NH Saturated Fat: Friend or Foe?
Is saturated fat really that bad for us?
Dr. Oz demystified
A UC Berkeley Campus Magazine
High Fructose Corn Syrup
Health implications we can draw from foods containing high fructose corn syrup How We Age
Exploring the free radical theory of aging and sources of antioxidants
My Chemical Romance The story of oxytocin
MaY â&#x20AC;˘ Spring 2012 â&#x20AC;˘ Issue 1
The Science of Wellness Magazine is a publication which features articles written by students on topics related to the chemistry of nutrition, food science, and health.
Letter from the Editor The Staff Editor in Chief Sheba Plamthottam Layout Designers Grant Hao-wei Lin Katherine Hsieh Hiro Kai Sheba Plamthottam Copy Editors Sonya Aggarwal Sree Chinreddy Jocelyn Lau Alyse Ritvo Jeremy Yip Writers Michelle Chen Danielle Hajj Aartika Maniktala Arjun Prabhakar Rajeswari Ramanathan Suravi Raychaudhuri Ruby Schuler Sophie Shevick Ashley R. Wang Alexandra Yesian Illustrator Gigi Lin Staff Advisor Michael Barnes A very special thank you to the ASUC and the BNC for their support Cover design by Grant Hao-wei Lin The Science of Wellness Magazine is not an ofﬁcial publication of the University of Callifornia, Berkeley, the ASUC, or the BNC. Opinions expressed are those of individual authors. Advertising, logos, and artwork are the sole responsibility of individual advertisers, not of the Science of Wellness. All rights reserved. Content may not be re-used without prior written permission from our editor. Letters to the editor, article proposals, and advertisements are welcome. They should be sent to email@example.com.
The Science of Wellness Magazine
Dear readers, Every day we get bombarded with false advertisements for questionably healthy food products, competing diet claims from medical professionals, or some new and very strange products that range from energy drinks to alcoholic beverages to even energy drinks that contain alcohol. (What happens when a stimulant like caffeine is mixed with alcohol? See Sophie Shevick’s feature on Four Lokos on page 15). Some products were claimed to be safe and then months later were taken off the market after detrimental side effects were found (e.g. the original Four Loko beverage). So then, how do you know who to trust? Rather than hanging on to every word of our health care professionals, we can take their advice with a grain of salt, and understand the science that led them to draw conclusions. On page 9, Michelle Chen wrote a special feature on an episode of the Dr. Oz Show, clarifying the statements he made and explaining the science behind his diet suggestions. On page 5, Alexandra Yesian wrote about a misconception that many of us may have about the saturated fats we consume in our diets. Studying Chemical Biology and Nutritional Science at UC Berkeley made me realize how intertwined the two subjects are. Making wise decisions about our health choices takes more than just looking at general trends in data and trusting media-advertised healthcare professionals. Understanding the science is important to make an informed decision for ourselves. Every decision we make affects our physical and mental health and wellness, and we each have an individual responsibility to ourselves and our future generations to make healthy lifestyle choices. The ﬁeld of nutrition is fascinating and is growing quickly, so this is a difﬁcult task to do in today’s world, because sometimes there are no correct answers to our questions. On page 3, Ruby Schuler writes about high fructose corn syrup, whose health implications are still under debate by many researchers. A curiosity about what we consume and the short and long-term effects of these foods help us take small steps in a positive direction to preventative health-care. This issue features an interview with UC Berkeley Professor of Public Health and Neuroscience Dr. William Jagust. On page 20, Danielle Hajj discusses the preventative measures we can take now, as students, that may help us avoid age-related diseases. Perhaps we have more inﬂuence on our well-being than we thought we did. The articles in our ﬁrst issue range from all aspects of wellness—from our social interactions with those close to us (page 12) to some surprising ﬁndings about coffee and diabetes (page 13). We hope you enjoy the inaugural issue of the Science of Wellness Magazine. We would love to hear your feedback. You may send your comments, questions, and critiques to firstname.lastname@example.org. Sincerely, Sheba Plamthottam Editor in Chief & Founder The Science of Wellness Magazine
Table of Contents 3
High Fructose Corn Syrup
Saturated Fat: Friend or Foe?
Dr. Oz Demystiﬁed
12 My Chemical Romance:
The Story of Oxytocin
13 Spilling the Coﬀee Beans 14
You Are Not an Alcoholic. Your Forefathers Were.
Are You Loco for them Lokos?
How We Age: Exploring the Free Radical Theory of Aging
Brain Aging: How to Delay the Inevitable
The Science of Wellness Magazine
High Fructose Corn Syrup vs. Sugar: Is high-fructose corn syrup really making us fat? These facts aren’t sugar-coated.
The Science of Wellness Magazine
by insulin, and leptin, which is responsible for signaling to your body that it is full and is released by the presence of insulin, thus causing you to want to stop eating. Fructose, on the other hand, does not signal insulin to be secreted, so leptin will not be triggered; your body will not tell you when it is full.1,6 The lack of insulin secretion also leads to the buildup of fructose in the liver, because the fructose won’t be able to be taken up by other tissues in your body without insulin present in your bloodstream. Your body wants to use this buildup of sugar for energy before it uses the fat in your body for energy, which can lead to weight gain due to this hierarchy of oxidation. Several recent studies have shown that fructose speciﬁcally increases visceral fat, or the fat that surrounds your organs in the abdominal area. This is cause for concern due to the negative eﬀects this belly fat can have on the body, mainly increasing risks for type 2 diabetes and heart disease.7 Observational data is what sparked the original hypothesis that HFCS was related to the rising obesity epidemic in the United States. The frequent use of HFCS in products in the United States really took oﬀ in the late 1960’s, around when its production method was being perfected. Obesity began to rise at approximately the same time as the increase in use of HFCS, causing some researchers to think that HFCS could be the cause of the
obesity epidemic.1 Some experiments have been tested to investigate the hypothesis that HFCS could be responsible for the increase in obesity; however, their results have shown that the hormones insulin, ghrelin, and leptin are not aﬀected any diﬀerently then they are by sucrose.6,8 Studies have been carried out that show that the consumption of sugary beverages, whether sweetened with HFCS or sucrose, both increase the amount of visceral fat gained due to the fructose alone.7 The portrayal of HFCS being an unhealthy alternative in foods compared to sucrose does not have any substantial evidence to prove it is true as of now. Chemically, they are made up of the same two monosaccharides, glucose and fructose, but until more research is completed that can explain how HFCS aﬀects the body, it would be wise to consume HFCS in moderation.1,2,5,6,7,8 Those who wish to avoid weight gain should be more concerned with the amount of added sugars they are consuming instead of the speciﬁc type, namely the amount of fructose, which has been shown to increase harmful belly fat.7
Ruby Schuler is an undergraduate student studying Nutritional Science, Dietetics at UC Berkeley.
igh-fructose corn syrup (HFCS) can be found in various products ranging from cookies, sodas, crackers, and cereals, which can make it hard to avoid when consuming processed foods and drinks.1 With all of the negative media attention HFCS gets, it is easy to think that it is not the healthiest of substances, yet it is hard to determine why HFCS is bad for you. Have you ever wondered why HFCS is in our food products instead of sugar? Is HFCS worse for you, health-wise, than table sugar? Is HFCS responsible for our country’s obesity epidemic? Take a look at the facts. HFCS is now commonly used in foods in lieu of table sugar (sucrose) because it is cheaper and more stable.2,3 More than half of the sugar in the United States is derived from the sugarbeet, which is grown in the cooler climates of the Midwest states.4 HFCS is made from American corn which is overly abundant and extremely cheap due to government subsidies.2 HFCS is a much more stable compound than table sugar for processed foods and beverages because it can withstand the acidic conditions these products go through when being shipped and subsequently left sitting on the shelf in a warehouse or grocery store.3 The stability of HFCS is due to its slightly diﬀerent chemical composition in comparison to sucrose. Sucrose is a disaccharide, meaning that it is composed of two diﬀerent single sugars that are connected. These two single sugars are known as glucose and fructose. HFCS is made up of glucose and fructose as well; however, in HFCS these two molecules are not connected.1,3 The way in which HFCS is made is what makes the diﬀerence in composition. The process of making HFCS was perfected in the late 1960’s in Japan and involves a multiple-use enzyme that catalyzes the conversion of about half of the glucose in corn into fructose. HFCS is made up of an almost 50:50 ratio of glucose to fructose, the same ratio as sucrose.1,2,5 The diﬀerence in the chemical structures between HFCS and sucrose has led some researchers to believe that HFCS is metabolized diﬀerently than sucrose by the body and therefore could be a cause for concern in its relationship to obesity in the United States.1,3,6 HFCS is made up of free— not connected, as in sucrose—glucose and fructose molecules.1,3 Glucose is important in signaling the regulating hormone insulin, which triggers either the release or inhibition of two other hormones that are important in appetite and satiety. These two hormones are ghrelin, which is responsible for telling your body when it is hungry and inhibited
HFCS is made up of glucose and frucose molecules, unlinked. Sucrose, or table sugar, is made up of linked glucose and fructose molecules.
