Google Buys a Quantum Computer.



and a corporation associated with NASA are forming a laboratory to study artificial intelligence by means of computers that use the unusual properties of quantum physics. Their quantum computer, which performs complex calculations thousands of times faster than existing supercomputers, is expected to be in active use in the third quarter of this year.

The Quantum Artificial Intelligence Lab, as the entity is called, will focus on machine learning, which is the way computers take note of patterns of information to improve their outputs. Personalized Internet search and predictions of traffic congestion based on GPS data are examples of machine learning. The field is particularly important for things like facial or voice recognition, biological behavior, or the management of very large and complex systems.

“If we want to create effective environmental policies, we need better models of what’s happening to our climate,” Google said in a blog postannouncing the partnership. “Classical computers aren’t well suited to these types of creative problems.”

Google said it had already devised machine-learning algorithms that work inside the quantum computer, which is made by D-Wave Systems of Burnaby, British Columbia. One could quickly recognize information, saving power on mobile devices, while another was successful at sorting out bad or mislabeled data. The most effective methods for using quantum computation, Google said, involved combining the advanced machines with its clouds of traditional computers.

Google bought the machine in cooperation with the Universities Space Research Association, a nonprofit research corporation that works with NASA and others to advance space science and technology. Outside researchers will be invited to the lab as well.

This year D-Wave sold its first commercial quantum computer to Lockheed Martin. Lockheed officials said the computer would be used for the test and measurement of things like jet aircraft designs, or the reliability of satellite systems.

The D-Wave computer works by framing complex problems in terms of optimal outcomes. The classic example of this type of problem is figuring out the most efficient way a traveling salesman can visit 10 customers, but real-world problems now include hundreds of such variables and contingencies. D-Wave’s machine frames the problem in terms of energy states, and uses quantum physics to rapidly determine an outcome that satisfies the variables with the least use of energy.

In tests last September, an independent researcher found that for some types of problems the quantum computer was 3,600 times faster than traditional supercomputers. According to a D-Wave official, the machine performed even better in Google’s tests, which involved 500 variables with different constraints.

“The tougher, more complex ones had better performance,” said Colin Williams, D-Wave’s director of business development. “For most problems, it was 11,000 times faster, but in the more difficult 50 percent, it was 33,000 times faster. In the top 25 percent, it was 50,000 times faster.” Google declined to comment, aside from the blog post.

The machine Google will use at NASA’s Ames Research facility, located near Google headquarters, makes use of the interactions of 512 quantum bits, or qubits, to determine optimization. They plan to upgrade the machine to 2,048 qubits when this becomes available, probably within the next year or two. That machine could be exponentially more powerful.

Google did not say how it might deploy a quantum computer into its existing global network of computer-intensive data centers, which are among the world’s largest. D-Wave, however, intends eventually for its quantum machine to hook into cloud computing systems, doing the exceptionally hard problems that can then be finished off by regular servers.

Potential applications include finance, health care, and national security, said Vern Brownell, D-Wave’s chief executive. “The long-term vision is the quantum cloud, with a few high-end systems in the back end,” he said. “You could use it to train an algorithm that goes into a phone, or do lots of simulations for a financial institution.”

Mr. Brownell, who founded a computer server company, was also the chief technical officer at Goldman Sachs. Goldman is an investor in D-Wave, with Jeff Bezos, the founder of Amazon Web Services is another global cloud, which rents data storage, computing, and applications to thousands of companies.

This month D-Wave established an American company, considered necessary for certain types of sales of national security technology to the United States government.

Source: NY times




Well, it seems to have happened again. A small vial of a potentially deadly strain known as the Guanarito virus has went missing from the University of Texas Medical Branch in Galveston. It is not known how long the vial has been unaccounted for so it is anyone’s guess as to where it is and what has been done with it.

The virus was discovered missing when an unidentified “official” noticed that one out of five vials was missing, even though they are “locked” in a bio-hazard freezer. As soon as it was noticed the CDC (Centers for Disease Control and Prevention) was notified of the risk. It has been a week since it has been reported and we have heard very little about this potential hazard, in fact it was hardly reported at all despite the curious circumstances behind the incident. Why would a vial of a potentially dangerous virus be missing from a U.S laboratory and who would want something so hazardous in their possession?

