MMR Doctor denies submitting kids to painful tests just to prove his Theories

Dr. Andrew Wakefield told a General Medical Council (GMC) disciplinary panel he did not submit young children to painful tests just to further his theories linking vaccinations to autism. He stressed that the tests were clinically necessary to diagnose and treat the young children - he said the children had autistic-like symptoms as well as debilitating bowel diseases.

A decade ago Dr. Wakefield said the MMR vaccine may cause autism.

Professor John Walker-Smith, the doctor of the young children, had ordered all the tests, according to Wakefield. The investigations - including painful colonoscopies, lumbar punctures (taking spinal fluid), brain scans, blood tests, and urine tests - were stopped when they could not reveal a link to the children's problems. He insisted that the well-being of the children was "our foremost consideration".

Dr. Wakefield is not a practicing clinician, he is an academic. He is accused of ordering tests against the children's best interests in order to further his own research - and by doing so breaking rules. However, he says he played no role whatsoever in deciding whether the tests should or should not take place. According to Wakefield, all the parents were very keen for their children to be included in the tests, and knew about the research program.

He said parents had told him about their 'normal' children who developed autism after receiving the MMR vaccine and started investigating a potential link in 1995. He had previously investigated a possible link between the MMR vaccine and Crohn's disease. "They were telling what turned out to be a remarkably consistent story of a normal child who they had lost, who had lost speech, communication, play, interaction with siblings, had sometimes become incontinent … was bloated, off their food, was losing weight, was failing to thrive."

While answering the Panel's questions (during the hearing) several supporters were gathered outside with banners indicating support for Wakefield. Professor Walker-Smith, Professor Simon Murch and Dr. Wakefield all deny serious professional conduct.

According to the Daily Mail, Dr. Wakefield charged over £150 ($300) per hour to a law firm that had planned to sue the vaccine's manufacturer. He invoiced Richard Barr, a lawyer, the hourly rate for investigating alleged dangerous side-effects of the MMR vaccine. Two years later Wakefield published his research paper, alleging a causal link between MMR and autism in young children. However, he did not disclose that he was being paid as an expert adviser for Mr. Barr, who was in legal proceedings against the manufacturers of the MMR vaccine - a clear conflict of interest.

Most of the children who were examined were represented by Mr. Barr. When Dr. Wakefield's report came out, it led to a dramatic drop in the number of children receiving the MMR jab, and a subsequent rise in children developing measles.

According to the Daily Mail, Dr. Wakefield "was also accused of dishonesty in applying for £55,000 of legal-aid money for his research, even though these costs had already been met by the NHS." According to Wakefield, he needed two funding sources for two separate investigations.

Wakefield told the Panel that the Royal Free Hospital's (London) ethics committee had fully approved the invasive tests on the children. Dr. Michael Pegg, who was the Committee's chairman said this was not true - Wakefield suggested that Dr. Pegg's memory is at fault.

The hearing continues.

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Contact Patterns and the Flow of Infectious Diseases

Researchers in Europe have analyzed and modeled social contact patterns in order to better understand the spread of respiratory infections. The study is published in the open-access journal PLoS Medicine.

It is common to use mathematical modeling techniques to understand and predict the impact of infectious diseases. The models help policy officials and researchers make recommendations regarding intervention, treatment, and prevention of infectious and contagious diseases. In assessing the likelihood that a disease will spread among a population, researchers use contact rates - how many people that a person contacts in a day - as a key predictor. Contact rates are usually assumed to follow a certain pattern, but researchers have not yet directly observed these patterns. To improve our understanding of contact rates and to analyze patterns among age groups and social settings, researchers have decided to directly ask people how many contacts they have in a day and then generated models based on these data.

Joël Mossong (Microbiology Unit, Laboratoire National de Santé, Luxembourg and Centre de Recherche Public Santé, Luxembourg) and colleagues from several European nations recruited 7,290 people from Belgium, Germany, Finland, Great Britain, Italy, Luxembourg, The Netherlands, and Poland. The participants recorded basic demographic information and noted physical (kiss, handshake, e.g.) and nonphysical (two-way conversation without skin-to-skin contact) contacts for one day.

