Lifestyle interventions targeted at obtaining/maintaining a healthy body weight and/or incorporating physical activity and healthy eating habits have great potential in improving outcomes in cancer survivors. Cancer diagnosis is a “teachable moment” wherein many patients are highly motivated to make changes (1). Furthermore, a balanced diet and moderate exercise can improve prognosis, quality of life, physical function, and survival across the cancer continuum. As such, groups such as the Amercian Cancer Society, National Comprehensive Cancer Network and the American College of Sports Medicine have released lifestyle guidelines for cancer survivors.

However, implementing changes in individuals and healthcare systems is challenging, to say the least. This is a recent topic covered by Karen Basen-Engquist and a number of colleagues as part of a special Issue of Obesity (Transdisciplinary Research on Energetics and Cancer)(2). Their article provides a 6-point agenda for translating research into clinical and community action, as follows:

  1. Increase the availability of different types of activities for weight management, nutrition counseling, and physical activity. One size will never fit all when it comes to improving health. Individual goals/preference, resources, and logistics all come into play, and cancer-specific programs may be needed.
  2. Improve screening and referral to lifestyle interventions. A system for evaluating and triaging patients for health programs should be developed. Importantly, an individual’s physical status, health needs, and goals should be considered.
  3. Improve the health care provider’s ability to screen, assess, and refer survivors for lifestyle programs. Oncology providers have a powerful role in helping cancer survivors; however, they often do not feel confident in screening, giving advice, or administering recommendations for lifestyle-related constructs. Implementation of processes such as the 5As (Ask, Advise, Assess, Assist, Arrange), which has been successful in tobacco cessation (3) and obesity management (4) might prove beneficial.
  4. Expand the support of oncology-specific professional training and certification. Professional organizations of dietitians, exercise professionals, psychiatrists, and physical therapists have additional certification programs for oncology or are working on developing one for its members. However, professionals with specific expertise in oncology are still greatly needed to address the unique needs of this population.
  5. Expand dissemination and implementation research. Many research programs do not address how a program could be implemented in a real-world setting (external validity). Dissemination of research findings with consideration of the sustainability and generalizability of programs is essential for broader impact.
  6. Advocate for health care policies that support lifestyle services for cancer survivors. Coverage for health programs is highly variable and often has barriers such as large co-payments, no coverage in grandfathered plans, and cost sharing. A potential solution could be incentivizing nutrition and exercise services, although more research is needed to determine the effectiveness of such actions.

As the authors eloquently articulate, the time has come to enable research into action for optimal healthcare in all cancer survivors.

References:

  1. Demark-Wahnefried W, Aziz NM, Rowland JH, Pinto BM. Riding the crest of the teachable moment: promoting long-term health after the diagnosis of cancer. J Clin Oncol 2005;23:5814–30.
  2. Basen-Engquist K, Alfano CM, Maitin-Shepard M, Thomas CA, Schmitz KH, Pinto BM, et al. Agenda for Translating Physical Activity, Nutrition,and Weight Management Interventions for Cancer Survivors into Clinical and Community Practice. Obesity 2017; 25, S9-S22.
  3. Siu AL, Force USPST. Behavioral and pharmacotherapy interventions for tobacco smoking cessation in adults, including pregnant women: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2015;163:622-634.
  4. Rueda-Clausen CF, Benterud E, Bond T, Olszowka R, Vallis MT, Sharma AM. Effect of implementing the 5As of Obesity Management framework on provider-patient interactions in primary care. Clin Obes 2013; 4, 39-44.

 

March 2017 Member Highlight Interview for ASN Nutrition Notes eNewsletter:

Interview with Juan Rivera Dommarco, Director of the National Institutes of Public Health (INSP) of Mexico, President of the Latin American Nutrition Society (SLAN), and Executive Board Member of the Ibero-American Nutrition Foundation (FINUT)

Dr. Rivera is the newly appointed Director of the National Institutes of Public Health, where he has been since 1993. There he founded the Center for Research in Nutrition and Health in 2001. He is also Professor of Nutrition in the School of Public Health of Mexico and Adjunct Professor at Emory University. Dr. Rivera has published more than 400 scientific articles, book chapters, and books, and made more than 500 presentations and conferences at scientific events. He is past recipient of the Kellogg International Nutrition Research Award from ASN, granted for active engagement in research to benefit populations in nonindustrialized countries, as demonstrated through publications in the scientific literature, and actively engaged in training new scientists for international nutrition research.

1. How did you first get involved in nutrition epidemiology and research? What made you interested in the field of nutrition science?

My original motivation was poverty and inequity. Most Latin American Countries, including Mexico have profound inequities. Since childhood, I felt social inequalities were morally wrong. During high school, I read several books about social injustice, including Josue de Castro’s recounts of inequity, and a direct indicator of inequity was hunger and undernutrition. After high school, I spent some time in an indigenous community in Chiapas, where I witnessed poverty very closely. That is when I decided to devote my life to fight undernutrition, hunger, and their health effects. My undergraduate training was in nutrition and food sciences at the Universidad Iberoamericana, a Jesuit University in Mexico City with a mystic about poverty alleviation. I did my internship training with Dr. Joaquín Cravioto, a prominent Mexican scientist interested in undernutrition and mental development. He inspired me to become a nutrition scientist. I started reading the works of Scrimshaw, Habicht, and Martorell at INCAP in Guatemala and I corresponded with Jean-Pierre Habicht, who invited me to visit the Division of Nutritional Sciences at Cornell. After my visit, I decided to undergo postgraduate training in Nutrition at that University.

