical benefits. The next diet is usually the SCD followed by the diets that eliminate special foods (elimination and rotation), food chemicals, e.g. phenolics, salicylates, glutamates, excitotoxins, etc. This can be followed by a “limited” low oxalate diet (not yet strict), the Body Ecology diet or the GAPS diet (Gut and Psychology Syndrome diet). The last diet many parents move to is a very “strict” low oxalate diet. NOTE THAT THERE IS NO ‘PERFECT ORDER’ AND DIFFERENT CHILDREN WOULD DO BETTER TO SWITCH THE ORDER. This is something that parents and their clinician could do together, though more often than not parents experiment on their own as they watch what works and what does not work for their child.
As stated, there are reasons that a child may need to skip over “the next usual diet to be added” to go farther down the list. These “skips” or “exceptions” are usually based on a child’s symptoms, a discussion too big and too specific to be covered in this comment. Trial and error is the tried and true method. Lab tests are very often misleading and confusing. In addition, lab tests are not always available for many of the different “mechanisms of action” that may be operative. Even if a lab test was possible to do, because there are so many different lab tests to look at all the different mechanisms — IgE “true” food allergy, IgG non-allergic “delayed” hypersensitivity, difficulty breaking down peptides, gastrointestinal enzymatic deficiencies, cytotoxicity, direct chemical reactions, toxic or intolerance reactions to food components or contaminants, etc — it is financially impossible and impractical to do them all. Therefore, the CLINICAL TRIAL IS THE BODY’S BEST LAB TEST, but only if done in a systematic and progressive manner.
In general the casein-free, gluten-free diet helps over 60% of children on the autism spectrum according to ARI data. Though such a diet has been historically mocked by our detractors as unproven, unhealthy, and ineffective, as time marches on more and more peer reviewed articles are appearing in respectable journals documenting this diet works for a significant subset of the children on the spectrum. The reasons discussed in the published papers why this diet works has a spectrum of its own ranging all the way from “unknown but definite” to “gastrointestinal” all the way to “immunological” reasons. One recently described but definite reason that milk may be playing a negative role in children on the spectrum is because of a cerebral folate deficiency. In the “absolute” deficiency syndrome there is an autoimmune reaction whereby the body produces antibodies against the folate receptors found at the choroid plexus, thus blocking the body’s ability to get reduced folic acid molecules across the blood brain barrier into the cerebral spinal fluid and ultimately into the neurons. It is becoming apparent that every child does not need to meet the criteria to be diagnosed with an “absolute” cerebral folate deficiency to be suffering similar negative neurological symptoms due to a “partial or incomplete” blockade of the same biochemical pathway. Cerebral folate deficiency studies show that when milk is present, the blocking antibodies rise, that when milk is taken out of a child’s diet the blocking antibodies fall substantially, and that when milk is reintroduced, the blocking antibodies once again rise very quickly! Research also shows that the longer one is exposed to milk, the higher the antibody levels become. Of special interest at the time of this post (August 2011) is that out of the 120 children we have tested so far in our clinic for folate receptor autoantibodies, 2/3 of them (65.8%) have been positive to either the blocking and/or binding folate receptor autoantibodies. Of even greater interest is that we can often do something to treat the problem effectively, occasionally even to the ‘Wow-degree’!
What is not well understood is that there are many different “mechanisms” as to why a certain food may cause problems in different subsets of individuals that look alike and have the same types of symptoms. Let’s use casein as one good example. Some patients cannot tolerate casein well because of the “OPIOID” MECHANISM which causes a drug-like reaction. This opioid-like phenomenon is due to the inability of “specific” enzymes that break down key bonds that occur between the molecules holding together certain parts of a casein molecule [also certain parts of a gluten molecule]. Therefore, “if” a patient lacks this specific enzyme, DPPIV ["DPP-four"], casein may not be broken down into its smallest common denominator (single amino acids named “peptides”) and thus remain as polypeptides or “dipeptides,” which are then absorbed and subsequently “misread” by the body’s opioid receptors with which they cross react as opioids [morphine-like drugs]. This “OPIOID REACTION” to casein/milk products is only “ONE SPECIFIC MECHANISM” to a host of mechanisms why dairy may not be good for a certain subset of children. The “ADENOSINE CONNECTION” is “ANOTHER SPECIFIC MECHANISM” whereby dairy products from milk (not eggs), acting through the DPPIV pathway, blocks the effectiveness of methyl-B12.
