Diet vs. exercise: Which should you focus on for weight loss? By Lainey Younkin, RD

Are you diligently exercising but seeing no results around your midsection? Good news: It’s not just you. Two new studies explain why many people who begin exercise programs often lose little to no weight.

In the first study published in PLoS, researchers from the U.S. and U.K. compared total daily energy expenditure (TEE) – how many calories are burned each day – between Westerners and the Hadza, a population of hunter-gatherers living in Northern Tanzania.

The Hadza hunt and forage for food without modern tools (e.g. vehicles or guns). According to the study, their diet consists mainly of “tubers, berries, small- and large-game, baobab fruit, and honey.”

Many believe that modern Western lifestyles lead to decreased energy expenditure, as people, in general, burn fewer calories than in the past because their lives have become more sedentary.

Researchers were interested in determining the difference, if any, in daily energy expenditure between the Hadza and Westerners. They measured the TEE of 30 Hadza adults over an 11-day period using the doubly labeled water (DLW) method and also calculated their physical activity levels (PALs). Then they compared the TEE of the Hadza to the TEE of individuals in Western countries (U.S. and Europe) by gathering TEE data from previous DLW studies and taking new measurements from 68 U.S. adults. They also gathered comparative data from non-Western market economies such as Siberia and from a farming population in Bolivia. There were 221 subjects from comparative datasets.

Not surprisingly, the Hadza were active, lean, and had lower body fat percentages than the average Westerner. They were also found to have greater PALs (calculated as TEE/estimated basal metabolic rate). Men walked about seven miles each day, while women walked an average of 3.5 miles. The researchers attributed the greater PAL to the differences in body size, as the Hadza are smaller in general than individuals in the West.

What was surprising was that the researchers found little difference in TEE  (calories burned) between the Hadza and their Western counterparts. Though the Hadza seem to be more active, both groups expended about the same amount of energy each day.

This means that minutes of physical activity per day may have little to no effect on the number of calories burned. So what does?

An important part of the equation is missing: energy intake. Since energy expenditure did not significantly differ between the Hadza and Westerners, the researchers concluded that “differences in obesity prevalence between populations result primarily from differences in energy intake rather than expenditure.” In other words, “active ‘traditional’ lifestyles may not protect against obesity if diets change to promote increased caloric consumption.”

Diets have indeed changed, especially in the West. It’s long been known though that in order to lose weight, you have to burn more calories than you consume. But why do so many people have trouble burning calories and keeping the weight away? The second study, published in Obesity Reviews, was a review on the effect of exercise interventions on body composition that revealed why people lose little weight when enrolled in exercise programs.

Contrary to popular belief, the researchers found that when people exercise and keep their energy intake (i.e. number of calories) constant, their resting metabolic rate (i.e. metabolism) is actually reduced. This was especially true of individuals who had a lower amount of lean body mass, which is the total mass of the body minus fat.

However, the researchers did find that aerobic exercise (e.g. running, cycling, swimming) caused people to lose more fat mass than lean body mass when keeping calorie intake constant. In addition, when people increased the number of calories they ate during aerobic training, they gained more lean body mass and less fat mass than previously predicted. But if you increase your calories by too much, it negates the effects of your hard work.

Therefore, the reason people lose less weight than expected when exercising is two-fold, according to the scientists. First, exercise programs may not lead to as much calorie-burn as you would think. Second, many people concomitantly increase their calories when exercising and may sometimes increase them too much. This could cause you to either gain weight while exercising or not lose as much weight as expected.


If you enroll in an exercise program or start a form of aerobic training to lose weight, you won’t succeed with the mentality “I can eat anything because I’ll burn it off later.” You will have better weight loss results if you choose a healthy diet of whole grains, fruits and vegetables, lean proteins, and healthy fats while exercising. And, though these two studies show that diet is more important than exercise for weight loss, don’t discount the other benefits of exercise, including decreased stress and anxiety, improved mood, and reduced risk of cardiovascular disease, diabetes, and some cancers.

Lainey Younkin, RD is starting her second year as a Nutrition Communication student at Friedman. She looks forward to learning more about diet and exercise and hopes to help people find a proper balance between the two.

Increase Your Metabolism with An Apple? By Lisa D’Agrosa, RD

In the heat of summer, the crisp, cool fall apple season might feel far away.  But it will be here before you know it, and there is good reason to celebrate this year: apple skins contain ursolic acid.  What’s that?  Ursolic acid is a compound found in the skins of apples, as well as cranberries, basil and some other fruits and vegetables, which may boost metabolism. New research published in the June 2012 issue of PLoS One finds that mice fed a high-fat diet with ursolic acid had faster metabolisms when compared to mice fed only the high-fat diet.

What was especially interesting was the mechanism in which metabolism was increased.  It was not due simply to an increase in muscle mass in the mice, which happened as well, but also to an increase in brown adipose tissue, or brown fat.  Brown fat is the type of fat involved in warming up the body and thus, unlike its white counterpart, it burns calories rather than storing them.

The researchers were especially excited by the increase in brown fat.  Brown fat is most active in newborns and helps them keep warm without shivering.  In past years, researchers have tried to uncover ways to increase brown fat in older adults but without much luck. Brown fat did increase when people were exposed to cold temperatures for long periods of time; presumably activated to help warm up the body.  However, it’s a lot easier to eat apples than stand outside in the cold.

The researchers were unsure how and why the brown fat was increased in the mice.  In past studies, brown fat has been increased in humans by placing them in extremely cold conditions for a long time.  Because brown fat burns calories, it has been a hot topic in recent years.  However, the long-term effects of boosting brown fat in humans remain unclear.  Would an increase in metabolism also increase appetite? Would the brown fat stay active for a long time?  Would there be other negative side effects?  The answers to these questions are not yet known.

In the study, the mice getting ursolic acid also exhibited lower rates of obesity, better blood glucose levels, and less fatty liver disease.  In addition, the mice had increased slow and fast twitch muscles and ran faster on a treadmill than their counterparts.  The research implies that ursolic acid essentially helped the mice gain less weight and get stronger and faster, all while minimizing the risk of certain diseases.  Sounds pretty great. However, the research is still very preliminary.

While the latest study done on ursolic acid in mice seems promising, so far no studies have been done to test the effects of ursolic acid in humans.  It’s a good idea to eat apples with the skin on, especially because apples are high in fiber and other vitamins and minerals, but there is no guarantee that they will keep the doctor away or boost your metabolism.

*sources available upon request

Lisa D’Agrosa is a second year nutrition communication student at Tufts.  She loves apples, especially with peanut butter or some nice sharp cheddar.  When she’s not chomping on her fruits and veggies, you can find her on a yoga mat or walking around the beautiful city of Boston.

Red Meat and Death? Seeing Through the Headlines

By Allison Knott, RD

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As with most nutrition topics, there is the constant desire to find the magic bullet – the one food, or group of foods, that will improve our health and lengthen our lives.  However, those who study nutrition know a single food is never the answer, but that a diet based on variety is important to health and well-being.  You wouldn’t know this, though, when a recent study connecting red meat and mortality was released in March.  The headlines read, “Death By Bacon” and “Will Red Meat Kill You?”  From CNN to the Huffington Post, every major news organization was reporting on a hot new study from Harvard.

Published in the Archives of Internal Medicine, researchers examined two prospective cohort studies, The Nurses’ Health Study and the Health Professionals Follow-up Study for an association between red meat consumption and mortality.  The researchers concluded “…a higher intake of red meat was associated with a significantly elevated risk of total, [cardiovascular disease] CVD and cancer mortality.”  Further, according to researcher An Pan, PhD in the Department of Nutrition at Harvard School of Public Health, “In the study population, if all the patients reduced their total red meat intake to less than 0.5 servings per day we estimate a 7-9% reduction in total mortality.”

Study participants submitted dietary intakes at baseline and again every four years in the form of a self-reported food frequency questionnaire between 1980 and 2006.  Total red meat consumption ranged from less than one serving to slightly more than two servings per day at baseline and decreased over time (one serving was equal to three ounces in the study population).  In addition to the association between red meat and mortality, the results also showed no statistically significant difference between processed and unprocessed red meat and total mortality.  However, one would be mistaken in assuming that cutting red meat from the diet would have a direct effect on lifespan.  More importantly, it is the other foods consumed in the diet that are most likely to have the greatest effect.  The study researchers found that people eating higher amounts of red meat were not eating the other things that have been shown to improve longevity like whole grains, fruits and vegetables.  “The question is not whether we should eat red meat or not,” explained Dr. Pan in a brief interview March 15th, “people can eat it definitely, but in the current American diet we are eating it too much and those with a higher red meat intake need to reduce it.  Also, people need to limit processed red meats and replace red meat with a healthier source of protein.”

