ESSAY - A TIMELINE REGARDING A DECISION TO PRESENT A HYPOTHESIS THAT STATES THAT ELECTRICAL EMISSIONS IN SOME INSTANCES ARE ASSOCIATED WITH THE DEVELOPMENT OF AMYOTROPHIC LATERAL SCLEROSIS (ALS)
BURTON A. WAISBREN SR. M.D. FACP
Epigram: There is nothing new under the sun, what happens once will happen again.(1)
Hypotheses do not spring like Athena from the forehead of Zeus. Rather in most instances they spring from a distillation of various experiences of their authors. It is in this frame of reference that this hypothesis is being presented. The statement of the hypothesis is that in some instances exposure to electrical emissions will result in the development of Amyotrophic Lateral Sclerosis (ALS). *
1955 - Gajdusak presented a paper at an Atlantic City medical meeting that I attended. He described a syndrome that he had observed while on a government sponsored mission in New Guinea (3). There he found a remote tribe whose members were dying of a disease that resembled Parkinsonism. It was called by the natives Kuru. The disease noted was similar to a disease in sheep called scrapies (4). The disease was found to be contagious only when members of the tribe, who were cannibals, ate the remains of its victims.
It’s cause was a new type of microorganism which is now called a Prion(5).
* ALS is used here in the context that is a disease of the motor neurons in the spinal cord that may have more than one cause (2).
1960 - Harold Simon published a book that detailed medical syndromes caused by attenuated micro organisms (6).
The works of Gajdusak and Simon awoke in me an interest in treating some diseases of unknown etiology with modalities that would either destroy attenuated organisms or would help the body to do so (3,6).
1961 - My friend and laboratory assistant developed rapidly progressing Multiple Sclerosis which was unaffected by the treatments being prescribed by several neurologists.
Accordingly, I discussed with him and his family the idea of treating him on an empirical basis with the immunomodulators I had been using for intractable cancers (7). These were BCG, transfer factor, and a mixed bacterial vaccine. The patient and his family agreed not only to immunomodutation treatment but to donate their blood so that its lymphocytes could be used to make the transfer factor.
All concerned understood that the basis of the treatment was the possibility that M.S. was caused by an attenuated infection which might respond to immunomodulation. We now know that M.S. is a acquired autoimmune disease. The response was so satisfactory that the treatment was continued for the next 30 years before he died of emphysema (8). Why the treatment might have helped is conjectural. Others in the community heard of his apparent response and presented themselves for similar treatment.
During the next 30 years about sixty patients with Multiple Sclerosis were treated in this manner. Some appeared to have been helped but their numbers prelude any attempt at a scientific evaluation (8). .
1980 – Phillip Milonic*, a patient who had progressive Multiple Sclerosis told me that he knew exactly when and how he got his Multiple Sclerosis. It was 10 days after he had received a vaccination against Swine flu disease in 1976 (9). His personal observation led to my now generally accepted finding that autoimmune disease can follow antigenic exposure to microbial vaccines (10,11,12).
1984 – A 35-year old former marine who’s ALS had developed after his being stationed in Guam requested treatment of his ALS of the type being used for M.S. (8). After a careful explanation that the idea was a “long shot” based on possibilities, we decided to start an immunodulation treatment but after several months he became discouraged and disappeared. We know now that ALS caught on Guam is not the “garden variety” type of ALS found in the United States.
1985 – Intrigued by this experience, I wrote to Dr. Forbes Norris who was at that time the accepted expert of ALS in this country and asked him if he would like to try using our transfer factor on some of his patients. He was, so we sent him enough transfer factor to treat ten patients. He wrote me six months later and informed me that the transfer factor had not helped any of the ten patients (13). So the matter was dropped. However, this is how ALS crept into my minds’ data bank.
