For a Healthier 2018!

Dancing together is good for your health!


By Jesica Levingston Mac leod, PhD


Social dancers know the amazing feeling that a synchronized dance could bring. When your follower or leader is connected and it feels like you are one mind and body following the music, it is mystical and magical… Well, it turns out that synchronized dancing is also good for your health. I started dancing salsa because a good friend was going crazy about it and she recommended it, this inspired me to join a class. At this point I was a solitary belly dancer only following in team dances where you have choreography and if you are coordinated enough you feel this celestial connection with the other dancers…but without any physical contact.

On the other hand, in social dances like salsa, bachata, tango, zouk or swing, the connection is the base of a good dance. Nobody wants to be the person stepping to the left when 5 other dancers moved to the right while performing in a stage in front of hundreds of people, as well as nobody enjoys turning to the wrong side for misreading your dance partner lead, or watching how a follower does a completely different step that the one the leader indicated. Furthermore, being “in sync” with the group or your direct dance partner may help to improve your health, science says. In a nutshell, a recent study found that synchronizing with others while dancing raised pain tolerance and encouraged people to feel closer to others.

This year, Dr. Burzynska et al., at Colorado State University, separated 174 healthy adults, 60s to 79 years old, who had no signs of memory loss or impairment, into 3 activity groups: walking, stretching and balance training, or dance classes. The activities were carry on for 6 months and three times a week, those in the dance group practiced and learned a country dance choreography. Brain scans were done on all participants and compared with scans taken before the activities began. Not surprisingly, the participants in the dancing group performed better and had less deterioration in their brains than the other groups. Their most recent study published in November: “The Dancing Brain: Structural and Functional Signatures of Expert Dance Training” showed that dancers’ brains differed from non-dancers’ at both functional- and structural-levels. Most of the group differences were skill-relevant and correlated with objective laboratory measures of dance skill and balance. Their results are promising in that long-term, versatile, combined motor and coordination training may induce neural alterations that support performance demands.” (link 2)

Moreover, It is well established that dancing-based therapies are providing outstanding results in the treatment of dementia, autism and Parkinson’s. Indeed, dance therapy improves motor and cognitive functions in patients with Parkinson’s disease. Dancing was suggested to be a powerful tool to improve motor-cognitive dual-task performance in adults. Dance movement therapy has known benefits for cancer patients’ physical and psychological health and quality of lifeAnother study by Domane and collaborators, working with a cohort of overweight and physically inactive women, showed that Zumba fitness is indeed an efficacious health-enhancing activity for adults. Park also concluded that “a 12-week low- to moderate-intensity exercise program appears to be beneficial for obese elderly women by improving risk factors for cardiovascular disease”.

Dancing helps generate positive connections with others and this is one of the evolutionary reasons you are “called” to the dance floor when a song you like starts playing, and probably you will start your dance by coordinating with or copying others. Probably this behavior signaled tribe membership for early humans and also got couples together in a more romantic way, creating emotional bonds. Coordinated dances are as old as music, and distributed in a lot of different cultures, for example, the nowadays Hakka, used by rugby players, was a native group dance that intimidates rival tribes.

Talking about the chemistry of dancing, as any other exercise, it releases endorphins (the hormones of happiness and pain relief). For example, a study from the University of London were anxiety-sufferers enrolled in one of four settings: exercise class, a music class, a math class and a dance class, showed that only the last group displayed “significantly reduced anxiety.”

In the most recent study done in the same London University by Tarr and collaborators, the researchers used pain thresholds as an indirect measure of endorphin realize (more endorphins mean we tolerate pain better) for 264 young people in Brazil. The volunteers were divided into groups of three, and they did either high or low-exertion dancing that was either synchronized or unsynchronized. The high exertion moves were standing, full-bodied movements, on the other hand, in the low-exertion groups did small hand movements sitting down. They measured the before and after feelings of closeness to each other via a questionnaire and their pain threshold by attaching and inflating a blood pressure cuff on their arm, and determining how much pressure they could stand.

