Mars Mining This Mars miner will probably never go home again. NASA
What Will Mars Medicine Be Like? Long Distance Robotic Surgery?
ScienceDaily.com, PopSci.com, The Huffington Post, October 28, 2010
With that goal in mind, writes PopSci, NASA and the Pentagon’s Defense Advanced Research Projects Agency (DARPA) are embarking on a “Hundred-Year Starship” program, which will bring space travelers to other planets and leave them there.
The first planet in sight? It may be Mars.
Worden expects the program to take off within the next two decades. “I think we’ll be on the moons of Mars by 2030 or so,” Worden said, according to Kurzweil AI.
So far, NASA has contributed $100,000 to the project, and DARPA has chipped in $1 million, according to Gear Log. That isn’t nearly enough for blast-off, but Worden hopes to convince additional individuals to invest.
“[Google co-founder] Larry [Page] asked me a couple weeks ago how much it would cost to send people one way to Mars and I told him $10 billion, and his response was, ‘Can you get it down to 1 or 2 billion?’ So now we’re starting to get a little argument over the price,” Worden said.
How feasible is a colony on Mars?
Story continues below
As PopSci points out, in the October-November edition of the Journal of Cosmology, a paper titled “To Boldly Go: A One-Way Human Mission to Mars” explains that Mars’s similarities to Earth make it an ideal site for human exploration and, possibly, settlement.
Dirk Schulze-Makuch and Paul Davies, who co-authored the paper, argue that a one-way mission is favorable for two reasons. First, writes Science Daily, “because the greatest portion of the expense is tied up in safely returning the crew and spacecraft to earth.” The second reason is that leaving people on Mars could lead to “long-term human colonization of the planet.”
In their paper, Schulze-Makuch and Davis compared potential settlers of a Martian colony to the first Europeans who explored uncharted North America, Science Daily reports. They predict that a Martian settlement could be extremely useful to researchers and may even serve as a “lifeboat” in case a “mega-catastrophe” occurs on Earth.
Buzz Aldrin argued “we can be well on our way to Mars by July 20, 2019” and believes in building a colony on Mars. He told Vanity Fair, “I’m convinced that sending people to Mars is so expensive that if you go once and bring the people back and then go again and bring the people back, we’re eventually going to run out of money. But what if we send people the first time and they don’t come back? What if they stay there?”
The pain gate: When we suffer pain–whether from a stubbed toe or a metastasized tumor–pain signals are transmitted to the brain from around the body through these groups of sensory neurons, called dorsal root ganglia (DRG). A new gene-therapy technique intercepts pain signals at the DRG using a gene for a naturally produced opiate-like chemical. On the right, the cells of a rat’s DRG glow green with a marker for the opiate-like gene one month after it was injected into the rat’s spinal fluid. On the left are DRG cells from a control rat injected with saline solution. Credit: PNAS
Researchers use gene therapy to stop pain signals before they reach the brain
MIT Technology Review, by Jocelyn Rice — A gene therapy developed at Mount Sinai School of Medicine could bring relief to patients suffering from chronic pain while bypassing many of the debilitating side effects associated with traditional painkillers.
Researchers at Mount Sinai School of Medicine injected a virus carrying the gene for an endogenous opioid–a chemical naturally produced by the body that has the same effect as opiate painkillers such as morphine–directly into the spinal fluid of rats. The injections were targeted to regions of the spinal cord called the dorsal root ganglia, which act as a “pain gate” by intercepting pain signals from the body on their way to the brain. “You can stop pain transmission at the spinal level so that pain impulses never reach the brain,” says project leader Andreas Beutler, an assistant professor of hematology and medical oncology at Mount Sinai.
The injection technique is equivalent to a spinal tap, a routine procedure that can be performed quickly at a patient’s bedside without general anesthesia.
Because it targets the spinal cord directly, this technique limits the opiate-like substance, and hence any side effects, to a contained area. Normally, when opiate drugs are administered orally or by injection, their effects are spread throughout the body and brain, where they cause unwanted side effects such as constipation, nausea, sedation, and decreased mental acuity.
