37 MILLION BEES FOUND DEAD In Ontario, Canada After Large GMO Corn Field Planted

Dead Bee

Local Ontario farmer, Nathan Carey, reported that this spring there were not enough bees on his farm. He believes, as do many others, that there is a strong correlation between the disappearance of bees and the use of insecticides. For the last seven consecutive years, honeybees have been in decline, something scientists have coined, “colony collapse disorder” (CCD).

GMO Corn Field Kills 37 Million Bees in Ontario

If the global honeybee population were to collapse, we would be in serious trouble. It’s estimated that one-third of everything we eat depends on honeybee pollination- that means bees contribute over 30 billion to the global economy. And for some things like almonds, bees do 100% of the work. No more bees equals no more almonds.

From the article:

“A new study published in the Journal Proceedings of the National Academy of Sciences revealed that neonicotinoid pesticides kill honeybees by damaging their immune system and making them unable to fight diseases and bacteria.”

And we can see that the pesticides linger; scientists have found 121 different pesticides in samples of bees, wax, and pollen. “We believe that some subtle interactions between nutrition, pesticide exposure, and other stressors are converging to kill colonies,” said Jeffery Pettis, of ARS’s bee research laboratory.

And why are the pesticides in bees, wax, and pollen? Because two of the best-selling pesticides, Imidacloprid and Clothianidin (by Bayer), are known to get into pollen and nectar. In fact, while these drugs were being marketed in Europe and the US, there were large-scale bee deaths in those places.

Thankfully, after large bee losses were reported- after exposure to Imidacloprid- it was banned for use on corn and sunflowers (as you can imagine Bayer protested this decision). And France rejected Bayer’s application for Clothianidin.

While we are happy for the common sense approach to bee and public health in Europe, it’s time that starts happening here.

Watch the video. URL:https://youtu.be/WnrpTHNPjaU

More Falls for Those Starting Newer Antipsychotics

Falls, fractures up 50% in patients with new prescriptions for atypical antipsychotics.

Receiving a new prescription for an atypical antipsychotic medicine was associated with more serious falls and more fractures in a new retrospective cohort study.

Adults ages 65 and older who received a new prescription had a 53% increased risk of falling and a 50% increased risk of nonvertebral osteoporotic fracture, found the study. It was published as a research letter in JAMA Internal Medicine on Jan. 13, 2015, and was led by Lisa-Ann Fraser, MD, from the University of Western Ontario in Canada.

“These findings call into question the widespread off-label use of atypical antipsychotic medications and support increasing evidence of safety concerns regarding their use in older adults,” Fraser and colleagues wrote.

In the retrospective study of 200,000 residents of Ontario, whose medical records are kept in a central database, those who received a new prescription for one of three atypical antipsychotics — quetiapine (Seroquel), risperidone (Risperdal), or olanzapine (Zyprexa) — from 2003 to 2011 were matched 1:1 with other Ontario residents who didn’t receive such a prescription. Controls were matched to cases for fracture risk factors. Medical encounters over the following 90 days were analyzed for fracture and fall outcomes.

Starting atypical antipsychotics was associated with increased rates of hip fracture (odds ratio 1.67, 95% CI 1.53-1.81), nonvertebral osteoporotic fracture (OR 1.51, 95% CI 1.41-1.60), and falls (OR 1.54 95% CI 1.47-1.61). The risk of fracture and falling wasn’t related to the type of atypical medication used, the dosage, or whether the individual lived in a long-term care facility.

The raw data indicated that 7.0% of those receiving antipsychotic prescriptions experienced fractures versus 5.5% of the controls. Similarly, falls occurred in 4.4% of the antipsychotic recipients compared with 2.9% of controls.

Antipsychotic medications have been found to be associated with fracture risk in some previous studies, although the strength and nature of the link has been debated.

“Atypical antipsychotic medications have been found previously to be associated with hypotension, sedation, and gait abnormalities; therefore, it is possible that falls are the mechanism by which these drugs increase fracture risk,” researchers wrote.

The authors noted limitations to the study. It was retrospective, observational, and based on administrative records; there may also have been unmeasured confounding factors. Also, the analysis did not examine use of first-generation antipsychotic drugs.

Even a Little Physical Activity May Prevent Depression.

Even low levels of physical activity may reduce the risk of developing depression in individuals of all ages, new research suggests.

