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Sunday, 26 September 2010

Training Humans And Dogs

Another long post, this one on the subject of behaviour problems in the young and the potential causes. It is from the Dr. Mercola web site of the USA. This one has its little ways and there are sales and products related, but often there are items of real substance relating to chemical and other issues..


Attention Deficit Disorder (ADD) and Attention-Deficit/Hyperactivity Disorder (ADHD) seem to have become more or less the catch-all designations for children who do not “behave well,” and as this study shows, this personal observation may have some merit.

As of 2006, at least 4.5 million American children under the age of 18 were diagnosed with ADHD, according to CDC statistics.

The study above, published in the Journal of Health Economics in June, determined that about 20 percent of these children have likely been misdiagnosed. That’s nearly one million children in the US alone.

The study found that many of the youngest children in any given grade level are perceived as exhibiting “symptoms” of ADHD, such as fidgeting and inability to concentrate, simply because they’re compared to more mature classmates.

How Do You Diagnose ADHD?

ADHD involves a cluster of symptoms that include inattention, hyperactivity, and impulsive behaviors. There is no definitive diagnostic tool, such as a brain scan, to determine if you have ADHD. There’s only subjective evaluation, and, for better or worse, teachers can play a significant role in this evaluation.

The term ADD has largely been replaced with ADHD, as it describes two of the most common symptoms of the condition, inattention and hyperactive-impulsive behavior.
Most children display a combination of these two traits, and may also show the following symptoms:

Frequent fidgeting or squirming
Feels restless or often runs and climbs excessively, or leaves his or her seat in the classroom when not appropriate
Has difficulty playing quietly
Talks excessively, interrupts often, and may blurt out answers to questions at inappropriate times
Always seems on the go
Has difficulty waiting his or her turn

As you can see, many of these “symptoms” could describe most children at one time or another! Therefore, only those who struggle with inattention and hyperactive or impulsive behaviors around the clock are candidates for the ADHD label.

Children who display these symptoms at school but not at home or with friends are not considered to have ADHD. Likewise, with children who display symptoms at home but not at school.

Is it ADHD, or Just Immaturity?

Since this behavioral disorder is so easily misdiagnosed, and the ramifications of a diagnosis so severe, it’s essential that you become actively involved and pay close attention to your child’s developmental progress.

The drugs prescribed for this condition are quite dangerous, and can lead to addiction and long-term health complications, including death. Drugs really should be a last resort, and not a knee-jerk consequence of immature or “poor” behavior.

The study found that the youngest students were 60 percent more likely to be diagnosed with ADHD than the oldest in the same grade. And when you take into account the maturity level, and in large part normal behavior of a 6 versus a 7-year old, you can easily see why.

Science Daily writes:

“… the "smoking gun" of the study is that ADHD diagnoses depend on a child's age relative to classmates and the teacher's perceptions of whether the child has symptoms.
"If a child is behaving poorly, if he's inattentive, if he can't sit still, it may simply be because he's 5 and the other kids are 6," said Elder, assistant professor of economics. "There's a big difference between a 5-year-old and a 6-year-old, and teachers and medical practitioners need to take that into account when evaluating whether children have ADHD."

In addition, it’s important for parents to remain in charge and make their own assessments known, as the study also concluded that,

“ A child’s birth date relative to the eligibility cutoff also strongly influences teachers’ assessments of whether the child exhibits ADHD symptoms but is only weakly associated with similarly measured parental assessments, suggesting that many diagnoses may be driven by teachers’ perceptions of poor behavior among the youngest children in a classroom.

These perceptions have long-lasting consequences: the youngest children in fifth and eighth grades are nearly twice as likely as their older classmates to regularly use stimulants prescribed to treat ADHD.”

What Causes ADHD?

There are a number of theories to explain the rise in ADHD diagnoses, including:

Sugars and Grains. Children who consume highly processed foods loaded with high fructose corn syrup and fruit juices tend to have a higher rate and severity of these symptoms. While organic whole grains are superior to processed ones, many children with ADHD do not respond well to most grains, especially wheat.

Genetic factors -- Some scientists are now aiming their research at finding genes that may make a person more susceptible to this disorder

Environmental toxins -- A 2006 study found that a mother's use of cigarettes, alcohol, or other drugs during pregnancy could increase the risk for ADHD. Exposure to lead and mercury may also cause ADHD symptoms, and pesticides and the industrial chemicals polychlorinated biphenyls (PCBs) have also been named as potential culprits.

Allergic reactions -- Chemically-sensitive people may exhibit ADHD symptoms when exposed to something as simple as clothing washed with perfumed and chemical-laden soap. Permanent press or stain-resistant products also contain chemicals that can initiate ADHD-like reactions in sensitive individuals.

Processed food additives – Certain food dyes and other additives may cause ADHD-like symptoms. These chemicals have a particularly pernicious synergy if they are combined with sugars such as fructose.

Increased number of childhood vaccinations – One 2007 survey found a strong correlation between rates of neurological disorders, such as ADHD, and childhood vaccinations. Vaccine adjuvants have also been associated with ADHD-type neurological problems.

Fluoridated water

Emotionally unstable home environments Stress is the frequently unappreciated and overlooked variable that can easily worsen ADHD. If the parents are having trouble in their relationship this can easily influence the child’s behavior.

