S.F.T.A.H.  Society For The Autistically Handicapped.

 Vaccines. FACT SHEET

MMR Vaccine, Thimerosal and Regressive or Late Onset Autism

(“Autistic Enterocolitis”)   

A Review of the Evidence for a Link Between Vaccination and Regressive Autism 

July 2005

 David Thrower,

49, Ackers Road,

Stockton Heath,

Warrington, England      

email david.throwerwarrington@ntlworld.com

 Contents 

Executive Summary 

Part A:     A Novel Syndrome 

1.       What Is Acquired Autism/Autistic Enterocolitis

2.       The New Syndrome

 Part B:     The Scale of the Autism Problem

 3.      The Financial Costs  -  Autism Is Costing The Taxpayer £$Billions

4.      Overall Cost Estimates

5.       Failure to Monitor Increases In UK Autism Numbers

6.     “Now Almost Everyone Knows Someone Who’s Autistic”

7.       Is Autism Increasing Due To Changes In Criteria?

8.       Autistic Disorder

9.       Pervasive Developmental Disorder Not Otherwise Specified

10.     Asperger’s

11.     Paper by Mark Blaxill, June 2001

12.     University of Cambridge Research

13.     University of Sunderland Research

14.     UK National Autistic Society Estimates

15.     Report by Fiona Loynes, UK All Party Parliamentary Group, Dec. 2001

16.     Report, “Autism In Schools”, UK National Autistic Society May 2002

17.     Autism in Scottish Schools

18.     Is Autism Increasing?  -  Some Official UK Pronouncements

19.     Autism In The USA

20.     The US Amish Community

21.     Autism Elsewhere

 Part C:     MMR

 22.     The Introduction of MMR

23.     Recognised Adverse Reactions to MMR

24.     US Vaccine Adverse Events Reporting System (VAERS)

25.     Contraindications To Receiving MMR

26.     The UK Department of Health’s Position over MMR and Autism

27.     Single Vaccines In The UK

28.     Measles In The UK and US

29.     Promotion of MMR In The UK After Wakefield “Early Report”

30.     Position of the US Centers For Disease Control on MMR/Autism

31.     The Parents Have Seen What They’ve Seen.....

 Part D:     The Thimerosal/Thiomersal* Issue

(*the two terms are interchangeable)

 32.     Thimerosal’s Possible Role

33.     Joint Statement by American Acad. Of Ped./PH  Service, July 1999

34.     Removal of Thimerosal

35.     Interview With Neal Halsey, Johns Hopkins University, Nov 2002

36.     Waters & Kraus Press Release, 2002

37.     Statement by Safe Minds group, US

38.     US Use of Thimerosal - Statement by Dr. Geier, 2004

39.     Thimerosal’s Use in the US

40.     UK Vaccines With Thimerosal

41.     UK Med. and Healthcare Regulatory Agency Position on Thimerosal

42.     UK Joint C’ttee on Vaccin & Immunisation Position on Thimerosal

43.     UK Department of Health’s Position on Thimerosal

44.     US CDC Thimerosal Studies

45.     Report, “Mercury In Medicines”, US C’ttee on Govt. Reform 2003

46.     Letter to Congress by the US Office of Special Counsel, 2004

47.     California Votes To Ban Thimerosal, June 2004

48.     US CDC’s Current Position on Thimerosal

49.     Memo by Merck

 Part E:     Evidence That Autism Increases Are Real

 50.     Paper by Mark Blaxill, The Rising Incidence of Autism    

51.     Close-Up On California

52.     The MIND Study, California

53.     Close-Up On New Jersey

54.     Atlanta Study, 2003

55.     Paper by Gurney, Fritz et al, Trends on ASD In Minnesota, 2003

56.     Paper by Yazbak, Autism In The US, J of A Phs & Surg 2003

57.     Paper by Yazbak, Autism In Quebec, 2004

 Part F:     Reviews Questioning the Autism Epidemic

 58.     Paper by Fombonne, UK Med Research Council, Pediatrics, Jan 2001

59.     Paper by Wing, Centre for Social & Commun. Disorders, London 2002

60.     Position of Dr. B. S. Siegal, University of California, 2002

61.     Study by Croen et al, July 2002

62.     Editorial by Fombonne, J of the American Medical Asscn., January 2003

63.     Paper by Jick et al, Boston Un Sch of Med, Pharmacotherapy, Dec 2003

64.     Study by Smeeth, Fombonne et al, November 2004

65.     Study by Barbarisi et al, January 2005

 Part G:   The MMR Original Safety Trials Debate

 66.     Wakefield & Montgomery “Through A Glass Darkly” (MMR safety)

67.     Dr. Peter Fletcher Commentary, J of Adverse Drug Reactions, 2001

68.     Dr. Stephen Dealler Commentary, J. of Adverse Drug Reactions, 2001

69.     Dr. F. E. Yazbak Commentary, J of Adverse Drug Reaction, 2001

70.     The Wakefield/Watson/Shattock Rebuttals

71.     The UK Dept of Health’s Repudiation of “Through A Glass Darkly”.

 Part H:   Studies and Papers That Point Towards The Plausibility Of Gut/Autism, MMR/Gut/Autism, Thimerosal/Autism and Autoimmunity/Autism Links

