Courtesy eshermanThe people of the world wait, their breath held, their tongues clenched between their teeth, open cans of Fresca frozen halfway to their mouths. What do you mean, JGordon? Does soda give me cancer? Or not?
Don’t worry, folks. It’s mostly “or not.” Or is it? Or not.
You may have heard (or read—I call it “hearing with your eyes”) that soft drinks might raise your chances of developing cancer. That was probably hard to hear (or read—I call “listening through your face-holes”), because I know you’re generally pro-soda, and generally anti-cancer, and you had been living your life in the hope that there would never be any conflict between the two. You can probably go on living like that, because it’s unlikely that pop is really going to give you cancer, but you should be aware that the world is a complicated place, and your soda and your cancer are sadly not excluded from the complications.
See, a the results of a study out of the University of Minnesota were recently published claiming that there seemed to be a link between the regular consumption of soft drinks (sugar-sweetened carbonated beverages) and a higher incidence of pancreatic cancer. Pancreatic cancer isn’t one of the fun cancers (like, ah, cancer of the… nothing). Although relatively rare, the three-year survival rate for people diagnosed with pancreatic cancer is about 30%, and the survival rate after five years is only 5%.
The study was based on a 14-year survey of 60,524 men and women in Singapore. Of that group, 142 people developed pancreatic cancer. Examining the lifestyles of those who did and did not develop cancer, the researchers found that people who drank two or more soft drinks a week (5 was the average) had an 87% increase in their chances of getting cancer. And because Singapore is a fairly wealthy country with good health care, the scientists think that the results could apply fairly well to western countries as well.
Oh, no! Right? I can’t give up RC Cola!
Well… eh. The thing to keep in mind is it’s all very complicated. Even if there was a direct link between sift drink consumption and pancreatic cancer, your chances of developing the cancer, even as a soda drinker, would still be very small. But, the thing is, there isn’t necessarily a direct link between the two; there’s an association here, but maybe not a causal link. That is, people who drink soda are more likely to get pancreatic cancer, but we don’t know it’s the soda that causes the cancer.
Soft drink consumption itself was associated with behavior like smoking and red meat consumption, so it’s difficult to say that it’s just the soft-drinking (as it were) that contributes to the increased cancer risk.
Researchers do think, however, that it’s possible that soda could be involved in a causal relationship with the cancer. The high sugar levels in soda probably contribute to increased insulin production and presence in the body, which may contribute to pancreatic cancer cell growth. The study also found, however, that there was no association between fruit juice consumption and pancreatic cancer, which sort of makes me wonder. Lots of fruit juice, after all, is very sugary (even if it’s not quite so sweet as most soda). So does it have something to do with the type of sweetener used? Most soda in this country is sweetened with corn syrup, but that’s not necessarily the case in other countries (see Coca Cola for an example), and there’s some debate as to how the body might react to different sweeteners.
Anyway, you aren’t completely taking your life in your hands if you finish that can of Fresca. (Fresca was probably a bad example, seeing as how it uses artificial sweeteners, and will probably give you a totally different kind of cancer.) You’re better off just taking the dip out of your mouth. It’s gross with Fresca anyhow.
Courtesy Wiki Media CommonsScience Buzz bloggers have been buzzing about this topic for some time, but as the time draws near, I thought I would jump in for those new to Science Buzz. The rapidly expanding field of DNA analysis is now being used to verify the genealogy of the great kings of Egypt. Zahi Hawass, chief of the Supreme Council of Antiquities in Egypt, has announced that on February 17th, 2010 he will be revealing the results of DNA testing on the famous mummy of the boy king, Tutankhamun. DNA testing has already been done on King Amenhotep III (who reigned from approximately 1388 to 1351 BCE) for comparison as he is believed to be either Tut’s father or grandfather. The mummy of Amenhotep’s son, Akhenaten (who could be Tut’s father), has yet to be found. Researchers also plan to test the DNA of two mummified fetuses found in the tomb to determine if they are related to Tut and shed light on whether King Tut’s bride, daughter of Akhenaten, was his full sister or half sister.
Despite the popularity of King Tut and the splendid artifacts found in his tomb, he is actually only a minor figure in the history of Egyptian pharaohs, reigning for a mere 10 years in a time of great unrest. The story of Akhenaten is more interesting. Akhenaten, who ruled from 1352 to 1336 BCE, is famous for changing both religion and artistic style in Egypt, what is now known as the Amarna Period. Akhenaton introduced a new monotheistic cult of worship surrounding the sun disc Aten and excluded all other Egyptian gods from being worshipped in an effort to suppress the powerful priesthood of Amun.