Increased rates of birth interventions. This can result in birth trauma and lack of oxygen in the newborn, which significantly increases the risk of developmental delay.
But the key factor, I believe, is nutrition, or rather lack thereof.

We know the food choices of most children -- and adults -- today are incredibly poor. How can you possibly expect a child to have normal behavior if he is fed refined grains, sugars, processed foods loaded with chemicals and genetically engineered ingredients, and juices and sodas instead of pure water?

Add to that the substandard amount of vegetables in most people’s diets -- up to 90 percent fewer than what is required for health -- an overabundance of highly processed, damaged omega-6 fats and a deficiency of omega-3 fats, and behavioral issues are not far behind.

You simply cannot have a healthy functioning brain when the proper ingredients to develop or maintain a healthy brain are not being given!

The ADHD “Epidemic” is Creating a Generation of Drug Addicts

Once a diagnosis has been made, the conventional approach typically involves drug therapy. Commonly prescribed drugs include:


Ritalin and Concerta contain different formulations of methylphenidate, a powerful psychostimulant drug that is in the same class as cocaine.

Adderall contains amphetamine (aka "speed") and dextroamphetamine.

Please understand that just because these drugs are by prescription does NOT make them safer than their illegal “street drug” counterparts.
Methylphenidate behaves similarly to highly addictive drugs. Ritalin, for example, has the same pharmacological profile as cocaine, yet its effects are even more potent. Using brain imaging, scientists have found that, in pill form, Ritalin occupies more of the neural transporters responsible for the “high” experienced by addicts than smoked or injected cocaine.
In essence, we have created a large body of new drug addicts, priming them for addiction from an extremely young age.
This is a particularly painful thought when you consider that, in all likelihood, nearly one million children are being drugged simply because they act their age! And even more children are likely receiving addictive drugs when what they really need is proper nutrition.
It’s also worth mentioning that, like antidepressants, some ADHD drugs have been linked to an increased probability of suicidal thoughts and behavior.
Strattera®, which contains atomoxetine hydrochloride, carries this warning. Hallucinations, increased aggressive behavior, heart attack and stroke are also possible side effects of ADHD drugs.
Ritalin Use in America is Out of Control
U.S. pharmacists distribute five times more Ritalin than the rest of the world combined, according to Dr. Samuel Epstein’s Cancer Prevention Coalition (CPC). In all, 60 percent to 90 percent of U.S. kids with attention deficit disorders are prescribed this powerful drug, which amounts to 3 percent to 5 percent of U.S. children and teens on Ritalin.
By definition, Ritalin stimulates your central nervous system, leading to side effects such as:
Increased blood pressure
Increased heart rate
Increased body temperature
Increased alertness
Suppressed appetite
Research has also linked Ritalin with more severe health problems such as cancer.
Natural Ways to Relieve ADHD Symptoms
It is my sincere hope that people will begin to realize that drug therapy, if at all necessary, should be a very last resort, after all other options have been exhausted – especially when it comes to behavioral problems such as ADHD.
Before you consider drugs, please consider implementing the following strategies first, in addition to making sure that your child is assessed in an age-appropriate manner:
Eliminate most grains and sugars from your child’s diet. Grains and sugars both tend to cause allergies in sensitive individuals. Even organic, whole grain can cause problems in many children so it would be wise to give them a grain holiday and see if their behavior improves.
Replace soft drinks (whether diet and regular), fruit juices, and pasteurized milk with pure, clean non-fluoridated water.
Increase omega-3 fats by taking a high quality animal-based omega-3 oil. Research has confirmed that something as simple as animal-based omega-3 fat can improve the symptoms of ADHD more effectively than drugs like Ritalin® and Concerta®. In my view, krill oil is the best option for this. It contains essential EPA and DHA in a double chain phospholipid structure that makes it far more absorbable than the omega-3s in fish oil.
Minimize your use of nearly all processed fats, especially trans fats as they disrupt nerve cell intercommunication.
Avoid all processed foods, especially those containing artificial colors, flavors and preservatives, which may trigger or worsen symptoms.
Clear your house of dangerous pesticides and other commercial chemicals. Pesticide exposure has been linked with ADHD.
Avoid commercial washing detergents and cleaning products used on clothes, and replace them with naturally derived cleaning products with no added perfumes, softeners, etc.
Spend more time in nature. Researchers have found that exposing ADHD children to nature is an affordable, healthy way of controlling symptoms.
Investigate sensory therapy and emotional wellness tools. Instead of looking for a quick fix, encourage ADHD sufferers to talk, and find out what emotions are causing issues. You may want to consider the energy tapping techniques to improve emotional coping and healing.


It is not just humans that are affected. According to press reports, including one in the Sunday Mail of 26 September, there is a plague of ill health amongst dogs, man’s best friend, who are now being fed largely on processed grain based foods.

Thursday, 23 September 2010

Genes And Asthma

This longish 1177 word item from escience dot com is about a possible genetic element in asthma in that some may be more vulnerable than others. If this is the case then it is likely that the more pollutants and the stronger in the air then the more the asthma. The study does not indicate whether amongst the remaining population there may be more people at the margins, but that is possible.