2. When and why did you first join ASN? What convinced you to join the organization?

I was first introduced to ASN in 1983, while I was a graduate student at Cornell University, and I officially became a member in 1991. My Committee Chair and mentor, Jean-Pierre Habicht, considered as part of the training of his students to attend the then called FASEB Meetings to present the results of our research. As many other of his students, I joined ASN and attended the meetings.

3. What aspects of ASN membership have you found most useful, professionally? What other aspects of your membership do you find useful as your career has progressed?
I appreciate the opportunity to keep up-to-date about new knowledge in the area of global nutrition, along with the high quality of the research results presented and lively discussions at Experimental Biology. I also advocate for ASN journals, in which I have published repeatedly, and I enjoy the opportunity to meet with colleagues and old friends during ASN meetings, where we often discuss new research and explore collaborations. More recently, ASN meetings have exposed my students to high quality works and allowed them to share the results of their studies with other nutrition scientists.

4. What aspects of your research do you foresee being most important for ASN members?

In Mexico, we face the double burden of undernutrition and obesity; therefore, we are conducting research aimed at solving these two problems, which together are of great interest to the Global Nutrition Council and to much of the ASN membership:
 We have been monitoring the magnitude and trends of the double burden of malnutrition in Mexico during the last 30 years through national nutrition surveys.
 We are conducting birth cohort studies looking at the relationship between maternal feeding and weight status and gain during gestation, as well as infant feeding practices and several outcomes at different points in time during childhood and adolescence, including appetite and satiety, growth, weight gain, cardiometabolic risks, and neurodevelopment.
 We are also generating knowledge for the design of policies for the prevention and control of the double burden of malnutrition, including programs for the prevention for stunting, anemia, and micronutrient deficiencies and policies for the prevention and control of obesity, including fiscal measures and school regulations, among others.
 Finally, we are conducting evaluations of the effects of several programs and policies applied by the Government for the prevention and control of the double burden of malnutrition.

5. Can you tell us more about your current position and the research activities in which you are involved?

On February 16, I was appointed as Director General of the Mexican National Public Health Institute (INSP), the research and training institution that houses the Mexican School of Public Health. We conduct research in several public health topics including: nutrition, obesity and non-communicable chronic diseases, infectious diseases, environmental health, health systems research, reproductive health, health promotion, etc. and we offer twenty-eight Masters and PhD programs. We have around 1,200 employees and close to 500 students in three campuses. I am personally involved in the research activities mentioned above: monitoring the double burden in the population, birth cohort studies to assess the effects of infant feeding practices, generation knowledge for the design of policies for the prevention and control of the double burden, and evaluating the effects of some of those policies applied by the Government.

6. What do you feel are the biggest challenges facing nutrition researchers today? Are there any areas where you would like to see more research?

One of the biggest challenges in Public Health Nutrition is translating research results into clinical and public health large-scale interventions and their rigorous evaluation for further improvement. To do this we need research from subcellular particles (molecular biology) to programs and policy. This includes linking the wealth of information coming from basic research, particularly from molecular biology, to clinical and public health innovative actions. We also need to study the drivers and determinants of the double burden of malnutrition and its health and environmental consequences using a systems approach, since nutrition problems are multifactorial and complex. We need to understand the food system but also the factors influencing behaviors (food and physical activity). We also need to study how to influence sound policy-making, including the roles of direct advising to policy makers and of social mobilization to generate demand for policy. Finally, we need to conduct rigorous evaluations in order to inform policy makers about improvements in current policies.
March 2017 ASN Nutrition Notes Member Highlight
Interview with Dr. Juan Rivera Dommarco – Page 3

7. Is there anything else you’d like to tell ASN members, especially students and postdocs?

To Students and postdocs: The phrase “First do no harm” (Latin Primum non nocere) is believed to have been part of the original Hippocratic oath taken by physicians. We nutritionists do not take a similar oath, but we should. You have the privilege to be a fraction of people in the world who have access to postgraduate training. You chose Nutritional Sciences, a field that can have a profound impact on the health and wellbeing of millions of people. You should be generous, because life has been generous to you. You should pay back to those in poverty, to the neediest persons in the world, for the privilege to have reached postgraduate training, in an activity that can change the lives of many. However, most importantly, do not harm the nutrition and health of people by promoting or endorsing unhealthy food and beverage products. To the general ASN membership, I would like to invite you to attend the SLAN Congress in Mexico in late 2018, showcasing the best nutrition research from Mexico and Latin America.

Dr. Rivera’s research interests include the epidemiology of stunting (under-nutrition and obesity), the short- and long-term effects of under-nutrition during early childhood, the effects of zinc and other micronutrient deficiencies on growth and health, the study of malnutrition in Mexico, and the design and evaluation of policies and programs to improve nutritional status of populations.