By Ashley Wang
BACKGROUND PHOTOGRAPH: TRAM LE
at lunch. Several moments later, pen to paper and then—BAM. Food coma. The powerful sleepy feeling creeps over you and you ﬁght it to no avail. Why does this always happen? Typically, students who eat a meal comprised mostly of carbohydrates, especially simple carbohydrates, will experience a surge in energy and then the dreaded “crash.” This “food coma” is both unhealthy and as we all know, quite uncomfortable. If we overeat, we stretch our stomachs (not to mention our waistlines),
and if we pack up on simple carbs, not only do they turn into sugar very quickly, but they also fail to provide enough nutrients, leading to a low-quality diet. Our very own Professor Nancy K. Amy, who retired just last year, gave an informative lecture about this phenomenon to her Nutritional Science 10 Class, stating that blood glucose levels rise immediately after a meal and “insulin is released, stimulating the uptake and storage of glucose.” Later, the blood glucose level drops, and as a result, the body must break down this stored glucose—
Illustration By Gigi Lin. Gigi is an undergraduate student studying Chemical Engineering at UC Berkeley.
known as glycogen—in order to try to bring blood sugar levels back to normal. This is why we phase out of a sleepy state into a suddenly alert state after a few hours of doing homework. The sugar levels in our body peak, and then drop, and then peak again—a roller coaster of energy levels for the unwary student. In addition, palmitic acid, a type of saturated fat in butter, cheese and red meat, blocks satiety hormones and increases appetite.1 For example, leptin, a hormone released by fat cells to signal the feeling of “fullness,” may go undetected by the body. These saturated fats can thus lead to a tendency to overeat and in turn, induce the dreaded “food coma.” It is beneﬁcial to ﬁll up on ﬁber-ﬁlled foods instead, such as apples, oatmeal, or carrots, which keep us fuller longer. Fiber is indigestible by our systems and slows the absorption of nutrients, thus gradually supplying energy to our bodies instead of giving us a “sugar high.” Protein, such as those in nuts, provides energy at four kilocalories per gram and, at smaller serving sizes, can induce more satiety than carbs. One of my personal favorites, yogurt, can serve as a healthy snack too, often providing live cultures that improve gastrointestinal motility and usually calcium, for our growing bodies. Next time you decide to have a study session after eating, drop that donut and instead, go pick from the plethora of healthy snack options.
Ashley R. Wang is an undergraduate student studying Molecular Environmental Biology at UC Berkeley.
The Science of Wellness Magazine
Saturated Fat Friend or Foe ? By Alexandra Yesian
Saturated fat is not as bad as we think it is. This, of course, is not to say that we should guiltlessly eat copious amounts of bacon and Alfredo sauce, as not all saturated fats are created equal.
â&#x20AC;&#x153;People in northern India consume 17 times more animal fat but have an incidence of coronary heart disease 7 times lower than people in southern India.â&#x20AC;? â&#x20AC;&#x201C; Sally Fallon, author of Nourishing Traditions
Americans have decreased their daily calories from fat from 40% to 30%, and fat from animal sources from 83% to 62%. However, obesity, diabetes, and heart disease rates are still increasing steadily.
hen many of us look at a stick of butter, we think of saturated fat, heart disease, and obesity. Over the past few decades Americans have been urged by public health officials to swap their butter for vegetable oils in an attempt to curb the epidemic spread of obesity and cardiovascular disease. Most of us accept the “fact” that saturated fat is bad for us without questioning where this correlation comes from. We continue to curb our fat intakes to meet the dietary guidelines set out for us by the government, but our waistlines are still expanding and our arteries are more clogged than ever. According to Gary Taubes, writing in Science magazine, the average American has decreased the percent of daily calories from fat from 40% to 34% since the 1970s. The percentage of dietary fats coming from saturated fats has dropped even more markedly; Sally Fallon, author of Nourishing Traditions cites that the amount of fat from animal sources plummeted from 83% to 62% between 1910 and 1970. This decrease, however, is coupled with a steady increase in obesity, diabetes, and heart disease rates. The current beliefs regarding the effects of saturated fats on health seem especially paradoxical when one considers the impeccable health of people such as the Masai of Africa. In her article “What if Bad Fat isn’t so Bad?” Nina Teicholz discusses how these native Kenyans may consume up to 60% of their calories from fat, mainly from meat, dairy, and blood. Despite this high-fat diet, heart disease and obesity are absent from their society. When a group of these
tribal people was placed on a reduced–fat “Western” diet, however, their cholesterol increased, initiating a cascade of associated health maladies. Similarly, Fallon states that “people in northern India consume 17 times more animal fat but have an incidence of coronary heart disease seven times lower than people in southern India,” despite their comparable lifestyles and genetic factors. Fallon says that this high-fat, low heart-disease trend is seen in various cultural groups, such as Puerto Ricans, Inuits, and Cretans. If people have survived for thousands of years on diets high in animal fats, how is it that saturated fat came to be incriminated as the source of so many modern health problems? It was not until the 1950s that any correlation was distinguished between saturated fat and heart disease. This association was coined the “lipid hypothesis” by a scientist named Ancel Keys in 1953. He conducted a study in which he compared the percent of calories from fat to the rate of heart disease in 22 different countries. However, when he reported his findings he cited data from only six of the countries. These included the United States, Japan, Canada, Australia, England, and Italy. These nations yielded data that conveniently fulfilled Keys’s hypothesis. The Americans, who consumed the most fat, had the highest rates of heart disease, while the Japanese consumed the least fat and had the fewest cases of cardiovascular problems. The other four countries followed this trend perfectly, with fat consumption
Lipid Hypothesis: “Cardiovascular disease is largely the result of high serum cholesterol levels brought on by a diet high in saturated fat.”
appearing to have a direct correlation with heart disease. This revolutionary finding took hold before anyone had a chance to question its legitimacy. In 1957, when UC Berkeley biostatistics professor Jacob Yerushalmy reanalyzed the data using all 22 countries, he found no real correlation between fat intake and heart disease at all! According to Teicholz, Yerushalmy found glaring contradictions; “for example, the death rate from heart disease in Finland was 24 times that of Mexico, even though fat-consumption rates in the two nations were similar.” A 2010 study published in The American Journal of Clinical Nutrition did followup analysis of 21 epidemiological studies which attempted to link heart disease to saturated fat; the researchers found “there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of coronary heart disease or cardiovascular disease.”
The Science of Wellness Magazine
PICTURE: GRANT LIN
We need HDL, or the “good cholesterol,” to transport the “bad cholesterol,” or LDL, to the liver for elimination. Mary Enig, author of Know Your Fats, and Fallon also point out that, on average, only 26% of the fat in a clogged artery is saturated! It is also highly unlikely that saturated fat contributes any more greatly to weight gain than unsaturated facts. In fact, the opposite may prove to be true. Saturated fats have short or mediumchain lengths. Enig explains that shortchain fatty acids are immediately available to use for energy because they do not have to be processed by the liver. Long-chain fatty acids, particularly polyunsaturated fats, must be emulsified by bile salts; this means they spend a longer time in transit in the body and have a greater chance of accumulating as body fat.