 72.     Paper by Nelson & Gottshall, Applied Microbiology, May 1967

73.     Paper by Eggers, Klinical Paediatrics, March 1976

74      Weizman, Weizmann et al Study, Am. J of Psychiatry, Nov. 1982

75.     Delgiudice-Asch and Hollander Study

76.     Paper by Dr. H. Fudenberg

77.     Paper by Dr. Reed Warren

78.     Warren and Singh Study, Immunogenetics, 1992

79.     Singh, Warren, Odell, Warren and Cole Paper, March 1993

80.     Singh, Warren, Odell et al Study, Brain Behaviour, March 1993

81.     Oleske and Zecca paper

82.     Binstock paper

83.     Anne-Marie Plesner Letter, Lancet, February 1995

84.     Paper by Thompson, Montgomery et al, Lancet, April 1995

85.     Gupta, Aggarwal & Heads Study, J of Autism and Dev Disorders, 1996

86.     Montinari, Favoino and Roberto paper, Naples conference May 1996

87.     Auwaerter & Griffin paper, Clin Immunol & Immunopath, May 1996

88.     Cook, Courchesne et al Paper, Molecular Psychiatry, May 1996

89.     Griffin and Hussy Study, Journal of Infectious Diseases, June 1996

90.     Martinez et al Study, Proceedings of National Acad of Sciences, 1997

91.     Paper by Zecca, Graffino et al, Meeting of Nat Inst of Health, Sept. 1997

92.     Weibel, Caserta and Evans Study, March 1998

93.     Wakefield et al “Early Report”, Lancet, February 1998

94.     Paper by Montgomery, Morris et al (pub. date/details not yet known)

95.     Sabra, Bellanti and Colon letter, Lancet, July 1998

96.     Further Paper by Singh and Yang, Pharmaceutical Jnl, October 1998

97.     Uhlmann, Sheils et al Paper

98.     Bitnun et al Study, Clinical Infectious Diseases Journal, October 1999

99.     Paper by Horvath, Papadimitriou et al, Journal of Pediatrics Nov 1999

100.   Paper by Singh to the US Committee on Govt Reform, April 2000

101.   O’Leary Paper Presented to Congressional Oversight C’ttee, April 2000

102.   Kawashima, Takayuki et al Study, Digestive Dis and Sciences, Apr 2000

103.   Confidential Review, US CDC, Simpsonwood, June 2000

104.   Hagenbuch, Kullak-Ublick et al Study, J of Pharm Exp Ther, July 2000

105.   Wakefield et al Paper, American J. of Gastroenterology, September 2000

106.   Statement by Professor Walter O. Spitzer, December 2000

107.   Furlano, Anthony et al Study, Journal of Pediatrics, 2001

108.   Paper by Enayati et al, Medical Hypotheses, 2001

109.   Study by Jyonouchi, Sun and Le, J. of Allergy & Clin. Immun., Feb. 2001

110.   Study by Jyonouchi, Sun and Le, J of Neuroimmunology, 2001

111.   Paper by Spitzer, Aitken et al, J of Adverse Drug Reactions & Tox., 2001

112.   Study by Holmes, Cave et al, June 2001

113.   Paper by Blaxill, Institute of Medicine, July 2001

114.   Paper by Dr. Ken Aitken to the Scottish Society for Autism, 2001

115.   Paper by Imani and Kehoe, Clinical Immunology, September 2001

116.   Paper by Redwood, Bernard et al, Neurotoxicology, October 2001

117.   Paper by Buie, Oasis 2001 Conference for Autism, Portland, US

118.   Paper by Uhlmann, Wakefield et al, J. of Clinical Pathology, Feb. 2002

119.   Paper by Singh and Nelson, February 2002

120.   Review by Wakefield, Pulestone et al, Aliment Pharm. Ther. 2002

121.   Report of Study, Comi et al, Johns Hopkins Hosp, Baltimore, Apr 2002

122.   Paper by Torrente, Ashwood, Day et al, Lancet, May 2002.

123.   Paper to 102nd GM of Am. Soc for Microbiology, Singh et al, May 2002

124.   Study by O’Leary et al to Path Soc of GB and Ireland July 2002

125.  Wakefield Paper Presented to US Govt Reform Committee, June 2002

126.   Paper to US Government Reform C’ttee by Dr Krigsman, June 2002

127.   Unpublished Research by Shattock, Un. of Sunderland, June 2002

128.   Paper by Sheils, Smyth, Martin & O’Leary, Trinity Coll Dublin, 2002

129.   Paper by Dr. Vijendra Singh, Utah State University, August 2002

130.   Paper by Finegold, Molitoris, Song, J. Of Clin. Infect. Dis., Sept 2002

131.   Further paper, Jyonouchi, Sun & Itokazu, Un. of Minnesota, Oct 2002

132.   Paper, Treat. of Late Onset Autism, Matarazzo, U.S-Paulo, Nov 2002

133.   Paper by Makani, Gollapudi et al, Genes & Immunity, 2002

134.   Paper by Westphal, Asgari et al, Arch of Toxicology, August 2002

135.   Unpublished letter by Wakefield to New Eng. J. of Medicine, Nov 2002

136.   Study by Croonenberghs et al, University of Antwerp, December 2002

137.   Paper by Holmes, Blaxill & Haley, Internat J of Toxicology 2003

138.   Paper by Singh and Jensen, Pediatric Neurology 2003

139.   Paper by Geier & Geier, Soc. for Experimental Biology & Med. 2003

140.   Study by Geier and Geier, International Pediatrics, May 2003

141.   Further Paper by Geier & Geier, Ped. Rehabilitation, Apr-June 2003

142.   Further Paper by Geier & Geier, J of Am Phys and Surg, Spring 2003

143.   Paper by Blaxill, Redwood & Bernard, Safe Minds

144.   Paper by Bradstreet, Geier et al, J of Am Phy and Surg Summer 2003

145.   Letter by Geier & Geier, J of Am Phys. & Surgeons, Summer 2003

146.   Paper by Baskin, Ngo et al, Toxicology Science Aug 2003

147.   Paper by Via, Nguyen et al, Envir. Health Perspectives August 2003

148.   Paper by Sweeten, Bowyer et al, Pediatrics, November 2003

149.   Paper by Ashwood, Murch et al, J of Clinical Immunology, Nov 2003

150.   Study by Ueha-Ashibishi, Oyama et al, Toxicology, Jan 2004

151.   Paper by Jyonouchi, Geng et al, Jan 2004

152.   Paper by Singh, presented to the Inst. of Med, Washington, Feb 2004

153.   Paper by Bradstreet, Inst of Medicine, Washington, Feb 2004

154.   Paper by Bradstreet, O’Leary et al, Inst of Medicine, Feb 2004

155.   Further Paper by Bradstreet, Institute of Medicine, Feb 2004

156.   Presentation by Geier and Geier to the Institute of Medicine, Feb 2004

157.   Letter by Geier, Genetic Centers of Am, to Pediatrics, March 2004

158.   Paper by De Water, Ahwood et al, MIND Instit, California, May 2004

159.   Study by Deth et al, Journal of Molecular Psychiatry, Apr 2004

160.   Paper by Torrente, Anthony et al, Am. J of Gastroenterology, Apr 2004

161.   Presentation by Prof. Boyd Haley, Canada Autism Conference, Apr 2004

162.   Paper by Bradstreet Dahr et al, J of Am Phys & Surg, Summer 2004

163.   Paper by Deth, Health & Wellness Committee, Sept 2004

164.   Paper by Hornig, Chian, Lipkin et al, Mol Psychiatry June 2004

165.   Paper by Wakefield et al, J of Clinical Immunology, November 2004

166.   Paper by Slikker et al, Neurotoxicology, December 2004

167.   Paper by the Environmental Working Group on Mercury, Dec 2004

168.   Paper by Havarinasab et al, Toxicology & App Pharmacology, 2005

169.   Paper by Burbacher et al, Environmental Health Perspectives, 2005

170.   Press Report, Los Angeles Times, February 2005

171.   Study by Palmer & Miller, Health and Place journal, March 2005

172.   Paper by Jyonouchi, Geng et al, Neuropsychobiology, February 2005

Part J:     Other Relevant Papers

173.   US Developmental Delay Registry Report, 1994

174.   Stratton et al Study, National Academy Press, 1994

175.   Paper by Carbone.

176.   Iizuka, Saito et al Study, Gut, May 2001 (Mumps Study)

177.   Statement by Spitzer, US Govt Reform Committee, April 2001  

178.   Statement by Dr. Jefferson, Cochrane Collaboration, Oxford, Oct 2002

179.   Paper by Sweeten et al, Pediatrics 2003

180.   Paper by Blaycock, JANA, Winter 2003

181.   Paper by Singh and Rivas, Jan 2004

182.  Paper by Richler, Luyster et al, Univ of Michigan Aut Center, 2004

 Part K.     Studies Seeking To Disprove Any MMR/Thimerosal/Autism Link

 183.   Limitations of Epidemiology - A Preface

184.   Stokes et al paper, J of American Medical Assoc. (JAMA), Oct. 1971

185.   Study by Peltola and Heinonen, Lancet, April 1986

186.   Paper by Miller, Miller et al, The Practitioner, January 1989

187    Gillberg Study, Sweden, British Journal of Psychiatry, 1991

188    Commentary by Gillberg and Heijbel, Autism, 1998

189.   Letter by Fombonne, Pediatrics, March 1998

190.   UK Committee on Safety of Medicines Study, June 1999

191.   Paper By Taylor, Miller and Farrington, Lancet, June 1999

192.   Paper by Miller & Farrington to US Govt Reform Committee, Apr 2000

193.   Patja, Peltola et al Study, Finland, Pediat. Infect Disease J. Dec. 2000

194    Kaye, Melero-Montez and Jick Study, British Medical Journal, 2000

195.   Dales, Hammer and Smith Study, JAMA, March 2001

196.   De Wilde, Carey & Richards Study, Br. J. of General Practice, Mar 2001

197.   Davis et al study, Archive Pediatrics Adolescent Medicine, 2001

198.   Further Paper by Farrington, Miller and Taylor, Vaccine Journal, 2001

199.   Fombonne & Chakrabarti Study, Pediatrics, October 2001

200.   Further Paper by Taylor, Miller et al, BMJ.com, February 2002

201.   Review by Donald and Muthu, Bazian Ltd, British Medical J. June 2002

202.   Study into Childhood Gastrointestinal Disorders and Autism, Aug 2002

203.   Madsen et al, Population-Based study, MMR/Autism, Denmark, Nov 2002

204.   Study on Mercury by Pichichero, Lancet, November 2002

205.   Study by Makela et al, Finland, Pediatrics November 2002

206.   Commentary by Nelson & Bauman, Pediatrics March 2003

207.   Paper, Madsen et al, Thimerosal/Aut in Denmark, Pediatrics, Sep 2003

208.   Paper by Hviid, Stellfeld et al, Denmark, J of Amer. Med Assoc Oct 2003

209.   Paper by Miller, Taylor et al, Archives of Diseases in Childhood 2003

210.   Paper by Taylor et al, Archives of Diseases in Childhood, 2003

211.   Article by Verstraeten et al, Pediatrics, Nov 2003

212.   Paper by Stehr-Green et al, American J of Preventative Medicine 2003

213.   Paper by DeStefano, Yeargin-Allsopp et al, Pediatrics, January 2004

214.   Paper by Williams et al, Aberdeen University, Neuroimage June 2004

215.   Paper by Smeeth, Cook, Fombonne et al, Lancet, September 2004

216.   Paper by Heron, Golding et al, Pediatrics, September 2004.

217.   Paper by Barbaresi et al, Arch of Ped & Adolescent Medicine, Jan 2005

218.   Paper by Honda & Rutter, J of Child Psychol & Psychiatry, March 2005

219.   Study by Seagroatt, British Med Journal, May 2005

Part L:     Reviews Claiming There Is No Evidence Of A Vaccine/Autism Link

220.   Medical Research Council Ad-Hoc Review, March 1998

221.   Presentation by Miller, UK All-Party Parl. Gp on Primary Health, 2000

222.   Medical Research Council Sub-Committee Report, March 2000

223.   Review by US Institute of Medicine, 2001

224.   Review by Strauss & Bigham, Health Canada/Un Of Br Columbia, 2001

225.   Elliman, Bedford & Miller Review, Arch. of Dis. in Childhood, Oct. 2001

226.   Medical Research Council Review, July-December 2001

227.   Further Review by US Institute of Medicine, February 2002

228.   Review of the Scottish Executive MMR Expert Group, April 2002

229.   Review by Wilson et al, Arch. of Ped. & Adol Med., July 2003

230.   Review by US Institute of Medicine, Washington, February 2004