Courtesy Hajor and Wiki Media CommonsArtwork during the Amarna Period took on a more naturalistic style and often emphasized affectionate family scenes of the Pharaoh with his wife Nefertiti and their children. Of interest to many art historians is the depiction of Akhenaten himself. He is represented with an accentuated feminine appearance, rounded protruding belly, wide hips, long slender limbs, and a long thin face. Some believe it is a purposeful political depiction stressing his belief in equality of the sexes, some suggest he was a hermaphrodite, and others suggest he had Marfan’s syndrome. People with Marfan’s syndrome are usually very tall with long thin arms and legs, have thin faces, and funnel shaped chests. Unfortunately, until his mummy is located this will remain a mystery.
When Akhenaten died, the priests of Amun regained power, striking Akhenaten’s name from Egyptian records, reversed all of his religious and governmental changes, and returned the capitol to Thebes. His son, Tutankhaten changed his name to Tutankhamun to honor Amun and became the now famous boy king ruling from 1336 to 1327 BCE.
Mr. Hawass has announced plans to test all the royal mummies using their new $5 million DNA lab in the Egyptian museum. However, there is some concern in the scientific field that he will not submit results to labs outside Egypt for independent verification as is common practice in DNA testing. For example, DNA results of Hatshepsut, Egypt’s famous, powerful and only female pharaoh have never been released. Our fascination with the pharaohs is sure to continue for many more centuries.
Courtesy Harvard University Gazette
"In the half-century since Henrietta Lacks' death, her ... cells ... have continually been used for research into cancer, AIDS, the effects of radiation and toxic substances, gene mapping, and countless other scientific pursuits".
The manufacture of replacement body parts just might happen this year. Organovo just took delivery of the world's first production grade 3D bio-printer developed for them by Invetech.
The printer includes two print heads, one for placing human cells, and the other for placing a hydrogel, scaffold, or support matrix. The position of a capillary tip, can position droplets of "ink" containing virtually any cell type, with micron accuracy.
"Invetech plans to ship a number of 3D bio-printers to Organovo during 2010 and 2011 as a part of the instrument development program. Organovo will be placing the printers globally with researchers in centers of excellence for medical research." Organovo press release
For the first time, a team led by Yale University researchers has used nanosensors to measure cancer biomarkers in whole blood. The new device is able to read out biomarker concentrations in a just a few minutes. Extremely small concentrations are being measured, the equivalent of detecting a single grain of salt within a swimming pool size volume of liquid.
"The new device could also be used to test for a wide range of biomarkers at the same time, from ovarian cancer to cardiovascular disease, Reed said. Science Daily.
Authors of the paper, "Label-free biomarker detection from whole blood", include Eric Stern, Aleksandar Vacic, Nitin Rajan, Jason Criscione, Jason Park, Mark Reed and Tarek Fahmy (all of Yale University); Bojan Ilic (Cornell University); David Mooney (Harvard University).
Distinct components within the sensor perform purification and detection. A microfluidic purification chip simultaneously captures multiple biomarkers from blood samples and releases them, after washing, into purified buffer for sensing by a silicon nanoribbon detector. This two-stage approach isolates the detector from the complex environment of whole blood, and reduces its minimum required sensitivity by effectively pre-concentrating the biomarkers. Nature Nanotechnology, Dec 13, 2009
Courtesy kristiewellsLately, there’s been a lot of hoopla in the news about the over-screening of certain cancers, particularly breast and prostrate cancers. Back in October, an opinion piece published in the journal of the American Medical Association (JAMA) by researchers at the University of California, San Francisco and San Antonio’s University of Texas Health Science Center, called for rethinking in the screening guidelines for those two cancers. Although the researchers admit the regular screenings are beneficial, Laura Esserman, MD at UCSF says, “The benefit is not nearly as much as we hoped and comes at the cost of over diagnosis and over treatment.”
In a New York Times story about the report, Dr. Otis Brawley, chief medical officer of the American Cancer Society (ACS) is quoted saying “We don’t want people to panic, but I’m admitting that American medicine has over-promised when it comes to screening. The advantages to screening have been exaggerated.”
The report went on to say the ACS was “quietly working on a message, to put on its Web site early next year, to emphasize that screening for breast and prostate cancer and certain other cancers can come with a real risk of over treating many small cancers while missing cancers that are deadly.”
