Image via Karl Diefenderfer.
A sundog – a piece of a larger halo around the sun or moon – is caused by tiny ice crystals in the upper air.
Learn more about sundogs, (plus see another great pic of Karl’s) here.
Image via Karl Diefenderfer.
A sundog – a piece of a larger halo around the sun or moon – is caused by tiny ice crystals in the upper air.
Learn more about sundogs, (plus see another great pic of Karl’s) here.
The number of people in the UK who say they now don’t drink alcohol at all.
Gabi
The number of people in the UK who say they now don’t drink alcohol at all.
Gabi
Tonight – May 6, 2017 – and for the next few evenings, watch for the moon and the dazzling planet Jupiter to pop out almost immediately after sunset. Then as dusk ebbs into nightfall, look for the star Spica to come out below Jupiter. On May 6, Spica is almost on line with the bright waxing gibbous moon and Jupiter.
The grand celestial procession on May 6-8, 2017 – the moon, Jupiter and Spica – will travel westward across the nighttime sky for the same reason that the sun goes westward during the day. It’s because the Earth spins from west-to-east on its rotational axis, causing the sun, moon, stars and planets to rise in the east, set in the west and to go westward across our sky each day.
But if you note the moon’s position at the same time each day, you’ll see that it actually moves eastward (in the direction of sunrise) relative to the backdrop stars and planets of the zodiac. In one hour, the moon travels about ½ degree (the moon’s diameter) eastward through the constellations of the zodiac; and in one day, the moon travels roughly 13o in front of the zodiacal constellations.
The moon’s daily change of position is due to the moon’s orbital motion around Earth.
Watch for yourself – and contemplate the moon moving in orbit around Earth – as the moon swings by Jupiter and then the star Spica over the next few days.
Our friend Tom Wildoner at LeisurelyScientist.com captured this image of Jupiter and Spica on April 26, 2017. As you can see, Jupiter is much brighter! But Spica is bright, too, brighter than most stars. Tom wrote: “Beautiful Jupiter and Spica rising over my backyard trees, which are still struggling to push out spring leaves.”
Bottom line: Use tonight’s moon – May 6, 2017 – to see a grand procession of celestial bodies. The moon and Jupiter are the evening sky’s brightest objects. The star Spica is also bright and noticeable nearby.
Tonight – May 6, 2017 – and for the next few evenings, watch for the moon and the dazzling planet Jupiter to pop out almost immediately after sunset. Then as dusk ebbs into nightfall, look for the star Spica to come out below Jupiter. On May 6, Spica is almost on line with the bright waxing gibbous moon and Jupiter.
The grand celestial procession on May 6-8, 2017 – the moon, Jupiter and Spica – will travel westward across the nighttime sky for the same reason that the sun goes westward during the day. It’s because the Earth spins from west-to-east on its rotational axis, causing the sun, moon, stars and planets to rise in the east, set in the west and to go westward across our sky each day.
But if you note the moon’s position at the same time each day, you’ll see that it actually moves eastward (in the direction of sunrise) relative to the backdrop stars and planets of the zodiac. In one hour, the moon travels about ½ degree (the moon’s diameter) eastward through the constellations of the zodiac; and in one day, the moon travels roughly 13o in front of the zodiacal constellations.
The moon’s daily change of position is due to the moon’s orbital motion around Earth.
Watch for yourself – and contemplate the moon moving in orbit around Earth – as the moon swings by Jupiter and then the star Spica over the next few days.
Our friend Tom Wildoner at LeisurelyScientist.com captured this image of Jupiter and Spica on April 26, 2017. As you can see, Jupiter is much brighter! But Spica is bright, too, brighter than most stars. Tom wrote: “Beautiful Jupiter and Spica rising over my backyard trees, which are still struggling to push out spring leaves.”
Bottom line: Use tonight’s moon – May 6, 2017 – to see a grand procession of celestial bodies. The moon and Jupiter are the evening sky’s brightest objects. The star Spica is also bright and noticeable nearby.
Right now, according to public health officials, about half a million U.S. kids have blood lead levels that could harm their health. However, new research finds many more children — hundreds of thousands more — are likely going unidentified.
In a study published last week in Pediatrics, researchers estimated that while 1.2 million cases of elevated blood lead levels (EBLL) likely occurred between 1999 and 2010, only 607,000 were reported to the Centers for Disease Control and Prevention. That data gap not only means kids are likely going without needed treatment and services, but that public health officials don’t have all the data they need to ensure prevention and remediation efforts reach everyone who needs them. And if — as the study suggests — public health officials don’t have complete data on where lead poisoning threats exist, it makes it difficult to pinpoint the sources of exposure and prevent additional poisonings in the future.