“ANOTHER SPECIFIC MECHANISM” why some children will do better without dairy products is because the child may have “TRUE FOOD ALLERGIES”, e.g. the IgE antibody response [accepted by all conventionally trained physicians]. Still “ANOTHER SPECIFIC MECHANISM” why some children will do better without dairy products is because the child may have “FOOD SENSITIVITIES/INTOLERANCES” e.g. the IgG antibody response [accepted by most alternative medicine practitioners but only a small percentage of conventionally trained physicians]. “ANOTHER SPECIFIC MECHANISM” would include AN ABNORMAL CYTOTOXIC RESPONSE when the nuclei of cells are directly incubated with casein. When this is done, the nuclei “get angry” by taking in a lot more blue dye and the nuclei look just like the sky before a thunderstorm instead of a pretty blue sky on a summer day. Still “ANOTHER SPECIFIC MECHANISM” would include LACTOSE INTOLERANCE whereby “a different enzyme” than the one described above cannot break down milk sugar. When this happens, the undigested milk sugar bypasses absorption in the small intestine and travels down to the large intestine where bacteria and yeast say, “Yippee, beer and pretzel time!” and have a party on the front lawn of the large intestine. Unfortunately the byproducts of bacteria and yeast being “overfed” is the production of hydrogen and methane gases resulting in the child feeling bloated, having flatulence, and possibly abdominal pain.
Many similar mechanisms are happening with a child that may be better on a gluten-free diet, e.g. the DPPIV opiod-mechanism, the IgE and IgG mechanisms, and the cytotoxic mechanism. An ADDITIONAL MECHANISM comes into play with gluten, that being the AUTOIMMUNE PHENOMENON known as CELIAC DISEASE. In this disorder the body makes an antibody against its own intestinal mucosa. The mucosal lining becomes damaged and therefore the absorptive surface becomes compromised which impairs the body’s ability to absorb. This can be pictured by opening one’s hand to observe the fingers and knuckles which we will define as absorptive surfaces. When antibodies destroy the surface lining, picture this by making a fist. Now compare the two – the first one has a tremendous surface area while the second one has very little. So it is with celiac disease.
A popular diet right now for children on the autistic spectrum is the Specific Carbohydrate Diet (SCD). The “mechanism” at work in this diet is still another enzyme deficiency — a specific class of enzymes that are supposed to break down starches or “two-part, two-molecule sugars.” The food classification known as “carbohydrate” is comprised of individual biochemical units known as sugars [these are "biochemical sugars" that are not the same as the lay term "sugar"]. These biochemical sugar molecules have common names, e.g. glucose, fructose, and galactose. Biochemically these individual units of biochemical sugars are called mono ["one"] saccharides ["sugar molecule"]. When two of these individual sugar molecules are combined, they are now called dissacharides ["two" "sugar molecules"]. When a single “glucose” biochemical sugar molecule combines with a single “galactose” biochemical sugar molecule, the result is the disaccharide lactose, commonly known as “milk sugar.” When a single glucose biochemical sugar molecule combines with a single fructose biochemical sugar molecule, the result is the disaccharide commonly known as “fruit sugar.” When a single glucose biochemical sugar molecule combines with another single glucose biochemical sugar molecule, the result is the disaccharide commonly known as a “starch.” Clinically it seems that there is a subclassification of enzymes that is unable to break down the “starchy” disaccharides [names like isomaltase -- a disaccharidase; palitinase -- a dissacharidase, etc]. These types of disaccharidases are especially hard on the intestinal tract [remember "ase" added to the end of a word just means an enzyme that digests the similarly named substrate, e.g. lactase digests the substrate lactose, etc.]. By simply removing these “relatively hotter disaccharides” from a child’s diet, the child may improve significantly.
Other diets include elimination diets based on “true allergy tests — IgE tests,” on “intolerance/sensitivity allergy tests — IgG tests,” “cytotoxic sensitivity tests — lymphoblastic activation,” or “chemical reactions to food substances,” e.g. the Feingold diet and other similar diets, “metabolic disorders,” e.g. avoidance of foods containing items like phenols, sulfur pathway offenders, tyramines, nightshades, the oxalate diet, etc. Each of these diets may work because of single mechanisms or alternatively because of combined synergistic mechanisms working together.
PLEASE NOTE THAT THE SINGLE MOST VALUABLE LABORATORY TEST is a child’s specific reaction to the introduction, restriction, and then reintroduction of a potentially offending substance. Therefore, When In Doubt, Cut It Out of the child’s diet and observe clinically for results. Understand that the removal of an item may not give clinical results that are easily observable. However, with the reintroduction of the food, symptoms or decompensation may then occur.
The only real exception to the general principle stated above is to the “big baddies,” things that are known to be life-threatening, things like peanuts, shrimp, etc. These are true IgE allergies and could have serious consequences if not respected. To these substances one should not consider reintroducing them just to see if the child has improved or can tolerate the substance or not. The problem is that if reintroduced, two things could happen. With the first reintroduction after being off the food for a period of time, the body may not have an outward reaction, though internally the body will lose what was a “temporary amnesic response” because it had avoided the food for a long period of time while it sets itself up for a serious reaction should the food be ingested again within a relatively short period of time. The second thing that could happen is that the child may react to the first reintroduction of the food and have a potentially life-threatening anaphylactic emergency.
Remember that each child is different and that each diet is different. The best way to determine when to start and when to stop a diet will be different, one child to the next. Therefore I always recommend professional help in these matters. As is standard for my practice, if I believe a result to starting a diet could be “very important,” or have significant benefits or side effects, I will recommend that the diet be started at a time when no other variables are being added or removed from the child’s program. The same general principle applies to the discontinuation of a diet.
