A Conversation with ASN Executive Officer John E. Courtney, PhD
By Teresa L. Johnson, MSPH, RD

The smile on Dr. John Courtney’s face says it all: ASN’s Scientific Sessions and Annual Meeting at EB 2015 is the place to be. Courtney, who is in his ninth year as ASN’s Executive Officer, sat down with me on a sunny afternoon in Boston and chatted about the meeting and ASN’s current and future status.

TJ: What’s your favorite thing about ASN’s Annual Meeting?
JC: It’s so great for bringing together the wide, diverse audience of ASN in one central convening area. We have members in basic, clinical, and translational nutrition, and they’re housed in academia, medicine, practice, and industry. So it’s exciting to give people an opportunity to develop and build partnerships and work together, not only to advance the science but their personal careers too.

TJ: Tell me about the changes ASN members can expect to see in 2018.
JC: ASN will convene a nutrition-focused Scientific Sessions and Annual Meeting for three years beginning in 2018. EB has been a great forum for people to work within, but we think that having a nutrition-focused meeting brings together members of the nutrition science community where they can all meet and convene. It will be a smaller meeting so it will be more open to networking, less confusing, and have less competition for scheduling to allow productive connections. I envision us having a lot more flexibility in how we structure our meeting. We’ll probably do it outside the academic year, and we’ll do it in a cool place!

TJ: What are you hearing from the members regarding this change?
JC: There’s been great support from our members, and a lot of excitement. Of course, our current president, Dr. Simin Nikbin Meydani (pictured below with Dr. Courtney) of Jean Mayer USDA HNRCA at Tufts University, is a fantastic leader with great skills in consensus-building. If you make changes, you really have to go the extra mile in seeking input and cultivating agreement, and she’s done that.

TJ: How will ASN maintain the same level of quality in its meeting?
JC: A lot of questions have been raised about how we can do it the best way. Some people are concerned because they like the EB model—they like the “cross-fertilization” of scientific disciplines—so one of the things we’re hearing loud and clear is that we need to keep that cross-fertilization. So we’ll offer programming that meets all the segments of ASN’s needs.

TJ: What will be unique about ASN’s meeting?
JC: I see us having a lot of different types of activities. We can take a look at how to offer sessions that reach out to the public. Right now we reach the researchers and the practitioners, but we want to take that next leap and start to engage the public.

We’re also planning sessions that are unrelated to nutrition. Maybe we’ll hear about the newest, hottest thing in the future of information technology or the potential role that robotics can play in personalized health!

Perhaps we’ll have an inspirational session that brings in that spectacular leader or renowned speaker who says, “This is what the world is going to look like in 2050,” and asks, “How can people working in nutrition prepare for the challenges and the opportunities that will be taking place then?”

TJ: How is ASN poised to address the next five years?
JC: We have a strategic map that focuses on positioning ASN as the global authoritative leader in nutrition science. We have an actionable dashboard that identifies what our key problematic areas are and we’ve developed strategies that fit and help us meet those challenges.

For example, one of the exciting strategies that our incoming president Dr. Patrick Stover, Cornell University, wants to focus on is positioning ASN for 2028—the 100th anniversary for the Society. So, rather than looking at what we want to be in five years, we’re asking what we want to do and be in 2028; then we’re breaking it into chunks that will get us there. We’re looking at an endpoint to best add the most value.

TJ: What kinds of initiatives do you anticipate ASN will launch here in the US and abroad?
JC: I expect we’ll have a lot more topical meetings throughout the world. We have meetings now in the Middle East, Central and South America, and Asia, but I see us really taking off so that ASN will have a presence in every major continent in the next five years. Although we have that presence now with members, we don’t offer a lot of programming outside of the States so that’s what we want to do—develop programs that meet those members’ needs and grow even more.

TJ: Will ASN still be called “American Society for Nutrition”?
JC: That’s a great question! We’ve dialogued about that and had a lot of good feedback about it. I don’t envision us changing ASN—I really don’t—but we’re a volunteer organization, and if our volunteers should wish to change it, perhaps we’ll simply refer to ourselves as “ASN.” When we say our name, we each have some vision of what that means, but what we really are is a global organization. We have over 5,200 members in 72 different countries, and approximately 28% of the meeting attendees are from outside the United States. Clearly we’re drawing a global audience.

TJ: What keeps ASN relevant?
JC: ASN really is the global leader in nutrition science. Our members, our authors, and our speakers are the preeminent leaders in nutrition. They’re the ones researching today’s problems, disseminating that research through our publications and our meeting-related activities, and then taking it and translating that to dietitians, medical practitioners, and public health advocates.

ASN is really on the move. We’ve more than doubled our membership, outreach, staffing and budget in the last 10 years. In the next 10 years I think we’ll see equivalent growth in terms of our revenue and our member service activities, so we’ll have more interaction on a grander scale.

For a first-person take on Dr. Courtney’s management style, watch his video interview with CEO Update here.