But the American Cancer Society responded with a claim that, despite the headlines, it wasn’t changing its guideline recommendations regarding screenings, and continued to stress that a mammogram was still “one of the best things a woman can do to protect her health.”
The story resurfaced again in late November when the United States Preventive Services Task Force issued new recommendations regarding breast cancer screenings, calling for postponing initial mammograms for women until the age of 50 rather than 40. The task force, a federal advisory board, made its decision to change the guidelines after reviewing evidence presented to it by a team of oncologists. The American Cancer Society opposes the new guidelines.
This whole story is somewhat confusing. And it’s that confusion that causes some in medical community to worry.
“I am concerned that the complex view of a changing landscape will be distilled by the public into yet another ‘screening does not work’ headline,” said Dr. Colin Begg a biostatistican at New York’s Memorial Sloan-Kettering Cancer Center. “The fact that population screening is no panacea does not mean that it is useless.”
On a recent post on the KevinMD blogsite, Dr. Amy Tuteur tries to unravel some of the confusion explaining why some medical experts think aggressive screening (and severe treatment) for breast and prostate cancer has done little to lower the death rate from these particular cancers. The PSA test, for instance, is utilized much more often in the United States than it is in the United Kingdom to screen for prostate cancer, yet the death rate from the cancer in each country is pretty much the same. It should be noted that for some cancers regular screenings are making a difference. Colon and cervical cancers are often treated successfully with early detection and by removal of cancerous or pre-cancerous tissue.
The problem is not all cancers behave the same way. Some can start small, grow slowly and if caught in the early stages, be treated (or removed) before they become fatal. And that’s been the classic cancer treatment paradigm for a long time. If all cancers behaved this way, aggressive screenings would be the way to go. But over the past decades doctors and researchers have learned a lot more about cancer biology. They now know certain cancers can erupt suddenly and explosively and become fatal very quickly. Others can appear and remain dormant - sometimes for years - and never become a problem during the lifetime of the patient. But because screening practices have become more agressive, more of the non-fatal tumors are being spotted and treated unnecessarily. At the same time the screenings can sometimes be missing some of the aggressive cancers because they’re detected too late to treat. What’s needed is for doctors to be able to find a way to determine which tumors will become fatal.
“Without the ability to distinguish cancers that pose minimal risk from those posing substantial risk and with highly sensitive screening tests, there is an increased risk that the population will be over-treated.” --Dr. Laura Esserman
This topic is of interest to me, particularly this month, because December is when I get to subject myself to various post-cancer screenings (CT scan, blood and urine tests) and an annual visit to my oncologist. Three years ago I had my first colonoscopy. I was 54 years old at the time, and 4 years beyond the recommended age for a first colonoscopy. Although no cancer or pre-cancerous polyps were found in the colon, during the procedure the gastroenterologist – who, lucky for me, was thorough enough to go beyond the end of the large colon - discovered a tumor at the very beginning of my small intestine. It turned out to be a rare cancer that can usually be cured with surgery if it’s not too advanced. In researching it, I read that it is usually a slow-growing cancer – you can have it for years without experiencing any symptoms - but the surgeon told me it could also be very aggressive. It just depends. Getting it removed was the most prudent thing to do (it’s amazing how quickly you want to rid it from your body when you learn you have cancer), so I had the surgery and fortunately the tumor was still contained and the cancer hadn’t spread elsewhere. No chemotherapy or radiation was necessary (my type of cancer doesn’t respond to it), and I’ll be considered cancer-free if I pass my annual screenings for four years. I just passed my third checkup on Wednesday.
But here’s my point: when I was first diagnosed, one of my friends chastised me for waiting so long to have my first colonoscopy. I admit I dragged my feet, despite my doctor’s recommendation. It’s my nature to avoid dealing with unpleasant things. But who knows? Had I not delayed having the procedure done, maybe the carcinoid tumor in my small intestine would have been too small to be detectable during a colonoscopy, and then much more advanced (or completely gone on its own) by the time I had my next screening. I have no way of knowing if that would be the case. But I’m not saying I’ll continue to buck my doctors’ recommendations for screenings (my oncologist set me up for another colonoscopy next month - so I got that going for me), but I can’t help but think – at least in my case – maybe some of it did come down to luck and timing.
The "flu shot" vaccine side effects are usually the normal common reactions, and usually minor. some reactions are: about one in three people get a sore arm, little redness, or low fever from the shot, and an average of 10-15% of people feel tired or get a headache. The flu itself can cause serious problems, including GBS (Guillain-Barré Syndrome); the body's immune system attacks part of the peripheral nervous system.
