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. https://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: Hassan S. Dashti, PhD

Small, frequent meals, also referred to as grazing, picking, nibbling, and snack-eating, is a dietary pattern characterized by consuming multiple meals throughout the day. This dietary pattern has been on a rise, thanks to aggressive marketing of snacks, decline in home-meal preparation, longer waking hours, among other reasons. But aside from convenience, does consuming 6 to 8 or even 10 meals per day instead of the traditional 3 meals per day confer health benefits?

It was commonly believed that having many small meals per day increases satiety. Supporting this notion are cross-sectional studies suggesting an inverse association between eating frequency and body weight in adults(1). Meanwhile, data from the NHANES suggest a positive association between eating frequency and energy intake in the healthy US population, whereby each additional ‘eating episode’ is estimated to contribute an additional ~200 kcal to overall energy intake potentially resulting in weight gain in the long-term (2). These findings, however, are greatly hindered as a result of underreporting of energy intake and meal frequency, particularly among nibblers (3).

The relationship between meal frequency and weight loss in overweight and obese individuals is also limited. A randomized, controlled trial in 2012 identified no differences in energy intake and BMI between participants randomized to either three or five meals per day (4). These findings were similar to other trials as well, which suggest no weight loss benefit from frequent meal intake (5). Meanwhile, in the healthy elderly, grazing may ensure adequate energy and micronutrient intake (6,7). While the contribution of small, frequent meals on energy balance remains equivocal, its influence should further be examined in the context of dietary quality and achieving adequate micronutrients intake.

Clinically, ‘small, frequent meals’ is perhaps the most commonly used medical nutrition therapy. Clinical nutrition guidelines generally recommend six to ten meals per day for patients experiencing early satiety and anorexia as they battle various diseases, such as pancreatitis and gastroparesis, or undergoing appetite suppressive treatment, such as chemotherapy, as recommended by the American Cancer Society(8). This eating pattern promises to decrease bloating, overcome early satiety and other symptoms, to help achieve adequate caloric intake (9). Grazing is also indicated post surgery for many gastrointestinal procedures including bariatric surgery and Whipple, to accommodate calories without abdominal distention and discomfort or dumping syndrome. Despite its short-term benefits, prolonging this dietary pattern post surgery may result in adverse health outcomes, such as less weight loss and eventual weight regain following bariatric surgery (10). These findings support the notion that this eating pattern more likely than not contributes to positive energy balance in the long-term. Yet this remains under examined, and whether the provision of small, frequent meals does indeed result in increased caloric intake in nutritionally at-risk individuals, such as those with pancreatitis, has yet to be elucidated.

An often-overlooked consequence of grazing is curtailed fasting duration. Clinical indications of small, frequent meals also include avoiding prolonged fasting, which is critical for cirrhotic patients, for example, to overcome the onset of endogenous protein breakdown for gluconeogenesis particularly during nocturnal fasting. However in healthy individuals, nocturnal fasting has been shown to provide various health benefits .

Several hurdles remain to be overcome in advancing our understanding of the relationships between grazing pattern and health. Among the most pressing limitations is the consistent use of a single definition for ‘meals’ for meaningful comparisons among studies. In addition, appropriate assessment tools, such as multiple food diaries –capturing meal size and time – in addition to nutrient intake, instead of food-frequency questionnaires should be adopted moving forward to accurately assess frequency.

The 2010 Dietary Guidelines of Americans concludes that there seems to be inadequate evidence to accurately evaluate the relationship between meal frequency and nutrient intakes. The current evidence does seem to suggest that unless clinically indicated, perhaps the general population should follow a more structured, 3 nutritious meals at regular times per day because of difficulty related to achieving energy balance without proper portion control. In addition, small, frequent meals often tend to be in the form of convenient snacks, which contribute refined carbohydrates, rather than fats and proteins, to the diet, and therefore add minimal nutrition to the diet for the most part. Thus, if necessary, provision of this dietary pattern should also be supplemented by an education focused on healthy meals/snacks and portion control.

References:

1.Kant AK. Evidence for efficacy and effectiveness of changes in eating frequency for body weight management. Adv Nutr. 2014 Nov;5(6):822–8.