Diets are very frustrating, no doubt. They are not “The American Way”! The right diet is not easy to find. And no diet is ever easy to do. It takes commitment by the parents and alters the family’s lifestyle, one of the hardest things for all of us to do – change! However, diets are worth investigating by every parent because when the correct diet is found, many of the troublesome symptoms associated with the autism spectrum will diminish or disappear completely~! Good luck on your journey. We are here to help you in any way we can along the way.
So many of the children we see at our office have issues other than just autism. Many children regress in the spring or in the fall. This is usually because of the increase of pollen triggering an allergic response and often in children on the spectrum — regression. So what options are out there?
I am including a comment we give to our patients as there are several choices available. This comment will discuss the various options as Dr. Neubrander views them and why he he picks LDA as a treatment for autism.
Dr. Neubrander’s comments to his patients:
When parent learn their child has a significant degree of environmental allergies (also called inhalant or airborne allergies), the parents are confronted with the question, “What’s the best way to help my child?” The options parents have are to do nothing, treat symptoms only, to desensitize with conventional allergy shots or by LDA shots. My bias is definitely to try to desensitize the child, either by conventional allergy shots, provocation/neutralization (P/N), serial endpoint titration (SET), or LDA shots rather than to just treat symptoms.
When one just treats the symptoms, it does nothing to get to the root of the problem and only gives short-term benefits. To desensitize gives long-term benefits and does get to the root of the problem. Provocation/neutralization or SET are hybrids between the two, conventional allergy shots and LDA. I have done all of these and for my ASD population, the best answer, relatively speaking and when speaking in accordance with these children’s fears and phobias and the need for repeated invasive treatment, is to opt for LDA.
Conventional allergy shots need to have a series of skin tests and then many desensitization shots over several years. This is definitely an invasive option that is usually not offered early by an allergist, and even more often not offered to young children. Provocation/neutralization or serial endpoint titration are also invasive and require a series of shots to diagnose the problem over several hours and often a couple of days. Treatment may then use shots or sublingual drops. LDA only needs to determine if allergies exist. Therefore, a simple blood test is adequate. The reason this is OK for LDA is because the treatment “generalizes” for types of allergenic stimuli. For conventional allergy shots, SET, or P/N, the treatment is a one-to-one treatment. You must test for a specific antigen, find the specific treatment dose, and then treat from the same vial, lot, and batch number. One tests for oak and treats for oak. The treatment will not “cross over” and treat for elm or maple or sycamore, etc. By contrast, LDA is able to determine one is sensitive to “tree pollens in general” and therefore desensitize to tree pollens in general, whether they come from New Jersey, Texas, or Oregon. Therefore, LDA offers current and future treatment for a great number of allergens that one is in contact with now, or may come in contact with in the future. This is not the case with any of the other types of desensitization.
For LDA to work “optimally”, it has been taught in the past that one needs to avoid certain things while having others in place. As I look back over my long history with LDA and its precursor, EPD, I see that many things we were taught as facts and absolutes are no longer the case. Rather than to go over such a list, let me make my point for today. In the past we have been taught to follow strict diets for LDA to work. We now know that LDA will work for most patients, specifically for this audience children on the spectrum, without having to be on the strict LDA diet. We have also been taught that patients should avoid taking many types of medications and supplements. What we have learned is that most patients do not have to be excessively strict with this as long as they continue to do the same thing as they were doing. We have learned that often it is just as much a “shock to the immune system” to stop something for a while and then restart it after being off for several days. Dr. Shrader, in personal communications with me on more than one occasion, has said that with LDA there is more to gain by doing it, even if we are not doing it perfectly (something we don’t know and change our minds about year after year) than to not do it at all. I have learned over the years that most of my patients who should not have had any results based on the “we gotta be perfect theory” which they couldn’t be on for a number of reasons did improve.
Therefore, because everything is relative when treating children with autism, and because it is rare for a parent to be perfect with anything they are doing, does that mean they shouldn’t try and scrap the whole thing? Take diet for example — there are almost always infractions so should one not do the diet? Take supplements for example — because a child cannot take everything all the time, or because a child cannot take much of what is recommended most of the time, does that mean one should quit? The obvious answer to both of these things is, “No!” So it is with LDA and “the things” that are taught for how to “make it perfect”. The rules and recommendations apply most to patients who are the most severely ill patients, e.g. those that see Dr. Shrader in New Mexico. For the rest of us, and from talking with other colleagues who give LDA to their patients, we do not want to be cavalier but at the same time we need to be practical with the ASD population and their families. The question arises, “What about vitamin C? If my child takes it, will it ruin the shot?” The answer is that it may blunt the total effectiveness of the shot somewhat, but definitely not make it to where the shot fails. The same can be said for the oils. If one wants, one can decrease the total amount of the supplements being taken by 1/2 or 1/8 for two to three days before up to two to three days after the shot if they have vitamin C or oils in them. However, I can say that if given according to the shot frequency schedule I have outlined for children on the spectrum, and if the shots are given for the full three years according to this schedule, and if one does not break the rules and “walk in the posies”, then the shots will still work for the vast majority of patients. Therefore it is my opinion, biased by years of successfully treating children on the spectrum, that the benefit of LDA, when compared to the other forms of therapy, even when not done perfectly, is a better option.