According to CDC, there’s no safe blood lead level in children, and even low levels of lead have been shown to impact IQ, attention and academic achievement. Other effects of childhood lead poisoning include damage to the nervous systems, slowed growth and development, behavioral issues, and hearing and speech problems. Research has found that investing in lead hazard control reaps significant benefits, both in preventing the high cost of special care and services and in protecting a child’s opportunity to succeed academically, which is often a predictor of future health, prosperity and longevity. In California alone, research shows that EBLL results in lost earnings of up to $11 billion over the lifetime of children born each year.
Study co-author Eric Roberts, a pediatrician and co-principal investigator of the California Environmental Health Tracking Program at the Public Health Institute, said that because the standards determining who should be tested for lead vary across states, he and colleagues had a hunch many at-risk and impacted children were being overlooked. According to the Pediatrics study, the American Academy of Pediatrics recommends clinicians refer to state and local lead screening guidelines, “but these recommendations are often difficult for clinicians to access and commonly defer to practitioners’ individual evaluations of EBLL risk in the communities they serve, a task for which few are equipped.” And while laws require lead testing for Medicaid and WIC enrollees, researchers said the requirement often goes unenforced. That means childhood lead testing is mostly left to the discretion of physicians.
“We did observe almost universally that when you ask state or local public health to quantify the amount of lead poisoning, they provide you with numbers of lead-exposed kids identified by physicians — and that always struck me as a circular argument,” Roberts told me. In other words, in communities where physicians do a lot of testing, the resulting data underscores the need to sustain and possibly expand such testing; if little testing is done, the resulting data can cause physicians to incorrectly believe testing isn’t necessary.
He added: “Right now, folks are just assuming that certain communities are at low risk. But the default should be for testing, especially for children 12 to 24 months old. …We now assume no risk until it’s found, and that policy is clearly failing to protect kids.”
To conduct the study, Roberts and colleagues used National Health and Nutrition Examination Survey (NHANES) data to estimate state-level EBLL prevalence among children ages 12 months to 5 years between 1999 and 2010. They then compared those estimates to diagnostic case numbers reported to CDC. They found that in 23 of the 39 states where data was available, more than half of children with EBLL weren’t being identified. Nationwide, according to the study, only 64 percent — or 607,000 cases — of children with EBLL were identified and reported to CDC.
Between 1999 and 2010, researchers estimated that about 1.2 million children had EBLL, but only those 607,000 cases were identified and reported to CDC. The researchers noted that about 45 percent of unreported cases happened in years when the particular state wasn’t reporting such data to CDC, and about 55 percent of unreported cases weren’t reported due to “incomplete case ascertainment.” At the regional level, the greatest number of reported EBLL cases occurred in the Midwest and Northeast, while the highest number of overall cases occurred in the South. At the state-level, 23 states reported fewer than half of expected EBLL cases, while 11 states reported less than 20 percent of expected cases. For example, in California, the study estimated that only 37 percent of children with EBLL were identified.
Researchers noted that because of changes to NHANES data collection in 2010, clinician testing has become the only source of information on EBLL prevalence. In addition, CDC’s Childhood Lead Poisoning and Healthy Homes Program had its budget cut in 2012 from $29 million to $2 million, which means states have much less capacity to do lead-related surveillance, outreach, education, prevention, assessment and enforcement.
Co-authors Roberts, Daniel Madrigal, Jhaqueline Valle, Galatea King and Linda Kite write:
American Academy of Pediatrics policy…explicitly defers to state and local health departments to decide when children should undergo BLL testing. This policy is based on two assumptions, however: that well-resourced public health agencies will communicate effectively with providers, enabling them to make data-directed decisions about when to test for EBLL, and that statutory requirements for testing would be accompanied by mechanisms and resources for enforcement. Both of these assumptions have proven to be false, with the effect that large numbers of children with EBLL (indeed, the majority of these children in many parts of the country) have been missed by clinicians.
“I think the fundamental message here for public health is that we need to realize that simply enumerating the number of kids found by pediatric care providers is not a scientific basis for knowing whether kids are at risk or not,” Roberts told me. “(Lead exposure) is a much wider-spread problem than we’ve been willing to admit.”
Roberts noted that while the most common route of child lead exposure is lead-based house paint — and that risk has been drastically reduced in recent decades — the drinking water crisis in Flint shows that lead remains a serious threat to children’s health. In fact, he said as aging infrastructures deteriorate, children could face new lead exposure risks, which are all the more reason for better surveillance, testing and data.
On the clinical side, he said groups like the American Academy of Pediatrics can make a difference by strengthening their practitioner guidelines for childhood lead testing, with the understanding that local public health data might not provide a complete picture of who’s at risk and who should be tested.
“What we’re doing when we allow kids to be exposed to lead is we’re sacrificing some portion of their futures,” Roberts said. “There’s a cost to doing nothing.”
For a copy of the new lead study, visit Pediatrics.