Part M:     Flawed UK Regulatory, Safety and Monitoring Systems

231.   Fighting Measles, Missing Autism, Overlooking Damage?

232.   Has the UK Medicines Control Agency Missed the Syndrome?

233.   Further Statement by Dr Jefferson, Cochrane Collaboration, Mar 2004 

234.   Has The UK C’ttee on Safety of Medicines Modified MMR Vaccine?

235.   UK Department of Health Re-Launch of MMR, January 2001   

236.   The Search For Alternatives To MMR

237.   Full Removal of Thimerosal from Childhood Vaccines

Part N: UK and US National Political Initiatives

238.     UK House of Commons Health Committee, Westminster

239      UK All Party Parliamentary Group on Autism, Westminster

240.     Scottish Parliament, Edinburgh

241.     UK Liberal Democrats

242.     UK Conservatives

243.     US House of Representatives C’ttee on Government Reform

244.   Commentary by Congressman David Weldon, February 2005

Part P:     Compensation and Litigation

245.     UK Legal Action

246.     UK Vaccine Damage Payment Scheme

247.     US Vaccine Injury Compensation Scheme (VICP)

248.     Families Taking Legal Action in the US over Thimerosal and Autism

249.     US Government Attempts To Block The Thimerosal/Autism Litigation

250.     MMR Litigation In Ireland

251.     MMR Litigation in Japan

252.     Litigation Elsewhere

Part Q:     Some Conclusions and Some Unanswered Questions

253.     Some Broad Conclusions

254.     Some Unanswered Questions

 EXECUTIVE SUMMARY

 Ÿ         This comprehensive review  -  which has been put together by the parent of a child who became autistic after immunisation  -  sets out the concerns of parents whose children have degenerated into an acquired-autistic state after MMR or other vaccines, and attempts to summarize the debate over thimerosal (or thiomersal) preservative used in vaccines other than MMR, and to highlight possible links between this mercury-based preservative and autism. It is possible, and increasingly likely, that the MMR and thimerosal factors overlap in the cause of late-onset degenerative autism.

 Ÿ         These are immense and complex subjects. This briefing does not attempt to cover every single piece of the available scientific literature for or against an MMR/autism or thimerosal/autism link, but it reviews about one hundred of the most recent, most pivotal, or most frequently-quoted studies and papers.

 Ÿ         Its key finding is that there has not been a single credible study that can robustly refute the claims of the parents that their children’s acquired autism has been caused by MMR or related measles-containing vaccines, or thimerosal-containing vaccines.

 Ÿ        The concept of vaccination is not the issue. No attempt is made here to criticize the principle of vaccination. It has been argued that vaccines have saved millions of lives, and continue to do so, particularly in the developing world.

 Ÿ         The issue here is, have a small minority of children been damaged by vaccines, in a way that has yet to be fully understood? Specifically, is a subset of the autism spectrum causally linked to certain types of vaccine, or vaccine ingredients? These are the questions that are addressed.

 Ÿ         This document is in no way an “anti-vaccine” tirade. But if there is a problem, even for a small sub-set of children, it must be investigated, and its consequences faced up to. We do not shrug-off air travel fatalities, or deaths of passengers traveling by rail. Yet possible vaccine damage seems to have been largely ignored in the past, and the issue of safety treated as a taboo subject. Vaccine safety monitoring, and even the wider issue of drug and pharmaceuticals safety, has been in need of major reform, for many years.

 Ÿ         Each of the studies that seeks to “disprove” an MMR/autism link or a thimerosal/autism link can be argued to be flawed in design or ambiguous in results. These flaws are discussed in detail in the text.

 Ÿ         It also notes that all but one of the studies that seek to disprove an MMR/autism or a thimerosal/autism link did not look at the actual children themselves, but rather were based upon statistical analyses of the medical records of the wider population. Such epidemiological studies are not appropriate to the identification of relatively-rare adverse outcomes, and have indeed been criticized by professional statisticians.

 Ÿ         Such studies also fail to address the problem  -  what was it that damaged the specific children that became autistic after MMR or thimerosal-containing vaccines?

 Ÿ         The one MMR study that has both claimed there is no MMR/autism link and also actually looked at information extracted from the medical records of a sub-set of UK damaged children was unable to prove or refute the suggested association with MMR on the basis of the information available  -  although it went on, despite this, to insist that MMR was safe. And  -  note  -  this was still not a clinical study. No children were actually clinically examined.

Ÿ         Parents who have scrutinised the studies quoted by the Department of Health as “proof” of there being no link between MMR or thiomersal and autism have found that such studies crumble away easily when pressed. To give just one example, the Finnish study by Patja, Peltola et al was very loudly heralded at the start of 2001 by the UK Department of Health as convincing and conclusive proof that MMR was safe. After intense critical scrutiny by parents and media, by the end of 2001 the Medical Research Council was forced to admit that Patja, Peltola et al’s original 1998 paper “did not examine the relationship of MMR and autistic spectrum disorders.....and does not therefore provide useful evidence on this point.” Of the subsequent paper by Patja, Peltola et al, the MRC admitted: “The findings need to be interpreted with some caution, as cases of autistic spectrum disorder or bowel disorders not considered at the time attributable to MMR would not necessarily have been reported”. Quite a retreat. Yet the study still continues to be regularly quoted by medical commentators and professionals as “proof” that MMR is safe.

Ÿ         In contrast, the parents find that there is a considerable, and growing, number of studies that suggest that MMR and/or thimerosal preservative (routinely used in very many vaccines until very recently, and still in widespread use in 2005) could be causing acquired autism (or “autistic enterocolitis”) in significant numbers of children.

Ÿ         Contrary to the claims of the authorities, particularly in the UK, not all of these studies originate from only one group of researchers (the former Wakefield team at the Royal Free Hospital London, and then Dr. Wakefield since his departure), as has sometimes been inaccurately asserted by those who defend MMR. The studies that point to a link have involved a growing number of research teams, in several countries. Other studies, whilst not specifically targeting MMR or thimerosal-containing vaccines, offer further clues as to what may be happening, and are consistent with an MMR and/or thimerosal involvement, implicating vaccines.

Ÿ         Furthermore, many of the studies that suggest that there is an MMR/autism or a thimerosal/autism link are based upon the scientific analysis of data gathered from detailed individual medical examination, and upon medical samples taken from the children concerned. These are the studies that actually seek to address the two key questions, “what is the damage sustained by this specific child, and what exactly precipitated the damage to this specific child?”.

Ÿ         A “house of cards” has thus been constructed by the UK Department of Health, the US Government health system and by other authorities and commentators in the medical establishment over the past five years, with repeated assurances being given to the public, but with these being based upon a lop-sided, highly partisan and culpably selective gathering and interpretation of the available evidence.

Ÿ         This briefing note also finds that there are other related concerns  -  from the regulatory bodies themselves  -  about the risk of permanent developmental damage from thimerosal-containing (or thiomersal-containing) vaccines, though it is not yet completely understood as to how these problems are directly interlinked biologically to the MMR/autism problems (we are told that MMR in itself does not contain thimerosal). Class-action lawsuits are now under way in the US (see later sections) over thimerosal/thiomersal and autism, just as they have been (or still are) in the UK and Ireland over MMR and autism.

Ÿ         Although complete and precise scientific proof of how the children have been damaged by vaccines and become autistic is still emerging, there have been numerous vital clues over the past six years and more  -  clues that all too often have been ignored, or, worse still, have been rejected out of hand by the authorities.

Ÿ         The medical establishment has repeatedly asked itself the wrong question. It has asked itself “Is MMR safe?”, and “is thimerosal safe?”, hoping for an affirmative answer. In contrast, researchers and parents have asked two very different questions: “What precisely is wrong with this child?”, and “Why did this child change from being healthy to being autistic?”. It is answering these latter two questions that should be the key issue.

Ÿ         The safety trials of MMR were undoubtedly very poor. That is an established fact. For the thimerosal issue, the picture is even more stark. The product appears to have had no proper safety trials since its introduction about 75 years ago, and its use appears to have lacked any appropriate back-checks on safety.

Ÿ         Much of the debate within the medical community appears to have been based around the simplistic assumption that, for example, if MMR caused autism, there should be matching graphs showing the uptake of MMR and the uptake of autism. For example, in Spring 2005, Dr. William Barbaresi of the Mayo Clinic, Rochester, Minnesota, commented that children had been given MMR for almost twenty years before there was a marked increase in US autism. The possibility that children had, for example, been damaged in gradually-increasing numbers by the introduction of MMR and then the later acceleration of the vaccination schedule using increased total burdens of thimerosal for each child, in combination, in combination, producing a delayed-action increase in autism numbers, does not seem to occur to the medical establishment. It is rather like road accidents. Accidents are caused by driver behaviour, vehicle design, vehicle speeds, road design, road condition, weather and other factors, in combination. You do not expect to find a precise historic straight-line linear relationship over decades between (say) “numbers of drivers” and “numbers of deaths”. Life is more complex than that.