Side effects are a major hurdle in treating chronic pain, which costs the United States around $100 billion annually in treatment and lost wages. While opiate drugs can be very effective, the doses required to successfully control pain are often too high for the patient to tolerate.
“The side effects can be as bad as the pain,” says Doris Cope, director of the University of Pittsburgh Medical Center’s Pain Medicine Program. Achieving the benefits of opiate treatment without their accompanying side effects, Cope says, would be a “huge step forward.”
Beutler hopes to do just that. “Our strategy was to harness the strength of opioids but target it to the pain gate, and thereby create pain relief without the side effects that you always get when you have systemic distribution of opioids,” he says.
Several groups have previously attempted to administer gene therapy for pain through spinal injections, but they failed to achieve powerful, long-lasting pain relief. The new technique produced results that lasted as long as three months from a single injection, and unpublished follow-up studies suggest that the effect could persist for a year or more.
Beutler credits his team’s success to the development of an improved virus for delivering the gene. The team uses a specially adapted version of adeno-associated virus, or AAV–a tiny virus whose genome is an unpaired strand of DNA. All the virus’s own genes are removed, and the human endogenous opioid gene is inserted in their place. Beutler’s team also mixed and matched components from various naturally occurring AAV strains and modified the genome into a double-stranded form. These tweaks likely allow the virus to infect nerve cells more easily and stick around longer.
Once the virus is injected into the spinal fluid and makes its way into the nerve cells of the pain gate, it uses the host cells’ machinery to churn out the opioid protein–which then goes to work blocking pain signals on their way to the brain. Normally, the gene is rarely activated. But the version used for therapy has no such limitations because the gene carried by the AAV has been modified to continuously produce the opioid chemical.
Cope says that using endogenous opioids is inherently superior to injecting synthetic opiate drugs directly into the spinal fluid, an approach that requires the installation of a pump in order to deliver the drugs over a long time period. “It’s kind of a holy grail,” she says. “If the body’s own system for pain control were activated by genetic expression, that would be superior to an artificial medication.”
In Beutler’s study, which was published in PNAS, rats were surgically modified to have a stronger than usual response to pressure on their paws, mimicking the effects of so-called neuropathic pain. The gene-therapy treatment effectively restored the rats to a normal level of pain sensitivity. The team also tested a nonopioid gene, which produced comparable pain relief through an entirely different mechanism. But while the opioid gene’s effects will likely extend to humans, who respond to opiates the same way rats do, the nonopioid’s effects may be rat specific.
The Stockholm-based company Diamyd Medical has been developing a different approach to gene therapy for chronic pain that also bypasses the side effects of standard pain treatment. The approach uses a deactivated version of herpes simplex virus (HSV). HSV can be administered straight through the skin as it naturally finds and infects peripheral nerves and travels to the spinal cord on its own. Darren Wolfe of Diamyd says that this method is superior to spinal injection because it’s safer and easier, and it can be administered repeatedly.
Because of these considerations, the HSV method may be preferable for treating localized pain. However, when chronic pain involves multiple areas of the body–as it often does with, for example, metastasized cancers–going straight to the pain gate could work more efficiently.
While both of these methods have proved effective in animal models of pain, their efficacy in human patients remains to be shown. Diamyd applied to the FDA to begin phase I clinical trials, and Beutler estimates that his approach could be tested on humans in as few as three years.
A Conceptual Drawing of the ‘Holometer’ via Symmetry
PopSci.com, October 28, 2010, by Clay Dillow — Researchers at Fermilab are building a “holometer” so they can disprove everything you thought you knew about the universe. More specifically, they are trying to either prove or disprove the somewhat mind-bending notion that the third dimension doesn’t exist at all, and that the 3-D universe we think we live in is nothing more than a hologram. To do so, they are building the most precise clock ever created.
The universe-as-hologram theory is predicated on the idea that spacetime is not perfectly smooth, but becomes discrete and pixelated as you zoom in further and further, like a low-res digital image. This idea isn’t novel; recent experiments in black-hole physics have offered evidence that this may be the case, and prominent physicists have proposed similar ideas. Under this theory, the universe actually exists in two dimensions and the third is an illusion produced by the intertwining of time and depth. But the false third dimension can’t be perceived as such, because nothing travels faster than light, so instruments can’t find its limits.