In 25 of 30 large studies examined in the systematic review, which included participants between the ages of 11 and 100 years, a “negative risk” was found between baseline physical activity (PA) and the future development of depression.

In addition, this inverse association was found in all levels of PA ― including less than 2.5 hours of walking per week.

“It was a little surprising that 25 of the studies found this protective effect, and that’s really promising,” lead author George Mammen, PhD candidate from the Faculty of Kinesiology and Physical Education Department at the University of Toronto in Ontario, Canada, told Medscape Medical News.

“We also did quality assessments on each study, and the majority were of high methodologic quality, which adds weight to the findings,” said Mammen.

He noted that the take-home message is that being active is important for more than just physical health.

“From a population health perspective, promoting PA may serve as a valuable mental health…strategy in reducing the risk of developing depression,” write the investigators.

The study was published in the November issue of the American Journal of Preventive Medicine.

Prevention Strategy Needed

Previous studies have shown a link between exercise and decreasing symptoms in patients with depression,including several reported by Medscape Medical News.

“However, with the high prevalence of depression worldwide and its burden on well-being and the healthcare system, intuitively, it would make more sense…to shift focus toward preventing the onset of depression,” the investigators write.

We need a prevention strategy now more than ever. Our health system is taxed. We need to…look for ways to fend off depression from the start,” added Mammen in a release.

After searching 6 of the top databases, including MEDLINE and PubMed, the researchers found 6263 worldwide citations of PA and depression. For this analysis, they selected 30 English-language studies that were published between January 1976 and December 2012.

All were prospective, longitudinal, and “examined relationships between PA and depression over at least two time intervals.” They had follow-up periods ranging from 1 to 27 years.

Results showed that 25 of the studies revealed a significant inverse effect between any PA reported at baseline and subsequent depression development.

Interestingly, 4 of these studies showed that women who reported baseline PA were less likely than men to develop depression.

“These studies postulate that psychological factors may explain these findings because women may benefit more from the social aspects of PA than men,” note the investigators.

Of the 5 studies that did not find a significant association between PA and depression, “only 1 was considered to be of high quality,” and 2 focused only on older adults.

Get Moving

Using data from the 7 studies that measured amounts of weekly PA participation, the researchers found that exercising more than 150 minutes per week was associated with a 19% to 27% decreased risk of developing depression.

Surprisingly, participating in less than 150 minutes per week of PA was associated with a 8% to 63% decreased depression risk compared with individuals who were sedentary. Still, the 63% decreased risk was found in one study of patients participating in 120 minutes of weekly PA.

37 Million Bees Found Dead In Ontario.

It was just a few weeks ago that 50,000 bees were found dead in an Oregon parking lot, and now the ongoing problem has hit north of the border in Ontario, Canada where more than 37 million bees have been found dead. 

In the past, many scientists have struggled to find the exact cause of the massive die-offs, a phenomenon they refer to as “colony collapse disorder” (CCD). In the United States, for seven consecutive years, honeybees are in terminal decline.The problem has brought beekeepers to crisis in an industry responsible for producing apples, broccoli, watermelon, onions, cherries and a hundred other fruits and vegetables. Commercial honeybee operations pollinate crops that make up one out of every three bites of food on our tables. 