Student Blogger for Global Nutrition Council at ASN’s Scientific Sessions and Annual Meeting at EB 2016

By: Sheela Sinharoy, MPH

A symposium called Biology of Linear Growth on Tuesday examined linear growth from the molecular to the population level, bringing perspectives from biology, physical anthropology, nutrition, and epidemiology

Are you familiar with the process of endochondral ossification? Julian Lui, MD PhD explained that this is the process that results in linear growth. It takes place in the growth plates, at the end of long bones such as the femur, and is subject to systemic regulation by endocrine, nutritional, and inflammatory cytokine factors as well as local regulation by paracrine factors and other cellular mechanisms. Malnourished children have lower levels of hormones like insulin-like growth factor 1 (IGF-1) and estrogen, as well as increased levels of glucocorticoids, leading to decreased linear growth. Dr. Liu explained that this allows the body to conserve resources and that, in situations of food insecurity, “Growth is something of a luxury that can be postponed until better times.”

Rather than growing continuously, children grow in saltations, meaning that – as many a parent has observed – a child may grow substantially overnight and then not at all for a number of days afterwards. Michelle Lampl, MD PhD stated that as children age, these saltations become less and less frequent, with older children growing much less often than infants. The amount and frequency of these growth saltations can be affected by environmental factors, which can interact with cellular effects. Maternal smoking, for example, has a well-documented inhibitory effect on growth, as does maternal alcohol consumption and stress.

Since linear growth happens most rapidly in early life, the first 1,000 days from conception to two years of age are considered a critical period. Parul Christian, DrPH presented results from a meta-analysis analyzing various maternal and child nutrition interventions targeting this 1,000-day window. Starting during pregnancy, balanced protein-energy, iron-folic acid, and multiple micronutrient supplementation were all found to increase birth weight. However, maternal supplementation during pregnancy was not associated with any long-term linear growth in children under five years old. For infants and young children, nutrition promotion and food supplementation showed promise as interventions with positive impacts on child height.

In the final talk of the symposium, Aryeh Stein, PhD addressed the question of linear catch-up growth: for those children whose growth has been suppressed by malnutrition, is it possible to catch up on missed growth, even after the first 1,000 days? A number of studies have provided different nutrients and foods to children ages two and older. Dr. Stein presented results from studies of protein, zinc, iron, iodine, calcium, multiple micronutrients, and food. Protein and some of the micronutrients may have promise, but several of the calcium studies reported negative effects, while food had no association with growth.

The symposium made it clear that nutrition has an important role to play in stimulating or inhibiting linear growth. However, a great deal remains to be learned about these complex biological processes and the most effective interventions to promote children’s optimal growth.

By Allison Dostal, PhD

Gastrointestinal problems are one of the most common unpleasant issues that we all experience at some time or another. But what if your upset stomach wasn’t just a passing discomfort? What if severe abdominal pain, cramping, fatigue, and diarrhea became more of your norm and less of a passing annoyance? For more than 1.4 million Americans, these symptoms typify their experience with inflammatory bowel disease (IBD), a disorder characterized by chronic inflammation of the gastrointestinal (GI) tract. The specific cause (or causes) of IBD remain unknown, but one leading hypothesis is that the bacteria that inhabit our GI system – termed the gut microbiome – play a central role. In this post, we’ll take a closer look at this condition and highlight research aimed at elucidating the impact of the microbiome in IBD development, progression, and treatment.

Characteristics, Diagnosis, and Treatment of IBD

Inflammatory bowel disease is unique in that its symptoms vary from person to person, and an individual’s own experience with their condition can differ markedly from another affected person. Most people are diagnosed with one of the two most common types of IBD, which are ulcerative colitis (UC) and Crohn’s disease (CD). The primary distinguishing factor between the subtypes is that in UC, symptoms are limited to the colon. In contrast, any part of the GI tract – from the mouth to the anus – can be affected in CD. In addition, UC only involves the innermost layer of the colon, while CD can extend deeper into the cell layers of the GI tract. Lastly, in CD, the inflammation can “skip”, leaving normal areas between patches of affected GI tract.

Making a clear IBD diagnosis isn’t always as easy as meeting – or not meeting – these criteria. There is no gold standard available for a clear-cut diagnosis, and 5-15% of cases do not meet strict criteria for either UC or CD. These patients fall into the “IBD type unclassified” (IBDU) group. And in up to 14% of patients, the diagnosis changes over time. Despite the difficulty in specific diagnosis, all subtypes of IBD have one strong feature in common: an abnormal response by the body’s immune system. The immune system is composed of various cells and proteins that usually protect our bodies from infection. However, in people suffering from IBD, the immune system reacts inappropriately, and mistakes benign or beneficial cells and bacteria for harmful foreign substances. When this happens, the immune system produces an inflammatory response within the GI tract and produces the symptoms of IBD. This adverse reaction is termed a “flare”, and can result in symptoms such as abdominal pain and cramping, diarrhea, fever, and blood in the stool. People with IBD often have deficiencies in vitamins, minerals and macronutrients stemming from loss of appetite, reduced food intake, and malabsorption from the GI tract. The lack of nutrients can lead to worsening of symptoms or development of new complications.

Treatment for IBD is centered around two goals: achievement of remission and prevention of flares. Anti-inflammatory drugs such as aminosalicylates and antibiotics are often the first line of treatment, and can be followed by corticosteroids, immunomodulators, and/or biologic agents. In severe cases, removal of the affected part of the GI tract is needed if a patient is not responsive to other treatments.