This is theoretical physics at its finest, drowning in complex mathematics but short on hard data. So Fermilab particle astrophysicist Craig Hogan and his team are building a “holometer” to magnify spacetime and see if it is indeed as noisy as the math suggests it might be at higher resolution. In Fermilab’s largest laser lab, Hogan and company are putting together what they call a “holographic interferometer,” which – like a classic interferometer – will split laser beams and measure the difference in frequencies between the two identical beams.
But unlike conventional interferometers, the holometer will measure for noise or interference in spacetime itself. It’s actually composed of two interferometers – built one atop the other – that produce data on the amount of interference or “holographic noise.” Since they are measuring the same volume of spacetime, they should show the same amount of correlated jitter in the fabric of the universe. It will produce the first direct experimental insight into the fundamental nature of space and time, and there’s no telling what researchers delving into that data might find out about the holographic nature of the universe.
So enjoy the third dimension while you still can. Construction on the first instrument is already underway, and Hogan thinks they will begin collecting data on the very nature of spacetime itself by next year.
Build Your Own Spacetime-Measuring ‘Holometer’ at Home: Just kidding. Don’t. Sam Waldman, MIT/Craig Hogan, Fermilab PAC
Buckyball named after Buckminster Fuller
FORBES.com, October 28, 2010, PASADENA, Calif. — A soccer ball-shaped carbon molecule that some scientists think may have helped seed life on Earth is more common in the universe than initially believed.
Using NASA’s Spitzer Space Telescope, researchers spotted the carbon spheres known as ‘buckyballs’ around three dying sun-like stars in the Milky Way and in the space between stars. The telescope also detected the cosmic balls floating around a dying star in a nearby galaxy.
The telescope previously found buckyballs only in one location in space.
The new findings appear online Thursday in the Astrophysical Journal Letters.
Scientists hope to better understand the role buckyballs play in the birth and death of stars and planets.
FORBES.com, October 28, 2010, By BRUCE UPBIN
Photo by Andy Morris
FORBES.com, October 28, 2010, By BRUCE UPBIN
The list of rich men obsessed with space exploration is as long as an Apollo rocket. The sums spent are long, too. Musk has put up an estimated $100M, Bezos is into the millions likely, Paul Allen spent $100M. Robert Bigelow, a budget hotel-chain mogul, built a life-size space station in his well-guarded Bigelow Aerospace factory in Nevada.
But Musk and Bigelow look like pikers next to James Lick. The wealthiest man in California (150 years ago), Lick spent more on a single telescope (in today’s dollars) than all of their investments combined. Lick made his fortune in real estate after the Gold Rush. He built most of downtown San Jose, Calif. and late in his life was moved to spend $700,000 on the Lick Observatory, finished in 1876 in San Jose at a cost of what would now be the equivalent of $1.2 billion (in 2008 dollars). The era of the tycoon-funded giant telescope lasted until the construction of the Palomar Observatory in 1928 with $6.5M from the Rockefellers. That’s $972M in 2008 GDP equivalent dollars (see methodology below). Most of these big scopes were built with private money, and most were built purely for scientific purposes. Musk and Bigelow seem like they’re in it for the money and the science. And why not go for-profit? The space industry is worth $250B, with great potential for entrepreneurs to take share from lazy, shiftless government programs.
These money comparisons were drawn out in a recent paper by NASA research economist Alexander C. MacDonald (yes, NASA has economists), who is working on an economic history of space exploration for his doctoral dissertation. He says the rich have always been a huge factor in space work.
“These [new] guys,” says MacDonald of Musk, Bigelow and Bezos, “already made their money so profit is not really their goal. They’re also doing it for personal reasons. They want to see space as an option for humanity. I mean, there are a lot of easier ways to make money than in the space industry.”
MacDonald’s paper is here. His thesis also validates the Obama administration’s agenda to encourage private space enterprise, which is smart because government efforts usually bloat up with taxpayer money that space bureaucrats merely had to ask for from Congress. While we don’t want to be dependent on billionaires for all our big-ticket science and engineering projects, we might as well reduce the barriers that hold back private efforts.