The Guanarito virus is part of a family of diseases that were discovered to have caused several deadly outbreaks in Venezuela and the government has made it a priority to study it, hence why the virus was apparently locked inside of a Texas University bio-hazard freezer in the first place. The reason the government has prioritized this virus to be studied is because “it can potentially be used by terrorists in a contagion attack”. Therfore, reports of this virus being “potentially” dangerous is likely because if the individual or organization that possesses the vial has ill intentions it can be used to cause an outbreak on a targeted population. It would not be hard for an insider of any given enemy government to enroll in a class at a University to have access and obtain deadly viruses to use on the American population. If this were to happen, it is unknown how severe the consequences could be which is why these “deadly” strains should be studied in more secure locations, and not on University campuses. This would significantly decrease the risk of something like this happening. In fact, “deadly” viruses should never be at a school in the first place, as it should be high level graduates that have access to these materials as opposed to people who are not even in the field yet. This is just one example of how to avoid risks like this from occurring in the future.

UTMB director Scott Weaver said that “Guanarito has been responsible for causing deadly diseases within the South American country (Venezuela)”. The symptoms of the missing virus (aside from death, as it has been classed as “deadly”), is a severe hemorrhagic fever which could lead to death. Essentially, your brain starts to bleed which can lead to death if not treated and since it is still being studied as a priority it is unknown if there is a cure for this virus. If you have ever watched the movie “Outbreak”, it has a similar plot to this real life event as a virus is released on the public that causes the exact symptom, “hemorrhagic fever”. It was also showing on television around the time the vial was reported to be missing. Coincidence?

The UTMB said that there was no security breach or break-in at the Texas facility, nor did they “believe” there was evidence of foul play and that the vial “could have” simply been broken during the labs cleaning process, all answers indicating they are clearly unsure of what exactly happened.

It is not clear if we will ever find out the answers as to where it could have ended up however the government wanted it studied due to it’s potential for being used by terrorists and this is a huge red flag for anyone who has followed the course of history even the slightest. Lyme disease was also released from a U.S laboratory (Plum Island) and was developed by a Nazi scientist who escaped persecution in a CIA plot called Project Paperclip, and was rewarded a new life in America to work on bio-hazard studies. He is now known for introducing Lyme disease on the population of the world as it escaped the laboratory in a similar unknown breach as the recent incident in Texas.

Worth noting is that in December of 2012, an unknown epidemic hazard was announced in Northern Ontario in a report by the Family Survival Protocol. This report stated:

“A woman was found dead on a Via Rail passenger train early Saturday morning. The company says the Vancouver-to-Toronto train stopped near Parry Sound, Ont., because four passengers were showing flu-like symptoms. Emergency crews boarded the train and confirmed that a woman who Via Rail described in a news release as elderly had died. The other three passengers were taken to hospital for treatment, according to the news release. The train was about six hours late getting to Toronto, according to the release. The train had left Vancouver on Christmas Day night. Via said a quarantine was placed on the two rooms the passengers were in, which is part of their standard procedures. It’s not believed anyone else was in those compartments, which will be sterilized. Health officials say it’s not believed that other passengers or the train’s crew were exposed to those taken off the train, which had 200 passengers and 13 crew members on board. The local coroner was trying to determine the cause of death and the Ontario Provincial Police say the woman’s identity was being withheld until all family members were notified.”

Similarly, in more recent reports (March 2013) it was claimed that a deadly new “Coronavirus” has been spreading throughout the Asia and Europe and has claimed lives in the Middle East, China, and has since worked its way North claiming lives in the UK as well. This virus is similar to, yet more deadly than SARS and originated from the Middle East.

“The SARS coronavirus infected very few animal cell lines. It was finally traced to bats and civets. But we may have a very hard time, as this new virus seems to be much more promiscuous,”, stated Yuen Kwok-yung, a microbiologist at the University of Hong Kong“The SARS coronavirus infects very few human cell lines. But this new virus can infect many types of human cell lines, and kill cells rapidly…If the new virus mutates further, it could cause a deadly pandemic” he warned.