Most of the volunteers who did full-bodied exertive dancing had higher pain thresholds compared with those who were in the low-exertion groups. Most importantly, synchronization led to higher pain thresholds, even if the synchronized movements were not exertive. Therefore when the volunteers saw that others were doing the equivalent movement at the same time, their pain thresholds increased.

The results also showed that synchronized activity encouraged bonding and closeness feelings more than unsynchronized dancing. Therefore, “Dance which combined high energy and synchrony had the greatest effects. So the next time you find yourself in an awkward Christmas party or at a wedding wondering whether or not to get up and groove, just do it”, claims Dr. Tarr.

Coming back to the dance floor, I had reached out for an opinion about the wellness of dancing to the best Bachata DJ: Brian el Matatan: “I enjoy the dancing for a few reasons. There’s the enjoyment & challenge of using what I’ve learned; socially as well as choreographed performance. Also, there is the rush of endorphins similar to “runner’s high”. There’s also the socializing aspect of dancing. It’s like having a conversation without speaking.” Well said DJ!
He also offered some advice for followers: dance with many different types of leaders if you’d like to improve your following. There are many different leads, and there is an experience to be gained in social dancing that would not be gained via dance class. Also, feel free to ask a leader to dance, & be courteous in how you decline a dance. Most importantly- communicate. Don’t “lead” a leader into thinking their lead is better than what it really is- for your sake & that of your fellow followers. For example, if he almost ended your life with that risky move, let him know so that he doesn’t try it on you or anyone else again (at least not without figuring out how to do the move properly). And some advice for leaders: be VERY  courteous in how you ask for a dance, try to not take rejection personally, be patient with follows who may not be on the same skill level as you, & don’t almost end her life with risky moves.

Lastly, I asked for the most sensual dancer, scientist, and project manager –  Debbie McCabe – for her advice for followers. She commented “The lady’s job is to surrender and connect to her partner…it is a 3-minute love affair and energy exchange. I love Bachata because I can get out of my head and just feel, express my sensuality, be playful and connect… it balances out my left brained day job.”

More than 20 years ago, scientists found a connection between music and enhancement of performance or changing of neuropsychological activity involving Mozart’s music from which the theory of “The Mozart Effect” was derived. The basis of The Mozart Effect lies at the super-organization of the cerebral cortex that might resonate with the superior architecture of Mozart’s music. Basically listening to Mozart K.448 enhances performance on spatial tasks for a period of approximately 20 min.

So dear reader, please stop complaining and making excuses and just dance! Or at least listen to music, as the outstanding jazz singer Tamar Korn once told me when I was in distress “music heals”.


This post was originally published on Dec 30, 2015 and was updated with new research on Dec 12, 2016 and on Dec 19, 2017.

How Can You Make Money and Help Others with Your Shit?

And other very important poop updates.


By Jesica Levingston Mac leod, PhD

First, you have to be a healthy pooper… Second, you have to live in the Boston area. Your stool can help a person suffering from recurrent C. difficile infections, which is a bacterium that affects 500,000 Americans every year.  Where antibiotic treatment has failed to help, a new treatment called “fecal microbiota transplantation” has shown a cure rate of 90%.  In this procedure, a fecal microbiota preparation using stool from a healthy donor is transplanted into the colon of the patient.  OpenBiome, the startup company based in Boston, helps facilitate this procedure by screening and processing fecal microbiota preparations for use in this treatment. After joining the registration you and your stool will be screened and if you are healthy and a good candidate you will became a donor. If you can succeed with all the tests and you can provide “supplies” quite often then you can exchange money for you poo.

Lately, the study of the human microbiota has been all over the news, specially related with weight control, pregnancy and the infant’s diet. In fact, it’s estimated that the human gut contains 100 trillion bacteria, or 10 times as many bacteria as cells in the human body. Yes, I know what you are thinking: “More of them that my own cells, that cannot be right, right?”

These bacteria, or microbiota, influence your health in many ways, from helping to extract energy from food to building the body’s immune system, to protecting against infection with harmful, disease-causing bacteria.