“Only 26% of the
fat in a clogged artery is saturated.
Though seemingly blasphemous, it may be reasonable to say that saturated fat is good for us. Saturated fat has many functions in our bodies; in addition to being a major component of cell membranes, saturated fat also plays a critical role in immune function; short and medium-chain fatty acids such as lauric acid serve as antimicrobial agents in the body. Enig also has found evidence that saturated fat is essential for bone health as it aids in calcium absorption. Another benefit of saturated fat is its ability to raise HDL, the “good” cholesterol which transports arterial plaque and LDL, “bad” cholesterol, to the liver for processing and
elimination. Because saturated fat plays so many roles in our bodies, it makes sense that its absence from our diets has caused more harm than good. Taubes argues that “the brain, for instance, is 70% fat, which chieﬂy serves to insulate neurons. Fat is also the primary component of cell membranes. Changing the proportion of saturated to unsaturated fats in the diet changes the fat composition in these membranes. This could conceivably change the membrane permeability, which controls the transport of everything from glucose, signaling proteins, and hormones to bacteria, viruses, and tumor-causing agents into and out of the cell.” This, of course, is not to say that we should guiltlessly eat copious amounts of bacon and Alfredo sauce, as not all saturated fats are created equal. Butter from grass fed cows, for example is far more nutrient-rich and wholesome than is butter from grain-fed cattle. Whole milk and butter from pasture-raised cows has a distinct yellow color because it contains high
“Today, a lipid hypothesis based on faulty data is accepted as true by governments, health organizations, the media, and industry, and we, the general population are left eating a recommended diet that just might be causing more harm than good.”
quantities of the fat-soluble vitamins A, D, E, and K, which are required for physiological necessities such as eyesight, bone health, and blood coagulation. Additionally, cows which eat grass produce milk that contains conjugated linoleic acid (CLA). These compounds have been shown to decrease body fat and promote muscle synthesis. In fact, bottles of CLA can be seen on pharmacy shelves in supplements that “support weight loss.” Coconut oil is highly saturated and is an especially rich source of the immune-bolstering lauric acid. A study done by Enig also demonstrated that consumption of coconut oil improves the blood serum ratio of HDL to LDL cholesterol. While it is impossible to say what the optimum diet is for the maintenance of a healthy weight and cardiovascular system may be, there is compelling evidence that this diet does not involve the complete elimination of saturated fat. Though it has been more than 50 years since Ancel Keys introduced the lipid hypothesis, it is not until now that we are finally starting to challenge the idea that saturated fat is detrimental to our health. Saturated fat has not been conclusively linked to cardiovascular disease or the obesity epidemic. Foods that are high in saturated fat have been safely consumed for thousands of years—they play a vital role in the proper functioning of the human body and should continue to be enjoyed in moderation.
Alexandra Yesian is an undergraduate student studying Nutritional Science, Dietetics at UC Berkeley.
The Science of Wellness Magazine
d e fi i t s y dem The Food Pharmacy By Michelle Chen
The Dr. Oz Show is a television talk show, hosted by Dr. Mehmet Oz, a cardiothoracic surgeon and author who became influential after his appearances on The Oprah Winfrey Show 99
TheThe Science Science of of Wellness Wellness Magazine Magazine
igh cholesterol is one of the many contributors to heart disease that has struck the United States. As a result, there have been many treatments advertised to the American public that claim to help resolve this issue. Dr. William Li, the head of the Angiogenesis Foundation—a nonproﬁt that is reconceptualiz-
What is cholesterol, and why is it bad for you? Cholesterol is a type of fat and is categorized into three diﬀerent types: low-density lipoprotein (LDL), very low-density lipoprotein (VLDL), and high density lipoprotein (HDL). LDL cholesterol can be damaging at high levels because it tends to stick to artery walls. Enough LDL built up in
ing global disease ﬁghting—guest starred on the Dr. Oz Show in a segment that featured various natural treatments of disease by consuming the right foods, especially in regards to preventing high cholesterol. Dr. Li claims that these foods can be just as eﬀective as the medication sold in pharmacies.
the arteries can develop into atherosclerosis, hardening of the arteries, which puts patients at a higher risk for a heart attack. HDL, on the other hand, is beneﬁcial to the body and is appropriately deemed the “good cholesterol.” Increased levels of HDL can actually remove LDLs from the bloodstream by transporting and disposing them through the liver.
Mustard Greens: 1-1/2 cup a day Mustard greens are the leaves of the same plant whose seeds are used to make Dijon mustard. These greens contain a phytochemical named sulforaphane, a compound that is also found in cruciferous vegetables such as broccoli, cauliﬂower, kale, cabbage and bok choy. Sulforaphane prevents the production of cholesterol in humans by acting as a bile acid binder. Bile acid is needed to make cholesterol and is produced in the liver. Bile acid binders bind to the bile acid in the intestine and prevent the bile acid from being reabsorbed into the blood, thereby reducing the amount of bile acid available to make cholesterol. Eating more bile acid binders, such as sulforaphane, can help decrease the amount of cholesterol circulating in the blood.
Sulforaphane, along with being a bile acid binder, has been a studied compound in cancer research as well. It is classiﬁed as a Phase 2 enzyme inducer in various research papers for its anti-carcinogenic activity. It works as a neutralizer to carcinogens before they can damage DNA and possibly cause cancer. One important factor not mentioned in this episode is the role insoluble ﬁber, a type of ﬁber that cannot be dissolved in your body (from cruciferous vegetables, including mustard greens), plays in decreasing cholesterol levels. Fiber itself does not contain any nutritional value, but can actually decrease the amount of fat being absorbed. Decreasing absorption of fat means less cholesterol can be produced.
The Science of Wellness Magazine
Dark Chicken Meat: 4 oz. a day lowers risk of fatal heart disease by 57%
Persimmons: Reduce atherosclerosis risk by 25%
Certain animal muscles appear darker in color because they are found in areas of the animal that are physically exercised more than the whiter areas. For example, chicken breast tends to have a lighter color than chicken thighs or legs because chickens use their legs more to run around. What gives the legs the darker coloring is the higher amount of myosin, a protein that holds oxygen for the muscles to use when needed. A recent women’s health study conducted by Dr. Yu Chen, Associate Professor of Epidemiology at NYU School of Medicine, has suggested that one of the components in dark meat, taurine, may provide protection against coronary heart disease for those with high cholesterol. Taurine is known to be related to the production of bile acid, which, as described earlier, is directly related to the production of cholesterol. The study found that women with high cholesterol and high levels of taurine were 60% less likely to die from coronary heart disease than those who had low levels of taurine. The ﬁndings are quite recent and call for further investigation on the matter, but they certainly open up new ﬁelds of research on dark meat that can be done to help people with cholesterol problems.
Persimmons contain a carotenoid called beta cryptoxanthin, a component of vitamin A. Carotenoids are fat-soluble and waterinsoluble, so they are able to circulate well with fats such as cholesterol. Carotenoids also exhibit antioxidant behavior that may help with heart problems related to high cholesterol, such as atherosclerosis. Oxidation of LDL can further develop atherosclerosis, so antioxidants are important in regulating the oxidation reaction of LDL to keep the atherosclerosis risk in check. Several studies have shown that higher levels of carotenoids are related to lower artery thickness. However, the causation is not clear because foods containing carotenoids also contain other factors that may induce this eﬀect. Vitamin A does have other beneﬁcial effects given its antioxidant activity. Vitamin A helps lower the amount of free radicals that can interfere with various biochemical reactions occurring in the human body. One of the many beneﬁcial eﬀects of this includes clearer skin.