Here’s the table from MacDonald’s paper listing costs then and now of space exploration projects from 100 or more years ago. Many were larger in today’s dollars than today’s space investments.
MacDonald ran his numbers using equivalent GDP ratio, which he says is a better method than inflation-adjusting when it comes to assessing relative historical impacts of megaprojects like telescopes or churches. MacDonald divided Lick’s $700,000 telescope budget by the U.S. GDP in 1876 and multiplied that number by 2008 GDP. Voila: $1.2 billion. NASA’s total annual space shuttle budget is $4 billion.
Backgrounder on the money today: Dennis Tito spent $20 million of his own money to become the world’s first space tourist in 2001. Microsoft cofounder Paul Allen spent $25 million on SpaceShipOne. PayPal cofounder Elon Musk put a reported $100 million of his own money into SpaceX, whose Falcon rockets are poised to take over cargo delivery duties from NASA to the International Space Station. Intel cofounder Gordon Moore has spent $24 million and pledged another $200 million through his foundation to build a giant $1.4 billion telescope in Mauna Kea, Hawaii. It will be able to peer to the very edge of the observable universe. Amazon founder Jeffrey Bezos has bankrolled with undisclosed millions a project called Blue Origin that has already received a separate $3.7 million in federal funds to develop an astronaut escape system for its manned New Shepherd rocket. The final frontier ain’t cheap.
Greetings from the TEDMED conference in San Diego, CA. Your blogger is at this conference for the week……….and will post some of the most interesting presentations on this BLOG, next week.
Pain killer: A new class of drugs proves exceedingly effective against the pain of osteoarthritis (seen here in the x-ray of a degenerating knee joint).
Credit: Courtesy of Nevit Dilmen/Wikimedia Commons
A new approach alleviates osteoarthritis pain better than any drug available
MIT Technology Review, October 26, 2010, by Lauren Gravitz — A new class of pain relievers that targets musculoskeletal pain receptors, instead of more general pain pathways, could alleviate osteoarthritis pain better than any drug now on the market, but hurdles remain before it’s approved by the U.S. Food and Drug Administration. Research on the new therapy was published yesterday in the New England Journal of Medicine.
Osteoarthritis occurs when joint cartilage wears down, with the worst cases requiring joint replacement surgery. The pain can be unrelenting, and there’s no real cure. Patients often get through the day by relying on pain relievers, typically starting with over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen. As the pain intensifies and people become inured to the drugs’ effects, they gradually work their way up to opioids such as oxycodone.
The new treatment, called tanezumab, acts on a completely different pathway. While NSAIDs inhibit an enzyme that produces inflammation, and opioids target specific receptors in the central nervous system, tanezumab homes in on musculoskeletal pain receptors. This approach promises fewer side effects, such as internal bleeding, liver damage, and the danger of addiction, which can accompany the alternatives.
Tanezumab, which was developed by Pfizer, is the first in a new class of pain relievers that inhibit sensory neurons, preventing them from transmitting pain signals to the brain. In a clinical trial to assess the intravenous medicine’s efficacy, patients on tanezumab experienced as much as a 62 percent reduction in pain–as much as 40 percent better than the placebo.
“Nothing out there works like this–this is a game-changing molecule,” says Nancy Lane, director of the Center for Healthy Aging at the University of California, Davis, and the study’s lead researcher. NSAIDs and opiates show about half the efficacy of tanezumab (although the current study only compared different tanezumab doses to a placebo rather than to currently available medications). Still, Lane says, “The efficacy was beyond belief.”
Tanezumab works by preventing a protein called nerve growth factor from attaching to sensory neurons, thereby stopping the neurons from transmitting pain signals to the brain. It’s a pathway specifically related to muscle and bone pain, and therefore provides an opportunity for targeted pain relief.
“This really represents a new class of drugs, and it’s been many decades since we’ve introduced a new class of agents for treating osteoarthritis,” says Patrick Mantyh, a professor of pharmacology at the University of Arizona. “It’s an outstanding paper, very thorough, and a beautiful case of coming up with a really novel approach for treating pain and showing a clinically significant result.”