What role does red meat have in the diet?

Alice H Lichtenstein, Senior Scientist and Director in the Cardiovascular Nutrition Laboratory at the Jean Mayer USDA HNRCA at Tufts University, shed some light on the study findings.

“The bottom line is that this study shows an association and cannot address the question of whether there is a cause and effect relationship,” explained Dr. Lichtenstein.  “We know that people who consume diets that are higher in red meat frequently engage in other dietary habits that can be associated with increased risk of cancer, cardiovascular disease, and mortality.”  The study confirmed, people consuming the most red meat were also more likely to be current smokers, to drink alcohol, have a higher body mass index, and to be less physically active.  “There is an attempt to statistically correct for all those factors,” explained Dr. Lichtenstein, “but you may be left with residual confounding, or factors that cannot necessarily be corrected for.”  For example, the group eating the highest amount of red meat reported eating 700-800 calories on average more per day.  Since the average body mass index (a measure of height compared to weight) were relatively similar across the groups, does that suggest that perhaps one group more completely reported their food intake?  Were that the case, how would it affect data interpretation?  So, while those study participants who ate a higher amount of red meat reduced their red meat consumption over time, they were additionally engaging in other activities that would increase their total mortality, as well as eating lower amounts of whole grains, fruits, vegetables, and fish.

Does this mean red meat leads to death?  No.  “The study confirms what we already know – diets low in fruits and vegetables and fish, and high in animal fat are associated with less favorable outcomes,” said Dr. Lichtenstein.  While the headlines claim red meat causes death, the take away message is not quite so simple.  If you are eating red meat, do so in moderation – choose lean cuts and moderate portion sizes.  Consider replacing red meat with poultry, fish, plant-based proteins, and eat plenty of fruits, vegetables, and whole grains.

Allison is a second year Nutrition Communication student and registered dietitian.  She has a passion for communicating sound nutrition information to the public.  Follow her kitchen blunders, triathlon adventures, and read nutrition advice on her blog, Choices.Habits.Lifestyle

Epigenetics 101 – Nature, Nurture, and Nutrition

By Lara Park, MS

Think that the DNA code you’re dealt is the be-all-end-all for disease risk? A body of research is now demonstrating that nutrition can change how your genome functions by altering the folding of your DNA. This regulation of packaging is called epigenetics, and it is shedding new light on the nature versus nurture debate.

Why do individuals have different susceptibilities to disease? In 2003 when the Human Genome Project was coming to a close, there was a belief that the field of medical research would become increasingly obsolete because all diseases were thought to originate from differences in DNA sequence. In the years since, it has become evident that how the DNA responds to the environment plays a critical role in determining disease susceptibility. DNA contains the blueprint to make every kind of protein in the body, but a library of blueprints is not very useful without any instructions about what to build and when to build it. Epigenetics are the instructions to the DNA blueprint. The food we eat serves as a daily environmental exposure that can modify which genes are turned on and off through changes in epigenetic patterns.

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Every single cell in our body contains over six feet of string-like DNA, which needs to fit inside the 15-micron nucleus. In order to fit, the DNA is wrapped around bead-like proteins called histones, and then these beads-on-a-string are tightly wound up into chromosomes. In order to turn on a gene, the packaging around this gene needs to be loosened by adding biochemical compounds to the histone beads. When the gene is turned off, the gene is tightly packaged by adding compounds such as methyl groups directly to the DNA. Epigenetics is the pattern of these compounds on the DNA and its supporting histone structure. This gives DNA two separate identities; one being the DNA code and the other the epigenetic packaging.

Individuals display highly variable epigenetic patterns. The cause of this variability appears to arise from our environment, blurring the distinctions between nature and nurture. Environmental exposures such as diet, pollution, and even stress, can alter epigenetic patterns changing which genes are turned on and off to ultimately affect physiological function. Studies in monozygotic twins with identical DNA demonstrated that older twins, who would have experienced more variable environments, had significantly different DNA methylation patterns compared to young twins. These differences were even more substantial for twins reared apart with a less shared environment. The researchers used a technique to make the DNA methylation patterns on one twin fluoresce green and the other twin fluoresce red, with regions where patterns were identical appeared yellow. While this study was correlational in nature, these visually striking results highlight potential roles of the environment on identical DNA.

DNA methylation in 3 year old twins (left) and 50 year old twins (right).

Nutrition is a daily environmental exposure that contributes to these variations in epigenetic patterns. Studies in cell culture, animal models and humans have identified many dietary compounds that affect epigenetics patterns. Diets deficient in the B vitamins such as folate and vitamin B12 are associated with increased cancer risk across many tissues because these nutrients are the source for methyl groups required for epigenetic DNA methylation. Changes in DNA methylation are one of the earliest steps in cancer development. Curcumin, a polyphenol in the Indian spice turmeric, interacts with the enzymes that place epigenetic marks on histone bead proteins to turn off inflammatory genes in blood cells when blood glucose is high, as seen with diabetes. This suggests that increased curcumin consumption may reduce some of the complications of diabetes, though this hasn’t been thoroughly investigated in humans yet. Similarly, sulfurophane compounds in cruciferous vegetables such as broccoli and brussel sprouts modify histone epigenetic marks at genes that prevent cancer development in colon and prostate cancer cells. While many of these studies suggest potential preventative (and delicious!) therapeutic approaches to disease, research supporting these mechanisms has been challenging in humans. This is in part due to variability in human metabolism, difficulty in quantifying dietary exposure and logistical challenges in acquiring informative tissue samples at appropriate timing in disease progression from free-living humans.

Environmentally induced epigenetic changes can persist even after the exposure is gone. Epigenetics has become particularly relevant to elucidate the mechanisms underlying the fetal origins of disease theory, famously known as the Barker hypothesis. In 1989, David Barker made the observation that low birth weight infants had an increased risk of coronary artery disease, stroke and type II diabetes later in life. A role for epigenetics in the Barker hypothesis was identifiedin the DNA methylation analysis of blood samples from adults who were in utero during the Dutch Hunger Winter when Germany imposed a food embargo on the Netherlands during World War II. Adults with pre-natal famine exposure had impaired glucose tolerance with reduced DNA methylation at the insulin-like growth-factor II (IGF2) gene compared to their non-famine exposed siblings. IGF2 plays a role in insulin signaling during fetal development, making it biologically plausible that it contributed to diabetes susceptibility later in life. These transgenerational epigenetics are hypothesized to contribute to the predictive adaptive response in which the fetus uses the in utero environment to prepare for the post-natal environment. Similar to the Dutch Hunger Winter, many studies have demonstrated that maternal malnutrition leads to fetal epigenetic programming that enhances storage of energy as fat, which turns out to be maladaptive in the post-natal life of food abundance.

The social environment has also been identified as an input in early-life epigenetic programming. Animal models with reduced maternal behaviors, quantified as time spent licking and grooming (LG) of offspring, demonstrated that low-LG offspring had differential DNA methylation of the glucocorticoid receptor in the brain. This turned on the glucocorticoid receptor gene, which functions to regulate the stress response. In humans, suicide victims who were exposed to early life adversity also demonstrated methylation differences at the glucocorticoid receptor gene in the brain compared to non-suicide victims without early life adversity. Taken together, this suggests that early social environments can lead to persistent epigenetic changes that may play a role in behavior.

So to answer our initial question, epigenetics encompasses biological, sociological and environmental inputs into our DNA to contribute to variability in disease risk. What do we do with this information? Well, we can spread the word by dancing about it, as seen in this Dance your PhD entry! On a more serious note, we can be cognizant that our lifestyle choices can impact our DNA such that our health outcomes are truly a balance between nature and nurture. Epigenetic patterns can be viewed as our life history on our DNA and serve as an empowering message to strive for a healthy lifestyle.