Remember how all those studies came out a few years ago telling us that the diet did not help/cure autism. Parents were imagining this as the studies showed that diet had no effect. The gut has nothing to do with the brain. Studies on well children prescreened to make sure that they had no bowel issues were administered the diet and wonders of wonders the diet did nothing for autism in children with no bowel issues. Well lately things are looking up for parents. So after years of being patronized by physicians and the scientific community, it is now being shown that the parents may not be crazy after all. Here are a few of the more recent articles to come out.
Nutr Neurosci. 2010 Apr;13(2):87-100.
The ScanBrit randomised, controlled, single-blind study of a gluten- and casein-free dietary intervention for children with autism spectrum disorders.
Dept of Pharmacy, Health & Well-being, Faculty of Applied Sciences, University of Sunderland, UK. email@example.com
There is increasing interest in the use of gluten- and casein-free diets for children with autism spectrum disorders (ASDs). We report results from a two-stage, 24-month, randomised, controlled trial incorporating an adaptive ‘catch-up’ design and interim analysis. Stage 1 of the trial saw 72 Danish children (aged 4 years to 10 years 11 months) assigned to diet (A) or non-diet (B) groups by stratified randomisation. Autism Diagnostic Observation Schedule (ADOS) and the Gilliam Autism Rating Scale (GARS) were used to assess core autism behaviours, Vineland Adaptive Behaviour Scales (VABS) to ascertain developmental level, and Attention-Deficit Hyperactivity Disorder – IV scale (ADHD-IV) to determine inattention and hyperactivity. Participants were tested at baseline, 8, and 12 months. Based on per protocol repeated measures analysis, data for 26 diet children and 29 controls were available at 12 months. At this point, there was a significant improvement to mean diet group scores (time*treatment interaction) on sub-domains of ADOS, GARS and ADHD-IV measures. Surpassing of predefined statistical thresholds as evidence of improvement in group A at 12 months sanctioned the re-assignment of group B participants to active dietary treatment. Stage 2 data for 18 group A and 17 group B participants were available at 24 months. Multiple scenario analysis based on inter- and intra-group comparisons showed some evidence of sustained clinical group improvements although possibly indicative of a plateau effect for intervention. Our results suggest that dietary intervention may positively affect developmental outcome for some children diagnosed with ASD. In the absence of a placebo condition to the current investigation, we are, however, unable to disqualify potential effects derived from intervention outside of dietary changes. Further studies are required to ascertain potential best- and non-responders to intervention. The study was registered with ClincialTrials.gov, number NCT00614198.
Notice there is increasing interest. For years parents have said… but only now is there increasing interest. Also the cover your butt conclusion “unable to disqualify potential effects”. So are there any other studies out there? it appears so. More and more studies are coming out showing that the GFCF diet does have a scientific reason for the reduction in symptoms.
J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.
Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives.
de Magistris L, Familiari V, Pascotto A, Sapone A, Frolli A, Iardino P, Carteni M, De Rosa M, Francavilla R, Riegler G, Militerni R, Bravaccio C.
Department Magrassi-Lanzara, Gastroenterology, Second University of Naples, Italy. firstname.lastname@example.org
Intestinal permeability (IPT) was investigated in patients with autism as well as in their first-degree relatives to investigate leaky gut hypothesis. Faecal calprotectin (FC) was also measured in patients with autism, either with or without gastrointestinal symptoms, and in their first-degree relatives.
PATIENTS AND METHODS:
IPT results, assessed by means of the lactulose/mannitol test, were compared with adult and child controls and with FC values.
A high percentage of abnormal IPT values were found among patients with autism (36.7%) and their relatives (21.2%) compared with normal subjects (4.8%). Patients with autism on a reported gluten-casein-free diet had significantly lower IPT values compared with those who were on an unrestricted diet and controls. Gastrointestinal symptoms were present in 46.7% of children with autism: constipation (45.5%), diarrhoea (34.1%), and others (alternating diarrhoea/constipation, abdominal pain, etc: 15.9%). FC was elevated in 24.4% of patients with autism and in 11.6% of their relatives; it was not, however, correlated with abnormal IPT values.
The results obtained support the leaky gut hypothesis and indicate that measuring IPT could help to identify a subgroup of patients with autism who could benefit from a gluten-free diet. The IPT alterations found in first-degree relatives suggest the presence of an intestinal (tight-junction linked) hereditary factor in the families of subjects with autism.
There are more but this one is one of my favorites.
Ann Clin Psychiatry. 2009 Oct-Dec;21(4):205-11.
The possibility and probability of a gut-to-brain connection in autism.
Reichelt KL, Knivsberg AM.
