Doctors behind ADHD study question drug treatment.

The co-authors of a 20-year-old study promoting the use of prescription drugs to combat the effects of attention deficit hyperactivity disorder (ADHD) are now claiming the report may have overstated medication’s benefits.

According to a report in the New York Times, at least two co-authors of the highly influential study – called the Multimodal Treatment Study of Children With ADHD – have come forward to express concern that the original report also downplayed the benefits of behavioral therapy.

“There was lost opportunity to give kids the advantage of both and develop more resources in schools to support the child — that value was dismissed,” said co-author Dr. Gene Arnold, a child psychiatrist and professor at Ohio State University.

“I hope it didn’t do irreparable damage,” added a second co-author, Dr. Lilly Hechtman of Montreal’s McGill University. “The people who pay the price in the end is the kids. That’s the biggest tragedy in all of this.”

The report originally claimed that not only was medication like Adderall and Ritalin more effective than therapy, but also that combining the two treatments offered little to no benefit to the patient. Even a 2001 report that showed a combination of medication and therapy effectively treating ADHD symptoms by 12 percent over medication only (68 – 56 percent) labeled the results“small by conventional standards.”

Boosted by marketing from pharmaceuticals, prescriptions for ADHD drugs have skyrocketed since the early 1990s, alongside a significant rise in the diagnosis of ADHD in general.

According to new data from the Centers for Disease Control and Prevention, 15 percent of high-school-age children have been diagnosed with the disorder, with roughly 3.5 million currently taking medication. These numbers stand in stark contrast to the 600,000 or so children diagnosed with ADHD in 1990.

“The numbers make it look like an epidemic. Well, it’s not. It’s preposterous,” Keith Conners, a psychologist and professor emeritus at Duke University, said to the Times earlier in December.“This is a concoction to justify the giving out of medication at unprecedented and unjustifiable levels.”

One of the reasons medication has been used so often to treat the disorder is that, at the cost of $200 a year, it’s significantly cheaper than therapy, which can run up to $1,000 a year or more and isn’t covered as comprehensively by insurance companies. While medication can be helpful, it also has its consequences – potential addiction, anxiety, depression, insomnia and, in some cases, suicidal tendencies and hallucinations.

Behavioral therapy, meanwhile, focuses on developing a child’s long-term academic and social skills. According to psychologist Ruth Hughes of the advocacy group Children and Adults With Attention-Deficit/Hyperactivity Disorder, medication may make a child ready to learn important skills, but it still requires someone to teach them.

Now, new studies are suggesting that the effects of medication begin to decrease once a child grows older, suggesting it’s extremely difficult to calculate how a child will react as they reach young adulthood. Some researchers pin the blame on the fact that many children stop taking the pills, while others say it demonstrates the inability of a medication-only approach to conclusively treat the disorder.

“My belief based on the science is that symptom reduction is a good thing, but adding skill-building is a better thing,” Stephen Hinshaw, a psychologist at the University of California, Berkeley, said to the Times. “If you don’t provide skills-based training, you’re doing the kid a disservice. I wish we had had a fairer test.”

Women’s breasts age faster than the rest of their body.

Breasts typically age more quickly than the rest of the female body. So suggests a system that may be the most accurate way yet of identifying a person’s age from a blood or tissue sample.

As we age, the pattern of chemical markings on our DNA changes. Each gene becomes more or less methylated, that is, they have methyl chemical groups added or removed. This generally increases or decreases gene expression. The whole process is known as epigenetics.

The question "how old are you?" just became a lot harder to answer <i>(Image: REX/Cultura)</i>

Steve Horvath at the University of California, Los Angeles, and his colleagues have used these changes to estimate a person’s age. To do so, they first performed a detailed statistical analysis of methylation patterns in 7844 healthy tissue samples from 51 different types of tissue. The tissue covered a range of ages – from fetuses to people 101 years old.