*Photo 2 source:  Fraga et al. Epigenetic differences arise during the lifetime of monozygotic twins. PNAS 2005; 102(30):10604-10609

Lara Park is a PhD student in the Biochemical and Molecular Nutrition program working in nutritional epigenetics with Dr. Sang-Woon Choi. Her thesis work is investigating how genome wide epigenetic patterns change with aging and whether a Western-style diet or calorie restricted diet can modify these patterns. Outside of the science world, Lara dances with Urbanity Dance, a Boston-based contemporary dance company.

Ancient Medicine, Modern Products, and Health Claims: The Success of Kombucha Tea

By Katie Andrews

Kombucha, a fermented black tea often referred to as the “champagne of life,” is marketed as a wellness panacea for everything from bodily cleansing, to improved energy and digestion, to a cure for cancer. Frequently called “tea fungus,” Kombucha was reportedly first consumed in Central Asia around 220 BC, and home brewing in health food circles in the United States was reported in the early 1990s. Kombucha is made by combining black tea, sugar, and a symbiotic yeast and bacteria combination often confused for a mushroom. During the 7-14 day fermentation process, the tea develops several organic acids, active enzymes, amino acids, polyphenols, and other compounds that provide its reported antioxidant and antimicrobial effects.

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Kombucha hit the commercial market in the early 2000s, and today, consumers can choose to brew their own by purchasing cultures online or can take the easier route of spending about $4 for a bottled product.

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However, the beautiful packaging of Kombucha hardly prepares the consumer for the putrid smell of fermented vinegar and chunks of floating “mother mushroom” bacteria. Upon stomaching your first bottle, the message seems to be: anything that smells this bad must be good for me.

The health claims associated with Kombucha cite the historical use of the tea as evidence of its efficacy, thereby feeding the social power of the product. A blogger known as “The Food Renegade” focuses on the detoxifying properties of the tea, claiming that the drink is “rich in the enzymes and bacterial acids your body produces and/or uses to detox your system, thus reducing your pancreatic load and easing the burden on your lives.”  Stuart Thomson, director of the online Gaia Research Institute, published a “scientific heath literature review” about Kombucha tea, claiming that Russian research dating back to the 1940s supports the tea’s use against aging and the associated comorbidities of rheumatism and gout.   “GT Dave” himself, the founder of GT’s Kombucha and a self-proclaimed “lifelong practitioner of health,” claims Kombucha all but cured his mother’s breast cancer. The truth is, she was diagnosed and received both chemotherapy and radiation to treat her cancer, but she alludes that it was her daily Kombucha habit that “kept her strong” throughout treatment.

Kombucha has gained popularity and power through these claims, even though the science behind them is limited or non-existent, particularly regarding human studies. A 2000 review compiled a list of the acetic acid bacteria and yeasts identified in tea fungus, but considering that each may be brewed differently and from a different “mother” source, metabolite concentrations are variable.

Additional research on Kombucha has included studying hepatoprotective properties, protection against phenol toxicity, gastric ulcer healing, and oxidative stress from environmental contaminants. However, each of these studies was conducted with mice or rats. Outside of historical personal claims, there are no scientific trials studying the effects of Kombucha consumption on humans.

While you may think that Kombucha devotees would fear a study discounting their magic elixir, true believers would welcome solid scientific evidence picking up where the Russian studies of the early 1940s left off. The theory as to why the tea hasn’t been studied further is a simple one: economics. “No one in the drug industry stands to profit from researching a beverage that the average consumer can make for as little as 50 cents,” “The Food Renegade” says.  Without an interested party to fund the research, the effects of Kombucha consumption remain untested.

While research to support the myriad of health claims associated with Kombucha is scarce, there are case studies reporting on the dangers of toxicity and infection related to Kombucha consumption. Reports of stomach upset, allergic reactions, hepatotoxicity and metabolic acidosis have been published, but the mechanisms as to why they occurred are still unclear. What seems most obvious is that when brewed at home, there are a multitude of things that can go wrong, such as introducing the wrong bacteria, over-extending the fermentation time, or allowing lead to leach in from storage vessels.

The greatest challenge in the safety of Kombucha is that the fermentation process is complex and not clearly elucidated. The production of ethanol occurs when the yeast cells hydrolyze sucrose into glucose and fructose as well as when acetic bacteria break down glucose to gluconic acid and ethanol.  This helps elucidate why one of the recorded effects of Kombucha is “reducing alcoholic’s craving for alcohol.”  Yet when you are selling a product on commercial shelves the problem becomes clear: just how much alcohol do these drinks contain?

While there is no way to regulate what people will make in their own homes, there are repercussions for the companies who are scientifically unable to control their products. In June 2010, national grocery chain Whole Foods pulled Kombucha from store shelves and in-store taps due to excessive alcohol content, even though less than three months earlier they had praised the product on their own blog for “its ability to promote good health” and its “excellent detoxifying, metabolic balancing and immune enhancing qualities.”  

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Because Kombucha is technically neither food nor drug, the FDA has no regulatory power, but in 1995 they did investigate the death of one woman and almost-fatal hospitalization of another who had been drinking home-brewed Kombucha from the same “mother” mushroom.  They have also stated that pasteurizing the product would help reduce the dangers of variable bacteria and alcohol content. However while one brand, Kombucha Wonder Drink, does pasteurize their products for safety, the processing kills the live cultures and bacteria believed to give Kombucha its antimicrobial and antioxidant power, thereby killing its social value.

Kombucha seems to be experiencing a Jekyll and Hyde identity: is it the miracle cure, centuries in the making, or a colony of bacteria posing potentially fatally consequences for trusting consumers? The product currently exudes such a shiny health halo that the research firm The Hartman Group applauded the “reawaken, rebirth, repurpose, redefine” statement on the GT’s Kombucha label for being a simple clean message of “physical benefits [that] extend to soulful, emotional benefits.”

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“GT Dave’s” story about his mother’s cancer was highlighted for exuding “authenticity,” even though the story is arguably untrue.  While research states that core health and wellness consumers pride themselves on “intense scrutiny of brands and their claims,” consumers also want “real and clean foods and beverages” to treat and prevent disease. And that authentic wellness ideal is exactly the niche market that Kombucha fits into.

Belief in a folk remedy, especially during a time of failing health, can be a much stronger form of advice than a professional source, even one with evidence-based research behind him. In addition, more and more consumers don’t feel they need science to teach them about nutrition.  But with a product like Kombucha, it is a thin line between an expensive bottle of sparkling tea and a potential negative health outcome. What was a niche market has grown to over $300 million as of 2010, meaning that even without the scientific evidence, the products are selling.  In this era of real, clean food, “scientifically proven” has lost some value within certain social realms, and the claims associated with Kombucha appear to be sending this product into a successful future.

*Sources available on request

Katie Andrews is a 2nd year Nutrition Communications student finishing her last semester at the Friedman School. An avid blogger, future registered dietitian, and commenter on all controversial things nutrition, you can find her at

Coffee May be Linked to Reduced Risk of Type 2 Diabetes

By Lainey Younkin, RD

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What began in the jungles of Ethiopia several hundred years ago now presents itself on every corner in both cities and suburbs.  It’s sold at Starbucks, Dunkin Donuts, Panera, and Au Bon Pain among others, and Americans rely on it to fuel their bodies and brains each day.  It’s one of the most popular nonalcoholic beverages in the world.  You guessed.  It’s coffee.

Coffee originates from coffee cherries whose seeds are roasted, creating a complex chemical composition.  Its makeup consists of over a thousand different chemicals including caffeine, chlorogenic acid, other polyphenols, carbohydrates, lipids, vitamins, minerals, nitrogenous compounds, and many others.

Coffee consumption has skyrocketed in recent years due to these “fast coffee” chains that are ever-present.  But with coffee’s growing popularity has come growing speculations about its effect on health.  Specifically, researchers have been interested in the effect of coffee on chronic disease risk, and according to a recent German study they may be one step closer to finding a link.

The European Prospective Investigation into Cancer and Nutrition (EPIC)-Germany Study results showed that coffee consumption does not increase the risk of chronic disease (type 2 diabetes, myocardial infarction, stroke, and cancer) but could lower the risk of type 2 diabetes (T2D).

The EPIC-Germany Study sought to determine the effects of caffeinated and decaffeinated coffee consumption on the risk of four chronic diseases: T2D, myocardial infarction (MI), stroke, and cancer. Participants were from two cities in Germany that are part of the larger EPIC study, a multicenter prospective cohort focused on associations between diet, lifestyle, and chronic disease risk.