Department of Pediatric Research, Rikshospitalet Medical Centre, University of Oslo, Oslo, Norway. email@example.com
We have shown that urine peptide increase is found in autism, and that some of these peptides have a dietary origin. To be explanatory for the disease process, a dietary effect on the brain must be shown to be possible and probable.
Diagnosis was based on DSM-III and DSM-IV criteria. We ran first morning urine samples equivalent to 250 nm creatinine on high-performance liquid chromatography (HPLC) reversed phase C18 columns using trifluoroacetic acid acetonitrile gradients. The elution patterns were registered using 215 nm absorption for largely peptide bonds, 280 nm for aromatic groups, and 325 nm for indolyl components. We referred to a series of published ability tests, including Raven’s Progressive Matrices and the Illinois Test of Psycholinguistic Ability, which were administered before and after dietary intervention. The literature was also reviewed to find evidence of a gut-to-brain connection.
In autistic syndromes, we can show marked increases in UV 215-absorbing material eluting after hippuric acid that are mostly peptides. We also show highly significant decreases after introducing a gluten- and casein-free diet with a duration of more than 1 year. We refer to previously published studies showing improvement in children on this diet who were followed for 4 years and a pairwise matched, randomly assigned study with highly significant changes. The literature shows abundant data pointing to the importance of a gut-to-brain connection.
An effect of diet on excreted compounds and behavior has been found. A gut-to-brain axis is both possible and probable.
The gut and diet CAN influence the brain! Shocking I know. Such a recent discovery except for the part of disregarding parental testimonies for 15 years or so. Maybe in the future, science will pay attention to parents and try to design studies that look for the why parents are seeing something rather than looking for the why a treatment could not work.
Recently it has come out that a subset of ASD kids have issues with recently discovered folate autoantibodies of the blocking and binding types. In spite of all the big words the prior sentence has, this actually opens up a new way of testing and treatment for those children that are in that subset. In plain English, the body is attacking itself by targeting the folate receptors. As anyone who has taken a high school health courses knows, antibodies are designed to fight the foreign invaders (bacteria, virus, or anything not considered part of the body) and utterly destroy them so the body can remain pure and healthy. But somehow, the body has been tricked into fighting itself and destroying the ability of folate to bind and be transported through the nervous system leading to a neurological impairment.
For the past several months, our clinic has been having children the doctor has suspected of having this issue tested for these antibodies and the findings have been surprising to say the least. Over half of the children tested are coming up positive! This has opened up a new line of treatment for these kids in that high doses of folinic acid have produced clinical benefit.
In spite of the fact that another issue with ASD has been identified and treatments exist for this problem, the real questions are…. Why is the body attacking itself? What triggered an autoimmune reaction? Is molecular mimicry to blame and if so, what started the initial assault? Was it something in the environment? Inquiring minds want to know.
This post will be my last for the present time on MB12. I will most likely return to this subject at a later date but I do not wish to lose the attention of my readers and so the next post will be on some of the other treatments we use at the clinic. But for today, I wish to focus on what Dr. Neubrander terms “A Really Cool Rat Study”.
So why would he get so excited about a study done on rats and what does it mean for the patient? Since 2002 Dr. Neubrander has been saying the MB12 given in high doses as an injection makes a difference for children with ASD. For several years it was his observations and parent anecdotes as the only confirmation that MB12 could make a difference. That all changed when this rat study came out. Now there is a bit of vindication for justifying the use of MB12 but with a slight drawback; the study did not mention autism. Through this study the benefits of MB12 on nerve and nerve repair is shown and may provide an insight into why it works on autism, but as usual, ‘more study is needed’.
I am including a comment that Dr. Neubrander gives to patients regarding the Okada study.
Please note that at the end of this comment I am including the abstract from a recent publication showing that the methyl analog from the cobalamin “family” (methyl, adenosyl, hydroxy, cyano, glutathionyl, and sulfito cobalamin) is the one that is the most biologically active. What is important to me from the article itself, not the abstract, is that though the methyl form is the most biologically active form, it is short-lived and the authors say that possibly a better delivery system is needed, e.g. “injections”. They also say that greater benefits or benefits at all are seen at the higher doses. I have been saying these exact same things for years — injections and daily shots!
Richard Deth, Ph.D. from Northeastern University in Boston, professor, colleague, and friend of mine dealing with the methylation phenomenon, is a world-renowned researcher in methionine synthase. As you know, methylcobalamin is the form of B12 that works hand-in-glove with methionine synthase. On March 31, 2010, Dr. Deth commented on the Okada article: “Although the article (Okada et al.) is basic science, it does provide some important insights into the effects of methyl-B12 (MeB12) on neurons and how it does it. Using neurons from rats, they showed that MeB12 increases the length of axons, the formation of neurites, and increases resistance to apoptosis. Together these effects indicate a significant role in development of networks among neurons. MeB12 was the best form of cobalamin for doing this, although others had activity, presumably because they were converted to MeCbl. They also showed that the effects of MeB12 reflected increased methylation, and adding SAM had similar, but weaker effects. MeB12 increased activation of the MAP kinase and PI3 kinase signaling pathways, indicating that it mimics the effects of neurotrophic growth factors. Finally, MeB12 improved the repair of transsected nerves as well as improved functional recovery of motor activity, in conjunction with increased myelination. All together a pretty impressive array of effects.“
The abstract on this study I posted below. You can look it up on pubmed, but I am listing it here for your convenience.