Pistachios: 1/3 cup a day lowers LDL by 11% Nuts are always a healthier alternative to junk food when it comes to snacking. They are a great source of protein and unsaturated fat, the better type of fat that can help reduce LDL levels in the body. An active ingredient in pistachios is lutein. There is limited information on the relationship between lutein
and cholesterol, but lutein has been known to play an important role in maintaining vision. Lutein helps ﬁlter blue light wavelengths from the eyes. These high-energy light wavelengths can induce free radicals in the eyes, so ﬁltering them out would be best to make your eyes last as long as possible. Lutein also acts as an antioxidant to remove free radicals from your eyes, helping prevent cataract, which is mainly caused by oxidation of eye lens.
Deﬁnite ways to lower cholesterol The sure-ﬁre way to ﬁx problems related to high cholesterol is lifestyle modiﬁcation. A low-fat diet in which total fat intake does not exceed 30 grams a day may help lower LDL and triglyceride levels. Increased exercise will ﬁx the good to bad cholesterol balance by increasing HDL levels and decreasing LDL levels. If three months of this new lifestyle does not lower cholesterol levels, medication is sug-
gested by most doctors, especially if LDL levels are particularly high. Doctors will typically prescribe a class of drugs called statins in order to inhibit an enzyme called HMG-CoA reductase, which is needed in the production of cholesterol. Red yeast rice is an over-the-counter herbal treatment that is known to work on patients who are looking for a more natural treatment, and has similar eﬀects as statin. Moreover, Niacin, also known as Vitamin B3, helps set the HDL-LDL balance, but many people cannot take it due to side eﬀects of ﬂushing.
Michelle Chen is an undergraduate student studying Public Health at UC Berkeley.
The Science of Wellness Magazine
My Chemical Romance: The Story of Oxytocin
s love just a chemical cocktail? Scientists have been trying to answer this question for decades. For a long time, the hormone oxytocin has been the answer. Proverbially termed the “love hormone” or “cuddle hormone,” oxytocin is a crucial part of social bonding between romantic partners and between parents and newborn babies. The “warm, fuzzy feeling” you feel when you see or touch a loved one is partially attributed to oxytocin. In addition, studies suggest that treatment with oxytocin can reduce the anxiety felt by romantic couples during a prolonged separation.1 Historically, oxytocin was associated with its ability to induce uterine contractions during childbirth in 1906 and to induce milk release during breastfeeding in 1910. The nine amino acids that make up oxytocin were sequenced and biochemically synthesized in 1953, making it the first polypeptide hormone ever sequenced and synthesized.2 Oxytocin is produced in all mammals and an oxytocin-like hormone is produced in virtually all vertebrates. Even invertebrates like leeches, snails, octopi, and earthworms produce hormones very similar to oxytocin. Oxytocin is even used in the dairy industry to increase milk production in cows.3 The fact that oxytocin is present in vastly diverse, evolutionarily different organisms suggests that it has a larger role than the name “cuddle hormone” suggests. Social Interactions Oxytocin acts as a chemical reinforcement for positive social interactions. Like many recreational drugs (such as ecstasy), it acts through the dopamine pathway.4 In animals, it has been demonstrated that oxytocin activates different dopamine receptors in situations of social contact or during interactions between mothers and offspring. For example, in prairie voles, a monogamous species of voles, the oxytocin released during sexual activity is crucial for the female vole to form a bond with her mate. Oxytocin blockers will stop the bond from forming, while administered oxytocin induces pair bonding without sexual activity.5
In humans, studies have found increased blood plasma oxytocin levels at orgasm in men and women.6 Increased oxytocin levels are also correlated with feelings of trust and empathy. When test subjects were being proposed with a risky transaction, those given a nasal spray of oxytocin demonstrated a higher likelihood to agreeing to the deal. This trend only occurred when the subject was dealing with another person, not a computer, suggesting that oxytocin increases trust in fellow human beings.7 Oxytocin is believed to aid wound healing by decreasing inflammation response. In a 2010 study, investigators
Oxytocin plays a significant role in pair-bonding interactions. recruited heterosexual couples and inflicted blisters on each partner’s arm. They found that couples that participated in positive communication exercises afterwards demonstrated higher oxytocin levels and faster wound healing.8
forehand. If a subject was working with an unknown partner, the oxytocin dose actually made him less likely to cooperate.9 Oxytocin is also reported to increase racial bias and ethnocentrism. In a 2011 study, Dutch subjects were given a scenario where they could save 5 people by sacrificing one person, who had either a Dutch, German, or Arab name. Subjects who were given a dose of oxytocin were more likely to protect the Dutch victim than the controls.10 In conclusion, oxytocin is a much more complex hormone than the nicknames “cuddle hormone” and “liquid trust” suggest. Oxytocin has significant physiological effects on sexual activity, childbirth, and breastfeeding. It also has intricate social effects, such as creating pair-bonding and increasing trust. Recent research is elucidating more sinister effects of oxytocin such as decreased trust of strangers and increased racial bias. Due to oxytocin’s effect on social behavior and feelings of trust and empathy, ongoing researchers are investigating possible therapeutic uses for conditions such as extreme social phobias and autism. Research on the social, physiological, and therapeutic effects of oxytocin continues, with the hope of bringing to light some of human kind’s most complex and mysterious emotions and interactions.
Suravi Raychaudhuri is an undergraduate student studying Chemical Biology at UC Berkeley.
The nine amino acids that make up the hormone oxytocin are shown below.
The Dark Side of Oxytocin Recent research has demonstrated that oxytocin does not unilaterally increase feelings of positive emotions, like trust. For example, a 2010 study showed that when playing a game with a partner, oxytocin made the subject more likely to cooperate only if he had met the partner be-
The Science of Wellness Magazine
Coffee Beans the
By Aartika Maniktala
ould your daily cup of Pike’s Place roast be the next wonder drug? In the case of diabetes, it just might. A new study conducted in China has recently revealed that drinking four or more cups of coﬀee per day signiﬁcantly lowers the risk of developing Type 2 diabetes. Type 2 diabetes, a metabolic condition, leads to high glucose levels in the body as a result of an ineﬀective insulin regulatory system. By drinking four cups of coﬀee a day, the risk of Type 2 diabetes is reduced by ﬁfty percent, and with each additional cup, the risk goes down by another seven percent. This study essentially suggests that the more coﬀee you consume, the less likely you are to develop this condition. But is coﬀee really the magic cure-all, or do its risks outweigh the beneﬁts? Coﬀee’s signiﬁcance in preventing Type 2 diabetes stems from its ability to block toxic aggregations in the body. After meals, the pancreas secretes a compound known as human islet amyloid polypeptide (hIAPP). By slowing down gastric emptying, inhibiting the secretion of digestive juices, and providing the feeling of “fullness,” hIAPP slows down the rate of appearance of glucose in the blood and contributes to glycemic control. But the problem with this regulatory compound is that it can sometimes aggregate, misfold, and polymerize to form amyloid ﬁbrils, or insoluble protein masses. These ﬁbrils consequently deposit in pancreatic islets and interfere with the glucose regulatory system. However, four or more cups of joe provide the compounds necessary to inhibit the production of these toxic deposits. In addition to caﬀeine, coﬀee also contains caﬀeic acid (CA) and chlorogenic acid (CGA), two compounds that are key to Type 2 diabetes prevention. Research from the study in China shows
The Science of Wellness Magazine
that CA and CGA interact with hIAPP to prevent polymerization, and subsequently inhibit production of amyloid ﬁbrils. Evidence also suggests that amyloids enter cell membranes and initiate apoptosis, or cell death. CA, shown to have antioxidant properties, works to prevent the cell death that contributes to Type 2 diabetes. Four or more cups of coﬀee deliver adequate amounts of CA and CGA to inhibit toxic aggregation of hIAPP and regulate blood glucose levels. Coﬀee seems to have positive eﬀects throughout the body. Similar research has shown that coﬀee lowers the risk of prostate cancer and estrogen receptor-negative breast cancer, while also increasing brain function. However, coﬀee does contain caﬀeine, which is notorious for causing anxiety, insomnia, and an elevated heart rate. Drinking four or more cups of coﬀee, which contain a noteworthy amount of caﬀeine, is certain to have adverse eﬀects. Researchers need to decide whether this tradeoﬀ is worth Type 2
diabetes prevention. This study certainly had its limitations, with the tests being performed in cells and not humans directly. The relationship between CA and CGA and Type 2 diabetes prevention has not been declared causal. Until the beneﬁts of CA and CGA are actually observed in human subjects, we cannot be sure that heavy coﬀee consumption is the answer to preventing Type 2 diabetes. Only further research will conﬁrm whether or not coﬀee is essential to avoiding this disease. So go ahead and enjoy your morning cup, and maybe a few more, but you might like to reconsider that ﬁfth cup.
