Does hygiene lead to a higher risk of Alzheimer’s Disease?

As a student who is passionate about studying psychology, I came across an article on the University of Cambridge’s research site that talks about Alzheimer’s disease, which can be defined as “a progressive disease that destroys memory and other important mental functions”. The article, titled “Better hygiene in wealthy nations may increase Alzheimer’s risk,” argues that there is a strong positive correlation between clean, industrialized countries and the prevalence of Alzheimer’s disease in the countries’ population. (Fox, 2013) While I was initially fascinated by this claim, I knew that I needed to be a little more objective when trusting these relatively one-sided claims. In doing so, then, I formulated the following question: To what extent does hygiene actually contribute to the development of Alzheimer’s disease? In other words, is there a direct cause-effect relationship between cleanliness and Alzheimer’s or is there simply a correlation between the two?

To me, the article seems to suggest that Alzheimer’s Disease (AD) is caused by high sanitation levels within a country because of limited contact with certain bacteria, viruses, and other microorganisms. Deficiency of contact with these microorganisms, they claim, can lead to an insufficient amount of T-cells, which are a form of white blood cells that effectively counteract “foreign substances and disease” (Apple dictionary). The resulting inflammation that occurs from a lack of T-cells is linked to the inflammation that is commonly found in the brains of Alzheimer’s patients. (Better hygiene in wealthy nations may increase Alzheimer’s risk, 2013) So in searching for a clearer answer to my question, I knew that I needed to understand the differences between the brain of an AD patient and a healthy brain, and break them down to their elemental, molecular level to understand exactly what could be the root cause of AD.

The brains of Alzheimer’s patients are characterized by 3 “hallmarks”: an abundance of amyloid plaques, an increase in neurofibrillary tangles, and the destruction of and loss of connection between the nerve cells. (National Institutes of Health, 2011) From this, I thought that perhaps the excess of amyloid plaques could be linked to the lack of T-cells in an Alzheimer’s brain. From here I came across a scientific study that related T-cells to the amyloid-beta proteins (that make up the plaques), and I found that “chronic stimulation by the amyloid-beta protein present in the blood” could be the cause of changes in the T-cells of AD patients that otherwise make us immune to bacteria and other microorganisms. (Mariavaleria et al., 2011) I then came across a second scientific study that claimed that T-cell immunity to bacteria and other microorganisms in AD patients decreased significantly in comparison to the T-cell immunity of healthy patients. (Giubilei et al., 2003) This research seemed to tell me that hygiene may not be the direct cause of AD, but rather that the build-up of amyloid-beta proteins in our brain could be a biological cause.

I followed through with this prediction – that the build-up of amyloid-beta proteins in our body causes AD – by trying to find out where the amyloid-beta protein comes from. Interestingly, I found that there are actually three types of amyloid-beta proteins that are processed from what is called the amyloid precursor protein (APP), which is found widely within the cells of our own bodies. Two types of amyloid-beta proteins (amyloid-beta 38 and amyloid-beta 40) are benign while the third type of amyloid-beta protein (amyloid-beta 42) is toxic and seems to be the one that causes brain damage in AD patients. (Khan) After identifying the type of amyloid-beta protein, then, I came across its chemical structure:


The molecular formula for amyloid-beta 42 is C203H311N55O60S (chemBlink); clearly, I can see that the molecular structure is quite large. It is also characteristic of a protein, as evidenced by the presence of primary, secondary, and tertiary amides that are part of the molecule. I found that this protein may actually be responsible for damaging the blood-brain barrier by making it more permeable. (Sharma et al., 2012)

From this, I thought that maybe the increase in permeability of the BBB could be linked to a less immune brain, which could connect back to the “hygiene hypothesis.” So I then decided to go back to investigating the immune system’s role in AD pathology by connecting it to its relation with the amyloid-beta 42. I found that the amyloid-beta 42 activates the production of one type of T-cells that “secrete pro-inflammatory cytokines, which cross the BBB and directly activate microglia and astrocytes in the brain, as well as indirectly induce inflammation by activating dendritic cells.” (Town et al., 2005 as cited in Fox et al., 2013) Microglia and astrocytes are “cellular components of the brain’s immune network” (Cohen, 2009); hence, I observe that T-cells modify the performance of these components in the immune system, which fosters the development of AD.

So in answering my question, I find that the amyloid-beta protein and the immune system of the brain are bidirectional in developing AD, and both play significant roles in the pathology of AD. That means that our immune system’s response to different levels of hygiene, along with our genetic predisposition (the presence of APP) both can contribute to increase risk in Alzheimer’s disease.

What are the implications, then, of my findings about AD? Well, since AD is the 5th leading cause of death for those aged 65 and older (Alzheimer’s Association, 2013), understanding the causes of AD can help us better find cures for this disease, which are not entirely ready as of yet. For example, realizing that the blood-brain barrier has increased permeability in AD patients tells drug developers that treating AD involves strengthening the blood-brain barrier so it does not allow toxic substances (such as cytokines) to enter and trigger inflammatory responses. (Sharma et al., 2012) In addition, after researching more thoroughly into the claims of the initial reading on AD, I now understand that certain claims can often turn out to be monochromatic and therefore they must be taken with a grain of salt. The health and diet claims that are so prevalent on the web must be, in my opinion, scrutinized and considered comprehensively in order to be trusted, especially since our well-being is directly at risk.

All in all, my investigation on AD has taught me more than just causes or effects of the disease. My findings have led me to understand that critical evaluation and rational judgment (the weighing of pros and cons) is often necessary when we are faced with decisions to make the best choices, both for ourselves and for our society.


Alzheimer’s facts and figures. (2013). Retrieved from

Alzheimer’s disease: Unraveling the mystery. (2008, September). Retrieved from

Brown, C., & Ford, M. (n.d.). Medicine and drugs. In Higher Level Chemistry: Developed specifically for the IB Diploma Pearson Baccalaureate.

Cohen, R. M. (2009). The role of the immune system in alzheimer’s disease. The journal of lifelong learning in psychiatry, 7(1), 28-35. Retrieved from

Fox, M. (2013, September 04). Better hygiene in wealth nations may increase alzheimer’s risk. Research at Cambridge. Retrieved from

Fox, M., Knapp, L.A., Andrews, P.W., & Fincher, C.L. (2013). Hygiene and the world distribution of alzheimer’s disease. Evolution, medicine, & public health, 2013(1), doi: 10.1093/emph/eot015

Giubelei, F., Antonini, G., Montesperelli, C., Sepe-Monti, M., Cannoni, S., Pichi, A., & Tisei, P. et al., US National Library of Medicine, National Institutes of Health. (2003). T cell response to amyloid-beta and to mitochondrial antigens in alzheimer. Retrieved from website:

Khan, A. (n.d.). The amyloid hypothesis and potential treatments for alzheimer’s disease. The Journal of Quality Research in Dementia, (4), Retrieved from

Mayo Clinic staff. (n.d.). Alzheimer’s: Causes. Retrieved from

Pellicano, M., Larbi, A., Goldeck, D., Colonna-Romano, G., Buffa, S., Bulati, M., Rubino, G., Iemolo., F., Candore, G., Caruso, C., Derhovanessian, E., & Pawelec, G. (2012). Journal of neuroimmunology, 242(1), 52-59. Retrieved from

Sharma, H. S., Castellani, R.J., Smith, M.A., Sharma, A., US National Library of Medicine, National Institutes of Health. (2012). The blood-brain barrier in alzheimer’s disease: Novel therapeutic targets and nanodrug delivery (10.1016/B978-0-12-386986-9.00003-X). Retrieved from website:

Image Resources:

Beta-Amyloid (1-42) human [Web Graphic]. Retrieved from

Is my sunblock poisonous?!