Kim Krisberg is a freelance public health writer living in Austin, Texas, and has been writing about public health for 15 years. Follow me on Twitter — @kkrisberg.
Right now, according to public health officials, about half a million U.S. kids have blood lead levels that could harm their health. However, new research finds many more children — hundreds of thousands more — are likely going unidentified.
In a study published last week in Pediatrics, researchers estimated that while 1.2 million cases of elevated blood lead levels (EBLL) likely occurred between 1999 and 2010, only 607,000 were reported to the Centers for Disease Control and Prevention. That data gap not only means kids are likely going without needed treatment and services, but that public health officials don’t have all the data they need to ensure prevention and remediation efforts reach everyone who needs them. And if — as the study suggests — public health officials don’t have complete data on where lead poisoning threats exist, it makes it difficult to pinpoint the sources of exposure and prevent additional poisonings in the future.
According to CDC, there’s no safe blood lead level in children, and even low levels of lead have been shown to impact IQ, attention and academic achievement. Other effects of childhood lead poisoning include damage to the nervous systems, slowed growth and development, behavioral issues, and hearing and speech problems. Research has found that investing in lead hazard control reaps significant benefits, both in preventing the high cost of special care and services and in protecting a child’s opportunity to succeed academically, which is often a predictor of future health, prosperity and longevity. In California alone, research shows that EBLL results in lost earnings of up to $11 billion over the lifetime of children born each year.
Study co-author Eric Roberts, a pediatrician and co-principal investigator of the California Environmental Health Tracking Program at the Public Health Institute, said that because the standards determining who should be tested for lead vary across states, he and colleagues had a hunch many at-risk and impacted children were being overlooked. According to the Pediatrics study, the American Academy of Pediatrics recommends clinicians refer to state and local lead screening guidelines, “but these recommendations are often difficult for clinicians to access and commonly defer to practitioners’ individual evaluations of EBLL risk in the communities they serve, a task for which few are equipped.” And while laws require lead testing for Medicaid and WIC enrollees, researchers said the requirement often goes unenforced. That means childhood lead testing is mostly left to the discretion of physicians.
“We did observe almost universally that when you ask state or local public health to quantify the amount of lead poisoning, they provide you with numbers of lead-exposed kids identified by physicians — and that always struck me as a circular argument,” Roberts told me. In other words, in communities where physicians do a lot of testing, the resulting data underscores the need to sustain and possibly expand such testing; if little testing is done, the resulting data can cause physicians to incorrectly believe testing isn’t necessary.
He added: “Right now, folks are just assuming that certain communities are at low risk. But the default should be for testing, especially for children 12 to 24 months old. …We now assume no risk until it’s found, and that policy is clearly failing to protect kids.”
To conduct the study, Roberts and colleagues used National Health and Nutrition Examination Survey (NHANES) data to estimate state-level EBLL prevalence among children ages 12 months to 5 years between 1999 and 2010. They then compared those estimates to diagnostic case numbers reported to CDC. They found that in 23 of the 39 states where data was available, more than half of children with EBLL weren’t being identified. Nationwide, according to the study, only 64 percent — or 607,000 cases — of children with EBLL were identified and reported to CDC.
Between 1999 and 2010, researchers estimated that about 1.2 million children had EBLL, but only those 607,000 cases were identified and reported to CDC. The researchers noted that about 45 percent of unreported cases happened in years when the particular state wasn’t reporting such data to CDC, and about 55 percent of unreported cases weren’t reported due to “incomplete case ascertainment.” At the regional level, the greatest number of reported EBLL cases occurred in the Midwest and Northeast, while the highest number of overall cases occurred in the South. At the state-level, 23 states reported fewer than half of expected EBLL cases, while 11 states reported less than 20 percent of expected cases. For example, in California, the study estimated that only 37 percent of children with EBLL were identified.
Researchers noted that because of changes to NHANES data collection in 2010, clinician testing has become the only source of information on EBLL prevalence. In addition, CDC’s Childhood Lead Poisoning and Healthy Homes Program had its budget cut in 2012 from $29 million to $2 million, which means states have much less capacity to do lead-related surveillance, outreach, education, prevention, assessment and enforcement.
Co-authors Roberts, Daniel Madrigal, Jhaqueline Valle, Galatea King and Linda Kite write:
American Academy of Pediatrics policy…explicitly defers to state and local health departments to decide when children should undergo BLL testing. This policy is based on two assumptions, however: that well-resourced public health agencies will communicate effectively with providers, enabling them to make data-directed decisions about when to test for EBLL, and that statutory requirements for testing would be accompanied by mechanisms and resources for enforcement. Both of these assumptions have proven to be false, with the effect that large numbers of children with EBLL (indeed, the majority of these children in many parts of the country) have been missed by clinicians.