Largest genetic study of asthma points towards better treatments

Published: Wednesday, September 22, 2010 - 16:32 in Health & Medicine

An international study looking at DNA from over 26,000 people has identified several genetic variants that substantially increase susceptibility to asthma in the population. The findings, published in the New England Journal of Medicine, will help scientists to focus their efforts to develop better therapies for the illness.

The study, which was co-ordinated by researchers from Imperial College London, was performed by the GABRIEL consortium, a collaboration of 164 scientists from 19 countries in Europe, along with other groups in the UK, Canada and Australia. It analysed DNA samples from 10,000 children and adults with asthma and 16,000 non-asthmatics.

The researchers performed more than half a million genetic tests on each subject, covering all the genes in the human genome. The study pinpointed seven locations on the genome where differences in the genetic code were associated with asthma.

One in seven children in the UK suffers from asthma. When the airway is irritated in a person with asthma, the airway narrows and the lining becomes inflamed, causing difficulty breathing. The causes of the disease are poorly understood, but genetic and environmental factors are thought to play roughly equal roles.

Today's research has a number of potential implications, according to the study team. It suggests that allergies are probably a consequence of asthma, rather than a cause of the disease. It also suggests that genetic testing would not help predict who is likely to develop the disease.

The new variants linked to asthma were found in more than a third of children with asthma in the study. The gene with the strongest effect on children did not affect adults, and adult-onset asthma was more weakly linked to other genetic differences, suggesting that it may differ biologically from childhood-onset asthma.

Childhood asthma, which affects boys more than girls and can persist throughout life, is often linked to allergies, and it has been assumed that these can trigger the condition.

However, the study found that genes controlling the levels of antibodies that cause allergies had little effect on the presence of asthma, suggesting that allergies are more likely to be a consequence of asthma than a cause.

Professor Miriam Moffatt, Professor of Human Genetics at Imperial College London and one of the study's leaders, said: "As a result of genetic studies we now know that allergies may develop as a result of defects of the lining of the airways in asthma. This does not mean that allergies are not important, but it does mean that concentrating therapies only on allergy will not effectively treat the whole disease."

Some of the genes identified are involved in signalling pathways that tell the immune system when the lining of the airways has been damaged. Other genes appear to control how quickly the airways heal after they have been injured. Identifying these genes should help direct research into new treatments for asthma, the researchers suggest.

"Asthma is a complex disease in which many different parts of the immune system can become activated," said Professor William Cookson, Director of Respiratory Sciences at Imperial College London, who co-ordinated the study.

"One of the problems with asthma research has been choosing where to intervene in the disease pathways. Our study now highlights targets for effective asthma therapies, and suggests that therapies against these targets will be of use to large numbers of asthmatics in the population. "

Professor David Strachan, Professor of Epidemiology at St Georges, University of London, who also co-authored the study, said: "Asthma has often been considered a single disease, but our genetic findings suggest that childhood-onset asthma may differ biologically from asthma that is acquired in adult life.

The GABRIEL consortium is now investigating whether the causes of asthma differ between people with and without these newly discovered genetic variants."

The study also found that the genes associated with asthma did not have strong enough effects to be useful for predicting early in life which children might eventually develop the disease. This indicates that environmental factors are also very important in causing asthma to develop.

The GABRIEL consortium is working to identify environmental exposures that could protect against the illness.

The study was primarily funded by the European Commission, the French Ministry for Higher Education and Research, the charity Asthma UK and the Wellcome Trust.

Although large multi-national collaborations are becoming the norm with the study of many complex genetic diseases, the GABRIEL study is unique in that nearly all of the 15 billion genetic tests were performed in a single institution, the Centre National de Genotypage near Paris.

Professor Mark Lathrop, the Director of the CEA-CNG and the Scientific Director of the Fondation Jean Dausset–Centre d'Etude du Polymorphisme Humain (CEPH), pointed out the crucial role of an integrated large-scale infrastructure like CEA-CNG which has the capacity to perform all the steps from receiving the biological samples, to high throughput genotyping, quality control and data analysis. The Fondation Jean Dausset – CEPH was also a major player in this study.

Professor Miriam Moffatt said: "It has been enormously gratifying to work with such a group of dedicated scientists from so many countries. This genetic study has taken five years from planning until completion, but it builds on many earlier years of work in which all the 26,000 volunteers were recruited and studied in great detail.

The study would not have been possible without the contribution of all of the GABRIEL members."

Professor Ivo Gut, former Deputy Director of the CEA-CNG and now Director of the Centro Nacional de Análisis Genómico in Barcelona, said: "These results constitute a huge leap forward in the understanding of asthma that will lead to major advances in the treatment and quality of life of people suffering from the disease. It has been an immense effort to get this far but is well worth it.

The generous support from the funding agencies, the kind donation of DNA by the research subjects and the huge personal dedication of the collaborators of the Gabriel consortium, have made this study possible."

Professor Florence Demenais, Director of the Genetic Variation and Human Diseases laboratory in Paris (UMR-946 Inserm-Université Paris Diderot, Fondation Jean Dausset), who led the statistical analysis that combined all of the data, said: "Large scale genetic studies, such as this one, provide a powerful tool to decipher the genetic mechanisms underlying asthma and to unravel different types of disease that make up the asthma syndrome."