Ever since I was little, my mom always made sure that I put on sunblock before going outdoors. She correctly believed that the purpose of sunblock was to prevent skin cancer, which according to the American Cancer Society is actually “the most common of all cancers, accounting for nearly half of all cancers in the United States”.  (2013). Now, as a habit, I wear sunblock every day before going outdoors for cross-country practice. My teammates make fun of me for being “paranoid”, but I think that taking precautions is important; I do not want skin cancer! I always argue about the importance of sunscreen. Thus, you can imagine the shock when I read an article called “Your sunscreen might be poisoning you” by Dr. Perry, an Adjunct Associate Professor at Columbia University on the Dr. Oz  TV show website. I was a bit hesitant about the reliability of claims from the Dr. Oz show, (an American TV talk show hosted by Dr. Oz, a teaching professor at Columbia University) since I assume from experience that TV shows are often more for entertainment and may misrepresent the truth. As a result, to clarify whether I have been poisoning myself for sixteen years, I decided to research the chemistry of sunblock: what are some common ingredients? How do they work? And most importantly, do they really harm us?

According to the University of California San Francisco School of Medicine,  there are two types of active ingredients in sun blocks: physical, which “reflect or scatter UV radiation before it reaches your skin” and chemical, which “work by absorbing the energy of UV radiation before it affects your skin.” (2013).

According to Dr. Elizabeth Hale of the Skin Cancer Foundation, the most common physical sunblock used is either zinc oxide or titanium oxide. (n.d.) In a sense, applying them is almost the equivalent of applying white paint, as they literally “block” the sunrays. (Hale, E. n.d.) For example, as seen in the image, zinc oxide is literally a white powder.

Image 1: Zinc Oxide

These physical sunblock ingredients absorb both UVA and UVB rays, which is known as “broad spectrum” (a term you should look for on your sunscreen labeling!) and are large enough particles that they do not enter into your bloodstream. (Hale E., n.d.)Thus, they are both harmless and effective. The drawback, however, is that they are not so visually pleasing unless you want to have a white layer on your face. I researched my own Avene sunblock and found it to be a physical sunblock; it is indeed very white are hard to spread apart—something I found annoying at first, but now I’m glad that at least I’m being effectively protected from the sun.

The consumers’ natural preference of a sunblock that wasn’t so “whitely” visible like a layer of paint on their faces therefore led to the development of chemical sunblock—and this is where the problem begins. One common chemical ingredient is called oxybenzone, which is a chemical that absorbs UV rays. It is so common, that according to a CNN article, “56% of beach and sport sunscreens contain the chemical oxybenzone.” (Dellorto D., 2012).

Image 2: Oxybenzone

Dr. Perry’s article on the possible poisonous effects of sunblock was referring to oxybenzone; he claimed that as an endocrine disruptor (an external compound that disrupts the physiological actions of our body’s natural hormones)(Aguirre C., n.d.), it “can cause abnormal development of fetuses and growing children… early puberty… low sperm counts and infertility… the development of breast and ovarian cancers…prostrate cancer…”. (Perry A., 2013) After reading this, I immediately looked for other sources’ claims on oxybenzone to confirm Dr. Perry’s claim. First, the CNN article referenced before reported that “The American Academy of Dermatology maintains that oxybenzone is safe.” (Dellorto D., 2012) After this, I thought, “Okay, so the government thinks that oxybenzone is safe. Then is this the Environmental Working Group and Dr. Perry crazy?”This is when I came upon an article by Dr. Claudia Aguirre of the International Dermal Institute,  which shed light on the studies causing people to blacklist oxybenzone. One study showed that the harmful effects of oxybenzone were done on rats that were ingesting oxybenzone in toxic amounts. Another study was on whether the chemical would penetrate deep into the dermis in the first place, and although the answer was yes, the study was done on skin samples in a lab—not on human beings. Finally, another study on oxybenzone “saw deleterious effects on humans”, but “the participants were asked to use about 6 times the recommended amount of sunscreen needed to prevent sunburn”. (Aguirre C., n.d.). Thus, in the end, Dr. Perry’s claim is true—but only if you use a crazy amount of sunscreen with oxybenzone.

After doing this research, I learned a lot about sunscreen, and I think it was interesting to research the chemical ingredients in our everyday products. I had always assumed that sunscreen was just some “magical” skin cancer preventer! Also, an important implication from this research is that we should never immediately trust claims made by articles online, even if the author, like Dr. Perry, is an adjunct professor at Columbia University. We should look more in depth into the studies that the claims are based on, and decide whether we want to use these products. Dr. Perry was too extreme in his claim, which confirms my initial assumption that people on TV shows tend to exaggerate and cannot always be trusted. Thus, we have to be careful to what extent we should believe in others’ claims, and of course, we should continue to use sunblock (use the recommended amount of the equivalent of a shotglass, or two tablespoons, to the face and body) (Hale, E., n.d.)!


Aguirre C. (n.d.). Shedding Light on Sun Safety – Part Two Retrieved from

American Cancer Society. (2013, March 25). Skin Cancer Facts. Retrieved from

Dellorto D. (2012, May 16). Avoid sunscreens with potentially harmful ingredients, group warns. Retrieved from

Hale, E. (n.d.) Ask the Expert: How much sunscreen should I be using on my face and body? Retrieved from

Perry, A. (2013, May 7). Your Sunscreen Might be Poisoning You. Retrieved from

University of California San Francisco School of Medicine. (2011, June 10). Sunblock. Retrieved from


Wikipedia Commons. n.d. Zinc Oxide. Graphic. Retrieved from

The Medical Dictionary. n.d. Oxybenzone. Graphic. Retrieved from

Fun in the Sun

I got my first sunburn this summer (ouch) because I forgot to put on sunscreen. Actually, I pretty much forgot to use sun protectant the whole summer. That got me thinking about sunscreen. It’s just something that we rub onto our bodies, so how does it protect our skin? So in this post I’m going to investigate how sunscreen works, why it’s important to protect your skin from the sun, and how to do so.

The reason we need to protect our skin is because of the UV rays that are present in sunlight. UV rays come in wavelengths from 10nm to 400nm, but there are 3 main categories: UVA (315-400nm), UVB (280-315nm), and UVC (100-280nm). UV radiation has “low penetration” so its effects are mainly limited to the skin. (Encyclopædia Britannica, 2013)

(Skin Cancer Foundation, 2013) – diagram of UV ray penetration of skin

UVC rays are completely absorbed by the Earth’s atmosphere, so we don’t need to worry about that. It’s the UVA and UVB rays that cause trouble. UVB rays are the ones responsible for sunburns and suntans. (Everyday Mysteries: Fun Science Facts from the Library of Congress, 2010) UVA rays, since they have a longer wavelength, penetrate deeper and are the main cause of wrinkles and age spots. (Bytesize Science, 2012) UVA rays can also penetrate through clouds and glass, and 99% of the UV rays that reach the Earth’s surface are UVA rays. (Encyclopædia Britannica, 2013) Both UVA and UVB rays can cause skin cancer. (US Food and Drug Administraton, 2011) Also, sun exposure is responsible for 90% of wrinkles! (Youtube, 2013)

To protect ourselves from these UV rays, sunscreens were invented. There are two types of sun protectants available: chemical and physical sunscreens. Physical sunscreens, also known as inorganic sunscreens, are made out of nanoparticles that are approximately 100nm. They act as tiny reflectors on the skin to deflect and scatter the UV rays that shine onto our skin. (PBS Newshour, 2010) The large particle size is also what attributes to the “white cast” look of sunscreen on the skin. ( Chemistry, n.d.) Typical ingredients in physical sunscreens are titanium dioxide and zinc oxide.

physical sunscreen

(Bytesize Science, 2012) – structures of titanium dioxide and zinc oxide

Chemical sunscreens, also known as organic sunscreens, are much smaller in size, around 40-50nm. The small sizes of the nanoparticles allow it to be more transparent than physical sunscreens. (PBS Newshour, 2010) The most common ingredients in chemical sunscreens are octinoxate and avobenzone. (Bytesize Science, 2012)

chemical sunscreen

(Bytesize Science, 2012) – skeletal structure of octinoxate and avobenzone

Unlike physical sunscreen, chemical sunscreens protect the skin by absorbing the UV rays instead of reflecting it. The molecules in the sunscreen absorb the high-energy UV photons, and the electrons become “excited.” When the molecule returns to its original state, the energy it absorbed is released as insignificant amounts of heat. This process can be done more than once, in a cycle. (Nonprescription Drug Manufacturers Association and Cosmetic, Toiletry, And Fragrance Association, 1998)

Yikes, those UV rays don’t sound nice at all. In the interest of having younger looking skin, not getting a nasty sunburn, and preventing skin cancer, protecting our skin from the sun is a must. Physical sunscreens can only defend our skin from UVB rays, but chemical sunscreens can protect our skin from both. So when buying sunscreen, look for products that are labeled “broad spectrum” or have a PA value because those indicate both UVB and UVA protection. (Youtube, 2013)

(Youngerberg, 2013) – sunblock that have UVA and UVB protection

SPF, which stands for “sun protection factor,” can be a useful way of determining the effects of sunscreen. If your skin can stand 10 minutes in the sun without burning, then a SPF of 30 will allow your skin to be out in the sun for 30×10, or 300 minutes (5 hours), before burning. ( Chemistry, 2010)  Keep in mind that most people don’t put on enough sunscreen (a shot glass worth, or 45mL, of sunscreen is what’s recommended to cover your body), and sweat and water can make the sunscreen less effective, so it is important to reapply sunscreen often (around every 2 hours if you’re active).