Previous studies yielded conflicting results surrounding coffee’s effect on chronic diseases.  Some studies suggest that drinking coffee raises the risk of many chronic diseases.  Randomized controlled trials have shown coffee consumption raises blood pressure, cholesterol levels, and homocysteine.  Other studies suggest coffee reduces the risk of chronic diseases, and still others claim there is no association.  Current dietary guidelines recommend drinking coffee in moderation, and the American Heart Association says that 1-2 cups per day does not seem to be harmful in relation to coronary heart disease.

One reason results are conflicting is because many factors must be taken into consideration when addressing this potential relationship.  Several previous studies did not differentiate between caffeinated and decaffeinated coffee.  Other studies failed to account for confounding variables such as smoking, alcohol intake, and physical activity.  Historically, smoking and coffee consumption have gone hand-in-hand, which presents the question of which is to blame for adverse health outcomes.

The EPIC-Germany Study analysis included 42,659 participants (mean age 49.7 y) recruited from 1994-1998 and followed for almost nine years.  Compared to drinking <1 cup/d of caffeinated coffee, they found that consuming >4 cups/d of caffeinated coffee was associated with a 23% lower risk of T2D.  The same amount of decaffeinated coffee (>4 cups/d) was found to be associated with a 30% lower risk of T2D.  One cup of coffee was defined as 150 mL, which is slightly more than 4 oz.

In addition, compared to drinking <1 cup/d of decaffeinated coffee, consuming >4 cups/d was positively associated with MI risk.  But, the investigators were quick to point out that this finding must be taken with caution since only 4.5% of the participants reported drinking solely decaffeinated coffee.  Also, it was likely that participants could have switched to decaffeinated coffee after diagnosis of CVD.  Therefore, the positive association could be due to the fact that participants already had an increased risk of MI from having had a previous heart attack.

All of these results were after adjustment for confounding factors including chronic disease risk, age, sex, city, alcohol intake, smoking status, BMI, and hypertension.

The researchers also found an interaction between drinking caffeinated coffee and smoking. For smokers, caffeinated coffee consumption did not decrease the risk of T2D. This is likely because the adverse effects of smoking may outweigh the potential benefits of coffee.

Prior to previous reports, the researchers found no relationship between caffeinated and decaffeinated coffee consumption and CVD risk. They believe this is due in part to previous studies not adjusting for smoking and alcohol intake.  Since this was an observational study, causality could not be determined.  The researchers also found no relationship between caffeinated or decaffeinated coffee consumption and total cancer risk.

While this study took both caffeinated and decaffeinated coffee into account, it had a few limitations.  It relied on self-reported coffee consumption, did not assess the method of preparation, and did not determine if anything was added to the coffee (sugar, milk, etc).

Clearly, more studies are needed on this hot topic.  Until further research proves otherwise, drink away, in moderation.

*Sources available on request

Lainey is a first year Nutrition Communication student and registered dietitian.  She loves drinking coffee and hopes to help people have a positive relationship with food (and drinks).  In addition, she has fun working at her jewelry business Stella and Dot and blogging at

Back to the Future: Is the Paleo Diet for Real?

By Max Prokopy

Six of the top seven causes of death in America are significantly impacted by diet and lifestyle.  However, there still exist small societies where such problems are rare.  In his 1939 book Nutrition and Physical Degeneration, Dr. Weston Price (a dentist by trade) noted the remarkable health of those who consumed indigenous diets free of “white man’s foods” like flour, sugar, white rice, and vegetable oils.  Contrary to Price’s Cleveland, OH patients, “primitives” from pole to pole were virtually unaffected by our biggest killers.  While most nutrition research ventured into low-fat and low-carbohydrate diets, some took a further interest in Price’s observations.  Sifting through fossil and climate records, scientists established dietary patterns of the Paleolithic humans (who lived approximately 2.5 million to 10,000 years ago).  This data helped researchers understand how food and culture shaped (or selected for) the human genome during our evolution.  Among the most notable of these scientists is Professor Loren Cordain, author of peer-reviewed manuscripts and books including The Paleo Diet.

The diet encourages readers to consume the foods we ate before concentrated agriculture appeared, about 10,000 years ago.  The eminent scientist Stephen Jay Gould stated:

“There’s been no biological change in humans in 40,000 or 50,000 years. Everything we call culture and civilization we’ve built with the same body and brain.”

Cordain hypothesizes if our genome hasn’t changed then we should still be eating the foods with which we co-evolved and eventually thrived.  Paleo foods are:

  • Fresh produce, especially organic and seasonal fibrous vegetables
  • Pastured or wild animal products, including organ meats and eggs
  • Fatty plants (avocados, olives, nuts, coconuts)
  • A few starchy plants such as carrots, squash, and sweet potatoes
  • Water and teas

The following staples of agrarian societies are notably absent:

  • Grains
  • Legumes, including peanuts
  • Potatoes
  • Salt
  • Dairy
  • Sugar and vegetable oils

The Good

Few experts would eschew the message of no processed foods, lots of fibrous vegetables, and naturally pastured/wild animal products.  Moreover, recently introduced foods (including processed plant oils) offer a radically new set of challenges to the body’s physiology.  Since 1909 (just 4 generations), North American plant oil consumption has increased ~500%.  Current rates of chronic disease suggest we’re not yet up to the task of handling “new” foods.

Boyd Eaton’s 1997 article in the European Journal of Clinical Nutrition estimated our Paleolithic ancestors consumed 104 grams of fiber/day without eating grains or legumes.  Although whole grain consumption has recently skyrocketed, Americans still average only ~15 grams/day.  In addition, pastured/wild animals have a fat profile superior to grain-fed feedlot animals.  Price estimated that 20th century Paleo-type “primitives” got 2-25 times the minerals and more than 10 times the animal-based fat-soluble vitamins as their westernized counterparts.  Importantly, Cordain’s paradigm encourages local, independent food systems with dramatic reductions in fossil fuel use.

The biggest controversy with The Paleo Diet is the elimination of grains, dairy, and legumes.  Epidemiological evidence suggests people who eat whole grains and legumes live longer, healthier lives.  This would appear to contradict the purported health benefits of the Paleo diet.  However, the disharmony is largely resolved in light of a few important observations.  First, epidemiological surveys compare diets rich in whole grains and legumes to diets even higher in processed foods, not lower as Paleo promotes.  Second, the surveys which support whole grains use unreliable tools to collect food data and poorly control for significant health factors like exercise.  Third, studies reveal grains, potatoes, and legumes are comparatively rich in deleterious components.  Among them are:

In essence, epidemiological evidence does not currently have the capacity to compare grain-rich and grain-free diets because these processed foods are consumed in such great abundance.  Where epidemiology has fallen short, a few small Paleo-type intervention trials better addressed the whole grain/legume critiques (follow links).  Human and animal studies indicated Paleo-type eating significantly improved:

  • Total, HDL, and LDL cholesterol
  • Body weight and waist circumference
  • Blood pressure
  • Triglycerides
  • HbA1C (long-term blood glucose)
  • HsC-RP (inflammation)
  • Insulin sensitivity

Contrast these results with a well-conducted 2008 study that fed participants either whole or refined grains for 12 weeks.  Whole grains were superior to refined grains in only two of 29 biomarkers examined.  Those who ate refined grains ironically showed bigger drops in blood pressure, weight, and waistline.  The authors note:

Whole-grain foods are recommended for prevention of CVD because they contain many cardioprotective compounds, including dietary fiber, trace minerals, phytoestrogens, and antioxidants.”

Except for controversial phytoestrogens, Cordain’s diet contains the aforementioned beneficial compounds in greater abundance.

Dairy has health implications that include casein lectins and an exaggerated insulin response.  This is true for both whole and skim milk.  There have also been dairy-free diet interventions to treat Autism.  For further exploration of the principles, watch this exhaustive video.  While Paleo has some science behind it, the diet has drawbacks.

The Bad

It’s not possible to eat identically to our hominid ancestors.  Anyone who has seen wild blueberries understands our current cultivars are a far cry from those of 100,000 years ago.  Weston A. Price did manage to find Paleo-type diets in healthy modern populations.  However, once those peoples became exposed to modern culture they invariably delighted in its delicacies.  So maybe the problem is that modern foods are very enticing, engineered to contain the fat, salt, and sugar combination we all crave.  The Paleo diet is hard to adhere to, with restaurants and parties being particularly troublesome.  One can usually find a high-protein salad but that invariably becomes dull.  It’s often said the best diet is one which people are likely to follow.  Paleo probably fails this test.