Universal ageing

The analysis allowed the team to weed out methylation patterns that varied between tissues, leaving just those that are common to all tissues. This enabled them to identify a subset of 353 specific regions of the genome that became either more or less methylated with age in almost all types of tissue.

By measuring the total amount of methylation in these regions, the team was able to create an algorithm that identified the age of the tissue.

The team validated the algorithm against thousands more samples of known age. Horvath says the method is twice as accurate as the next best method of ageing tissue, which is based on the length of telomeres – tips of chromosomes that “burn down” with age like candle wicks. He says that his method has a 96 per cent chance of accurately identifying someone’s age to within 3.6 years compared with around 53 per cent for telomeres.

“What’s unique about this study is the idea that there’s a signature of ageing common across tissues in spite of the significant tissue specificity of DNA methylation patterns,” comments Moshe Szyf, who studies methylation at McGill University in Montreal, Canada. “The data point to the possibility that DNA methylation signatures could be used as robust markers of biological ageing.”

Young at heart

Horvath says that, remarkably, their analysis shows that some parts of the body age at different rates. When they used their algorithm on healthy breast tissue from a group of women of average age 46, for example, it churned out a result that was on average two to three years older than the woman’s actual age. Whereas in two groups aged 55 and 60 across both sexes, heart tissue appeared nine years younger than true age.

If it is known where the sample comes from, it is still possible to accurately predict age after some straightforward adjustment, says Horvath. However, in general, the algorithm is most accurate for samples from people under 30 years of age. “The older one gets, the less accurate it becomes,” he says.

Horvath thinks that breast tissue ages more quickly because of its constant exposure to hormones. Heart tissue may remain younger, by contrast, because it is constantly regenerated by stem cells.

Cancerous tissue also appeared to age prematurely, coming out at 36 years older than the person’s actual age on average across 20 cancers from 20 different organs.

Because ageing is a risk factor for all cancers, Horvath suggests that the premature ageing of breast tissue might explain why it is the most common cancer in women. “It could be so prevalent because that part of the female body is older,” he says.

Blood work

Because the method also works on blood it might have the potential to be used forensically, to reveal the age of a murder suspect, suggests Horvath. It might also be used to diagnose cancer, by revealing accelerated ageing in tissue biopsies.

“The data raises questions about whether these DNA methylation changes play a causal role in ageing and, if so, whether epigenetic interventions could reverse these and therefore slow down ageing,” says Szyf. “The chemical robustness of DNA methylation and the ability to accurately measure it make it a very attractive tool to study ageing, which could well be superior to measuring telomere length, which is the current practice.”

Horvath says that further studies comparing telomere and epigenetic ageingcould be useful, and hopes the two can be complementary. He also says that the software for his algorithm is openly available so that other researchers can try validating it on their own tissue samples.

Journal reference: Genome Biology, DOI: 10.1186/gb-2013-14-10r115

Florbetapir Approved: Now How Do We Use It?

April 19, 2012 — Florbetapir (Amyvid, Eli Lilly/Avid Radiopharmaceuticals), a new agent to detect beta-amyloid plaques in living patients with possible Alzheimer’s disease (AD), has just been approved by the US Food and Drug Administration (FDA). The question now is how this imaging option will be used in practice.

Although they are for the most part enthusiastically awaiting access to this new agent, expected to be available by June, many neurologists are also striking a cautionary note. Cost, availability, the need for expert interpretation of scans using the florbetapir tracer, and what it really means for a diagnosis of AD are a few of the concerns being raised.

Medscape Medical News polled experts in the field of AD to see how they view the approval and how they see this diagnostic tool may fit into their clinical practice.

Diagnostic Dilemmas

Florbetapir is a diagnostic agent tagged with a radioisotope, fluorine-18. Used with positron emission tomography (PET), it binds to amyloid plaques in the brain. Approved by the FDA on April 9, florbetapir is 1 of 3 imaging agents in various stages of development; others are florbetaben (Bayer/Piramal Imaging SA) and flutemetamol (GE Healthcare). All are reported to detect amyloid deposition in the living brain.