“I think the fundamental message here for public health is that we need to realize that simply enumerating the number of kids found by pediatric care providers is not a scientific basis for knowing whether kids are at risk or not,” Roberts told me. “(Lead exposure) is a much wider-spread problem than we’ve been willing to admit.”
Roberts noted that while the most common route of child lead exposure is lead-based house paint — and that risk has been drastically reduced in recent decades — the drinking water crisis in Flint shows that lead remains a serious threat to children’s health. In fact, he said as aging infrastructures deteriorate, children could face new lead exposure risks, which are all the more reason for better surveillance, testing and data.
On the clinical side, he said groups like the American Academy of Pediatrics can make a difference by strengthening their practitioner guidelines for childhood lead testing, with the understanding that local public health data might not provide a complete picture of who’s at risk and who should be tested.
“What we’re doing when we allow kids to be exposed to lead is we’re sacrificing some portion of their futures,” Roberts said. “There’s a cost to doing nothing.”
For a copy of the new lead study, visit Pediatrics.
Kim Krisberg is a freelance public health writer living in Austin, Texas, and has been writing about public health for 15 years. Follow me on Twitter — @kkrisberg.
Via a VV comment at ATTP I discover How a professional climate change denier discovered the lies and decided to fight for really long headlines which is fair enough, but via that I discover the far more interesting Taking Property Rights Seriously: The Case of Climate Change by Jonathan H. Adler1, a friend of said reformed denier.
This is interesting for two reasons: the arguments it puts forwards, and FME4 itself. Here’s its abstract:
The dominant approach to environmental policy endorsed by conservative and libertarian policy thinkers, so-called “free market environmentalism” (FME), is grounded in the recognition and protection of property rights in environmental resources. Despite this normative commitment to property rights, most self-described advocates of FME adopt a utilitarian, welfare-maximization, approach to climate change policy, arguing that the costs of mitigation measures could outweigh the costs of climate change itself. Yet even if anthropogenic climate change is decidedly less than catastrophic – indeed, even if it net beneficial to the globe as whole – human-induced climate change is likely to contribute to environmental changes that violate traditional conceptions of property rights… It may well be that aggregate human welfare would be maximized in a warmer, wealthier world, or that the gains from climate change will offset environmental losses. Such claims, even if demonstrated, would not address the normative concern that the consequences of anthropogenic global warming would infringe upon the rights of people in less-developed nations. A true FME approach to climate change policy should be grounded in a normative commitment to property rights. As a consequence, this paper suggests a complete rethinking of the conventional conservative and libertarian approach to climate change.
The use of property rights is probably not going to be favourably received on the “left”, but that doesn’t matter, because for the moment we’re discussing an argument to be made to the “right”. We being by reminding ourselves of an old court case:
As understood by FME proponents, common law principles prohibit the forcible imposition of pollution or other harms onto the persons or property of others, even if such a forced exchange of rights would be net beneficial. For example, in one famous case from New York, the state’s highest court upheld an injunction shutting down a $1 million pulp mill employing several hundred workers in order to protect the riparian rights of a single farmer. “Although the damage to the plaintiff may be slight compared with the defendant’s expense of abating the condition,” the court held, “that is not a good reason for refusing the injunction.” Such a ruling, the court explained, “would deprive the poor litigant of his little property by giving it to those already rich.”
The application to the case of GW is obvious: just because the world overall might gain from burning lots of nice fossil fuels, living in nice warm houses, and whizzing around in cars and planes, doesn’t mean that individual harm (perhaps, stretching things slightly, harm-in-the-future; or maybe you just discount) is permissible, regardless of whether the net effect – if that could even be calculated – is positive or not.
This represents a completely different approach to the usual one where, a-la-Tol-etc, we compute a global damage function, with all it’s attendant problems. Before stopping to think of some of the problems, let’s extend and simplify this slightly, as Adler does, and split the world into those who emit lots of CO2 and gain from it: call them W. And those who emit less and will lose overall: call them T (this is a gross simplification for the sake of illustration of the usual assertion that those who emit least CO2, are poor, and will probably suffer most damage). We now imagine a global court in which T sue W for (a) damages and (b) injunctive relief, the latter meaning “you must stop emitting CO2”. If we look to the simple example of our riparian farmer and his enemy the pulp mill, we might expect them to get both. But, no. At least according to Adler; on the “clean hands” principle, T (even though emitting less CO2 than W), cannot claim to be emitting little or none, and so aren’t entitled to ask W to stop. Instead, they just get (a), viz damages2.
I should now consider some of the obvious problems with this approach, which even Adler admits is only a thought experiment. Firstly, no global court exists. Second, it is not possible to specify damage with precision, even assuming the most simple form of change he considers, sea level rise3. Third, assuming a simplifying aggregation into just two blocks is implausible. Some of these problems might in principle be resolved, some seem insurmountable. But that doesn’t necessarily matter. The point is not to setup such a system: recall that we’re only talking to the “right” here who believe in strong property rights. Those who believe in utilitarianism might not even accept the principle. But for those who do claim to believe in FME, it provides a philosophical underpinning for wealth xfer to those who would lose under GW.