37 Million Bees Found Dead In Ontario

According to the annual survey by the Apiary Inspectors of America and the US government’s Agricultural Research Service (ARS), The number of managed honeybee colonies has fallen by over 30%.US scientists have found 121 different pesticides in samples of bees, wax and pollen, lending credence to the notion that pesticides are a key problem. “We believe that some subtle interactions between nutrition, pesticide exposure and other stressors are converging to kill colonies,” said Jeffery Pettis, of the ARS’s bee research laboratory.The collapse in the global honeybee population is a major threat to crops. It is estimated that a third of everything we eat depends upon honeybee pollination, which means that bees contribute over 30 billion to the global economy. 37 Million Bees Dead in Ontario Dave Schuit, who runs a honey operation in Elmwood, Ontario says he’s lost more than 600 hives — that’s more than 37 million bees — in 2012 alone. Schuit says he’s been seeing his bees die at a rapid rate every spring in the last few years. “This is how they die,” Schuit explained to The Toronto Star, pointing with a broad hand to a bee that’s gone haywire, flailing erratically in the grass. “Their tongue sticks out and the venom drips out their backside.” According to the 48-year-old apiarist, neonicotinoid pesticides are to blame for the loss. The Collective Evolution finds that the deaths occur after the pesticide dust is blown into the air (used to coat corn seed with air seeders). A study from the Proceedings of the National Academy of Sciences (PNAS) shows that the causes of CCD may be more varied than scientists expect. The bees may be dying not from a single toxin or disease but rather from an assault directed by a collection of pathogens. A research team led by entomologist May Berenbaum at the University of Illinois compared the whole genome of honeybees that came from hives that had suffered from CCD with hives that were healthy. The sick bees exhibited genetic damage that could account for the die-off, and that damage indicated that they might be afflicted with multiple viruses simultaneously. This could weaken them enough to trigger CCD. “It’s like a perfect storm,” says Berenbaum. Health Canada’s Pest Management Regulatory Industry began taking samples from dead bees in Ontario and Quebec. Schuit’s bee’s were a part of that study and now the agency is now “re-evaluating” the pesticides status while analyzing more samples this year. Bayer Pesticides Long Implicated in Colony Collapse Disorder Two of Bayer’s best-selling pesticides, Imidacloprid and Clothianidin, are known to get into pollen and nectar, and can damage beneficial insects such as bees. The marketing of these drugs also coincided with the occurrence of large-scale bee deaths in many European countries and the United States.

The non-profit group NRDC filed a lawsuit in August 2008 to force the U.S. government to release the studies it ordered on the effect of clothianidin on honeybees. NRDC attorneys believed the EPA already had evidence of a link between pesticides and the mass honeybee die-offs, yet was not making the information public. NRDC is now being allowed to look through the studies. There is some information already publicly available, though, and that’s the EPA’s fact sheet on clothianidin. It says right there in black and white that: “Clothianidin has the potential for toxic chronic exposure to honey bees, as well as other nontarget pollinators, through the translocation of clothianidin residues in nectar and pollen…In honey bees, the effects of this toxic chronic exposure may include lethal and/or sub-lethal effects in the larvae and reproductive effects on the queen.”

Unfortunately, the EPA approved neonicotinoid pesticides on the basis that the amounts found in pollen and nectar are not enough to kill bees. This says nothing of their potential to impact the bees on a non-lethal level, and, in fact, studies have shown that the substances can impair bees’ learning and memory even at low doses. France, meanwhile, after reporting large losses of bees after exposure to Imidacloprid, banned it for use on corn and sunflowers, despite protests by Bayer. In another smart move, France also rejected Bayer’s application for Clothianidin, and other countries, such as Italy, have banned certain neonicotinoids as well. After record-breaking honeybee deaths in the UK, the European Union has banned multiple pesticides, including neonicotinoid pesticides. Sources: thestar.com – mercola.com – guardian.co.uk 

What Will It Take to Wipe Out Superbugs?


Superbugs are making public health experts very nervous. Image courtesy of the Centers for Disease Control.

We have a drug problem.

Only this time we need drugs, specifically antibiotics. The problem is that more germs are becoming resistant to the antibiotics doctors have been using for a long time, resulting in “superbugs” from which even the National Institutes of Health couldn’t protect itself.

One reason, as the Centers for Disease Control (CDC) warned yet again in a report last month, is that doctors continue to be overzealous in prescribing antibiotics. Case in point: A new study at Brigham and Women’s Hospital in Boston found that doctors prescribed antibiotics in 60 percent of the cases where people came in complaining of sore throats—this despite the fact that only 10 percent of those patients had strep throat, the only sore throat antibiotics can cure.

On top of that, Big Agriculture aggressively uses antibiotics both to keep healthy animals from getting sick and to help them grow faster. And while all this excessive use of antibiotics is making them less and less effective, the pharmaceutical industry has dramatically scaled back research into new infection-fighting drugs because it’s not a very profitable line of business.

Some public health experts fear that unless scientists are able to develop new antibiotics soon, we could regress into pre-penicillin days, when everyday infections killed people. Even the CDC, which points out that more than 23,000 people in America die from infections caused by resistant bacteria every year, says we could be facing “potentially catastrophic consequences.”

Turning drugs off

There’s the conventional strategy to dealing with the threat—earlier this year the U.S. Department of Health and Human Services committed to pay the pharmaceutical firm GlaxoSmithKline as much as $200 million over the next five years to try to develop new antibiotics.

