I’m excited to be working at the American Geophysical Union. My science writer internship with the public information office is just starting. The team here is great and I’m learning a lot about everything earth, space (in our solar system) and geoscience.
I’ll be posting links to the blogs and press releases I write here on my blog.
I hate this commercial. As a science journalist, and a generally curious person, I always want to hear and understand the complicated explanation. It’s hard for me to hear the tone of the commercial as reassuring, instead of condescending.
I don’t think people need partial, glossy truths. I believe that more often than not oversimplifying a topic just creates confusion. But too much information is equally confusing. It’s a tricky thing to balance clarity, accuracy, and simplicity when explaining science. And I think that when discussing dietary sugar, the simple explanations aren’t doing us any favors.
One of the challenges of writing about food and food science is that nutrition is such a big part of both topics. Last year an editorial in the journal Nature talked about the power of simple messages and the issues with loss of detail for the sake of sound bites in nutrition:
“It is risky to oversimplify science for the sake of a clear public-health message. . . . [S]imple messages and themes are seductive. . . . Black-and-white messages can cause confusion of their own.”
I’m not a nutritionist, or a dietician, nor do I want my writing to be prescriptive. But I do want it to be clear. So, with that very large caveat, here is some of what we do and don’t know about the difference between how our bodies process added sugar versus intrinsic sugars.
Added sugars vs. intrinsic sugars
Sugar is important. Sugar provides fuel for cellular processes and body functions. Sugar is delicious and we are programmed to enjoy it.
However, like other carbohydrates, sugars aren’t considered essential nutrients. (Essential nutrients are molecules that the body can’t create by itself or are needed in large amounts to maintain health.)
Americans get the bulk of their added dietary sugar in two different forms; sucrose (table sugar) or high fructose corn syrup (HFCS). Processing sugar cane and, more recently, sugar beets yields sucrose. Corn, naturally, is processed into HFCS.
High fructose corn syrup first emerged in the 1960s, thanks to technological advances creating the capacity to convert corn-derived glucose into fructose. Despite it’s name, the resulting syrup is composed of almost equal portions of glucose and fructose.
Sucrose consists of the two simple sugars glucose and fructose. Glucose and fructose have same chemical formula but they differ slightly in structure and greatly in sweetness. Fructose is twice as sweet as glucose.
Both sucrose and HFCS are composed of the same approximate 1:1 ratio of glucose and fructose. But, again, the significant difference between the two is structural. Sucrose: glucose and fructose are chained together. HFCS: glucose and fructose are unconnected and free floating.
During digestion sucrase, an enzyme in the intestines, breaks sucrose into glucose and fructose for processing.
When we digest sucrose the enzymes in our small intestine must break the sucrose molecules into glucose and fructose to be used for energy. At first glance, it looks like the sugars in HFCS would be absorbed faster the simple sugars in sucrose (since HFCS basically skips that digestive step). But because sucrose is converted to glucose and fructose in just a few seconds, HFCS and sucrose appear to behave the same way metabolically.
After converting sucrose (and not converting HFCS) the glucose and fructose in the small intestine is then ready to be absorbed into the bloodstream. But first both simple sugars head to the liver and here is where their paths diverge.
Before letting glucose flood the bloodstream, an specific enzyme (phosphofructokinase) checks to make sure that the liver has enough energy. If the liver doesn’t need energy, it sends the glucose into the bloodstream.
Our bodies exert strict control over the amount of glucose in our blood. Glucose is basically our default “fuel”. It used by every cell in body and is especially important for brain function. The brain uses up to 20% of the energy used by the human body, and can only use energy in the form of glucose. When your blood glucose levels drop, so does brain function.
Too much glucose in the bloodstream is also a problem. Over abundant blood glucose signals the pancreas to secrete insulin which removes excess glucose from the blood. Excess glucose also promotes the release of leptin, a hormone which suppresses feelings of hunger.
Fructose’s first stop is also the liver. Fructose is not immediately useful to most cells, and is largely metabolized through the liver, where it is converted into glucose and lactate. But unless you have no energy reserves at all and energy is needed elsewhere in the body, the fuel created from fructose seems to stay in the liver (even when it doesn’t need that extra energy). In the liver, some fructose might be converted into glycogen for short-term storage, and some fructose is changed into fat for long term storage.
Unlike glucose, fructose doesn’t promote insulin production. Instead it promotes the release of grehlin, a hormone that reinforces feelings of hunger. This has led some researchers to suggest that ingesting large amounts of fructose might lead to overeating.
A recent trend has been to say that all sugar is toxic, when in fact most researchers who are pushing that message are only referring to fructose. There are many studies that look at individual harmful aspects of fructose metabolization, and it can seem as though fructose is inherently harmful.