* These conservatives want to convince you that climate change is real
1. Not being familiar with it, I poked around for discussion of it. I found a ref to it at Climate Etc. but as you’d expect there’s little of interest there.
2. OIANAL. If you want all the right words used in the proper order, read Adler’s original.
3. See-also Impacts – IX – Sea Level 4 – Sinking Megacities May 2, 2017 by scienceofdoom.
4. Also known as “Fuck My Environment”, by analogy with FML.
Via a VV comment at ATTP I discover How a professional climate change denier discovered the lies and decided to fight for really long headlines which is fair enough, but via that I discover the far more interesting Taking Property Rights Seriously: The Case of Climate Change by Jonathan H. Adler1, a friend of said reformed denier.
This is interesting for two reasons: the arguments it puts forwards, and FME4 itself. Here’s its abstract:
The dominant approach to environmental policy endorsed by conservative and libertarian policy thinkers, so-called “free market environmentalism” (FME), is grounded in the recognition and protection of property rights in environmental resources. Despite this normative commitment to property rights, most self-described advocates of FME adopt a utilitarian, welfare-maximization, approach to climate change policy, arguing that the costs of mitigation measures could outweigh the costs of climate change itself. Yet even if anthropogenic climate change is decidedly less than catastrophic – indeed, even if it net beneficial to the globe as whole – human-induced climate change is likely to contribute to environmental changes that violate traditional conceptions of property rights… It may well be that aggregate human welfare would be maximized in a warmer, wealthier world, or that the gains from climate change will offset environmental losses. Such claims, even if demonstrated, would not address the normative concern that the consequences of anthropogenic global warming would infringe upon the rights of people in less-developed nations. A true FME approach to climate change policy should be grounded in a normative commitment to property rights. As a consequence, this paper suggests a complete rethinking of the conventional conservative and libertarian approach to climate change.
The use of property rights is probably not going to be favourably received on the “left”, but that doesn’t matter, because for the moment we’re discussing an argument to be made to the “right”. We being by reminding ourselves of an old court case:
As understood by FME proponents, common law principles prohibit the forcible imposition of pollution or other harms onto the persons or property of others, even if such a forced exchange of rights would be net beneficial. For example, in one famous case from New York, the state’s highest court upheld an injunction shutting down a $1 million pulp mill employing several hundred workers in order to protect the riparian rights of a single farmer. “Although the damage to the plaintiff may be slight compared with the defendant’s expense of abating the condition,” the court held, “that is not a good reason for refusing the injunction.” Such a ruling, the court explained, “would deprive the poor litigant of his little property by giving it to those already rich.”
The application to the case of GW is obvious: just because the world overall might gain from burning lots of nice fossil fuels, living in nice warm houses, and whizzing around in cars and planes, doesn’t mean that individual harm (perhaps, stretching things slightly, harm-in-the-future; or maybe you just discount) is permissible, regardless of whether the net effect – if that could even be calculated – is positive or not.
This represents a completely different approach to the usual one where, a-la-Tol-etc, we compute a global damage function, with all it’s attendant problems. Before stopping to think of some of the problems, let’s extend and simplify this slightly, as Adler does, and split the world into those who emit lots of CO2 and gain from it: call them W. And those who emit less and will lose overall: call them T (this is a gross simplification for the sake of illustration of the usual assertion that those who emit least CO2, are poor, and will probably suffer most damage). We now imagine a global court in which T sue W for (a) damages and (b) injunctive relief, the latter meaning “you must stop emitting CO2”. If we look to the simple example of our riparian farmer and his enemy the pulp mill, we might expect them to get both. But, no. At least according to Adler; on the “clean hands” principle, T (even though emitting less CO2 than W), cannot claim to be emitting little or none, and so aren’t entitled to ask W to stop. Instead, they just get (a), viz damages2.
I should now consider some of the obvious problems with this approach, which even Adler admits is only a thought experiment. Firstly, no global court exists. Second, it is not possible to specify damage with precision, even assuming the most simple form of change he considers, sea level rise3. Third, assuming a simplifying aggregation into just two blocks is implausible. Some of these problems might in principle be resolved, some seem insurmountable. But that doesn’t necessarily matter. The point is not to setup such a system: recall that we’re only talking to the “right” here who believe in strong property rights. Those who believe in utilitarianism might not even accept the principle. But for those who do claim to believe in FME, it provides a philosophical underpinning for wealth xfer to those who would lose under GW.
* These conservatives want to convince you that climate change is real
1. Not being familiar with it, I poked around for discussion of it. I found a ref to it at Climate Etc. but as you’d expect there’s little of interest there.