*Mr. Milonic and the other patients mentioned in this essay gave their permission for their names to be mentioned in any reports about our activities
1986 - A patient, Ronald Shinabery, appeared for a consultation regarding treatment for his early ALS. He had heard of our treating diseases of unknown etiology for possibilities rather than probabilities. He told me that he knew what caused his ALS. He had purchased an electric powered recliner in which he sat watching television for the several years before he developed ALS.
He was an electrical engineer and it had occurred to him that electrical emissions from his recliner were the cause of his disease. He was trained to study electrical emissions and found his recliner to be defective in that respect. His initial research on the subject caused him to find the fact that three members of the San Francisco professional football team had developed ALS (14). A retired quarterback, Robert Waters, was still alive and Mr. Shinabery contacted him. Mr. Waters confirmed Mr. Shinabery’s hunch that he had spent many hours having his aches and pains treated in the training facility of his football teams. I contacted Mr. Waters, who then was coaching a college team. He confirmed that he had spent many hours exposed to diathermy and other electrical devices during his football career. In fact he had heard of other football players suffering from ALS. Because of this, Milorganite the fertilizer in use on football fields had been suggested by some to be the cause of ALS (15). Mr. Waters told me that when he had asked someone in the central office of his team about the electrical safety of their training facility they broke off all contact with him. Mr. Shinabery found Mr. Waters because he was featured in a story in a sports magazine (14).
I then wrote to both the San Francisco 49ers and to the Professional Football Union inquiring about safety checks of the electrical equipment in their training facilities. I received no answer.
1988 - Dr. Wortman, a physician in New Jersey, published a letter in the Journal of the American Medical Association in which he said that he had developed ALS shortly after he had received a severe shock from a defective handheld drill (16).
1989 - An electrical engineer in Canada who had heard of my interest in ALS called me and asked if his ALS could have been caused by his occupation which was involved in working with and diagnosing malfunctioning electrical equipment. He had received many shocks in connection with his work. I told him that I thought that this was possible. I never heard from him again, perhaps because I told him the association could not be proven at that time.
Mr. Ronald Shinabery, the electrical engineer, and Robert Waters, the football player, agreed to co-author a letter that we submitted to the Journal of the American Medical Association. It was entitled “The Possible Relationship between Electrical Exposure and Amyotrophic Lateral Sclerosis” (17). The letter was rejected for publication with no comment.
1989 - My interest in ALS was further stimulated when the son of a woman who was on a respirator and dying of ALS asked me the following question: Since his mother had suffered a serious case of documented Lyme disease just before the onset of her ALS would it be reasonable to treat her Lyme disease as possibly related to her ALS? I told him that I thought there was nothing to lose and that if her personal physician at the nursing home where she was and the family would agree, it was a reasonable thing to try. Accordingly, the patient was given 2 grams of Ceftriaxone intravenously for two weeks when she suddenly died. During the two weeks, all concerned felt that she had improved greatly. It was thought at the time that she died due to her ALS, but in our present state of knowledge her death might have been to a Jerish-Herxheimer reaction (18).
I couldn’t resist following up on the idea that her Lyme disease might have some relationship to ALS. I had heard that Dr. Cashman, a professor of neurology at the University of Wisconsin Medical School in Madison, had saved 54 frozen sera from patients with ALS with the hope that they might eventually be useful. I contacted him and he agreed to have the sera tested by Dr. Snell, a microbiology professor at his medical school for antibodies against Lyme disease. Five of the sera tested positive. This finding was published in the Lancet, a peer reviewed medical journal (19). In the article the suggestion was made that it might be worthwhile to treat some cases of ALS with Ceftriaxone, an antibiotic that had recently been found to be active against the spirochete that causes Lyme disease.
2001 – Rothstein, a brilliant scientist who heads the ALS service at John Hopkins Medical School, made a landmark observation that a glutamate elevation in the motor nerve cells of ALS patients seriously damaged them to the point that the muscles they stimulate became paralyzed (20,21,22). Furthermore, he found that this was due to the failure of a feedback enzyme (EAATZ), in the cells which control the intracellular levels of glutamate (21,22).
