Eat your Oranges!

Eat your Oranges!

            From a current publishing in Science there is new found data that vitamin C can be used to help prevent cancer and prolong survival rate.  They found in mice that vitamin C can kill tumor cells, which are specific to certain mutations.  In the 1970’s and 80’s Linus Pauling and other researchers were trying to figure out how to show vitamin C could cure many diseases, including cancer but they were ridiculed by fellow scientists because there was little proof.  But within the past five years there have been findings that intravenous vitamin C can prolong the survival of patients with pancreatic and ovarian cancer, when also treated with chemotherapy. 

            Vitamin C is a water soluble vitamin and uses passive diffusion to cross the plasma membrane.  Oxidized vitamin C, dehydroascorbic acid (DHA), is a key player in Jihye Yun’s research into its effect on free radicals within the cell.  Certain colon cancers arising from mutations in genes KRAS or BRAF yield large quantities of GLUT1, which aids in transporting glucose through the plasma membrane.  GLUT1 also transports DHA into the cell as well and once in the cell DHA inhibits the cells ability to reduce free radicals.  For normal cells this is harmful but researchers have found that especially for colon cancers specified by KRAS and BRAF mutations it is an opportunity to attack the cancer.  By administering high doses of vitamin C and targeting tumor cells it causes a high enough concentration of free radicals to destroy the cells, specifically inhibiting the enzymes needed to metabolize glucose and therefore halting energy production. 

            Using vitamin C as a treatment has a lot of potential because colon cancers with KRAS mutations make up around 40% of patients.  Furthermore, KRAS mutations have also been found to be the culprit of certain pancreatic cancers.  Also a fun fact from the findings is that when they mentioned high doses of vitamin C, it is the equivalent of eating 300 oranges.  Moral of the story is to eat oranges, not only are they yummy but they also can help prevent cancer.

Reference: news.sciencemag.org/chemistry/2015/11/vitamin-c-kills-tumor-cells-hard-treat-mutation

Tooth Erosion by Sugar Free Drinks

Common sense say sugar lead to oral cavity but it actually the acid that produce by the bacteria that lead to oral cavity. Any drinks that are acidic, whether they contain sugar or not can also be bad for our teeth. The acid actually attacks the teeth by dissolving the outer layers of tooth enamel. In a study testing twenty-three different types of sugar free drinks, including soft drinks and sports drinks. The study found that those contain acidic additives and those with low pH levels cause measurable damage to tooth enamel, even if they have no sugar. Interesting this study also found flavored mineral waters can cause a measurable loss of tooth enamel too. Expert suggest quenching thirst with water is a much healthier alternative to soft drinks or any sugar free beverage. 
So if you see any sugar-free confectionery products in the grocery store that are labelled 'toothfriendly', do not trust the label because when tested they were found to be erosive to enamel. 

Reference: Briefing paper: The potential of sugar-free beverages, sugar-free confectionery and sports drinks to cause dental erosion, Oral Health Cooperative Research Centre, Melbourne, Australia, published online 26 November 2015.

Horror Movies and the Brain!

Halloween is probably my favorite holidays of the year. I can sit and watch horror movies all day without hesitation! Besides all of the brilliant classics out there like Nightmare On Elm Street and Scream, my favorite horror film right now is Sinister. It involves an ancient pagan Babylonian deity that consumes the souls of children and essentially makes them kill their families in sickening ways. Twisted but so intriguing and scary! A few nights ago I made a friend of mine watch it and she was absolutely horrified. Closing her eyes during the anticipated horror scenes with her heart beating out of her chest. This led me to question what the difference was between us. What is happening in my brain to make me love horror movies as much as she hated them? I did some research.