The Role of the Microbiome in IBD

In recent years, it has become clear that the microbes in our gut have a key role in IBD, but the bacteria involved and their associated functions remain largely unknown. An imbalance of the normal gut bactera due to loss or overabundance of certain species is important in the persistence of the inflammatory responses seen in IBD. The role of the gut microbiota in IBD pathogenesis has been demonstrated by studies showing that antibiotic use can reduce or prevent inflammation – antibiotics work by reducing the number and types of bacteria found in the gut, therefore killing microbes that are causing IBD symptoms. Also, results from studies with UC patients who underwent a transfer of stool collected from healthy donors – called a fecal microbiota transplant – had notable disease remission. However, results have not been consistent between studies, due to differences in populations studied, official diagnosis, treatment methods and doses, and methods of assessing study endpoints. Therefore, no consensus on the microbiome’s relationship to IBD has been reached.

Research Endeavors

As you can imagine, the combination of unpleasant, potentially severe symptoms and an uncertain diagnosis or treatment can result in significant stress on IBD sufferers, their caregivers, and health care providers. The scientific efforts dedicated to identifying causes and cures for IBD have rapidly expanded in recent years due to advances in technology that allow researchers to work toward refining a clear diagnosis, map specific gut bacteria associated with disease development and symptoms, and identify defined targets for therapy. One of these initiatives is the Crohn’s and Colitis Foundation of America (CCFA) Microbiome Initiative, which is dedicated to understanding the role of the gut microbes in IBD, IBD families, and disease flares. Thus far, there are 7 active projects and 30 published manuscripts stemming from the Initiative, which have determined that different subsets of IBD are characterized by signature bacterial compositions and that people carrying different IBD genes have different microbiome compositions, among other accomplishments.

Other organizations are also supporting IBD research endeavors, including the Kenneth Rainin Foundation, whose Innovator Awards program provides $100,000 grants for one-year research projects conducted at non-profit research institutions, and the NIH’s Human Microbiome Project, which has funded several projects aimed at genetic and metabolomic elucidation of risk for Crohn’s disease. Several randomized trials are ongoing at this time, and their results will inform future directions for diagnosis, treatment, and eventual resolution of IBD.

References

Borody TJ, Warren EF, Leis SM, Surace R, Ashman O, Siarakas S. Bacteriotherapy using fecal flora: toying with human motions. J Clin Gastroenterol.2004;38(6):475–483.

Bull MJ, Plummer NT. Part 1: The Human Gut Microbiome in Health and Disease. Integr Med. 2014 Dec; 13(6):17-22.

Crohn’s and Colitis Foundation of America:http://www.ccfa.org/

Swidsinski A, Weber J, Loening-Baucke V, Hale LP, Lochs H. Spatial organization and composition of the mucosal flora in patients with inflammatory bowel disease.J Clin Microbiol. 2005;43(7):3380–3389.

Tontini GE, Vecchi M, Pastorelli L, Neurath MF, Neumann H. Differential diagnosis in inflammatory bowel disease colitis: state of the art and future perspectives. World J Gastroenterol. 2015 Jan 7;21(1):21-46.

By Celez Suratos, MS, RD, ACCN15 Blogger

An individual only needs two things to easily access a myriad of information: a device that has the ability to connect to the internet, and an internet connection. Such information may be as simple as finding nearby show times for a movie, or something more complex, such as trying to self-diagnosis when exhibiting symptoms of a particular disease. This concept is the same when it comes to how the general public may be finding nutrition information. Along with the ease of access of internet searches however, is a high potential of inaccurate or incomplete nutrition information that’s widely distributed.

This can be further exhibited when it comes to myths surrounding carbohydrate (CHO) intake in people with diabetes mellitus (DM). DM is a complex disease in and of itself.Add the ever-evolving nutrition recommendations, such as the diabetic exchange list, glycemic index, and CHO counting into the mix, and one may be more sympathetic as to why a patient may struggle with compliance and management of his or her diabetes.

Alison Evert, MS, RD, CDE from the University of Washington Medical Center approached some of the frequent concerns that arise from patients and healthcare providers when it comes to DM and CHO intake at the 2015 Advances and Controversies in Clinical Nutrition conference. From the presentation and based on a 2005 Dietary Reference Intake report, individuals need to consume at least approximately 139 gram (g) of CHO per day (this does not include creating glucose through pathophysiological processes, such as gluconeogenesis) in order to meet minimum obligatory glucose needs. Ms. Evert reports recent data of median intake of CHO as 220-330 g/day by men and 180-230 g/day by women. Moreover, data from a 2014 National Health and Nutrition Examination Survey (NHANES) reports that adults (20 years and older) without diabetes consume 48 to 50 percent of their daily calories from CHOs. This information tells consumers that intake of CHOs is a necessity, whether or not he or she has DM. It also communicates to nutrition educators that there may not be an ideal percentage of calories that should be consumed from a single macronutrient.

This begs the question, is current and best practice to make percentage recommendations of macronutrient intake based off of total calories, or is this an archaic and irrelevant practice? During her session, Ms. Evert reflected on her time as a dietetic intern in which she made specific calculations on g of CHO a diabetic should consume per day, and passed on a meal plan to patients based on this information. Imagine trying to explain a generic serving recommendation, such as “eat 13 to 17 servings of CHO per day” to an ill and perhaps non-compliant, underserved, or even under-educated patient.