It seems that I’ve found the fountain of youth – sunscreen! The next time you’re out in the sun, remember to protect yourself from those pesky UV rays, and do yourself a favor by putting on sunscreen. You’ll thank yourself when you’re older!

References Chemistry (n.d.). How Does Sunscreen Work?. [online] Retrieved from: [Accessed: 19 Sep 2013]. Chemistry (2010). How to Choose the Best Sunscreen. [online] Retrieved from: [Accessed: 19 Sep 2013]. Pediatrics (2010). SPF – Sun Protection Factor and Sunscreen. [online] Retrieved from: [Accessed: 19 Sep 2013].

Bytesize Science (2012). Repelling the Rays: The Chemistry of Sunscreen – Bytesize Science. Available at: [Accessed: 19 Sep 2013].

Discovery Fit and Health (n.d.). What do SPF numbers mean?. [online] Retrieved from: [Accessed: 19 Sep 2013].

Everyday Mysteries: Fun Science Facts from the Library of Congress (2010). How does sunscreen work?. [online] Retrieved from: [Accessed: 19 Sep 2013].

Gizmodo (2013). How Sunscreen Works (And Why You’re Wrong About It). [online] Retrieved from: [Accessed: 19 Sep 2013].

Live Science (2010). How Does Sunscreen Work?. [online] Retrieved from: [Accessed: 19 Sep 2013].

Nonprescription Drug Manufacturers Association and Cosmetic, Toiletry, And Fragrance Association (1998). Tentative Final Monograph for OTC Sunscreen. [e-book] Food and Drug Administration. Available through: [Accessed: 19 Sep 2013].

PBS Newsroom (2010). Just Ask: How Does Sunscreen Work?. [online] Retrieved from: [Accessed: 19 Sep 2013].

Science & Engineering News (2002). C&EN: WHAT’S THAT STUFF? – SUNSCREENS. [online] Retrieved from: [Accessed: 19 Sep 2013].

ultraviolet radiation. (2013). In Encyclopædia Britannica. Retrieved from

US Food and Drug Administration (2011). How Sunscreen Works. Available at: [Accessed: 19 Sep 2013].

Youtube (2013). The Ultimate Guide to Sunscreen. Available at: [Accessed: 19 Sep 2013].


Bytesize Science (2012). Repelling the Rays: The Chemistry of Sunscreen – Bytesize Science. [image online] Available at: [Accessed: 19 Sep 2013].

Bytesize Science (2012). Repelling the Rays: The Chemistry of Sunscreen – Bytesize Science. [image online] Available at: [Accessed: 19 Sep 2013].

Skin Cancer Foundation (2013). Untitled. [image online] Available at: [Accessed: 22 Sep 2013].

Youngerberg, E. (2013). Untitled. [image online] Available at: [Accessed: 22 Sep 2013].

Exceptional Bioethanol

One of the videos that particularly struck me from Chemistry class was “Bioethanol,” from the Periodic Table of Videos. In the video, Professor Poliakoff discusses his travels in Brazil, a country known for its high use of ethanol fuel, as well as his discovery regarding the use of bioethanol versus common gasoline. He found that while Brazilians domestically produced an abundant supply of ethanol fuel for use, most citizens continued to use regular gasoline to fuel their cars because it was more cost-effective (meaning that their cars could run on more kilometers per gallon with gasoline than with ethanol, and the difference in price between the two fuels was minimal). Poliakoff then went on to provide an economic explanation for this – because ethanol is fermented from sugar, and because sugar is also consumed in the diet, there is an increasing demand for sugar in both industries. Thus, the costs of producing bioethanol from sugar increase, and in turn, its price as a fuel increases. He then briefly mentioned that an alternative to using sugar in the production of ethanol could be cellulose, a material that is not specifically used for food (Haran, n.d.).Upon mentioning this, he piqued my interest and I decided to further investigate bioethanol and cellulose. This brought me to my question: How is bioethanol manufactured from cellulose, and to what extent is the use of cellulosic ethanol a cost-effective solution to preserve our environment?

(Bioethanol for Sustainable Transport, n.d.)
(Bioethanol for Sustainable Transport, n.d.)

To begin, I conducted background research on bioethanol, otherwise known as ethanol. Ethanol, whose chemical formula is C2H5OH, belongs to the chemical family of alcohols. It is “a colorless liquid and has a strong odor.” (European Biomass Industry Association, n.d.) A number of incentives have fostered the use of ethanol as an alternative fuel source. Among the most pressing of these include the increasing greenhouse gas emissions and harmful pollutants such as carbon monoxide and nitrogen oxide to the environment (Derry et al., 2008), the increasing scarcity of fossil fuel resources, and the growing dependence on foreign imports of oil (CropEnergies AG, 2011). All these concerns for developed countries, such the United States and those in the EU, that result from excessive consumption of fossil fuels contribute to the utilization of ethanol as a cleaner alternative energy source for automobiles. Ethanol releases energy according to the following equation when combusted:

CH3CH2OH (l) + 3O2 (g) –> 2CO2 (g) + 3H2O (g)

(Derry et al., 2008)

There are three main steps in manufacturing ethanol. The first is the formation of “a solution of fermentable sugars,” the second is the “fermentation of these sugars to ethanol,” and the third requires the “separation and purification of the ethanol, usually by distillation.” (Badger, 2002) Traditionally, the fermentable sugars used to produce ethanol come from either sugar crops, such as sugar cane or sugar beet, or cereal crops, such as maize or wheat (European Biomass Industry Association, n.d.). Fermentation of these sugars occurs when microorganisms, such as yeast, ferment the C-6 sugars (commonly glucose) obtained from the crops by using them as food and producing byproducts that include ethanol (Badger, 2002). However, because these sugar crops and cereal crops are also necessary for human consumption, they can be relatively expensive to use for production of ethanol.

(Warner & Mosier, 2008)

So, a third mechanism of developing ethanol for fuel has been developed, using cellulose, the waste residues from forests and the parts of plants that are not needed for food. Also known as Lignocellulosic or Cellulosic bioethanol, this biofuel is considered less expensive and “more energy-efficient than today’s ethanol because it can be made from low-cost feedstocks, including sawdust, forest thinnings, waste paper, grasses, and farm residues (i.e. corn stalks, wheat straw, and rice straw).” (Detchon, 2007) As a person who never likes when things go to waste, I was delighted at the fact that we could create fuel from cellulose, which in turn helps to save so many of our natural resources and eliminate much of our waste. To my dismay, however, I discovered that this advantage is accompanied with many costly limitations.

Cellulose, like starch, is composed of long polymers of glucose, which can be used for fermentation in producing ethanol. However, the structural configuration of cellulose is different from that of starch, and this, combined with its encapsulation by lignin, a material that covers the cellulose molecules, makes hydrolysis of cellulosic materials very difficult because the process requires the aid of enzymes or specific reaction conditions or equipment (Badger, 2002).