A large proportion of the world population will get H1N1 and the vaccine side effect risk is far smaller than the sickness. When vaccines are approved, which includes the H1N1 vaccine, they are guaranteed to be much less risky than the sickness they prevent. "There could be unknown side effects. Something could happen, but it hasn't, but we think that is highly unlikely," infectious disease and vaccine expert Mark Mulligan, MD, executive director of the Hope Clinic of the Emory Vaccine Center in Atlanta.
An interview with the health teacher, Mr. Mcginnis at Central Sr. high school, gave a new direction for this topic. He explained to me that when people encounter the H1N1 flu, teenagers and young adults are not in the high level of complications and death. As to the age range of an elder, or 7 and under, are at the high risk. Students at Central Sr. high have encounter with the H1N1, and at least 1 in 10 people at Central knows who has or had it. Teenagers to get the H1N1 vaccine aren't on the top of the list but, as a matter of fact they really don't need it. Their bodies can fight it off and can get it out of their body systems. There has been little deaths so far relating teens dying from this vaccine. Mr. Mcginnis added that "we should still stay home when we have signs of the flu. It could happen to be something else, and getting the vaccine should be kept a priority to get done for everyone."
Interview with a staff member Edward Cullen*, was a first hand look at the H1N1 virus. He had recently encounter the H1N1 late October in 2009. He first came down with the symptoms after the school homecoming game. The next morning he had a very high fever of 104 degrees, and all the symptoms of a regular cold. After about four days he scheduled an appointment with his doctor, and after about a few questions it was confirmed that he has had the H1N1 for about the last 4 days. He was given Tylenol, Advil, and Delsym to treat the virus. Looking back now he says "it was horrible and hope to never experience it ever again." Adding on he missed a whole week of school, and the teachers compromised for him to catch up on assignments. As to his plans to get the H1N1 shot, he doesn't need it. The virus is already immune to his system. Edward Cullen's* advice to everyone is to " GET THE H1N1 VACCINE!".
All vaccines aren't safe, but we've been using them for years so adding the H1N1 vaccine doesn't make a difference. The vaccines we have used and still using has side effects but people still get the shots for it. The H1N1 has not shown any real side effects other then the usual side effects of the other vaccines. It should be fine and be used to stop the spread of the H1N1. Have you gotten the shot? Do you know someone who has the H1N1? What are your plans to not get the H1N1?
* Name has been changed.
Courtesy sirgabeThere’s something I want to get out of the way straight off the bat: the original title for this post was “Monday Nutrition Extravaganza: Chemicals in your food, playing with your manhood!” And while that has a certain whimsical charm, a re-read revealed hidden, disturbing meaning in those words. And I didn’t want to subject you Buzzketeers to that. I just thought you should know.
So, moving on, what’s this stuff playing with our manhood, now?
Chemicalz in our foodz! And stuff.
Earlier today, I came across this study about how there seems to be a correlation between high levels of chemicals call phthalates in pregnant mothers’ urine, and a lowered incidence of “masculine play” in their male children. (“Girls’ play behavior” didn’t seem to be affected.)
Phthalates are a group of chemicals added to plastics to make them softer and more pliable. We all like soft plastic—no one is arguing that!—but phthalates are all over the place, and increased exposure to them (all sorts of products and packaging use phthalates) is raising concerns about how those chemicals affect us, particularly during childhood development. See, phthalates are antiandrogens, meaning that they mess with the way your body works with hormones like testosterone. Testosterone plays an important role in how we physically develop, and perhaps in how we act. The boys whose mothers had higher levels of a couple kinds of phthalates demonstrated less “male-typical” behavior. The study looked a preferred toy types (trucks versus dolls), activities (“rough-and-tumble play”), and “child characteristics.”
Now, these are slightly sticky things to go judging kids on. Some folks might argue that these characteristics aren’t linked to biology so much as social conditioning. And it feels a little weird quantifying characteristics in children (and, let’s be honest here, characteristics which may not have a solidly identified “norm,” but nonetheless have all sorts of social and sexual baggage that we are uncomfortable with and often deal with in the worst ways). However, there does seem to be some statistical association here, whatever the causal relationship is. One hypothesis is that phthalates alter fetal production of testosterone at an important period of development, affecting “brain sexual differentiation.” It’s not so hard to imagine—a year ago I did a post on how certain common chemicals in pregnant mothers seemed to be causing penis deformities in their male children. The culprit there? Phthalates. The women in that story, however, had had exceptionally high exposure to phthalates (their jobs had them in constant contact with phthalate-containing hairspray), so it’s probably not something to lose sleep over, but it’s worth knowing.