By Teresa L. Johnson, MSPH, RD

“A calorie is a calorie, but the body’s physiological response to that calorie might be different depending on the circadian phase the body is exposed to,” said Frank Sheer, PhD, an assistant professor of medicine at Harvard Medical School. Sheer spoke during ASN’s scientific symposium titled “Is ‘When’ We Eat As Important As ‘What’ We Eat?—Chronobiological aspects of food intake.” He opened his discussion by asking why we should care about circadian biology, and then pointed to its possible influence on metabolic processes, meal timing, and disease risk. He explained that an internal “circadian clock”—present in nearly all the body’s cells—regulates the body’s rhythms based on feedback from the brain. We can uncouple those rhythms and choose to be awake, but at a cost, possibly increasing our risk of some chronic diseases, like type 2 diabetes.

Jonathan Johnston, PhD, an associate professor at University of Surrey, “flipped the question on its head,” so to speak, and asked what effect meal timing might have on the body’s internal clock. Johnston explained that circadian rhythms are endogenous and self-sustaining even without external cues, like light and darkness. “Clocks are everywhere,” Johnston said, “and they function like an orchestra.” All the “musicians”—the various clocks—have to be synchronized to function properly, he said. Johnston’s data, gleaned from gene expression studies in human adipose tissue, suggest that modifying meal times might help synchronize the body’s clocks, a possible treatment for the circadian dyssynchrony commonly observed with shift work, jet lag, blindness, and sleep disorders.

“Humans are the only species that disobeys their biological clocks,” said Fred Turek, PhD, a professor at Northwestern University, and the downstream effects might be enormous. We have become “night creatures,” he said, and he and his colleagues are wondering how that affects human health. Turek pointed out that at least 10 to 30 percent of gene expression in the human body is under circadian control including genes in tissues like the brain, liver, and muscle—key players in metabolism—and likely influences disease risk, gut permeability, and the gut microbiota. He suggested that science is at a tipping point with regard to circadian medicine and health, adding that the field of circadian biology is growing and spans many different disciplines, including immunology, oncology, cardiology, and nutrition. “I think it’s the next frontier in medicine,” Turek said.

Jose Ordovás, PhD, a professor at Tufts, explained that circadian rhythms extend beyond 24-hour cycles to monthly and seasonal patterns, a phenomenon now ingrained in human physiology. Ordovás suggested that humans’ ancestral genes were more like the genes of the laboratory animals he studies, which respond to regular cycles of light and dark. Migration away from humans’ equatorial origins likely has altered human circadian biology and, in fact, circadian clocks now vary depending on geographical location. Ordovás speculated on the potential application of circadian biology in personalized or precision medicine as a means to identify those at risk for nutritional disease, and added, “Know your genome and act accordingly.”

By Ann Liu, PhD

Historically, immunology and metabolism have been distinct disciplines. However in recent decades we have learned that metabolic diseases such as obesity and type 2 diabetes result in major changes in inflammation and the immune response. Conversely, it has also become clear that certain behaviors and properties of lymphocytes are regulated by internal metabolic processes. Thus the new field of immunometabolism has emerged to examine the crosstalk between immune and metabolic processes. Speakers at the symposium “Diet and Immunometabolism,” co-sponsored by the Nutritional Immunology and Obesity RIS, highlighted the role of nutrients and metabolites in inflammatory processes on March 31.

While we may traditionally think of iron’s role in anemia and fetal development, it is also required for proper immune function and adipogenesis. Elevated serum ferritin levels are associated with type 2 diabetes, gestational diabetes, and metabolic syndrome. Excess iron also induces lipolysis and insulin resistance. Dr. Alyssa Hasty from Vanderbilt University School of Medicine presented data from mouse models indicating that iron homeostasis is disrupted during obesity. Iron is traditionally stored in the liver, however during obesity it appears that iron levels decrease in the liver and increase in adipocytes.

These changes may be related to changes in macrophage populations, which are important mediators of adipose tissue inflammation. Hasty identified two distinct macrophage populations based on their iron content. Some macrophages have high iron content which allows them to be isolated using a magnet while others have low iron content. Lean animals have both types of macrophages. However obese animals have increased levels of macrophages with low iron content.

This indicates that iron levels are changing in both adipocyte and macrophage populations during obesity and suggests that the ability of macrophages to sequester iron may be impaired. Further study is needed to identify the mechanisms of crosstalk between macrophages and adipocytes and examine potential functional consequences.

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.

By Teresa Johnson, MSPH, RD

Robert Waterland, PhD, an associate professor at Baylor College of Medicine, described nutritional influences on human developmental epigenetics. Waterland defined epigenetics as “mitotically heritable stable alterations in gene expression potential that are not caused by changes in DNA sequence.” Multiple factors likely contribute to epigenetic changes, including cytosine methylation, histone modification, auto-regulatory transcription factors, and non-coding RNAs, Waterland pointed out, and they tend to work in a synergistic fashion to influence gene transcription. Waterland said he is particularly interested in DNA methylation because methylation requires dietary donors and cofactors, which is influenced by nutritional factors. He presented data demonstrating that periconceptual maternal nutrition status predicts hypomethylation in a mother’s infant. These changes are stable and maintained over a lifetime, Waterland said, and may point to evidence of metabolic imprinting as an adaptive response to early nutrition.