Researchers are only just beginning to understand how differences in the composition of gut bacteria may influence human health. From what we know so far, here are five ways gut flora can affect your wellness:


Weight Changes

Yes, your gut bacteria affect your eating disorders (or orders if you are lucky). For example the diversity of gut bacteria is higher in lean people compared to obese people. Also, some specific bacteria groups, the Firmicutes and the Bacteroidetes, are linked with obesity. The famous study were they transplanted gut bacteria from obese and lean people to mice, making the host of the first kind of poo gain more weigh that the mice who received the “lean fecal bacteria”, was a shocking confirmation of the importance of the gut bacteria in the body weight regulation. They discovered that the gut bacteria from obese people increase the production of some amino acids, while the material from lean people increases the metabolism of “burning” carbohydrates.


Preterm Labor

Realman and col. found that pregnant women with lower levels of bacteria Lactobacillus in their vagina had an increased risk of preterm labor, compared with women whose vaginal bacterial communities were rich in Lactobacillus. Apparently, the absence of Lactobacillus allows the grown of other species that would have different effects in the pregnancy.


Crying Babies

In a funny study on how diet may affect babies, Pertty and col. showed that giving probiotics to your baby does not change the daily crying time, around 173 minutes, compare to the placebo group (174 min), according to the parental diary. They enrolled 30 infants with colic during the first 6 weeks of life.  However, parents reported a decrease of 68% in daily crying in the probiotic and 49% in the placebo group.


Heart Attacks

Gut Bacteria produce compounds can even affect your heart. One of these compounds is the trimethylamine-N-oxide (TMAO), and the presence of it in the blood of the subjects of a recent research study, increased 2.5 times the probability of having a heart attack, stroke or to die over a three-year period compared with people with low levels of TMAO. They have also shown that the metabolism of the gut bacteria changes according of the host’s (your) diet. For example, the consumption of high cholesterol and fatty food can increase the bacterial production of TMAO.


The Immune System

A recent review published in Cell rang the alarm about the negative effect of the “rich countries” diet in the microbiota influencing the immune system. In ideal and normal conditions the immune system-microbiota association allows the induction of protective responses to pathogens and the maintenance of regulatory pathways involved in the maintenance of tolerance to innocuous antigens. In rich countries, overuse of antibiotics, changes in diet, and elimination of constitutive partners, such as nematodes, may have selected for a microbiota that lack the resilience and diversity required to establish balanced immune responses. This phenomenon is proposed to account for some of the dramatic rise in autoimmune and inflammatory disorders in parts of the world where our symbiotic relationship with the microbiota has been the most affected.


Lungs and Asthma

The gut bacteria can affect your lungs: The low levels of 4 gut bacteria strains (FaecalibacteriumLachnospiraVeillonella, and Rothia) in kids was been recently related to an increase in the risk for developing debilitating asthma. The introduction of these 4 bacteria in mice induced to suffered asthma shown protection as the mice’s lungs did not present inflammation.

The question is: how bacteria IN the guts can affect your other tissues and organs? One study that was just published shows  that these bacteria produce chemicals that may help the immune system to battle against other germs. Without this training, the immune system could fail and create inflammation in the lungs. As a follow up from the latest research it may be possible in the near future to predict asthma, and other diseases, as well as cure some illnesses with gut bacteria.

Be ready to give a shit about your shit.

’Tis the Season for Weight Loss!


By Robert Thorn

It is that time of year again. 2014 is coming to an end and it is time to think about our past year and make our New Year’s resolutions for 2015. If you are like me (and many others), one of your 2014 resolutions was weight loss, and perhaps you haven’t quite met your goals. A quick search of weight loss supplements on the internet will lead you to a myriad of “miracle” weight loss solutions. Its so simple, just put lemon in your water, drink 5 glasses of ice cold water a day, and/or replace one meal a day with a shake/bar/handful of nuts. Well, now it’s time to throw away all those snake oil voodoo weight loss “solutions” because there may be a new molecule in town to help cut the pounds.