One question remains…Why do laboratories “create” deadly viruses again? It just does not make any sense to me whatsoever.

Cardiovascular Safety of Inhaled Long-Acting Bronchodilators in Individuals With Chronic Obstructive Pulmonary Disease.

Importance  Chronic obstructive pulmonary disease (COPD) is a common and deadly disease. Long-acting inhaled β-agonists and anticholinergics, first-line medications for COPD, have been associated with increased risk of cardiovascular outcomes. When choosing between the medications, patients and physicians would benefit from knowing which has the least risk.

Objective  To assess the association of these classes of medications with the risk of hospitalizations and emergency department visits for cardiovascular events.

Design  We conducted a nested case-control analysis of a retrospective cohort study. We compared the risk of events between patients newly prescribed inhaled long-acting β-agonists and anticholinergics, after matching and adjusting for prognostic factors.

Setting  Health care databases from Ontario, the largest province of Canada, with a multicultural population of approximately 13 million.

Participants  All individuals 66 years or older meeting a validated case definition of COPD, based on health administrative data, and treated for COPD from September 1, 2003, through March 31, 2009.

Exposure  New use of an inhaled long-acting β-agonist or long-acting anticholinergic.

Main Outcome and Measures  An emergency department visit or a hospitalization for a cardiovascular event.

Results  Of 191 005 eligible patients, 53 532 (28.0%) had a hospitalization or an emergency department visit for a cardiovascular event. Newly prescribed long-acting inhaled β-agonists and anticholinergics were associated with a higher risk of an event compared with nonuse of those medications (respective adjusted odds ratios, 1.31 [95% CI, 1.12-1.52; P < .001] and 1.14 [1.01-1.28;P = .03]). We found no significant difference in events between the 2 medications (adjusted odds ratio of long-acting inhaled β-agonists compared with anticholinergics, 1.15 [95% CI, 0.95-1.38;P = .16]).

Conclusions and Relevance  Among older individuals with COPD, new use of long-acting β-agonists and anticholinergics is associated with similar increased risks of cardiovascular events. Close monitoring of COPD patients requiring long-acting bronchodilators is needed regardless of drug class.


Source: JAMA





Fortunately, the Swiss National Advisory Commission on Biomedical Ethics (NEK, President: Otfried Höffe) critically commented on the use of the ADHD drug Ritalin in its opinion of 22 November 2011 titled Human enhancement by means of pharmacological agents: The consumption of pharmacological agents altered the child’s behavior without any contribution on his or her part.

That amounted to interference in the child’s freedom and personal rights, because pharmacological agents induced behavioral changes but failed to educate the child on how to achieve these behavioral changes independently. The child was thus deprived of an essential learning experience to act autonomously and emphatically which “considerably curtails children’s freedom and impairs their personality development”, the NEK criticized.

The alarmed critics of the Ritalin disaster are now getting support from an entirely different side. The German weekly Der Spiegel quoted in its cover story on 2 February 2012 the US American psychiatrist Leon Eisenberg, born in 1922 as the son of Russian Jewish immigrants, who was the “scientific father of ADHD” and who said at the age of 87, seven months before his death in his last interview: “ADHD is a prime example of a fictitious disease”

Since 1968, however, some 40 years, Leon Eisenberg’s “disease” haunted the diagnostic and statistical manuals, first as “hyperkinetic reaction of childhood”, now called “ADHD”. The use of ADHD medications in Germany rose in only eighteen years from 34 kg (in 1993) to a record of no less than 1760 kg (in 2011) – which is a 51-fold increase in sales! In the United States every tenth boy among ten year-olds already swallows an ADHD medication on a daily basis. With an increasing tendency.