Of greater concern, the Paleo diet lies distinctly at odds with the reality of earth’s population.  Estimates indicate the U.S. wouldn’t grow enough produce if every American decided to follow the “eat 5 a day” program, let alone a Paleo diet.  The entire world population feeding on organic produce and pastured animals requires an unimaginable devotion of land and labor, plus redistribution of population centers.  And even if concentrated agriculture has worsened our health, hasn’t it accelerated our culture?  Without the ability to feed many people with grains, our entire civilization (not to mention this computer), is doubtful to have arisen.  I have yet to see these issues adequately addressed by Paleo advocates.

On a scientific level, our genome may have been stable since the Paleolithic era but the field of epigenetics has proven our DNA structure to be malleable.  Environmental factors like diet and pollution can change which genes are expressed within a single generation.  Further, early hominids had far more physical activity than current humans.  Is diet the only health-related variable to have changed with the advent of agriculture?  Certainly not.  Parsing out those factors is a vague exercise at best.  Paleo advocates must understand the industrialized world will never approach their ancestors’ activity levels.

The Ugly

The diet makes little exception for vegetarians.  While Paleo has science and history to claim health benefits, many vegetarians eat for ethical or religious reasons.  Cordain should better address this population.  The Paleo diet will also put a hit on your wallet and lies out of reach for most people.  Grains cost less per calorie while organic and pastured products command premium prices.  Americans already skimp on nutritious foods in favor of economic savings.  So even if they have the discipline, few can afford to eat this way.


In general, Paleo is poorly characterized and often confused with Atkins.  Countless blogs contain advocates and detractors.  Unfortunately, there is a paucity of funded science researching the concepts.  While this may owe to our grain centrism, common sense and several studies support Cordain’s approach.  Our food culture is set up around central processed grains and their oils.  Chemical- and petroleum-dependent networks sustain cheap calories with massive health and environmental costs.  The current system opposes our 2+ million years of evolution but is it the only way to feed the world’s population?  Paleo is difficult to follow, expensive, and restrictive.  However, if people so choose it represents a paradigm to bring ancient health and food back to the future.

*Photo source

Max Prokopy is a first-year Biochemical and Molecular Nutrition PhD student who has certifications and experience with training collegiate and professional athletes with a particular focus on ice hockey.

A Tax on Sweetness?

By Jenn LaVardera

Imagine getting carded the next time you buy a soda. As ludicrous as that might sound, it may become a reality.

According to the United Nations, chronic diseases including heart disease, cancer, and diabetes have become more of a health burden on society than infectious diseases. In September 2011, the UN convened in New York for a High-Level Meeting to discuss prevention and control of the four main non-communicable diseases – cardiovascular disease, cancer, chronic lung disease, and diabetes. Tobacco, alcohol, and diet were targeted as the major risk factors for the development of these diseases. As stated in the Summary Report of the Secretary-General, the best interventions strategies include “tobacco-control measures, including raising taxes and bans on advertising and smoking in public places; raising taxes on alcohol and enforcing bans on alcohol advertising; reducing salt intake; replacing trans-fats in foods with polyunsaturated fats; promoting public awareness about diet and physical activity…”

If tobacco and alcohol can be regulated by the government to protect public health, does it make sense to regulate the other major risk factor – poor diet – in order to prevent disease? Food is essential, unlike tobacco and alcohol, and the regulation process would be different than those of non-essential substances. However, there may in fact be aspects of the Western diet that should be monitored for health purposes according to some experts.

A position paper by leading obesity researchers Robert H. Lustig, Laura A. Schmidt, and Claire D. Brindis from the University of California, San Francisco School of Medicine published in the journal Nature on February 2, 2012 addresses this issue. They contend that sugar consumption is linked to a rise in non-communicable disease; sugar’s effects on the body are similar to those of alcohol; and that regulation could therefore include tax, limiting sales during school hours, and placing age limits on purchase of sugary products.

The team references psychologist Thomas Barbor, who in his 2003 book Alcohol: No Ordinary Commodity presented four criteria that justify the regulation of alcohol. Running through his checklist, it seems that sugar may not be as ordinary as it appears.

1. Unavoidability / Pervasiveness throughout society: Due to the evolution of processed foods, sugar is now in the majority of packaged food products in grocery stores, which limits a consumer’s decision to avoid products with added sugars. Worldwide, people consume an average of 500 calories or more per day from added sugar alone. In the United States the average is well over 600 calories.

2. Toxicity: Sugar not only adds extra calories to the diet but induces all diseases associated with metabolic syndrome, including hypertension and diabetes. It can be reasoned that fructose, a form of sugar widely used in processed foods, has toxic effects on the liver similar to those of alcohol; it raises uric acid and causes damage to lipids, proteins, and DNA through non-enzymatic binding to these molecules.

3. Potential for abuse: Sugar suppresses the hormone ghrelin, which signals hunger to the brain, interferes with leptin, the hormone which produces the feeling of fullness. It also decreases dopamine signaling, which reduces the amount of pleasure experienced from eating and thereby promotes overconsumption.

4. Negative impact on society: The U.S. spends an annual $65 billion in lost productivity and $150 billion on health-care resources for side effects of metabolic syndrome.

This proposition has generated considerable debate. Ron Boswell, senator for Queensland, Australia, responded to Nature claiming “To describe sugar as ‘toxic’ is extreme, as is its ludicrous comparison with alcohol…There is no evidence to suggest that reducing sugar consumption will halt the rise in obesity. The contributing factors are far more complex.” A Canadian group of medical experts subsequently disputed that Lustig et al “are directing attention away from the problem of general overconsumption.”

Commenters to Nature also argued that it is misleading to put sugars in a regulatory league with alcohol and tobacco because sugars do not cause behavioral intoxication nor have second-hand proximity effects. Some suggest that the authors should have recommended individuals to manage a balanced diet with exercise rather than demonize sugar. However, one could also argue that these types of message do exist, and society rarely listens to them.

Though it might seem odd paying an extra tax for a sugary cereal, getting carded to buy a soda, or not being able to purchase a box of doughnuts after a certain hour, sugar and alcohol may not be all too different. Maybe the purchasing of these items should be treated in the same way. Sure, a tax on sugar will likely not solve all of the health problems of the world, but it may be a good start to get people to reach for a bottled water instead of a Coke.

*Photo source

Jenn is a first year Nutrition Communication student with plans to complete her Dietetic Internship post graduation. Her hobbies include running, trying new restaurants, doing cross word puzzles, and attending Dave Matthews Band concerts around the country.

Research Spotlight: Daily D Study

By Lainey Younkin, RD

While you’re still snoozing at 5:00 am, the Daily D team has already started their day collecting data with elementary and middle school students.  The Daily D study kicked off this past fall 2011, and visits to the schools are filled with pubertal status questionnaires, height and weight measurements, and skin color and blood samples.  An interview with the Project Coordinator, Elizabeth Olson, provided insight into the reasoning behind the study, specifics about the target population, and details regarding data collection.

Why was the Daily D study initiated?

Blood samples from the FIT study (John Hancock Research Center, PI Jennifer Sacheck, PhD), conducted from 2008-2011 in Somerville, found that 97% of 4th-8th graders were vitamin D insufficient during the late winter.

Vitamin D is important for bone health, muscle strength, and immunity.  Vitamin D deficiency is associated with lower HDL and elevated LDL in children and adolescents and is linked to the development of cardiovascular disease.  It is estimated that 6 million children in the U.S. are vitamin D deficient.

Vitamin D deficiency is even more common in northern latitudes, among some people with darker skin pigmentation, and in those who are overweight or obese.

The Institute of Medicine recommends 600 IU/day of vitamin D for children, but it is difficult for many children to consume this amount.  Many suggest that vitamin D supplementation might be necessary.

What is the study objective?

The overall objective is to determine the appropriate vitamin D supplementation requirements for children with various risk factors who live at northern latitudes.

Who is your target population?

The target population is 4th-8th grade children in Everett, Malden, and Somerville.  We have worked to recruit children who are racially diverse, have high obesity rates, and are disadvantaged socioeconomically.  To date, the first wave of the study has enrolled over 300 children.