A paper recently published in Nature Medicine from a group in Germany has shown that there may be a way to trick your body into losing weight by mimicking hormones that normally help regulate the body’s response to food. They aimed to affect three hormones that are known to be important for the regulation of weight in obesity. The three hormones are glucagon-like peptide-1 (GLP-1), glucose-dependent insulin tropic polypeptide (GIP) and glucagon. These three hormones have been studied by themselves to determine if they could have any positive effect in controlling obesity. Scientists have created molecules, called agonists, that are able to activate the receptors that are normally activated by either glucagon, GIP or GLP-1. By themselves these agonists allow a modest benefit to obesity, but also came with negative side effects that would make them unpleasant to use. It has been hypothesized that regulating all three of these hormones at once would allow for greater anti obesity effects with less unpleasant side effects.


First, the group decided to test how using three agonists at once, one each for GLP-1, GIP and glucagon, would alter weight loss in a mouse model with an altered diet high in sucrose to induce obesity. The tests showed a synergistic effect by using all three, versus using each one individually in weight lose in this mouse model. Next, they decided to attempt to create a single molecule that would be an agonist to each of the 3 hormones at once (aka a triagonist). Previously, coagonist molecules that affected different combinations of the three pathways had been designed and by using these sequences and structures they were able to rationally design a triagonist to all thee hormones. Once designed and synthesized, the triagonist was tested for activity with the intended receptors (i.e. the receptors for GLP-1, GIP and glucagon) and for non-intended receptors. These tests showed that the triagnoist was effective in activating all 3 intended receptors and when tested against a set of other receptors it showed no cross reactivity, suggesting that the triagonist is a specific triagonist of GLP-1, GIP and glucagon.


Once in vitro studies showed that the triagonist interacted with receptors as they were designed to be, the group moved on to testing in mice. They again used the diet induce obesity mouse model to test the triagonist. Both short term and long term exposure to the triagonist showed a decrease in overall body fat in the mice, without any hypoglycemia. Remarkably, this difference was even greater than the difference previously seen with coagonists. In addition to the weight reduction, treatment with the triagonist was also able to slow the progression of type II diabetes in these mice. To further test the triagonist, rat models of both obesity and diabetes were treated with the triagonist. In both of these models the triagonist was able to alleviate the effects of both obesity and diabetes respectively. To date, there have been other triagonists designed and tested by other groups, but none have shown such robots anti-obesity and anti-diabetes effects as this triagonist.


This level of weight loss from a single molecule is extremely promising as a way to fight the ever-growing obesity epidemic. Not only does the increased obesity negatively affect individuals who are obese, but it also can act as a burden on public health. This triagonist could serve as a safer, non-invasive alternative to biatric surgery, which is oftentimes the only solution for some cases of obesity. While all this information is very promising, it is important to note that mouse models don’t always translate perfectly to human trials but it is definitely possible that in the next few years we may very well have a “miracle” weight loss solution that actually works!

‘Tis The Season of Food Follies, Fa-la-la-la-la…


By Lori Bystrom, PhD


“Sleigh bells ring, are you listening?” It is hard not to hear the lyrics of these and other seasonal songs during the holidays, just as it is difficult to ignore the colorful array of decorations, and the aroma of pine trees, cinnamon, ginger, and cloves. Engulfed by the sensory overload of the holidays, many of us cannot help but become overzealous consumers of holiday foods. As one might imagine, however, this is not good for our health.


In fact, there is evidence that the dietary choices we make during the holidays or the days leading up to big festivities, such as Christmas and New Year’s, can take a toll on our health. Holiday overconsumption can especially pose a problem in developed countries, where obesity is on the rise and is linked to numerous health problems. A recent study in PLOS ONE, for example, has shown that during the 2010-2011 American holiday period (Thanksgiving to New Year’s) food expenditures increased 15% compared to the pre-holiday period (July to Thanksgiving). Moreover, 75% of this increase was due to expenses on less-healthy food.


