An unhealthy shift in your gut microbes might cause you to gain weight by changing how many calories you burn while you sleep, a new study with mice suggests.
When researchers used a drug to change the gut microbiome in mice, they saw a reduction in resting metabolic rate—the rate at which calories are burned while sleeping or resting.
“Our research leads to the conclusion that it is probably bacteria (in the gut) that are responsible for the calories you burn while you are asleep,” says John Kirby, professor of microbiology and urology at the University of Iowa Carver College of Medicine and one of the authors of the study in eBiomedicine.
DRUG FOR AUTISM AND BIOPOLAR
Kirby and his colleagues focused on the effects of risperidone, an antipsychotic drug that causes significant weight gain in patients. Risperidone is used to treat various psychiatric disorders in adults and children, including autism, bipolar disorder, and schizophrenia, and prescribing rates for children have increased nearly eight-fold over the last two decades.
In an earlier study, Kirby and Chadi Calarge, a University of Iowa pediatric psychiatrist, compared patients taking risperidone long-term to patients who were not on the drug. They found that weight gain was correlated with a significant shift in the composition of the patients’ gut microbiomes. These results were published in Translational Psychiatry.
In the new study, Kirby teamed up with Justin Grobe, assistant professor of pharmacology, to find out how this risperidone-induced microbiome shift causes weight gain. Mirroring the human studies, the researchers showed that risperidone causes weight gain in mice (an extra 2.5 grams, or approximately 10 percent of the total body mass, over two months, compared to controls) and significantly alters the bacterial composition of the mouse microbiome.
They then showed that the altered microbiome causes a reduction in resting metabolic rate that is entirely responsible for the excess weight gain.
“The control mice gain a little weight as they age and their microbiome undergoes a ‘healthy shift’ due to aging. With the risperidone, the mice become obese and exhibit an alternative, less healthy shift in their microbiome,” Kirby says. “With this study, we now have a mechanism for how a shift in the microbiome contributes to weight gain, and it’s to do with changes to the resting metabolic rate.”
In fact, the scientists found that the amount of weight gain was pretty alarming, continue to the next page to see what their research uncovered.
If you need one more thing to put on the list of things about your life that you can blame on your parents, then here’s one everyone can add: face mites. Yes, believe it or not, everyone has them, you can’t get rid of them, and you get them from your parents. Well, you also exchange them with anyone else you brush faces with, but here’s the good news: they are harmless.
So breathe a sigh of relief and read about what a fascinating article from the WIRED website tells us about these benign facial hitchhikers:
New research out today in the Proceedings of the National Academy of Sciences reveals four distinct lineages of the face mite Demodex folliculorum that correspond to different regions of the world. African faces have genetically distinct African mites, Asian faces have Asian mites, and so too do Europeans and Latin Americans have their own varieties. Even if your family moved to a different continent long ago, your forebears passed down their brand of mites to their children, who themselves passed them on down the line.
Looking even farther back, the research also hints at how face mites hitchhiked on early humans out of Africa, evolving along with them into lineages specialized for certain groups of people around the planet. It seems we’ve had face mites for a long, long while, passing them back and forth between our family members and love-ahs with a kiss—and a little bit of face-to-face skin contact.
Leading the research was entomologist Michelle Trautwein of the California Academy of Sciences, who with her colleagues scraped people’s faces—hey, there are worse ways to make a living—then analyzed the DNA of all the mites they’d gathered. “We found four major lineages,” says Trautwein, “and the first three lineages were restricted to people of African, Asian, and Latin American ancestry.”
The fourth lineage, the European variety, is a bit different. It’s not restricted—it shows up in the three other groups of peoples. But Europeans tend to have only European mites, not picking up the mites of African, Asian, or Latin American folks. (It should be noted that the study didn’t delve into the face mites of all the world’s peoples. The researchers didn’t test populations like Aboriginal Australians, for instance, so there may be still more lineages beyond the four.)
So what’s going on here? Well, ever since Homo sapiensradiated out of Africa, those four groups of people have evolved in their isolation in obvious ways, like developing darker or lighter skin color. But more subtly, all manner of microorganisms have evolved right alongside humans. And with different skin types come different environments for tiny critters like mites.