Ÿ         The children that have been damaged have had their lives ruined. They were previously completely healthy. They now have seventy or eighty years of mental handicap ahead. Whether their sacrifice is justified in the interests of wider public health is not the point at issue. What is at issue is, what changed for these children, through what processes, involving what susceptibility factors and trigger factors. And how can further cases of damage be headed-off?

Ÿ         This briefing note also poses a number of unanswered questions about MMR, about thimerosal,  and about the children that are believed to have been severely damaged by vaccine administration. The damage involved is not confined to regressive autism.

Ÿ         Finally, it is emphasized that this note is the result of a search of the published (and sometimes unpublished) studies and other information. It does not offer medical advice. Parents considering vaccinating their children with MMR or with thimerosal-containing vaccines must form their own conclusions as to whether to proceed, and are urged to gather the maximum amount of hard information before making their own choice. It is hoped that this Briefing Note offers a useful start, and is useful for journalists.

PART A

A NOVEL SYNDROME

1:     What Is Acquired Autism/Autistic Enterocolitis?

Ÿ         Autism is not an illness in itself, so much as a manifestation of a dysfunction in certain parts of the central nervous system, particularly affecting language, cognitive and intellectual development and the ability to relate to others. It is an effect, and a consequence, not a cause in itself. Everything has a cause. Autism is not some mysterious illness that comes out of the sky, to strike children at random. It is a global term, all too loose, to describe a set of characteristics.

Ÿ         The “classic” form of autism was first described by Dr. Leo Kanner. These children were different from normally-developing children from birth.

Ÿ         However, a very different form of autism, formerly a minority variant, has now begun to predominate. In this, children develop normally, passing all their developmental milestones, and then later acquire an autistic-like condition. They lose their previously-demonstrated speech, learned behaviour and social skills. In effect, they dissolve into a state of mental impairment, of varying severity. Often the damage is severe or very severe, and usually the damage appears to be permanent, although some remedial treatments are claimed to be able to reverse some aspects of damage to a modest degree.

Ÿ         This late onset of autism typically follows the receipt of MMR vaccination, but also appears to sometimes follow measles-containing vaccines such as monovalent (so-called “single”) vaccine, or measles-rubella (MR) vaccine, and sometimes other vaccines such as DPT (diptheria-pertussis-tetanus).

Ÿ         It does not necessarily occur immediately after MMR  -  onset of autism is not in any case an “acute” reaction  -  and there are now grounds for believing that onset following vaccination may be very gradual indeed, spread over at least many weeks, more probably several or many months, or even in some cases several years. The rate of deterioration seems to vary considerably. It has been a consistent error of the medical authorities to view autism as an alleged acute, immediate, reaction, although many parents have certainly reported than some form of immediate or near-immediate (within 24 hours) adverse reactions, such as high-pitched screaming and high temperatures, have occurred. Some parents have reported a rapid change in their child’s behaviour, whereas others have seen a slower decline. Typically, the child’s mood has changed, they have become quiet and withdrawn, speech has been lost and skills have vanished. Sleep patterns have often disintegrated.

Ÿ         Crucially, the onset of this acquired form of regressive autism is accompanied by other visible and associated physical manifestations of problems. These include bright red ears and dark rings under the eyes after certain foods, acute gluten and casein intolerances, prolonged hyperactivity, night sweating and loss of temperature control, and chronically poor sleep patterns.

Ÿ         The arrival of these problems and the degeneration of the child into autism as a “package” strongly suggests that they are interconnected

Ÿ         The timing of onset following vaccination  -  not just MMR  -  is described by the UK Department of Health as a coincidence. Their argument is that autism is “noticed” around this time, because this is a time when child development is most rapid, and therefore any failure most noticeable. The thinking behind this stance appears to be that either autism was always there, all along, or that it is akin to some sort of delayed-action genetic “bomb”, primed in certain individuals to detonate just after receipt of MMR or thimerosal-containing vaccines, or around that time.

Ÿ         The gross implausibility of this argument, that it is highly unlikely in the extreme that previous problems would have been missed, and at a time where children receive constant devoted attention and close scrutiny regarding their development, is ignored. The concept that genetics alone could be responsible for sudden devastating decline in a developing infant is equally implausible.

Ÿ         Photographic and video evidence, together with child health and developmental records and the accounts of relatives, friends and visitors, that contradicts the authorities’ arguments, is also routinely ignored, without even a superficial investigation to verify their accuracy.

Ÿ         However, very significantly, much older children have also degenerated into autism after MMR or other vaccination. If degeneration in affected children always follows immunisation with MMR or measles-containing vaccine, regardless of the age of the child, then it implies that the link is not coincidental.

Ÿ         Also, no cases are known, at least to campaigning parents, of any children who have rapidly become autistic just before MMR or thimerosal-containing vaccines. This clearly implies that such cases are much fewer in number.

Ÿ         Also, it is not simply a failure to develop. The children have developed normally, then inexplicably acquired their autistic state. This protracted event has been directly observed by parents and relatives, and in many cases recorded on photographs and video footage.

Ÿ         There is also the issue of double-regression, where children have been normal, have been vaccinated, have regressed, have made some remedial progress, have been re-vaccinated (as a booster) and have severely regressed again. This principle is known as challenge-rechallenge. The US Institute of Medicine has stated that evidence of challenge-rechallenge would constitute powerful support for a causal link between vaccines and regressive autism. There are many UK children (and presumably US children, too) who offer such evidence, but the IoM has not yet accepted that its self-declared criteria has been fulfilled.

 Ÿ         No credible alternative explanation for why a previously-healthy child should become severely autistic has been put forward. The unheralded acquisition of a state of severe disability, in a substantial number of hitherto-healthy children, has to have a significant causal trigger. A growing number of scientists, as well as parents, believe that the trigger is either MMR, or thimerosal, or both acting in synergy.

 Ÿ         Undoubtedly there are other factors involved, pointing to a predisposition of certain children to be vulnerable to damage, of varying severity. Research should be trying to pinpoint those factors, but patently is not. Research is being held up by the refusal of the medical establishment in the UK and US to recognise the problem, or even to recognise the reality of a steep increase in autism.

 Ÿ         Also coinciding with the late onset of autism in many of the children (or other severe damage  -  autism is not the only manifestation of there being a problem), has come gastrointestinal problems such as alternating bouts of diarrhoea and constipation, chronic abdominal pains and bloating.

 Ÿ         Examination of children, initially but not exclusively at the Royal Free Hospital, London, has identified a novel form of inflammatory bowel disease, ileal-lymphoid nodular hyperplasia. This has emerged after ileocolonoscopy of affected children and analysis of samples. The pioneer research the Royal Free has now been confirmed by researchers at other centres in Ireland and the US.

 Ÿ         The simultaneous onset of these problems after a normal early development suggests that it is highly likely that these other elements are linked into the biological explanatory sequence of autism, notably through the pathway of gut damage and either the penetration of the blood-brain barrier or the triggering of some other process, such as serious myelin damage (in basic terms, the myelin sheath is the “insulation” around the neurons or “wires” of the brain).

Ÿ         Research reported by Dr. Jeff Bradstreet to the US Institute of Medicine on 9th February 2004 found that, when the cerebrospinal fluid of 28 regressive-autistic children was analysed, measles virus was found in 19 of the 28 cases. When 37 non-autistic control-group children were analysed, only one child was found to have measles virus. All 65 of these children had received MMR, and none had any recorded history of wild measles infection. This more recent research is powerful statistical evidence of a measles virus complicity in the pathogenesis of regressive autism. This research therefore strongly endorses the anecdotal evidence of the parents, that their children became autistic after MMR. For many children, MMR thus remains the prime suspect.

2:     The New Syndrome

This is a very brief summary of the new syndromes of autistic enterocolitis and/or mercury damage:

Ÿ         In a 200-strong cohort of children examined through ileocolonoscopy at the Royal Free Hospital, London, an almost 100% incidence of ileal-lymphoid nodular hyperplasia has been found. This condition manifests itself as swollen lumps throughout the intestinal tissue of autistic children. The condition is very rare in non-autistic children.

Ÿ         The condition is believed to have developed in each case in the period following MMR immunisation

Ÿ         Because of the swollen and hyperplasic condition of the intestinal wall, undigested toxins , having not been stopped by either the intestine or the liver (which can also be damaged) may then be able to attack the central nervous system. The evidence for the complete pathway of damage is uncertain at present, due to lack of research.