Interestingly, the study also found that the sales of healthy foods increased by 29.4% during the post-holiday periods (New Year’s to March), while the sales of less-healthy food remained the same as the holiday period. As a result, the calories purchased/week increased by 9.3% compared to the holiday period, and by 20.2% compared to the pre-holiday (baseline) period. Such behavior does not bode well, given that there is an ongoing obesity epidemic in many developed countries.


Although it would appear we have little control over our behavior during the holiday season –many of us acting like zombie consumers enticed by the smells, sights, and sounds of the holidays— there must be a way we can control these festive compulsions. Perhaps one way to tackle the obesity epidemic would be to reduce the cumulative increase of calories/unhealthy food that result from the holidays. But how do we resist the many temptations of the holidays? And, if we cannot resist, how can we undo the effects of our holiday choices afterwards?


In a recent report by PBS NEWSHOUR, Sendhil Mullainathan, an economics professor at Harvard University and cofounder of the behavioral economics consultancy ideas42, discusses several holiday gifts that might improve our unhealthy behaviors during the holidays and beyond.


He suggests buying smaller plates (similar to the standard plate size of the 1960s) to reduce the amount of food we consume at one sitting. In addition, he recommends a product made by Meal Measure that is used to control the amount of starches, vegetables, fruits, and protein put on your plate. Furthermore, could a candy/cookie jar that locks you out for a few minutes after opening stop you from eating more candy or cookies? The makers of The Kitchen Safe think so.


Other gadgets that may help prevent or reduce holiday weight gain include the Fitbit  or the Jawbone UP, which help you keep track of your exercise, sleep, and food intake patterns. And, if you find yourself too sluggish after the holidays, then perhaps Clocky or Tocky  the runaway alarm clock will get your day started sooner and keep you more active.


It remains to be seen whether or not any of these products actually help us control our holiday food intake or weight gain. Regardless, understanding our dietary patterns before, during, and after the holidays is likely to help researchers/ product innovators develop new strategies that may improve our unhealthy holiday/everyday dietary habits.


For now, as we fa-la-la-la our way through the holidays, it might be best to be mindful of our food intake or at least to make more effective New Year’s resolutions so we can fa-la-la away our holiday food follies.

Let Us Eat Real Food


By Kelly Jamieson Thomas, PhD

Sugar, which is undeniably highly addictive, is the number one additive in our food. Food manufacturers are hiding added sugar in almost every food including pizza, juice, bread, ketchup, and even baby formula. Added sugar consumption causes several diseases, including obesity, cardiovascular disease, diabetes, gout, fatty liver disease, some cancers, and tooth decay. What are added sugars? Those not found naturally in foods. When you eat an apple, it’s sweet, but the sugar in an apple isn’t added. But, when you drink a soda or eat an energy bar, the sugar in both of those is added. Prior to 1950, there were no added sugars in food. Since then, with the onset of added sugar in our food, Americans consume 39% more sugar. On average, we are eating 152 pounds of sugar per year, which is 2/3 of a cup per day! With such an astounding increase in our sugar intake, it’s certainly not surprising we are seeing a hefty increase in diseases related to sugar consumption, specifically obesity.


Is there a true link between increased sugar intake and increased body weight, specifically, body fat content? In an attempt to answer this highly debated question, the World Health Organization (WHO) analyzed thousands of studies and selected the most reliable. They focused on identifying an overall indication of how population changes in added sugar consumption affects our health. The resounding results—yes, increased sugar intake leads to increased body fat (adiposity). In children, this was especially relevant to consumption of sugary beverages, such as soda. Just as Bloomberg faced backlash for attempting to rid New York of large soda bottles, WHO has also received similar resistance for encouraging us to consume 5% of our calories from added sugar. The guideline has been officially set at 10%, which is equivalent to approximately one 12-ounce soda per day.