2.Kant AK, Schatzkin A, Graubard BI, Ballard-Barbash R. Frequency of eating occasions and weight change in the NHANES I Epidemiologic Follow-up Study. Int J Obes Relat Metab Disord. 1995 Jul;19(7):468–74.

3.McCrory MA, Campbell WW. Effects of eating frequency, snacking, and breakfast skipping on energy regulation: symposium overview. J Nutr. 2011 Jan;141(1):144–7.

4.Bachman JL, Raynor HA. Effects of manipulating eating frequency during a behavioral weight loss intervention: a pilot randomized controlled trial. Obesity (Silver Spring). 2012 May;20(5):985–92.

5.Kulovitz MG, Kravitz LR, Mermier C, Gibson AL, Conn CA, Kolkmeyer D, et al. Potential role of meal frequency as a strategy for weight loss and health in overweight or obese adults. Nutrition. 2014 Apr;30(4):386–92.

6.Zizza CA, Tayie FA, Lino M. Benefits of snacking in older Americans. J Am Diet Assoc. 2007 May;107(5):800–6.

7.Zizza CA, Arsiwalla DD, Ellison KJ. Contribution of snacking to older adults’ vitamin, carotenoid, and mineral intakes. J Am Diet Assoc. 2010 May;110(5):768–72.

8. https://www.cancer.org/acs/groups/cid/documents/webcontent/002903-pdf.pdf

9. https://espen.info/documents/enpancreas.pdf

10.ConceiÇão EM, Mitchell JE, Engel SG, Machado PPP, Lancaster K, Wonderlich SA. What is “grazing?” Reviewing its definition, frequency, clinical characteristics, and impact on bariatric surgery outcomes, and proposing a standardized definition. Surg Obes Relat Dis. 2014 Sep;10(5):973–82.

11.Marinac CR, Natarajan L, Sears DD, Gallo LC, Hartman SJ, Arredondo E, et al. Prolonged Nightly Fasting and Breast Cancer Risk: Findings from NHANES (2009-2010). Cancer Epidemiol Biomarkers Prev. 2015 May;24(5):783–9.

By Caitlin Dow, PhD

Breakfast is often considered the “most important meal of the day,” and if you are looking to lose weight, you mustn’t skip breakfast… or so the story goes. This idea is widely believed in popular culture as well as by many nutrition scientists and government bodies and is repeated so often that many in the field consider it health dogma. Indeed, the Dietary Guidelines for Americans even recommend breakfast consumption as an important tool for weight loss. But what does the science say?

Observational studies indicate that breakfast consumption is linked to lower weight. Data from the National Weight Control Registry demonstrated that 78% of the nearly 3,000 subjects included in the analysis (adults who had lost at least 13 kg and kept the weight off for a year or more) reported eating breakfast everyday and only 4% reported never eating breakfast [1]. Further, a recent meta-analysis of observational studies that have evaluated the relation between weight and breakfast consumption found that skipping breakfast was associated with a 55% increased odds of having overweight or obesity [2]. These findings are likely the reason many tout breakfast consumption as an important weight loss modality, despite these studies not actually testing that outcome.

Observational studies can only describe associations, but are not appropriate to determine causation. Thus, randomized controlled trials (RCTs) have sought to test whether breakfast consumption directly impacts weight. In one of the first RCTs to evaluate the role of breakfast in weight loss, Schlundt et al. [3]studied women with obesity who were self-reported breakfast eaters or skippers.Within each group, women were randomized to eat or skip breakfast in addition to following a 1200 kcal/day diet for 12 weeks. All groups lost at least 6 kg, but interestingly, those who were randomized to switch their breakfast condition (e.g. ate breakfast at baseline, then started skipping) lost more weight than those who maintained their breakfast habit. These results suggest that changing an eating behavior in addition to following a reduced calorie diet may accelerate weight loss. However, the results from a study by Dhurandhar et al. did not corroborate those findings. Adults with overweight and obesity were randomized to one of three conditions in which all groups received a USDA pamphlet on healthy eating practices: the control group received no other information, one group received additional instructions to consume breakfast, and the third group was instructed to not eat breakfast [4]. After 16 weeks, there was no observed effect of treatment assignment on weight loss.Contrary to the results from the Schlundt study, baseline breakfast eating habit was not related to weight change, though this study didn’t evaluate breakfast consumption in conjunction with a reduced calorie diet.Finally, in a recently published 4-week study, adults with overweight and obesity were randomized to three different breakfast conditions: water (control), frosted flakes, or oatmeal [5].Interestingly, skipping breakfast resulted in an average weight loss of 1.2 kg, while those randomized to either breakfast condition demonstrated no significant weight change.However, total cholesterol also increased in the control group, suggesting that skipping breakfast may result in slight weight loss, but have detrimental effects on cardiometabolic health.