Ÿ         An alternative pathway of damage may be that the virus(es) in the vaccine, or other constituents of the vaccine, may be inflicting the actual damage, or interfering with the brain’s further development by damaging myelinisation. Comprehensive studies to determine this have also yet to be undertaken.

Ÿ         It is also possible that thimerosal, a mercury-based preservative that has been routinely used in a number of vaccines, may have played a role. The resultant damage closely resembles that of mercury poisoning. Again, adequate research has not yet been done.

Ÿ         Damage may in the event be via either, or a combination, of these pathways.

PART B

THE SCALE OF THE AUTISM PROBLEM

3:     The Financial Costs  -  Autism Is Costing The Taxpayer £$Billions

Quite apart from the immense social costs of autism for individual families, there are the huge financial costs. Autism effects every UK and US taxpayer, not just the families with the children. In the UK, the costs comprise:

Ÿ         Health costs  -  specialist hospital visits, GP visits, prescriptions, exclusion diet costs  -  passed on to the taxpayer

Ÿ         Major education costs  -  special schools, extra teachers, extra teaching assistants, extra training, management  -  passed on to the taxpayer

Ÿ         Transport costs for schooling and respite  -  taxis plus drivers and escorts, plus local authority management costs, plus environmental/congestion costs of extra traffic  -  passed on to the taxpayer

Ÿ         Significant childhood social services costs  -  respite care staff costs, management, inspection, reviews  -  passed on to the taxpayer

Ÿ         Later special transport costs in adult life (during lifelong care)  -  funded by the taxpayer, as the person with autism will almost certainly have no income

Ÿ         The immense costs of sheltered accommodation during adult life (lifelong costs), again including social services, management, inspection, and also including furniture and other allowances, all passed on to the taxpayer

Ÿ         The immense loss of earnings of the affected person (lifelong)

Ÿ         The loss to the Government of their national tax revenues (lifelong)

Ÿ         The loss to local government of their Council Tax revenues (lifelong)

Ÿ         Loss of earnings of parents whilst acting as carers

Ÿ         Loss of the parents’ tax revenues whilst caring

Ÿ         Carers allowances (paid to parents when they are acting as carers), the costs of which are passed on to the taxpayer

Ÿ         Disability living allowances, often at the higher rate (lifelong), including care and mobility components, passed on to the taxpayer

Ÿ         Incapacity benefit (lifelong beyond age 16), passed on to the taxpayer

Ÿ         Wider economic costs  -  other losses of gross domestic product and other non-financial contributions to the national economy

It would be interesting to know if the UK (or US) Treasury had a view on these costs, and whether sufficient resources were being devoted to investigating acquired autism and other forms of autism, as they represent a massive loss to the local and national taxpayer and the national economy.

These costs will grow as more and more children become autistic and as more of the existing children reach adulthood and leave home. The affected people almost certainly won’t be paying these costs as children, nor even as adults, as they almost certainly won’t have any income. And once the children reach adulthood, the parents won’t be paying them, either.

As these costs soar, the question becomes, “is autism too important to be left to the Department of Health, a Department that has done virtually nothing to investigate its causes”?  -  or to its counterparts in the US and elsewhere? Is this just a private matter for the medical community, or a matter for a wider audience? And, for the medical safety regulators, “who guards the guards”? Does a Minister control his/her advisers, or do his/her advisers control the Minister?

4:     Overall Cost Estimates

In June 2000 a study for the UK Mental Health Foundation found that

Ÿ         the annual costs of autistic disorder in the UK were at least £1 billion

Ÿ         individual lifetime costs per child affected could run to £2.94 million each.

The full costs, taking into account wider economic costs, are probably considerably higher still.

If one reduces the £2.94m per child by an arbitrary 33%, to allow for the fact that many children are less severely damaged than the maximum, and will thus cost less to care for, one is still facing a bill of £2m for lifelong care, not counting other wider costs such as loss of tax revenues from the autistic person an (when their parents care for them) their carers, plus other costs such as carers’ allowances (a UK scheme). The degree of severity and precise costings could be debated at length, but are clearly extremely large for severe cases.

Another way of looking at it is to compare the UK with the US, which has hard State-collected data. According to the Individuals With Disabilities Education Act data, the US autism numbers (with four times the population) stood at 120,000 in early 2003 (amongst 6-21 year olds in full time education).

If UK cases currently run to around a quarter of this figure, 30,000 to 35,000, then total economic costs for the UK could be immense. A reasonable estimate would be that 35,000 cases would cost the UK taxpayer somewhere between £35 billion and £100 billion spread over perhaps seven decades, or between £500m and £1.4 billion per annum. A mid-range answer probably lies in the £20 billion to £40 billion-plus range, spread over five to six decades, and even that latter figure works out at £700 million per year. And that is only for the UK.

Even if these costs are being seriously overestimated here, they are still immense. And they could represent an underestimate, especially if there is economic damage from the milder cases that are probably not included in the statistics. There is also the prospect of cases being added to the total, all the time, now. Any annual increase in cases of, say, ten per cent would lead to all these estimates having to be re-doubled a decade on.

And this is wholly irrespective of any MMR-autism or thimerosal-autism link being proved, because the children already exist, even if the cause of their illness remains disputed. The children are out there, now, and these bills are being passed to the taxpayer, now, today. The costs meter is already running, but the immense scale of the bill is partly obscured by it being spread amongst many central and local government (or Federal and State) budget headings, and amongst numerous lesser authorities.

5.     Failure To Monitor Increases In UK Autism Numbers

Ÿ         There has been a consistent argument on the part of the authorities, and those seeking to defend MMR, that the apparent rise in autism may be largely a matter of better recognition. This has received some backing from autism researchers. But where hard UK or US data is available, increases are far too steep, and in far too short a timescale, to be credibly ascribed to better recognition alone..

Ÿ         For this to be “better recognition” or “improved diagnosis”, this would have required these children to have been missed, simultaneously, by their parents, their relatives, their doctors and their teachers in the past This is simply not credible. For example, the increase in autism 1992-99 in Wakefield, West Yorkshire, UK, local education authority was from 5 cases to 111 cases. If increased autism is down to better recognition, it would mean that, back in 1992, there really were 111 cases, but only 5 were recognised, and the remaining 106 were missed, and by all the parties  -  parents, doctors, health visitors, teachers  -  concerned. This is completely implausible.

Ÿ         Undoubtedly there has been some degree of better recognition and reclassification, following introduction of ICD-10 (international classification of diseases/disorders) criteria in 1992, and DSM-IV (diagnostic statistics manual) criteria in 1995. But this will account for only a minority of the growth.

Ÿ         The UK Department of Health has failed to monitor autism, and is still failing to (despite a specific 1997 recommendation of the House of Commons Health Committee to do so). Is it now afraid of what it might find? If it does decide to monitor autism, will it find that numbers are high and then claim it has always historically been so?

Ÿ         UK Health Boards/Authorities are also failing to monitor autism locally. Health Boards/Authorities have little data and no consistent approach. At the health authority level, official figures vary wildly, by factor of 300-fold, i.e. 300-times (not 300%). The data is an extraordinary mess.

Ÿ         In fact, most UK data is actually non-existent. In the year 2000, only 1 in 6 UK Boards/Authorities had any credible figures at all. Most used estimates from textbooks.

Ÿ         The Scottish schools census now includes autism. The census commenced in 1998. The 1998 figure was around 750, but by year 2000 this had climbed steeply to about 1,250, and by 2002 it stood at approaching 2,200.

Ÿ         There are other indications of the level of increases: Kaye et al paper (see later) found a sevenfold increase 1988-99 in UK. An unpublished 1999 paper by Dr. Fiona Scott, Autism Research Unit, Cambridge, indicated autism at eleven times the expected level (1 in 174)  -  see later.

Ÿ         The 2001 Medical Research Council review found autism to be at 1 in 166, many times higher than hitherto thought. Sixteen studies published between 1966 and 1991 found rates of between 1 in 3030 and 1 in 625. A rate of 1 in 166 is nearly four times higher than 1 in 625, itself the highest of these sixteen, and only from a relatively-recent study in 1983. If you take a rate of 1 in 1830 as being the mid-point of these historic rates, then a rate of 1 in 166 is eleven times higher.

The repeated official line that the apparent increase is down to better recognition is little more than a counsel of complacency.

In December 2002, a Parliamentary Written Question (84502) confirmed that there is now in place a “Good Practice Guidance on Autistic Spectrum Disorders”, in the UK, published by the Government’s Departments of Education & Skills and of Health. This is intended to raise awareness amongst schools and local education authorities. However, it is probably just one of many thousands of such well-intentioned documents, is non-statutory, and is probably lost in the stream of paper raining down on local government from central government.

UK schools and local education authorities have a duty to identify, assess and make suitable provision for children with special educational needs. However, there seems to have been no duty upon either the health authorities at the local level or the Department of Health at Government level to improve the data position over autism  -  doubtless to the latter’s relief. Perhaps centrally-collated figures showing steep increases would beg uncomfortable questions as to the causes. The UK Department of Health seems to regard autism as a problem for local education authorities  -  not for the Department.