But most experts seem to think that fructose is not inherently harmful and what is more important is the amount of sugar in a person’s diet as a whole and the form the sugar is consumed in.
Drinking a soda is a classic example of ingesting “empty” calories. A coke provides a lot of energy with very little digestive effort, zero fiber, and almost no nutrients. Very shortly after drinking a soda sweetened by either sucrose or HFCS, fructose floods the intestines and is shuttled to the liver to be broken down.
But eating an apple requires significantly more digestive energy than harvesting free sugars from a soda. The fiber (cellulose) structure of the fruit slows down digestion while digestive enzymes break down cell walls to get to the sugars inside. It takes time for the freed fructose from the fruit to reach the liver, and it arrives in more of a trickle than a flood.
So it’s not just about the actual sugar content, but the structure of the food. Added sugars, which aren’t part of the cellular structure of a food, are absorbed almost instantly by our bodies. While intrinsic sugars, like those in fruits, take more time and effort to harvest.
Finally, foods with intrinsic sugars are usually more nutritionally dense and lower in calories, making them a better choice for your daily sugar quota overall.
Following is a loose transcript of the conversation that took place.
Eva: I’ve never been to Boston, but have been part of the Science Online community for long time. I was at the first Science Online conference in 2007, and went back in 2009. I want to go back again. I haven’t met a lot of the new communities – I’m excited to meet people only seen online. My new job, as outreach director for F1000 Research (@F1000Research) started 6 weeks ago. The journal is also new (which is why they needed her).
The journal launched last year to solve problems in scientific publishing. For example…
(Many) researchers want to publish, but are not aiming to publish in Nature. (But) even in PLOS one, for example, it can often take months or up to a year for the paper to go into print from submission. Which is ridiculous, it shouldn’t take so long.
How can we speed it up? We can speed up the peer review process, but that still takes a while.
Instead of publishing after the paper has passed peer review, the paper goes online at the start of the peer review process.
This allows people to clearly see what happens, revisions being made, and who the peer reviewers are. This encourages peer reviewers to submit accurate reviews and to not take an excessively long time.
Average time from submission of a paper to going online is about 6 days, including author delays (where the author didn’t reply).
So far they have published (put online) around 180 papers. Not all of those are indexed, in PubMed – or external databases. Half-finished (still not peer-reviewed) papers don’t get sent to those databases.
Eva’s question for science writers:
So when do you send out press releases? With the paper is online – by the time it finishes peer review it has been online several weeks. As writers, if it has been published online already, a press release several weeks later – is that too late?
Do writers want to be notified when a paper goes up?
Do writers want something to track papers as they go up and then when they are finished with peer review?
Another way that F1000Research is different: Data
They require ALL data to be included, though there are some exceptions (such as medical studies with private patient data). Data can be included in data repositories like Figshare, when too large or complicated for F1000 Research’s servers. But that data is embedded in the papers.
F1000Research publishes articles that aren’t “traditional”
You can submit an article that is just a single experiment (an addition to a previous paper).
Positive results are really easy to publish, negative results are impossible to publish. Often doctors prescribe drugs based on positive study results, but there may also be negative study results that didn’t get published.
Replication studies are also difficult to publish. For example often labs do an experiment to verify another lab’s original published findings. So publishing replication studies allows them to publish their results…
Questions from the audience:
Q: Do you accept articles among all subject areas?
A: We started out with the areas covered by F1000Prime – biology and medicine. So our editorial board has many biologists and medical doctors and reviewers. If we can find a reviewer for a paper we will publish it.
David E: My field is risk – and that gets press attention because it is controversial. That could be dangerous with F1000 model (of putting papers online before the peer review process).
A: Once you’re on the paper’s page it is obvious it hasn’t been peer- reviewed. Once it passes peer review – that is also obvious.
Peanut Gallery:(I couldn’t keep track of everyone talking here – sorry!)
“At the moment we also have situations where people are writing in the mainstream media about papers that haven’t gone through peer review yet. So maybe the bigger issue is making the public aware of something being peer reviewed or not…”
@biochembelle: How do we get the public to understand what peer review means? There are current problems with peer review, even within the scientific community there is a concept that peer review is altruistic, but really also peer review that is vindictive (some no better than grammar checking).
From our end – what we could do is send out a press release only if something has passed peer review.
Haley Bridger – What about sending a pitch rather than a press release?
“There is an interesting story there. Maybe writing about watching the scientific process unfold and any controversy… “
“Already a false idea that when a paper is published that is the news..”
“You’re not gonna get rid of bad journalism. I don’t think there is anything – other than an onus on the journalist – to do their own journalistic checks. Make it clear in the story.”
