Archive for the ‘Health’ Category
Seasonal Affective Disorder affects quite a few people, and it’s interesting that using a bright lamp to combat it also helps with regular (non-seasonal) depression. Jorden Pearson reports at Motherboard:
There’s a familiar ritual for people suffering from seasonal affective disorder, or SAD, a very real condition that leaves people feeling depressed in the slushy depths of winter: you wake up, the world still dark and frigid, and you flip on a little lamp that tricks your brain into thinking you’re absorbing sunlight. It’s a treatment with some serious techno-dystopian vibes, yet research has shown for decades that it works.
But according to new research, those dorky little lamps aren’t only useful for people with SAD. In a study that tested the efficacy of SAD lightboxes alongside antidepressants on people with non-seasonal depression, researchers at the University of British Columbia concluded that those little lamps can help with regular old non-winter related clinical depression, too.
“We always think of seasonal depression as a different type of depression for all kinds of good reasons, so people haven’t considered light therapy as a way to treat non-seasonal depression,” Dr. Raymond Lam, the psychiatrist at the University of British Columbia who led the study, told me over the phone. “We thought it was time for a good study, so that’s what we did.”
Although some of the earliest studies on the effectiveness of SAD lamps involved people without SAD itself, these studies were small—just seven subjects, in some cases—and unsatisfactory, Lam said.
The study, published on Wednesday in JAMA Psychiatry, split 121 subjects into four test groups. The first group got the lamp with a placebo antidepressant, the second got the lamp with a real pill, the third group used a switched-off negative ion generator—effectively a placebo, since it’s hard to fake light—and an antidepressant, and the final group got a real negative ion generator with a fake pill.
Negative ion generators are machines that fill the air with electrically-charged air molecules, which supposedly have an effect that may help with depression. But for the purposes of this study, Lam said, they just had to look fancy and make a nice noise.
After eight weeks of treatment, subjects with the real lamp and fake pills reported feeling much better, while those with the lamps and real pills reported feeling the best out of all the groups. Sorry, folks with ion generators. . .
Light boxes for treating SAD have come down a lot in price over the past several years.
Jen Hayden has an excellent post at Daily Kos. From it:
Who could’ve seen this coming? When you don’t teach kids about safe sex, they tend to have sex anyway, minus the safe part: . . .
And later she quotes:
Abstinence-only programs have been an enormous failure, despite heavy funding from the George W. Bush administration and conservative legislatures:
Abstinence-only-until-marriage programs don’t work.
To date, 11 states have evaluated the impact of their abstinence-only-until-marriage programs. None has been shown to reduce teen sexual activity.
Virginity pledgers have found “loopholes” to keep their pledges intact—engaging in risky oral or anal sex—and neglecting to use condoms when they do begin to have vaginal intercourse, according to research from Peter Bearman at Columbia University.
A 2007 federally-funded evaluation of these programs found that youth in the control group were no more likely to have abstained from sex and, among those who reported having sex, had a similar number of partners and had initiated sex at the same age.
Astounding. This takes self-investigation and self-policing to a new level, and raises serious questions about the EPA’s ability to do its mission—and indeed about EPA’s understanding of its mission. Sharon Lerner reports in The Intercept:
The Environmental Protection Agency concluded in June that there was “no convincing evidence” that glyphosate, the most widely used herbicide in the U.S. and the world, is an endocrine disruptor.
On the face of it, this was great news, given that some 300 million pounds of the chemical were used on U.S. crops in 2012, the most recent year measured, and endocrine disruption has been linked to a range of serious health effects, including cancer, infertility, and diabetes. Monsanto, which sells glyphosate under the name Roundup, certainly felt good about it. “I was happy to see that the safety profile of one of our products was upheld by an independent regulatory agency,” wrote Steve Levine on Monsanto’s blog.