Exp Neurol. 2010 Apr;222(2):191-203. Epub 2010 Jan 4.
Methylcobalamin increases Erk1/2 and Akt activities through the methylation cycle and promotes nerve regeneration in a rat sciatic nerve injury model.
Okada K, Tanaka H, Temporin K, Okamoto M, Kuroda Y, Moritomo H, Murase T, Yoshikawa H.
Department of Orthopaedics, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Methylcobalamin is a vitamin B12 analog and is necessary for the maintenance of the nervous system. Although some previous studies have referred to the effects of methylcobalamin on neurons, the precise mechanism of this effect remains obscure. Here we show that methylcobalamin at concentrations above 100 nM promotes neurite outgrowth and neuronal survival and that these effects are mediated by the methylation cycle, a metabolic pathway involving methylation reactions. We also demonstrate that methylcobalamin increases Erk1/2 and Akt activities through the methylation cycle. In a rat sciatic nerve injury model, continuous administration of high doses of methylcobalamin improves nerve regeneration and functional recovery. Therefore, methylcobalamin may provide the basis for better treatments of nervous disorders through effective systemic or local delivery of high doses of methylcobalamin to target organs. Copyright 2009 Elsevier Inc. All rights reserved.
PMID: 20045411 [PubMed - indexed for MEDLINE]
In continuing the series on the use of MB12 in autism, I am going to discuss the role of MTHFR and Glutathione. The last article showed that the MTHFR mutation is more common in people with ASD than in the regular population. The study listed below makes a correlation between MTHFR and low levels of Glutathione in the blood.
Experimental Biology 2005. April 2. San Diego . Abstract
Low plasma methionine, cysteine, and glutathione levels are associated with increased frequency of common polymorphisms affecting methylation and glutathione pathways in children with autism
S. Jill James, Stepan Melnyk, Stefanie Jernigan. Pediatrics, University of Arkansas for Medical Sciences, 1120 Marshall St. , Slot 512.40B, Little Rock , AR , 72202
Autism is a complex neurodevelopmental disorder that is thought to involve both genetic and environmental factors. The 10-fold increase in the prevalence of autism in the last 15 years is a major public health concern. Although abnormal thiol metabolism has been associated with other neurologic diseases, these pathways and related polymorphisms have not been evaluated in autistic children. Plasma levels of metabolites in methionine transmethylation and transsulfuration pathways were measured in 90 autistic and 45 control children using HPLC with electrochemical detection. Polymorphic variants in transcobalamin II (TCII), methylene- tetrahydrofolate reductase (MTHFR), methionine synthase reductase (MTRR), catecholamine-O-methyltransferase (COMT), and glutathione-S-transferase (GST) M1/T1 were evaluated in 233 autistic children and 183 controls. The results indicated that mean levels of methionine, cysteine, total glutathione, and the ratio of oxidized to reduced glutathione were significantly decreased among the autistic children. The frequency of MTHFR 677CT/1298AG heterozygosity, TCII 776GG, COMT 1947GG, and the GST M1/T1 double null genotype was increased in the autistic children relative to controls. We hypothesize that an increased vulnerability to oxidative stress (environmental and/or intracellular) may contribute to the development and clinical manifestations of autism.
So what does this mean for a patient? Glutathione is the body’s natural detoxification mechanism. Its job is to move ‘bad stuff’ out of the body. If you do not have enough, then harmful substances can accumulate and thus affect health; or if the toxins get too high, they can affect brain function. So how does glutathione affect the brain and what does this have to do with MB12? The following is a comment that Dr. Neubrander gives to his patients that (while a bit technical) may explain some of the processes involved.
According to the work of Dr. Richard Deth, methyl-B12 seems to work better in the brain, especially the cortex, than it does in the liver. This is probably because glutathione is very abundant in the liver but limited in the brain and methionine synthase in the brain is configured differently than in the liver. The methyl-B12-requiring form of the methionine synthase enzyme will only be active when there is enough glutathione around to synthesize methyl-B12. Of course the first step is the conversion of hydroxy-B12 to glutathionyl-B12. This occurs spontaneously when hyroxy-B12 and glutathione are simply mixed together. It’s limited only by the glutathione level, which is how nature designed it. So in tissues like the brain (neurons) where glutathione is scarce, methionine synthase activity will only be turned on when glutathione is adequate. Otherwise homocysteine will be continuously diverted toward glutathione synthesis. Thus methylation (i.e. D4 receptor activity) in the brain is only allowed to occur when there is enough glutathione. Things that lower glutathione (e.g. mercury) will therefore particularly lower methylation activity in the brain. SAM is also required for methyl-B12 synthesis, but does not seem to be as critical a limiting factor as glutathione.