The Centers for Disease Control and Prevention conservatively estimates that about 27 million people in the U.S. suffer from osteoarthritis–a number that represents a huge opportunity for any company that can improve upon existing pain relief. At least four American pharmaceutical companies have therapies in development that inhibit either nerve growth factor or the receptor to which it binds; all are intensely watching Pfizer’s progress.
The study’s results come with a word of caution. Lane and her colleagues completed the trial in 2007. In the years since, Pfizer started a number of phase II and III trials, but has since been ordered by the FDA to suspend them: Ensuing osteoarthritis trials caused a small number of participants to experience so much tissue degeneration that they required joint replacement surgery, and not necessarily on the joint they were undergoing treatment for.
More studies need to be done to determine whether the joint damage occurred because tanezumab was somehow affecting bone or because it was just so effective that the subjects were more active than they should have been and didn’t feel pain to warn them of serious injury. Lane believes it’s the latter. “It works so well that people are going to need to be counseled. Just because they don’t feel pain doesn’t mean their disease is gone,” she says. “Pain is good; it keeps us from doing too much. And this medication is very good, so good that it allows people to do more than they should.”
Getting pain relievers approved by the FDA has always been difficult, since there are so many drugs with a proven safety record and relatively good efficacy already commercially available. In the post-Vioxx era (the drug was approved then taken off the market after it was shown to increase risk of stroke and heart attack), the FDA sets the bar even higher.
Even if it turns out that tanezumab is acting on bone and doesn’t make it through the approval process, Mantyh says, the research is no less important: It proves nerve growth factor has an important role in driving skeletal pain and is thus a good target for pain relief. “In the end, if the drug doesn’t get approved for whatever reason, they have provided clinical data to show that [nerve growth factor] is a major player in driving the pain of osteoarthritis.”
Kevin Koch, the chief scientific officer and president of Boulder, Colorado-based Array Biopharma, says Pfizer should be congratulated on moving this aggressively. “Being the first is always the hardest,” he says. Array is working on its own type of nerve-growth-factor inhibitor, an orally administered version that lasts only 12 hours, rather than eight weeks. So he’s particularly interested in the outcome of tanezumab trials and the FDA’s approval process. “This is a very exciting mechanism,” Koch says. “This is by far the most effective new pain therapy I’ve seen.”
Pain relief: Scientists at MicroTransponder are developing a novel neuro stimulator to treat chronic pain. Small electrodes (blue circles) are injected near the spinal cord, and a PDA controls an external coil on the surface of the skin, powering the electrodes. Credit: MicroTransponder
RFID technology allows neural stimulators to get really small.
MIT Technology Review, by Emily Singer — A tiny injectable implant, smaller than a grain of rice, might one day take the place of large neural stimulators used to treat chronic pain and other neurological disorders. The novel device, under development by MicroTransponder, a Dallas-based startup, owes its small size to the use of RFID (radio-frequency identification) technology like that used to tag clothes to prevent shoplifting.
The device works similarly to spinal-cord stimulators for managing chronic pain. The idea is that the electrical jolts delivered by the device override the neural pain signals being transmitted to the spinal cord. However, the precise mechanism is not yet clear.
Existing devices have a battery and controller implanted beneath the skin, which delivers electrical pulses to a connected set of leads placed near the spinal cord. The MicroTransponder device, in contrast, is wireless and has no batteries. The implanted portion consists of small electrodes and a small coil, which is powered by an external battery-powered coil worn like a cuff on the arm or leg. The stimulation parameters are programmed via laptop or PDA and would be tailored to the individual patient.
Like some cochlear implants and other medical devices, the implant is powered with radio-frequency transmission. Radio waves transmitted by the external coil generate a magnetic field in the internal coil, which powers the electrodes. Adopting technologies from the rapidly advancing RFID world has allowed the researchers to further shrink the device. “Instead of trying to transfer energy from two coupled antennas to do telemetry, which is a common approach for medical devices, RFID is geared to have very small transponders, so you don’t need a large coil,” says Joseph Pancrazio, a program director at the National Institute for Neurological Disorders and Stroke, a government funding agency, in Bethesda, MD, that has given the company small business loans.