Professor Erika von Mutius at the University of Munich and co-coordinator of GABRIEL said: "The puzzle now is to work out what is causing the damage to the airway lining in asthma.

The GABRIEL study has also been busy looking for clues as to the environmental causes of asthma, particularly by dissecting the strong protective effects of living on a farm.

In the next year we will be combining the results from the genetic and environmental wings of the GABRIEL study, and we are greatly looking forward to what we may find."

Source: Imperial College London


The rise in the numbers and severity of asthma cases promises to become a plague in the developed world, yet the authorities seem to be careless as to some of the most likely causes.

Saturday, 18 September 2010

What Can You Believe?

If you might wonder why so many of us are getting sick, losing our capability and the air is thick with muck as are the products we buy or are medically treated with read the article below. I was just going to link to it but it is here in full with the attribution


Medical ghostwriters who build a brand.

There are no rules against this, just traditions, good faith, and leaky regulations.

Ben Goldacre, The Guardian, Saturday 18th September 2010

If I tell you that Katie Price did not, necessarily, write her own book, this is not a revelation. From academics I have slightly higher expectations, but now the legal system has spat out another skip full of documents: we get a new insight into the strange phenomenon of medical ghostwriting.

Attributed authorial assistance is one thing. This is different, and more cynical. A commercial medical writing company is employed by a drug company to produce papers that can be rolled out in academic journals to build a brand message.

After copywriters write the articles, in collaboration with the drug company, to their specifications, the ghostwriting company finds some academics willing to put their names to them, perhaps after modest changes.

The latest documents come from a court case brought against Wyeth by around 14,000 patients who developed breast cancer while taking Prempro, the hormone replacement therapy (HRT).

The open access journal PLoS Medicine, acting with the New York Times, argued successfully in court that 1,500 documents which detailed the ghostwriting should be placed in the public domain, because they represent information on a potential threat to public health.

Now, PLoS has published the first academic analysis of these documents, which is free to access online.

HRT has a rocky history. Initially the panacea to all ills, by 1998 the HERS trial showed it did not prevent cardiovascular events and by 2002 the Women's Health Initiative showed it increased the risk of breast cancer and stroke. We now know it increases the risk of dementia and incontinence.

Survey data shows that even today many gynaecologists have beliefs about the efficacy of HRT that are in excess of the evidence. Reading how the literature was engineered, it is not hard to see why.

The medical communications company DesignWrite boasts that over 12 years they have "planned, created, and/or managed hundreds of advisory boards, a thousand abstracts and posters, 500 clinical papers, over 10,000 speakers' bureau programmes, over 200 satellite symposia, 60 international programmes, dozens of websites, and a broad array of ancillary printed and electronic materials".

They proposed a "planned publication programme" to Wyeth, of review articles, case reports, letters, editorials, commentaries and more, using the medical literature as a marketing tool.

DesignWrite wrote the first drafts, and sent them to Wyeth, who advised on the creation of a second draft. Only then was the paper sent to the academic who would appear as the "author".
The academics were not paid cash, but they did get an easy publication in an academic journal for their CV. And once the publication process was in train, the chap from Wyeth's marketing department provided comments and suggestions for the authors to use in response to peer reviewers' comments.

The PLoS documents show DesignWrite sold Wyeth more than 50 peer reviewed journal articles for HRT, and a similar number of conference posters, slide kits, symposia, and journal supplements.

Adriane Fugh-Berman, associate professor in the department of physiology at Georgetown University Medical Centre in Washington DC, who analysed the documents (who appeared against Wyeth in the class action) found that these publications variously promoted unproven and unlicensed benefits of Wyeth's HRT drug, undermined its competitors, and downplayed its harms.

There are no rules against this. There are traditions, good faith, and leaky regulations. It's illegal, for example, to promote a drug for "off label" use, which means selling it to treat a medical problem for which it has no licence.

In the case of Wyeth's HRT drug, they could not market it for preventing Alzheimer's, Parkinson's, and wrinkles, to name but a few. Fugh-Berman's analysis found that many articles promoted the drug's use for exactly these conditions: but academic journal publications are not regarded as promotional activity, so this was all legal.

Worst of all is the complicity of the academics. There is no possible way they could persuade themselves what they were doing was correct. "Research shows high clinician reliance on journal articles for credible product information," said DesignWrite. They're right: when you read an academic paper, you trust it was written by the person whose name is on it.

There are simple solutions. If a commercial writer employed by a pharmaceutical company writes a paper, their name and their company's name should be on it. If the authors on a paper did not write or lead on it, they should say so. Universities could take a lead, but do not, and so these problems will persist, because they are complicated, and hidden from public scrutiny.

That's why you should read about them in PLoS, talk about them, crane your neck over, scratch your chin, and mutter in astonishment. Nobody in a regulatory role is interested. Our only hope is the power of shame.


It takes a worried man to sing a worried song……..

Tuesday, 14 September 2010

Anti This And Anti That

This is a long one, over 1100 words but of interest. It deals with antibiotics and bacteria suggesting that bodily bacterial balance can be disrupted by repeated treatments over months. Many products now contain antibacterial properties routinely as a “healthy” marketing feature. Is it possible that prolonged and continual application of these in products could have some form of similar effect?


Repeated antibiotic use alters gut's composition of beneficial microbes, Stanford study shows.