The researchers found that the participants averaged 13.4 contacts per day (97,904 contacts in total). The diversity of contact information is summarized below:

* Children had more contacts than adults
* People who live in large households had more contacts
* People had more contacts on weekdays than on Sundays
* Longer duration and higher frequency contact tended to be physical
* People of the same age tended to mix more frequently than people of different ages
* About 70% of daily contacts lasted less longer an hour
* About 75% of contacts with strangers lasted less than 15 minutes

"One of the most important findings of our study is that the age and intensity patterns of contact are remarkably similar across different European countries even though the average number of contacts recorded differed. This similarity implies that the results may well be applicable to other European countries, and that the initial phase of spread of newly emerging infections in susceptible populations, such as SARS was in 2003, is likely to be very similar across Europe and in countries with similar social structures," write the authors.

Mossong and colleagues then modeled the contact patterns using mathematical and statistical techniques. They were also able to create a model of how a respiratory infection epidemic may spread throughout a population. Results predicted that during the initial spread of a respiratory infection, 5- to 19-year olds would suffer the greatest burden. These younger people have many more contacts per day and more contacts within their own age group.

The authors conclude: "Our survey is, to our knowledge, the first population-based prospective survey of mixing patterns pertinent to the spread of airborne and close-contact infectious diseases performed in several European countries using a similar diary methodology. The quantification of these mixing patterns shows a remarkable similarity in degree of assortativeness, which likely results in similar patterns of spread in different populations. This finding represents a significant advance in our understanding of the spread of these infectious diseases and should help to improve the parameterization of mathematical models used to design control strategies."

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Dementia Risk in Old Age linked to Belly Size in Midlife

A new study by researchers from the US and Sweden showed that having a large belly in midlife increased the risk of having dementia in old age, with overweight and obese people with large bellies having double or triple the risk. In other words, while being overweight and obese was a risk factor, the study showed this was significantly affected by where the weight was carried in midlife.

The study is published in the online issue of the journal Neurology, and was conducted by Dr. Rachel Whitmer, who is a research scientist at the Kaiser Permanente Division of Research in Oakland, California, and colleagues.

Previous research has linked waist circumference or central obesity and body mass index (BMI) in elderly people to the risk of developing dementia, and it has also shown that having a large abdomen in midlife is linked to higher risk of heart disease, stroke and diabetes.

But this is the first study to show a link between belly fat in midlife and the risk of developing dementia decades later.

Whitmer and colleagues studied 6,583 health plan members of Kaiser Permanente living in Northern California who had had their sagittal abdominal diameter (SAD) measured between 1964 and 1973 when they were aged between 40 and 45.

SAD, which is a measure of belly density, is taken using a caliper that measures the distance from the back to the upper abdomen, when positioned midway between the top of the pelvis and the bottom of the ribcage.

The researchers explained that the size of the belly at this point is an indicator of the amount of fat tissue that is wrapped around the organs in the abdomen.

By examining medical records between 1994 and 2006, the researchers established that 16 per cent (1,049) of the participants had dementia an average of 36 years later.

Using statistical techniques and adjusting for age, sex, race, education, blood pressure, stroke, and other medical and demographic variables, they examined the links between midlife SAD and dementia incidence.

The results showed that:

* Participants who were overweight and had a large belly in midlife were 2.3 times more likely to develop dementia some 30 years later than those who were of normal weight and belly size.

* Participants who were obese and also had a large belly in midlife were 3.6 times more likely to develop dementia later in life compared with those of normal weight and belly size.

* Participants who were overweight or obese but did not have a large belly in midlife, had an 80 per cent increased risk of dementia.

* Having a high SAD measure, ie larger than normal abdomen, in midlife appeared to increase the risk of dementia regardless of whether the person had normal overall weight, was overweight or obese, and regardless of existing health conditions, including diabetes, stroke and cardiovascular disease.

* Being non-white, having high blood pressure, high cholesterol or diabetes, and less than a high school level of education was closely linked to higher abdominal obesity.