Concurrently, it was found by Rothstein that Ceftriaxone, the antibiotic that happened to be effective against Lyme disease, prevented glutamate from damaging nerve cells (22). Because of this he proposed that a study be done to determine if Ceftriaxone would help patients with ALS. He was able to get government funding for this study which is now going on at many ALS centers in the U.S. (23).
Either because of Rothsteins’ work or because of the possible relationship to Lyme disease to ALS, there have been a number of ALS patients treated with Ceftriaxone with no scientific reports regarding its efficacy. However, there has been some “internet murmurings” regarding its effectiveness (24,25,26).
All of this is being mentioned here because it fits in with the concept of treating diseases of unknown etiology or the basis of possibility rather than probability (27). Here there are three possibilities. One is that ALS and Lyme disease are related, another is that coincidently Ceftriaxone may be effective in this syndrome because of a metabolic rather than on an microbial basis, and third could be electrical emissions are a co-factor with Lyme disease in causing ALS. This last idea surfaced because two similar cases have surfaced at this clinic and in both instances they had chronic Lyme disease and laptop computer exposure.
2008 – The timeline regarding the decision to present this hypothesis ended in February of 2008. This is because if this hypothesis it true it may result in some cases of ALS being prevented and it also will reveal methods to study ALS by electrical inducement of the metabolic abnormalities of the disease by surrogate methods that use animal models of the disease or cell culture models of the disease (28,29,30). By surrogate methods is meant methods that may either substantiate a hypothesis or tend to denigrate it.
A description of the key case follows: The patient is a 52-year-old computer specialist, who in September of 2006, began to notice progressive weakness of both lower legs. He saw three neurologists both of whom felt that he had early ALS. His EMR was positive for this disease. A spinal tap and MRIs of his brain and spinal cord were negative. He had previously been in excellent health. He presented himself to me because my website had discussed neurological complications from Hepatitis B vaccinations which he had had because of the travels necessary for his occupation. He also lived in a Lyme county and had tick exposure and had read about treatment of ALS for Lyme disease on my website. He was in a wheelchair because of the severe weakness of his legs.
My examination showed leg weakness, absent abdominal reflexes, and depressed ankle and knee jerks. All of the serologic tests done to diagnose Lyme disease were negative.
During a post-examination conference with the patient, I shared with him the experiences I have discussed above in regards to electrical emissions and ALS. At that point his face lit up and he told me that for the past 3 years he had spent almost every working day with his laptop computer on his lap. He asked if this could have caused his problem.
At this point, after hearing his hypothesis about his laptop computer, I decided again to share my hypothesis with my colleagues, that electrical emissions could be involved in ALS (17). This is because even a brief review of the literature and the internet suggests that electrical exposure may be involved in ALS (31,32). Computers are known to express electrical fields, and the proximity of the of the laptop computer when it is held on the lap is so close to the nerves of the spinal cord that it is reasonable to conclude that if electrical impulses are involved in ALS that motor nerves might be damaged by electrical impulses. The patent office of the United States evidently thought that a problem exists because they granted a patent for a device that would reduce computer RF emissions (33).
I then discussed with the patient the possibility that his conclusion might be correct and that if that was so, some treatment based on Rothsteins’ recent findings might be in order.
Then, when and if, electrical emissions of some magnitude could be demonstrated to be put out by his computer, actions dictated by Rothsteins’ studies would be done (26). First would be determinations of the glutamate and EAATZ levels in his spinal fluid. Then if these determinations revealed abnormal findings, second opinions would be sought before empirical treatment with Ceftriaxone would be started.
When all of this is being considered, what are the options of the key patients? Should he enter into the multicenter study regarding Ceftriaxone use in the treatment of ALS? (33) Should he accept an unblinded approach to a 6 gram daily dose of Ceftriaxone given intravenously for at least 6 months? Should he try oral antibiotic treatment for ALS? Should he get further consultation before making a decision? (He is already doing this.) Should he except conventional wisdom and take Rilutec and hope something better will surface in the future? It goes without saying that in situations such as this, patients will have to make their own decision on what course to follow.