Aartika Maniktala is an undergraduate student studying Integrative Biology and Psychology at UC Berkeley. PI C T U RE: G R
You are not an alcoholic.
Your forefathers were.
By Rajeswari Ramanathan Alcohol is one thing most college students cannot avoid. In fact, at Berkeley, freshmen go through a mandatory alcohol education program to help them become aware of the dangers of alcohol. Yet what may be causing college students to drink is not just the fact that they have a sudden freedom, but also because it is a genetic calling. As unreal as it may seem, having zealous excitement for alcoholic beverages is not something new. More than 100,000 years ago, organisms in our planet had the same interest in ethyl alcohol, the form of alcohol found in alcoholic beverages. Archeologist Patrick McGovern of the University of Pennsylvania Museum in Philadelphia conducted several studies related to understanding how the ancient cultures created and used fermented drinks. His most recent work shows that the earliest fermented beverage, an herbal wine, originated as far back as 6,000 BCE during the predynastic period in Egypt. He has used radiocarbon dating, cesium magnometer surveying, and colorant analysis on various pottery and glasses to understand how the drinks were used thousands of years ago. What began as a common drink centuries ago is still a staple in today’s society.
However, Professor Robert Dudley from the Department of Integrative Biology at UC Berkeley, proposed that humans tend to drink more because the need to consume alcohol is encoded in our genes. Difficult to believe? Well, his proposal, known as the “Drunk Monkey Hypothesis,” explains that early primates survived by eating ripe fruits that contained ethanol. It was found that unripe fruits had zero ethanol content in comparison to ripe ones. As fruit ripen, yeast on the skin produce ethanol. This ethanol diffuses into the fruit releasing an odor. The scent of alcohol signaled the animals that the fruit was ripe and ready to be consumed. Professor Dudley believes that organisms really liked the ripe fruits because it gave them instant energy, as alcohol beverages do today. Since ripe fruits were tastier and healthier than their unripe counterparts, animals then competed to get as many ripe fruits as possible. Professor of Pathology and Laboratory Medicine at the University of Texas Health Center, Dr. Amitava Daspguta, found that “natural selection favored primates who
had a keen appreciation for the smell and taste of alcohol.” In fact, fossilized teeth show evidence that fruits were a vital part of many primates’ diets, including those of orangutans, gorillas, and chimpanzees. So next time someone calls you a reckless teenager for drinking, you can blame it on your ancestors. However, alcoholic beverages consumed today come in much higher concentrations of ethanol and other substances, which can have adverse effects on our bodies. Since ethanol is such a small compound (2 carbons, 6 hydrogens, and an oxygen) and is water soluble, it easily diffuses through the membranes in the body and quickly enters the bloodstream. This is why many teenagers are easily susceptible to fainting or blacking out after consuming a few drinks. In Dr. Dasgupta’s study, she explains that monkeys prefer ripe fruits with one to four percent alcohol content. While this may seem like a lot for a fruit, the popular Skyy Vodka that many students drink actually has 40 percent alcohol content. Having Blood Alcohol Content (BAC) higher than 0.08% is dangerous, because past this limit, a person will not have a balanced motion, proper sight, and decision making abilities. Depending on your body size, having more than four drinks a day may lead to severe health problems, and could even be fatal. Students are obviously at a higher risk of facing health problems than are primates.
Rajeswari Ramanathan is an undergraduate student studying Integrative Biology at UC Berkeley.
The Science of Wellness Magazine
m e h t r o f o
? s o k o L Blackout
c o l you
By Sophie Shevick
in a can -
That was the extent to which most college students understood the content of these fruity malted beverages. Looking at these potent alcoholic energy drinks in more depth actually makes these “blackouts” a little more clear. In no particular order…
Taurine is a component of many energy drinks and supplements, including the original Four Loko beverages, as well as Red Bulls. Tuarine (2-aminoethanesulfuric acid) is an amino acid abundant in muscle tissues; while it is essential for healthy bodily functions, it can be biosynthesized from other amino acids in a healthy diet. It is present in high levels in seafood, but it can also be purchased as a nutritional supplement at any health store. Its roles in the body span from bile acid conjugation, detoxification, membrane stabilization, osmoregulation and control of cellular calcium levels.1 Energy drinks and supplements favor the use of taurine because of its supposed role in increasing muscle strength and reducing damage to muscles caused by exercise.2
The Science of Wellness Magazine
Pantothenic Acid Niacin
These ingredients are also included in many energy drink beverages, such as Red Bull and Monster. All of these compounds are essential for the body’s central metabolism (i.e. biosynthesis of compounds used in the citric acid cycle, or the breakdown of sugar into usable energy for cells), amino acid metabolism, and metabolic electron transfer compounds (i.e. NAD, NADP). However, these energy drinks should not be considered a significant source of these vitamins; these vitamins are abundant in a healthy diet. Consuming an excess of these compounds will not make you healthier—any excess of these compounds in your body will be excreted through urine.3 However, energy drink manufacturers infuse drinks with these compounds for different reasons aside from the claimed health benefits—they will fluoresce under UV light. These compounds are aromatic compounds (think: benzene rings) that will absorb and emit neon light when subjected to UV light. On a side-note, you do not need to buy these energy drinks to have drinks that will glow under a black light—just drink a gin and tonic! The quinone in tonic water, which is a natural malarial prophylactic, will exhibit the same fluorescence under a black light.
Guarana (Paullinia cupia) is a plant naturally found in the Amazon Basin, particularly Brazil. It contains a complicated mixture of compounds—including methylxanthine, theophylline or theobromine, and tannins—but its most notable extractable compound is caffeine. In fact, it contains two to three times the amount of caffeine than an equivalent amount of coffee beans. Generally, energy drink manufacturers will use guarana as a masked way to increase the caffeine content of their beverage.