Although the presence of amyloid on the scan doesn’t necessarily mean the patient has AD, a scan showing little amyloid deposition, “is inconsistent with a neuropathological diagnosis,” of AD, a press release from the company at the time of approval notes. The statement added that the safety and effectiveness of florbetapir have not been established for predicting development of dementia or other neurologic conditions, or for monitoring responses to therapies.

Still, the use of florbetapir may clear up some diagnostic dilemmas, said Sandra Black, MD, professor, Department of Medicine, Division of Neurology, University of Toronto, Ontario, Canada. “It might help in situations where you’re not quite sure what’s going on — when you don’t know whether this is aphasia due to AD or a frontal temporal dementia-type thing.”

Pedro Rosa-Neto, MD, assistant professor, neurology, neurosurgery and psychiatry, McGill University, Montreal, Quebec, Canada, felt that the new tracer could be informative in the investigation of patients with early onset or atypical presentations of dementia to rule out AD, and in cases of rapidly progressive dementia.

“Rapidly progressive Alzheimer’s disease is a highly neglected condition, frequently misdiagnosed as Creutzfeldt-Jakob disease,” Dr. Rosa-Neto noted. For these selected cases, he sees PET using florbetapir adding to the information gained from the clinical history, various magnetic resonance imaging (MRI) modalities, including fluid-attenuated inversion recovery and diffusion-weighted imaging, cerebrospinal fluid sampling, and neuropsychological and genetic evaluations.

Although the tracer could be of assistance in patients with dementia in whom it’s unclear whether amyloid is a cause of cognitive deterioration, it would not be as useful an addition in cases where all clinical, cognitive, and imaging findings strongly point to the presence of AD, said Liana Apostolova, MD, Alzheimer’s Disease Research Center, University of California, Los Angeles.

“While the test could be useful to confirm that presumption, dementia specialists can already diagnose AD under these circumstances with high sensitivity,” she said. “This is when I might say, ‘I’m pretty certain what’s going on at this point; I don’t need to subject the patient to this expensive diagnostic procedure.”

Role in Mild Cognitive Impairment?

Some clinicians agreed that there is a place for the new biomarker in patients with mild cognitive impairment (MCI). Ronald Petersen, MD, PhD, director, Alzheimer’s Disease Research Center, Mayo Clinic, Rochester, Minnesota, credited with developing the concept of MCI, said the tracer “will be helpful” to see whether amyloid can explain memory problems experienced by these patients. “It will not make the diagnosis, but it will help the clinician sort out the cause of the symptoms.”

Dr. Petersen pointed out that many patients with MCI — perhaps up to 40% — don’t have AD as the underlying cause of their cognitive problems.

For Steven T. DeKosky, MD, vice president and dean, University of Virginia School of Medicine, Charlottesville, the new biomarker “seems like a reasonably accurate detector” of whether MCI is AD in development or whether it relates to some other cause.

Other physicians said they wanted to avoid using the new tracer in cases of MCI.

“Although I think a positive amyloid imaging study would increase the likelihood that the person will decline, that is not known for certain,” said David Knopman, MD, Department of Neurology, also at Mayo Clinic Rochester, Minnesota. “So, I would definitely not do an amyloid scan routinely.”

Doctors stressed that a positive scan does not necessarily mean an asymptomatic patient will develop AD. “Many cognitively normal elderly will show amyloid deposition in their brains as the disease is believed to have an asymptomatic stage that lasts up to 20 years,” pointed out Dr. Apostolova.

“I don’t think we know enough about the prognostic factors of a positive amyloid scan,” said Adam S. Fleisher MD, director of brain imaging, Banner Alzheimer Institute, Phoenix, Arizona, during a Web-based debate on the role of neuroimaging in the diagnosis of AD earlier this year.