The take-away message Ms. Evert’s presentation is that patients with DM need individualized nutrition recommendations/meals plans, particularly as there are major differences in type 1 versus type 2 DM, the spectrum of type 2 DM progression among patients, and medications that affect glycemic control. Her suggestion – make it a point to discuss what our food sources of CHO are and focus on lifestyle behavior change.

By Caitlin Dow, PhD

If you’ve spent any time on the internet in the last couple of months, you’ve likely heard about the recent statement on red and processed meat from the World Health Organization (WHO).The statement was produced by a Working Group of 22 scientists who gathered together at the International Agency for Research on Cancer (IARC), with the goal of considering all data from over 800 epidemiological studies on red and processed meat in order to determine their potential carcinogenicity. The group defines red meat as “mammalian muscle meat – such as beef, veal, pork, lamb, mutton, horse, or goat” and processed meat as “meat that has been transformed through salting, curing, fermentation, smoking, or other processes to enhance flavour or improve preservation” (1). Based on the available data, the Working Group concluded that “that there is sufficient evidence in human beings for the carcinogenicity of the consumption of processed meat.” And then the internet exploded. But what exactly does this mean?

The IARC is responsible for categorizing chemical compounds based on the strength of evidence that said chemical may be carcinogenic. In this statement, they categorized processed meat as a Group 1 carcinogen and red meat as a Group 2B carcinogen.These categorizations are used to describe the strength of evidence that these compounds may be carcinogens; thus, Group 1 is used to distinguish “established carcinogens” [e.g. acetaldehyde (a metabolite of alcohol), oral contraceptives, formaldehyde, and sawdust], whereas Group 2B includes compounds that are considered “possible carcinogens” [e.g. benzofuran (a compound in coal tar), butylated hydroxyanisole (an additive found in foods, cosmetics, rubber, etc.)] (2).And while these classifications are important, they are easily misconstrued, as was the case in this statement by the IARC. These classifications simply tell us that a compound could be hazardous to human health. What they don’t tell us is degree of risk.That’s important because lots of things can be hazardous without posing a significant risk.For example, UV radiation is a hazard, but it is only a risk if one is exposed to excessive amounts of UV radiation.That is, risk is the product of hazard multiplied by exposure. Reduce your exposure, reduce your risk. That’s where most people got confused with this IARC statement.

The media jumped on the statement and let out a warcry against red and processed meats.But what most of them failed to mention is the all-important question: how much red and processed meat need be consumed to increase risk for developing cancer? One meta-analysis found that risk of colorectal cancer increased with increasing intake of red and processed meats up to 140 g/day (~5 oz/day) (3). Further, risk of developing colon cancer in response to consuming red/processed meat increases by ~25% for every additional 100g consumed/day. Thus, this study was evaluating risk in consumers who eat A LOT of red and processed meats.Importantly, these effects were strongest in European (29% elevated risk/100 g/day increase in intake) compared to North American (11% elevated risk/100 g/day increase in intake) and especially to Asia-Pacific studies that observed a non-significantly reduced risk (6% reduced risk/100 g/day increase in intake). These results indicate that not all populations are equally affected, which is likely due to differences in genetics and/or lifestyle. And what about people who don’t even eat red/processed meat everyday? Are they at risk just by eating these foods once in awhile? A meta-analysis by Norat, et al. (4) estimated that reducing red meat consumption to 70 g/week (~one 3 oz. serving/week) would reduce colorectal cancer rates by 7-24% in regions with high intake.That is, eating red or processed meat once a week likely does not increase risk for colorectal cancer.

At the end of the day, the IARC added processed and red meat to their list of carcinogens.But in terms of translating that into a public health message, they didn’t do a great job.Yes, red and processed meats are hazards to health. If you choose to eat them, keep your exposure low and your risk will likely also be low. As always, eat a varied diet, high in fruits and vegetables, whole grains, legumes, nuts and seeds to ensure high antioxidant and anti-inflammatory compound intake to protect against potential damage that red and processed meats may pose.

References

1.Bouvard, et al. on behalf of the International Agency for Research on Cancer Monograph Working Group.Carcinogenicity of consumption of red and processed meat. Lancet: Oncology. 2015 Dec;16(16):1599-1600.

2.American Cancer Society. Known and Probably Human Carginogens. http://www.cancer.org/cancer/cancercauses/othercarcinogens/generalinformationaboutcarcinogens/known-and-probable-human-carcinogens. 2015 Oct.

3.Chan DS, et al. Red and Processed Meat and Colorectal Cancer Incidence: Meta-Analysis of Prospective Studies. PLoS One. 2011;6(6):e20456.

4.Norat T, et al. Meat consumption and colorectal cancer risk: dose-response meta-analysis of epidemiological studies. Int J Cancer. 2002 Mar;98(2):241-56.

By: Emma Partridge, MS Candidate

Green tea contains a high concentration of polyphenols, most of which are flavanols. Flavanols are commonly known as catechins, the most active catechin being epigallocatechin-3-gallate (EGCG).1 Within the world of nutrition, green tea is consistently touted as a beverage with a plethora of health benefits. These benefits are far-reaching and specific roles of green tea have been identified to improve symptoms or reverse disease damage amongst people with autoimmune disease, heart disease, cancer, liver disorders, smoking complications, chronic inflammation, and more. The roles of green tea often overlap and while green tea consumption is important for those with various diseases, the consumption of green tea by healthy individuals may be integral in the prevention of many of the following diseases.