Eva: One thing we are thinking of doing is allowing you to subscribe to a paper, so you could be notified when it has been reviewed or revisions go up. Theoretically you could put new versions up forever if peer reviewed and indexed – you could also put new results up and update findings.
“Maybe make the non-peer reviewed ones harder to find!”
Trina: About the initial review process..? If Wakefield sends a manuscript and 1000 dollars will it go up on the site?
Eva: The in-house editors do a “sanity check”. I don’t know if he passes a “sanity check” or not. They look to see if they can send it out in good conscience to peer reviewers. Right now (for papers that don’t pass) it’s usually problems with bad English (for writers who are non-native speakers), missing data or other crucial information, or cases where it was immediately obvious even before peer review that the work did not meet basic scientific standards.
Answering a question about how people tend to review papers knowing that their name is publicly on record.
Eva: They tend to be much more accurate, and their tone is friendlier. We publish the negative peer review comments as well as positive peer review. So there are implications to being direct and honest about work. Often in anonymous review papers are passed on to post-docs or students and the reviewers don’t actually do the work. But when their name is on it they are encouraged to take ownership of the reviews they submit.
(At this point her talk was over and everyone started chatting with each other)
Suggested edits from Eva were made on 5/2/2013 to more accurately reflect on F1000Research.
Recently researchers shared a rare glimpse of life on the ocean floor – posting video compiled from high resolution videos at a depth of 100 meters (or 328 feet) of aquatic life in an Australian marine sanctuary.
The researchers, who are participating in a collaborative project between Deakin University and Parks Victoria, recorded the sea floor videos from various sites in the Discovery Bay Marine National Park. The footage is part of a project to understand the connections between seafloor habitats and fish communities across Victoria’s marine national parks and sanctuaries.
Their data shows that drinking spikes in college students during holidays, measured by drinks per week.
Most of this drinking occurs off campus.
I was curious to see if the Alcohol Enforcement Patrol data followed similar trends.
Unfortunately, data is only available up to the 10th weekend of this academic year. In addition – the data published is not how many drinks students had, but instead how many students got into trouble each weekend.
Assuming enforcement was consistent, this still doesn’t show how much drinking was going on or by who – just who got caught.
data compiled from BU Alcohol Enforcement Patrols - published in BU Today
The most obvious similarity here is the spike at week 3, and what looks like an upward trend at week 10 (towards a spike at week 11).
data compiled from BU Alcohol Enforcement Patrols - published in BU Today
It’s still hard to see what all the graphs look like in comparison. Especially since the first graph is so small, and low quality.
Here’s a scaled comparison:
Comparing these graphs next to each other – it seems that hospital transports and number of alcohol related violations follow the drinks per week chart fairly well.
data compiled from BU Alcohol Enforcement Patrols - published in BU Today
data compiled from BU Alcohol Enforcement Patrols - published in BU Today
Finally – combined data from for the most major data points…
If the patterns of students getting into trouble for alcohol related incidents, and the number of drinks per week in across the academic year are correlated at BU – the police could expect to see a really large spike in activity coming up at the end of this semester and again when students return for the beginning of Spring.
When seeking accommodations at my university as an undergrad, I had to get re-diagnosed or re-assesed again as an adult. The Disability Services Office only accepted testing paperwork that was less than five years old.
Then, when I needed accommodations to take the GRE to get into graduate school last year, I had to get tested *again* to satisfy their paperwork requirements.
It’s frustrating and expensive to have to go through testing again and again. It’s also exhausting, since the tests force you to try to concentrate and pay attention for long periods of time.
Diagnosing ADHD is still rather complicated. It’s not enough to just meet the criteria that the DSM-IV-TR sets for ADHD. Before ADHD can be identified as a problem other condition have to be ruled out, through differential diagnostic testing. Once other conditions are ruled out, ADHD can be considered as a diagnosis.
In adults, the symptoms must affect the ability to function in daily life and persist from childhood. ADHD can be confused with a number of other conditions such as emotional and adjustment problems, behavioral problems, depression, bipolar anxiety, obsessive-compulsive disorder, tic disorders, abuse, other medical problems, or learning disorders. Sometimes it is also co-morbid with one or more of these conditions.
ADHD diagnostic testing depends on a battery of psychological, intelligence, cognitive and performance tests. These are backed up by self-surveys of the person and their friends or family, to show how the patient is impaired functionally at home, school and work.
People do not get their brains scanned to diagnose ADHD.
From time to time everyone gets distracted, has problems concentrating or paying attention, or exhibits other “classic ADHD” symptoms. Modern lifestyles contribute to these problems. Dr. Edward Hallowell, an established expert on ADHD, calls this “pseudo-ADHD”.