On the other hand, a negative scan may not mean a patient is out of the woods because there could be another explanation for their cognitive problems, such as vascular dementia.

“We will have to be very careful using amyloid imaging and making sure patients understand that a negative scan is not necessarily a cause to celebrate,” said James B. Brewer, MD, PhD, associate professor, radiology and neurosciences, Human Memory Laboratory, University of California at San Diego, who also participated in the Webinar.

Possible other causes of cognitive decline could include stroke, thyroid problems, drug interactions, chronic alcoholism, and vitamin deficiencies. Psychiatric disorders such as depression can masquerade as dementia as well.

The Alzheimer’s Association acknowledged that FDA approval of florbetapir is a “double-edged sword,” although it supports the move.

…the fact that all of the potential uses of this product are not crystal clear tempers our enthusiasm.

In a statement, the Association said that although the approval will expand the clinical and research opportunities for amyloid imaging, “the fact that all of the potential uses of this product are not crystal clear tempers our enthusiasm.” Additional research is needed to clarify the role of florbetapir-PET imaging in Alzheimer’s, it added.

Worried Well

Physicians weighing in agreed that amyloid measurements alone are not enough — that other imaging tests, including MRI, should also be part of the diagnostic equation. Many talked about the “multi-modal use” of this and other emerging amyloid biomarkers.

And, as Dr. Brewer pointed out, the new amyloid tracer does not measure tau, which some experts believe plays a crucial role in AD. Another agent under development by researchers at the University of California, Los Angeles, called FDDNP, images both tau and amyloid on PET.

All doctors also emphasized the importance of patient counseling before ordering an amyloid test.

“You have to have a good understanding of how that’s going to influence discussions with the patient, and your treatment and prognostic decision-making,” said Dr. Fleisher. He added that the test results could be quite anxiety provoking for a patient.

Doctors who spoke to Medscape Medical News also expressed a concern about “direct to patient” advertising and about “worried well” patients asking for this test. Many called for caution about using this new biomarker in cognitively normal patients who are anxious about their amyloid status.

The Alzheimer’s Association, too, warns of “less than scrupulous” imaging operators who make unrealistic promises to such patients about the value of florbetapir imaging. It recommends that the test be accessible only in the context of a complete evaluation of medical/neurologic status and with appropriate expert consultation.

Cost Issues

Cost may be a significant issue in determining whom to scan using this new biomarker, doctors agreed. The price tag for the radioactive compound alone appears to be in the neighborhood of $1600, said Dr. Apostolova.

“Then there will be the added cost of getting the PET scan which in most places will be between $1000 and $1500. So I think we are looking at a cost of about $2500 to $3000 per scan here.”

Because the tracer will be costly, “we have to use it with caution and only when it’s really necessary,’ said Dr. Apostolova, “Is it going to tell me anything beyond what I already know?”

As for insurance coverage, Dr. Petersen said that it’s unclear at this time who will pay for this new agent when it becomes available in June. Dr. Knopman commented that that “to start with, no insurer will pay for it.” The agent is also not currently eligible for coverage by the Centers for Medicare and Medicaid Services (CMS) because of its specific policy on reimbursement for PET procedures.

During a press conference after approval of the agent, Stephanie Prodouz, manager of Eli Lilly Bio-Medicines Communications, said that, “Although Amyvid will not be eligible for coverage, it’s important to note that Lilly is working with a broad group of stakeholders to explore and collaborate with CMS to find a new policy for PET coverage.”

Treatment Lacking

Although there is palpable excitement among some neurologists about the diagnostic possibilities of this new tracer, their enthusiasm is also tempered by the lack of available AD treatments.

“From a scientific viewpoint, the development of amyloid imaging was huge [but] the commercial availability is less so, unless it can be tied to finding better therapeutics,” said Dr. Knopman. “Until there are better therapeutics for AD, amyloid imaging does not change the landscape in clinical practice.”

Until there are better therapeutics for AD, amyloid imaging does not change the landscape in clinical practice.