“Some [skin types] do show different levels of hydration, and different levels of oil production, and different density of glands,” Trautwein says. “All kinds of differences.” So African mites may have evolved with uniquely African skin, while on the other side of the globe Latin American mites evolved with Latin American skin. As for those European mites, which show up on faces around the world, their spread is probably a side effect of imperialism and globalization. When Europeans occupied new countries, from Brazil to the Philippines, they brought along their face mites.
The populations of different lineages on our skin, though, are by no means static. Kiss your grandma on the cheek and you could exchange mites. “If you do have multiple people in your family that you spend a lot of time being physically close to, if you have multiple romantic partners across your life, there’s all these different opportunities to be colonized,” says Trautwein. Because families tend to be more kissy with each other than strangers, their blends of mites may persist for generations. But it’s always a give and take, mites coming and going, as cheeks hit cheeks.
So just remember during this holiday season, you are not only exchanging gifts with your beloved family, but you are very likely also going to be exchanging face mites under the mistletoe… For more of the grossly fascinating details of these weird arachnids, see the excellent article on the WIRED web site.
After much research, scientists discovered there were just 30 genes that played a major roll in longevity and overall health. These thirty genes were discovered in all three of the animals they tested on, but they are also in humans. Altering any one of these genes can cause better health and longevity.
In order to detect these genes, the researchers examined around 40,000 genes in the nematode C. elegans, zebrafish, and mice. By screening them, the scientists wanted to determine which genes are regulated in an identical manner in all three organisms during each comparable aging stage: young, mature, and old.
As a measure of gene activity, the researchers measured the amount of messenger RNA (mRNA) molecules found in the cells of these animals. mRNA is the transcript of a gene and the blueprint of a protein. When there are many copies of an mRNA of a specific gene, it is very active; the gene is unregulated.
By conducting experiments in which the mRNA of the corresponding genes were selectively blocked, the researchers pinpointed their effect on the aging process in nematodes. With a dozen of these genes, blocking them extended lifespan.
One of these genes proved to be particularly influential: the bcat-1 gene. “When we blocked the effect of this gene, it significantly extended the mean lifespan of the nematode by up to 25 percent,” says Ristow.
Our understanding of the natural world is now so great we can manipulate the DNA blueprints for any living thing on Earth. We can replace genes for traits we don’t like with others we prefer and even add genes that don’t occur naturally in an organism. Over the last few years, scientists have developed several methods for editing genes in this way and excitement over one in particular, the CRISPR-Cas9 system, has reached fever pitch.
We have also developed a way to introduce these gene changes to an entire population of a species. This “gene drive” process has most recently been used to alter the DNA of small groups of mosquitoes so that they no longer carry the malaria parasite, raising the possibility of eliminating the disease altogether. But meddling with nature in this way carries huge implications that need careful consideration.
Gene editing
Gene-editing techniques involving cutting genes at specific sites in the DNA of an embryo in order to disrupt those genes’ function or insert other genes. For instance, the CRISPR-Cas9 system uses enzymes that can cut specific gene sequences from DNA, guided by a similar molecule known as RNA. Natural gene repair mechanisms then kick in and can be used to disrupt the function of the original gene or replace it with a completely different one.
CRISPR systems actually aren’t new – they have existed in nature for millions of years. Bacteria use them to fend off viral infections by adding part of the virus’s DNA to their own. So why all the fuss? CRISPR-Cas9 makes artifical gene-editing much easier and cheaper, enabling scientist to target specific bits of DNA. By comparison, another method known as TALENS requires the construction of complex proteins. As a result, CRISPR gene-editing is heralding advances in biomedicine such as cancer treatments and protecting individuals from infections
But there are other ways gene-editing has the potential to help in the fight against infectious diseases. Very recently, CRISPR methods have been used to make mosquitoes resistant to malaria infections and coupled with a “chain reaction” to drive this gene modification (the resistance to malaria parasite) through the population.
Gene drive
This process is referred to as a “gene drive”, and again is not new: nature spreads evolutionary changes through a population all the time. It doesn’t mean changing the DNA of all living individuals in a population. Instead it’s about ensuring a specific genotype (a certain version of a gene) is passed on to the descendants of modified individuals.
A sexually reproducing organism usually has a 50% chance of inheriting a specific genotype from one of its parents. Using a gene drive can bias the inheritance pattern to increase that chance to nearly 100%, ensuring almost all descendants possess the genotype. As those descendants mate and produce their own offspring, the proportion of organisms with the genotype increases until it can be found in the entire population.