When it comes to the proven repertoire of Edward Bernays, the father of propaganda, to sell the First World War to his people with the help of his uncle’s psychoanalysis and to distort science and the faith in science to increase profits of the industry – what about investigating on whose behalf the “scientific father of ADHD” conducted science? His career was remarkably steep, and his “fictitious disease” led to the best sales increases. And after all, he served in the “Committee for DSM V and ICD XII, American Psychiatric Association” from 2006 to 2009. After all, Leon Eisenberg received “the Ruane Prize for Child and Adolescent Psychiatry Research. He has been a leader in child psychiatry for more than 40 years through his work in pharmacological trials, research, teaching, and social policy And after all, Eisenberg was a member of the “Organizing Committee for Women and Medicine Conference, Bahamas, November 29 – December 3, 2006, Josiah Macy Foundation (2006)”. The Josiah Macy Foundation organized conferences with intelligence agents of the OSS, later CIA, such as Gregory Bateson and Heinz von Foerster during and long after World War II. Have such groups marketed the diagnosis of ADHD in the service of the pharmaceutical market and tailor-made for him with a lot of propaganda and public relations? It is this issue that the American psychologist Lisa Cosgrove and others investigated in their study Financial Ties between DSM-IV Panel Members and the Pharmaceutical Industry7. They found that “Of the 170 DSM panel members 95 (56%) had one or more financial associations with companies in the pharmaceutical industry. One hundred percent of the members of the panels on ‘Mood Disorders’ and ‘Schizophrenia and Other Psychotic Disorders’ had financial ties to drug companies. The connections are especially strong in those diagnostic areas where drugs are the first line of treatment for mental disorders.” In the next edition of the manual, the situation is unchanged. “Of the 137 DSM-V panel members who have posted disclosure statements, 56% have reported industry ties – no improvement over the percent of DSM-IV members.” “The very vocabulary of psychiatry is now defined at all levels by the pharmaceutical industry,” said Dr Irwin Savodnik, an assistant clinical professor of psychiatry at the University of California at Los Angeles. and for his theories of autism and social medicine”.

This is well paid. Just one example: The Assistant Director of the Pediatric Psychopharmacology Unit at Massachusetts General Hospital and Associate Professor of Psychiatry at Harvard Medical School received “$1 million in earnings from drug companies between 2000 and 2007”. In any case, no one can easily get around the testimony of the father of ADHD: “ADHD is a prime example of a fictitious disease.”

The task of psychologists, educators and doctors is not to put children on the “chemical lead” because the entire society cannot handle the products of its misguided theories of man and raising children, and instead hands over our children to the free pharmaceutical market. Let us return to the basic matter of personal psychology and education: The child is to acquire personal responsibility and emphatic behavior under expert guidance – and that takes the family and the school: In these fields, the child should be able to lead off mentally. This constitutes the core of the human person.




New evidence suggests some birds gave up flight to become better swimmers.


An international team of wildlife researchers has found evidence to support the theory that some birds, such as penguins, lost the ability to fly because of adaptations that allowed for better swimming. In their paper published in Proceedings of the National Academy of Sciences, the team describes the results of testing energy efficiency levels of birds that both fly and dive as compared to birds that have lost the ability to fly.

To gain a better understanding of the factors that led to flightlessness in some birds, the team traveled to two remote locations: Nanavuk, Canada and Middleton Island in Alaska. By attaching sensors to captured cormorants and murres, the team was able to measure energy efficiency in both species. Both kinds of birds are able to fly and both find prey by diving underwater and swimming. Cormorants use their webbed feet to maneuver underwater, while the murres use their wings.

In analyzing the data from the sensors, the researchers found that murres are relatively efficient swimmers—the amount of energy they burn is just 30 percent lower than that of similar sized penguins. In the air, however, things were quite different. The birds set a new record for inefficiency—they burned 31 times more energy when flying than when sitting still—the highest ever seen in a bird. Studying murres is particularly important when looking to find why penguins lost the ability to fly because they are so similar to their non-flying cousins. Because of their coloring and body shape, they actually look like flying penguins.