At least theoretically, there could indeed be people for whom hydroxy-B12 might be better than methyl-B12. Making methyl-B12 available all the time removes the glutathione contingency for methionine synthase activity. It does guarantee that the D4 receptor phospholipid methylation mechanism will always be operating at better efficiency, despite lower glutathione levels, which is probably the main cognitive benefit of methyl-B12. However, allowing hydroxy-B12 to be converted to glutathionyl-B12 by glutathione may be important for other aspects of methylation. For example, consider DNA methylation. When methionine synthase stays turned off, homocysteine and SAH accumulate. The SAH will inhibit DNA methylation and “turn on” some genes that used to be silenced by methylation. Some of these genes may serve a useful role in combating oxidative stress. When methyl-B12 is given it will tend to lower homocysteine and SAH, which will tend to increase DNA methylation. Of course at this time we can only speculate about what genes might be involved, so this is just a theoretical perspective.
In general there is the possibility that too much methyl-B12 could be a problem, so finding the right dose and right duration of therapy for a given individual remains an important consideration. Hopefully in the near future there will be laboratory tests allowing us to discriminate between who needs methyl-B12 or hydroxy-B12 and who doesn’t.
Since May of 2002, Dr. Neubrander has been stressing the importance of MB12 for children on the spectrum. His initial finding of MB12′s benefits came by accident. In treating a non-verbal seven-year-old autistic patient, he decided to try a new form of B12 to help with some of the nutritional issues seen in this particular patient. One week later, in the middle of a huge storm that was hitting New Jersey, the parents of that child came unannounced to the office and ran down the hall shouting, “What was that you gave our child? He started speaking!” Thus history was made that day.
So why does MB12 help so many on the spectrum? This first series of blog posts will go through the various aspects of why MB12 is needed and how it helps. To start the series, I will be getting a little scientific but hopefully can explain it in such a way that an ordinary, non-medical person can understand.
First I am going to discuss the MTHFR mutation. I will probably be touching on this subject in future posts, but today I will start off with one study showing that people with ASD have a higher rate of mutation in the MTHFR gene, and then will follow with the doctor’s explanation of how this impacts persons with the mutation. Dr. Neubrander has written a preface for the study that we give our patients and I will begin with that comment, follow with the abstract, and end with an explanation of what this means in lay-terms.
JUNE 2009: Preface by Dr. Neubrander to the following published study – Please note that in my practice I have been testing most patients for MTHFR and homocysteine status. Though I have not yet officially tabulated the results from my patient population, I can definitely say by “seat-of-the-pants science” that the incidence of the MTHFR mutations, whether C677T or A1298C, are much higher than what was reported in this study. I can also say that most of my patients have at least one mutation; many have two. It has been my observation that children with the C677T homozygous (double) mutation are the most likely to respond to MB12 and with some of the best “initial intensities of response”. Children who have a single (heterozygous) mutation of the C677T allele or who have two single mutations on the two different alleles, C677T (heterozygous) and A1298C (heterozygous) or who have double mutations (homozygous) of the A1298 allele are the next most likely group of children to respond to MB12 injections. As a general rule, this group of children demonstrate responses fewer in number and of a lesser intensity when present. Children with a single (heterozygous) mutation of the A1298C allele represent the group of children whose responses, though present, are usually the fewest in number and of the least intensity. It is interesting to hypothesize why some of the best responders, both in number of responses and intensity of responses, have no MTHFR mutations.
Psychiatr Genet. 2009 May 13. [Epub ahead of print]
Aberrations in folate metabolic pathway and altered susceptibility to autism.
Mohammad NS, Jain JM, Chintakindi KP, Singh RP, Naik U, Akella RR.
a. Center for DNA Fingerprinting and Diagnostics
b.Institute of Child Health, Niloufer Hospital, Hyderabad, India.
OBJECTIVE: To investigate whether genetic polymorphisms are the underlying causes for aberrations in folate pathway that was reported in autistic children. BASIC METHODS: A total of 138 children diagnosed as autistic based on Diagnostic and Statistical Manual of Mental Disorders, fourth edition criteria and Autism Behavior Checklist scoring and 138 age and sex matched children who are nonautistic were tested for five genetic polymorphisms, that is, cytosolic serine hydroxyl methyl transferase (SHMT1 C1420T), methylene tetrahydrofolate reductase (MTHFR C677T and MTHFR A1298C), methionine synthase reductase (MTRR A66G), methionine synthase (MS A2756G) using PCR-restriction fragment length polymorphism methods. Fisher’s exact test and logistic regression analysis were used for statistical analyses. RESULTS: MTHFR 677T-allele frequency was found to be higher in autistic children compared with nonautistic children (16.3 vs. 6.5%) with 2.79-fold increased risk for autism [95% confidence interval (CI): 1.58-4.93]. The frequencies of MTRR 66A allele (12.7 vs. 21.0%) and SHMT 1420T allele (27.9 vs. 45.3%) were lower in autistic group compared with nonautistic group with odds ratios 0.55 (95% CI: 0.35-0.86) and 0.44 (95% CI: 0.31-0.62), respectively, indicating reduced risk. MTHFR 1298C-allele frequency was similar in both the groups (53.3 vs. 53.6%) and hence individually not associated with any risk. However, this allele was found to act additively in the presence of MTHFR 677T allele as evidenced by 8.11-fold (95% CI: 2.84-22.92) risk associated with MTHFR 677CT+TT/1298AC+CC genotypes cumulatively. CONCLUSION: MTHFR C677T is a risk factor, whereas MTRR A66G and SHMT C1420T polymorphisms reduce risk for autism. MTHFR A1298C acts additively in increasing the risk for autism.