Chronic Inflammatory Disease
EGCG may be most important flavanol when it comes to inflammation control.2 EGCG has been shown to suppress the production of cytokines, pro-inflammatory mediators. Suppressing cytokines decreases long-term inflammation and has been shown to improve inflammation-related symptoms in arthritis models.3,4

Autoimmune Disease
In addition to helping to control the chronic inflammation associated with most autoimmune diseases, EGCG has been shown to suppress auto-reactive T cell proliferation. Auto-reactive T cells act against the body, resulting in various forms of autoimmune diseases. EGCG may also help to regulate T-helper cell balance, which may decrease the pathogenesis of arthritic diseases, especially rheumatoid arthritis.3

Type 2 Diabetes Risk
Type 2 Diabetes is sweeping America, and food production practices, availability, and affordability are making it harder for people to access healthy options. The ease of accessing and affording unhealthy foods is increasing the risk of diabetes among populations. Green tea, as well as coffee, has been associated with lowering the risk of type 2 diabetes, though the mechanism is unknown and the data inconsistent. However, in a study of 40,000+ people followed for 10 years, researchers found that daily consumption of at least three cups of coffee or tea may lower type 2 diabetes risk.5

Heart Disease & Stroke Risk
In an article published by the American Heart Association, researchers found that people who drank two to three cups of green tea per day had a 14% lower risk of stoke.6 The research on green tea and stroke risk comes on the wake of multiple studies finding links between green tea and heart health. Multiple studies found green tea consumption to lower risk of death from heart attacks by 26% and lower risk of coronary artery disease by 28%.7

Cancer & Tumor Growth
Cancer is a leading cause of death in the United States, behind heart disease. Green tea has already been shown to be beneficial in preventing the leading cause of death; now studies have now shown that the EGCG may affect transformed cells by inhibiting the growth of certain cell lines, inducing apoptosis, and altering gene expression to prevent transformed cells from becoming cancerous.8

Smoking
The polyphenols in green tea have shown to work against carcinogens, while the antioxidant effects may reverse endothelial dysfunction in healthy smokers.8 The reversal of endothelial dysfunction in smokers is important because it plays a role in the pathogenesis of atherosclerosis and cardiovascular disease.9

Liver Disease
Green tea’s aforementioned anti-carcinogenic affect may play a role in preventing liver disease. Active polyphenols detoxify reactive oxygen species, preventing oxygen free radicals from destroying hepatocytes and causing oxidative DNA damage. Multiple studies have shown that, most likely via this method, green tea intake can attenuate liver disease or liver cancer.10

Weight Loss & Weight Maintenance
Green tea’s affect on weight loss may be attributed to two components: EGCG and caffeine. Caffeine alone does play some role in increasing energy expenditure, but when combined with EGCG, the mixture stimulates energy expenditure and fat oxidation to a greater degree. This may trigger weight loss, and additional evidence reveals that continual green tea consumption can further help to maintain weight.11

In determining whether or not green tea is for you, the answer is likely yes. While there are risks by way of overconsumption, a few glasses a day has been shown to be beneficial for the all-around healthy person in preventing disease and for the person suffering from various diseases or ailments.

1.Ehrlich SD. Green Tea. 2011; http://umm.edu/health/medical/altmed/herb/green-tea.
2.Hamer M. The beneficial effects of tea on immune function and inflammation: a review of evidence from in vitro, animal, and human research. Nutrition Research. 2007;27(7):373-379.
3.Wu DY, Wang JP, Pae M, Meydani SN. Green tea EGCG, T cells, and T cell-mediated autoimmune diseases. Molecular Aspects of Medicine. 2012;33(1):107-118.
4.Kim HR, Rajaiah R, Wu QL, et al. Green Tea Protects Rats against Autoimmune Arthritis by Modulating Disease-Related Immune Events. Journal of Nutrition. 2008;138(11):2111-2116.
5.van Dieren S, Uiterwaal C, van der Schouw YT, et al. Coffee and tea consumption and risk of type 2 diabetes. Diabetologia. 2009;52(12):2561-2569.
6.Green tea, coffee may help lower stroke risk. 2013; http://newsroom.heart.org/news/green-tea-coffee-may-help-lower-stroke-risk.
7.Green tea may lower heart disease risk. Harvard Heart Letter 2012; http://www.health.harvard.edu/heart-health/green-tea-may-lower-heart-disease-risk.
8.Chen ZP, Schell JB, Ho CT, Chen KY. Green tea epigallocatechin gallate shows a pronounced growth inhibitory effect on cancerous cells but not on their normal counterparts. Cancer Letters. 1998;129(2):173-179.
9.Nagaya N, Yamamoto H, Uematsu M, et al. Green tea reverses endothelial dysfunction in healthy smokers. Heart. 2004;90(12):1485-1486.
10.Jin X, Zheng R-h, Li Y-m. Green tea consumption and liver disease: a systematic review. Liver International. 2008;28(7):990-996.
11.Hursel R, Viechtbauer W, Westerterp-Plantenga MS. The effects of green tea on weight loss and weight maintenance: a meta-analysis. International Journal of Obesity. 2009;33(9):956-961.

By Marion Roche, PhD

The target set out by the World Health Assembly is to reduce the anemia in all women of reproductive age by 50% by 2025. Women make up about 3.5 billion in population on our planet. In order to reach this World Health Assembly target, it will be essential to address anemia in the 600 million adolescent girls in the world and recently their nutrition has been getting more attention.