The research is still in an early stage. Researchers have developed a prototype device, which they are testing in rats. The device can effectively stimulate peripheral nerves in rats, although it’s not yet clear whether the electrical stimulation alleviates chronic pain. (Scientists assess chronic pain in rats by recording how much the animals eat; a rat in pain won’t eat as much.)
Some scientists are skeptical that the device will be powerful enough to deliver a therapeutic level of stimulation. “The main limitation of any electronic device small enough to be injected into the body is that it must receive enough power to operate its circuitry and provide the required stimulation parameters,” says Gerald Loeb, director of the Medical Device Development Facility at the University of Southern California, in Los Angeles. Loeb has also developed an injectable radio-powered microstimulator, which he says has encountered substantial limitations in range and power.
“We believe we can do it with less power,” says Scott Armstrong, MicroTransponder’s chief technical officer. However, he declined to give further details of the technology for proprietary reasons.
If it does prove successful, the device could have a number of applications. Researchers at MicroTransponder plan to test it as a treatment for tinnitus, a perceived ringing in the ears that is particularly common among veterans with head injuries.
Medscape.com, by Lisa Nainggoian, October 22, 2010 (Sheffield, United Kingdom) — Among men who have coronary heart disease, mortality was doubled in those with low testosterone levels compared with those who had normal levels, a new observational study has shown. Dr Chris J Malkin (Royal Hallamshire Hospital, Sheffield, UK) and colleagues report their findings in Heart. 
“This is the fourth epidemiologic study to have shown that low testosterone is a marker of early mortality,” senior author Dr Kevin S Channer (Royal Hallamshire Hospital, Sheffield, UK) told heartwire . “But most crucially, it is the first in men with vascular disease; all of the other epidemiologic follow-up studies of testosterone have excluded this patient population.”
In an accompanying editorial , Drs Ronald CW Ma and Peter CY Tong (Prince of Wales Hospital, Shatin, Hong Kong) describe the history of studies on testosterone and cardiovascular disease and say the new trial “adds to the emerging picture” by making it clear that the link between reduced testosterone and increased mortality extends to subjects with established cardiovascular disease.
Channer says a long-term (5 to 10 years) prospective randomized placebo-controlled trial of testosterone replacement therapy is now needed in patients with heart disease, to assess its effects on mortality: “If you replace the testosterone, can you push that Kaplan-Meier survival curve back to the normal line?”
The editorialists agree. While Ma and Tong say there are some risks from testosterone–it might increase the risk of prostatic diseases and erthrocytosis, and exacerbate sleep apnea–overall, “The encouraging results from clinical studies so far support investigating the effects of testosterone supplementation on cardiovascular disease in larger clinical trials.”
20% of Men Were Testosterone-Deficient
To examine the effect of testosterone levels on survival, Malkin et al followed 930 consecutive men with coronary disease referred for angiography for a two-year period from June 2000, with a mean follow-up of almost seven years. The main variables were all-cause and vascular mortality and the presence of testosterone deficiency.
The overall prevalence of biochemical testosterone deficiency was 20.9% using a measure of bioavailable testosterone <2.6 nmol/L; 16.9% using total testosterone <8.1 nmol/L; and using either measure it was 24%.
Adjusted all-cause and vascular mortality was more than doubled among those with low bioavailable testosterone (HR 2.2. p<0.0001 for all-cause mortality; HR 2.2, p=0.007 for vascular mortality) compared with those who had normal levels of the hormone.
Low serum testosterone was one of only four variables found to influence time to all-cause and vascular mortality in multivariate analyses (HR 2.27), along with the presence of left ventricular dysfunction (HR 3.85), aspirin therapy (HR 0.63), and beta-blocker therapy (HR 0.45).
“In patients with coronary disease, testosterone deficiency is common and impacts negatively on survival. Prospective trials of testosterone replacement are needed to assess the effect of treatment on survival,” the authors conclude.
Testosterone Not Like Female HRT, No Money for a Big Trial
Channer explains that testosterone replacement therapy can be given in a number of ways. Testosterone is not suitable for oral therapy, because “It undergoes high first-pass metabolism through the liver,” he explains. But it is available in slow-release injection formulations, as a three-month depot injection, as transdermal patches, and as a gel. He says his team has had some problems with the skin patch because it causes a rash and men tend not to like it, but they have had more success with the three-month depot injections, which they have been able to keep people on for a year. However, “We desperately need some other formulations,” he says.