What is the timeline of the study?

The study will be conducted over two, 12-month waves spanning from the fall of 2011 to the fall of 2014.  We have been and will continue to be in the schools every three months taking various measures such as height and weight, questionnaires, skin color, and blood samples.

Can you comment on the study design and the outcomes being measured?

This is a double-blind study in which participants are randomized to one of three different doses of vitamin D: 600 IU, 1000 IU, and 2000 IU.  Researchers will measure the impact of a 6-month “vitamin D intervention” on changes in vitamin D status and cardiometabolic risk factors in these children.

Tell me about the Daily D Study Team.

We have one Primary Investigator, Jennifer Sacheck, PhD and five co-investigators.  There are three fulltime staff members, including myself, who implement the study with the help of several translators, phlebotomists, and research assistants.

As the Project Coordinator, I work on the budget, logistics and planning, identifying and recruiting new communities and schools, and some data collection and management.

What goes on “behind the scenes” when you’re not out collecting data?

When we are not collecting data, we are coordinating adherence phone-calls with the participants, answering any questions, and addressing issues that come up.  Additionally, we continuously work on recruitment and retention strategies for current and future participants.  We are always researching potential communities and schools in which to implement the study.  Finally, there is a dearth of data to be entered, cleaned, and reconciled, which our core staff is always working on.

What reactions have you received from community members regarding involvement in the study?

School principals, nurses, teachers and parents have responded positively.  This is likely due to having heard about vitamin D deficiency from their doctors and/or in the news.  The schools are often proud to have their kids enrolled in the study, and parents often cite both the importance of their children’s health and aiding research as to why they enroll their children.

What do you hope to do with the results in terms of “real-world application” or public health interventions?

Results of this work will inform the development of evidence-based recommendations and guidelines regarding vitamin D supplementation to: maintain optimal vitamin D levels, reduce cardiometabolic risk, and help better understand a number of interactions between childhood obesity and Vitamin D.

*This interview was edited and condensed

*Photo courtesy of the Daily D Research Staff

Lainey is a first year Nutrition Communication student and registered dietitian.  She loves working with kids and has enjoyed being a research assistant for the Daily D study.  In addition, she has fun working at her jewelry business Stella and Dot and blogging at

2012 Student Research Conference: “7 Billion Strong: Approaches to Feeding the World”

By Lainey Younkin, RD

The 6th annual Future of Food and Nutrition Graduate Student Research Conference is quickly approaching.  If you’re a first-year Friedman student, like me, you may have heard rumblings about the upcoming event, but perhaps you are just as clueless as I am about what it entails.  For this reason, I met up with Johanna Andrews and Brooke Smith, co-chairs of the event.  They were filled with practical and exciting information about the upcoming conference.

Abstracts are due soon (February 10), so keep reading if you think you may be interested in participating!

What is the Future of Food and Nutrition Graduate Student Research Conference?

This student run conference is a venue for students to present original research from any discipline related to food and nutrition.  This year’s title is “7 Billion Strong: Approaches to Feeding the World.”  This topic was chosen because members of the team felt it was important to recognize that our population recently hit 7 billion people and the importance of nutrition in our rapidly growing population.

At the conference students will have the opportunity to share, as well as engage in a lively discussion of new research covering domestic and international topics, from both the biological and social sciences.  As a presenter or attendee, students will gain valuable professional experience presenting and discussing novel, multidisciplinary research and will also have the opportunity to network with colleagues and future leaders in the field.  Relevant research includes projects conducted as part of thesis work, internships, capstone papers, or directed studies. Conference participants can attend the student presentations, poster sessions, and an expert panel that will talk about “7 Billion Strong: Approaches to Feeding the World.”

Who runs this event?

The conference is organized by ten graduate students from the Tufts University Friedman School of Nutrition Science and Policy.

Who participates and who attends?

This is a student-focused conference, showcasing student research from universities across the country.  Although Friedman hosts the event, you can expect to see research from a wide range of schools.  Students, professors, and professionals from the field attend the event.

When and where will the conference be held?

The conference will be held March 31, 2012 at the Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at 150 Harrison Ave, Boston, MA 02111.

How can I participate?

The abstract submission deadline has been extended to February 10, 2012.  To submit an abstract use the online form or email the abstract submission form to

If you’d like to attend the event, sign up by March 16th to take advantage of the discounted early bird rate of $25.00.  After that, admission will be $35.00.  Breakfast, snacks and lunch are included in the registration fee.  You can register here.

Anything else you would like to share about the conference?

Last year, over 200 graduate students came together to hear students from 28 universities present research from fields as diverse as anthropology and nutritional epidemiology!

Check for ongoing updates here.

Have any questions?  Email the conference committee at:

Lainey is a first year Nutrition Communication student and registered dietitian.  She enjoys writing about various events around Boston and Friedman.  When not event-hopping or writing, she enjoys working at her jewelry business – Stella and Dot.

Mortality and Supplement Use

By Max Prokopy

Photo Source

Large-scale scientific studies are geared towards evaluating complex questions about health and human behavior.  Using surveys, the lifestyles of thousands of people are tracked for decades.  Then researchers use statistical methods to associate behaviors (e.g., smoking) with health outcomes (e.g., cancer risk).  A common side effect of this analysis is to either reinforce or challenge conventional practices (e.g., taking a daily vitamin).  Occasionally, the findings are weighty enough to provoke national media scrutiny or behavioral and policy changes.

An October 2011 paper published in the Archives of Internal Medicine by Mursu et al. perfectly illustrates how the media filters the complex intersection of statistical methods and public health practices.  The paper comes to the following conclusion: “In older women, several commonly used dietary vitamin and mineral supplements may be associated with increased total mortality risk.”

Media outlets like USA Today, Reuters, the Associated Press, and CNN responded with splashy headlines like “Vitamins linked to higher risk of death.”  These headlines have the power to simultaneously attract and scare readers.  But is it really true?  Does this recent study slam the door on decades of conventional wisdom?  To help shed light on the results of this controversial study, I enlisted the help of Dr. Paul Jacques, Director of the Nutritional Epidemiology Laboratory at Tufts.

Study Design and Authors’ Conclusions

Does taking a vitamin/mineral supplement affect people’s risk of death?  Most people  assume common daily supplements improve health outcomes, or at least do no harm.  However, data from the Iowa Women’s Health Initiative suggest the opposite is true.  The article used surveys to track about 40,000 older women from 1986 to 2004.  Supplement use was correlated with mortality rate.  The higher the correlation, the stronger the relationship is between the two factors.  For example: driving fast on the highway increases your chances of getting a traffic citation.  Statisticians used the data to construct hazard ratios which assign “normal” behavior a risk of 1.0.  Normal behavior was no supplement use at any of the three surveyed time points.  People who used supplements had their mortality risk evaluated relative to the 1.0 reference.  Risks above 1.0 (e.g., 1.1) indicate that group of people carried a greater risk of death.  Likewise, risk values below 1.0 pertain to a reduced mortality rate.

Several surprising results were reported.  Multivitamin users had a risk ratio of 1.06, meaning they had a higher mortality rate than those who did not take a multivitamin.  Other supplements were more strongly associated: vitamin B6 = 1.10, folate (B9) = 1.15, iron = 1.10, and copper = 1.45.  A couple supplements seemed to confer benefits to users: calcium = 0.91, and vitamin B complex = 0.91.  If you’ve been reading carefully the results are curious. Two B vitamins taken alone associated with greater risk while a B complex supplement appeared beneficial.  Moreover, multivitamins have B-complexes as part of the formula.

The authors conclude the following: “Based on existing evidence, we see little justification for the general and widespread use of dietary supplements…our study raises a concern regarding their long-term safety.”  These statements seem damaging to the billion-dollar supplement industry and the media was quick to report on the potential pitfalls.  However, inconsistencies exist.  Understanding the methodology and statistical analyses becomes paramount to digesting the implications of this study.

Upon Further Review

Statistics don’t lie; they are simply calculations.  However, the methods of data collection and controls significantly affect the outcome.  The study has significant flaws in these regards.  Supplement use was evaluated by survey at only three time points in 18 years.  While surveys can have significant inaccuracies, Dr. Jacques notes that errors can offset one another.  Researchers hope equal numbers of people under- and over-report supplement use.  The fact remains that supplement use was evaluated infrequently and changes in usage could be entirely missed.  Is it likely for people take the same supplement combinations for 18 years?