But new treatments are on the horizon, according to Marwan Sabbagh, MD, director, Banner Sun Health Research institute, Sun City, Arizona. “Later this year, you will see 2 large immunotherapy studies — bapineuzumab and solanezumab — reporting their data to the world on their phase 3 trials, so the game changing elements here are perfectly timed in anticipation of these potential disease modifying agents.”

Bapineuzumab and solanezumab are both monoclonal antibodies that bind to and clear beta amyloid. Dr. Sabbagh is an investigator on both trials and serves on the steering committee for the bapineuzumab study.

Still, it’s unclear what role the amyloid plays and whether clearing it will result in any change in cognitive status. However, if safe and effective treatments become available, “that changes the whole ball game,” commented Dr. Brewer.

Dr. Apostolova agreed. “If we can find an agent that can halt the disease progression, before symptoms occur, this [florbetapir] will become the single most useful diagnostic and prognostic test out there,” she added.

For his part, Dr. DeKosky said that if an effective AD drug were available, the amyloid test could be used not necessarily to rule out AD but to determine that the cognitive impairment a patient experiences is indeed AD, so that drug could be administered.

Still, even in the absence of more effective amyloid treatments, many doctors felt that the test could nevertheless be useful. For example, said Dr. Brewer, it provides physicians with an opportunity to educate patients, help them manage risk factors and perhaps get them enrolled in a clinical trial.

As well, said Dr. Apostolova, the test results may spur patients to make necessary work-related arrangements or put their personal affairs in order. “Knowledge is power,” she said.

Clinical Studies

According to Eli Lilly, the information on scans using the new tracer correlates highly with what is seen on autopsy. In a study that used the majority interpretation of 5 readers, there were 96% sensitivity and 100% specificity in patients who underwent scanning within a year of death.

Dr. Black called this autopsy correlation research “elegant.” “It showed that indeed they were really picking up the amyloid” prior to death in these patients, she said.

The clinical studies also showed that the new diagnostic tracer appears to be very safe. The most common adverse reactions reported in these trials were headache (1.8%), musculoskeletal pain (0.8%), fatigue (0.6%), nausea (0.6%), anxiety (0.4%), back pain (0.4%), increased blood pressure (0.4%), claustrophobia (0.4%), feeling cold (0.4%), insomnia (0.4%), and neck pain (0.4%).

The studies are outlined in more detail in the product prescribing information.

But although the new imaging agent is safe and promises to be helpful diagnostically, training of interpreters will be key. Florbetapir was approved only with the proviso that Eli Lilly improve education initiatives for readers of the images. In January 2011, the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee voted 13 to 3 against recommending approval for the tracer, but in a second unofficial vote, the committee voted 16 to 0 in favor of approval if the company would agree to structured training for those reading the scans.

“There was a fear that radiologists would not know how to interpret the scans, as well as a concern about what would be an appropriate use of this agent,” said Dr. Black.

After working with the FDA and nuclear medicine experts, Eli Lilly developed both an online and an in-person training program for physicians. According to the company, images should be interpreted only by readers who have successfully completed a training course. The company cautions that errors may occur in the estimation of plaque density during image interpretation.

“This is a new kid on the block; it’s a new technique” that requires training, commented Dr. Apostolova, who carries out imaging research. “It’s not the case that one day, all of a sudden, one’s brain’s tissue becomes full of amyloid. It’s a slow protracted continuous build up.”

Patients will fall on a continuum, with some having minimal amyloid binding and others moderate or severe amounts, she added. “The last ones would be the easiest to call, but there will be many intermediate cases where we have to decide on a threshold that we will be using to call a scan positive versus calling it negative.”

Not Straightforward

The lack of familiarity in reading scans could pose “a big problem” for clinicians since “it’s not straightforward,” commented Dr. Petersen.