With clear evidence linking excess added sugar intake to the rapidly growing obesity epidemic, it’s in our best interest to seriously consider how sugar may ruin our long-term health. If we don’t change our habit and instead continue to gorge on added sugar, we will continue to see a rise in obesity. Currently, in the US, about 78 million adults (more than 37%) and 12.5 million (17%) youths are obese. Obesity incidence has risen from 14.5% to 30.9%, more than doubling, between 1971 and 2000. Obesity, the leading cause of preventable death, poses a significant risk for decreased life expectancy, type 2-diabetes, heart disease, osteoarthritis and some cancers. Not only are we making ourselves fat, but we are also creating an enormous burden in healthcare costs. If the obesity rate continues to grow at current rates, healthcare costs attributable to obesity, which were $147 billion in 2008, are predicted to increase to $957 billion dollars by 2030, a startling 18% of total US health expenses.


What are we doing to make a change? Recently, the FDA has set new standards for food labeling. Information about added sugars will be required and serving size portions will be adjusted to reflect our larger portion size. Unfortunately, to our dismay, food manufacturers will not be forced to limit added sugars, nor will 20-ounce sodas and other sugary drinks be banned from the markets. With such strong evidence supporting the link between our increased consumption of added sugars and obesity, it’s time we wean off added sugars. Clearly, we can’t rely on processed foods to help us do this. The bottom line: let’s eat real food! Have some strawberries instead of strawberry ice cream. Ditch that soda for sparkling water with fresh lemon in it. If we consider that our food is our fuel, would you want to run on processed junk or naturally nourishing fuel?

Can a Mutation Protect You From Diabetes?


Evelyn Litwinoff

For the first time in diabetes research history, researchers have found mutations in a gene that is associated with a 65% decrease in risk of developing type 2 diabetes (T2D).  What’s even more astounding is that only one copy of the gene has to be mutated to show this protection.  The gene of interest is SLC30A8, which encodes a zinc transporter in pancreatic islet cells.  (A quick brush up on your cellular anatomy: Pancreatic islet cells produce insulin, which the body uses to uptake glucose into cells.  Zinc plays an important role in the uptake, secretion, and structure of insulin.) This study found not 1, not 2, but 12(!) different loss-of-function mutations, all in SLC30A8 and all predicted to result in a shortened protein, that associates with protection from T2D risk.


Most of this study is based upon sequencing genes that were previously associated with a risk of developing T2D.  Overall, the authors looked at about 150,000 individuals from various ethnic populations in order to obtain statistical significance for their associations.  Their results are surprising since previous studies had linked mutations in SLC30A8 with an increased risk of T2D.


However, this study does not address how a decrease in function of the zinc transporter, named ZnT8, could lead to protection from a disease state.  The authors did conduct one mechanistic-ish experiment, but this was only to see if the mutations in ZnT8 actually affect the activity of the protein.  To this end, the authors overexpressed 4 different mutated versions of ZnT8 in HeLa cells and saw a decrease in protein levels in 2 out of the 4 versions.  Furthermore, they showed that the increased protein degradation could be part of the reason for the observed decrease in amount of protein.  Their main conclusion from these cell experiments show that some of the mutations in ZnT8 result in an unstable protein, which would help us understand how the zinc transporter is not working, but it does not explain why the dysfunctional protein protects from T2D.  Hopefully, this paper will spark others to investigate a mechanism for the associated protection.


Currently, Pfizer and Amgen are starting to develop drugs that mimic this mutation to see if they can replicate the protection.  Although a new diabetes drug based on this study could be 10-20 years down the road, this study still makes a big splash in the diabetes research community.

Leafing through the Literature

Thalyana Smith-Vikos

Highlighting recently published articles in molecular biology, genetics, and other hot topics

Can I get some of your gut bacteria?

While there have been many reports popping up in the literature that demonstrate a connection between gut microbiome and diet, Ridaura et al. have elegantly showed how the mammalian microbiome affects diet in a specific yet alterable manner that can be transmitted across individuals. The researchers transplanted fecal microbiota from adult murine female twins (one obsess, one lean) into mice fed diets of varying levels of saturated fats, fruits and vegetables. Body and fat mass did depend on fecal bacterial composition. Strikingly, mice that had been given the obese twin’s microbiota did not develop an increase in body mass or obesity-related phenotypes when situated next to mice that had been given the lean twin’s microbiota. The researchers saw that, for certain diets, there was a transmission of specific bacteria from the lean mouse to the obese mouse’s microbiota.