2. OIANAL. If you want all the right words used in the proper order, read Adler’s original.
3. See-also Impacts – IX – Sea Level 4 – Sinking Megacities May 2, 2017 by scienceofdoom.
4. Also known as “Fuck My Environment”, by analogy with FML.
In 2015, we wrote about some fascinating research from one of our scientists based at our Cambridge Institute, Dr Jason Carroll.
Carroll and his team uncovered a possible explanation for why women whose breast cancer cells carry two key molecules – called the oestrogen and progesterone receptors – do better than those whose cells only carry the oestrogen receptor. Even when they receive the same treatment.
They revealed that when signals were sent through the progesterone receptor it slowed down the growth of breast cancer cells. To find out if this had potential as a treatment, the researchers tested a new combination of hormone therapies and found it slowed down tumour growth in mice.
This was a really important study, but had only been carried out in mice, so it was too early to say whether it could help treat women with breast cancer.
Now, just 2 years after the discovery from Carroll’s team, 3 clinical trials are set to open that will test this new approach in people.
Carroll’s study was instrumental in understanding how the progesterone receptor works in breast cancer, and how it can act as a handbrake on cancer cells’ growth. The team’s results have now led to a possible new approach for stopping double positive breast cancer cells growing.
Normally, women whose breast cancer cells carry the oestrogen receptor (so-called ER positive) are treated with drugs that cut off oestrogen or directly block the oestrogen receptor. This will either be tamoxifen or aromatase inhibitors, depending on whether the woman is pre- or post-menopausal.
Dr Jason Carroll
But Carroll’s results showed that treating mice with those oestrogen-blocking drugs and a dose of the hormone progesterone had an even bigger effect compared to the oestrogen-blocking drugs alone.
Progesterone changes the genes that oestrogen turns on and off by forcing the oestrogen receptor to sit in different positions in the genome, and according to Carroll this means the combined treatment offers a safety net.
“It’s like a double blow,” he says. “We cut off oestrogen, and as an insurance policy we use progesterone to pull the oestrogen receptor away from the genes that support cancer’s growth.”
This was the evidence that was needed to take the research into early clinical trials.
When the results were published, they caused quite a stir. Carroll says they challenged how people thought these different types of breast cancer worked at the time.
“For years there’d been a lot of confusion over whether progesterone encourages cancer to grow, and this has largely come from population studies looking into hormone replacement therapy (HRT),” he says
Some women choose to take HRT to ease symptoms caused by the menopause. There are different types, and the combined form contains a man-made version of progesterone called medroxyprogesterone acetate (or similar versions).
It’s this combined form of HRT in particular that is linked to an increased risk of developing breast cancer.
“This led to the popular belief that progesterone encourages breast cancer to grow,” says Carroll. “But it’s not that simple. Different versions of man-made progesterone seem to have different effects on cells compared to the natural hormone.
“Plus we were trying to understand what role progesterone plays after a breast cancer has developed, rather than looking at how it affects risk of cancer beginning in the first place.”
Just 6 months after the findings were published, Carroll was approached by Dr Richard Baird, a clinical trials specialist based at our Cambridge Centre, to discuss possible trials.
Because the drugs we want to test have been used by doctors for years for a variety of reasons, we know they are safe and what doses to use them at. Plus they have the benefit of being cheap.
– Dr Jason Carroll
“A clinical trial from Brazil showed that around 40% of women whose cancer had stopped responding to standard oestrogen-blocking therapies, including tamoxifen and anastrozole, still responded to a man-made progesterone called megestrol acetate,” says Carroll.
Their idea was to try the combination of oestrogen-blocking drug and progesterone as the first therapy women receive. And setting up the trial was surprisingly simple.
“Because the drugs we want to test have been used by doctors for years for a variety of reasons, including in the treatment of late stage metastatic breast cancer, we know they are safe and what doses to use them at. Plus they have the benefit of being cheap,” says Carroll.
The Pioneer trial is being led by Carroll and Baird, and will start enrolling women with early stage breast cancer in June 2017.
Women joining the trial will still get the gold standard of care treatment that all women with early breast cancer receive, but the team will test the combination in a gap that exists between diagnosis and surgery.
“What happens is there’s normally a few weeks’ wait between a women having a biopsy and then having surgery to remove her tumour.
“In our trial, we’re going to ask women to take the combination of an oestrogen-blocking drug – in our case anastrozole – and the man-made progesterone (megestrol acetate) during this wait. Then we can study the biopsy sample and a sample of the tumour removed during surgery to see the effects of the combination treatment on the cancer cells.”
Carroll and Baird are focusing on post-menopausal women in their trial, but there are 2 other trials that have been set up in partnership that look at slightly different things.