It is understood that from January 2004, a first survey in England will be undertaken of disabilities amongst children receiving special needs education. This will be the UK (England-only) Pupil Level Annual Schools Census (PLASC). English local education authorities and the schools in their areas have to supply data about the numbers of pupils with different types of special educational need, including autistic-spectrum disorders.

However, it may be some time before data is available, and obviously it will be several years before any clear trend emerges. Any past steep rise during the 1988-2004 period will therefore of course have been missed, although some idea of increases may be available if data is stratified by age (this is not known at time of writing).

There has been a similar failure to monitor numbers closely in the US, although the data position is considerably better, as will be explained later. The data position elsewhere is not known, but is almost certainly either very poor or non-existent.

6.     “Now Almost Everyone Knows Someone Who’s Autistic”

Autism was a very rare condition, but is now almost regarded as commonplace. Very many cases are now of late-onset autism, whereas almost all used to be cases from birth. We have to ask why this is.

Some UK research noted the sharp increases in autism in the 1990s. A paper by Powell et al, Department of Public Health and Epidemiology, University of Birmingham, UK, Changes in the Incidence of Childhood Autism and Other Autistic Spectrum Disorders in Pre-School Children from Two Areas of the West Midlands, UK, was published in Developments in Medicine and Child Neurology, September 2000. This looked at the incidence of childhood autism and ASD in pre-school children between 1991 and 1996.

The study found that there were year-on-year increases in classical autism during this period of 18%, but for “other ASDs” the annual increase was no less than 55%. But the study then concluded that this was due to clinicians being increasingly able or willing to make a diagnosis. The possibility of an underlying genuine increase, and any follow-on question as to causes, does not appear to have occurred to the study team.

But parents of children believe to have been damaged by MMR strongly believe that part of the increase is down to a new phenomena, autistic enterocolitis.

It is not the autism of the past. Such a severe acquired regressive syndrome after a normal early childhood would have been noticed at once in the past by parents, and recognised medically, and also reflected in much higher historic rates of prevalence/incidence. Regressive autism used to be a minority variant: Now it is clearly the predominant form, by a very wide margin.

Dr. Bernard Rimland, President of the US Autism Research Institute, has concluded, after a thorough analysis of the ARI database: “Late onset autism (starting in the second year) was almost unheard of in the 1950s, 1960s and 1970s. Today, such cases outnumber early onset cases by five to one, with the increase paralleling the increase in required vaccines”.

In the parents’ view, there is clear evidence of recent dramatic rates/increases in autism:

Ÿ         Some UK examples  -  an East Surrey 1/69 rate amongst three year old boys, 1/139 rate amongst three year old boys+girls combined (source: personal communication of 10/6/99 from Caroline Clark, Commissioning Manager, Learning Disability Services, East Surrey Health Authority). The letter from East Surrey stated: “In the remaining half of the District, it is estimated that there are at least 50 children on the autistic spectrum under the age of five. A special needs audit has been undertaken of children aged three by the community paediatrician. This is the age where the paediatrician expects to identify children at the more severe end of the autistic spectrum. Thirty-six children have been identified during the last two years as presenting with autism, of which twenty-nine were between the ages of two and three, with seven children slightly older. The general population is around 2,500 children (born) per year in this part of the District. The prevalence of autism indicated by the audit is 0.72% (1 in 139) but with 1.44% (1 in 69) for young boys.”

Ÿ         Bromley Autistic Trust figures show a 1990-94 increase of 280% over 1980-84 figures (source: personal communication of 16/9/99 from Miss C. M.  Povey, Services Director, Bromley Autistic Trust)

           A local survey carried out in the Inverness area in 2003 found that 1 in 49 children was on the autistic spectrum.

 Ÿ         Wakefield LEA autism pupils rose from 5 to 111 in seven years (source: survey by David Brown, a specially-seconded headmaster from the Park School, Wakefield, on behalf of Wakefield Local Education Authority, 1999)

 Ÿ         Telford health data up from 4 new cases per year in 1990 to 17 per year 1998 and again 1999 (source: personal communication of 20/11/00 by Dr F. R. J.  Hinde, Consultant Paediatrician, Princess Royal Hospital, Telford)

 Ÿ         As noted, Scottish schools census, repeatedly up year-on-year, and by a large margin each year; from around 750 in 1998 to well over 2000 in 2002 (source: Scottish Annual School Censuses, available from Scottish Education Office, tel 0131 556 8400)

 The problem isn’t confined to autism. On December 22nd 2002, the (UK) Observer newspaper carried a report on the apparent epidemic of behavioural problems amongst UK schoolchildren. Whilst not autism (the report cited hyperactivity and attention-deficit disorder), the Observer’s report suggested a steep rise in the incidence of problems. Figures obtained by the newspaper suggested that numbers of schoolchildren with attention-deficit disorder (ADD) or attention-deficit hyperactivity disorder (ADHD) had reached 345,000, and that one child in twenty between the ages of 6 and 16 years had one or other condition. The Observer also found out that prescriptions for Ritalin, to counter these disorders, had increased markedly, from 91,100 in 1997 to 208,500 in 2001.

 In the US, the Brown University Child & Adolescent Behavioural Letter (18(3): 1: 304, 2002) carried the following details:

 Ÿ              A study into attention deficit hyperactivity disorder (ADHD) was undertaken, based on parent and teacher reports concerning 6,099 children in 17 public elementary schools. The study was undertaken by researchers working for the National Institute of Environmental Health Sciences in North Carolina

 Ÿ              When the researchers surveyed parents in a typical county of rural and suburban communities  -  Johnston County, North Carolina  -  the parents reported that more than 15% of boys in grades 1st through 5th had a diagnosis of ADHD, with about 10& (i.e. two-thirds of those diagnosed) receiving medication.

 Although ADHD is not autism, it may share some common causal pathways, particularly multiple food allergies and gut permeability. The finding is thus of interest to the MMR/autism debate.

 7.     Is Autism Increasing Due To Changes In Criteria?

 This has become a hotly-contested topic, as it is central to the vaccine/autism controversy. But gradually, sheer numbers are silencing, or at least weakening, the position of those who doubt that autism has greatly increased in a very short space of time.

 It has frequently been asserted by Governments, some researchers and elements of the medical establishment that the apparent increases in numbers of children with autism can be ascribed to “looser” criteria for inclusion. This latter point is demonstrably not the case. The criteria have in fact tightened-up.

 Kanner’s original concept of autism included five diagnostic features:

 ·        A profound lack of affective contact.

 ·        obsessive desire for the preservation of sameness

 ·        Fascination for objects

 ·        mutism or language that does not seem suited to interpersonal communication

 ·        feats of memory, or skills in performance tests

Kanner and Eisenberg, in 1956, emphasized two diagnostic criteria:

·        profound lack of affective contact.

 ·        repetitive ritualistic elaborate behaviour

They considered that if these two key features were present, the other typical features would also be found.

In 1980, the DSM-III (Diagnostic and Statistical Manual III) criteria were introduced. These included:

·        “pervasive developmental disorder” for the general category of autism.

 ·        “infantile autism”

 the category of infantile autism was defined as:

 ·        lack of responsiveness to others.

·        language absence or abnormalities.

·        resistance to change and/or attachment to objects.

·        the absence of schizophrenic features.

·        onset before age 30 months

In 1994, DSM-IV criteria were introduced. These criteria are more restrictive than DSM-III, and so an increase in numbers between the DSM-III era and the DSM-IV era cannot be explained by looser criteria, as the very opposite is the case. For example, in Washington State, autism numbers actually fell when DSM-IV was introduced.

It is worth setting out in detail the criteria for autism and relating autistic-spectrum disorder (ASD) conditions:

8.     Autistic Disorder

For DSM-IV, a total of six or more items from the following lists of (1), (2) and (3) is necessary, with at least two items having to come from (1), and one each from (2) and (3):

(at least two from)

(1)     Qualitative impairment in social interaction as manifested by:

*     marked impairment in the use of multiple non-verbal behaviours, such as eye-to-eye gaze, facial expression, body postures and gestures to regulate social interaction.

*     failure to develop peer relationships appropriate to developmental level.

*     a lack of spontaneous seeking to share enjoyment, interests or achievements with others (eg by a lack of showing, bringing or pointing-out objects of interest.