Dr. Knopman agreed, saying he’s “very concerned” about the scan interpretation issues. “I am dubious that radiologists who don’t do a lot of them will misinterpret them,” he said. “Even after nuclear medicine physicians have taken the course provided by Lilly, if they have low instances of contact with the test, they are likely to make mistakes in interpretation.”

He added that he’s particularly worried about the risk for overdiagnosis of Alzheimer’s, especially when the amyloid imaging is not interpreted in light of the clinical history.

“For example, up to 30% of cognitively normal people over age 70 years are expected to have a ‘positive’ scan,” he said. “I’m worried that a normalperson will hear that their amyloid scan shows ‘Alzheimer’s disease’ and will conclude that they have the disease and are at imminent risk of losing their memories. In fact, an abnormal amyloid scan should be interpreted as showing amyloidosis, not Alzheimer’s.”

Dr. Black said her “hunch” is that florbetapir will be more likely to be used in specialty memory clinics that have access to experts who can properly interpret the scans than in general family practices.

Longer Half-Life

One of the advantages of the new agent is its versatility. Florbetapir has a half-life of almost 2 hours, compared to a half-life of 20 minutes for the currently available amyloid imaging agent, carbon 11–labeled Pittsburgh compound B (C-PiB).

The discovery of PiB was truly ground-breaking and set the stage for the current series of amyloid tracers now hitting the market, said Dr. DeKosky, who led the clinical trials of PiB.

“PiB was 7 years ahead of all these others,” he said. “We were able to find a way to non-invasively detect amyloid in living people harmlessly, and then several people found a way to develop different compounds. They are all to be congratulated, but the first one is always the one for which there’s romance,” he says wryly.

But because even florbetapir still loses over half of its radioactivity every 2 hours, it must be distributed in a timely fashion from a radiopharmacy to an imaging center. To address this problem, Siemens PETNET Solutions, a subsidiary of Siemens Medical Solutions USA Inc, announced last week a manufacturing and distribution agreement with Eli Lilly.

Beginning in June, Siemens will supply florbetapir to imaging centers in limited US markets. By the end of the year, the company anticipates having 25 manufacturing centers and co-located radiopharmacies offering the compound.

Dr. Apostolova pointed out that to administer florbetapir, a center must also have a PET scanner. In addition to the manufacturing and distribution of florbetapir, Siemens announced its new Biograph mCT PET/CT (computed tomography) scanner, and related software.

Many neurologists said they have faith that the distribution network used by Lilly/Avid will make the agent widely available to clinicians.

“Now we have PET scanners everywhere, which we didn’t have maybe 7 or 8 years ago,” Dr. Black noted. “And now we have an 18-fluorine compound and there are others that should be emerging soon.”

This widening and promising landscape, she said, “is very exciting.”


Women are more vulnerable to infections.

Public-health officials discount role of sex in people’s response to flu and other infections.

Sabra Klein came to the annual meeting of the Society for the Study of Reproduction this week armed with a message that might seem obvious to scientists who obsess over sex: men and women are different. But it is a fact often overlooked by health researchers, says Klein, an immunologist at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland.


Her research on influenza viruses in mice, presented at the meeting in Montreal, Canada, helps explain why women are more susceptible to death and disease from infectious pathogens — and the reason is intimately linked with reproduction. “She’s one of the people that really gets the bigger picture as far as why do we see these patterns,” says Marlene Zuk, an evolutionary biologist at the University of Minnesota, Twin Cities, in St. Paul.

Women generally suffer more severe flu symptoms than men, for example, despite the fact that they tend to have fewer viruses during an infection. To Klein, this suggests that women quickly mount a substantial immune-system attack to clear infections — and suffer the consequences of the inflammatory responses that flood their systems. “This is where females run into trouble,” Klein says.

She and her collaborators have found this disparity in mice infected with flu viruses1. But when the researchers castrated the males and removed the ovaries from the females, the difference disappeared as the males became more sensitive to infection.

But testes are not simply protective. Klein found that giving the neutered females the female sex hormones oestrogen and progesterone actually protected them from disease.