(Warner & Mosier, 2008)
(Warner & Mosier, 2008)

The three main methods of cellulosic hydrolysis are acid, thermochemical, and enzymatic hydrolysis (Badger, 2002). For the purposes of this blog post, I will focus on the latter form, involving enzymes, which are “biological catalysts.” Enzymes are introduced into a reaction to provide an alternative pathway with a lower activation energy so that the reaction can take place (Derry et al., 2008). However, enzymes must be able to make contact with the reactants of the reaction, which is quite difficult to achieve with cellulose molecules. Thus, a “pretreatment process” is needed to separate the tightly-bound sugars that comprise cellulose. These processes are often energy-intensive, and are thus associated with high costs (Badger, 2002). In addition, the costs of the enzymes are also currently quite high, although biotechnology research is gradually decreasing their costs (Novozymes, as cited in Detchon, 2007) The National Renewable Energy Laboratory (NREL) uses a process known as simultaneous saccharification and co-fermentation (SSCF) to hydrolyze cellulose. A “dilute acid pretreatment” to “dissolve the crystalline structure” of the cellulose is first employed. A portion of the “slurry” that results is then placed into a vessel that grows a cellulase enzyme, while another portion is placed into another vessel to grow a yeast culture (Badger, 2002). In this process, sugar conversion and fermentation occur simultaneously, rather than consequentially, to yield the product of ethanol as quickly as possible, usually a few days (Lynd, 1999 as cited in Warner & Mosier, 2008). However, SSCF still requires expensive enzymes in order to occur, and because the process lasts a few days, the reactor vessels must run for long periods of time (Badger, 2002).

So, simply from observing the process of SSCF, I realize that the industrial creation of ethanol from cellulose is a tiresome process. The reactions needed to convert a molecule of cellulose into its glucose constituents are both costly and time-consuming, contrary to what I had believed would have been quite simply a breaking down of a polymer of glucose. There are numerous implications to this issue, and this brings me to the second part of my question: to what extent is the use of cellulosic ethanol a cost-effective solution to safeguard the environment? Here I discovered the advantages and disadvantages of cellulosic bioethanol. Firstly, greenhouse gas emissions from ethanol-fueled cars are reduced by 85% to 94% compared to those running on regular gasoline. Cheap feedstock that is non-related to food materials is another added benefit of bioethanol created from cellulose, since the question of food vs. fuel is eliminated. And, much of the infrastructure adapted for ethanol fuel use is already in place – roughly 2,000 stations serving E85 (a fuel containing 85% ethanol and 15% petrol) and most automobiles are already built to run on both gasoline or ethanol-based fuel. What’s even more favorable to the environment from using bioethanol is that because ethanol is an organic compound, it is highly biodegradable, making fuel spills much less hazardous than regular gasoline spills (Green the Future, 2008).

Furthermore, the overall benefits gained from using bioethanol made from any other means also cannot be ignored – for example, lower carbon emissions, less reliance on foreign oil reserves, and conservation of finite fossil fuel resources (CropEnergies AG, 2011).

These pros do no exist without their cons, however. I also found that in addition to the high costs of production of cellulosic ethanol that may make it relatively expensive for consumers, there were other disadvantages as well. Commercialization of this type of ethanol is limited, as most production plants are pilot plants and find it difficult to transition to full-scale commercial plants. In addition, because ethanol absorbs water, it is easily contaminated as a fuel and thus is difficult to transport. The high costs of production also could not be outweighed by ethanol-run automobile performance, since it takes about 1.4 gallons of E85 to run the same distance as it would take 1 gallon of regular gasoline (Green the Future, 2008). This was also the main reason, as stated by Poliakoff, that Brazilians continued to use regular gasoline as opposed to bioethanol – their cars simply ran more efficiently on petrol.

From analyzing both sides of the argument, I have come to the conclusion that even though bioethanol seems to have its many disadvantages, the biofuel has come a long way in improving the welfare of our environment. The implications of a better environment per se are perhaps enough to convince me to purchase ethanol as the source of fuel for my car (when I get one, eventually). But also, because cellulosic materials are often wasted and abundant in nature, I find it simply fascinating that we have come across yet another resource with which to provide energy to sustain our lifestyles. Of course, though, I am careful not to jump to the conclusion that this is a panacea to the global peril of climate change, because I know that exploitation of our environment will lead to destruction of it. But now I have understood that even the smallest of steps taken to achieve ecological sustainability can have drastic rewards for the wellbeing of society.


Badger, P.C. (2002). Ethanol from Cellulose: A General Review. Trends in new crops and new uses, 1, 17-21. Retrieved from

CropEnergies. (2011). Bioethanol report [Brochure/report]. Retrieved from

Derry, L., Clark, F., Janette, E., Jeffery, F. Jordan, C., Ellett, B., & O’Shea, P. (2008). Chemistry for use with the IB diploma programme: Standard level. Port Melbourne, Victoria: Pearson Education Australia.

Detchon, R. (2007). The Biofuels FAQs: The Facts about biofuels: ethanol from cellulose. Retrieved from

European Biomass Industry Association. (n.d.). Bioethanol Production and use [Brochure]. Retrieved from

Green the Future. (2008). Cellulosic Ethanol: Pros and cons. Retrieved from

Haran, B (Producer). (n.d.). Bioethanol [Video episode]. United Kingdom: University of Nottingham. Retrieved from

Warner, R.E. & Mosier, N.S. (2008). Ethanol from Cellulose Resources. Retrieved from

Image Sources:

Bioethanol for Sustainable Transport. (n.d.). CO2 cycle for bioethanol [Image]. Retrieved from

Warner, R.E. & Mosier, N.S. (2008). Fermentation of glucose to carbon dioxide and ethanol [Image]. Retrieved from

Warner, R.E. & Mosier, N.S. (2008). Structure of cellulose polymer [Image]. Retrieved from

Fermented Food

Everyday at dinner, my mother would bring Kimchi to the table. I myself am not a big fan of the taste of Kimchi, but in my opinion, my mother, like all Koreans, might be. During the SARS outbreak 11 years ago, my uncle convinced me to eat Kimchi by telling me that the reason Korea was not affected by SARS was that all Koreans ate Kimchi. 11 years later, I am still asking myself what is so special about this fermented vegetable that Koreans and a few foreigners are crazy about. So I came up with the research question for this blog post: What are the positive and negative effects of consuming fermented food, and what is the chemistry behind them?

Kimchi is not the only type of food that has been through fermentation. Our favorites such as cheese, yoghurt, and smoked salmon have also been through this process. So, to begin, what is the definition of fermented food? According to Peter Sahlin at Lund Institute of Technology, fermented food is any foods influenced by lactic acid producing microorganisms. Similarly, fermentation was categorized by the World Health Organization as a “technique for preparation/storage of food.” This is because in the developing countries, one tenth of the children below the age of five die because of dehydration because of diarrhoea caused by unhygienic conditions. In this case, lactic acid fermentation has been discovered to “reduce the risk of having pathogenic microorganisms grow in the food.” (Sahlin, 1999)

Fermentation of foods has been an ancient traditional practice. Tiberius the Roman emperor always had a barrel of sauerkraut when he traveled to the Middle East because Romans knew of the effects of lactic acid that included protection from intestine infections. (Schachter, R. ) Over the years, fermented foods have continued to be known to create beneficial probiotics to our guts. Having healthier guts lead to healthier digestion, which means having better absorption of nutrients, vitamins and minerals, improving overall health. In addition, fermented foods have helped in relief from lactose intolerance, prevention of colon cancer and  prevention of reoccurrence of bowel disease. (Sisson, M., n.d.)

The beneficial effects of fermented food are caused by the lactic acid bacteria that form during fermentation which increases the acidity of the food (decrease the pH) as the bacteria convert energy from sugars and starches into lactic acid. (Erickson, Fayet, Kakumanu & Davis) Lactic acid bacteria, according to Sally Fellon, writer of Nourishing Traditions are ‘beneficial organisms that produce numerous helpful enzymes as well as antibiotic and an anti-carcinogenic substances.” (Pickl-It., n.d.) From what I have previously learned, acids such as lemon are able to kill harmful bacteria. When I connect this fact to my research, I could most likely conclude that when fermenting food, the food is not only stored at a state where harmful bacteria are not able to cultivate, but also the production of beneficial enzymes are not interfered, hence resulting in the beneficial effects of fermented food, such as improvement in digestion.

Figure 1: Lactic Acid Structure

However, when fermented food are over consumed, there can be negative health impacts.