“We live in a microbial world,” said Dingding An, PhD, a researcher at Boston Children’s Hospital. An elaborated on the role of early life gut microflora in immune system development, and explained that microbial exposure begins at birth and influences our risk for chronic diseases such as inflammatory bowel disease, asthma, arthritis, and autism later in life. Many early-life factors impact the makeup of the gut microbial population in particular, such as nutrition, hygiene, and antibiotic use. An presented data indicating that some gut microbes enhance immune cell maturation and immune response. But the timing of microbial exposure is critical, An added, because later exposure diminishes the response, indicating that key windows of regulation have been missed.

Deborah Sloboda, PhD, an associate professor at McMaster University, provided insights into the impacts of fructose consumption during pregnancy. Fructose is a monosaccharide present in honey, maple syrup, and fruit sugar, and is widely available in processed foods. Fructose consumption differs by sex and age, Sloboda said, with highest consumption reported among lower socioeconomic status females during their reproductive years. This is important, Sloboda said, because “the early-life environment plays a very big role in determining health and disease risk later in life.” Her data from animal models indicate that high fructose intake during pregnancy induces changes in the offspring’s metabolic response. Taurine supplementation reversed fructose-induced adverse metabolic programming, Sloboda said, but not in the presence of a high fat diet, emphasizing the importance of correctly identifying the population in need of intervention.

Growing up in the now well-studied Swedish village Överkalix strongly influenced the research of Lars Bygren, MD, PhD, a professor at University of Umea. Bygren, who addressed the topic of transgenerational outcomes associated with paternal nutrition, explained that human responses to early-life exposures, especially in males, have the potential to impact development for multiple generations. In particular, exposure to high food availability during slow-growth periods negatively affects the health of subsequent generations, and could explain the present day prevalence of many chronic diseases. Byrgen said data from other studies, including the Taiwan betel nut study and the ALSCAP study, lend support to these conclusions.

By Sheela Sinharoy

Tuesday’s minisymposium ‘Nutrition and Inflammation’ covered a wide range of topics and research designs from clinical, lab, and public health perspectives.

Starting with clinical research, Wendy Ward of Brock University (Canada) presented on associations of dietary intake with periodontal healing. She explained that 42% of adults in the US are affected by periodontal disease, which is characterized by inflammation of tissues around the teeth that can eventually lead to loss of alveolar bone. One treatment is the mechanical removal of bacteria below the gum line through sanative therapy. Dr. Ward’s group found that higher dietary intakes of fruits and vegetables, β-carotene, vitamin E, and α-linolenic acid were associated with greater healing following sanative therapy.

Taking a more public health-oriented perspective, Mercedes Sotos Prieto of Harvard University spoke about the development of a healthy lifestyle score (HLS) and its association with inflammatory markers among Puerto Rican adults in Boston. The HLS included five components: diet, physical activity, smoking, social network and support, and sleep. Dr. Sotos Prieto found that a 20-unit increase in the HLS was associated with a decrease in the inflammatory biomarkers IL-6 and TNF-α when adjusted for a number of covariates. These in turn were associated with obesity and hypertension but not with diabetes or heart disease.

Presentations from Yaw Addo and Leila Larson of Emory University also had clear public health implications. They looked at biomarkers of iron and vitamin A status, respectively, and their relationship with biomarkers of inflammation. First, Dr. Addo explained that transferrin receptor was strongly associated with α-1 acid glycoprotein (AGP) in women of reproductive age across six countries, though the magnitude of the association varied by country. Next, Ms. Larson showed that retinol binding protein (RBP) was significantly associated with both C-reactive protein (CRP) and AGP among preschool children in Liberia. Both of these analyses suggested that it may be important to account for inflammation, particularly with RBP, where adjusting for inflammation through linear regression decreased the prevalence of vitamin A deficiency by almost 20 percentage points.

Moving to lab studies, Marie-Caroline Michalski of the University of Lyon (France) presented research on the effects of dietary lipids on plasma endotoxins and lipopolysaccharides (LPS), which contribute to low-grade inflammation. She showed that in a sample of normal weight and obese men, ingestion of a higher-fat test meal led to postprandial endotoxemia only in obese subjects. Qiaozhu Su of the University of Nebraska then presented data showing that the cAMP responsive element binding protein H (CREBH), which is activated by the inflammatory cytokine TNF-α, induces expression of apolipoprotein B. This in turn increases secretion of very low density lipoproteins (VLDL) and may play a role in hepatic steatosis, hyperlipidemia, and insulin resistance. Finally, Sadiq Umar of Washington State University showed that thymoquinone, a compound derived from Nigella sativa, or black cumin, inhibits TNFα-induced production of the inflammatory cytokines IL-6 and IL-8 as well as the pro-inflammatory mediator ASK1.

Given the associations between inflammation and many chronic diseases, we will likely hear a great deal more about these topics in years to come.