Possibly the most controversial ingredient in the original Four Lokos, it is one of the most important. Caffeine is the most widely used legal drug; it exhibits psychoactive, stimulatory effects on the body’s central nervous system. If consumed in enormous excess it can be lethal—for a rat the lethal oral dosage (LC50) is 192 mg/kg.4 For a 150-lb. college student the lethal dosage corresponds to about 13 grams of caffeine, or 65 cups of coffee (which, come finals time, is about the amount of coffee a Berkeley student drinks). Although most college students are familiar with the effects of drinking coffee, caffeine takes effect within an hour of consumption (one to two cups has about 150-250 mg); a student may exhibit clearer and more rapid thought, greater sustained intellectual effort, increased motor activity and delayed feelings of drowsiness and fatigue. Because of its stimulatory effect, its consumption can also be followed by a slight let down (i.e. fatigue and lethargy), although it can have severe withdrawal symptoms in heavy caffeine users.5 Although the original recipe for Four Loko contained about the same amount of caffeine in a cup of coffee (260 mg), it has a considerably different effect when consumed with alcohol.6
Clearly the most notorious ingredient in the Four Loko concoction. Unlike caffeine, alcohol is a depressant. In one can of Four Loko, there are approximately five 12-oz. cans of Coors Light (or your beer of choice). A 150-lb. male drinking a can of Four Loko over an hour-and-a-half time period would have a BAC of about 0.102; comparatively, a 125-lb. female drinking a single can of Four Loko over a two hour time period would have a BAC of 0.137.* (Note: alcohol metabolism is highly variable depending on the person in question. It depends on genetic make-up, health and recent food consumption. These numbers are approximate and meant to give an idea of the level of intoxication possible.7) At this BAC (0.9-0.25), effects of alcohol become observable; the loss of critical judgment, impairment of perception, reduced visual acuity, sensory-motor incoordination and impaired balance.8 *In order to calculate levels of intoxication, scientists measure the Blood Alcohol Content (BAC) in either grams of alcohol per 100 mL of blood, or grams of alcohol per 210 L of breath. In the state of California, the legal limit before a person is considered too drunk to drive is 0.08.8
The Science of Wellness Magazine
Despite the fact that caffeine and alcohol have opposing effects on the central nervous system, caffeine actually masks the physiological effects of alcohol —it does not “cancel” it out. Although it is too dangerous to test the limits of mixing caffeine and alcohol in humans, most scientists agree that caffeine delays the drowsiness brought on by alcohol consumption, enabling consumers to drink past a reasonable limit. Interviews with college bar patrons showed that those who had drunk alcoholic energy drinks were more likely to stay out later, drink for longer periods of time, ingest more alcohol, and express an interest in driving after drinking than those students who drank only alcoholic beverages.9 In November 2010, Phusion LLC, the makers of Four Loko, announced that they were changing the composition of the Four Loko drinks by removing the taurine, guarana and caffeine. Four Lokos are still sold today, without caffeine, although the alcohol content has remained the same.10 Four Lokos are not the first mixture of a stimulant with alcohol. In fact, in the 1800s, a French chemist named Angelo Mariani created a potent wine, Vin Mariani, that was actually a Bordeaux wine infused with cocaine. This “cocawine” was consumed in a slightly different setting than the Four Lokos of today; instead, it was drunk at intellectual gatherings attended by Jules Verne, Thomas Edison, and even President Ulysses S. Grant.11 Much less was known about cocaine at the time, but one fact remains the same—the search for a safe alcoholic beverage combined with a stimulant is far from over.
Sophie Shevick is an undergraduate student studying Chemical Biology at UC Berkeley.
The Science of Wellness Magazine
How We Age Exploring the Free Radical Theory of Aging By Arjun Prabhakar
The free radicals that are responsible for aging processes can come from a variety of sources, both internal and external.
The Science of Wellness Magazine
Top sources of antioxidants in common food items
eople these days get overly conscious about their appearances as they ask themselves in the mirror, “Am I getting old?” But here is a diﬀerent question that most people don’t ponder: What biological factors lead to aging? Despite the important role that aging plays in our lives, the ﬁeld of gerontology, or the study of aging, is relatively new and scientiﬁc research has yet to uncover the mystery behind this ubiquitous biological process. Scientists have proposed more than 300 diﬀerent theories to explain the aging phenomenon. However, studies in the past few decades supported a particular aging hypothesis that is growing in acceptance as a potential explanation of the chemistry behind the concept of aging: the free radical theory. The free radical theory introduces a fundamental idea in chemistry called a free radical, which is a classiﬁcation of a group of chemically highly reactive species that lack the stability of paired electrons in the valence shells of the atoms in the molecule. Hoping to eventually pair up, this unpaired electron from the free radical will then interact with the paired electrons of a stable molecule to destabilize that molecule into another free radical. This ultimately leads to a series of radical reactions that can drastically aﬀect the chemical properties of organic molecules in the vicinity. This type of chemical can have deleterious eﬀects in a biological environment as it will damage the diﬀerent biomolecules like carbohydrates, proteins, lipids, and nucleic acids that are responsible for normal cellular function. This free radical theory states that oxygenderived free radicals are responsible for the aging symptoms through damage at the cellular and tissue levels. HO
Sources of Antioxidants
Blueberries, blackberries, raspberries, strawberries, cranberries
Walnuts, pistachios, pecans, hazelnuts, almonds
Red, kidney, pinto, black
Artichokes, spinach, red cabbage, red and white potatoes, sweet potatoes, broccoli
Green tea, coffee, red wine, fruit juices
Cloves, cinnamon, ginger, dried oregano leaf, turmeric powder
These oxygen-derived free radicals are also known as reactive oxygen species. Most of them are produced in the mitochondria, the organelle in a cell that functions to generate cellular energy through metabolism of food molecules. What is interesting is that these reactive oxygen species are regularly produced in the mitochondria during the chemical reduction of oxygen into water during cellular respiration. Thus, this controlled process of aging must be inﬂuenced by both the oxidative stress of the free radical and the counteracting force that inhibits or delays oxidation, known as an antioxidant. Your body naturally produces antioxidants to slow down the impairment in the cellular functions caused by the reactive oxygen species. However, under normal conditions, every day about 1% of these reactive oxygen species escapes the control of the antioxidant defenses and contributes to oxidative damage of surrounding tissues. This, as a result, promotes the aging process. The most important source of antioxidants that alleviate the aging process is provided by nutrition. Nutritional antioxidants are quite diﬀerent from the endogenous kind for their distinct mechanisms in neutralizing free radicals directly, reducing
concentrations of harmful oxidants like peroxides, and repairing the oxidized cell membranes. Although a wide variety of antioxidants exist in our diets, some of the most common ones include vitamin C, vitamin E, and beta-carotene. Some research has shown that antioxidants not only help as anti-aging components but also provide protection against heart disease, cancer, and other chronic conditions; however, substantial evidence is forthcoming to show clearly that this is in fact true. Despite the lack of scientiﬁc validity of the roles of antioxidants, the media and the supplement and food industries have already begun to hype the beneﬁts of antioxidants. Further trials need to be conducted to provide a conclusive result on the real eﬀects of antioxidants, but perhaps people should already start to take advantage of this knowledge and help themselves live better lives by eating fruits, vegetables, and whole grains—all rich in networks of antioxidants and their helper molecules.
Arjun Prabhakar is an undergraduate student studying Chemical Biology at UC Berkeley.
PICTURES (TOP TO BOTTOM): SHYB, SAMELI, KAJINO, BENNER
Vitamin C OH
Beta-Carotene Chemical structures of common antioxidants
The Science of Wellness Magazine
Berries, walnuts, and grean tea are great sources of antioxidants.
Brain Aging Ho w to th del ei ne aY vit ab
By Danielle Hajj
PICTURE: LE BLANC
Interview with Professor William Jagust
Synaptic density refers to the number of synapses associated with one neuron. More synapses per neuron are thought to indicate a richer ability of representation and adaption. As we age, decreasing synaptic density may be responsible for neurological degeneration and slowing of cognitive activity.may be responsible for neurological degeneration and slowing of cognitive activity.