The global birth rate has declined over the past decade, except when analyzing the rate for adolescent girls, with 17-20 million adolescent pregnancies per year. Eleven percent of all pregnancies are to adolescents and 95% of these adolescent pregnancies are occurring in developing countries.

Complications from pregnancy and child birth are the second greatest contributor to mortality for girls 15-19 years of age. Young maternal age increases the risk for anemia during pregnancy, yet adolescent women are less likely to be covered by health services, including micronutrient supplementation, than older women. Compared with older mothers, pregnancy during adolescence is associated with a 50% increased risk of stillbirths and neonatal deaths, and greater risk of preterm birth, low birth weight and small for gestational age (SGA) (Bhutta et al, 2013; Kozuki et al, 2013; Gibbs et al, 2012).

Reducing anemia in adolescents is often motivated by efforts to improve maternal and newborn health outcomes for pregnant adolescents; however, benefits for improving adolescent school performance and productivity at work and in their personal lives should also be valued.

Globally, iron deficiency anaemia is the third most important cause of lost disability adjusted life years (DALYs) in adolescents worldwide at 3%, behind alcohol and unsafe sex (Sawyer et al, 2012).

Adolescents have among the highest energy needs in their diets, yet in developing countries many of them struggle to meet their micronutrient needs. The World Health Organization recommends intermittent or weekly Iron Folic Acid Supplements for non-pregnant women of reproductive age, including adolescent girls. IFA supplementation programs have often been designed to be delivered through the existing health systems, without specific strategies for reaching adolescent girls.

I have heard adolescence referred to as “the awkward years” when individuals explore self-expression and autonomy, but it is also definitely an awkward period for public health services in terms of delivering nutrition, as we often fail to reach this age group.

There have been examples of programs going beyond the health system to reach adolescent girls, such as through schools, peer outreach, factory settings where adolescents work in some countries and even sales in private pharmacies to target middle and upper income adolescent girls.
The Micronutrient Initiative implemented a pilot project with promising results in Chhattisgarh, India where teachers distributed the IFA supplements to 66,709 female students once per week during the school year over a 2 year pilot.

It was new for the schools to become involved in distribution of health commodities, but engaged teachers proved to be effective advocates. There were also efforts to reach the even more vulnerable out of school girls through the integrated child development centers, yet this proved to be a more challenging group of adolescents to reach. Peer to peer outreach by the school girls offered a potential strategy. The current project is being scaled up to reach over 3.5 million school girls.

Adolescent girls have much to offer to their friends, families and communities beyond being potential future mothers. It is time to get them the nutrients they need to thrive in school, work and life.

By Kevin Klatt

Colorectal cancers are the third most common worldwide, and represent one of the major areas of prevention research. Rates of these cancers increase with industrialization, and are uncommon in Africa and much of Asia. A number of potential nutritional targets have been posited, based on preclinical and epidemiological data; however, these remain controversial. The American Institute of Cancer Research’s 2011 report (1) on Colorectal Cancer states that there is convincing evidence that foods high in fiber decrease risk and red and processed meats increase risk of colon cancer. However, there are few controlled feeding studies in humans have corroborated these associations; indeed, a large body of literature (2-7) focusing on dietary fiber supplementation back in the late 90’s and early 2000’s did not show any support for any positive effects of high fiber/low-fat diets on recurrent adenomas . However, these studies can/have been criticized for: 1. not being long enough 2. fail to capture of a window of true prevention (as subjects already had adenomas) 3. The dose/type of fiber. Since these trials, considerable experimental data (8,9) has been generated to suggest that the type of fiber, its dose, and the type/amount of short chain fatty acid fermentation products likely add some complexity to the inconsistent epidemiological associations between fiber intake and colorectal cancer risk.

A recent study published in Nature Communications (10) provides a novel perspective on this contentious topic of high-fiber diets and colon. The study employed a food-based dietary intervention in 2 populations: African Americans and rural South Africans (a sensible population to study given Burkitt’s original observations that rural Africans are nearly free of large bowel diseases). Twenty healthy, middle-aged African Americans and 20 rural Africans were first examine in their home environments for 2 weeks, to examine their normal food intake, before being housed in their respective research facilities for the 2 weeks of the dietary intervention (to ensure compliance). African Americans were given the ‘African style’ diet that was low in fat (16% kcals) and high in fiber (55g/day). Participants from Africa were given a western style diet that was higher in fat (52% kcals) and lower in fiber (12g/day). Notably, the high fiber diet was achieved using HiMaize, a purified resistant starch product. The authors look at outcomes related to mucosal epithelial cell proliferation (Ki67 staining) and markers of inflammation (CD3+ intraepithelial lymphocyte and CD68+ lamina propria macrophage staining), to examine the effect of diet on predicted neoplastic change and increased risk of colon cancer. They further look at alterations in microbial composition, highlighting changes in microbes with the baiCD gene, responsible for the deconjugation of bile acids and production of their carcinogenic, secondary metabolites. Their results quite nicely show that the high fiber intervention alters biomarkers in directions that suggest a protective effect against colorectal cancer, while also finding some interesting nuances related to amino acid and choline metabolism.