And while phthalates aren’t supposed to be in food packaging, the next article I came across (this is an extravaganza, after all) deals with another plastic additive, BPA, that is found in food packaging, and which may also cause some hormone-related havoc.
BPA has come up on Science Buzz before. It’s in all sorts of packaging and bottles (it’s the reason your over protective mother doesn’t want you to use nalgene bottles) and it may affect tissue development, potentially increasing cancer risks.
We don’t care about that, though, right? Sure, cancer is out there, but in the future, not right now, you know? I know. But BPA’s latest appearance in the news may bring some immediacy to the concern over its use. Concern for some people. For men, I mean.
Chemical BPA in workers related to sex problems, says the Washington Post. “Sex problems”? We don’t want those! Chinese men working in a factory that uses BPA were found to have high rates of sexual problems. (I won’t be defining what “sexual problems” are because whatever you just imagined was probably correct.) Now, these guys have BPA levels about 50 times higher than the average American. But, still, something like 90% of Americans have detectable levels of BPA in their urine. Again, probably nothing to lose a lot of sleep over, but something worth knowing about. This professor is of the opinion that BPAs should be banned, even though most of us will probably never be exposed to dangerous levels of it, because a) it’s not a natural part of our diet; b) it’s not actually necessary in plastics processing; c) it accumulates in the body, and we still don’t know what level at which it begins to become harmful (ask those Chinese guys); and d) it’d be relatively easy to get it out of the food and water supply, unlike some other potentially harmful chemicals.
Accepting that scientific studies are necessarily very focused to eliminate variables, both of these stories still left me wondering what affect phthalates and BPAs have on women and girls. On one hand, one tries to avoid the mindset that average human physiology=male physiology, but on the other hand it’s usually just males that have penises, making their medical problems a little more hilarious.
There are so many… things out there, and they’re all doing… stuff! Interesting to know.
Courtesy Jiju Kurian Punnoose
In the embryo, the pancreas and liver tissue develop from the same family of cells. Crucial for the creation of the pancreas in the embryo, is the Pdx-1 gene.
By infecting adult human liver cells with a harmless virus engineered to carry Pdx-1, the liver cells began produced Pdx-1 protein.
Sarah Ferber and her colleagues at the Sheba Medical Center in Tel Hashomer, Israel, showed that the gene deactivates a range of genes relevant to the cell's function in the liver, as well as activating unexpressed genes vital for beta cell function (beta cells produce insulin).
The ultimate plan is to take liver cells from people with diabetes, reprogram the cells and reinject them. Because they are the patient's own, the cells should escape rejection by the immune system, sparing the individual a lifetime of daily insulin injections. "Potentially, patients can be donors of their own therapeutic tissue," says Ferber. New Scientist
Ferber is presenting the work on July 9 at an International Society for Stem Cell Research (ISSCR) meeting in Barcelona, Spain.
Courtesy USDALets say you are walking in the woods and you see a 12 point deer ahead of you. You sneek up quietly but not quietly enough. The deer hears you looks right at you and begins to charge. Before you know it its right antler has sheered off your arm! What do you do? Well if you were a salamander you would simple re-grow it.
For centuries scientist have wondered how salamanders regenerate limbs. In recent history they believed the tissue around the injury regressed into pluripotent stem cells (the kind we have all heard about that can morph into many different types of cells) and they reform into each cell type needed to create the limb.
This research was conducted to help understand how the salamander was able to do this amazing feat so that we could apply it to humans. Unfortunately, stem cells are not the easiest thing to work with but, that is old news now.
New research has shown that the salamander's cells do not regress but have memory that allows them to grow into what they once were. The memory is so good that the cartilage from the lower limb re-grows in the lower limb again.
The way scientist were able to do this was by engineering a florescent protein in a group of salamanders and transplanted only a select cells (skin, bone, muscle, etc) into embryos. After the embryos had grown, a limb was amputated. When it re-grew scientists observed that the glowing cells were not spread out amongst all the different cell types, as it would be if the cells had regressed into blank slates, but the florescent protein was only found in the original transplanted cell type.
Good new for us humans. This new finding may, although most likely not in our life time, make it easier to regenerate human organs.