PICTURE: LINH TA
n a society that spends around 80 billion dollars on anti-aging products, therapeutic measures such as Botox and wrinkle creams are ﬂourishing.10 Preserving the beauty of one’s youth has become a top priority for women aged thirty and over. However, society has neglected to pay necessary attention to the most dangerous type of aging: brain aging. Brain aging is not only severely debilitating but also has the ability to decrease the longevity of one’s life. Today’s youth must understand that maintaining a higher cognitive state at a young age means that neurological decline can remain at the high end of the low spectrum in old age. 6 In order to combat aging eﬀects, it is imperative to understand the research investigating speciﬁc measures that may delay the “slowing” down accompanied by age. 6 What exactly is brain aging? While scientists have not been able to coin a single, speciﬁc deﬁnition to this phenomenon, they are able to study the trend of “normal” aging, which gives them indications of the cognitive changes that can be expected in healthy individuals.3 Most deﬁnitions encompass the idea of brain structures and function declining in relation to an increase in age. 6 It is important to note that great individual variation is present when studying these aging eﬀects in the elderly.3,6 Although it may seem that aging is accompanied by neuronal loss, shrinking neurons and decreasing synaptic density hold more responsibility in neurological degeneration.6 With declining synaptic density comes a decrease in the amount of neural connections your brain can make. Less neural connections can indicate slowing of cognitive activity and memory problems.6 Additionally, neurochemical changes of acetylcholine, dopamine and serotonin are also causes of deteriorating function. 8 Another determinant of brain aging is oxidative stress.5,7 This occurs as free radicals (extremely unstable chemicals known as reactive oxygen intermediates (ROIs)) are produced from cellular respiration—an unavoidable biological process your body undergoes.7 ROIs are damaging to lipids, carbohydrates, proteins and nucleic acid.5 They cause DNA damage through oxidation of mtDNA and are, consequently, impairing to the brain. 5,3 With all of the knowledge, the next question is whether or not there are
measures to be taken that can combat these neurochemical changes and slow the brain aging process. In an interview with neurologist and UC Berkeley professor Dr. William Jagust, he noted the studies done on preventative measures “are only observational studies showing associations. No large study has been done revealing large cognitive beneﬁts.” However, Dr. Jagust acknowledges that the observational studies done on animals regarding physical activity and on humans regarding mental activity are “strong suggestions” that these are measures to preserve neurological function. Staying mentally active throughout one’s lifetime is the best way to exercise the mind and strengthen neural connections.4,9 One study using animal models concluded that aerobic exercise increased brain-derived neutrophic factor (BDNF). The study concluded exercise to accelerate synaptic activity and beneﬁt the overall structure of the neuron through generating BDNF.1 Along with physical and mental exercise, caloric restriction and other dietary additions have been associated with higher cognitive ability at an older age. In studies done by the National Institute of Aging, scientists observed a correlation between caloric restriction and a delay of the “onset of age-related disease and…normal age-related decline.” Scientists believe that decreasing metabolic activity, therefore reducing oxidative stress, is one of the mechanisms that explain the correlation.3 Due to possible negative eﬀects of caloric restriction, studies have been done to ﬁnd chemicals that mimic this eﬀect on oxidative stress.7 Resveratrol is one of the mimicry chemicals and has been found to have antioxidant
“While staying as sharp as a 20-year-old is not feasible, delaying the onset of severe age-related diseases and delaying the effects of normal aging is within reach.” 21
The Science of Wellness Magazine
and anti-inﬂammatory properties, scavenging the damaging free radicals.2 Since the body’s production of natural antioxidants decreases with age, consuming antioxidants is very beneﬁcial. In a study sponsored by the National Institute of Health, resveratrol was found to have “neuroprotective” characteristics.2 By activating a target called SIRT1, it is able to protect speciﬁc cells from oxidative damage.2,7 Red grapes, wine, grains and other various fruits and vegetables all contain resveratrol.2 As the eﬀects of aging take their toll on your brain, understanding the implications behind preventative measures and healthy behaviors has the power to extend a person’s quality of life by preserving optimal cognitive function. While staying as sharp as a 20-year-old is not feasible, delaying the onset of severe age-related diseases and delaying the eﬀects of normal aging is within reach. 9 Exhibiting the suggested protective behaviors at a young age may prove to be a main contributing factor to conserving maximum neurological ability.3,9 Dr. Jagust reminds us that in addition to practicing helpful behaviors, avoiding unhealthy behaviors throughout our lifetime is another method to combatting the neurological damage of aging. Stop stressing, stop being a couch potato and resist engaging in any activities that compromise your health, trust me in ﬁfty years you’ll thank yourself.
A special thanks to Professor Jagust for his interview and lectures. Danielle Hajj is an undergraduate student studying Public Health at UC Berkeley.
References High Fructose Corn Syrup vs. Sugar 1. Bray, G. A., Nielsen, S. J., & Popkin, B. M. (January 01, 2004). Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. The American Journal of Clinical Nutrition, 79, 4, 537-43. 2. Casey, J. P. (January 01, 1977). High Fructose Corn Syrup. A Case History of Innovation. Starch Stärke, 29, 6, 196-204. 3. White, J. S. (January 01, 2008). Straight talk about high-fructose corn syrup: what it is and what it ain’t. The American Journal of Clinical Nutrition, 88, 6. 4. Ali, Mir B. (October 01, 2004). Characteristics and Production Costs of U.S. Sugarbeet Farms. United States Department of Agriculture: Economic Research Service, 974-8. 5. Bemiller, J. N. (September 23, 2009). One hundred years of commercial food carbohydrates in the United States. Journal of Agricultural and Food Chemistry, 57, 18, 8125-8129. 6. Melanson, K. J., Zukley, L., Lowndes, J., Nguyen, V., Angelopoulos, T. J., & Rippe, J. M. (February 01, 2007). Eﬀects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normalweight women. Nutrition, 23, 2, 103-112. 7. Liebman, Bonnie (April 01, 2012). Sugar Belly: How Much Sugar is Too Much Sugar? Nutrition Action, 3-7. 8. Stanhope, K. L., Swarbrick, M. M., Havel, P. J., Bair, B. R., Griﬀen, S. C., & Keim, N. L. (May 01, 2008). Twenty-four-hour endocrine and metabolic proﬁles following consumption of high-fructose corn syrup-, sucrose-, fructose-, and glucosesweetened beverages with meals. American Journal of Clinical Nutrition, 87, 5, 1194-1203. Food Coma 1. Amy, Nancy K. “Carbohydrates.” University of California, Berkeley. Wheeler Auditorium, Berkeley, CA. 7 Sep. 2010. Nutritional Sciences 10 Lecture. 2. Benoit, Stephen C., Christopher J. Kemp, Carol F. Elias, William Abplanalp, James P. Herman, Stephanie Migrenne, Anne-Laure Lefevre, Céline Cruciani-Guglielmacci, Christophe Magnan, Fang Yu, Kevin Niswender, Boman G. Irani, William L. Holland, and Deborah J. Clegg. “Palmitic Acid Mediates Hypothalamic Insulin Resistance by Altering PKC-θ Subcellular Localization in Rodents.” Journal of Clinical Investigation 119.9 (2009): 2577-589. Print. Dr. Oz Demystiﬁed 1. Chen, MD, Patricia. Telephone interview. 5 Feb. 2012. 2. “Bile Acid Sequestrants for High Cholesterol.” WebMD - Better Information. Better Health. Web MD, 2 July 2010. Web. 06 Feb. 2012. 3. “Phytochemicals.” Phytochemicals. Top Cultures. Web. 06 Feb. 2012. 4. “Sulforaphane.” Phytochemicals. Top Cultures. Web. 06 Feb. 2012. 5. Choi, Christina, and Rian Ervin Medill. “A Nutrient That May Lower a Woman’s Risk of Heart Disease.” Nwitimes.com. The Times, 8 Mar. 2012. Web. 18 Mar. 2012. 6. Wanjek, Christopher. “Dark Meat Can Be Heart Healthy, Study Shows.” LiveScience.com. TechMedia Network, 6 Mar. 2012. Web. 18 Mar. 2012. 7. Hidgon, PhD, Jane, and Victoria J. Drake, PhD. “Carotenoids.” Micronutrient Information Center. Linus Pauling Institute, Dec. 2005. Web. 06 Feb. 2012. 8. “Lutein & Zeaxanthin | American Optometric Association.” American Optometric Association. American Optometric Association. Web. 06 Feb. 2012. 9. Berliner, Judith, Mohamad Navab, and Alan Fogelman. “Atherosclerosis: Basic Mechanisms:
