VESTIBULOCOCHLEAR TOXICITY IN A PAIR OF SIBLINGS [DOCTOR & NURSE] 15 YEARS APART SECONDARY TO ASPARTAME: TWO CASE REPORTS


Compiled By Rich Murray, MA
Room For All
1943 Otowi Road
Santa Fe, New Mexico 87505 USA
Telephone: 505-501-2298
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Posted: 06 May 2010


Vestibulocochlear toxicity in a pair of siblings [doctor & nurse] 15 years apart secondary to aspartame: two case reports, Paul Pisarik & Dasha Kai, Cases J 2009.09.15 free full text: Rich Murray 2010.05.04
http://rmforall.blogspot.com/2010_05_01_archive.htm
Tuesday, May 4, 2010
http://groups.yahoo.com/group/aspartameNM/message/1600

_______________________________________________

"For both, subsequent intentional challenges with aspartame and unintentional exposures brought back each of their respective symptoms."

"After the last occurrence of her nausea, headaches, and vertigo, she has since not consumed aspartame in any product or form and has been symptom free for 22 years."

"Except for six mild reoccurrences of his symptoms within 24 hours of unintentionally consuming something with aspartame (hypoesthesia anterior to the tragus and mild tinnitus) lasting 2-4 hours, he has been symptom free for over six years now."

Cases J. 2009 Sep 15; 2: 9237.
Vestibulocochlear toxicity in a pair of siblings 15 years apart secondary to aspartame: two case reports.
Pisarik P, Kai D.
University of Oklahoma College of Medicine, Tulsa
1111 S. St. Louis Ave. Tulsa, OK 74120-5440, USA.

Abstract

INTRODUCTION:

Aspartame may have idiosyncratic toxic effects for some people; however, there are few case reports published in the medical literature. We present two case reports in a pair of siblings, one with a vestibular and the other with a cochlear toxicity to aspartame. The cochlear toxicity is the first case to be reported, while the vestibular toxicity is the second case to be reported.

CASE PRESENTATION:

A 29-year-old white female had a 20-month history of nausea and headache, progressively getting worse with time and eventually to also involve vomiting, vertigo, and ataxia. She was extensively evaluated and diagnosed with a vestibular neuronitis versus a chronic labyrinthitis and treated symptomatically with limited success. In response to a newspaper article, she stopped her aspartame consumption with total cessation of her symptoms.

Fifteen years later, her then 47-year-old white brother had a 30-month history of an intermittent, initially 5-10 minute long episode of a mild sensorineural hearing loss in his right ear that progressed over time to several hour episodes of a moderately severe high-frequency sensorineural hearing loss to include tinnitus and a hypoesthetic area in front of his right tragus. After a negative magnetic resonance scan of the brain, he remembered his sister's experience with aspartame and stopped his consumption of aspartame with resolution of his symptoms, although the very high frequency hearing loss took at least 15 months to resolve. For both, subsequent intentional challenges with aspartame and unintentional exposures brought back each of their respective symptoms.

CONCLUSION:

Aspartame had a vestibulocochlear toxicity in a pair of siblings, suggesting a genetic susceptibility to aspartame toxicity. Even though the yield may be low, asking patients with dizziness, vertigo, tinnitus, or high-frequency hearing loss about their aspartame consumption and suggesting cessation of its use, may prove helpful for some.
PMID: 20126318 [PubMed - in process]
PMCID: PMC2815650
Free PMC Article

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815650/pdf/1757-1626-0002-0000009237.pdf
4 pages 165 KB

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815650/?tool=pubmed

Cases J. 2009; 2: 9237.
Published online 2009 September 15.
doi: 10.4076/1757-1626-2-9237.
PMCID: PMC2815650
Copyright (c)2009 Pisarik and Kai
licensee Cases Network Ltd. licensee BioMed Central Ltd.

Vestibulocochlear toxicity in a pair of siblings 15 years apart secondary to aspartame: two case reports
Paul Pisarik 1 and Dasha Kai 2
1 University of Oklahoma College of Medicine, Tulsa
1111 S. St. Louis Ave. Tulsa, OK 74120-5440, USA
2 University Physician's Hospital
2800 E. Ajo Way, Tucson, AZ 85713, USA Paul Pisarik: paul-pisarik@ouhsc.edu
Dasha Kai: dasha456@comcast.net
Received January 2, 2009; Accepted August 25, 2009.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/3.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Introduction

Aspartame was approved by the United States Food and Drug Administration (FDA) in 1981 for use in dry products such as breakfast cereal and as a tabletop sweetener [1]. Later in 1983 it was approved for use in sodas and in 1995 as a general sweetener in all foods and drinks. Because of its very sweet taste, aspartame has been extensively used as a food additive. It is included in over 6000 products and consumed by 200 million people around the world [2]. Because of its ubiquity in our food supply, the FDA has received many complaints over the years that allege that aspartame was responsible for a myriad of consumers' illnesses.