Even though aldehydes are not toxic substances, if one encounters a high toxic level of aldehydes through foods such as kombucha tea, some pickles, wine and beer, one’s health may be damaged. Aldehydes are a type of organic compound produced by fermenting organisms, or oxidation of alcohols. They commonly contaminate cigarette and other smoke such as smog, vehicle and factory exhaust, synthetic fragrances, and others. (Schachter, R., n.d.) The human body has enzymes that are able to convert the aldehydes into a less-harmful substance, but when there is a high level of aldehydes, the aldehydes can become toxic and travel to the brain, causing neurological diseases. Another harmful effect of aldehydes is that it damages red blood cell membranes. What this  means is that red blood cells will become “less flexible in passing through tiny capillaries, altering hemoglobin” (oxygen transporter in RBC). In other words, there will be less oxygen available to the cells in the body, especially the brain. (Pierini, C., ASCP, C., & CNC. n.d.)

Figure 2: Aldehyde Structure
Figure 2: Aldehyde Structure

Despite that my sources suggest both negative and positive health implications of fermented food, they are not clear about the specific diseases that can be caused by the negative impacts of fermented food, but only clear about the specific diseases that can be prevented by the positive impacts. From this, I may be able to assume that the positive consequences of eating fermented food may be greater than the negative consequences, and if I would like to avoid the negative consequences, I may need to avoid certain types, such as alcohol, although this may not be a problem as I am not an alcohol consumer.

After learning about the effects of fermented foods, I realized that it was no coincidence that my mother had intestinal problems. I learned that all this time, when my mother was bringing Kimchi to dinner table, she was eating the fermented vegetable for her health rather than for the taste.

Figure 3: Kimchi


1. Erickson, L., Fayet, E., Kakumanu, B., & Davis, L. (n.d.). Retrieved from Files/CH 5 – Lactic Acid Fermentation.pdf

2. Pickl-It: What is lactic acid?. (n.d.). Pickl-It. Retrieved September 15, 2013, from

3. Pierini, C., (ASCP), C., & CNC. (n.d.). A Health-Destroying Toxin We Can’t Avoid And Must Detoxify. Vitamin                         Research Products. Retrieved September 16, 2013, from http://


4. Sahlin, P. (1999). Fermentation as a method of food processing. Retrieved from:

5. Schachter, R. (n.d.). Risks and Benefits of Fermented Foods Consumption | Wake Up World. Wake Up World.

Retrieved September 14, 2013, from

benefits- of-fermented-foods-consumption/

6. Sisson, M. (n.d.). The Health Benefits of Fermented Foods | Mark’s Daily Apple. Mark’s Daily Apple. Retrieved                     September 14, 2013, from


7. Aldehydes and Ketones. (n.d.). Boundless. Retrieved September 15, 2013, from–2/functional-group-names-


8. Healthy Kimchi Burritos | Hungry Girl in Korea. (n.d.). Hungry Girl in Korea | The blog about healthy cooking and baking in Korea. Retrieved September 16, 2013, from

9. Helmenstine, A. M., & Ph.D.. (n.d.). Lactic Acid Chemical Structure. Chemistry – Chemistry Projects, Homework Help, Periodic Table. Retrieved September 16, 2013, from—L/Lactic-Acid.htm

Zingiber officinale

Growing up with a Chinese mother, one of the worst parts about getting sick wasn’t just the symptoms, but the ingestion of traditional Chinese remedies. The ginger root was (and still is) the worst one in my opinion however at the same time it was the most effective. Whenever I get sick, my mom will either make me eat solid cut up ginger root or she would put it in into Coca-Cola for me to drink and for some reason it is surprisingly effective. This got me wondering, what chemical process lies behind this home remedy and how does it work?

The ginger (Zingiber officinale) root, or rhizome, has been used as herbal medicine in its native Asian continent for thousands of years. It has been known to mainly help cure ailments such as a common cold and those involving the stomach, such as: stomach aches, motion sickness, morning sickness, diarrhea and nausea to name a few. However, it has also been known to be a pain reliever, relieving chest pain, low back pain, arthritis and muscle soreness, nature’s very own analgesic if you will.[1][2] Doctor’s also prescribe ginger pre-surgery to alleviate post-surgery nausea and it is also used post-chemotherapy operations for similar reasons. [1]


Figure 1: Foster, S. Zingiber Officinale

Surprisingly enough, even though this natural remedy has been in use for thousands of years, scientists still don’t have a clear idea on how it acts on our body on the micro level. What is known is that the active ingredients in the ginger root are non-volatile pungent components oleoresin, grouped into gingerols and shogaols. Gingerols are a series of homologues with varied unbranched alkyl chain length, whereas shogaols are a series of homologues derived from gingerols with dehydration at the C-5 and C-4. The most active gingerols and shogaols are the 6-, 8- and 10-, gingerols and 6- shogoal.[5]

Gingerols & shogoals

Figure 2:

Diagrams of 6-, 8-, 10- gingerols & 6- shogaols compared to internal standard PAV

Part of a study conducted by Yanke Yu. et,al took twenty high-risk subjects developing colorectal cancer and randomly placed them in half. Half of them would receive 250mg ginger extract and half of them would receive a placebo. The study found that 6- gingerols in particular was found in high-concentrations in the colon among high-risk sample subjects that ingested dried powdered ginger. This lead to the assumption that 6- gingerols were a necessary factor in the health of the colon and thus is being investigated as a possible treatment for patients with colon cancer.

However, despite all of the positive (albeit vague) effects that ginger has on the body, there also possible side-effects of ingesting ginger. MedlinePlus suggests that ginger affects fetal sex hormones and thus it is advised that pregnant women avoid eating ginger. Breast-feeding women, people with various bleeding disorders (hemophilia), diabetics and people with heart conditions should stay away from eating ginger. The effects of ginger interacting with prescribed medication have also raised some questions for people with similar cases as previously stated. Ginger shouldn’t be used with anti-coagulative / anti-platelet drugs as ginger “might” slow blood clotting, such medications include ibuprofen and aspirin. Medications for diabetes and high blood pressure should also not be ingested with ginger as ginger might reduce blood sugar concentration.

What vexes me most about this investigation is how vague my sources are. I find that although my question has been answered on mainly a macro level. I still do not know how the 6-, 8-, 10- gingerols and 6- shogaols interacts with various bacteria and other pathogens. However, I do observe that the structures of the gingerols and shogaols do contain an alcohol hydroxyl functional group. Drawing upon my everyday experiences and previous knowledge, I know that alcohols do have anti-septic properties and this functional group might play a role in how gingerols and shogaols interact with various bacteria and pathogens in the human body. Also, the gingerols and shogaols have a non-polar structure, I assume that this allows them to pass through blood-membrane barriers more easily than other polar substances, however this is pure speculation.

The implications of this lack of knowledge is that, until we know more about how gingerols and shogaols found in ginger interact with our bodies’ systems, we will be putting more people with colorectal cancer at risk. It has been found in the study previously stated that the gingerols and shogaols found in ginger are necessary in our bodies gastro-intestinal tract (specifically in the colon) and could play a vital role in aiding people with colorectal cancer. Also, if we know how the gingerols and shogaols interact with various pathogens and with our body in general, it could be possible to create more effective medical solutions for common day sicknesses and reduce the risk of additional side effects with other medications.

Reference list:

[1] University of Maryland Medical Center. (2013). Ginger. Retrieved from:

[2] United States National Library of Medicine. (2013). Ginger. Retrieved from:

[3] National Center for Complementary and Alternative Medicine. (2013). Herbs at a glance: Ginger. Retrieved from:

[4] Inc. (2013) ginger (zingiber officinale) – oral. Retrieved from:

[5]Yu, Yangke., Zick, Susanna., Li, Xiaoqin., Peng, Zhou., Wright, Benjamin., Sun, Duxin., (2011). Examination of the Pharmacokinetics of Active Ingredients of Ginger in Humans. Retrieved from:!po=2.50000

[6] National Library of Medicine. (2013). Diagram of structures of 6-, 8-, 10- gingerols and 6- shogoal compared to standard internal PAV. Retrieved from: (picture)

[7] Sabina, E.P., Pragasam, S.J., Kumar, S., Rasool, M., (2011). 6- gingerol, an active ingredient of ginger, protects acetaminophen-induced hepatotoxicity in mice. Retrived from:

Soil Chemistry

The large-scale deforestation of tropical rainforest has had a great impact towards the environment, from the loss of habitats, to driving climate change. However what one often neglects is destruction of soil as a result of deforestation. Recently while watching a documentary about the deforestation in the Amazon I’ve noticed that the deforested areas were like deserts, which strongly contrasted with the lush lives among the rainforest floors. This is seen in the image below taken by John Michael Fay of National Geographic.