For females, infections appear to throw these cycling sex hormones out of whack. They elongate the oestrus cycle in non-neutered female mice — stretching the part of the cycle associated with the lowest amounts of oestrogen from 4-5 days to 8-9 days.

Researchers have long known that immunological cells have receptors for sex hormones, and that autoimmune disease strikes women more frequently than men. Nevertheless, Klein says that her work should have implications for current public-health practices.

Women, who are often less likely than men to get vaccinated against flu, should be encouraged to do so, she says. And researchers may want to examine whether hormone-replacement therapies and contraceptive drugs have unintended — possibly positive — effects on some types of infectious disease.

But most importantly, Klein says, medical studies should take sex differences into account. Many epidemiological studies do not break down results by sex, a practice that she has found can obscure crucial trends2. And clinical trials have traditionally worked around the female oestrus cycle, because it can interfere with results.

To Zuk, Klein has provided a voice of reason here. “Why is it viewed as interference when you have interaction with the endocrine system or some other aspect of the reproductive system?” she asks.

“The age-old answer we get is that funding is tight and if we’re going to compare sexes, we’ll have to double the groups,” says Klein. But on the basis of her work, she says, “I don’t know that that’s actually true”.

Source Nature


Calcium intake may protect against mortality among women.

Calcium supplements, up to 1,000 mg daily, and increased dietary calcium intake may reduce the risk for mortality among women, according to data from a recent Canadian study. Researchers also studied vitamin D intake but found no evidence of harm or benefit associated with daily doses.

In the Canadian Multicentre Osteoporosis Study, 9,033 men and women were followed for 10 years, during which time 1,160 people died.

Among women, per 500 mg increase in total daily calcium intake, the HR for mortality was 0.95 (95% CI, 0.89-1.01). Additionally, the risk for mortality was lower among women who used calcium supplements vs. those who did not (HR=0.78; 95% CI, 0.66-0.92), although the researchers reported no dose-response effect.

Among men, there were no statistical benefits.

“Our study found daily use of calcium supplements was associated with a lower risk of death among women,” study researcher David Goltzman, MD,professor in the department of medicine at McGill University in Montreal, said in a press release. “Higher amounts of calcium were potentially linked to longer life spans in women, regardless of the source of the calcium.”

Based on their findings, including a lack of evidence that vitamin D intake affects the association between calcium and mortality, Goltzman and colleagues recommend assessing dietary intake to meet calcium and vitamin D needs for bone health and to consider supplements, when necessary, to meet these requirements.

Source: Endocrine today

Is your bottled water polluted with addictive chemicals?


Does your Bottled Water Contain Nicotine?

How about Pharmaceuticals?


Research published last year determined that commercial bottled water in Spain had over 50 pharmaceutically-active chemicals in it, as well as the highly addictive drug nicotine. Is your (or your children’s) bottled water polluted ?

It looks like it very well may be. And we’re not talking about nicotine-supplemented water meant to help wean smokers off of nicotine. We’re talking the kind of bottled water people drink to avoid the pollutants found in municipal drinking water supplies.

Researchers from the School of Public Health, Immunology and Medical Microbiology of Spain’s Rey Juan Carlos University analyzed ten brand of commercially available bottled waters.

The researchers were surprised to learn that the bottled water contained 58 active pharmaceuticals, and five of the ten brands contained significant amounts of nicotine.

The nicotine content of these five brands ranged from 7 nanograms per liter to 15 ng/L. The researchers admitted that these levels were low. However, they added:

Despite the low nicotine concentration measured, the presence of this compound in bottled water still raises concern. Health risk assessment researchers have postulated that the risk to adult healthy humans from oral intake of nicotine at low levels is negligible. However, no studies have been conducted to assess the human health risk of vulnerable populations such as pregnant women and newborns. This population is the target of advertising on the purity and quality characteristics of bottled mineral water.