The study concluded that:

"Central obesity in midlife increases risk of dementia independent of diabetes and cardiovascular comorbidities. Fifty percent of adults have central obesity; therefore, mechanisms linking central obesity to dementia need to be unveiled."

Whitmer suggested that measuring midlife belly size may be a better indicator of long term disruption of metabolism that leads to dementia than using abdominal size in older people because as people age they lose muscle and bone mass and their belly becomes proportionally larger.

She said this was a disturbing finding, considering that 50 per cent of adult Americans have abdominal obesity.

"It is well known that being overweight in midlife and beyond increases risk factors for disease," said Whitmer.

"However, where one carries the weight, especially in midlife, appears to be an important predictor for dementia risk," she added.

Changes in the brain that lead to Alzheimer's can start in young to middle adulthood, as autopsies have revealed, explained Whitmer. Research has also shown that high abdominal fat in older people is linked to higher rate of brain atrophy. However, Whitmer said that:

"These findings imply that the dangerous effects of abdominal obesity on the brain may start long before the signs of dementia appear."

However, the researchers also cautioned that, as with all observational studies, you cannot say these results show that belly size drives dementia risk, the more likely explanation is that it is one of a complex set of inter-related health factors and behaviors.

The researchers called for further studies to investigate the underlying mechanisms that link belly size in midlife to risk of developing dementia later.

Dementia is not a specific disease, it is an umbrella term for a group of symptoms caused by a range of brain disorders that prevents people getting on with everyday life such as eating and getting dressed or going shopping. It impairs memory, language, ability to solve problems, and control emotions, and can change a person's personality or make them anxious or see things that aren't there.

Alzheimer's disease and stroke are two examples of diseases that can cause dementia. Drugs can slow or improve some of the symptoms but there is no cure.

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The Far-Reaching Role of Nanominerals: From Ocean to Atmosphere to Biosphere

The ubiquity of tiny particles of minerals--mineral nanoparticles--in oceans and rivers, atmosphere and soils, and in living cells are providing scientists with new ways of understanding Earth's workings. Our planet's physical, chemical, and biological processes are influenced or driven by the properties of these minerals.

So states a team of researchers from seven universities in a paper published in this week's issue of the journal Science: "Nanominerals, Mineral Nanoparticles, and Earth Systems."

The way in which these infinitesimally small minerals influence Earth's systems is more complex than previously thought, the scientists say. Their work is funded by the National Science Foundation (NSF).

"This is an excellent summary of the relevance of natural nanoparticles in the Earth system," said Enriqueta Barrera, program director in NSF's Division of Earth Sciences. "It shows that there is much to be learned about the role of nanominerals, and points to the need for future research."

Minerals have an enormous range of physical and chemical properties due to a wide range of composition and structure, including particle size. Each mineral has a set of specific physical and chemical properties. Nanominerals, however, have one critical difference: a range of physical and chemical properties, depending on their size and shape.

"This difference changes our view of the diversity and complexity of minerals, and how they influence Earth systems," said Michael Hochella of the Virginia Polytechnic Institute and State University in Blacksburg, Va.

The role of nanominerals is far-reaching, said Hochella. Nanominerals are widely distributed throughout the atmosphere, oceans, surface and underground waters, and soils, and in most living organisms, even within proteins.

Nanoparticles play an important role in the lives of ocean-dwelling phytoplankton, for example, which remove carbon dioxide from the atmosphere. Phytoplankton growth is limited by iron availability. Iron in the ocean is composed of nanocolloids, nanominerals, and mineral nanoparticles, supplied by rivers, glaciers and deposition from the atmosphere. Nanoscale reactions resulting in the formation of phytoplankton biominerals, such as calcium carbonate, are important influences on oceanic and global carbon cycling.

On land, nanometer-scale hematite catalyzes the oxidation of manganese, resulting in the rapid formation of minerals that absorb heavy metals in water and soils. The rate of oxidation is increased when nanoparticles are present.