Figure 1: Deforested Amazon Rainforest (Fay, J.M., n.d. )

This led me to my question, what is the main factor(s) which determine the health of the soil or the extent of soil degradation?

Rainforest soil have little or no nutrients as they are rapidly used up by the flourishing plant life (Sayre, 1994). However a tropical rainforest has its own nutrient cycle, where it recycles the nutrients released by the decomposition of the organic matter on the forest floor. The Nitrogen cycle and Water cycles within the Tropical Rainforest, are the 2 major cycles which allows the rich existence of life among the forest (Witherick, M.E., 2010).

As learned from GCSE Biology, Nitrogen is a essential element for all living things. This is because the enzymes in and living organism which facilitates all kinds of reaction and processes is a form of protein. And from IB Chemistry we know that a protein molecule is identified by the functional group of an amine.

Figure 2: A Protein Molecule (University of New Mexico, n.d.)

Although the air is composed of 79% Nitrogen gas, but it is in a chemical form which is inaccessible to the  majority of living organisms. (Kiera, S., 2009). This form of Nitrogen can be converted to the usable form of nitrates and nitrites through Nitrogen Fixation, a process limited to some microorganisms. (Nitrogen Cycle, n.d.). The nitrogen fixation mechanism is undergone exclusively with prokaryotes using the complex enzyme of nitrogenase and can be seen from the following equation (Deacon, J., n.d.):

N2 + 8H+ + 8e + 16 ATP ↔ 2NH3 + H2 + 16ADP + 16 Pi

As seen with the visible layer of humus and rotting leaves of the rainforest floor,the hot and humid climate of the rainforest, this creates an ideal condition for decomposition. The decaying leaves, animal and insect droppings are decomposed by fungi and bacteria, which releases Ammonium (NH4+). Then through the process of Nitrification by bacteria, nitrate and nitrite compounds can be formed and assimilated into plants. This cycle is represented in the following diagram by Sierra Kiera, 2009:

Figure 3: The Nitrogen Cycle (Sierra Kiera, 2009).

Water is also an essential substance for all living organism as it is a component of aerobic respiration. The water cycle consist of the processes of: evaporation, precipitation, transpiration, through flow, surface runoff. In the diagram below by BBC Bitesize, it shows the uniqueness of the water cycle and the features that help the rainforest retain and store the precious water.

Figure 4: The Rainforest Water Cycle (BBC, n.d.)

These cycles are examples of close systems. As we have just learned in Chemistry, the closed system allows the rainforest to sustain a natural occurring equilibrium of its nutrient usage and creation and water storage and transfer. By removing the trees from the cycle, we are in fact “opening” the system, creating an imbalance in nature, interfering with the equilibrium. Since the trees are a large store of water in the cycle and prevent direct rainfall, the removal of the trees will cause the rain to wash away any nutrients and physically erode the soil. Since there are no more decaying roots and leaves from trees, there will be a lack of supply to nitrogen, which inhibits the growth of other organism. Also the lack of decomposition of these organic substances, will cause problems with water retention. Water plays a vital role not just in aerobic respiration but assimilating important dissolved minerals such as calcium and magnesium into plants. Due to the copious amount of rain in a tropical climate, the remaining nutrients in the soil is quickly washed away, leaving a sheet of bare land with no capability of plant growth.

In conclusion, the ratio of organic matter in soil is a major factor in determining the fertility of the soil. The decomposers (fungi and bacteria), the amount of nutrients, the decaying matter, and the water retention rate are all necessities in soil for the growth of plants. (Lewandowski, A., 2002). With the lack of either component, the soil can be easily susceptible to erosion, degrading the soil, in the long-run causing desertification. This poses a threat to the available arable land available for crops and other agricultural use, which directly affects our supply of food.


Sayre, April Pulley. Exploring Earth’s Biomes: Tropical Rainforest. New York: Henry Holt and Company, Inc, 1994, pp.1-56

Nitrogen Cycle. (n.d.). Microbiology The Beginning. Retrieved September 5, 2013, from

Kiera, S. (2009, October 13). Nitrogen Cycle in the Rainforest. Biology of Tropical Rainforest. Retrieved September 5, 2013, from

ACEER. (n.d.). Water Cycle. West Chester University. Retrieved September 5, 2013, from

Lewandowski, A. (2002). Organic Matter Management – Soil Scientist. University of Minnesota Extension. Retrieved September 5, 2013, from

BBC. (n.d.). BBC – GCSE Bitesize: Rainforest water and nutrient cycles. BBC – Homepage. Retrieved September 5, 2013, from

Deacon, Jim. “The Microbial World: The Nitrogen cycle and Nitrogen fixation.” Biology. The University of Edinburgh, n.d. Web. 5 Sept. 2013. <>.

Witherick, M. E., & Milner, S. (2010). Edexcel IGCSE geography. Harlow: Edexcel.

BBC – GCSE Bitesize: What are enzymes?. (n.d.). BBC – Homepage. Retrieved September 10, 2013, from

Image Citations:

“Biological Macromolecules.” UNM Biology Department Home Page. N.p., n.d. Web. 5 Sept. 2013. <>.

Fay, J.M., n.d. Retrieved from:

Analgesic Properties of …. Snail Venom?

I know what you’re probably thinking; snails have venom? This was exactly what I had thought when I came across a post on the popular social media website, Reddit. I was intrigued because I didn’t even know that snails have venoms and that they could even be used as painkillers. Turns out, the post wasn’t referring to the typical snails you find in a garden, but instead, the cone snails that are typically found in warm and tropical seas and oceans. Interested by the topic, I decided to investigate more on how exactly the snail venom can act as an analgesic, and its possible significance in the medical field.
Analgesics are commonly known as painkillers, and are divided into two types, mild and strong. Mild analgesics, such as aspirin and paracetamol, are used to treat the typical headaches, toothaches, or sore throats by, “preventing the stimulation of nerve endings at the site of pain and by inhibiting the release of prostaglandins, the chemical responsible for the widening of blood vessels near the site of the injury, from the site of injury to provide relief to inflammation, fever and pain” (Brown, Ford, 2008). For more severe pains, strong analgesics bind to opioid receptors in the brain to alter the perception of pain by blocking the transmission of pain signals between brain cells (Brown, Ford, 2008). Today, many cancer patients, diabetic patients, and other victims of chronic pain are treated with strong analgesics like morphine and heroine. The problem is that these opioids are highly addictive and repeated usage can lead to tolerance, which a reduced response to the drug. Scientists have discovered that the venom found in cone snails have analgesic properties that are 10000 times more powerful than morphine, and the best part about the venom is that it is not addictive. (National Geographic, n.d.) Since cone snail venom is clearly a better analgesic than opioids, I questioned why isn’t it replacing morphine and heroine as the common analgesics to treat victims with chronic pain?
deadly cone

Figure 1: Image of a Marble Cone Snail (National Geographic, (n.d.))