He is keen to stress that testosterone is a whole different ballgame from female hormone replacement therapy: “Men are given testosterone, the same hormone as they make themselves, and we monitor levels and titrate to physiologic levels. This is not like female hormones, where women were given doses of a drug and the physicians didn’t know whether they were physiological, super-physiological, or what; it’s totally different.”
But he does not hold his breath when it comes to a big trial. He and his colleagues have had every request for funding for such a large study turned down, he says, adding: “The problem is that none of the drug companies that make testosterone are big enough to fund such a study, because it would cost millions.”
Concerns Dismissed: Testosterone “Like Thyroid Hormone”
Channer also doesn’t understand what he sees as reticence from some quarters when testosterone as a potential therapy is discussed. “I’ve struggled to understand why endocrinologists don’t just accept that replacing testosterone is the same as replacing thyroid hormone, for example, what’s the matter with that?”
And he dismisses any concerns arising from a US National Institutes of Health study in elderly men, which was stopped early because testosterone treatment was associated with an increased risk of cardiovascular events; the paper was published in the New England Journal of Medicine earlier this year.
“We were very surprised that NEJM published that paper. The end points were very soft indeed,” he comments. “Yes, there were a few more deaths, but these were elderly men and you wouldn’t expect in the duration of that study for the testosterone to have had that kind of effect. We’ve been doing studies for 15 years with testosterone in men with known heart disease, angina, and heart failure, and we haven’t had any [serious] adverse reactions.”
Neither the authors nor the editorialists report any conflict of interest.
- Malkin CJ, Pugh PJ, Morris PD, et al. Low serum testosterone and increased mortality in men with coronary heart disease. Heart 2010 DOI: 10.1136/hrt.2010.195412
- Ma RCW and Tong PCY. Testosterone levels and cardiovascular disease. Heart 2010;96:1787-1788.
FORBES.com, October 25, 2010, by Randolph E. Schmid –WASHINGTON — The ability to taste isn’t limited to the mouth, and researchers say that discovery might one day lead to better treatments for diseases such as asthma.
It turns out that receptors for bitter tastes are also found in the smooth muscles of the lungs and airways. These muscles relax when they’re exposed to bitter tastes, according to a report Sunday from researchers from the University of Maryland College of Medicine in Baltimore in the online edition of the journal Nature Medicine.
That surprised Dr. Stephen B. Liggett, a lung expert who noted that bitter tastes often are associated with poisonous plants, causing people to avoid them.
Liggett said he expected the bitter-taste receptors in the lungs to produce a “fight or flight” reaction, causing chest tightness and coughing so people would leave the toxic environment.
“But that’s not what we found,” Liggett said.
Instead, when scientists tested some nontoxic bitter compounds on mice and on human airways in the laboratory, the airways relaxed and opened more widely.
The compounds “all opened the airway more profoundly than any known drug that we have for treatment of asthma or chronic obstructive pulmonary disease,” Liggett said.
“That’s the fun of science, when you find something you didn’t expect,” he said in a telephone interview.
Liggett, who hopes to begin tests in humans within a year, said that eating bitter tasting foods or compounds would not help in the treatment of asthma. Instead, he said, to get a sufficient dose people will need to use aerosolized compounds, which can be inhaled.
Fortunately there are thousands of compounds known to have a bitter taste, such as quinine and many drugs, he said. So researchers can begin testing them to determine which have the best result without few or no side effects.
The presence of bitter taste receptors on the hair-like cilia in the airways was reported last year by Michael J. Welsh of the University of Iowa. It was suggested that the cilia might react by moving to push a noxious aerosol out of the airways, and Liggett said that may be the case.
But the new research by Deepak A. Deshpande and Liggett centers on receptors in the smooth muscles, rather than the cilia. The lung receptors were limited to bitter tastes, Liggett said, and did not include the ability to sense salty, sour, sweet and savory tastes, which the tongue can detect.
Unlike the taste receptors in the tongue, the ones in the airways react to the taste but do not send signals to the brain.
The research was supported by the U.S. National Heart, Lung and Blood Institute.