Want to keep up with gut microbiota? Create your feed!


In vivo reprogramming

Abad et al. have performed reprogramming of adult cells into induced pluripotent stem cells (iPSCs) in vivo. By activating the transcription factor cocktail of Oct4, Sox2, Klf4 and c-Myc in mice, the researchers observed teratomas forming in multiple organs, and the pluripotency marker NANOG was expressed in the stomach, intestine, pancreas and kidney. Hematopoietic cells were also de-differentiated via bone marrow transplantation. Additionally, the iPSCs generated in vivo were more similar to embryonic stem cells than in vitro iPSCs by comparing transcriptomes. The authors also report that in vivo iPSCs display totipotency features.

Want to keep up with Abad et al.? Create your feed!


Connection between pluripotency and embryonic development

Lee and colleagues have discovered that some of the same pluripotency factors (Nanog, Oct4/Pou5f1 and SoxB1) are also required for the transition from maternal to zygotic gene activation in early development. Using zebrafish as a model, the authors identified several hundred genes that are activated during this transition period, which is required for gastrulation and removal of maternal mRNAs in the zebrafish embryo. In fact, nanogsox19b and pou5f1 were the top translated transcription factors prior to this transition, and a triple knockdown prevented embryonic development, as well as the activation of many zygotic genes. One of the genes that failed to activate was miR-430, which the authors have previously shown is required for the maternal to zygotic transition. Thus, Nanog, Oct4 and SoxB1 induce the maternal to zygotic transition by activating miR-430.


A microRNA promotes sugar stability

Pederson and colleagues report that a C. elegans microRNA, miR-79, targets two factors critical for proteoglycan biosynthesis, namely a chondroitin synthesis and a uridine 5′-diphosphate-sugar transporter. Loss-of-function mir-79 mutants display neurodevelopmental abnormalities due to altered expression of these biosynthesis factors. The researchers discovered that this dysregulation of the two miR-79 targets leads to a disruption of neuronal migration through the glypican pathway, identifying the crucial impact of this conserved microRNA on proteoglycan homeostasis.

Struggling to keep up with all the mIRs? Create your feed for miR-430 or miR-79.


Establishing heterochromatin in Drosophila

It is known that RNAi and heterochromatin factor HP1 are required for organizing heterochromatin structures and silencing transposons in S. pombe. Gu and Elgin built on this information by studying loss of function mutants and shRNA lines of genes of interest in an animal model, Drosophila, during early and late development. The Piwi protein (involved in piRNA function) appeared to only be required in early embryonic stages for silencing chromatin in somatic cells.  Loss of Piwi leads to decreased HP1a, and the authors concluded that Piwi targets HP1a when heterochromatin structures are first established, but this targeting does not continue in later cell divisions. However, HP1a was required for primary assembly of heterochromatin structures and maintenance during subsequent cell divisions.


The glutamate receptor has a role in Alzheimer’s

Um and colleagues conducted a screen of transmembrane postsynaptic density proteins that might be able to couple amyloid-β oligomers (Aβo) bound by cellular prion protein (PrPC) with Fyn kinase, which disrupts synapses and triggers Alzheimer’s when activated by Aβo-PrPC . The researchers found that only the metabotropic glutamate receptor, mGluR5, allowed Aβo-PrPC  to activate intracellular Fyn. They further showed a physical interaction between PrPC and mGluR5, and that Fyn is found in complex with mGluR5. In Xenopus oocytes and neurons, Aβo-PrPC caused an increase in intracellular calcium dependent on mGluR5. Further, the Aβo-PrPC-mGluR5 complex resulted in dendritic spine loss. As a possible therapeutic, an mGluR5 antagonist given to a mouse model of inherited Alzheimer’s reversed the loss in synapse density and recovered learning and memory loss.


Keep playing those video games!