Although they are only about four to six inches long, these carnivorous mollusks they have venoms poisonous enough to kill 15 adult human beings (Compassionate Healthcare Network, 2004). To do this, the cone snails have teeth that are similar to hypodermic needles that inject venom into their preys. The venom instantly paralyzes the victims by interfering with the communications of the nervous systems. In a typical nervous system, the neurons transmit chemical signals to another neuron through ion channels. The chemical signals are repeatedly transmitted from neuron to neuron until it reaches a muscle cell and tells it to contract. The venom of cone snails contain hundreds of thousands of short polypeptide proteins that blocks specific ion channels to prevent neurons from transmitting chemical signals, inhibiting muscle movement, leading to paralysis (Chadwick, 2013)(Discovery News, 2013).
So how can something so deadly be beneficial to humans? For many years, scientists have studied several hundreds of the short polypeptide proteins, called conotoxins, before the isolating analgesic conotoxin agent and creating the synthetic version named Ziconotide, or often known by the name Prialt. Unlike other analgesics, Ziconotide inhibits pain in a different way. People feel pain because electrical signals are carried across a synapse from the pain fibers to the nerve cells in the spinal cord that signals the brain. In order for the electrical signals to cross the synapses, electrical signals has to be converted into a chemical signal with the help of calcium. Ziconotide blocks the calcium gateways in the nerve fibers so that the chemical signals cannot cross the synapse to reach the nerve cells in the spinal cord. As a result, the brain does not receive the signal and therefore, one does not perceive pain (Compassionate Healthcare Network, 2004).
Although Ziconotide is 10000 times more powerful than morphine and is non-addictive, it is not commonly use to treat patients with chronic pain. This is because like any other drug, Ziconotide comes with many side effects such as abnormal vision, amnesia, vertigo, anxiety and possibly more undiscovered side effects. Furthermore, ziconotide cannot be administered orally because the body will break down the swallowed ziconotide before it can reach the receptors they need to reach. Therefore, zinconotide is currently administered with a direct injection into the spinal cord, a costly and invasive method of drug delivery.

Figure 2: Structure of Ziconotide (ChemBlink, (n.d.))

The discovery of Ziconotide has many implications in the medical field. Firstly, future research can be synthesized or modified Ziconotide to withstand the digestive processes of the body so that zinconotide can be taken more conveniently and without economic strain. In fact, scientists have already engineered a circular shaped synthetic Ziconotide conotoxin that is more stable to be administered orally (Discovery News, 2013). Ziconotide that can be administered orally will be more accessible to patients with chronic pain that have developed tolerance to morphine and heroine and need stronger analgesics to suppress the pain. Secondly, the discovery of Ziconotide suggest a bigger picture that many medical issues that people face today could possibly be cured by something in nature. There are so many microorganisms, animals and plants on Earth that have not yet been discovered. Perhaps, the secret to the cures of cancer and other illnesses lie in the Amazon jungle or at the bottom of the Mirana Trench.

Brown, C., Ford, M. (2008). Higher Level Chemistry Developed Specifically for
the IB Diploma. England: Pearson Education Limited.

Chadwick, A. (2013). Venom. The Cone Snail. Retrieved September 5, 2013, from

Compassionate Healthcare Network. (2004). Cone Snail Venom Attacking Pain.
Compassionate Healthcare Network. Retrieved September 5, 2013 from

Discovery News. (2013, February 11). Snail Venom Inspires Powerful Pain
Reliever. Discovery News. Retrieved September 5, 2013, from

National Geographic. (n.d.). Geographic Cone Snail. National Geographic.
Retrieved September 5, 2013, from

Marble Cone Snail [Web Graphic]. (n.d.) Retrieved September 5, 2013 from

Wikipedia. (n.d.). Conus. Wikipedia. Retrieved September 5, 2013 from

Wikipedia. (n.d.). Zinconotide. Wikipedia. Retrieved September 5, 2013 from

Ziconotide Acetate [Web Graphic]. (n.d.). Retrieved September 5, 2013 from

A Silver Bullet?

When my sister went to get her ears pierced over the summer, my mother recounted how, instead of using devices like the sterilized piercing guns used today, Indian people used to use thin wires of silver to pierce their ears because of its supposed antimicrobial properties. This intrigued me. Of course I had heard of molecules like penicillin that could kill off bacteria, but never before had I considered that a single, naturally occurring element would be able to accomplish the same. How does this seemingly benign molecule cause so much damage?

The transition metal itself is biologically inert; the real structural damage stems from its Ag+ ion. This is released when Ag comes into contact with moisture (Kenyon University & Garduque), and does its work inside the microbe itself. I stopped as soon as I read that last part. Something didn’t seem right. I had learned from my AP Biology class that the majority of cell membranes are hydrophobic. They consist mainly of a phospholipid bilayer with the polar hydrophilic heads facing outwards into the environment and inwards towards the cell’s cytoplasm, and the long, non-polar hydrophobic tails made of hydrocarbons chains in-between. These tails don’t like to let polar atoms and molecules in and out by themselves, and I thought it highly unlikely that microbes would have special protein channels built to let in damaging substances. So how did these Ag+ molecules get in in the first place?


Figure 1: The Phospholipid Bilayer

(Midlands Technical College, n.d.)

A while of digging later, I had no definitive answer. Some research hypothesized that the ions got through via protein channels made for other ions (Kenyon University & Garduque), but since there wasn’t any conclusive evidence I still remained somewhat skeptical. I continued to research the effects of the Ag+ ions, tough, and the evidence I found in favor of its microbial properties was strong enough for me to overlook this tiny blip.

What I found was that Ag+ works in three major ways: by reacting with the disulfide (R-S-S-R) and sulfhydryl (R-S-H) groups of microbial protein structures, by interacting with the microbial DNA, and by damaging the membrane structures of the cells. In the first method, the interactions of the ion change the quaternary (outer) structure of some of the microbes key proteins and enzyme, leaving it unable to function properly. The ion reacts to form, “a stable S-Ag” bond with the sulfhydryl-containing compounds, which are involved in, “trans-membrane energy generation and ion transport,” located in the microbial cell membrane, and are also believed to, “take part in catalytic oxidation reactions that result in the formation of disulfide bonds,” which are key components of a protein’s outer structure. The latter doesn’t involve Ag+ acting as reactant, but rather as a catalyst between existing the oxygen and hydrogen portions of the sulfhydryl groups. This reaction also ends up releasing H2O as a product (Jung, Koo, Kim, Shin, Kim & Park)


Figure 2:“Structure of the protein 1EFN, with focus on the quaternary structure.”

(Wikipedia, 2012)

Next, while it is clear that the Ag+ ions do have effects on microbial DNA, it is unclear exactly how it interacts with the DNA. Some scientists suggest that, “…they interact preferentially with bases in the DNA (Jung, Koo, Kim, Shin, Kim & Park),” while others think that the ions’ various other reactions in the cell, “…lead to an increased production of reactive oxygen species,” that in turn damages the microbe’s DNA, eventually leading to its death (Morones-Ramirez, Winkler, Spina & Collins, 2013). Finally, the microbe’s increased cell membrane permeability, which is also said to occur as a byproduct of these reactions and subsequent metabolic disruption and homeostatic iron levels, which, “…[restores] antibiotic susceptibility to a resistant bacterial strain (Morones-Ramirez, Winkler, Spina & Collins, 2013).”It is important to note, however, that this does not reverse the bacterial resistance, only temporarily weakens it.


Figure 3: “Figure 3. Treatment of cells with Ag+ results in DNA condensation, cell wall damage, and silver granule formation. (A) E. coli and (B) S. aureus cells with and without Ag+ treatment were observed with transmission electron microscopy (Feng et al., 2000).”

(Kenyon University, n.d.)

As much as it would be great to regard the Ag+ ion as an end to all our troubles, it’s not without its side effects. Some people are allergic to silver (Elsner & Hipler, 2006), and those that aren’t are in danger of having the element accumulate in their bodies (Fung & Bowen, 1996). Long-term intake can lead to increased levels of skin silver and/or silver sulfide particle levels. Sunlight causes these particles to darken, leading to a skin discoloration known as argyria (Elsner & Hipler, 2006). Furthermore, silver is no different from traditional antibiotics in that it is simply ‘another chemical’ in action. As such, it is plausible that overuse of it may eventually lead to increased silver resistance in bacteria, and then we would simply end up in the same place we are now with the antibiotic resistance problem; at best we’ll just delay our troubles. Still, since there’s little doubt in the actual antimicrobial properties of silver, all of this doesn’t completely take it off the table. If it were possible to distribute the dosages in a way to avoid some of the adverse side effects, we could take advantage of the aforementioned delay. Time is arguably the most valuable resource for humans, and with all of the major medical advances taking place in the modern age, that extra time might be just what we need to come up with a true solution.