While this is the first study to document bottled waters containing these chemicals, there are other studies, even newer, confirming identifiable concentrations of nicotine, pharmaceuticals and pesticide chemicals in municipal drinking water.

In the UK for example, the British Geological Survey analyzed and tested ground water and drinking watersupplies and also found nicotine along with caffeine and a variety of pharmaceuticals – such as carbamazepine and triclosan.

And many bottled waters are merely municipal tap water, sometimes run through a filtration unit. However, these filtration systems are typically designed to remove macro-pollutants such as lead and arsenic, but they may not filter out micropollutants such as pharmaceuticals and nicotine.

Studies finding pharmaceuticals in drinking water began to be published in the last decade. These were no fluke, however. And newer studies are confirming a growing problem among the world’s drinking water supplies.

For example, this year research from the Czech Republic’s Department of Water Hygiene at the National Institute of Public Health collected samples from 92 drinking water supplies, feeding half of Czech population.

They found the highest levels of pharmaceuticals to be ibuprofen, carbamazepine, naproxen, and diclofenac. These concentrations ranged from 0.5 to 20.7 nanograms per liter.

Another recent study – from Serbia’s University of Novi Sad Medical School – found trace levels of several antibiotics among their drinking water supplies.

Most municipal water treatment facilities do not filter out pharmaceuticals or other microtoxin metabolites from pesticides and other chemicals. New oxidation-driven systems are being tested, but these are not online in most municipalities. Micro-filtration units are also a possibility.

A study last year from Germany’s Free University Berlin found that the psychoactive drugs primidone and phenobarbital were found in drinking water supplies. Oxazepam and others were found in wastewater streams – likely soon to be in the drinking water supplies.

Another study from Spain – this from the Pharmacy Department of the University of Valencia – found numerous pharmaceuticals among the region’s ground water and drinking water supplies. They found 94% of the sediment and 80% of farming soils were polluted with carbamazepine, acetaminophen and others. They also found much of the drinking water supplies, pharmaceuticals were present at levels as high as 112 nanograms per liter. Soils contained lower concentrations, 15 nanograms per liter.

The researchers also pointed out high levels of fluoroquinolones and ibuprofen are threatening fish and otherwise contaminating the environment.

Meanwhile, last fall Polish researchers found the presence of beta-blockers and beta-agonists among their waterways.

And researchers from Australia’s University of Queensland studied waterways and water supplies close by hospitals. They found 57 different pharmaceuticals among these waterways, including many antibiotics – which entered into the system from hospitals and residential areas alike.

Researchers from the Netherlands found 12 pharmaceuticals in the drinking water supplies, as well as seven transformation products (metabolites that form other toxins).

Swedish researchers tested four waterways in the Montreal, Canada region between 2007 and 2009. They found significant levels of caffeine and a number of pharmaceuticals drugs – including carbamazepine, naproxen, gemfibrozil, and trimethoprim. They also found progesterone, estrone, and estradiol, along with the herbicide triazine – with atrazine, deethylatrazine, deisopropylatrazine, simazine, and cyanazine.

Researchers from the U.S. Geological Survey’s California Water Science Center analyzed ground water supplies that feed numerous drinking water systems throughout California. They found pharmaceuticals affecting two to three percent of the 1231 ground water systems tested. However, in this study only 14 pharmaceutical compounds were tested for, out of hundreds possible. And out of these 14 tested, seven were found in concentrations that were equal or greater to detection limits. These seven included acetaminophen, caffeine, carbamazepine, the highly addictive codeine, the caffeine metabolite p-xanthine, and the antibiotics sulfamethoxazole and trimethoprim. The samples also contained various pesticides, VOCs (volatile organic compounds) and others.

The research found that ground water supplies in the Los Angeles area were much more likely to contain pharmaceuticals, and contain higher levels of them.

It should be noted that several brands of commercial bottled waters (and many other foods and beverages containing water) are packaged in the Los Angeles area.