Published: esciencenews, Monday, September 13, 2010 - 15:16 in Biology & Nature

Repeated use of an antibiotic that is considered generally benign, because users seldom incur obvious side effects, induces cumulative and persistent changes in the composition of the beneficial microbial species inhabiting the human gut, researchers at the Stanford University School of Medicine have found.

By a conservative estimate, something like 1,000 different varieties of microbes coexist harmoniously within a typical healthy person's gut, said David Relman, MD, professor of medicine and of microbiology and immunology at the medical school and chief of the infectious diseases division at the Veterans Affairs Palo Alto Health Care System. Relman is the senior author of a paper, which will appear online Sept. 13 in Proceedings of the National Academy of Sciences.

The study examined the effects of ciprofloxacin (trade name Cipro), an antibiotic that is widely prescribed for intestinal, urinary and a variety of systemic infections. In an earlier, short-term study, Relman's group had concluded that people's intestinal microbial communities seem to bounce back reasonably well within weeks after a five-day regimen of ciprofloxacin.

This new study involved two courses of antibiotic administration, six months apart, and it revealed more-subtle, long-term effects of ciprofloxacin use - such as the replacement of multiple resident bacterial species by other, closely related varieties and the occasional complete eradication of a species.

The infrequent occurrence of easily visible side effects such as bloating and diarrhea from ciprofloxacin use has given rise to an assumption that the drug spares most beneficial gut-dwelling bacteria. Overall similarities between pre-regimen gut bacterial strains and their post-regimen replacements explain why such side effects aren't typically seen after ciprofloxacin use.

Still, the more nuanced differences between the pre-existing communities and those that appear in the wake of this repeated disturbance present a new set of problems, said Relman, who is also the Thomas C. and Joan M. Merigan Professor at the medical school.

A bacterial species whose presence was lost or diminished may have been performing a valuable job - for example, secreting a protein that's toxic to a particular pathogen - that is shirked by its replacement. The abandoned function might not be noticed until, perhaps, years later when the pathogen in question invaded the person's gut.

While the study's findings shouldn't be interpreted to mean that ciprofloxacin is dangerous and should be avoided, Relman said, they do raise questions about possible long-term effects of antibiotic administration, in addition to concerns about spurring the evolution of drug-resistant organisms.

The new findings underscore the desirability of finding ways to pinpoint not just which bacteria have been lost or whose numbers were diminished by an antibiotic, but also which important beneficial functions performed by the patient's gut microbial community as a whole have been impaired - such as signaling cells of the intestinal lining, which are constantly turning over, to maintain an appropriate barrier against ingested toxic compounds, or secreting anti-inflammatory substances that may prevent allergic or autoimmune diseases.

For this study, the Stanford scientists collected more than 50 stool samples from each of three healthy adult females over a period of 10 months. Then they used advanced, molecular techniques to count the number of different microbial species represented in each sample, as well as relative population sizes of the different species in that sample.

Twice during this 10-month period, the researchers perturbed their subjects' gut ecosystems by giving them five-day courses of ciprofloxacin at a standard dose. During the first course, overall bacterial populations in each subject - which had previously waxed and waned but, on the whole, been quite stable - plummeted and remained depressed for about a week.

Roughly one-third to one-half of the resident species' populations declined, with some disappearing entirely. A few originally less-abundant species grew in number, as they filled in the ecological niche abandoned by bugs adversely affected by the drug.

Within a week after the first course's completion, two of the three subjects' internal microbial ecosystems had largely returned to a state fairly similar to that before the regimen, as measured by the broad classes to which the microbial constituents belonged. One subject's overall ecosystem, however, still had not recovered even by that rough measure a full six months later.

The second course of antibiotic administration produced a stronger effect. "Even the one subject whose gut bacterial community fully recovered after the first ciprofloxacin course experienced an incomplete recovery after the second one," said Relman.

The communities in the other two subjects partially recovered from the second course, but never returned to their original state. In essence, each subject's community of gut-dwelling microbes shifted to a new, "alternative" state and remained in that state for at least two months after the second antibiotic course had been completed.

Thus, all three subjects experienced significant and lasting changes in the specific membership of their internal microbial communities at the end of the 10-month study period.

"Ecologists have found that an ecosystem, such as a wildlife refuge, that is quite capable of rebounding from even huge occasional perturbations - forest fire, volcanic eruption, pests - may yet be undone by too rapid a series of such perturbations," said Les Dethlefsen, PhD, a research scientist in Relman's lab and the study's first author.

"In the same way, recurring antibiotic use may produce a cumulative effect on our internal microbial ecosystems with potentially debilitating, if as yet unpredictable, consequences."

"It's as if your beneficial bacteria 'remember' the bad things done to them in the past," said Relman. "Clinical signs and symptoms may be the last thing to show up."
The precise counts of gut-dwelling microbes in this study were made possible by a new technique, pioneered in recent years by Relman and others.

The older method - growing the microbes in culture - simply doesn't work for many species and, even when it does, rare species are often swamped by more common ones and don't get counted. The new technique reads short, telltale DNA snippets that distinguish microbes both from human cells and one from another.

This allowed the Stanford researchers to assess both the total number of different microbial varieties and the relative size of each variety's population.