People can fall into two categories when watching movies: high sensation seekers and low sensation seekers. In a study by Straube et al., high and low sensation seekers were shown horror movie scenes and neutral movie scenes to analyze the differences in brain activation. They picked scenes from movies such as The Shining, Aliens, Silence of the Lambs and The Others (all amazing movies you should watch). High sensation seekers, like myself, have a significant increase in brain activation when exposed to horror movie scenes as shown by fMRI scans. They specifically showed high brain activation in the right thalamus and the right anterior insula, which are involved in corticol arousal, emotion, and self-awareness amongst other things. In low sensation seekers, there was brain activation of those areas but it was much less. When these sensation seekers were exposed to neutral scenes they showed less activation than low sensation seekers decreasing their insular activation and disrupting the optimal homeostatic level of interoceptive sensation. The idea is that because high sensation seekers experience this hypoactivation of those brain regions when exposed to low intense stimulation, they seek to compensate for it. This is why they exhibit hyperactivation and intense sensation when watching a horror movie, which is what they prefer. Low sensation seekers, however, still exhibit activation during neutral scenes because they are already anticipating danger and increased anxiety. So next time you are trying to force someone to watch a horror movie (as I do all the time), remember they are not a chicken, they truly are terrified!

http://onlinelibrary.wiley.com/doi/10.1002/hbm.20843/epdf    

Phantom limb pain: The (figurative) salt in the (actual) wound

Phantom limb sensation (PLS) is a very well-documented yet poorly understood phenomenon. The most common examples occur in wounded veterans that suffer limb loss, and it has been estimated that around 80% of amputees have experienced some sort of PLS. It has also been reported that 64% of amputees experience phantom limb pain (PLP). Of this group, the symptoms and severity can vary widely. Onset of PLP can be instantaneous, can become gradually worse over time, or patients can experience sudden onset after 25 years from the original amputation. The pain has been described as “stabbing,” “stinging,” “itching,” and “burning,” as well as a whole host of other uncomfortable adjectives, and can last anywhere from seconds to hours. Studies have shown the relationship between time of original onset and degree of pain to be negative, that is, PLP generally gets better over time, although this still remains hotly disputed.

Interestingly, people born without limbs have much lower instances of both PLS and PLP (8-18%). This is evidence that PLP is a result of remapping after an amputation and not just a secondary route that existed but was not used before amputation.

Another interesting aspect of PLS and PLP is referred sensation, which occurs when the neural connections accidentally rewire to a different area of the body. For example, arm amputees commonly report feeling phantom sensations when touched around the face, especially the lips. The theory that attempts to describe this phenomenon is called maladaptive plasticity theory, and it’s not without its critics. One of the biggest unanswered questions is something of a chicken and egg conundrum: does the cortical rewiring cause the sensation of pain or does the pain provide incentive for rewiring as a coping mechanism? As medical technology becomes more advanced using MRI and other imaging technologies, hopefully we will get closer to understanding the way PLP comes about, thus bringing us one step closer to finding the best treatment.

Mohlman, Jan, et.al. From Symptom to Synapse: A Neurocognitive Perspective on Clinical Psychology. Routledge, Taylor and Francis Group. New York, New York. 2015.

http://www.painresearchforum.org/news/25670-new-challenge-maladaptive-plasticity-theory-phantom-limb-pain

What Sport is the Best for Your Body?

Playing any sport competitively isn’t easy on one’s body. Repeated motions and the exertion of practices and games cause havoc on one’s body. I know many former collegiate athletes that have been thoroughly ‘beaten up’ by the sport they used to play so intensely. Most have decreased activity levels and quality of life because they wore out their bodies when they were young and they are paying for it now. However, are there some sports that one can play that are less detrimental to your body in the long run? A 2015 PubMed study may provide the answer. This study finds that soccer players have the greatest increase of cytokines and C- reactive protein in the blood after competition comparatively to volleyball, basketball, and handball. Cytokines are a good measure of the stress of a sport on the body because cytokines are an inflammatory response to threat and stress on the body. Muscle damage and metabolic stress was also highest in soccer players. These measured increased to astoundingly high levels right after a match was played. Volleyball had the lowest stress on the body after a match. So, if you want to protect your body from degradation so it can last you your whole lifetime, you should choose your sport carefully. If you want a body that will withstand the wears and tears of a sport, I would suggest staying away from soccer and instead, embrace a less physically stressful sport such as volleyball!  