One of the trials, led by Dr Carlo Palmieri at the University of Liverpool, is being funded by us. The approach is similar to that of Carroll and Baird, but Palmieri’s trial will involve pre-menopausal women who will be given a combination of tamoxifen and man-made progesterone instead.
The third trial will be opening in Australia, testing a combination of aromatase inhibitors and natural progesterone in post-menopausal women.
If the trials show that the combination treatment is effective by studying tumour samples, the next steps would be extending the studies into larger trials so women are given the combination after surgery too, to see if it improves survival and doesn’t cause any harms in the long-term.
Another interesting angle to the trials is finding out if adding progesterone to oestrogen-blocking drugs helps reduce the side effects of treatment.
“For the maximum effect, women should take oestrogen-blocking drugs for the recommended time period after surgery,” says Carroll. “But unpleasant side effects mean many women stop their treatment early, and this increases the risk of their cancer returning.
“As part of this trial, we’re also finding out if a lower dose of progesterone routinely used to alleviate menopausal symptoms works as well as the higher dose. This could make the side effects of hormone therapy more manageable and improve the fraction of women that stay on their standard treatments.”
The clinical trials are only just opening, so we’ll need to wait until they’ve got some results before knowing if this will benefit women with double positive breast cancer and could be made widely available.
But thanks to some excellent lab research by Carroll and his team, and our funding, the trials are up and running and we’re another step closer to an answer.
Emma
In 2015, we wrote about some fascinating research from one of our scientists based at our Cambridge Institute, Dr Jason Carroll.
Carroll and his team uncovered a possible explanation for why women whose breast cancer cells carry two key molecules – called the oestrogen and progesterone receptors – do better than those whose cells only carry the oestrogen receptor. Even when they receive the same treatment.
They revealed that when signals were sent through the progesterone receptor it slowed down the growth of breast cancer cells. To find out if this had potential as a treatment, the researchers tested a new combination of hormone therapies and found it slowed down tumour growth in mice.
This was a really important study, but had only been carried out in mice, so it was too early to say whether it could help treat women with breast cancer.
Now, just 2 years after the discovery from Carroll’s team, 3 clinical trials are set to open that will test this new approach in people.
Carroll’s study was instrumental in understanding how the progesterone receptor works in breast cancer, and how it can act as a handbrake on cancer cells’ growth. The team’s results have now led to a possible new approach for stopping double positive breast cancer cells growing.
Normally, women whose breast cancer cells carry the oestrogen receptor (so-called ER positive) are treated with drugs that cut off oestrogen or directly block the oestrogen receptor. This will either be tamoxifen or aromatase inhibitors, depending on whether the woman is pre- or post-menopausal.
Dr Jason Carroll
But Carroll’s results showed that treating mice with those oestrogen-blocking drugs and a dose of the hormone progesterone had an even bigger effect compared to the oestrogen-blocking drugs alone.
Progesterone changes the genes that oestrogen turns on and off by forcing the oestrogen receptor to sit in different positions in the genome, and according to Carroll this means the combined treatment offers a safety net.
“It’s like a double blow,” he says. “We cut off oestrogen, and as an insurance policy we use progesterone to pull the oestrogen receptor away from the genes that support cancer’s growth.”
This was the evidence that was needed to take the research into early clinical trials.
When the results were published, they caused quite a stir. Carroll says they challenged how people thought these different types of breast cancer worked at the time.
“For years there’d been a lot of confusion over whether progesterone encourages cancer to grow, and this has largely come from population studies looking into hormone replacement therapy (HRT),” he says
Some women choose to take HRT to ease symptoms caused by the menopause. There are different types, and the combined form contains a man-made version of progesterone called medroxyprogesterone acetate (or similar versions).
It’s this combined form of HRT in particular that is linked to an increased risk of developing breast cancer.
“This led to the popular belief that progesterone encourages breast cancer to grow,” says Carroll. “But it’s not that simple. Different versions of man-made progesterone seem to have different effects on cells compared to the natural hormone.
“Plus we were trying to understand what role progesterone plays after a breast cancer has developed, rather than looking at how it affects risk of cancer beginning in the first place.”
Just 6 months after the findings were published, Carroll was approached by Dr Richard Baird, a clinical trials specialist based at our Cambridge Centre, to discuss possible trials.
Because the drugs we want to test have been used by doctors for years for a variety of reasons, we know they are safe and what doses to use them at. Plus they have the benefit of being cheap.
– Dr Jason Carroll
“A clinical trial from Brazil showed that around 40% of women whose cancer had stopped responding to standard oestrogen-blocking therapies, including tamoxifen and anastrozole, still responded to a man-made progesterone called megestrol acetate,” says Carroll.
Their idea was to try the combination of oestrogen-blocking drug and progesterone as the first therapy women receive. And setting up the trial was surprisingly simple.