Anguera et al. investigated whether multitasking abilities can be improved in aging individuals, as these skills have become increasingly necessary in today’s world. The scientists developed a video game called NeuroRacer to test multitasking performance on individuals aged 20 to 79, and they observed that there is an initial decline in this ability with age. However, by playing a version of NeuroRacer in a multitasking training mode, individuals aged 60-85 achieved levels higher than that of 20-year-olds who had not used the training mode, and these successes persisted over the course of 6 months. This training in older adults improved cognitive control, attention and memory, and the enhancement in multitasking was still apparent 6 months later. The results from playing this video game indicate that the cognitive control system in the brains of aging individuals can be improved with simple training.

Want to stay in the game? Create your feeds and stay current with what’s sizzling.


Sugar: Generally Recognized As Safe?

Kelly Jamieson Thomas

We all are all cognizant that added dietary sugars aren’t good for us. How little added sugar is too much? And, how may low levels of added sugars in our diet affect our long term health? This August, both Nature Communications and National Geographic highlighted the negative effects of sugar consumption through two different approaches, bringing the sweet toxin into the spotlight. In National Geographic’s article “Sugar Love“, author Rich Cohen loosely maps the history of how added sugar and subsequently high fructose corn sugar (HFCS) found its way into our diet over the past 10,000 years. He highlights Haven Emerson’s observation that deaths from diabetes between 1900-1920 spiked with sugar consumption, and John Yudkin’s experiments demonstrate that added dietary sugar in mice and animals leads to increased levels of fat and insulin in the blood. Both of these factors are well known risks for heart disease and diabetes. Unfortunately, the war on saturated fat has historically overshadowed that on sugar, and, while fat comprises a smaller portion of the American diet than 20 years ago, added dietary sugar in the diet (primarily HFCS) has increased.


In an article published in Nature Communications entitled, “Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in mice“, the authors Ruff et al. demonstrate the deleterious effects of low levels of added sugar (given as a HFCS mimetic) on mice, suggesting that the current standards, which we currently regard as acceptable levels of added sugar in our food, is harmful. The authors utilize Organismal Performance Assays to prove that low levels of added sugar in the mouse diet result in harmful clinical defects such as increased mortality, decreased litter size, decreased glucose clearance, and increased fasting cholesterol. These findings are significant because they represent the lowest level of sugar consumption shown to adversely affect mammalian health.


Over the past few decades, we’ve seen a dramatic 100% increase in diabetes and obesity incidence. In the National Geographic article, Cohen quotes Richard Johnson, a nephrologist at the University of Colorado Denver. Johnson asks, “Why is it that one-third of adults [worldwide] have high blood pressure, when in 1900 only 5 percent had high blood pressure?” He continues, “Why did 153 million people have diabetes in 1980, and now we’re up to 347 million? Why are more and more Americans obese? Sugar, we believe, is one of the culprits, if not the major culprit.” Cohen has a point. Consumption of added sugar, primarily in the form of HFCS, is becoming more commonly recognized as a major contributor to the onset of metabolic syndrome. Metabolic syndrome, characterized by factors including increased blood pressure, high blood sugar level, excess body fat around the waist and abnormal cholesterol levels, is a major contributor to all three maladies Cohen questions–high blood pressure (which contributes to heart disease), diabetes and obesity.


Currently, both sucrose and high fructose corn syrup are both listed as food additives in the “Generally Recognized As Safe (GRAS)” list provided by the U.S. Food and Drug Administration. This means that companies who produce processed foods, which include any food in a can, bag or box, can add copious amounts of either to the “food” we are consuming. The two articles cited here represent a fraction of the literature supporting the negative health effects on added dietary sugar consumption. IT’S TIME to reset the baseline to zero added sugar.




Shake What Your Mama Gave You!

Sally Burn

If you eat five portions of fruit and vegetables a day, exercise, and don’t smoke then you are well on the way to becoming an optimally functioning human. Pat on the back. Extra points if you drink alcohol within guidelines, get eight hours sleep, and don’t go on regular processed meat benders. Deduct ten points for every time you’ve stressed out, rolled giddily in asbestos, or ate your own weight in cake. Continue reading “Shake What Your Mama Gave You!”