Oxidation, Inﬂammation, and Genetics.” ACC Current Journal Review 5.3 (1996): 37. Print. My Chemical Romance: The Story of Oxytocin 1. Marazziti D, Dell’Osso B, Baroni S, Mungai F, Catena M, Rucci P, Albanese F, Giannaccini G, Betti L, Fabbrini L, Italiani P, Del Debbio A, Lucacchini A, Dell’Osso L. A relationship between oxytocin and anxiety of romantic attachment. Clin Pract Epidemiol Ment Health. 2006. 2: 28. doi:10.1186/1745-0179-2-28. 2. du Vigneaud V, Ressler C, Trippett S”The sequence of amino acids in oxytocin, with a proposal for the structure of oxytocin”. J. Biol. Chem. December 1953. 205 (2): 949–57. 3. Lactation - Oxytocin.” Animal Sciences Classes. Web. 2 Apr. 2012. 4. Dara K. Shahrokh, Tie-Yuan Zhang, Josie Diorio, Alain Gratton and Michael J. Meaney. Oxytocin-Dopamine Interactions Mediate Variations in Maternal Behavior in the Rat. Endocrinology. May 1, 2010. 151(5): 2276-2286. 5. Y Liu, Z.X Wang. Nucleus accumbens oxytocin and dopamine interact to regulate pair bond formation in female prairie voles. Neuroscience. 15 October 2003. 121(3): 537-544. 6. Carmichael MS, Humbert R, Dixen J, Palmisano G, Greenleaf W, Davidson JM. Plasma oxytocin increases in the human sexual response. J Clin Endocrinol Metab. 1987 Jan. 64(1):27-31. 7. Kosfeld M, Heinrichs M, Zak PJ, Fischbacher U, Fehr E. Oxytocin increases trust in humans. Nature. June 2005. 435 (7042): 673–6. 8. Jean-Philippe Gouin, C. Sue Carter, Hossein PournajaﬁNazarloo, Ronald Glaser, William B. Malarkey, Timothy J. Loving, Jeﬀrey Stowell, Janice K. Kiecolt-Glaser. Marital behavior, oxytocin, vasopressin, and wound healing. Psychoneuroendocrinology. August 2010. 35 (7): 1082-1090. 9. Carolyn H. Declerck, Christophe Boone, Toko Kiyonari. Oxytocin and cooperation under conditions of uncertainty: The modulating role of incentives and social information. Hormones and Behavior. March 2010. 57(3): 368-374. 10. K. Carsten, W.De Dreu, Lindred L. Greer, Gerben A. Van Kleef, Shaul Shalvi, and Michel J. J. Handgraaf. Oxytocin promotes human ethnocentrism. PNAS. 2011. 108 (4): 1262-1266. Spilling the Coﬀee Beans 1. Biao Cheng, Xinran Liu, Hao Gong, Lianqi Huang, Hong Chen, Xin Zhang, Chuanzhou Li, Muyang Yang, Bingjun Ma, Lihua Jiao, Ling Zheng, and Kun Huang. “Coﬀee Components Inhibit Amyloid Formation of Human Islet Amyloid Polypeptide in Vitro: Possible Link between Coﬀee Consumption and Diabetes Mellitus”, Journal of Agricultural and Food Chemistry, Volume 59, Issue 24, 7 November 2011, Pages 13147-13155. 2. American Chemical Society. «Why coﬀee drinking reduces the risk of Type 2 diabetes. ScienceDaily, 11 January 2012. 3. Pittner RA, Albrandt K, Beaumont K, et al. “Molecular physiology of amylin”. J. Cell. Biochem. 55 Suppl: 19–28. You are not an alcoholic. Your Forefathers Were. 1. Dasgupta, Amitava. *The Science of Drinking: How Alcohol Aﬀects Your Body and Mind*. Lanham, MD: Rowman & Littleﬁeld, 2011. Print. 2. Keany, LeeAndrua. “Health & Medicine / Drugs & Addiction.” 20 Things You Didn’t Know About... Alcohol. Discover Magazine, 10 Jan. 2012. Web. Feb. 2012. 3. “Patrick E. McGovern.” Penn Museum. Web. 4. Stephens, Dustin, and Robert Dudley. “The Drunken Monkey Hypothesis: The Study of Fruit-eating Animals Could Lead to an Evolutionary Understanding of Human Alcohol Abuse.” CBS Interactive. CBS Interactive Business Network, 01 Dec. 2004. Web. Feb. 2012. Are You Loco for Them Lokos? 1. Eby, G. and Halcomb, W. “Of elimination of cardiac arrhythmias using oral 3 taurine with l-arginine with case histories: 4 hypothesis for nitric oxide stabilization of the sinus node.” Medical Hypothesis (2006): 3-4.
2. Seedman, J. and Seedman, J. “Nutrional Supplements: Taurine.” 3. Pitkin, et al. “Dietary reference intakes for thiamin, riboﬂavin, naicin, vitamin b6, folate,vitamin b12, pantothenic acid, biotin, and choline.” Washington D.C: National Academy Press, 1998. 4. “Caﬀeine.” Material Safety Data Sheet. SigmaAldrich, 08 Feb 2012. 5. Bolton, S. and Null, G. “Caﬀeine psychological effects, use and abuse.” Orthomolecular Psychiatry 10.3 (1981): 202-211. 6. Ringus, D. “The crazy science behind four loko.” The Cornell Daily Sun. 1 Dec 2010. 7. “Blood alcohol calculator.” The Original Blood Alcohol Calculator, 2010. 8. “Alcohol and the human body.” Intoximeters, Inc, 2012. 9. Shrieves, L. “Dangerous alcohol-caﬀeine mix not fully understood.” The Washington Post. 18 Jan 2011. 10. Phusion Projects. “Phusion projects to remove caﬀeine, guarana and taurine from products.” 16 Nov 2010. 11. Smith, P. “Watch your mouth: Four loko and the search for a safe caﬀeinated booze.” Good: Lifestyle. 25 Aug 2011. How we age: Exploring the free radical theory of aging 1. “Antioxidants: Beyond the Hype.” The Nutrition Source. Harvard School of Public Health. Web. 22 Feb. 2012. 2. Hensrud, Donald. “Food Sources the Best Choice for Antioxidants.” Medical Edge Newspaper Column. Mayo Clinic, 5 June 2009. Web. 22 Feb. 2012. 3. Yu, Byung P. “Aging and Oxidative Stress: Modulation by Dietary Restriction.” Review. Free Radical Biology & Medicine 21.5 (1996): 651-68. Print. 4. Fusco, Domenico, Giuseppe Colloca, Maria R.L. Monaco, and Matteo Cesari. “Eﬀects of Antioxidant Supplementation on the Aging Process.” Review. Clinical Interventions in Aging 2.3 (2007): 377-87. Print. Brain Aging: How to Delay the Inevitable 1. Carl W. Cotman, Nicole C. Berchtold, Exercise: a behavioral intervention to enhance brain health and plasticity, Trends in Neurosciences, Volume 25, Issue 6, 1 June 2002, Pages 295-301. 2. Albert Sun, Qun Wang, Agnes Simonyi, Grace Sun, Resveratrol as a Therapeutic Agent for Neurodegenerative Diseases, Molecular Neurobiology, Humana Press Inc., Volume 4, Issue 2, June 2010, Pages 375-383. 3. “Biology of Aging | National Institute on Aging.” National Institute on Aging | The Leader in Aging Research. National Institutes of Health, Nov. 2011. Web. 09 Feb. 2012. 4. Anderson, Virginia. “Senior Brain Boosters: Tips for Avoiding Age-Related Memory Loss.” WebMD - Better Information. Better Health. WebMd, June 2009. Web. 09 Feb. 2012. 5. Russell H. Swerdlow, Brain aging, Alzheimer’s disease, and mitochondria, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1812, Issue 12, December 2011, Pages 1630-1639, ISSN 09254439, 10.1016/j.bbadis.2011.08.012. 6. Jagust, William. “Newer Concepts of Cognitive Aging.” Morgan Hall, Berkeley. Feb. 2012. Lecture. 7. Jagust, William. “Revisiting Why We Age.” Morgan Hall, Berkeley. Feb. 2012. Lecture. 8. Jagust, William. “Changes in Neurochemistry with Aging.” Morgan Hall, Berkeley. Feb. 2012. Lecture. 9. Jagust, William. “Diﬀerent Types of Aging.” Morgan Hall, Berkeley. Feb. 2012. Lecture. 10. Jagust, William. “Deﬁnitions of Aging.” Morgan Hall, Berkeley. Feb. 20120. Lecture.
The Science of Wellness Magazine