DISCUSSION and CONCLUSIONS
This case study and its discussion is being presented here and briefly on the internet because this observation may cause to be revealed other cases of ALS among computer users. Hopefully if this occurs, they will be shared by those who observe them with their colleagues either by case reports or internet discussions. If similar cases surface, those who are exposed to excessive laptop computer use may want to seek protection from radiation put out by their computers (23). Manufactures and government agencies might want to add additional manufacturing requirements and warnings designed to decrease potential dangers from electrical exposure from computers.
After coming to the conclusion that it was timely to share this hypothesis with my colleagues I felt that the next order of business was to turn to the computer which was under suspicion as the cause of my patients difficulties. Not being trained in or conversant in the field of electrical emissions or tests to determine them, I searched out two renowned experts in this field. I found Dr. James DeMeo M.D. and PhD on the internet and Dr. Sam Milham M.D., DPhD through Mr. Louis Slesin editor of Microwave News.
I contacted both of them and they both graciously offered to help me. They have given me permission to share with my website readers their e-mails.
Comments on Dr. DeMeo’s e-mail:
“I have been working in the field of environmental protection from ’low-level’ EM fields for over 30 years, and so would recommend firstly that any of your patients who use a ’laptop’ computer, never, never use then on their lap. While the LCD screen of the typical laptop computer has a fairly low emission and is not significantly measurable at the usual distances from screen to head, the case of the laptop is filled with all sorts of electronics which give off fairly strong fields -- and since the person puts it on their lap, they get a fairly high exposure from that. They should be used on a table-top only. Also for the more sensitive people, resting their hands on the laptop also gives problems, as the hands are exposed. This can be dramatically reduced by using a typical USB type of external keyboard -- not a ’wireless’ one which should be avoided at all costs, but one with a hard wire. Also to never use ’wireless’ systems which work in the microwave bands”
Dr. Milhams’ classic article is worth reading. *
*Milham G and Morgan LL. A new electric magnetic exposure meter- High frequency voltage transcients associate with increase cancer incidence in teachers in California. Amer. J. Industr. Med. Published on line www.intersciencewiley.com 1-8.
Dr. Milhams e-mails follow:
Dear Dr. Waisbren,
I was referred to your website by Louis Slesin, editor of Microwave News. I’m convinced that ALS is caused by electrical exposure. Years ago Deapen et al showed that ALS was more common in people who had received a serious electrical shock and it is more common in electrical workers. I think that it will ultimately be related to high frequency voltage transients (dirty power). Laptops and a lot of other modern electrical equipment generate dirty power. I’m attaching a copy of a paper about dirty power https://fortress.wa.gov/doh/occmort.
Dear Dr. Waisbren,
I bought a meter which measures the WiFi fields put out by laptops. It is an Electrosmog Meter available from www.lessemf.com for $199. Its readings agree with those of my other meters, but this one automatically changes the readout units with a press of the button. If you got one of these meters, you could easily measure any laptop. Just make sure that the WiFi switch is on.
Mr. Henke’s IBM Thinkpad laptop emits microwave radiation in the band 60MHZ to 3.5GHZ at a maximum intensity of 8.67 V/M electric field, 23 mA/m and 19.95 uW/cm squared. The magnetic field readings were 12 mG with a Bell triaxial meter and 3.5 ,G with your Trifield meter. The Russian standard at these frequencies is 2.5 V/M based on human experimentation and biologic end points. There is no US standard.
I think that you should be very careful in associating nerve damage with computer exposure. Only when a laptop was used extensively on switch on, but my wife’s Dell doesn’t unless she is in a WiFi environment.
I’ll pack the laptop and return it tomorrow. Best, Sam Milham
Dr. DeMeo provided me with a Trifield meter which Dr. Milham included in his analysis of the computers health.