A PubMed search only shows only 14 case reports or case series regarding potential aspartame toxicity. The neurotoxic reactions reported include migraines, carpal tunnel syndrome, a movement disorder of the arms and legs, an orofacial sensitivity reaction, vertigo and ataxia, and seizure and mania. This will be the first paper to show a sensorineural hearing loss temporally related to aspartame and the second to show a vestibular toxicity temporally related to aspartame [3].

Case presentation

Case report 1

The first case was a 29-year-old white non-Hispanic female nurse (one of the authors) who started experiencing nausea and vomiting 3 weeks after conceiving her first pregnancy that persisted throughout her pregnancy. Her pregnancy was complicated with a 114-pound weight gain and pre-eclampsia. Her delivery was complicated with shoulder dystocia and post partum hemorrhage. After her delivery in January 1985, her symptoms got better in that she only had nausea in the mornings that cleared by 1 or 2 P.M. She also had headaches on awakening in the morning up to 3 days a week.

She was on no medications and had no allergies to medications. She denied use of alcohol, cigarettes, or any other drugs. Her past medical history was significant for intermittent hypertension. She had multiple right eye surgeries for strabismus in the early 1960s and a tonsillectomy and adenoidectomy in 1965. She was 5 foot and 11 inches tall and weighed 165 lbs prior to her pregnancy, 264 lbs just after her delivery that decreased over the time to 180 lbs at time of her self-diagnosis.

She went to see her physician in July 1985 with these symptoms. Her physician treated her with oral prochlorperazine and meclizine; however, these medications did not have much effect on her.

In January 1986, she again saw her physician with the same complaints. The neurological exam was normal except for showing a few beats of nystagmus on lateral gaze. She was again treated symptomatically with metoclopramide and trimethobenzamide. Over the next several months, the nausea progressed to encompass the entire day along with some vomiting. In addition, she was experiencing vertigo with motion and lying in bed.

She saw her physician in June 1986 and was noted to have nonfatiguing nystagmus on looking to the right. She had audiologic testing that was normal but had an electronystagmograph (ENG) that showed a direction-fixed right-beating positional nystagmus of about six degrees. She was referred to an otolaryngologist who noted a positioning nystagmus consistent with the ENG that was easily reproduced and persistent. Radiographs of the internal auditory canals were normal. Because of the persistence of her symptoms, she was then referred to a neurologist. He ordered a brainstem auditory evoked response test and a magnetic resonance imaging scan of the brain, both of which were normal. His final diagnosis was a vestibular neuronitis versus a chronic labyrinthitis and he gave her diazepam to take as needed.

Over the next two months, her symptoms got worse to where she was experiencing problems with muscle coordination manifested by occasionally not being able to negotiate doorways and occasionally not being able to place a spoon squarely in her mouth.

In September 1986, she read a doctor-advice column in the local paper that mentioned aspartame was anecdotally associated with nausea and headaches. She had first begun to drink an aspartame-sweetened drink -- Crystal Light (R) -- right after the birth of her son and was drinking 16 to 32 ounces per day, sipping on it throughout the day. She made sure that she did not consume it during her pregnancy.

After reading the article, she stopped drinking Crystal Light (R), her only source of aspartame, and within a week, she was symptom free. About a month later, she challenged herself with 8 ounces of Crystal Light (R) and within 1 to 2 hours started having nausea, headaches, and vertigo that lasted for 48 hours. About 3 to 4 weeks later she drank a 12-ounce can of Diet Pepsi (R) and within 1 hour started to have the exact same symptoms, again lasting about 48 hours. She had a recurrence of the symptoms two times after that, each time after accidentally drinking a beverage with aspartame in it. After the last occurrence of her nausea, headaches, and vertigo, she has since not consumed aspartame in any product or form and has been symptom free for 22 years.

Primary diagnosis is a vestibular neuronitis versus chronic labyrinthitis secondary to aspartame. Secondary diagnosis is nausea and vomiting of pregnancy.