But the EPA’s exoneration — which means that the agency will not require additional tests of the chemical’s effects on the hormonal system — is undercut by the fact that the decision was based almost entirely on pesticide industry studies. Only five independently funded studies were considered in the review of whether glyphosate interferes with the endocrine system. Twenty-seven out of 32 studies that looked at glyphosate’s effect on hormones and were cited in the June review — most of which are not publicly available and were obtained by The Intercept through a Freedom of Information Act request — were either conducted or funded by industry. Most of the studies were sponsored by Monsanto or an industry group called the Joint Glyphosate Task Force. One study was by Syngenta, which sells its own glyphosate-containing herbicide, Touchdown.
Findings of Harm Were Dismissed
Who pays for studies matters, according to The Intercept’s review of the evidence used in the EPA’s decision. Of the small minority of independently funded studies that the agency considered in determining whether the chemical poses a danger to the endocrine system, three of five found that it did. One, for instance, found that exposure to glyphosate-Roundup “may induce significant adverse effects on the reproductive system of male Wistar rats at puberty and during adulthood.” Another concluded that “low and environmentally relevant concentrations of glyphosate possessed estrogenic activity.” And a review of the literature turns up many more peer-reviewed studies finding glyphosate can interfere with hormones, affecting such things as hormonal activity in human liver cells, functioning of rat sperm, and the sex ratio of exposed tadpoles.
Yet, of the 27 industry studies, none concluded that glyphosate caused harm. Only one admitted that the pesticide might have had a role in causing the health problems observed in lab animals exposed to it. Some rats that consumed it were more likely to have to have soft stools, reduced body weight, and smaller litters. But because that evidence didn’t meet a test of statistical significance, the authors of the Monsanto study deemed it “equivocal.”
Indeed, many of the industry-funded studies contained data that suggested that exposure to glyphosate had serious effects, including a decrease in the number of viable fetuses and fetal body weight in rats; inflammation of hormone-producing cells in the pancreas of rats; and increases in the number of pancreatic cancers in rats. Each is an endocrine-related outcome. Yet in each case, sometimes even after animals died, the scientists found reasons to discount the findings — or to simply dismiss them.
When rats exposed to glyphosate had a decreased number of pregnancies that implanted, for instance, the authors of a 1980 Monsanto-sponsored study explained that “since ovulation and implantation occurred prior to treatment, the decreases … were not considered to be treatment related.” Although they noted that the decrease in implantations and viable fetuses was “statistically significant,” the authors nonetheless concluded that the decrease in implantations was a random occurrence.
While recent research has shown that very low doses of endocrine disruptors can not only have health effects but effects that are more dramatic than those caused by higher doses, some of the studies dismiss clear examples of harm because they occur in animals given relatively low doses of the substance. A study prepared by Monsanto in 1990, for instance, . . .
Trigger warning: Vivid.
If you’re ever locked in a cage in a gingerbread house, screaming in terror as you’re menaced by a wicked witch, take heart: she isn’t planning to eat you.
At least, not if she wants you to taste good. That’s because when animals (and presumably humans) have been frightened or stressed out before death, it actually affects the quality of their meat.
The scientific basis for the phenomenon is well-established, and it’s frequently been discussed as a reason to make slaughterhouse practices more humane. The key ingredient here is lactic acid: in an unstressed animal, after death, muscle glycogen is converted into lactic acid, which helps keep meat tender, pink, and flavorful. Adrenaline released by stress before slaughter uses up glycogen, which means there’s not enough lactic acid produced postmortem. This affects different kind of meat in different ways, but in general it’ll be tough, tasteless, and high in pH, and will go bad quicker than unstressed meat. (Lactic acid helps slow the growth of spoilage bacteria.)
In pigs, . . .
Veronique Greenwood reports in Quanta:
“Think of a deck of cards,” said Dan Larremore. Now, take a pair of scissors and chop the 52 cards into chunks. Throw them in the air. Card confetti rains down, so the pieces are nowhere near where they started. Now tape them into 52 new cards, each one a mosaic of the original cards. After 48 hours, repeat.
You have just reenacted the process that Plasmodium falciparum uses to avoid the immune system. P. falciparum is the world’s most dangerous malaria parasite, causing 600,000 deaths every year and killing more children under the age of 5 than any other infectious disease on the planet. Larremore, an applied mathematician, was introduced to its promiscuous habits while doing postdoctoral research at what is now the Harvard T.H. Chan School of Public Health.