The data shows, the researchers claim, that penguins and other flightless birds almost certainly lost the ability to fly as their swimming abilities grew stronger. You can’t have both, they note—becoming better at swimming causes wings to slowly morph into flippers, which of course won’t allow for flight. They suggest that murres are at a crossroads—just good enough to get by in both the air and water. If the need arises to dive deeper, the team notes, the murres could also lose the ability to fly. On the other hand, if the need to avoid predators by flying away remains critical, they could become bet


Flight is a key adaptive trait. Despite its advantages, flight has been lost in several groups of birds, notably among seabirds, where flightlessness has evolved independently in at least five lineages. One hypothesis for the loss of flight among seabirds is that animals moving between different media face tradeoffs between maximizing function in one medium relative to the other. In particular, biomechanical models of energy costs during flying and diving suggest that a wing designed for optimal diving performance should lead to enormous energy costs when flying in air. Costs of flying and diving have been measured in free-living animals that use their wings to fly or to propel their dives, but not both. Animals that both fly and dive might approach the functional boundary between flight and nonflight. We show that flight costs for thick-billed murres (Uria lomvia), which are wing-propelled divers, and pelagic cormorants (Phalacrocorax pelagicus) (foot-propelled divers), are the highest recorded for vertebrates. Dive costs are high for cormorants and low for murres, but the latter are still higher than for flightless wing-propelled diving birds (penguins). For murres, flight costs were higher than predicted from biomechanical modeling, and the oxygen consumption rate during dives decreased with depth at a faster rate than estimated biomechanical costs. These results strongly support the hypothesis that function constrains form in diving birds, and that optimizing wing shape and form for wing-propelled diving leads to such high flight costs that flying ceases to be an option in larger wing-propelled diving seabirds, including penguins.


Journal reference: Proceedings of the National Academy of science.


Friendly Viruses Protect Us Against Bacteria

Bacteria can be friends and foes—causing infection and disease, but also helping us slim down and even combating acne. Now, a new study reveals that viruses have a dual nature as well. For the first time, researchers have shown that they can help our bodies fight off invading microbes.

“This is a very important story,” says Marilyn Roossinck, a viral ecologist at Pennsylvania State University, University Park, who was not involved in the work. “We don’t have all that many examples of beneficial viruses.”

One of our most important lines of defense against bacterial invaders is mucus. The slimy substance coats the inside of the mouth, nose, eyelids, and digestive tract, to name just a few places, creating a barrier to the outside world.

“Mucus is actually a really cool and complex substance,” says Jeremy Barr, a microbiologist at San Diego State University in California and lead author of the new study. Its gel-like consistency is thanks to mucins, large, bottle brush-shaped molecules made of a protein backbone surrounded by strings of sugars. In between the mucins is a soup of nutrients and chemicals adapted to keep germs close, but not too close. Microbes such as bacteria live near the surface of the layer, whereas the mucus at the bottom, near the cells that produced it, is almost sterile.

Mucus is also home to phages, viruses that infect and kill bacteria. They can be found wherever bacteria reside, but Barr and his colleagues noticed that there were even more phages in mucus than in mucus-free areas just millimeters away. The saliva surrounding human gums, for example, had about five phages to every bacterial cell, while the ratio at the mucosal surface of the gum itself was closer to 40 to 1. “That spurred the question,” Barr says. “What are these phages doing? Are they protecting the host?”

To find out, Barr and his colleagues grew human lung tissue in the lab. Lungs are one of the body surfaces that is protected by mucus, but the researchers also had a version of the lung cells where the ability to make mucus had been knocked out. When incubated overnight with the bacterium Escherichia coli, about half the cells in each culture died; the mucus made no difference to their survival. But when the researchers added a phage that targets E. coli to the cultures, survival rates skyrocketed for the mucus-producing cells. This disparity shows that phages can kill harmful bacteria, Barr says, but it’s not clear whether they help or hurt beneficial bacteria; that may depend on which types of phages are present.

In a related series of experiments, the team found that the phages are studded with antibodylike molecules that grab onto the sugar chains in mucins. This keeps the phages in the mucus, where they have access to bacteria, and suggests that the viruses and the mucus-producing tissue have adapted to be compatible with each other, the team reports online today in the Proceedings of the National Academy of Sciences.

Mucus-covered surfaces aren’t unique to our insides; the slime can be found throughout the animal kingdom. It protects the whole bodies of fish, worms, and corals, for example. Protective phages seem to be equally widespread: Barr and his colleagues found dense populations of phages in every species they sampled. “It’s a novel immune system that we think is applicable to all mucosal surfaces, and it’s one of the first examples of a direct symbiosis between phages and an animal host,” Barr says.