Case report 2

In January of 2002 at the age of 47, a non-Hispanic white male physician (one of the authors and brother of case report 1) had an intermittent right-sided tinnitus associated with a hearing loss that would last 6-8 hours at a time. In addition, at the same time, he had a 1.5 cm diameter area of hypoesthesia in the region just anterior to the tragus of his right ear. He had noted a very minor right-sided hearing loss for at least two years prior to this, but it would never last more than for a few minutes, perhaps once a month, and he never thought much about it. There was no vertigo, nausea, headaches, or other neurological symptoms associated with this.

He was 6' 3'' tall and weighed 180 pounds. His past medical history was pertinent for benign prostatic hypertrophy treated with finasteride since January 1998. He had no allergies to medications. He denied use of alcohol, cigarettes, or other drugs. His past surgical history was pertinent for a tonsillectomy and adenoidectomy in 1963 and an open reduction and internal fixation of a comminuted left distal radius fracture in May of 2001 with subsequent removal of hardware in August of 2001. Family history was pertinent for a sister 15 years earlier having a vestibular neuronitis versus chronic labyrinthitis secondary to aspartame.

Between January and August 5, 2002, he had five such prolonged episodes, along with the episodes that lasted for a few minutes. On August 5th, he woke up with one such episode that lasted 10 hours before it went away. On August 8th, he had another episode that started at noon and unlike his previous episodes, lasted three days with a severe tinnitus and hearing loss. He contacted an otolaryngologist and was started on prednisone. He had an audiogram on August 9th that showed a right-sided high frequency sensorineural hearing loss. By the time he saw the otolaryngologist on August 12th, the hearing loss resolved clinically and another audiogram was done and was much improved and similar to a previous audiogram he had done in 1987, except for a remaining 35-decibel loss at 8000 Hertz (Hz).

At the time of his otolaryngologist appointment, his physical exam was normal. A magnetic resonance imaging scan of the brain with and without gadolinium was normal.

Hearing threshold levels in dB (re: ANSI-1969) of case report 2 for each ear at different points in time.

When the otolaryngologist did not have an explanation for his symptoms, the patient remembered that his sister had the adverse reaction to aspartame 15 years earlier. Up until now, he had consumed foods with aspartame, undeterred by his sister's experience. At this time, he was consuming aspartame in the form of one to two cans of Caffeine Free Diet Coke(r) along with a bowl of Fiberall (R) cereal a day. Thereafter he stopped consuming aspartame in any form. Over the next two months, he had no more severe episodes of tinnitus and hearing loss but did have two further episodes of milder right-sided tinnitus and hearing loss (30% of prior intensity) and only lasting 3-4 hours.

Thinking that it might not be due to aspartame, he drank a can of Caffeine-free Diet Coke(r) a day for four days in a row. On each of these days, he had a mild episode of right-sided tinnitus and hearing loss for 2-3 hours each day. He permanently stopped his aspartame consumption after that. He had one milder episode of tinnitus and hearing loss a couple of weeks after he finished his challenge.

Follow-up audiograms showed a slowly improving 8000 Hz hearing loss: November of 2002 showed only a 20 decibel loss compared to 1987 and November of 2003 showed a 10 decibel loss compared to 1987.

Primary diagnosis is tinnitus and sensorineural healing loss secondary to aspartame.

Except for six mild reoccurrences of his symptoms within 24 hours of unintentionally consuming something with aspartame (hypoesthesia anterior to the tragus and mild tinnitus) lasting 2-4 hours, he has been symptom free for over six years now.

Conclusion

Aspartame had a vestibulocochlear toxicity in a pair of siblings suggesting an idiosyncratic genetic predisposition to aspartame toxicity. In addition, the cochlear toxicity in case report 2 took at least 15 months to clear after his cessation of aspartame use suggesting that aspartame's cochlear toxicity can be long lasting.

Patients with dizziness, vertigo, tinnitus, and hearing loss present not only to otolaryngologists and neurologists, but also to primary care clinicians frequently. Even though the yield may be low, asking them about their aspartame consumption and suggesting cessation of its use, may prove helpful for some.

Abbreviations

ENG: electronystagmograph
FDA: Food and Drug Administration.

Consent

Written informed consent was obtained from the patients for publication of these case reports. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

DK obtained copies of her medical records when her health clinic closed down in the late 1980s and contributed both subjective and objective findings to case report 1. PP contributed to case report 2 and did the literature search. All authors read and approved the final manuscript.

References

US FDA.
Artificial Sweeteners: No Calories ... Sweet!
FDA Consumer Magazine. July-August 2006.