But more innovative approaches are also taking shape. Consider the research of a team of scientists in the Netherlands. They’re focusing on a way to deactivate antibiotics after they’ve been used, so that they no longer accumulate in the environment, which is what spurs the development of resistant superbugs. They’ve determined that if the molecules in antibiotics can be made to change their shape, they become ineffective. And the researchers have found they can use heat or light to do just that. In short, they’re developing ways to turn off antibiotics before they break bad.

Or take the researchers at McMaster University in Ontario who argue that the typical practice of growing bacteria in a nutrient-rich lab environment doesn’t really reflect what happens when we get an infection. Our bodies can be far less hospitable than that, forcing bacteria to grow their own nutrients. The researchers did an exhaustive search of 30,000 chemical compounds, with the goal of identifying some that block the ability of bacteria to create nutrients. They honed in on three. But they feel pretty good about those three. Now the trick is to see if they can be turned into effective antibiotics.

As one scientist put it, the McMaster researchers went “fishing in a new pond.” With luck, that might be what it takes.

Germ warfare

Here’s more recent research on the battle against bacteria:

  • That inner glow: It’s not unusual for bacteria to attach themselves to medical implants, such as bone screws, and develop into serious infections before anyone notices. A team of researchers in the Netherlands, however, may have developed an early warning system. By injecting fluorescent dye into an antibiotic, they were able to see where bacteria was growing. The process could lead to a far less invasive way to check for infections with surgery involving implants.
  • Thinking small: Scientists at Oregon State are taking yet another approach to attacking bacteria—they’ve narrowed their targeting down to the gene level. That’s seen as a much more precise way to battle infections, one that’s less likely to cause collateral damage. Said lead researcher Bruce Geller: “Molecular medicine is the way of the future.”
  • Say no to drugs: At Duke University, scientists say they’ve developed a blood test that can identify viral infections in people with serious respiratory problems. The test, they say, could significantly reduce the overuse of antibiotics. Since it can be hard to distinguish between viral sore throats, such as those that come with a cold, and bacterial infections, such as strep throat, a lot of doctors still prescribe antibiotics that end up not doing any good. The blood test could take the guessing—and pointless antibiotics—out of the treatment.
  • Now will you eat your yogurt?: It figures that one way to fight the bad side effects of some antibiotics would be by loading up on probiotics. Research published earlier this year found that probiotic supplements reduced the risk of antibiotic-related diarrhea by 64 percent.
  • All this and super lice, too?: Public health officials in the U.S. have told doctors to be on the lookout for a new strain of “super lice” that have become immune to shampoos and medications containing antibiotics.
  • Then again, they are termites: According to scientists at the University of Florida, the reason termites are so disease-resistant is that they use their own feces in building their nests. That promotes the growth of bacteria, which stifles pathogens. The researchers said that their findings could eventually result in new antibiotics for humans, but it might be better if they spare us the details.

Women’s intentions to breastfeed: a population-based cohort study.


Given that intention to breastfeed is a strong predictor of breastfeeding initiation and duration, the objectives of this study were to estimate the population-based prevalence and the factors associated with the intention to breastfeed.


Retrospective population-based cohort study.


All hospitals in Ontario, Canada (1 April 2009–31 March 2010).


Women who gave birth to live, term, singletons/twins.


Patient, healthcare provider, and hospital factors that may be associated with intention to breastfeed were analysed using univariable and multivariable regression.

Main outcome measures

Population-based prevalence of intention to breastfeed and its associated factors.


The study included 92 364 women, of whom 78 806 (85.3%) intended to breastfeed. The odds of intending to breastfeed were higher amongst older women with no health problems and women who were cared for exclusively by midwives (adjusted OR 3.64, 95% CI 3.13–4.23). Being pregnant with twins (adjusted OR 0.73, 95% CI 0.57–0.94), not attending antenatal classes (adjusted OR 0.58, 95% CI 0.54–0.62), having previous term or preterm births (adjusted OR 0.79, 95% CI 0.78–0.81, and adjusted OR 0.87, 95% CI 0.82–0.93, respectively), and delivering in a level–1 hospital (adjusted OR 0.85, 95% CI 0.77–0.93) were associated with a lower intention to breastfeed.


In this population-based study ~85% of women intended to breastfeed their babies. Key factors that are associated with the intention to breastfeed were identified, which can now be targeted for intervention programmes aimed at increasing the prevalence of breastfeeding and improving overall child and maternal health.


Should We Set a Higher Bar for Coronary Angiography?

Compared with Ontario, obstructive disease is less common in patients who undergo catheterization in New York.