Dr. Sam Milham e-mails speak for themselves. He was kind enough to agree to study the computer and his second e-mail sent after he did this makes available baseline information which should be valuable for those who want to follow up on this hypothesis by exposing animal models of ALS and astrocytes in cell cultures to dosages of magnetic radiations comparable to those received by the key patient over a 3 year period. Alternatively, those interested might just want to put a laptop computer whose electrical emissions are equal to the computer we tested in with ALS animal models and human astrocyte cell cultures to see if their glutamate levels increase.
Since becoming involved with this project I have asked each patient I see about their exposure to laptop computers. To my surprise I have found several other patients with bizarre neurologic findings who spend hours each day with their laptop computers. (There cases will eventually be shared with my colleagues.)
In view of all of the above, what might the future bring? Excessive laptop computer users and for that matter other types of compulsive computer users might want to have the electrical health of their computers determined. They might want to be sure that electrical emission guidelines already present regarding the manufacturing and exporting of their computers have been met. Both government agencies and sellers of computers might be required to label their computers in this regard.
When a situation such as has been described here occurs, patients may ask their physicians to look into this matter as it is unfolding. Hopefully, there may be those in the scientific community stimulated to undergo the surrogate studies that have been suggested here (28,29). This is because epidemiologic studies regarding extremely rare situations such as in this case cannot be expected to help in this matter. The reason for this is the tremendous numbers of patients that have to be involved in epidemiologic studies designed to prove a “rare, needle in the haystack” type of reaction will not be found for epidemiologic study (28,29,30).
Where do I hope the readers of this essay will go from here? Already I have found that there are many who want to check their electrical environment. To this end, with professional help, “a do it yourself electrical check program” is being prepared for inclusion on this website as soon as it is carefully worked out. With it individuals may want to check their electrical environment that may be influenced by things such as high-bred cars, cell phones, hearing aids and many other appliances now in use.
Furthermore, if the biblical quotation which is mentioned in our epigraph is valid some professionals should come across cases similar to the one presented here. Hopefully, they will share these cases with their colleagues as case reports or essays on the internet. In addition, there might be some who want to have labels attesting to the electrical health of their computers and other electrical devices with which they come in contact. To make this come about purveyors of computers would have to agree (perhaps due to legal requirements) to have a label on each computer or electrical device they sell in regard to its electrical health. This regulation would have to include computers imported from China, where the majority of computers sold in the United States are made. At the least, they may want to assure their customers that regulations already in place regarding the importation of computers are met (33,34).
Finally, there may be those in the internet family who want to do the surrogate experiments with animal models and cell cultures that use glutamate metabolism as an end point to indirectly check on this hypothesis (28,29,30). They might want to use a surrogate method of checking this because it is well known that searching for “needles in a haystack” complications of any type by epidemiologic methods usually run into the dictum “absence of proof is not proof of absence” (36,37).
I wish to acknowledge the role patients played in the development of this hypothesis. In 1983, Carl Strelitzer’s willingness to accept ammunomodulation therapy for his M.S. resulted in most of these patients being seen in this clinic (26). In 1979, Philip Milonic told me that a vaccination for Swine Flu influenza caused his M.S. (his observation has been confirmed in regard to vaccines being able to cause acquired autoimmune diseases (10,11,12). In 1986, Mr. Shinabery and Coach Waters agreed that electrical treatments might have caused their ALS (9). In 1988, Mr. Thresh suggested that his mothers Lyme disease should be treated with Ceftriaxone because her ALS started after she developed Lyme disease. Because of this she was the first patient treated with Ceftriaxone (19) Thomas Henke suggested to me while I was discussing my experiences with ALS that his laptop computer may have been cause of his difficulties. All of these patients agreed to their names being made public.
Finally, I would like to acknowledge the help and suggestions of Dr. John DeMeo and Dr. Samuel Milham who have helped me immeasurably in my approach to this problem. Their websites and publications will explain why.
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