In this study, the researchers chose the phage and the bacterium, but it’s possible that the animal host selects specific phages to control specific types of bacteria, such as by outfitting mucins with particular sugars that those phages recognize. The next step, Barr says, is to explore how this symbiosis works in real-life mucosal surfaces of all types, where many different types of phages and bacteria are interacting.

“This is a novel take on the whole microbiome-host relationship,” adds Michael McGuckin, a mucosal biologist from Mater Research, a medical research institute in South Brisbane, Australia, who was not involved in the work. The finding, he says, could provide insights into conditions such as inflammatory bowel disease (IBD). We all have an ecosystem of hundreds of bacterial species in our gut, but patients with IBD have a disrupted ecosystem with different dominant species. These diseases, which include Crohn’s disease and ulcerative colitis, also involve a breakdown in the mucus lining of the gut, he says, and this new study suggests that a failure in phage-based immunity might be the link between those symptoms.

McGuckin is intrigued by the idea that phages may help select the types of bacteria that live inside us. “There’s tons of questions around just how this whole system might control microbial populations in the gut, which have increasingly been shown to be important in obesity and diabetes, and all sorts of human conditions.”

It may also be possible to design a mucus-compatible phage that could fight infection or alter the body’s microbial balance, although that possibility is still very distant. This work, Barr says, “forces us to reevaluate the role of phages. Hopefully this will get people thinking about what they do and how we can use them to help us and combat disease.”


Source: Science Now



Hormone Imbalance,Thyroid Regulation & Bipolar Disorder.

Here are two reasons to care about thyroid:

1. There is a clear connection between the process of thyroid hormoneregulation and bipolar disorder.  The problem is, this connection is only just now beginning to become evident, and how the connection works is basically a mystery.  Two studies recently showed a strikingly high rate of autoimmune-caused thyroid problems in people with bipolar disorder, far more than you would expect to find.Vonk, Kupka  Thyroid problems are more common in the complex forms of bipolar disorder (mixed states and rapid cycling) than in classic bipolar manic patients.Chang  Signs of thyroid auto-immunity are much more common in people with anxiety and depression, particularly the forms of anxiety which don’t easily fit into typical “anxiety disorder” labels.Carta

2. Two studies have shown that people with bipolar depression were less likely to get better if they had low thyroid levels, whereas the ones with higher levels responded pretty well.Cole, Frye . The same phenomenon was recently shown even in “unipolar” depression.Gitlin.  These three studies are the basis for a treatment approach you could consider, particularly if depression is your main problem:  gently pushing your thyroid status over toward the “hyperthyroid” end of normal, if you happen now to be toward the hypothyroid end of normal (the lab testing we use to place you on this spectrum is explained below). Update 4/2008: this approach, using just a little bit of the standard form of thyroid hormone — T4, explained below — was recently tested directly.  The results were very positive, but it was a preliminary test with no control group.Lojko

Update 10/09: another research team recently concluded that “reduction in thyroid function can exacerbate bipolar symptoms even in euthyroid subjects.” Frye In other words, people who are in the normal range (“euthyroid”) can see their bipolar symptoms getting worse if their thyroid levels get low, even if that reduction leaves them still in the normal range.

(Finally, you should also know that some people think the standard lab testing for thyroid status does not do a good job of figuring out who’s “normal” and who’s not.  In other words, they think that people who are not normal, who are low on thyroid hormone, will actually test “normal” using the standard measures.  More on that controversy below).

Most doctors will not raise this option of adding thyroid unless you are clearly already low. It certainly isn’t the first thing to try for depression. But if you have tried several approaches and are considering what to do next; and if you have enough “bipolarity” to make antidepressants a concern, then it might be worth considering this approach, for this reason:  as long as you and your doctor are careful, and don’t bump you right up into hyperthyroidism, there is no risk in trying this approach — just a series of bloodtests, which a lot of people hate. And there is some risk if you end up hyperthyroid.