Souglis A, Bogdanis GC, Giannopoulou I, Papadopoulos Ch, Apostolidis N. Comparison of inflammatory responses and muscle damage indices following a soccer, basketball, volleyball and handball game at an elite competitive level. Res Sports Med. 2015;23(1):59-72.

Asking for trouble: Can using antibiotics create a breeding ground for super-duper bugs?

When battling multiple antibiotic resistant infections, what should we do when our last line of defense fails us? We may be frantically searching for an answer a bit sooner than we’d hoped: New research published just a few weeks ago shows that plasmid-mediated resistance to colistin has been discovered amongst livestock in China. Uhh…Colistin? Well, there’s probably a reason you’ve never heard of it. Colistin belongs to a very strong class of polymyxin antibiotics, which have cationic polypeptide structure, and are reserved for only the most serious infectious disease cases. Notably, colistin is not a new antibiotic, but side effects like kidney damage and bleeding discouraged widespread use since its discovery in 1959. Unfortunately, it has been more widely used in livestock, particularly in developing countries like China. (Side note: 8 out of 10 of the largest world colistin producers are Chinese.) Some of the most serious livestock infections are the result of carbapenemase-producing Enterobacteriaceae, treatable only with colistin. Up until now, colistin resistance was due to chromosomal mutations, but the huge rise in resistance in China has recently been determined to be plasmid-mediated. What’s the big deal with that? Plasmid transmission allows the easy spread of the resistance gene from cell to cell and even across species. The resistance gene mcr-1 has been transferred in plasmid pHNSHP45 between strains of E. coli, K. pneumoniae, and P. aeruginosa, and researchers have even found the resistance gene present in human samples collected at an inpatient facility in Guangdong, China.

This brings us to the paradox of using antibiotics: if we use them, are we fated to eventually create more dangerous strains of antibiotic-resistant bacteria? Does using antibiotics at the rate we do ensure that we find ourselves in a pre-antibiotic era?

http://www.sciencedirect.com/science/article/pii/S1473309915004247

http://phenomena.nationalgeographic.com/2015/11/21/mcr-gene-colistin/

Physiological Starbucks Advertising: What you want to know about coffee

So I don't know about you all but I am fairly dependent on that daily cup of jo. We've all heard about its effects on your teeth and the enormous amount of caffeine content and can’t stop drinking despite all that. Seeing as my personal productivity is directly linked to that first cup of coffee, many college students could use another excuse to justify this minor addiction. A study done at the Harvard T.H. Chan School of Public Health looked into the long-term effects of daily coffee consumption. Surprisingly, a significant correlation was seen between coffee drinkers and lowered risk of mortality due to cardiovascular and neurological disease as well as suicide. Unfortunately, there was no significant data supporting caffeinated coffee over decaf so we'll have to keep a different way to validate our exponential caffeine intake. Even so, the findings essentially suggested: coffee will make you live longer. 

Now I was a bit skeptical about how they were able to ascertain valid data and make such a blanket statement. My qualms were laid to rest when I found their study began in 1976 with a primarily adult female population size of nearly 300,000 participants who were surveyed throughout the years on their coffee intake among other life-style details, general health and diet. Anyway, back to the science. They propose that chlorogenic acid, the component in coffee hypothesized to play a role in prevention of type II diabetes, may also play a role in decreased CVD since the two often share common pathologies and mechanisms. They also suggest the decreased neurological risks could be due to caffeine attenuating to the neurotoxin MPTP, which has been known to play a role in neurological cases. How does this affect us? Coffee is not only what gets us up in the morning but it also may be beneficial long term. So next time you're feeling guilty about that $3 latte just remind yourself that coffee could be a lifesaver.

The link for the full article is listed below!

Reference:

http://circ.ahajournals.org/content/early/2015/11/10/CIRCULATIONAHA.115.017341.full.pdf+html