Similar techniques now make it possible to assess, before and after antibiotic administration, the abundance in a patient's gut of microbial genes known to code for important functions performed by one or more members of the patient's gut community, Relman said.

In the future, if it becomes known that a key function has been impaired, clinicians might perhaps restore that function by prescribing specific probiotics or nutrients that encourage the return of appropriate beneficial bugs.

Source: Stanford University Medical Center


We seem to be finding more and more just how vulnerable the body systems are to too many interventions either for “medical” or cosmetic reasons.

Saturday, 11 September 2010

Coughing For Life

There is now a good deal of work being done on causes and nature of lung problems around the world. Unluckily, precious little in the UK where research is governed by the funding requirements for “added value” in strictly commercial terms and added shareholder value related to the relevant companies.

This item is one I found interesting in that an implication is that there could be numbers of people from a young age who already very vulnerable to a wide range of possible causes of inflammation.

Quote from esciencenews dot com:

Research and insights on severe asthma in children

Published: Thursday, September 9, 2010 - 10:18 in Health & Medicine

A subset of children with asthma suffers from severe, treatment-resistant disease associated with more illness and greater allergic hypersensitivity, according to the results of the National Heart, Blood, and Lung Institute's Severe Asthma Research Program (SARP), presented in a recently published article in Pediatric Allergy, Immunology, and Pulmonology, a peer-reviewed journal published by Mary Ann Liebert, Inc. (

The article is available free online at Asthma is the most common chronic lung disease of children, with more than 6.6 million affected in the U.S. Although relatively few children have severe asthma, they account for almost half of asthma related expenditures.

SARP compared severe, therapy-resistant asthma in children and adults and identified age-specific characteristics of the disease. The results suggest that there are distinguishable clinical features of severe asthma that can be identified early in life.

Authors Anne Fitzpatrick, PhD from Emory University (Atlanta, GA) and William Gerald Teague, MD from the University of Virginia (Charlottesville) review the highlights of the SARP findings in an article entitled "Severe Asthma in Children: Insights from the National Heart, Lung, and Blood Institute's Severe Asthma Research Program".

They conclude that children with severe, therapy-resistant asthma are more likely to have poorer lung function and higher levels of allergic sensitization and to be of African American or mixed ancestry.

Their findings suggest that children as young as 6 years with severe asthma may already have structural airway changes.

"Identifying the features associated with severe, treatment-resistant asthma in children will allow us to better understand this illness and develop better treatments for these children who spend so much time struggling to breathe," says Harold Farber, MD, MSPH, Editor of Pediatric Allergy, Immunology, and Pulmonology, and Associate Professor of Pediatrics, Section of Pulmonology, Baylor College of Medicine, Houston, TX.

Source – Mary Liebhart, Genetic Engineering News


This all adds to the picture of complexity and uncertainty in relation to the developing problems. The more pollution and contamination the more serious and widespread the problems become.

Thursday, 9 September 2010

Burning Question

The connection between wood smoke, a sort of “natural” stuff in the air, tobacco and other extensive airborne pollutants may be a loose and debatable one. But to my simple mind if there is a lot of stuff in the air all of which does no good at all to the lungs then the more complex and the more general it is then the more lung issues that will arise in more people.


Wood Smoke Exposure Multiplies Damage from Smoking, Increases Risk of COPD

ScienceDaily (July 16, 2010)

Smokers who are exposed to wood smoke, either through home heating and cooking or through ambient neighborhood pollution, are not only at increased risk of COPD, but are also more likely to have epigenetic changes in the DNA that further increase their risk of COPD and related pulmonary problems.

Together, smoking, wood smoke exposure and these epigenetic changes can increase an individual's risk of COPD fourfold.

"When cigarette smokers are exposed to wood smoke their risk of having reduced lung function increases," explained lead author Yohannes Tesfaigzi, Ph.D. senior scientist and director of COPD Program at the Lovelace Respiratory Research Institute, where the research was completed.

"Cigarette smokers who have both changes in sputum DNA and are exposed to wood smoke have a synergistically increased risk of having reduced lung function and other indicators of COPD such as chronic mucous hypersecretion. "

The research was published online ahead of the print edition of the American Thoracic Society's American Journal of Respiratory and Critical Care Medicine.

Dr. Tesfaigzi and colleagues administered questionnaires to more than 1800 current and former smokers between 40 and 75 years old, and obtained demographic and smoke exposure information, as well as sputum samples which were analyzed for epigenetic changes to eight genes known to be associated with lung cancer.

They found that wood smoke exposure was significantly and independently associated with an increased risk of respiratory disease, especially among current smokers, non-Hispanic whites and men.

Furthermore, wood smoke exposure was associated with specific COPD outcomes in people who had aberrantly methylated p16 or GATA4 genes, and both factors together increased the risk more than the additive of the two risk factors together.

They also found that people with more than two of the eight genes analyzed showing methylation were also significantly more likely to have a lower than predicted FEV1 than those with fewer than two methylated genes.

"Because exposure to wood smoke appears to increase the risk of reducing lung function, cigarette smokers should try to avoid heating their homes or cooking with wood stoves and try to avoid environments where wood smoke is likely (for example, neighborhoods where wood smoke is common)," said Dr. Tesfaigzi.