Each card represents a gene for a protein that attaches to the walls of the host’s blood vessels, anchoring the parasite so that it cannot be dragged into the spleen, where it would be detected and destroyed. Each falciparum parasite has 50 to 60 of these vargenes, as they are called, and as time passes the parasite uses first one, then another, presenting a constantly morphing face to immune cells that might spot it clinging to the blood vessel. The crowning glory of this tactic, though, is that when the parasite divides, which it does every couple of days, chunks and snippets of the genes swap places up and down the chromosomes. In one out of every 500 parasites, this process will generate an entirely new gene. With the number of parasites out there, that adds up quickly. “It’s crazy. It means the total number of var gene sequences in the world is millions and millions — virtually infinite,” said Antoine Claessens, a malaria researcher with the Medical Research Council, The Gambia Unit, in Fajara.
New evidence from Larremore and his collaborators, however, reveals a paradoxical stability in these genes. In a recent paper in Nature Communications,they show that while var genes themselves are never repeated, short sequences of DNA in them — pieces of cut-up card — are shared between species that have been separate for millions of years. It’s a finding that has made some malaria researchers feel hopeful, because it suggests that there are limits on the crazy remaking of thevar genes, which could mean that vaccines can be developed to fight them.
Slicing and Dicing
“We want to know basic stuff,” said Caroline Buckee, an epidemiologist at the Harvard T.H. Chan School of Public Health and a co-author of the new study. “Are there certain parasites that cause disease more than others? Are they evolutionarily related to each other? … These questions, which in most pathogens we can figure out how to answer, have no answer [in malaria], because we don’t know how to compare these genes to each other.”
The usual tool for such a task is a phylogenetic tree. At the tree’s base is the oldest version of a gene, and as its daughters accrue small differences — a single DNA base change here, a single base change there — they become separate branches. Trees are built by lining the genes up next to each other and checking for differences at each DNA base. The trees have been helpful in studying the divergence of genes in viruses like the flu, which changes via just such a process of mutation.
Malaria researchers have used them as well, but with mixed results. A pair of var genes might have a chunk of 30 DNA bases in common, but if that chunk is at the beginning of one gene and at the end of another — which happens all the time in the shuffling process — a tree will call it a difference instead of a commonality. If the chunk does happen to be in the same place in both genes, a tree will say that the genes recently diverged, but the chunk could just as well have arrived two days ago in one gene and a year ago in another. All of this means that trees built from var genes are at best difficult to interpret, and at worst misleading, implying relationships where none exist. “It’s a mush. That’s the technical term,” joked Martine Zilversmit, a malaria researcher at the American Museum of Natural History in New York City.
If you want to compare these genes, though, there aren’t many other options. “It was a case of ‘this is the tool we have,’ and everyone kind of jamming their data into the tool,” said Buckee, who first began to talk about an alternative approach with collaboratorAaron Clauset, now a professor of computer science at the University of Colorado, Boulder, when the two were postdocs.
In 2012, Larremore, now at the Santa Fe Institute in New Mexico, took a postdoc position with Buckee and Clauset to try and see whether network analysis, a field he knew well, could help provide an alternative way to track the history of malaria parasites. Network analysis involves drawing links between nodes that have something in common, generating a diagram that can reveal underlying patterns. Linked nodes might be people who are friends in a social network, diseases that afflict the same people, or genes that share chunks of sequence.
If you make a network in which var genes are only connected if they share chunks of a certain length, the commonalities leap out. Buckee, Larremore and Clauset published a paper in 2013 showing that such networks could pick out identical sequences shared byP. falciparum parasites from different continents. Being able to clearly see these relationships helps researchers in their efforts to figure out how and why they arose. A greater number of common chunks in a pair of genes could mean that they share a recent ancestor, or it could indicate that the proteins they produce have a similar way of interacting with the immune system. The chunks could also be evidence of an ancestral cache of cut-up card pieces that modern parasites still carry around.