A recent study indicated that more cardiac catheterizations are performed per capita in New York State than in Ontario, Canada). Now, the same investigators have compared the prevalence of obstructive coronary artery disease (CAD) — defined as diameter stenosis ≥50% in the left main or ≥70% in a major epicardial vessel — in patients undergoing the procedure in the two regions.

Obstructive CAD was found in significantly more of approximately 55,000 patients undergoing a first elective cardiac catheterization during 2008–2011 in Ontario than in some 18,000 such patients in New York (45% and 30%, respectively). Compared with the Canadian patients, the New Yorkers were younger and more likely to be women or to have no or atypical symptoms; the prevalence of several other risk factors also differed significantly between the two groups. Fewer patients in New York than in Ontario had noninvasive evaluations (63% vs. 75%, P<0.001), and the predicted preprocedure probability of obstructive CAD was significantly lower in New York.

Among patients with obstructive CAD, those in New York were significantly more likely than those in Ontario to undergo revascularization (percutaneous coronary intervention, 55% vs. 35%; coronary artery bypass grafting, 20% vs. 14%). Higher crude 30-day mortality in New York than in Ontario was mainly attributable to higher mortality in patients without obstructive CAD.


These findings suggest that the relatively high cardiac catheterization rate in New York results primarily from selecting patients at lower predicted probabilities of obstructive coronary artery disease. The investigators could not control for regional differences in patient, societal, and physician characteristics, preferences, and expectations; nor could they assess which catheterization rate is more appropriate. Nonetheless, the higher prevalence of interventionalists and cardiac invasive capabilities — as well as market-oriented financing — in New York seems likely to account for much, if not all, of the disparity; if so, these data illuminate an opportunity to reduce unnecessary healthcare expenditures.

Source: NEJM

Risk of incident diabetes among patients treated with statins: population based study.


Objective To examine the risk of new onset diabetes among patients treated with different HMG-CoA reductase inhibitors (statins).

Design Population based cohort study with time to event analyses to estimate the relation between use of particular statins and incident diabetes. Hazard ratios were calculated to determine the effect of dose and type of statin on the risk of incident diabetes.

Setting Ontario, Canada.

Participants All patients aged 66 or older without diabetes who started treatment with statins from 1 August 1997 to 31 March 2010. The analysis was restricted to new users who had not been prescribed a statin in at least the preceding year. Patients with established diabetes before the start of treatment were excluded.

Interventions Treatment with statins.

Main outcome measure Incident diabetes.

Results Compared with pravastatin (the reference drug in all analyses), there was an increased risk of incident diabetes with atorvastatin (adjusted hazard ratio 1.22, 95% confidence interval 1.15 to 1.29), rosuvastatin (1.18, 1.10 to 1.26), and simvastatin (1.10, 1.04 to 1.17). There was no significantly increased risk among people who received fluvastatin (0.95, 0.81 to 1.11) or lovastatin (0.99, 0.86 to 1.14). The absolute risk for incident diabetes was about 31 and 34 events per 1000 person years for atorvastatin and rosuvastatin, respectively. There was a slightly lower absolute risk with simvastatin (26 outcomes per 1000 person years) compared with pravastatin (23 outcomes per 1000 person years). Our findings were consistent regardless of whether statins were used for primary or secondary prevention of cardiovascular disease. Although similar results were observed when statins were grouped by potency, the risk of incident diabetes associated with use of rosuvastatin became non-significant (adjusted hazard ratio 1.01, 0.94 to 1.09) when dose was taken into account.

Conclusions Compared with pravastatin, treatment with higher potency statins, especially atorvastatin and simvastatin, might be associated with an increased risk of new onset diabetes.


In this population based study, we found that patients treated with atorvastatin, rosuvastatin, or simvastatin were at increased risk of new onset diabetes compared with those treated with pravastatin. No such risk was evident with fluvastatin or lovastatin. The risk associated with rosuvastatin could depend on dose and duration of treatment. The risk of incident diabetes was similar whether statins were being used for primary or secondary prevention.