While providing encouraging results for the role of nutrition in colorectal cancer development, the study leaves us with more hypotheses to test, and a renewed interest in the way in which fiber and its fermentative products might act to buffer against colorectal cancer. Without hard clinical outcomes, it’s difficult to get too excited about the results in light of the multiple fiber interventions that have failed in the past. The biomarkers chosen are not without their scrutiny, as it has been noted that decreases in apoptosis rather than increased cell proliferation better predict tumorigenesis in animal models of colorectal cancer (11). Regardless of one’s enthusiasm about biomarker changes over 2 weeks, it does force us to critically think about previous study designs that have cast doubt on fiber’s role in colon cancer. The authors in this current study employ highly butyrogenic starches, at doses not tested in the trials that have failed before. There is consistent molecular evidence that butyrate works in a paradoxical manner, both stimulating cell proliferation at low concentrations and inhibiting it at high (12), leaving open the possibility that the previous doses of fiber were too low to see a beneficial effect.

Given the Western diets low concentrations of dietary fiber, particularly resistant starches (13), as well as the increased enthusiasm to fortify the food supply with added fibers, further research examining the role of particular fibers, their appropriate doses, and their relationship to clinical outcomes appear warranted. The type 2 resistant starch utilized in this study is uncommon in the food supply, coming largely from raw potatoes, unripe bananas, and some legumes and represents a potential area for food technologists to significantly alter the food supply for better health (14).

References
1. http://www.aicr.org/continuous-update-project/colorectal-cancer.html
2. http://www.ncbi.nlm.nih.gov/pubmed/11073017
3. http://www.ncbi.nlm.nih.gov/pubmed/10770979
4. http://www.ncbi.nlm.nih.gov/pubmed/10770980
5. http://www.ncbi.nlm.nih.gov/pubmed/7730878
6. http://www.ncbi.nlm.nih.gov/pubmed/7473832
7. http://www.nejm.org/doi/pdf/10.1056/NEJM199901213400301
8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926973/
9. http://www.ncbi.nlm.nih.gov/pubmed/20937167
10. http://www.nature.com/ncomms/2015/150428/ncomms7342/full/ncomms7342.html
11. http://carcin.oxfordjournals.org/content/18/4/721.abstract
12. http://jn.nutrition.org/content/134/2/479.full
13. http://linkinghub.elsevier.com/retrieve/pii/S0002-8223(07)01932-3
14. http://advances.nutrition.org/content/4/3/351S.full

By Teresa L. Johnson, MSPH, RD

W. Allan Walker, MD, and Emeran Mayer, MD chaired a symposium during ASN’s Scientific Sessions and Annual Meeting on March 30 that considered the role the gut microbiome plays in human behavior.

Mark Lyte, PhD, MS, a professor at Texas Tech University, provided insights into aspects of gut-brain communication pathways. He introduced the idea that gut bacteria, as neuroendocrine organisms, are more interactive with their human hosts than previously believed. Lyte then pointed out that the gut is highly innervated, and information flows in a bi-directional but asymmetrical fashion between the gut and the brain, with as much as 90 percent of the information flowing from the gut. He suggested that neuroendocrine chemicals naturally present in foods might influence gut bacteria responses, and mechanisms that were previously considered immunological might be neuroendocrinal instead. The take-home message, Lyte said, was that these food-derived neurochemicals, when absorbed in gut, likely interact with the microbiota. In response, the microbiota produce neurochemicals that affect behavior and cognition in a sort of feedback loop. He cautioned that much of the data are correlational, and causation cannot be assigned.

Sarkis Mazmanian, PhD, California Institute of Technology, focused his remarks on specific molecular communications between the gut and brain. He explained that our bodies are in contact with trillions of microbes. “This microbial fingerprint has effects on many aspects of our biology,” said Mazmanian. He noted that in recent decades, the prevalence of autism spectrum disorder (ASD) has increased dramatically, and he presented data demonstrating that in rodents, maternal immune activation during pregnancy yields offspring with ASD and dysbiosis, suggesting a possible gut-microbiome-brain connection in ASD.

Premysl Bercik, MD, a gastroenterologist and associate professor at McMaster University, noted that while individuals with inflammatory bowel disorders commonly have abnormal gut function and low-grade inflammation, they also experience psychiatric comorbidities such as depression, stress, and anxiety. The trigger for this chain of events has not been identified, Bercik said, but some have hypothesized that infections or abnormal gut flora might be responsible. He then presented data from animal models that demonstrate the bi-directional communication between the gut and brain, and described recent research indicating that both microbial and host factors influence behavior.

Mayer, a professor at the David Geffen School of Medicine at UCLA, began his presentation with a historical perspective on the perceived gut-brain connection, which dates back several millennia. He then described notable limitations to using rodent models to study the gut-brain connection due to structural differences between rodent and human brains, and added that the germ-free mouse, a common model for understanding gut microbiome function, introduces many confounders into the research due to its altered metabolism. Mayer presented data that indicate that pre- and post-natal stress alters the gut microbiome in animals, as evidenced by both behavioral and biological changes, and he raised the idea that the gut microbial organization might influence brain structure. Attempts to modulate behavior with probiotics are promising, Mayer said, because intake blunts the reactivity of several internal organs, including those in the gut. Mayer concluded his presentation by cautioning that although enthusiasm to extrapolate findings from rodent models to human conditions including obesity, autism, and others is high, many questions remain about the role the gut microbiome plays in human health.