Supplements are rarely used in isolation.  For example, only 229 people (0.59%) reported using copper alone as a supplement.  The high relative risk for this subset (1.45) could be due to the supplement, a small sample size, or confounding factors.  A person that would supplement with only copper probably has other unusual behaviors or filled out the surveys incorrectly.  In other words, it may not be the copper that’s the problem.

The issue of confounding has long plagued large-scale studies like this one.  How can you account for the fact that vitamin users tend to be more educated and wealthy?  According to Dr. Jacques, statisticians accurately account for these factors if they are measured well.  Smoking, which is easily measured with accuracy, can be reliably controlled in statistical analyses.  Physical activity, which is difficult to measure, is not easily removed from the calculation.  Confounders can be neutralized somewhat by having a very large sample size.  This practice is common to epidemiology but is not without its shortcomings.

Methodological Questions

Let’s assume confounders were handled correctly.  There remain several unnerving aspects as to how the study was conducted.  No blood tests were administered.  Thus, it’s impossible to tell if anyone who reported taking a supplement actually derived any physiological change from it.  It’s spurious to associate supplements with mortality if there is no data to corroborate the survey tool.

Over 15,000 (40%) of the women in the study had died by 2008.  That means many were sick while being surveyed.  It’s a well-known phenomenon that people begin supplement use upon diagnosis of a disease.  For example, diagnosis of heart disease can prompt a change in diet and initiate the use of aspirin, vitamins, and fish oils.  Those supplements are widely regarded as preventive tools, not treatments.  The people who died from heart disease probably did not die because of the supplements or diet.  They began the practices after it was “too late.”  However, the methodology wouldn’t account for that and the death would be tied to supplement use.

Final Thoughts

Weeding through the data of a massive health survey is complicated.  National media reports on vitamins are likely premature and this study had significant flaws.  However, studies like this provide a platform for connecting the dots between test tubes, animal models, small human randomized-controlled trials, and large uncontrolled trials.  The hope is that a pattern can be gleaned from all levels of research.  Such patterns can be turned into successful public health campaigns.  For example, folate fortification successfully reduced the incidence of birth defects.

Amidst the furor and frustration over the vitamins study, try to keep the following in mind:

  • This study underscores growing concerns over iron and copper supplementation.
  • Correlation is not causation.
  • Take large survey results with a grain of salt.  Many of the aforementioned study designs show vitamins to be beneficial, which calls the survey results into question.
  • Vitamin supplementation is but one health concern.  Smoking and exercise behaviors are better-established factors in longevity.

If a national health headline worries you, carefully read the study it’s based on before allowing it to change your life.  It pays to read the fine print.  Understanding the original publication can be difficult.  Don’t be afraid to get a bit of help in translation.

Max Prokopy is a first-year Biochemical and Molecular Nutrition PhD student who has certifications and experience with training prep, collegiate and professional athletes with a particular focus on ice hockey.

Stop Sugarcoating It: Georgia’s Bittersweet Childhood Obesity Campaign

By Lauren Todd

The State of Georgia has launched a new public health campaign that takes a tough-love approach to combat childhood obesity. Strong4Life, created by the Children’s Healthcare of Atlanta, is a series of PSAs that feature overweight children alongside blunt comments and the phrase, “Stop Sugarcoating It, Georgia.” These ads address the finding that 75% of parents of overweight children do not recognize a problem. With nearly 40% of Georgia’s children overweight or obese, Strong4Life aims to scare families into making changes. While the ads certainly turn heads, they may blame the victim instead of offer manageable solutions.

Many professionals in the nutrition field feel that the campaign provides necessary shock value. Childhood obesity has taken the spotlight, featured in every medium from academic resources to popular media. Yet despite the nation’s war against obesity, many families deny a problem at home. “It pains me to say that while I think it is startling and unfortunate, it is what we need,” said Dr. Miriam Nelson of the John Hancock Research Center on Physical Activity, Nutrition, and Obesity Prevention. “Many don’t understand that it is happening to them, their nieces and nephews, or the kids at school.” These campaigns seem to have alerted families, but it is uncertain whether they will engender positive change.

Like other child-oriented campaigns, Strong4Life has drawn attention to bullying. In one PSA, Tina states, “I don’t like going to school because the other kids pick on me.” Unfortunately, this is a common occurrence: a 2009 study published by Fox and Farrow in the Journal of Adolescence found that overweight kids were more likely to be verbally and physically bullied, a phenomenon mediated by the victim’s low self-worth and self-esteem. However, the Strong4Life campaign places blame on the victims instead of the bullies. If Tina wants to stop being picked on, Tina needs to lose weight. Blaming overweight children may generate helplessness instead of confidence. Shortly after these PSAs went live, The National Eating Disorders Association released a statement saying, “the ad campaign is most successful at shaming youth who are overweight and reinforcing societal prejudice against children who do not have an ‘ideal’ body type.” Should children be encouraged to lose weight as a means to fend off bullies or gain friends?

Bullying aside, the Strong4Life campaign hits on potential health implications associated with childhood obesity. In another PSA, Jaden says, “Being fat takes the fun out of being a kid.” It is common knowledge that obesity, even in children, is correlated with type II diabetes and hypertension. These diseases are traumatic when diagnosed in adults, let alone children. However, the ads focus primarily on losing weight as opposed to being more healthful. This can be problematic because low weight does not necessitate good health, nor does high weight necessitate poor health.

Aside from physical health, Strong4Life implies that thinner kids are happier kids. According to the journal, Pediatrics, BeLue and colleagues found that an increase in BMI was associated with an increased prevalence of emotional problems, including depression, anxiety, and suicide ideation among youth aged 12 to 17. However, little research has been conducted to evaluate how weight loss in children influences psychological health, unless the child gets an eating disorder. Suggesting that losing weight will positively influence emotional health may be a false promise.

Finally, there are multiple reasons for the obesity epidemic related to policy, environment, and culture that an individual, especially a child has little control over. Placing the blame on the victim without direction decreases self-efficacy. At best, the child walks away wanting to make a change, but ill-equipped to do so. At worst, the child walks away feeling guilty and powerless. However, the next step in the campaign will seek to provide solutions to promote healthful diets and increase physical activity. Hopefully, focusing on action instead of blaming will empower families.

While the Strong4Life ads have succeeded in bringing attention to an issue, they have not encouraged children to make positive changes. Although the health of America’s youth needs to be improved, the jury is still out regarding how to tackle this issue. Ostracizing individuals may not be the best way to fight disease.

Lauren Todd is a second year student in the Nutrition Communication program at the Friedman School.  Her professional interests are in eating disorder prevention.  She likes to procrastinate by painting and playing fantasy football.

Nutrition Talk Radio: Taking a closer look at the new MyPlate

By Sarah Gold

Nutrition Talk Radio, a program of the Tufts Nutrition Internet Radio Project, is a conglomerate of podcasts covering a variety of nutrition science, policy, and recent news topics. Each semester, students work with assistant professor Paul Giguere to develop an hour-long podcast similar to the format of the popular National Public Radio (NPR) program “This American Life.” Students work together throughout the semester to develop a topic, write a script, recruit experts for interviews, and edit the podcast to professional quality. Students gain knowledge in writing and editing radio scripts as well as editing in Apple’s garage band while earning a half-credit towards their degree.

This semester, I worked with Rachel Perez, Tracy Pui, and Utchima Spirachya-anunt to develop a radio program about the USDA’s recently released dietary icon, MyPlate.

In the latest episode of Nutrition Talk, host Rachel Perez explores the implications of MyPlate, the new image meant to represent the important messages of the 2010 Dietary Guidelines. She first talks with Dr. Robert Post, the Deputy Director of the Center for Nutrition Policy and Promotion, about the agency’s communication plan for MyPlate. After that, Emily Biever, RD, a dietitian at the Tufts Floating Hospital for Children and owner of private practice Integralfuel, joins Rachel to talk about the different uses for MyPlate when meeting with clients at her dietetics practice. Lastly, Rachel talks with Dr. Chris Peters, Assistant Professor at the Friedman School, about the agricultural implications of MyPlate and the land needed to achieve the dietary recommendations.

To listen to this episode, visit the Nutrition Talk website or download the episode for free on iTunes (search Tufts Nutrition Talk).  If interested in Nutrition Talk as a directed study, contact Paul Giguere.