Overall, we observed a 10-22% increased risk of diabetes for some statins that is consistent with findings from previously published meta-analyses of clinical trials. The increased risk with rosuvastatin significantly decreased after covariate adjustment and became non-significant once dose was taken into consideration. This could possibly represent greater use of rosuvastatin in patients with lower cardiovascular risk.3 In 2009, an analysis of five placebo controlled trials (n=57 593) found a 13% (relative risk 1.13, 95% confidence interval 1.03 to 1.23) increased incidence of diabetes in people taking statins compared with placebo over an average 3.9 years of follow-up,9 with a subsequent analysis of 13 placebo controlled trials (n=91 140) showing a 9% (odds ratio 1.09, 95% confidence interval 1.02 to 1.17) increased incidence of diabetes over four years of follow-up.10 More recently, two meta-analyses have suggested a dose dependent effect for patients receiving high dose atorvastatin or simvastatin treatment versus moderate dose treatment (odds ratio 1.12, 95% confidence interval 1.04 to 1.22) and when considering only atorvastatin trials.11 12 Our results differ from those of the Women’s Health Initiative study, which showed a nearly 50% increase in new onset diabetes with statins compared with placebo (hazard ratio 1.48, 95% confidence interval 1.38 to 1.59), with no differential risk among low potency (fluvastatin, lovastatin, pravastatin) and high potency (simvastatin, atorvastatin) statins.14 Our findings, however, are consistent with the findings of Zaharan and colleagues in 2012, who found an increased risk with atorvastatin (hazard ratio 1.25, 1.21 to 1.28), rosuvastatin (1.42, 1.33 to 1.52), and simvastatin (1.14, 1.06 to 1.23).30 Our population based assessment adds to the discussion of risk when doctors are considering starting statin treatment in a patient for primary versus secondary prevention.

Possible mechanisms

Several factors could explain the increased risk of new onset diabetes among patients receiving certain statins.2 7 15 The increased production of plasma derived low density lipoprotein (LDL) cholesterol as a compensatory response to de novo cholesterol synthesis inhibition might result in direct inflammation and oxidation within the β cell. Consequently, the functional and structural integrity of β cells is compromized, impairing insulin secretion as a result of cellular apoptosis.15Additionally, metabolic receptor effects interfere with cellular glucose uptake, energy production, and insulin secretion.2 7 15 16 Statins can also inhibit calcium mediated pancreatic insulin release and decrease expression of the β cell glucose transporters GLUT-2 and GLUT-4.15 Finally, statins are also known to interfere with the synthesis of ubiquinone (CoQ10), which could independently alter insulin secretion.15 16 The degree to which statins are involved in these respective mechanisms of diabetes onset is variable and supports why some statins pose a higher risk than pravastatin.7 As shown in our dose and potency analyses, the risk could be greater for atorvastatin and simvastatin, regardless of the dose prescribed.

Limitations and strengths

Some limitations of our study merit emphasis. We could not identify and account for potentially important risk factors for diabetes such as weight, ethnicity, and family history. Newer statins might be preferentially used in patients at higher risk of diabetes, though the characteristics of patients in our study were highly similar across study groups. Secondly, data on blood lipids, hemoglobin A1C concentration, or triglyceride concentrations were unavailable, and therefore we could not use these measures for risk stratification or diagnostic purposes. The ODD, however, has been shown to be both sensitive (86-90%) and specific (92-97%).19 Furthermore, we had no data on marketing or promotional efforts nor did we have data on physicians’ preferences for particular statins. Although the statin groups were well balanced with respect to a wide variety of demographic and clinical variables, we cannot exclude the possibility of residual confounding.

Our study also had several strengths including a large sample size, use of pravastatin as an active comparator reference group, and a population based design. Our findings suggest that older patients treated with certain statins are at increased risk for incident diabetes, regardless of dose or whether treatment is used for primary or secondary prevention. The risk seems to be greatest with atorvastatin, rosuvastatin, and simvastatin. After adjustment for dose, however, the risk did not seem to persist among rosuvastatin users. Clinicians should consider this risk when they are contemplating statin treatment for individual patients. Preferential use of pravastatin, and potentially fluvastatin or lovastatin, while recognizing the limited efficacy data and increased risk of drug interactions with these two agents, might be warranted. Pravastatin might have a preferential benefit among primary prevention patients at high risk of diabetes.

What is already known on this topic

  • Given the widespread use of statins to manage hypercholesterolemia, small effects in their efficacy and safety profiles can have important population impact.
  • Statins have previously been associated with an increased risk of incident diabetes, though there is controversy around whether this risk differs among drugs
  • When compared with pravastatin, atorvastatin, rosuvastatin, and simvastatin are associated with a greater risk of new onset diabetes, regardless of their use for primary or secondary prevention of cardiovascular events
  • The risk for rosuvastatin users might depend on the dose prescribed

What this study adds



Source: BMJ


2.6 Billion-Year-Old Water Found in Deep Mine.


One and a half miles beneath the surface of Earth in a Canadian mine, researchers have found pockets of water in rocks that have been isolated from the surface for some two billion years.