“Because the drugs we want to test have been used by doctors for years for a variety of reasons, including in the treatment of late stage metastatic breast cancer, we know they are safe and what doses to use them at. Plus they have the benefit of being cheap,” says Carroll.
The Pioneer trial is being led by Carroll and Baird, and will start enrolling women with early stage breast cancer in June 2017.
Women joining the trial will still get the gold standard of care treatment that all women with early breast cancer receive, but the team will test the combination in a gap that exists between diagnosis and surgery.
“What happens is there’s normally a few weeks’ wait between a women having a biopsy and then having surgery to remove her tumour.
“In our trial, we’re going to ask women to take the combination of an oestrogen-blocking drug – in our case anastrozole – and the man-made progesterone (megestrol acetate) during this wait. Then we can study the biopsy sample and a sample of the tumour removed during surgery to see the effects of the combination treatment on the cancer cells.”
Carroll and Baird are focusing on post-menopausal women in their trial, but there are 2 other trials that have been set up in partnership that look at slightly different things.
One of the trials, led by Dr Carlo Palmieri at the University of Liverpool, is being funded by us. The approach is similar to that of Carroll and Baird, but Palmieri’s trial will involve pre-menopausal women who will be given a combination of tamoxifen and man-made progesterone instead.
The third trial will be opening in Australia, testing a combination of aromatase inhibitors and natural progesterone in post-menopausal women.
If the trials show that the combination treatment is effective by studying tumour samples, the next steps would be extending the studies into larger trials so women are given the combination after surgery too, to see if it improves survival and doesn’t cause any harms in the long-term.
Another interesting angle to the trials is finding out if adding progesterone to oestrogen-blocking drugs helps reduce the side effects of treatment.
“For the maximum effect, women should take oestrogen-blocking drugs for the recommended time period after surgery,” says Carroll. “But unpleasant side effects mean many women stop their treatment early, and this increases the risk of their cancer returning.
“As part of this trial, we’re also finding out if a lower dose of progesterone routinely used to alleviate menopausal symptoms works as well as the higher dose. This could make the side effects of hormone therapy more manageable and improve the fraction of women that stay on their standard treatments.”
The clinical trials are only just opening, so we’ll need to wait until they’ve got some results before knowing if this will benefit women with double positive breast cancer and could be made widely available.
But thanks to some excellent lab research by Carroll and his team, and our funding, the trials are up and running and we’re another step closer to an answer.
Emma
“End? No, the journey doesn’t end here. Death is just another path, one that we all must take. The grey rain-curtain of this world rolls back, and all turns to silver glass, and then you see it.” -J.R.R. Tolkien
Stars live for a variety of ages, from just a million or two years for some to tens of trillions of years for others. But even after a star has run out of its fuel and died, its stellar corpse continues to shine on. Neutron stars and white dwarfs are both extremely massive, but very small in volume compared to a star. As a result, they cool very slowly, so slow that a single one has not yet gone dark in all the Universe.
An accurate size/color comparison of a white dwarf (L), Earth reflecting our Sun’s light (middle), and a black dwarf (R). Image credit: BBC / GCSE (L) / SunflowerCosmos (R).
So how long will it take, and who will get there first: neutron stars or white dwarfs? Believe it or not, there’s still enough uncertainty about how neutron stars cool, mostly due to uncertainties in neutrino physics, that we think we know the answer to be white dwarfs — and 10^14 or 10^15 years — but we’re not entirely sure!
Forming from the remnant of a massive star that’s gone supernova, a neutron star is the collapsed core that remains behind. Image credit: NASA.
Come find out what we know about finding the first truly dark star in the Universe today.
“End? No, the journey doesn’t end here. Death is just another path, one that we all must take. The grey rain-curtain of this world rolls back, and all turns to silver glass, and then you see it.” -J.R.R. Tolkien
Stars live for a variety of ages, from just a million or two years for some to tens of trillions of years for others. But even after a star has run out of its fuel and died, its stellar corpse continues to shine on. Neutron stars and white dwarfs are both extremely massive, but very small in volume compared to a star. As a result, they cool very slowly, so slow that a single one has not yet gone dark in all the Universe.
An accurate size/color comparison of a white dwarf (L), Earth reflecting our Sun’s light (middle), and a black dwarf (R). Image credit: BBC / GCSE (L) / SunflowerCosmos (R).
So how long will it take, and who will get there first: neutron stars or white dwarfs? Believe it or not, there’s still enough uncertainty about how neutron stars cool, mostly due to uncertainties in neutrino physics, that we think we know the answer to be white dwarfs — and 10^14 or 10^15 years — but we’re not entirely sure!
Forming from the remnant of a massive star that’s gone supernova, a neutron star is the collapsed core that remains behind. Image credit: NASA.
Come find out what we know about finding the first truly dark star in the Universe today.