"Because the same gene changes were associated with increased risk for lung cancer one would assume that wood smoke exposure also increases the risk of developing lung cancer. Future studies may show that it would be appropriate to screen patients for lung cancer if these exposures were present for prolonged periods."

Based on these findings, Dr. Tesfaigzi and colleagues established an animal model that will be able to further test whether both wood and tobacco smoke exposure cause more damage to the lung than either one of the exposures alone.

"We observed increased inflammatory response in mice that were exposed to both cigarette smoke and low concentrations of wood smoke compared to those exposed to cigarette smoke only. We would like to use this animal model to determine the mechanisms underlying this exacerbation," said Dr. Tesfaigzi.

Because wood smoke exposure was documented by self-report and was not quantified in this study, in the future Dr. Tesfaigzi also intends to characterize the type and amount of wood smoke the participants were exposed to. Such studies will help to further refine the analysis and provide intervention strategies.


I am just going out to light the bonfire, have a cigar and to cover the smell will give myself a good big dose of deodorant. If I cough it must be that strong coffee.

Monday, 6 September 2010

A Simple Question

This item is from over six years ago. So how much progress have the relevant authorities made in the UK to address the increasing problems?


Chemical Sensitivities and Perfume
Medical News Today – 10 June 2004

Fragrances are now used in almost every cleaning, laundry, and personal-care product on the market. Since people have been using perfumes for hundreds of years. It's reasonable to wonder why the problem of using scents has surfaced only recently.

Until the 20th century, perfumes were made from natural ingredients derived directly from plants and animals, and as fragrances became cheaper and more widespread, they also became more synthetic.

The National Academy of Sciences reports that 95% of the chemicals used in fragrances today are synthetic compounds derived from petroleum, including known toxins capable of causing cancer, birth defects, central nervous system disorders and allergic reactions.

We have been brainwashed by the industry to feel we must cover up our natural scents with toxic chemicals. Many of the same chemicals in perfumes are the same chemicals that are in cigarette smoke.

You would think the government would protect people by attempting to regulate the industries that are causing harm; however, the cosmetic industry is self regulated and isn't required to give formulations, test results, safety data or consumer complaints to the FDA.

When you use perfume or cologne, remember you are using powerful chemicals regulated solely by the industry that sells them. Just because they don't affect you now doesn't mean they won't affect someone in line next to you (giving them a migraine or sinus problems), or that you will always be immune to their effects. These chemicals go directly into the blood stream when applied to our skin, and are also absorbed into the skin from our clothing.

We also inhale these chemical fumes that go straight to our brains where they can do major harm, and many of these chemical fumes have a "narcotic" effect. ("Smelling Good But Feeling Bad, Synthetic Perfumes, Colognes and Scents Are Turning Up Noses," Green Living Your Health, and "The Health Risks of Perfume and Other Scented Products," - March 2002} Author's comment:

These effects from scents can surface days after the exposure, and many people do not connect the strong perfume/cologne smell on the lady or gentleman next to them at the opera to their headache or upset stomach days later.

One of the big toxic offenders is perfume and other scented products. Did you know that many of the ingredients in your perfume are the exact same ingredients found in gasoline???!! The scary thing is that the perfume industry is not regulated at all, and they can put any number of chemicals in fragrance without revealing what those chemicals are, and how they affect humans.

We humans are all participating in a giant "lab" experiment against our knowledge and against our will, and it is making some of us very sick.

{"Multiple Chemical Sensitivity - Environmental Illness," - April 2002}

Fragrance-free policies are beginning to take hold in work places across the United States and Canada. Here are just a few examples:

Evergreen State College in Olympia, Washington, asked its employees and students to refrain voluntarily from wearing scented products.

The entire Halifax Regional Municipality in Nova Scotia has a "scent-awareness" program that urges the use of unscented products only.

Alacrity Ventures, a Berkeley, California-based venture-capital firm, not only encourages its employees to go fragrance-free but also uses only unscented janitorial products.

Many businesses, at the request of their employees, are voluntarily creating fragrance-free policies, says Tracie Saab, a consultant with the "Job Accommodation Network," a Morgantown, West Virginia group that educates disabled workers and their employers.

These policies are applauded by people with asthma, allergies, and the controversial disorder called multiple chemical sensitivity, in which even low levels of exposure to chemicals (from pesticides to perfumes) can trigger headaches, fatigue and other symptoms.

"It is easier for businesses to enact these policies than to risk legal action somewhere down the line," says Saab.

{"Stink-Free Office Mates," Natural Health, Nov./Dec. 2000}

Many migraineurs are so sensitive to fragrance that people wearing perfumes and colognes around them trigger an immediate and severe migraine attack. You can make your house a fragrance-free zone, and if you have a visitor who is either not aware of this or forgets, most of the fragrance can be removed with alcohol wipes if it has been put on the skin and not the clothing.

{"Fragrance Triggers," Teri Roberts: Beating Headaches, on Headaches/Migraines on - Dec. 2001}


In answer to the question at the top, almost nothing.

Saturday, 4 September 2010

Collateral Damage Hurts Just As Much

Another item relating to the lungs. This one relates to how the immune system can be adversely affected by damage to the lungs. This concerns tobacco, a pollutant that is receiving a great deal of attention. But it does raise questions about other common pollutants in the air that may have more complex and powerful effects.