*Image source

Sarah is a second year student completing a dual degree in Nutrition Communication and the Didactic Program in Dietetics. Through her writing Sarah hopes to share her passion for nutrition, good food and exercise.  Sarah enjoys running, teaching spin, and testing out new recipes to share with friends and family! Read more from Sarah at

First All-Friedman Journal Club Discusses Controversial Article on Neighborhoods and the Obesity Connection

By Allison Knott, RD

The Friedman School of Nutrition Science and Policy held its first all student journal club last month.  It brought together students from multiple programs within the school to discuss a recent article published in The New England Journal of Medicine about neighborhoods and their effect on obesity and health.  The article, titled “Neighborhoods, Obesity, and Diabetes – A Randomized Social Experiment,” is quite unique because it applies to all programs in the Friedman School.  Students from the Food Policy and Applied Nutrition program, the Nutrition Communication program, the Bimolecular Nutrition program, and the Agriculture, Food, and Environment program contributed to the discussion making for a lively, educational debate.

The study investigated the relationship between neighborhood environments and their contribution to obesity and diabetes development.  The Department of Housing and Urban Development distributed housing vouchers between 1994 and 1998 to 4498 women with children in public housing.  The women were randomly assigned to one of three groups: vouchers redeemable without any restrictions or counseling, vouchers redeemable only if the person moved to a low poverty census tract and received counseling, and a group without any vouchers.  Body mass index and hemoglobin A1c were primary outcome measures.  The researchers found that living in a neighborhood with lower poverty rates was associated with a reduction in “extreme obesity and diabetes.”

Will Masters, Professor and Chair of the Department of Food and Nutrition Policy, along with Ed Saltzman, MD and Chair of the Department of Nutrition Sciences, initiated and organized the presentation.  Four students facilitated the discussion: Sarah Silwa, MS, Whitney Evans, MS RD, LDN, Phil Karl, MS, RD, CSSD, LDN, and Rebecca Nemec, a second year Agriculture, Food, and Environment student.  The students meticulously combed through the article and provided a review of the background, methods, results, and conclusions.  The discussion that followed was informative, but not conclusive.  Though the study had the benefit of randomization, many Tufts faculty members found the statistical analysis to be less than perfect.  In addition, students and faculty questioned the study’s set definition of a “community,” and addressed the potential for confirmation bias.

The diverse areas of study at the Friedman School make it hard to find research that touches on multiple topics that all Friedman students can relate to.  However when the opportunity arose, Will Masters and Ed Saltzman thought it was important to discuss the article as a student body.  The success of the presentation and large turnout of students indicated a desire to continue group discussions in the future.  Examining a topic from all sides, something the Friedman student body is capable of doing due to its diversified programs, provides additional insight into a specific issue and/or academic study.  Many students who attended were overhead saying how much they enjoyed the discussions and hoped that it would happen in the future.  And Will Masters expressed a desire to continue such group meetings and journal clubs as articles are published.

Overall, I think targeting the entire Friedman population was a successful strategy that should continue in the future.  Through school-wide journal clubs such as this, we have the unique advantage to promote an environment that fosters a diversified view of the nutrition field.

Allison is a second year Nutrition Communication student and registered dietitian.  She has a passion for communicating sound nutrition information to the public.  Follow her kitchen blunders, triathlon adventures, and read nutrition advice on her blog, Choices.Habits.Lifestyle.

Resveratrol Supplements Replace Diet and Exercise? Not so Fast.

By Alisha Mehta

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For many years red wine has been touted as the “heart-healthy” drink and recent discoveries have popularized several additional health benefits. The most prominently studied compound in red wine is resveratrol, the antioxidant present in grape skins. Unlike white wine, red wine uses the skins, seeds, and stems during the fermentation process, which preserves the resveratrol, accounting for many of these proposed health benefits. However, white wine also contains compounds presumed to have some benefits as well. Other food sources of resveratrol include peanuts, blueberries, bilberries, and cocoa beans.

Resveratrol, or the “compound du jour”, as Stephen Taylor, a researcher from the University of Queensland called it, offers many potential health benefits. Studies have shown that resveratrol may be able to prolong life due to its beneficial effects on cholesterol, heart disease, cancer, obesity, diabetes, and even other diseases. The latest study, which received a lot of media attention, touts resveratrol for its ability to decrease the metabolic effects of obesity and thus helps prevent the onset of age-related disease.

What’s the latest hype on resveratrol?  A small Dutch study published in the November issue of Cell Metabolism shows that resveratrol may mimic the effects of diet and exercise on the metabolism of obese men.  Previous findings have shown improved metabolic effects in rats fed high calorie diets, as well as with isolated human fat cells. However, this is the first study to show promising results in a clinical trial.

In this study, a small group of eleven obese, but otherwise healthy men were given 150 mg/day resveratrol supplements for thirty days. Twenty-nine bottles of the richest red wine would have to be consumed to obtain an equivalent dose. The findings showed improvements in blood pressure, blood glucose levels, decreased liver fat, and increased insulin sensitivity. In addition, sleeping and resting metabolic rates were lowered, indicating improved metabolic efficiency. The researchers found resveratrol supplements mimicked the effects of calorie restriction or endurance training. Thus, resveratrol supplementation may have the potential to improve metabolic health in individuals and delay the onset of obesity-related disease, including, cardiovascular disease and diabetes.

For years, we have been hearing that red wine, when consumed in moderation, may play a role in lowering cholesterol and preventing heart disease. Resveratrol has been studied for its role in a number of cardiovascular problems, such as myocardial infarction, hypertension, and atherosclerosis. A 2009 review of animal and cell studies in Alcoholism: Clinical and Experimental Research showed that resveratrol activates SIRT1, an enzyme important for several aspects of lifespan regulation, cellular response to stress, glucose homeostasis, insulin secretion and homeostasis, vascular tone and endothelial dysfunction. The effect of resveratrol on SIRT1 seems to be the mechanism responsible for many of the cardioprotective outcomes. Through its roles in reducing LDL cholesterol, preventing damage done to blood vessels by LDL cholesterol, preventing blood clots, and reducing inflammation that can lead to heart disease, resveratrol has won a lot of attention.

As an antioxidant, resveratrol plays several roles in reducing oxidative stress, possibly preventing the onset or further development of cancer. By increasing nitric oxide bioavailability, resveratrol may reduce oxidative stress to protect against exposure to UV radiation, free radicals, and damage to DNA. Resveratrol has been said to be effective against both precancerous and cancerous cells because of its potential role in attacking free radicals before they become harmful.  The protective effects of resveratrol have been studied in vitro (outside the body in a petri dish) as well as in mice. To date, studies in humans have not shown the same results but resveratrol has the potential to work as a cancer chemoprevention treatment. Resveratrol may also benefit the immune system by aiding the production of cytokines, white blood cells essential for the response to infections in their role in reproduction, growth, immunity, and tolerance. Researchers are still perplexed by the apparent contradiction of resveratrol both serving as a cardioprotective and neuroprotective agent, yet killing cancer cells. It is thought that there are dose-dependent effects and low-dose resveratrol is protective, while high doses initiate cell death signals. However, clinical trial data to support this is not yet available.

Though these findings are exciting, research studies such as these always need to be regarded with caution. Can a resveratrol supplement replace diet and regular exercise? Of course not. Most previous studies have been based on animal studies or cells in culture, while the actual effects could vary in humans. Furthermore, the effects of long-term supplementation are yet unknown. However as the first human study demonstrating the use of resveratrol in alleviating the problems associated with age-related diseases, the results are promising.


  1. Brown et al. The Biological Responses to Resveratrol and Other Polyphenols From Alcoholic Beverages. Alcoholism Clinical and Experimental Research, 2009; DOI: 10.1111/j.1530-0277.2009.00989.x
  2. Timmers, et al. Calorie Restriction-like Effects of 30 Days of Resveratrol Supplementation on Energy Metabolism and Metabolic Profile in Obese Humans. Cell Metabolism, 2011; DOI 10.1016/j.cmet.2011.10.002

Alisha is in her second year at the Friedman School as a dual Nutrition Communications/DPD student and is excited to soon become a Double Jumbo. She is a true California girl, enjoys traveling, trying different types of fitness classes, and attempting to create healthier versions of recipes. Alisha records her recipes she finds blog-worthy at SavortheFlavour.


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