Butchko HH, Stargel WW.
Aspartame: scientific evaluation in the postmarketing period.
Regul Toxicol Pharmacol. 2001;34:221-233.
doi: 10.1006/rtph.2001.1500. [PubMed]

Gulya AJ, Sessions RB, Troost TR.
Aspartame and dizziness: preliminary results of a prospective, nonblinded, prevalence and attempted cross-over study.
Am J Otol. 1992;13:438-442. [PubMed]

Articles from Cases Journal are provided here courtesy of BioMed Central

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recent aspartame (methanol, formaldehyde, formic acid) symptoms in English professor: Kristi Siegel: Rich Murray 2010.04.17
http://rmforall.blogspot.com/2010_04_01_archive.htm
Saturday, April 17, 2010
http://groups.yahoo.com/group/aspartameNM/message/1599

"Shortly after seeing the ophthalmologist and about two weeks or so into my Crystal Light regimen, I had my first episode of vision loss. [last week of January] This incident was completely different in degree and kind than the normal visual problems (increased far-sightedness and visual lability) I had been experiencing. Rather abruptly, I lost the visual field of the left hemisphere of my left eye. The vision loss lasted for about 20 or 30 minutes and after approximately 15 minutes, I started to develop a crushing headache which lasted for hours. I've never had a history of headaches, so the intensity and duration of this headache was unusual."


Formaldehyde from 11% methanol part of aspartame causes severe allergic dermatitis in boy, JE Jacob et al, Pediatric Dermatology 2009 Nov: Rich Murray 2010.03.30
http://rmforall.blogspot.com/2010_03_01_archive.htm
Tuesday, March 30, 2010
http://groups.yahoo.com/group/aspartameNM/message/1597

Pediatric Dermatology. 2009 Nov-Dec;26(6):739-43. Systematized contact dermatitis and montelukast in an atopic boy.

Castanedo-Tardan MP
González ME
Connelly EA
Giordano K
Jacob SE
University of Miami, Miller School of Medicine, Department of Dermatology and Cutaneous Surgery, Miami, Florida, USA.

Upon ingestion, the artificial sweetener, aspartame is metabolized to formaldehyde in the body and has been reportedly associated with systemic contact dermatitis in patients exquisitely sensitive to formaldehyde.

We present a case of a 9-year-old Caucasian boy with a history of mild atopic dermatitis that experienced severe systematized dermatitis after being started on montelukast chewable tablets containing aspartame.

Patch testing revealed multiple chemical sensitivities which included a positive reaction to formaldehyde.

Notably, resolution of his systemic dermatitis only occurred with discontinuation of the montelukast chewables. PMID: 20199453

Four Murray AspartameNM reviews in SE Jacob & SA Stechschulte debate with EG Abegaz & RG Bursey of Ajinomoto re migraines from formaldehyde from aspartame, Dermatitis 2009 May: TE Hugli -- folic acid with V-C protects: Rich Murray 2009.08.12
http://rmforall.blogspot.com/2009_08_01_archive.htm
Wednesday, August 12, 2009
http://groups.yahoo.com/group/aspartameNM/message/1582
extracts]


Formaldehyde, aspartame, migraines: a possible connection.
Abegaz EG, Bursey RG.
Dermatitis. 2009 May-Jun;20(3):176-7; author reply 177-9.
No abstract available. PMID: 19470307

Eyassu G. Abegaz *
Robert G. Bursey
Ajinomoto Corporate Services LLC, Scientific & Regulatory Affairs
1120 Connecticut Ave., N.W., Suite 1010
Washington, DC 20036
* Corresponding author. Tel.: +1 202 457 0284
fax: +1 202 457 0107
abegazee@ajiusa.com (E.G. Abegaz)
burseyb@ajiusa.com (R.G. Bursey)

"For example, fruit juices, coffee, and alcoholic beverages produce significantly greater quantities of formaldehyde than aspartame-containing products. [6]"

"[6] Magnuson BA, Burdock GA, Doull J, et al. Aspartame: a safety evaluation based on current use levels, regulations, and toxicological and epidemiological studies. Crit Rev Toxicol 2007;37:629-727"

[Two detailed critiques of industry affiliations and biased science in 99 page review with 415 references by BA Magnuson, GA Burdock and 8 more, Critical Reviews in Toxicology, 2007 Sept.: Mark D Gold 13 page: also Rich Murray 2007.09.15: 2008.03.24
http://rmforall.blogspot.com/2008_03_01_archive.htm
Monday, March 24, 2008
http://groups.yahoo.com/group/aspartameNM/message/1531

"Nearly every section of the Magnuson (2007) review has research that is misrepresented and/or crucial pieces of information are left out.