I think that this, along with the lack of a “hard biological test” for ADHD is a big part of the reason why there is still so much controversy about ADHD.
Some people still don’t think it exists. A lot of people still don’t understand that it can affect adults, and think ADHD is something that people grow out of. Just as a sidenote – the CDC page on AD doesn’t mention adult ADHD at all.
There have been many neurological studies that show differences in the ADHD brain. These show functional differences in how the brain operates, as well as structural differences. There is biological evidence of the existence of ADHD – and strong evidence of heredity of ADHD.
What is it like to have ADHD?
This is always hard for me to explain to people. There are some simulations – but they don’t really capture the full essence…
The Hendra virus is a zoonotic virus, or a virus that can infect humans and animals. The Henda virus is in thehenipavirusfamily (which is a sub group of the paramyxoviridae family of viruses). This virus is a relatively new threat to humans, and because it has an animal reservoir in the fruit bat – it is hard to eradicate the virus.
For fruit bats, a viral infection is largely asymptomatic – however an infected fruit bat releases a large number of viruses in its urine and feces.
Dog faced Fruit Bat -photo by radiospike photography on Flickr
The virus can then be inhaled, or ingested, and infect another host.
Hendra virus infects both horses and humans. The virus can spread from horse-to-horse (probably through saliva), or from horse-to-human (through aerosol inhalation), but so far no cases of human-to-human infection have been documented.
Hendra virus emerged in Australia, where there have been 14 known Hendra outbreaks in Australia since 1994, and has killed more than 40 horses. Sixty percent of the horses infected die. Horses are thought to get the infection by eating fruit or other foods, or drinking water that has been contaminated by bat droppings.
In humans, the symptoms of the virus are flu-like. People infected with the virus can experience brain inflammation, high fevers, headache and drowsiness.
Recent research done by scientists from the University of Texas Medical Branch at Galveston, Rocky Mountain Laboratories, the National Institute of Allergy and Infectious Diseases, the National Institutes of Health, the Uniformed Services University of the Health Sciences, the National Cancer Institute, and the Boston University School of Medicine – is a major step forward in developing better ways to combat this virus. Their research is published in Science Translational Medicine.
Researchers used anti-virus human monoclonal antibody therapy after exposure to Hendra virus to protect animals from exposure to the virus. Basically the researchers took human antibodies formed from exposure to the virus, cloned them and gave them to animals. These allowed the immune systems of the animals to recognize the virus.
In order to conduct the experiments safely the researchers had to do their work a biosafety level 4 “spacesuit” lab, because there are no therapies, medecines or vaccines to treat humans currently if infected.
“These findings are really quite promising and appear to offer a real potential treatment for Hendra virus infection in people,” said Christopher C. Broder, PhD, professor of microbiology at USU and study corresponding author in a statement.
This is one step closer to nipping this emerging zoonotic disease in the bud before it has a chance to become a real problem for humans, and one step closer to developing a way to treat this virus in humans.
While doing research for another blog post (about laundry chemistry) I came across a press release on Labspaces.
Apparently scientists have found that washing machine waste-water could be a major source for microplastic pollution, according to research described in their paper, “Accumulation of Microplastic on Shorelines Woldwide: Sources and Sinks”. In particular, tiny pieces of acrylic and polyester shred from clothing during wash cycles. The paper was published in ACS’ journalEnvironmental Science & Technology on the web September 6 of this year.
This research suggests new ways that microplastics might form and travel to global waters.
Mark Browne and his colleagues defined microplastics as plastics smaller than 1 millimeter (or 1/32 inch). The scientists found polyester, acrylic, polyproplylene, polyethylene and polyamide fibers at 18 different sites around the world. Large amounts of microplastics could be seen near highly populated areas.
The researchers compared microplastics found in water released from sewage treatment plants with microplastic found on shores, to confirm that wastewater from washing machines could be a source of microplastic fibers. They also washed polyester blankets, fleeces, and shirts to see how many fibers were shed per garment. All the garments washed released more thatn 100 microplastic fibers/liter of water. Some garments shed up to 1900 fibers in one wash.
The researchers warn that as the global population grows, larger amounts of sewage will be created. In order to prevent more microplastics from being released through washing machine wast-water, they suggest that future washing machines could be designed to filter out these fibers. Sewage treatment plants with ultrafiltration systems could also prevent these fibers from reaching water habitats.
The researchers emphasized that more work needs to be done to further our understanding of how microplastics get into water habitats. Hopefully, this kind research will eventually lead to new ways to stop microplastics from contaminating the oceans, streams and other waters.