Works Cited

Elsner, P., & Hipler, U. -. (2006). Silver in health care: Antimicrobial effects and

safety in use. Biofunctional Textiles and the Skin, 33, 17-34. doi: 10.1159/000093928

Retrieved from

Fung, M. C., & Bowen, D. L. (1996). Silver products for medical indications: Risk-

benefit assessment. Clinical Toxicology, 34(1), 119-126. doi: 10.3109/15563659609020246

Retrieved from

Jung, W., Koo, H., Kim, K., Shin, S., Kim, S., & Park, Y.

(2008). Antibacterial Activity and Mechanism of Action of the Silver Ion in Staphylococcus aureus and Escherichia coli. Applied Environmental Microbiology, 74(7), 2171-2178 doi:10.11.28/AEM.02001-07.

Retrieved from

Kenyon University. , & Garduque, G. (n.d.). Silver as an antimicrobial agent.

Retrieved from

Midlands Technical College. (Producer). The Phospholipid

Bilayer [Web Graphic]. Retrieved from

Morones-Ramirez, J. R., Winkler, J. A., Spina, C. S., & Collins,

J. J. (2013). Silver enhances antibiotic activity against gram-negative bacteria. Science Translational Medicine, 5(190), 198ra81. doi: 10.1126/scitranslmed.3006276

Retrieved from:

Wikipedia. (Producer). (2012, August 27). Protein structure with focus on the

quaternary structure [Web Graphic]. Retrieved from

The Physiology and Effects of Stress

As an IB student, I am undoubtedly subjected to a large amount of stress, ranging from academic to social pressures. Not only do I have to worry about college applications and final examinations as a senior, but I also have to consider balancing out my sports and extracurricular activities, my social life and sleep. My parents and even doctor have told me repeatedly that I need to watch out for my stress level because too much stress can cause negative repercussions. However, this made me wonder, how exactly does stress work in our bodies, and to what extent is it harmful for us? Thus, this post will first examine the physiology of stress, and then lead to an evaluation between its pros and cons.

To begin, the science behind stress is coincidentally linked to our current IB chemistry study on the topic of equilibrium. In Chemistry, stress is defined as something that interferes with a system’s equilibrium, such as a change in temperature, number of moles or volume. (Brucat, 2008) Similarly, this equilibrium state can also exists in our body. In fact, homeostasis within our bodies is defined as, “an elusive state of metabolic equilibrium between the stimulating and the tranquilizing chemical forces.” (The Franklin Institute, 2004) Ultimately, stress disturbs this homeostasis. The automatic nervous system (ANS), which controls all the involuntary activities and functions of our body, such as digestion and blood pressure, consists of two branches. The first branch, the sympathetic nervous system (SNS) is the fight-or-flight response that becomes automatically activated when our brain perceives danger or stress. The other branch, the parasympathetic nervous system (PNS), is responsible for restoring the body back to homeostasis after the threat is over. To best explain the physiology of stress, I shall use an example.

Imagine you are strolling casually in a forest when you suddenly notice a menacing lion gazing at you. Immediately, your hypothalamus in the brain sends a blazing “DANGER!” message through the nervous system to the other body systems. The hypothalamus also signals the endocrine system to start secreting hormones, mainly adrenalin and cortisol, into the bloodstream so that the every cell in your body gets ready for the fight-or-flight response. While the systems necessary for increasing power and speed are emphasized, the other systems, such as the digestive and immune system, are inhibited to allow for the extra work of the vital systems. (Olpin) Under our medicine and drugs unit in IB Chemistry, we studied the adrenaline hormone and its effects on our body, such as increased heart rate, blood flow to the brain and muscles, and mental awareness. (Ford & Brown, 2007) Thus, I will focus on the other primary stress hormone, cortisol, which is secreted by the adrenal cortex.

Cortisol affects the entire body and contributes to the physiological changes that occur when the ANS or fight-or-flight is activated. One of these effects is the metabolic process of gluconeogenesis, which makes “glucose from oxaloacetate” (Randall, 2011, p.1). Cortisol also prompts glucose synthesis in the liver. Altogether, it is responsible for regulating the bloodstream’s glucose level, which is essential when you demand a lot of energy trying to fight or run away from the angry lion, because cortisol ensures a continual supply of glucose. As aforementioned, other unneeded systems, like the immune system, are suppressed to divert more oxygen and blood to the systems that require them. Cortisol helps put this into effect by suppressing the immune system. It prevents the multiplication of T-cells and the secretion of histamine (a lack of histamine inhibits inflammations). (Randall, 2011)

Functional groups: Carboxylic acid, alcohol (2), carbonyl
Functional groups: Carboxylic acid, alcohol (2), carbonyl

(Structure of Cortisol, 2010)

Although stress seems to be widely accepted as something that is bad, our fight-or-flight response is evolutionary beneficial for our survival.  In situations of acute stress, an immediate and temporary disruption of our homeostasis is necessary for us to react more powerfully and rapidly to life-threatening situations, like an angry lion chasing us. Without the increased flow of adrenaline and other hormones in your bloodstream, an adequate supply of oxygen, glucose and fatty acids can’t be pumped fast enough to your muscles and brain during the emergency. Therefore, stress and our body’s response to it is not necessarily deleterious. (Olpin)

However, the problem is our stress reaction is only advantageous for the ephemeral demands. It is not everyday that we get attacked by an animal or experience a life-threatening emergency like an earthquake. The emotional and social stresses that we do face on a daily basis cause the stress response to be activated for a much longer time, as our brain does not perceive the challenge to be over. This persistent activation of the SNS is termed “chronic stress”, which has been found to bring harm to our health. Since our body is kept in the fight-or-flight response and not reverted back to homeostasis, the physiological activities that occur during the response are also prolonged. (Olpin) It is not difficult to realize why our body starts to deteriorate when you remember that cortisol suppresses our immune system, which makes us susceptible to diseases. Furthermore, as “the hippocampus, the region of the brain where memories are processed and stored, contains many cortisol receptors,” (Randall, 2011, p.1) exorbitant levels of cortisol can lead to atrophy of the hippocampus, causing memory loss and the brain’s inability to form new memories. These health claims came from credible sources made for educational purposes, such as the Dartmouth Undergraduate Journal of Science, so I have confidence in their reliability.


Therefore, stress works in our body by disrupting our internal equilibrium. In the short run, this response characterized by an activation of our SNS proves valuable, as it helps us react fast enough to urgent situations and stimulates our brains during challenges. However, in the long run, chronic stress prevents our body from functioning normally at homeostasis, leading to the breakdown of our organ systems. This understanding of stress, especially chronic stress, is definitely significant for me, students and adults all over the world, because current troubles may cause long-term, irreversible consequences on our body. Thus, when making decisions in commitments and decisions, one should consider the amount of stress that might be involved as to not overwhelm oneself. In addition, with the finding that an increase in the stress hormone cortisol for an extended amount of time is adverse to the body, another significant application of this knowledge would be to reduce other activities that also raise cortisol levels. (Randall, 2011) In my research, I found that sleep deprivation, caffeine, alcohol, too little exercise and too much eating could all elevate cortisol levels (Gahr, 2008). Hence, people already under chronic stress are even more at risk when they react to it by pulling all-nighters and gulping down cups and cups of coffee. In conclusion, the physiology of stress and the effects of chronic stress on health tremendously emphasize the importance of stress management. In order to best benefit from our body’s stress response, we must alter our lifestyle and behavior accordingly.


Brucat, P. (2008, April 27). Advancement, stress, and chemical equilibrium. Retrieved from

Ford, M., & Brown, C. (2007). Chemistry developed specifically for the ib diploma. (pp. 639-641). International Baccalaureate Organization.

The Franklin Institute. (2004). The human brain. Retrieved from

Gahr, T. (2008, October 28). The science behind stress. The Cornell Daily Sun. Retrieved from

Olpin, M. (n.d.). Retrieved from

Randall, M. (2011). The physiology of stress: Cortisol and the hypothalamic-pituitary-adrenal axis.Dartmouth Undergraduate Journal of Science, Retrieved from


Olpin, M. Chronic Stress. N.d. Graphic. Weber State UniversityWeb. 3 Sep 2013. <>.

Structure of Cortisol. 2010. Graphic. Dartmouth Undergraduate Journal of ScienceWeb. 3 Sep 2013. <