To investigate whether var genes exist in other parasite species and, if they do, whether they share any chunks with P. falciparum, the researchers analyzed samples of malaria parasites from wild apes. They used parasites from feces collected in the jungle and from the blood of sanctuary chimps, assembling DNA sequences from five Plasmodiumspecies that infect gorillas and chimps, including one that had already been found to have var genes.
They were in luck: The var gene marker they searched for cropped up in at least three of the species. That in itself is interesting, because it means the vargene family is old — ancient, even, according to Thomas Lavstsen, a biologist at the University of Copenhagen in Denmark, who studies the genes but was not involved in the research.
When the team created their networks, they saw something else striking. . .
Moises Valsquez-Manoff writes in the NY Times:
BY last August, my 1-year-old son had taken five courses of antibiotics for recurrent ear infections. That was alarming. By age 10, the average American child has had about 10 courses, and some microbiologists argue that even one course a year is too many — that it might damage our native microbial ecosystem, with far-reaching consequences.
My son was off to a worrisome start. Why, I wondered, didn’t doctors work harder to prevent this collateral damage, not with store-bought probiotics, but with “microbial restoration”? Why didn’t we reinfuse patients with their own microbes after antibiotics?
The scientific term for this is “autologous fecal transplant.” In theory, it could work like a system reboot disk works for your computer. You’d freeze your feces, which are roughly half microbes, and when your microbiome became corrupted or was depleted with antimicrobials, you could “reinstall” it from a backup copy.
That damage from antibiotics may not be trivial. Studies have linked antibiotic use early in life with a modestly increased risk of asthma,inflammatory bowel disease, obesity and rheumatoid arthritis. These are associations, of course; they don’t prove that antibiotics cause disease.
Many microbiologists, however, take the possibility seriously that antibiotics could contribute to the development of those diseases. That’s because, in animal studies, depleting certain microbes early in life — microbes that may promote gut health and soothe the immune system — makes rodents more susceptible to inflammatory disease later.
The “self-transplant” isn’t a new idea. In the late 1950s, a medical technologist named Stanley Falkow practiced what he called “fecal reconstitution.” Gut troubles often plagued surgery patients during recovery. They’d received antibiotics prophylactically, depleting their native gut microbes. So Mr. Falkow, working with an internist, began giving these patients capsules containing their own feces, collected and frozen before treatment. It helped tremendously. But when the hospital administrator found out — patients didn’t know what they were swallowing — he fired Mr. Falkow. (Mr. Falkow, now Dr. Falkow, an emeritus microbiology professor at Stanford, was rehired soon thereafter, but had to abandon the project.)
Almost 60 years later, the “fecal transplant” is a cutting-edge treatment for the pathogen Clostridium difficile, a bug that kills 29,000 yearly and infects nearly half a million. “C. diff” tends to strike after antibiotics deplete the microbes that naturally inhabit the gut, leaving us vulnerable to invasion. So far, fecal transplants seem to be more than 90 percent effective at curing these infections.
As currently practiced, however, the transplant material usually comes from someone else. Even with careful screening, that presents some risk. It’s theoretically safer to receive one’s own microbes. North York General Hospital in Toronto recently completed a pilot study banking incoming patients’ own stool. Should any of these patients develop infections after antibiotics, their own microbes were on hand for reconstitution.
None fell sick in this case, so the transplants weren’t needed. But the project proved feasibility, and achieved a processing time — gathering, blending and freezing — of less than one hour.
Memorial Sloan Kettering Cancer Center in New York has also started a proactive stool-banking study. Most of the subjects are patients with leukemia. Before stem cell transplants, patients receive antibiotics andchemotherapy, often wiping out their microbiota.
Dr. Eric Pamer, a physician and scientist at Memorial Sloan Kettering, has discovered that the diversity of the microbiota just after the stem cell transplant predicts well-being and survival. After excluding death from leukemia recurrence, those with the least diverse microbiomes after surgery were five times less likely to remain alive three years later, when compared with those with the most diverse. . .