So what does this mean? Of what importance is MTHFR to ASD? I am including a comment we give our patients to explain in simpler terms what MTHFR does.
The way that the MTHFR enzymatic defect fits into this whole scenario is that folic acid family members from food must travel down a biochemical pathway and present itself to the enzyme MTHFR [methyltetrahydrofolate reductase]. This enzyme then will catalyze the biochemical reaction that allows the precursor “unmethylated” folic acid molecule to grab onto extra hydrogen atoms and now become a “methylated” folic acid molecule [5-methyltetrahyrdofolic acid]. It is the methyl group from this methylated folic acid molecule that can now donate the methyl group to “rabbit B12″ — the plain ole’ ordinary B12 that comes from food or supplements – so that rabbit B12 now becomes “methyl”-B12. It is this methyl-B12, whose methyl group originated from the “MTHFR processing plant”, that will react with the enzyme methionine synthase to go on to donate this same methyl group to homocysteine to now become “methylated homocysteine” whose “other name” is methionine. It is this methionine that moves on to eventually donate this same methyl group to the brain to make proper functioning RNA, DNA, neurotransmitters, speech and language molecules [creatine], and nervous signal synchronization molecules [phospholipids]. Once this methyl group has been donated, the “methyl carrier molecule — metabolic smoke” eventually winds up to become homocysteine again. Once homocysteine is formed, it acts like a traffic cop deciding to send traffic to the left or to the right. “About” half the time homocysteine goes back to get another methyl group from “the next” methyl-B12 that shows up as the process described above repeats itself. “About” the other half of the time homocysteine decides to become glutathione which is the body’s major intracellular antioxidant and one of the body’s major way to detoxify many types of poison, only one of which is mercury.
The MTHFR enzyme has legs just like we have legs. We call our legs “left leg — right leg”. On both legs we are supposed to have ankles and knees. MTHFR’s legs have funny names. The name of one leg is C677T and the name of the other leg is A1298T. The name of MTHFR’s ankles and legs are C and T or A and T. Now here’s what’s happening. When we try to run, we do very well if we have two legs with knees and ankles. If we have an amputation of one ankle, we can still get around but we will definitely be slowed down. If we have an amputation above the knee, we will still be able to get around but much, much slower. If we had an amputation of a knee or ankle on the other leg, once again we would get around much, much slower. So it is with the ankles and legs on the MTHFR enzyme. If there is a single mutation, called heterozygous, one of the legs will have been amputated at the ankle. It there is a double mutation on the same leg, called homozygous, that leg will have been amputated above the knee. Combinations of heterozygous and homozygous mutations [analogous here to "amputations"] can occur.
What the developing research is finding is that mutations of the MTHFR enzyme occur quite frequently in children on the autistic spectrum. Therefore, as you can now see, these children will have a “slowed ability” to produce the methylated folic acid molecules that are required to form “enough” methyl-B12 at the rate necessary to make “brain things” and to make “detoxification things”. Therefore, in order to bypass this defect, methyl-B12 must be administered on a continual steady-state basis. This is the reason that injectable methyl-B12 into the subcutaneous tissue accomplishes this goal. By being in the subcutaneous tissue it slowly leaches out and provides a continual supply of “just a little bit” of methyl-B12 to be available for methionine synthase to use to recycle homocysteine.
Along with a new website, we have decided to put out a blog that will post information about the various biomedical treatments that we have found useful in our practice. This blog will not only address treatments for autism, but I intend to post articles that will address other issues that demonstrate biomedicine’s benefit in restoring health.
Our society is sick! When I grew up, I did not know of one person with autism, peanut allergy, or asthma. Now in almost any classroom, teachers will have a child with at least one of the above issues. Autism has risen steadily at alarming rates since the mid to late 80s. Asthma has also increased at an astounding rate. Schools today have had to ban any peanut products since there now exists such a high statistical chance that a student could enter into anaphylactic shock. What is happening to us as a society? Why has sickness increased so much when modern medicine has “progressed” so much?
There are so many theories as to why this is happening. I have several opinions I think may contribute to the current rise, but as they are opinions this blog will not be used to discuss matters that as of today cannot be proven one way or another. Instead, this blog will be used to discuss how our health can be affected using biomed.
Going forward, we will attempt to bring articles to your attention that discuss how a treatment can affect your child both positively and if any side effects are noted. We will also welcome suggestions on articles you would like to see the doctor address. I intend to post one to two articles a month.
This first post is an introduction. Please share your thoughts so that we can make this site a useful tool for each of you.