The chemistry of the water could support life, the team reports today in the journal Nature — a tantalizing discovery that raises the possibility that life-supporting water might also lie in similar kinds of rocks deep beneath the surface of Mars.

Because the water was trapped at a time when Earth was very different than it is today, the new findings also lend insight into the evolution of the early atmosphere and the habitability of the deep Earth. Until now, the oldest known reservoirs of underground water dated back just tens of millions of years.

“For the first time, we found that waters of this age can be preserved on our planet,” said Barbara Sherwood Lollar, an isotope geochemist at the University of Toronto. “Really, it’s a whole new world, a whole new hydrosphere on our planet. We didn’t know it was possible to trap this amount of fluid and gas for this kind of time scale.”

Miners have long known that water sometimes flows out of fractures in rocks deep underground, Sherwood Lollar said. As scientists have more recently become interested in the phenomenon, they have discovered that these fluids are often very salty, with salinity levels 10 times higher than seawater.

Deep isolated waters also contain large amounts of dissolved hydrogen, making it possible that they might sustain microorganisms like the ones that live around hydrothermal vents. In 2006, in fact, Sherwood Lollar and colleagues found a community of microbes living deep below South Africa in isolated waters that were tens of millions of years old.

“I refer to hydrogen as the jelly donuts of the microbe world,” Sherwood Lollar said. “If it’s there, they want to eat it.”

For the new study, the researchers lowered a tube-shaped device into pre-drilled boreholes in a mine in Ontario. Water flowed through the device, which separated the gas from the fluid and collected both.

In laboratories in Canada and the United Kingdom, scientists then measured levels of hydrogen, carbon, nitrogen and other stable elements as well as noble gasses such as helium, xenon and krypton. Knowing how quickly chemical reactions proceed over time between rocks and water, the team could then use the levels of those components to determine how long the fluid had been trapped in the deep crust.

Results showed that the water was between one billion and 2.6 billion years old — orders of magnitude older than the South African samples.

The water dates back to a time before the Great Oxygenation Event that filled Earth’s atmosphere with oxygen, making it possible for higher life forms to evolve, said planetary scientist Michael Mumma, director of the Goddard Center for Astrobiology at the NASA Goddard Space Flight Center.

Now, the search is on for signs of life in the ancient Canadian waters. If microbes turn up there and they are as old as the water is, the discovery could offer new places to look for life on Mars, which has rocks of similar age to those looked at in the new study.

“I think this is quite a profound finding,” Mumma said. “In a similar environment, a tectonically quiet environment on Mars, such reservoirs of these trapped gasses could in fact host a population of microbes of similar nature. And we could still find evidence that they were there at one time or in fact still do exist.”

Source: Discovery channel

Chest Pain: What Happens After the Emergency Department?

Patients who follow up with cardiologists do best.


Researchers examined patterns of follow-up care and outcomes in high-risk patients with chest pain who presented to Ontario emergency departments (EDs) from 2004 to 2010. High risk was defined as having a prior diagnosis of cardiovascular disease, diabetes, or both. The primary outcome was a composite of all-cause death and hospitalization for myocardial infarction within 1 year after the index visit.

Of nearly 57,000 patients, 17% followed up with a cardiologist (with or without a visit to primary care) within 30 days after ED discharge, 57% followed up with a primary care practitioner only, and 25% did not have a visit to a physician recorded. After adjustment for clinical, demographic, and hospital characteristics, the cardiologist group had a significantly lower hazard ratio for the composite outcome (HR, 0.79; P<0.001) than the no–follow-up group and the PCP-only group (HR, 0.85; P<0.001). PCP-only follow-up was significantly beneficial compared to no follow-up (HR, 0.93; P<0.023). Patients seen by cardiologists underwent more testing and received more evidence-based therapies within 100 days after discharge.

Comment: These robust results demonstrate that what happens after the emergency department visit is as important as what happens during the ED visit, and that postdischarge care for patients with high-risk chest pain should include timely assessment by a cardiologist.


Source: Journal Watch Emergency Medicine