In addition to the misrepresentation of the research, readers (including medical professionals) are often not told that this review was funded by the aspartame manufacturer, Ajinomoto, and the reviewers had enormous conflicts of interest."]


http://www.medscape.com/viewarticle/579335

Dermatitis. 2008; 19(3): E10-E11.
(c) 2008 American Contact Dermatitis Society
Formaldehyde, Aspartame, and Migraines: A Possible Connection
Sharon E. Jacob; Sarah Stechschulte
Published: 09/17/2008
[Extract]

Abstract

Aspartame is a widely used artificial sweetener that has been linked to pediatric and adolescent migraines. Upon ingestion, aspartame is broken, converted, and oxidized into formaldehyde in various tissues. We present the first case series of aspartame-associated migraines related to clinically relevant positive reactions to formaldehyde on patch testing.

Case Series

Six patients (ages 16 to 75 years) were referred for evaluation of recalcitrant dermatitis. By history, five of the patients were noted to have developed migraines following aspartame consumption; the sixth reported dermatitis flares associated with diet cola consumption of >2 liters/day.

All six patients had current environmental exposures to formaldehyde or formaldehyde-releasing preservatives in their personal hygiene products and/or regular consumption of "sugar-free food" artificially sweetened with aspartame.

Based on their histories and clinical presentations, these patients were patch-tested with the North American Contact Dermatitis Group 65-allergen Standard Screening Series and selected chemicals from the University of Miami vehicle, fragrance, bakery, and textile trays.

All six patients had positive reactions to formaldehyde, and four had additional positive reactions to formaldehyde-releasing preservatives (FRPs). Expert counseling on allergen avoidance (including avoidance of formaldehyde, FRPs, and aspartame) and alternative product recommendations were provided to the patients.

At their follow-up appointments (between 8 and 12 weeks), all the patients showed clearance of their dermatitis. Four patients (two inadvertently) resumed their consumption of aspartame and subsequently returned for an additional follow-up visit. Three of the first five patients had recurrences of both their migraines and their dermatitis; the sixth patient (who had no migraines) had a positive rechallenge dermatitis. These four patients were again counseled on avoidance regimen.

Formaldehyde, aspartame, and migraines, the first case series, Sharon E Jacob-Soo, Sarah A Stechschulte, UCSD, Dermatitis 2008 May: Rich Murray 2008.07.18
http://rmforall.blogspot.com/2008_07_01_archive.htm
Friday, July 18, 2008
http://groups.yahoo.com/group/aspartameNM/message/1553

Formaldehyde from many sources, including aspartame, is major cause of Allergic Contact Dermatitis, SE Jacob, T Steele, G Rodriguez, Skin and Aging 2005 Dec.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1533

"For example, diet soda and yogurt containing aspartame (Nutrasweet), release formaldehyde in their natural biological degradation.

One of aspartame's metabolites, aspartic acid methyl ester, is converted to methanol in the body, which is oxidized to formaldehyde in all organs, including the liver and eyes. 22

Patients with a contact dermatitis to formaldehyde have been seen to improve once aspartame is avoided. 22

Notably, the case that Hill and Belsito reported had a 6-month history of eyelid dermatitis that subsided after 1 week of avoiding diet soda. 22"

Avoiding formaldehyde allergic reactions in children, aspartame, vitamins, shampoo, conditioners, hair gel, baby wipes, Sharon E Jacob, MD, Tace Steele, U. Miami, Pediatric Annals 2007 Jan.: eyelid contact dermatitis, AM Hill, DV Belsito, 2003 Nov.: Murray 2008.03.27
http://rmforall.blogspot.com/2008_03_01_archive.htm
Thursday, March 27, 2008
http://groups.yahoo.com/group/aspartameNM/message/1532

Sharon E. Jacob, MD, Assistant Professor of Medicine
(Dermatology)
University of California, San Diego
200 W. Arbor Drive, #8420
San Diego, CA 92103-8420
Tel: 858-552-8585 ×3504 Fax: 305-675-8317
sjacob@contactderm.net
Sarah A. Stechschulte, BA sstechschulte@gmail.com


Methanol (11% of aspartame), made by body into formaldehyde in many vulnerable tissues, causes modern diseases of civilization, summary of a century of research, Woodrow C Monte PhD, Medical Hypotheses journal: Rich Murray 2009.11.15
http://rmforall.blogspot.com/2009_11_01_archive.htm
Sunday, November 15, 2009
http://groups.yahoo.com/group/aspartameNM/message/1589

_______________________________________________

Rich Murray, MA
Boston University Graduate School 1967 psychology,
BS MIT 1964, history and physics,
1943 Otowi Road
Santa Fe, New Mexico 87505
505-501-2298
rmforall@comcast.net

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