      *     lack of social or emotional reciprocity

(at least one from)

(2)     Qualitative impairments in communication, as manifested by at least one of the following:

*     delay in, or total lack of, the development of spoken language (not accompanied by an attempt to compensate through alternative modes of communication such as gesture or mime)

*     in individuals with adequate speech, marked impairment in the ability to initiate or sustain a conversation with others

*     stereotyped and repetitive use of language or idiosyncratic language

*     lack of varied, spontaneous make-believe play or social imitative play appropriate to developmental level

(at least one from)

(3)     Restricted, repetitive and stereotyped patterns of behaviour, interests and activities as manifested by at least one of the following:

*     encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus

*     apparent inflexible adherence to specific non-functional routines or rituals

*     stereotyped and repetitive motor mannerisms (eg had or finger-flapping or twisting or complex whole-body movements)

*     persistent preoccupation with parts of objects

9.     Pervasive Development Disorder  -  Not Otherwise Specified (PDD-NOS)

The DSM-IV criteria also included criteria for “pervasive development disorder-not otherwise specified”, or PDD-NOS. This category applies to cases where there is a severe and pervasive impairment in the development of reciprocal social interaction or verbal and non-verbal communications skills, or when stereotyped behaviour, interests and activities are present, but the criteria are not met for a specific pervasive developmental disorder, or schizophrenia, or schizotypal personality disorder, or avoidant personality disorder.

For example, PDD-NOS includes “atypical autism”, presentations that do not meet the criteria for autistic disorder because of late age of onset, atypical symptomatology, or sub-threshold symptomatology, or all of these.

10.     Asperger’s

The DSM-IV criteria for Asperger’s Disorder (or syndrome) are as follows:

Qualitative impairment in social interaction as manifested by at least two of the following:

*     marked impairment in the use of multiple non-verbal behaviours such as eye-to-eye gaze, facial expression, body postures and gestures to regulate social interaction.

*     failure to develop peer relationships appropriate to developmental level

*     lack of spontaneous seeking to share enjoyment, interests or achievements with other people

*     lack of social or emotional reciprocity

Restricted, repetitive and stereotyped patters of behaviour, interests and activities as manifested by at least one of the following:

*     encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal in intensity or focus

*     apparently inflexible adherence to specific nonfunctional routines or rituals

*     stereotyped and repetitive motor  mannerisms such as had or finger-flapping or twisting, or complex whole-body movements

*     persistent preoccupation with parts of objects

The disturbance causes clinically-significant impairment in social, occupational or other important areas of functioning. There is no clinically-significant general delay in language, eg single words are used by age two years, communicative phrases used by age three years). There is no clinically-significant delay in cognitive development or in the development of age-appropriate self-help skills, in adaptive behaviour (other than in social interaction) and in curiosity about the environment in childhood. Criteria are not met for another specific pervasive developmental disorder, or schizophrenia.

11.     Paper by Mark Blaxill, June 2001

The issue of diagnostic criteria was also considered in a long and detailed paper, “The Rising Incidence of Autism”, by a parent, Mark Blaxill, in June 2001. This paper covered a number of aspects of the vaccine/autism controversy, and is reported in several sections of this document. Coverage of diagnostic criteria  -  and whether changes in criteria have produced a “false impression” of an epidemic, were summarised in the paper.

The five most influential criteria groups that have formed a backdrop to the work of epidemiologists have been:

*     Kanner’s original work. Kanner’s criteria were abandoned in the 1970s.

*     Rutter’s attempt to modify and refine Kanner’s work with the introduction of a categorical approach

*     the codification of Rutter’s approach within the Diagnostic Statistical Manual (DSM) series, termed DSM-III

*     the modification of DSM-III into DSM-IIIR (“r” for revised)

*     attempts at producing an international standard, with the use of DSM-IV and ICD-10 (International Disease Classification-10)

From Rutter onwards, all the criteria have attempted a categorical approach. A child must exhibit specific significant impairments. Of the above four categorical methods, differences can be compared as follows:

(Social category)

*   Rutter 1978, “impaired social development which has a number of special characteristics (that are) out of keeping with the child’s (normal expected) intellectual level”

*   DSM-III 1980, “lack of responsiveness to others”

*   DSM-IIIR 1987, “qualitative impairment in reciprocal social interaction”, defined more specifically by the fulfillment of at least two out of five criteria from a checklist

*   DSM-IV 1994 “qualitative impairments in social interaction” which are now defined by meeting two out of four criteria from a checklist. These criteria include lack of eye contact, inability to form friendships, lack of awareness of the feelings of others, and lack of spontaneous play

(Language/communication category)

*   Rutter 1978, “delayed and deviant language development that also has certain defined features and is out of keeping with the child’s intellectual level”

*   DSM-III 1980, “language absence or abnormalities”

*   DSM-IIIR 1987, “qualitative impairment in verbal and non-verbal communication, and in imaginative activity”, which was defined as including at least one item from a list of six abnormalities. This included lack of language, abnormal speech patterns, lack of eye contact, abnormal play skills, abnormal conversation patterns and echolalia

*   DSM-IV 1994, “qualitative impairments in communication” which are now defined as any of four areas, including language absence or delay, abnormal conversation skills, echolalia or abnormal pretend play

(Behaviour category)

*   Rutter 1978, “insistence on sameness as shown by stereotyped play patterns, abnormal preoccupation or resistance to change

*   DSM-III 1980, “resistance to change or attachment to objects”

*   DSM-IIIR 1987, “markedly restrictive repertoire of activities and interests”, which require meeting one of five conditions, including self-stimulatory body movements, unreasonable insistence upon routines, distress over small changes in the environment, preoccupation with parts of objects and unusual preoccupation with narrow subject areas”

*   DSM-IV 1994,”restricted repetitive and stereotyped patterns of behaviour interests and activities” which requires meeting one of four criteria, including self-stimulatory body movements, unreasonable insistence on routines, preoccupations with parts of objects or unreasonable preoccupation with narrow patterns of interest

Blaxill notes that all four of these approaches share a great deal in common and reflect relatively few differences. He concludes that it is very difficult to make the case that a discontinuity in diagnostic concepts between 1978 (when Rutter’s criteria replaced Kanner’s) and the present time (then 2001) could produce increases of the magnitude recently reported. In other words, the major rises in autism numbers cannot be solely explained by changes in the diagnostic criteria, as is so often asserted by the medical establishment and by the US and UK Governments.

12.     University of Cambridge Research

On 18/2/01, the UK Sunday Telegraph reported on research undertaken by Dr. Fiona Scott at the Autism Research Centre at the UK University of Cambridge. The research, Prevalence of Autism Spectrum Conditions in Children Aged 5-11 Years in Cambridgeshire UK, by Scott, Baron-Cohen et al, which is due to be published shortly, was undertaken across schools in Cambridgeshire.

The study aimed to establish prevalence of the broader autistic spectrum, including Asperger syndrome in 5-11 year olds in Cambridgeshire, UK. Cases of diagnosed autism spectrum condition in children who were in Cambridgeshire schools and aged 5-11 on 31st December 1999 were sought out using public records, screening instruments, educational psychology and special educational needs coordinator records.

It found that:

Ÿ         One in 175 (58/10,000) children was autistic, whereas previous studies had pointed to a rate of 1 in 2000 (5/10,000)

Ÿ         This was 11 times higher than the rate of classic autism, but in line with other recent national and international rates for the broader spectrum.

Ÿ         In responding mainstream schools, the prevalence was 1 in 300. In the responding special schools, the prevalence was 1 in 8.

Ÿ         Extrapolated across the UK, that would imply 30,000 primary school (age 5-11) children with autism

Ÿ         The overall sex ratio of the children was 4 to 1 male to female, but in mainstream schools it as 8 to 1.

Ÿ         Linking these rates to estimated costs of education and care for sufferers would give a figure of as high as £5 billion per year, year after year. The Cambridge autism figures were described as “if anything an under-estimate”. They included only children with a definite clinical diagnosis. Any child who had only been “statemented” (= educational needs-assessed) as autistic, but not yet clinically diagnosed, was not counted

Ÿ         One in eight children with special educational needs was suffering from some form of autistic spectrum disorder. The increase of actual numbers over previously-assumed numbers would have enormous cost implications for central and local Government

Ÿ         A year-2000 report for the UK Mental Health Foundation by Professor Martin Knapp for the UK Institute of Psychiatry used the earlier “textbook” rate of autism of 5/10,000 to put the total UK economic cost of autism at £1bn. The Knapp report estimated the lifetime cost of a severely-affected child at £3m, for a high-functioning autism child at £0.8m, and for an Asperger’s syndrome child at £0.5m. The revised £5bn per year estimate is based upon these costs.

13.     University of Sunderland Research

An unpublished study by the UK University of Sunderland found a tenfold increase in diagnosis of autism, during the years 1989-93. Further details are awaited.

14.     UK National Autistic Society Estimates

The NAS issued a factsheet in early 1997 which gave the following prevalence rates:

Ÿ         People with Kanner syndrome (IQ less than 70)          5/10,000, or 1 in 2,000

Ÿ         Other spectrum disorders (IQ less than 70)                15/10,000, or 1 in 666

Ÿ         Asperger’s (IQ 70 or above)                                         36/10,000, or 1 in 278

Ÿ         Other spectrum disorders (IQ 70 or above)               35/10,000, or 1 in 286

Combined total of above four groups                                91/10,000, or 1 in 110

The above implies a very high level of autism in the UK, and the previously-described studies seem to bear this out.