Conversely, harmful heavy metals may disperse widely, courtesy of nanominerals. In research at the Clark Fork River Superfund Complex in Montana, Hochella discovered a nanomineral involved in the movement of lead, arsenic, copper, and zinc through hundred of miles of Clark River drainage basin.

Nanominerals can also move radioactive substances. Research at one of the most contaminated nuclear sites in the world, a nuclear waste reprocessing plant in Mayak, Russian, has shown that plutonium travels in local groundwater, carried by mineral nanoparticles.

In the atmosphere, mineral nanoparticles impact heating and cooling. Such particles act as water droplet growth centers, which lead to cloud formation. The size and density of droplets influences solar radiation and cloud longevity, which in turn influence average global temperatures.

"The biogeochemical and ecological impact of natural and synthetic nanomaterials is one of the fastest growing areas of research, with not only vital scientific, but also large environmental, economic, and political consequences," the authors conclude.

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Genetics Research in Zebrafish has Potential to Reduce Birth Defects in Humans

By injecting a customized "genetic patch" into early stage fish embryos, researchers at Washington University School of Medicine in St. Louis were able to correct a genetic mutation so the embryos developed normally.

The research could lead to the prevention of up to one-fifth of birth defects in humans caused by genetic mutations, according to the authors.

Erik C. Madsen, first author and an M.D./Ph.D. student in the Medical Scientist Training Program at Washington University School of Medicine, made the groundbreaking discovery using a zebrafish model of Menkes disease, a rare, inherited disorder of copper metabolism caused by a mutation in the human version of the ATP7A gene. Zebrafish are vertebrates that develop similarly to humans, and their transparency allows researchers to observe embryonic development.

Children who have Menkes disease have seizures, extensive neurodegeneration in the gray matter of the brain, abnormal bone development and kinky, colorless hair. Most children with Menkes die before age 10, and treatment with copper is largely ineffective.

The research is published this month in the Proceedings of the National Academy of Sciences' advance online edition.

The development of organs in the fetus is nearly complete at a very early stage. By that time, the mutation causing Menkes disease has already affected brain and nerve development.

Madsen and Bryce Mendelsohn, also an M.D./Ph.D. student at the School of Medicine, wondered if they could prevent the Menkes-like disease in zebrafish by correcting genetic mutations that impair copper metabolism during the brief period in which organs develop. Both students work in the lab of Jonathan D. Gitlin, M.D., the Helene B. Roberson Professor of Pediatrics at the School of Medicine and director of Genetics and Genomic Medicine at St. Louis Children's Hospital.

The researchers used zebrafish with two different mutations in the ATP7A gene, resulting in a disease in the fish that has many of the same characteristics of the human Menkes disease. Madsen designed a specific therapy to correct each mutation with morpholinos, synthetic molecules that modify gene expression. The zebrafish embryos were injected with the customized therapy during the critical window of development, and the researchers found that the zebrafish hatched and grew without any discernible defects.

"This method of copper delivery suggests that the prevention of the neurodegenerative features in Menkes disease in children may be possible with therapeutic interventions that correct the genetic defect within a specific developmental window," Madsen said.

The genetic mutations Madsen and the researchers worked with are caused by splicing defects, or an interruption in genetic code. The morpholinos prevent that interruption by patching over the defect so the gene can generate its normal product.

"Consider the genetic code as a book, and someone has put in random letters or gibberish in the middle of the book," Madsen said. "To be able to read the book, you have to ignore the gibberish. If we can make cells ignore the gibberish, or the splicing defect, the fetus can develop normally."

Up to 20 percent of genetic diseases are caused by splicing defects, Madsen said, so this treatment method could potentially be used for many other genetic diseases.

"The idea is that we can modify the treatment to target a specific mutation and design molecules to alter gene function in the same way the morpholino oligonucleotides can," Gitlin said.

The work is an important step toward personalized medicine, which can tailor treatment to an individual's genetic makeup.

"Eventually we would like to know each person's genome sequence so we know what mutations each person has that may lead to disease," Gitlin said. "That way, you don't get a drug for cancer that works against any kind of cancer, you get a drug for the specific mutation that causes your cancer. That's what personalized medicine is all about."

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