As a former military man I am well aware of the meaning of collateral damage


Protecting the Lungs Against 'Collateral Damage' from the Immune System

ScienceDaily Science News (Sep. 2, 2010)

A study published September 2 in the journal Science shows how our bodies try to minimise potential 'collateral damage' caused by our immune system when fighting infection. The research may also provide new clues to why cigarette smoke is a significant risk factor for developing diseases of the lung such as chronic bronchitis and emphysema.

When bacteria or viruses enter the body, our immune system fights back to neutralise any danger. One of the key 'soldiers' working for the immune system is a particular type of cell known as a neutrophil, which releases toxic enzymes to kill the invading organism. But these enzymes can cause collateral damage to surrounding tissue, and so the neutrophils need to act swiftly and leave the site of infection as quickly as possible.

"Neutrophils are powerful at fighting infection, but if left unchecked, they can cause damage to our own bodies," explains Dr Robert Snelgrove, a Sir Henry Wellcome Postdoctoral Fellow at Imperial College London, who carried out the study together with colleagues from the University of Alabama at Birmingham, USA.

"We know that their persistence contributes to the development and severity of many chronic lung diseases such as chronic obstructive pulmonary disease and cystic fibrosis."

The enzymes released by neutrophils can cause particular damage in the lung, where they can attack the collagen which makes up the lung's architecture, selectively cutting out a molecular fragment known as PGP. This fragment in turn recruits more neutrophils, potentially leading to a vicious circle of damage.

However, in research just published and part-funded by the Wellcome Trust, Dr Snelgrove and colleagues show how another enzyme released by the lungs -- LTA4H -- degrades PGP, breaking the cycle and preventing damage.

In a second experiment, the researchers also showed that chemicals found in cigarette smoke can have a negative effect on this process, modifying PGP in a way that increases its ability to recruit more neutrophils and protecting it from degradation, and inhibiting the performance of LTA4H.

Patients with diseases such as chronic bronchitis and emphysema, which are collectively known as chronic obstructive pulmonary disease (COPD), tend to have persistent neutrophils in the lungs.

"We have known for some time now that there is a link between smoking and COPD," says Dr Snelgrove. "Here we have shown that cigarette smoke can severely limit the effectiveness of an enzyme which contributes to the clearance of these rogue immune cells. This may be a contributing factor to damage to the lungs which affects a person's ability to breathe easily."
There are an estimated three million people in the UK living with diseases such as chronic bronchitis and emphysema, which are collectively known as chronic obstructive pulmonary disease (COPD).

This condition is caused by damage to the lungs, most commonly as a result of smoking, and leads to an inability to breathe properly.

The researchers believe that the research may have implications for the development of new drugs aimed at treating acute and inflammatory diseases. As well as working to reduce inflammation, LTA4H more commonly works to promote inflammation.

However, drugs aimed at inhibiting the pro-inflammatory activity of LTA4H could have repercussions for preventing degradation of PGP, causing potential lung damage, they caution.


Given the increasing extent, range, and power of odour products, just how much collateral damage are they doing to our immune systems?

Thursday, 2 September 2010

The Importance Of Lungs

The article below discusses the effect of silica based dusts on the lungs. This is in the context of work. Many personal products now used similar content to fix other chemicals to the skin or clothing by sprays that entail breathing in the product.


New discovery suggests our lungs are 'innately prone' to silicosis and related diseases.

Published in esciencenews dot com on Tuesday, August 31, 2010 - 09:29 in Health & Medicine

For the nearly 2 million U.S. workers exposed to silica dust each year, a new discovery may help prevent or treat the development of chronic lung diseases related to this exposure.

In the September 2010 issue of the Journal of Leukocyte Biology ( scientists from Montana and Texas use mice to show for the first time that the part of our immune system responsible for keeping airways clean and free of contaminants (innate immunity) can cause inflammation and symptoms of disease.

This study is significant because it is generally believed that reducing chronic inflammation will improve the quality of life for patients.

"Some of the most difficult lung diseases to treat are those that involve chronic inflammation and exposure to harmful particulates," said Celine A. Beamer, Ph.D., a researcher from University of Montana, Center for Environmental Health Sciences who was involved in the work.

"Hopefully, the information from this study will move us a step closer to curbing dangerous airway and lung inflammation."

To make this discovery, scientists treated two groups of mice with silica, a common mineral often found in sand or quartz, and then measured for the development of silicosis. The first group consisted of normal mice with a normal immune system, while the second group included mice with an inactive adaptive immune system.

The normal mice developed silicosis as expected, but the disease was even more prevalent in the mice without the adaptive immune system. Silicosis is a chronic lung disease caused by breathing in dust containing silica, often setting the stage for tuberculosis.

"The lungs are very complex and delicate organs, and many different kinds of chronic inflammation in the respiratory tract can lead to difficulty with normal daily activities," said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology.

"For many people, chronic inflammation is a problem that leads to the destruction of this tissue. This study gives us a much better understanding of how this inflammation occurs, and as a result, new avenues for stopping it."

Source: Federation of American Societies for Experimental Biology


Persistent or chronic inflammation of the lungs can be progressive and impact not only on breathing but on blood flow to the brain.