The NAS reach its 91 in 10,000 or 1 in 110 rate by taking the Wing & Gould study (Camberwell, London) of 1979, which looked at children with an IQ of under 70 and found a rate of 20 per 10,000, and adding this to the study by Ehlers & Gillberg (Sweden) of 1993 which looked at autistic children with an IQ of over 70 and found a rate of 71 per 10,000 (1 in 141).

The 91/10,000 rate is thus “merged data”, collected in two different countries and some years apart, and thus needs to be treated with caution, particularly if rates have since been rising further. The Wing & Gould study is now over two decades out of date, and also pre-dates MMR introduction into the UK.

15.     Report by Fiona Loynes, UK All-Party Parliamentary Group on Autism, Dec. 2001

The purposes of this report included:

Ÿ         To establish numbers of children with autistic spectrum disorders

 Ÿ         To learn whether UK local education authorities believed there had been a recent increase in the last five years

 Ÿ         To ascertain whether LEAs routinely collected data

 The findings included the following:

 Ÿ         100 out of 115 LEAs reported an increase in autism in the past five years. Some reported small increases, others reported far higher increases, in one case by 77%.

 Ÿ         The study compared the expected prevalence rate of all autistic spectrum disorders in each LEA (91 in 10,000 or 1 in 110) with the actual recorded number of children with ASD and a Statement of Educational Needs (21 in 10,000 or 1 in 476). If the estimated numbers are correct, then the implication is that 75% of children with autism do not become included in the Statement data, because they have no Statement.

Ÿ         Only 44 out of the 100 LEAs reporting an increase had actual data. Some of these reported dramatic increases, up to 400% in four years.

16.     Report, “Autism In Schools  -  Crisis or Challenge”, National Autistic Society UK, May 2002

This report was complied from the findings of a survey carried out in seven local education authorities across England, Wales and Scotland, although the Scottish findings were reported separately. The England and Wales survey involved 373 individual surveys, with a response rate of over 30%, covering a pupil population of 133,000. The study found that:

Ÿ         1 in 86 children in mainstream schools had special educational needs that were related to ASD.

Ÿ         The rate of ASD is three times higher in primary than in secondary schools. In primary it is 1 in 80, in secondary it is 1 in 268.

Ÿ         This is in addition to children with ASD in special schools. In special schools, 1 in 3 children has ASD-related needs.

17.     Autism In Scottish Schools

Although there is no proper UK database on autism, comparable to the US’s Individuals With Disabilities Education Act (IDEA) database, and the Department for Education and Employment does not have any breakdown of its total numbers of children in England with special educational needs, the position is rather better in Scotland. There, a Scottish Schools Census was implemented by the Scottish Executive in 1998, and this annual survey gives a picture of rising numbers within Scottish schools. The census covers both junior and senior schools, and identifies (by sex) scholars with special educational needs, counting those with a primary diagnosis of autism as “autistic” (they may also have other disabilities). The data available is (totals):

This gives a rise over five successive years after 1998 of 225%. The criteria for inclusion have not been changed during that time, and although greater awareness and improved diagnosis may have made a minority contribution to the increase, it seems inconceivable that there isn’t an underlying real increase in these figures, matching the similar rises reported in the US by the IDEA database.

18.     Is Autism Increasing?  -  Some UK Pronouncements

These are some recent, and sometimes self-contradicting, statements:

Ÿ         “There is no good evidence that the frequency of autism has increased since the introduction of MMR” - Tessa Jowell, then Minister for Public Health, October 1997 (personal communication to David Thrower)

 Ÿ         “The true incidence of autism is uncertain” - Sir Kenneth Calman, then Chief Medical Officer, March 1998

 Ÿ         The apparent rise in autism in the UK began more than ten years before the introduction of MMR” - Tessa Jowell, in June 1998

 Ÿ         “Rates of autism are rising, but not because of MMR” (Committee on Safety of Medicines, June 1999)

 Ÿ         “There is no robust data on the prevalence of autism before and after MMR’s introduction” - Brent Taylor, in a June 1999 study heavily quoted by the Department of Health

 Ÿ         “Numbers of cases of autism are rising, but the reason for this is unclear” - John Hutton, Minister for Public Health, December 2000

Ÿ         “Methodological differences between studies, changes in diagnostic practice and public and professional awareness are likely causes of increases in prevalence. Whether these factors are sufficient to account for increased numbers of identified individuals, or whether there has been a rise in actual numbers, is as yet unclear” - Medical Research Council 2001 review, quoted by the Scottish Parliament Expert Group May 2002.

Ÿ         “Two thirds of (surveyed) teachers felt that there were more children with ASD now than five years ago. This (is) consistent across age groups and in all types of education provision, special and mainstream” (Report of the National Autistic Society, May 2002)

Ÿ         “The vast majority of the increase is due to the fact that we’re much better at detecting autism now (and) we include many more things in the spectrum for autistic spectrum disorders.....There’s a far wider spectrum, so that’s one of the factors.” - Dr. Stephen Ladyman, Health Minister for England, in Epolitix, 14th October 2003

But then Dr. Ladyman hedged his bets a little.....

Ÿ              “And underlying that, I think there may well be some sort of underlying increase in the number as well.....But what I am as certain of as I can be is that it has nothing to do with MMR and there is no reliable piece of science that links MMR and autism.”

  and

Ÿ              “In my view, it is clear from the literature available that more people with autism have bowel disorders compared to the rest of the population” (extract from All Party Parliamentary Group On Autism minutes, address by the Minister).

19.     Autism In The USA

The UK Department of Health is fond of saying how MMR is safely used in 32 countries, including the USA, as though its use elsewhere is proof, in itself, that it is safe. Recent claims have even referred to 100 countries. A similar attitude prevails over thimerosal.

But the USA, at least, has clear evidence of an autism epidemic. Other countries may also be becoming aware of increases, for example Finland, where a 400% increase in cases has been alleged since was MMR introduced.

The US has IDEA (Individuals with Disabilities Education Act). The Act was passed in 1975 to ensure equal educational opportunities for children with disabilities. The US Department of Education is mandated to report annually to Congress. Initially, autism cases were few, but in 1991 it was decided to specifically list autism separately. Numbers were (US-wide) 5,415 in 1991-92.

This system therefore picks up numbers of schoolchildren with developmental problems, and illustrates a huge increase in autism numbers in a very short space of time. Autistic pupils ages 6-21 have now increased from 5,415 in 1991-92 to 140,920 in 2003-2004 (Source: US IDEA State data). Thus for every case there was in the IDEA system in 1991-92, there were 26 cases by 2004.

Since the introduction of the more restrictive DSM-IV criteria from 1994 onwards, the rise in US numbers has continued unabated:

 (source: Individuals With Disabilities Education Act)

 Ÿ         To the above total also has to be added the further cases of autism amongst children aged 3-5 years. As at year 2000, this was 15,581 (this number will have since increased further).

 Ÿ         There were huge increases in some States between 1992-1993 and 2002-2003  -  up 968% in Connecticut, 779% in Florida, 1,131% (repeat: one thousand one hundred and thirty-one per cent) in Idaho, 1,086% in Kansas, 1,291% in Minnesota, all in just ten years (Source: US State data, Individuals with Disabilities Education Act). The rises have continued into 2004.

Ÿ         Many of the increases in individual States can only be described as alarming.

  Florida, ages 6-21

   Illinois, ages 6-21

   Indiana, ages 6-21

   Massachusetts, ages 6-21

   Minnesota, ages 6-21

   New Jersey, ages 6-21

  Ohio, ages 6-21

  Oregon, ages 6-21

  Virginia, ages 6-21

  Wisconsin, ages 6-21

(source of all tables: US Individuals With Disabilities Education Act, by State)

Ÿ         It is also interesting that individual towns such as Round Rock, Texas, are reported to be up from 6 cases to 115 cases in eight years  -  very much like Wakefield Local Education Authority in West Yorkshire UK (up from 5 to 111 in seven years). This suggests that UK increases may very closely match those in the USA.

Ÿ         It has been alleged that Brick Township (New Jersey) has manifested an “autism cluster”. Some 40 of Brick Township’s 6,000 3-10 year olds have autistic spectrum disorder. It has made Brick Township the “autism capital of the USA” (but note, East Surrey rates in the UK are higher still). In Brick Township, Federal investigators collected data on surface and ground water, sites of industrial spillages and waste dumping, and also ensured that there had been correct diagnosis of the actual children. They have found nothing untoward. Their findings were reported in April 2000.

The following, covering the most recent one-year increases, covers children classified as having a primary diagnosis of autism and covered by the Individuals With Disabilities Education Act database, and covers ages 3-5: