Discussing and documenting resuscitation status

DNR discussions are challenging. Through the years I've noticed several common mistakes which form barriers to meaningful decision making:

Use of medical jargon. Patients and their families watch TV and read newspapers, and think they understand this terminology, but they often don't.

Misunderstanding of clinical issues. A lack of understanding of the patient's disease processes on the part of the person leading the discussion may lead to over or under estimation of the prognosis.

Cursory or hurried discussions. Pressure to adhere to a regulatory or institutional policy may drive such discussions, which are not informative to patients and families.

Discussions postponed until the moment of crisis.

Vague and overly subjective discussions. Early in the conference the patient may say something like “Do whatever you have to if you think it will help” and there ends the discussion. Individual modalities of resuscitation and their anticipated benefits are often not addressed specifically.

Shared assumptions that DNR status means giving up. DNR patients may still warrant aggressive care, including ICU care. At Mayo Clinic, for example, (see below link) DNR status does not preclude the option of intubation and mechanical ventilation for patients who develop respiratory failure.

Issues concerning DNR discussions are reviewed in a recent issue of the Green Journal.

Behavioural signs of autism become evident between the ages of 6 and 12 months

By UC Davis MIND Institute, [RxPG] A study of the development of autism in infants, comparing the behavior of the siblings of children diagnosed with autism to that of babies developing normally, has found that the nascent symptoms of the condition — a lack of shared eye contact, smiling and communicative babbling — are not present at 6 months, but emerge gradually and only become apparent during the latter part of the first year of life.

Researchers conducted the study over five years by painstakingly counting each instance of smiling, babbling and eye contact during examinations until the children were 3. They found that by 12 months the two groups’ development had diverged significantly. Intentional social and communicative behavior among children developing normally increased while among infants later diagnosed with autism it decreased dramatically. The study is published online early and will appear in the March issue of the Journal of the American Academy of Child & Adolescent Psychiatry.

“This study provides an answer to when the first behavioral signs of autism become evident,” said Sally Ozonoff, the study’s lead author, a professor of psychiatry and behavioral sciences and a researcher with the UC Davis MIND Institute. “Contrary to what we used to think, the behavioral signs of autism appear later in the first year of life for most children with autism. Most babies are born looking relatively normal in terms of their social abilities but then, through a process of gradual decline in social responsiveness, the symptoms of autism begin to emerge between 6 and 12 months of age.”

Autism is a pervasive developmental disorder of deficits in social skills and communication, as well as in repetitive and restricted behaviors, with onset occurring prior to age 3. Abnormal brain development, probably beginning prenatally, is known to be fundamental to the behaviors that characterize autism. Current estimates place the condition’s incidence at between 1 in 100 and 1 in 110 children in the United States.

Children with a sibling already diagnosed with autism are known to be among those at greatest risk of developing the disorder. The current study included 25 high-risk children who met criteria for autism at 3 years of age, matched with 25 low-risk peers who were developing normally. It was conducted at the MIND Institute and the University of California, Los Angeles. The sole inclusion criterion for the high-risk group was having a sibling with autism; low-risk participants had to have been born after 36 weeks gestation and have no autistic family members.

The children’s development was evaluated at 6, 12, 18, 24 and 36 months of age using a series of widely implemented diagnostic tools, including the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview-Revised (ADI-R). Examiners were not told which babies were at high- or low-risk when evaluating the participants’ development.

The researchers found that there were few discernable differences between the two groups at the outset but that after six months, 86 percent of the infants who developed autism showed declines in social communication that were outside the range for typical development. “After six months,” the study found, “the autism spectrum disorder group showed a rapid decline in eye contact, social smiling, and examiner-rated social responsiveness.” Group differences were significant by 12 months in eye contact and social smiling and all other measures by 18 months, the study found.

The study is notable because of the accuracy and precision of its prospective methodology, assiduously recording exact numbers of social and communicative behaviors during lab visits. Previously, researchers have constructed evidence of autism’s earliest manifestations by interviewing parents about when they believed their children’s symptoms first arose or by reviewing home movies for clues to when children begin exhibiting symptoms of autism.

"Until now, research has relied on asking parents when their child reached developmental milestones. But that can be really difficult to recall, and there is a phenomenon called the “telescoping effect” where people usually say that they remember something happening more recently than when it occurred,” Ozonoff said. In addition parents frequently will turn off the video camera when their children are behaving poorly — precisely when autistic symptoms may appear.

Ozonoff said that the study provides a deeper understanding for parents, caregivers and health-care providers and for future research of the developmental trajectory for very young children with autism.

“We need to be careful about how we screen, and we need to know what we’re looking for,” Ozonoff said. “This study tells us that screening for autism early in the first year of life probably is not going to be successful because there isn’t going to be anything to notice. It also tells us that we should be focusing on social behaviors in our screening, since that is what declines early in life.”

“This study also found that the loss of skills continues into the second and third year of life,” she said. “So it may not be adequate, as the American Academy of Pediatrics currently suggests, that providers screen for autism twice before the end of the second year. Autism has a slow, gradual onset of symptoms, rather than a very abrupt loss of skills.”

“Screening may need to continue into the third year of life, since symptom emergence takes place over a long time. If a child starts exhibiting a declining trajectory and a sustained reduction in social communication we want to refer them into therapy, especially if they are at risk,” Ozonoff said, “even before we might be able to make a definitive diagnosis.”

Ozonoff said that the study does not address the etiology of autism or causality. In this study, the infants who participated were at high risk due to having strong family histories of autism, suggesting that genetics plays a major role in the later autism diagnoses, despite the fact that their symptoms were not apparent at birth.

Did Malaria, Bone Disease Kill King Tut?

Feb. 16, 2010 -- Malaria and bone disease may have contributed to the death of King Tut more than 3,300 years ago, a new DNA analysis and other scientific methods indicate.

Many theories have been raised about the death of Tutankhamun, or King Tut, one of Egypt's most famous pharaohs, since his mummy was discovered in 1922. The theories include suggestions that he was murdered or died from an infection after breaking a leg in a fall.

But scientists who used a number of modern methods, including DNA analysis and radiological scans of mummies of Tut and probable close relatives, now report a variety of possible causes of death of Tutankhamun and others, including his grandparents, father, and siblings.

The study, led by Zahi Hawass, PhD, head of Egypt's Supreme Council of Antiquities, includes these points:

• King Tut suffered from avascular bone necrosis, a condition in which poor blood supply to the bone leads to weakening or destruction of an area of bone. This may have been from a rare condition called Kohler's disease that affects the foot.
• He was also found to have a club foot.
• Along with three mummies identified as Tutankhamun's close relatives, Tutankhamun had suffered at some time from malaria, possibly before death, but also perhaps at the time of his demise.
• The researchers write that the bone condition alone would not cause death but in addition to a malaria infection would be a likely cause. "These results suggest avascular bone necrosis in conjunction with the malarial infection as the most likely cause of death of Tutankhamun."

The researchers write that the discovery of several canes and sticks in Tut's tomb, some appearing to have been worn down by use, supports the idea that he had walking problems.

Tutankhamun died in the ninth year of his reign, about 1324 BC, at the age of 19, the researchers say. His mummy was discovered in 1922, and artifacts in the tomb have provided many clues about his life and his family's.

DNA Analysis of Mummy Yields New Clues to Pharaoh's Death

Searching for the Cause of King Tut's Death

Hawass and colleagues studied 11 royal mummies to search for pathological features attributable to inherited disorders, infectious diseases, and blood relationships. They also looked for evidence about what caused King Tut's death. Their research appears in the Feb. 15 issue of The Journal of the American Medical Association.

Some researchers have speculated that he died from complications from an injury, blood poisoning, or an embolism caused by a leg fracture or blow to the head. Others have said the young king may have been murdered because previous research has suggested death from a blow to the back of the head or possibly a fall from a chariot.

Between September 2007 and October 2009, royal mummies underwent detailed genetic, radiological, and anthropological studies. DNA also was extracted from the mummies.

Goodbye false balance over vaccines and autism! May you stay gone!

Category: Alternative medicine • Antivaccination lunacy • Autism • Entertainment/culture • Medicine • Popular culture • Television
Posted on: February 17, 2010 12:00 AM, by Orac

I realize that Chris Mooney is a polarizing figure here on the ol' ScienceBlogs, but I have to give him props for doing a damned fine job handling questions about vaccines, autism, and Andrew Wakefield's utterly discredited 1998 Lancet study, which was retracted by the Lancet's editors last week:

Visit msnbc.com for breaking news, world news, and news about the economy

I wish I could say the same thing for Nancy Snyderman. Although she was mostly right, I cringed--big time--when she insisted that there are no studies that show a link between vaccines and autism. Wrong, wrong, wrong, wrong! What she should have said is that there exist studies that show a link between vaccines and autism, but that they are all crap and many of them are published in highly dubious journals. Heck, I've even blogged about such crappy studies myself on multiple occasions over the years. I suppose you could argue that it's all semantics and that, technically Snyderman is correct, but the way she says it makes it sound as though there are no studies out there on the other side, which is simply not true. The studies touted by the antivaccine propagandists as showing a link between vaccines and autism are all either preliminary studies refuted by later studies or bad science. Let's also not forget that none of Wakefield's followup studies to his 1998 Lancet article has been retracted. They're still out there in the medical literature, even though, as Stephen Bustin showed, they are in essence false positives because the lab that ran the PCR on Wakefield's samples was incompetently run. In any case, Snyderman's statement grated on me and is the sort of thing that plays right into anti-vaccinationists' hands.

It's also interesting to note that Joe Scarborough, who, as you may remember, appeared to buy into the whole refuted thimerosal-autism link back in 2005 when Robert F. Kennedy, Jr. was pushing the link far and wide thrugh the media, appears to have rejoined the reality-based world. He seems to have spit out the Kool Aid and no longer appears to buy into the pseudoscience that falsely links vaccines to autism. I wouldn't have thought it possible five years ago.

Finally, do you notice one more good thing about this video? That's right, there's no balance! There are no boosters of pseudoscience pushing the vaccine-autism link and pulling vaccine Gish gallop.

Even though Chris Mooney is right that the supporters of a vaccine-autism link won't give up (heck, I've already written about that a couple of times), I see reason for optimism. The lazy journalistic trope of false "balance" seems to be giving way to letting the science speak.

A guy can dream, can't he?

In any case, whatever you think of Chris Mooney, be aware that I'm giving him props here. He handled himself well in this case.

What ailed King Tut?

I admit that I am a bit of an Egyptophile (is this a word?). It was great fun to read “Ancestry and Pathology in King Tutankhamun’s Family”, in JAMA’s February 17 issue. King Tut, made famous by the Steve Martin song of the same name, was portrayed in tomb art (statues/reliefs/sculptures) as androgynous and having a “bizarre form of gynecomastia.”

The authors of the article examined several mummies thought to be related to Tutankhamun via radiological and genetic studies. They developed a family tree, and surprise, surprise, the Tutankhamun family intermarried. Turns out the boy king was the product of a brother sister relationship, and he in turn, likely married his sister. Tut’s apparent grandpappy, Amenhotep had a club foot,which he passed on to Tut. In addition, Tut’s father, the beleaguered Akhenaten, had a cleft palate, which Tut had too. Scoliosus ran rampant as well.

In addition, King Tut had evidence of Plasmodium falciparuminfection, as well as juvenile aseptic bone necrosis, and had may have had to use a cane for much of his life. Images of Tutankhamun frequently show him sitting during activities in which one would usually stand, like hunting. When Tut’s tomb was opened over 130 canes were found, showing signs of wear.

As for the bizarre body type seen it statuary and artistic renderings of the period? The authors found no evidence of inherited syndromes that would cause androgynous features and “bizarre” gynecomastia. The authors conclude that the artistic representations of Akenaten and Tutankhamun were likely stylized and idealized according to the wishes of the king.

The great thing is, the boy king is not likely to sue if the authors are wrong!

Photo

Tags: diseases, King Tut

Travellers Beware: UQ Research Shows Canecutter's Disease On The Rise

A team led by PhD researcher Dr Colleen Lau from the School of Population Health http://www.sph.uq.edu.au/, has discovered the disease, known medically as leptospirosis, was traditionally a concern for males working in the agricultural and livestock industries, as it is contracted from contact with the urine of host animals.

Ms Lau said recreational exposure and international travel have emerged as increasingly important sources of infection over the past decade.

"Many of the areas with a high incidence of leptospirosis are popular destinations for domestic and international travellers," Dr Lau said.

"With the increasing popularity of ecotourism and outdoor adventure activities, travellers are likely to become increasingly exposed through activities that involve contact with freshwater, soil and animals."

Leptospirosis causes influenza-like symptoms such as fever, chills, headache and jaundice but can lead to more serious illness including kidney failure, liver failure, lung haemorrhage, brain infections, and can occasionally be fatal.

Called canecutter's disease in Queensland due to the spread of the disease by canefield rats, the study, published in the journal Travel Medicine and Infectious Disease (click here for abstract), has opened up a new way of looking at the spread of the disease.

As an under-diagnosed cause of fever in adventure seekers and returned travellers, Dr Lau and her co-authors, Professor Phil Weinstein and Lee Smythe, urged clinicians to change their perceptions of the population at risk of contracting leptospirosis, even if they do not fit the mould of a male agricultural worker.

"Early recognition, diagnosis, and treatment will reduce the incidence of severe illness and deaths," she said.

Known high-risk areas for leptospirosis include tropical and subtropical regions such as Queensland, New Zealand, the Pacific Islands, parts of South East Asia and the Caribbean.

Dr Lau is working in one such island, American Samoa, to complete her PhD on an analysis of risk factors for contracting leptospirosis.

Source:
Jeann Wong
Research Australia

A common thread links multiple human cognitive disorders

February 14, 2010 by admin

Contact: Cathleen Genova
cgenova@cell.com
617-397-2802
Cell Press
A new study reveals that a common underlying mechanism is shared by a group of previously unrelated disorders which all cause complex defects in brain development and function. Rett syndrome (RTT), Cornelia de Lange syndrome (CdLS) and Alpha-Thalassemia mental Retardation, X-linked syndrome (ATR-X) have each been linked with distinct abnormalities in chromatin, the spools of proteins and DNA that make up chromosomes and control how genetic information is read in a cell. Now, research, published by Cell Press in the February 16th issue of the journal Developmental Cell, helps to explain why these different chromatin abnormalities all interfere with proper gene expression patterns necessary for normal development and mature brain function.

“Although clearly distinct from one another, human developmental disorders that are linked with chromatin dysfunction often share similar cognitive clinical features,” explains senior study author, Dr. Nathalie Brub from the University of Western Ontario. “Whether the overlapping cognitive symptoms are due to underlying interlinked molecular mechanisms is still poorly understood.” Her work now demonstrates that chromatin proteins defective in RTT, CdLS, and ATR-X syndromes are all associated with each other and are required for one another’s function at certain “imprinted genes” in the developing mouse brain. Imprinted genes are a relatively rare type of gene that carries different information depending on whether it is inherited from the mother or the father. The results support the conclusion that ATRX (the chromatin protein that is defective in ATR-X syndrome) and its binding partners regulate expression of imprinted genes, and likely other genes required for normal brain development, by controlling chromatin structure.

“Our findings provide the first glimpse of the cooperation between ATRX and multiple other disease proteins in the regulation of common gene targets, perhaps explaining similarities between the associated human syndromes,” says Dr. Brub. “The failure to properly suppress genes that are essential during embryonic development, but potentially detrimental in the mature brain, might contribute to cognitive deficiencies characteristic of RTT, CdLS and ATR-X syndromes. Further studies are needed to gain a better understanding of the specific role of these chromatin proteins and the molecular pathogenesis of the associated human disorders.”

###

The researchers include Kristin D. Kernohan, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; Yan Jiang, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; Deanna C. Tremblay, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; Anne C. Bonvissuto, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; James H. Eubanks, Toronto Western Research Institute, Toronto, Canada; Mellissa R.W. Mann, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada; and Nathalie G. Berube, University of Western Ontario, Victoria Research Laboratories, London, Ontario, Canada.

Causes of Liver Cirrhosis Mnemonic

Causes of Liver Cirrhosis Mnemonic

A - Alfa 1 antitrypsin deficiency
B - Budd Chiary Syndrome - Hepatitis B Virus - Biliary cirrhosis - Bilharzia
C - Hepatitis C Virus - Cystic fibrosis - copper overload
D - Drugs
E - Ethanol
F - Fe overload
G - Glycogen storage disease


and while we are at it, lets review the complications:

• Bruising and bleeding due to decreased production of coagulation factors.
• Jaundice due to decreased processing of bilirubin.
• Itching (pruritus) due to bile salts products deposited in the skin.
• Hepatic encephalopathy.
• Sensitivity to medication due to decreased metabolism of the active compounds.
• Hepatocellular carcinoma
• Portal hypertension
• Ascites
• Esophageal varices
• Immune system dysfunction, leading to infection.
• Hepatorenal syndrome - insufficient blood supply to the kidneys, causing acute renal failure.
• Hepatopulmonary syndrome, leading to cyanosis and dyspnea (shortness of breath), characteristically worse on sitting up.

Autism's earliest symptoms not evident in children under 6 months


Anonymous's picture

(SACRAMENTO, Calif.) -- A study of the development of autism in infants, comparing the behavior of the siblings of children diagnosed with autism to that of babies developing normally, has found that the nascent symptoms of the condition -- a lack of shared eye contact, smiling and communicative babbling -- are not present at 6 months, but emerge gradually and only become apparent during the latter part of the first year of life.

Researchers conducted the study over five years by painstakingly counting each instance of smiling, babbling and eye contact during examinations until the children were 3. They found that by 12 months the two groups' development had diverged significantly. Intentional social and communicative behavior among children developing normally increased while among infants later diagnosed with autism it decreased dramatically. The study is published online early and will appear in the March issue of the Journal of the American Academy of Child & Adolescent Psychiatry.

"This study provides an answer to when the first behavioral signs of autism become evident," said Sally Ozonoff, the study's lead author, a professor of psychiatry and behavioral sciences and a researcher with the UC Davis MIND Institute. "Contrary to what we used to think, the behavioral signs of autism appear later in the first year of life for most children with autism. Most babies are born looking relatively normal in terms of their social abilities but then, through a process of gradual decline in social responsiveness, the symptoms of autism begin to emerge between 6 and 12 months of age."

Autism is a pervasive developmental disorder of deficits in social skills and communication, as well as in repetitive and restricted behaviors, with onset occurring prior to age 3. Abnormal brain development, probably beginning prenatally, is known to be fundamental to the behaviors that characterize autism. Current estimates place the condition's incidence at between 1 in 100 and 1 in 110 children in the United States.

Children with a sibling already diagnosed with autism are known to be among those at greatest risk of developing the disorder. The current study included 25 high-risk children who met criteria for autism at 3 years of age, matched with 25 low risk peers who were developing normally. It was conducted at the MIND Institute and the University of California, Los Angeles. The sole inclusion criterion for the high-risk group was having a sibling with autism; low-risk participants had to have been born after 36 weeks gestation and have no autistic family members.

The children's development was evaluated at 6, 12, 18, 24 and 36 months of age using a series of widely implemented diagnostic tools, including the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview-Revised (ADI-R). Examiners were not told which babies were at high- or low-risk when evaluating the participants' development.

The researchers found that there were few discernable differences between the two groups at the outset but that after six months, 86 percent of the infants who developed autism showed declines in social communication that were outside the range for typical development. "After six months," the study found, "the autism spectrum disorder group showed a rapid decline in eye contact, social smiling, and examiner-rated social responsiveness." Group differences were significant by 12 months in eye contact and social smiling and all other measures by 18 months, the study found.

The study is notable because of the accuracy and precision of its prospective methodology, assiduously recording exact numbers of social and communicative behaviors during lab visits. Previously, researchers have constructed evidence of autism's earliest manifestations by interviewing parents about when they believed their children's symptoms first arose or by reviewing home movies for clues to when children begin exhibiting symptoms of autism.

"Until now, research has relied on asking parents when their child reached developmental milestones. But that can be really difficult to recall, and there is a phenomenon called the "telescoping effect" where people usually say that they remember something happening more recently than when it occurred," Ozonoff said. In addition parents frequently will turn off the video camera when their children are behaving poorly ? precisely when autistic symptoms may appear.

Ozonoff said that the study provides a deeper understanding for parents, caregivers and health-care providers and for future research of the developmental trajectory for very young children with autism.

"We need to be careful about how we screen, and we need to know what we're looking for," Ozonoff said. "This study tells us that screening for autism early in the first year of life probably is not going to be successful because there isn't going to be anything to notice. It also tells us that we should be focusing on social behaviors in our screening, since that is what declines early in life."

"This study also found that the loss of skills continues into the second and third year of life," she said. "So it may not be adequate, as the American Academy of Pediatrics currently suggests, that providers screen for autism twice before the end of the second year. Autism has a slow, gradual onset of symptoms, rather than a very abrupt loss of skills."

"Screening may need to continue into the third year of life, since symptom emergence takes place over a long time. If a child starts exhibiting a declining trajectory and a sustained reduction in social communication we want to refer them into therapy, especially if they are at risk," Ozonoff said, "even before we might be able to make a definitive diagnosis."

Ozonoff said that the study does not address the etiology of autism or causality. In this study, the infants who participated were at high risk due to having strong family histories of autism, suggesting that genetics play a major role in the later autism diagnoses, despite the fact that their symptoms were not apparent at birth.

Other study authors include Ana-Maria Iosif, Fam Baguio, Ian C. Cook, Monique Moore Hill, Mary Beth Steinfeld, Sally J. Rogers, Sarabjit Sangha and Gregory S. Young of UC Davis and Ted Hutman, Agata Rozga and Marian Sigman of the University of California, Los Angeles.

The study was funded by grants from the National Institute of Mental Health of the National Institutes of Health.

The UC Davis M.I.N.D. Institute, in Sacramento, Calif., was founded in 1998 as a unique interdisciplinary research center where parents, community leaders, researchers, clinicians and volunteers collaborate to study and treat autism and other neurodevelopmental disorders. More information about the institute is available on the Web at http://www.ucdmc.ucdavis.edu/mindinstitute/.

Link:

http://www.ucdmc.ucdavis.edu

Franchising autism "biomed" woo

Remember Mark and David Geier?

I wouldn't be surprised if regular readers may have forgotten about this father-son tag team of anti-vaccine lunacy and autism woo. After all, I haven't written about them since journalist Trine Tsouderos did her expose of their "Lupron protocol" for the Chicago Tribune nine months ago. Long time readers, however, will remember the Geiers. They were one of the very first autism-related topics I wrote about after joining ScienceBlogs four years ago, when I wrote about them in a little ditty I called Why not just castrate them? The reason that I gave my post the title I did was to express my shock at the Geiers' use of a powerful anti-sex hormone drug Lupron, which is most commonly used to reduce testosterone to castrate levels in men with prostate cancer or to shut down female sex hormones as a part of in vitro fertilization cycles so that the process is completely controlled by exogenously administered hormones, on autistic children. It is not called chemical castration for nothing. It's also used sometimes to treat precocious puberty, but that is a rare diagnosis in real pediatric endocrinologists' offices. Unfortunately, in the Geiers' office, it's a very common diagnosis, even in children who are clearly too old for the diagnosis.

Even more incredible is the rationale they use to justify their woo. Basically, they claim that testosterone forms "sheets" that bind to mercury (left in the brain by those evil vaccines, of course!) and that these "testosterone sheets" make mercury harder to chelate. By lowering testosterone levels, claim the Geiers in a feat of armchair science, they get rid of the testosterone sheets and make mercury easier to chelate. What they fail to mention is that the only time testosterone-mercury complexes have ever been observed experimentally involved dissolving equal parts of mercuric chloride and testosterone in benzene. Obviously, this is a condition never seen in living tissues, much less brains, although one wonders whether Mark and David Geiers' brains have been soaked in hot benzene.

Benzene or no benzene, there are apparently a lot of parents of autistic children out there who are either desperate enough or gullible enough or, more likely both, and the Geiers have no compunction whatsoever about taking advantage of that combination. In fact, I just learned that they are apparently advertising for their franchise. In an e-mail that's gone out to some "biomed" mailing lists (nicely forwarded to me by my spies), we find out that the Geiers are still at it:

For Immed. Release
February 15, 2010

PRESS RELEASE CONTACTS:
Mark R. Geier, MD, PhD, FACMG, FACE
Founder & Medical Director
Tel. : 301-989-0548
E-mail: mgeier@comcast.net

WASHINGTON, DC - ASD Centers LLC is proud to announce its NEW web site: http://www.AutismTreatmentClinics.com as well as the opening of new treatment clinics in both Florida and Kentucky.

ASD Centers, LLC is committed to providing each patient with an exceptional level of care and attention. At the ASD Centers, LLC we are proud to be physician owned and operated.

Our dedicated staff works together as a team to provide high-quality comprehensive care.

Our compassionate and understanding doctors take pride in paying close attention to each patient's needs. ASD Centers is committed to:

a. Listening to the concerns of the parents of those who are not competent and/or unable to speak for each person we treat as well those patients who are able speak for themselves,

b. Clinically assessing and then addressing each of our patient's clinically identified medical issues and

c. Helping those who have a diagnosis of an autism spectrum, or related disorders, to recover from the underlying medical issues that produce the clinical symptoms of the diagnosed medical conditions for which we have clinically sound therapies.

Testing/Treatment Areas:

** Genetic Markers (DNA Fragile X Syndrome, Blood Chromosome, Chromosome Microarrays, DNA Rett Syndrome, Angelman/Prader Willi Syndrome)

** Mitochondrial Dysfunction (Carnitine, Lactic Acid, Ammonia, Hand Muscle-strength Testing)

** Hormone Imbalances (Total Testosterone, Free Testosterone, DHEA, DHEA-S, Andros- tenedione, Dihydrotestosterone, Total Estrogens, Estrone, Estradiol, ACTH, Aldosterone, Prolactin, FSH, LH)

** Oxidative Stress/Inflammation (Neopterin, Lipid Peroxides)

** Detoxification Pathways (Glutathione, Cystathionine, Homocysteine, Methionine)

** Immune System Function (Immune Deficiency Profile, HLA-Testing, Immune Complexes, Food Allergies, Celiac's Disease)

** Heavy Metals (Porphyrins, Blood Metals, Urinary Metals)

** Neurological Dysfunction (Brain MRI scans, Brain SPECT scans)

** General Health Status (Comphrensive Metabolic Panel)

## A significant portion of all the net revenues that are generated by the ASD Centers are donated to the non-profit 501(c)(3) Institute of Chronic Illnesses, Inc. and to the non-profit 501(c)(3) CoMeD, Inc., which are corporations dedicated to autism research and advocacy efforts.

That's nice. The Institute of Chronic Illnesses, as longtime readers may recall, is the Geiers' elusive institute, the institute through which the Geiers, using an institutional review board (IRB) packed with Geier cronies and headed by Mark Geier himself, "reviewed" the Geiers' Lupron "studies" and--surprise! surprise!--approved them as being ethical when clearly they were not. The conflict of interest was astounding, given that Mark Geier chaired the committee that was evaluating his own study. Even if the proposed study had a sound basis in science (which it did not), such an arrangement contravenes federal regulations and represents a conflict of interest that would make a big pharma executive blush. All the attention over the last couple of weeks has been on Andrew Wakefield, whose 1998 Lancet study was bankrolled by trial lawyers, who flouted research ethics by performing medically unnecessary invasive procedures on autistic children in the name of bogus "research," and who paid children £5 at a birthday party to let him draw their blood. However, compared to the Geiers, Andrew Wakefield seems almost ethical and reasonable. Almost.

The Geiers are also apparently a lot more entrepreneurial. Whereas Andrew Wakefield only has Thoughtful House, as this page on their website shows, in addition to their newest locations in Florida and Kentucky the Geiers have metastasized to many states, including Maryland, Illinois, New Jersey, Texas, Missouri, and Indiana. They're franchising like McDonald's. I looked at the staff who are heading up the Geier franchises and wonder ow they get away with it. Of all of them, only one (Dr. Georgia Davis, who really should know better but apparently doesn't) is a pediatrician. Otherwise we have a neuroradiologist (Dr. David A. Clayman), a "genetic counselor" (Dr. Mark Geier), and an OB/GYN (Dr. John L. Young). None of the rest are physicians, although one is a Ph.D. analytical chemist, who also really should know better, at least about the Geiers' claims about testosterone and mercury.

Of course, being a chemist, he may have no clue about the rest of the motherlode of autism woo on the Geiers' website. It's all there: "hormone imbalances" (i.e., allegedly precocious puberty and elevated testosterone levels), "detoxification" pathways, immune system "dysfunction," and, of course, "heavy metal toxicity." It's a veritable cornucopia of autism "biomed" woo. In any case, given the lack of expertise in endocrinology, I find it astounding that the Geiers can make the claim that they offer "assistance for patients diagnosed on the autism spectrum in the areas of genetics, endocrinology, neurology, psychiatry, internal medicine, nuclear medicine, radiology, and reproductive medicine."

So what we have here is, as Mike Stanton points out, a nasty little franchise, and that franchise is metastasizing. Even more dubious, as mentioned in the press release above, a "significant portion of all the net revenues" generated from the ASD Centers will be funneled into Institute of Chronic Illnesses, Inc. and CoMeD, Inc., the former of which lists Mark Geier as its President and David Geier as its Vice-President and the latter of which lists Geiers crony Lisa Sykes as its President and lists as its address 14 Redgate Court, Silver Spring, Maryland 20905, which happens to be Mark Geiers home. Ironically enough, this is the same address listed as the ICI's address too. Nice arrangement, eh? The money from ASD Centers is "donated" to the ICI and CoMeD, both of which are controlled by either the Geiers or their cronies. This money then goes into more dubious "research."

After reading this press release, I've concluded that there's one thing I fear, and that is that Andrew Wakefield will see what the Geiers have done and get the idea to franchise his Thoughtful House woo throughout the country. Before long we could have two major franchises pushing autism "biomed" throughout the country.

I think I just scared myself. Certainly parents of autistic children should be scared. Heck, all parents should be scared, because the promotion of anti-vaccine views through such franchises could result in lower vaccination rates for all and the return of vaccine-preventable diseases.

Autism and snake oil

For me, one of the most interesting things about the retraction last week by the Lancet of its discredited 1998 study linking vaccines and autism was the consensus that those who have believed the study will continue to have faith in it, despite the retraction.

That's why, with the help of Star health reporter Megan Ogilvie, who wrote the paper's original story on the retraction, I began asking around why people clung to scientific studies long after they have been discredited. The result was a story in Tuesday's paper.

I spoke with Jeanette Holden, a geneticist at Queen's University specializing in autism and whose brother is autistic.

As a scientist, Holden knows every rational reason why a discredited 1998 study, by Andrew Wakefield of London's Royal Free Hospital, linking autism to vaccines is poor science – vaccines have no connection to autism, she says – but can find little fault in the families of autistic children who remain loyal to it.

"This does provide some sort of an answer," she says.

I also spoke with Paul Offit, a Philadelphia pediatrician whose book Autism's False Prophets takes aim at the anti- vaccination movement, who said that people such as Wakefield offers patients and their families the glimmer of something he and other scientists so far cannot: hope.

And hope can be a powerful thing. "They love him because he offers them something," Offit says.

The story has generated some e-mails to Ogilvie and I, with one reader from the United States this morning passionately defending Wakefield and assailing his critics.

Offit, he says, has a conflict of interest because he created a vaccine and stands to lose financially if vaccines are shown to cause autism. However, Wakefield had his own conflicts of interest, having been paid by a law firm suing vaccine makers to conduct the study. The firm also provided some of the research subjects.

Wakefield was the lead author of the report. He wrote that the parents of eight of the 12 children blamed MMR: they said symptoms of autism had set in within days of vaccination. The Sunday Times has now established that four, probably five, of these children were covered by the legal aid study. And Wakefield himself had been awarded up to £55,000 to assist their case by finding scientific evidence of the link.

Wakefield did not tell his colleagues or medical authorities of this conflict of interest either during or after the research.The children were subjected to a battery of invasive procedures, including colonoscopies and lumbar punctures.

In the months that followed the examination of the first children, many more were channelled through the hospital. The parents of many were clients of one solicitor, Richard Barr, of King's Lynn, Norfolk, who was leading the legal attack and had organised Wakefield's funding from the Legal Aid Board (now the Legal Services Commission).

The writer also disputes the description in the story that autism as "relatively rare," pointing out that diagnoses of the condition have been increasing rapidly. I have no way of knowing, however, if that's due to more cases, or better diagnostics. The write ends the e-mail by saying that parents love Wakefiled because he listens to them, which is essentially what Holden and Offit said.

Holden said the only way such family members might finally break with the vaccine study is if Wakefield himself disavows it. She doesn't, however, expect that to happen.