That is all supposed to sound pretty weak, as a justification for this approach.  It is weak.  But some people with bipolar depression need to know of every option they might try before turning to antidepressants, as explained in the essay entitled Antidepressants That Aren’t Antidepressants. If that’s not you, don’t go carrying this thyroid page to your doctor, she might scoff at you, as there is a long history of unsupported use of thyroid hormone and you don’t want to get branded as “one of those people”.  Even so, the relationship of mood and thyroid is extremely complex, almost mysterious.

Let’s take a quick look at that complexity before turning back to why you might want to learn more about thyroid and bipolar disorder. There are reports linking the entire stress hormone system (here are some basics on stress and depression) to changes in thyroid function.  This part is really complicated.  The short version, translating from two amazing reviews of stress and mental health, is that stress hormones interfere with the production of thyroid hormone and with the conversion of thyroid hormone to its active form. Tsigos, Charmandari

It is also clear that people whose symptoms look the kinds of “bipolar disorder” explained on this website, have thyroid problems — and family members with thyroid problems — at a greater rate than would be expected.  Is that because the thyroid problems somehow actually cause “bipolar”-like symptoms?  Could it be that some of what looks like “bipolar” is actually a thyroid problem?  There may be some such folks.  In addition, there are clearly cases which seem to be “bipolar disorder” for sure, that get better with thyroid hormones as part of the treatment.  In many of these cases it is clear that thyroid hormone was not enough, by itself, to make mood “normal”.  So, for now I think it is safe to say that bipolar disorder has something to do with thyroid regulation in many cases, though not the majority; and that treating with thyroid alone is only rarely going to lead to full remission of symptoms (with a few notable exceptions…).

So, you need to know about thyroid and bipolar disorder for several reasons:

1. There is some relationship between the two, though poorly understood.

2. You need to make sure your thyroid is okay before you begin treatment for bipolar disorder, because

  • if it’s not okay, you might not respond fully to treatment; and
  • it’s usually pretty easy to get your thyroid hormone in the right place, which by itself could help your symptoms somewhat.

3. Thyroid hormone is sometimes used as a treatment for bipolar disorder, even if your thyroid is “normal” (by lab tests, anyway).

4.  And finally, lithium commonly interferes with the thyroid system, so you’ll need to understand a bit about thyroid if you’re going to take lithium.






Use of Prone Positioning During Ventilatory Support Found Superior in ARDS.

In patients with acute respiratory distress syndrome (ARDS), use of the prone position during ventilatory support roughly doubled survival at the 1- and 3-month marks, according to a New England Journal of Medicinestudy.

Researchers followed outcomes in nearly 500 patients with severe ARDS who were randomized either to prone positioning for at least 16 consecutive hours a day, or to being left supine. By 28 days, mortality was 16% in the prone group, versus 33% in the supine group; at 90 days, the prone-positioning advantage held: 24% versus 41%.

An editorialist calls the results “compelling,” and the treatment effect “virtually unprecedented in modern medicine.” He cautions, however, that the logistics of turning patients to the prone position from supine requires teamwork to avoid kinking and extubation. The article includes a video showing how this can be accomplished with three people.

Source: NEJM 

Vigorous Sports OK for Some Patients with ICDs.



Many patients with implantable cardioverter-defibrillators (ICDs) can safely participate in vigorous sports, despite recommendations against such activity, a Circulation study finds.

Researchers followed nearly 400 athletes (aged 10 to 60) with ICDs for about 2.5 years; participants were involved in either organized or high-risk sports (most commonly, running, basketball, soccer, and skiing). Overall, no one experienced the primary endpoint, defined as tachyarrhythmic death, resuscitated tachyarrhythmia, or severe injury resulting from arrhythmia-related syncope or shock. Participants were not significantly more likely to receive shocks during sporting activities (10%) than during other recreational activities (8%). The ICD terminated all arrhythmia episodes.

The researchers conclude: “Many athletes with ICDs can engage in vigorous and competitive sports without physical injury or failure to terminate the arrhythmia. … These data provide a basis for more informed physician and patient decision making in terms of sports participation for athletes with ICDs.”

Soure: Circulation