Gene warfare on malaria. Shutterstock
The idea that you can “replace” a population’s genotype is particularly appealing when that population is responsible for spreading disease, as mosquitoes are with malaria. Malaria is preventable and curable but still kills over 400,000 people each year.
The potential for using a gene drive to engineer insects (particularly mosquitoes) was discovered in the 1960s. But the advent of CRISPR’s cheap and easy gene-editing puts this research onto a whole new footing. Researchers at the University of California, Irvine, recently published a proof-of-princple study demonstrating the techniques can alter a population of the main type of mosquito that carries malaria in urban India, Anopheles stephensi.
Putting into practice
The longer term aim, in this instance, might be to release a persistent, modified mosquito into the environment to assist in the control a public health problem. This would be an area-wide release programme to compliment existing control interventions that would require case-by-case assessment of all the cost and benefits. For example, mathematical modelling would be needed to work out how many modified mosquitoes to release, how long it would take for the mosquito population to be clearly affected and how long it would take to impact public health.
One obstacle to the practical use of gene-drives is the need for relevant regulations, or at least the application of existing laws on genetic modifications. Gene-drive technologies are still some way off from the necessary environmental risk assessments for field trials and releases that would sufficiently scrutinise the risks to the environment and/or human health. These sorts of CRISPR-based modifications might even need a whole new set of regulatory structures that require a fuller debate about novel biotechnological advances.
Rapidly targeting genome modifications has the power to advance many aspects of basic and translational biomedical sciences. The potential benefits to reducing the impact of infectious disease and genetic disorders, including cancers, and improving the way the immune system works are huge. But the technology isn’t without pitfalls.
CRISPR systems rely on a guide molecule to make sure the DNA sequence is cut in exactly the right place. Getting this wrong will probably cause damage to non-target genes that could harm the organism. And just because we can edit the DNA within a species doesn’t mean we should. We need strong leadership at all levels – ethical, scientific, political – and appropriate regulations to ensure these new technologies can prosper without unintended consequences.
It’s interesting: with all of the advances in medical science on so many fronts, what is it about menstruation in women that has had it remain so under studied? Did you know that among mammals, female monthly menstruation is not common? In fact, in many other mammal species, nothing like the human equivalent of menstruation happens at all.
An incredibly insightful article on Live Science’s website reports the results of a recent survey of the past 40 years of medical research on this topic:
“There’s so much we don’t understand about why this repeated event of shedding and repair happens,” said Dr. Hilary Critchley, an ob-gyn and reproductive health researcher at the University of Edinburgh in Scotland. “It’s so crucial for the reproduction of our species. But it’s not a popular topic to study. There’s a big to-do around talking about problems that people don’t see.”
In a paper to be published in an upcoming issue of the journal Human Reproduction Update, Critchley and a colleague at the university, researcher Jacqueline Maybin, combed the scientific literature published over the last 40 years on all aspects of menstruation, medically defined as the loss of the endometrium, or the tissue that lines the inside of the uterus.
Their conclusion? There’s a lot that researchers still don’t know about menstruation and how it affects women’s health.
For example, some women who have heavy bleeding during menstruation also have certain conditions, such as uterine fibroids(which are noncancerous growths in the uterus) or endometriosis (a condition in which bits of endometrium appear outside of the uterus). But some women with heavy bleeding seem to have no other related problems.
Researchers aren’t sure whether the cause of heavy bleeding lies in the lining of the uterus itself or in the mechanisms that normally control the bleeding. Moreover, researchers don’t know whether the cause of heavy bleeding is the same in women with fibroids as in those with endometriosis, or in women without either condition.
But finding the answers would help millions of women; heavy bleeding can be a major disruption in a woman’s life, Critchley said. Normally, women lose about 1.2 ounces (35 milliliters) of blood monthly, she said. When blood loss approaches 2 ounces (60 ml), women are at risk for anemia. Women with blood loss of 2.7 ounces (80 ml) or more are diagnosed with the clinical condition called heavy menstrual bleeding, or HMB, she said.
However, some women lose 13.5 ounces (400 ml) of blood every month. For comparison, when people give blood to a blood bank, they donate about 17 ounces (500 ml), and donations are allowed only every eight weeks.
“These women with heavy menstrual bleeding are just debilitated. They are miserable. They can’t go out of the house,” Critchley said. “This dominates their social lives, their holidays, their weekends.”
Really understanding the biological process of menstruation would be a benefit in so many ways. Continue on to the next page to learn more about that…