Thus, the results from the few RCTs completed in adults with overweight and obesity, to date, do not support the notion that breakfast consumption should be part of a weight loss regimen. Importantly, though, the results are also not compelling to suggest that eating breakfast hinders weight loss. This field is still young and many questions remain unanswered. I look forward to more RCTs evaluating breakfast consumption (and potentially, breakfast quality) on various facets of weight and metabolic health.

References

1.Wyatt, H.R., et al., Long-term weight loss and breakfast in subjects in the National Weight Control Registry. Obes Res, 2002. 10(2): p. 78-82.

2.Brown, A.W., M.M. Bohan Brown, and D.B. Allison, Belief beyond the evidence: using the proposed effect of breakfast on obesity to show 2 practices that distort scientific evidence. Am J Clin Nutr, 2013. 98(5): p. 1298-308.

3.Schlundt, D.G., et al., The role of breakfast in the treatment of obesity: a randomized clinical trial. Am J Clin Nutr, 1992. 55(3): p. 645-51.

4.Dhurandhar, E.J., et al., The effectiveness of breakfast recommendations on weight loss: a randomized controlled trial. Am J Clin Nutr, 2014. 100(2): p. 507-13.

5.Geliebter, A., et al., Skipping breakfast leads to weight loss but also elevated cholesterol compared with consuming daily breakfasts of oat porridge or frosted cornflakes in overweight individuals: a randomised controlled trial. J Nutr Sci, 2014. 3: p. e56.

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; https://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; https://newsroom.heart.org/news/green-tea-coffee-may-help-lower-stroke-risk.
7.Green tea may lower heart disease risk. Harvard Heart Letter 2012; https://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 Banaz Al-khalidi

Losing weight is hard enough. Keeping it off is even harder. Despite decades of scientific advancement in our understanding of energy intake and energy expenditure, weight regain after weight loss remains a major issue in obesity treatment. What could we be missing in this energy balance equation? Rethinking this problem, I think it is worth asking ourselves whether we live to eat or eat to live. There is a huge difference. Given the abundance of food in our environment, the majority of us will live to eat. But what drives this motivation or simply put, what are the determinants of healthy versus unhealthy behaviors?

Generally, healthy lifestyle interventions including diet, exercise, and behavioral strategies, such as keeping a food log, have proven to be effective for weight loss in the short term. However, participants’ lack of adherence to the intervention coupled with subsistence of unhealthy behaviors result in weight regain in the long term. According to a research on cardiovascular health behaviors and health factor changes in the US population from 1988 to 2008, healthy diet scores changed minimally (from 0.3% to 1.4% between 1999 and 2008), and physical inactivity levels decreased by only 7-10% from 1999 to 2006. Furthermore, by 2020, it is estimated that 43% of American men and 42% of American women will have a BMI of ≥ 30 kg/m2 (i.e., obese category). Despite the established risks and benefits associated with diet and physical activity, it seems that health behaviors tend to be incredibly resistant to change.

A recent report from a panel of obesity experts convened at the National Institutes of Health discussed the issue of weight regain after weight loss. The authors highlighted the problem of behavioral fatigue, in which patients grow weary of strict lifestyle regimens, especially when weight loss declines after the first 6 months. Specifically, the authors mentioned that “Initially, the positive consequences of weight loss (e.g., sense of accomplishment, better fit of clothes) outweigh the cognitive and the physical effort needed to lose the weight. Later, when the goal is to maintain lost weight, the positive feedback is less compared to the effort required to keep adhering to the same regimen. Thus, the benefits no longer seem to justify the costs”. In other words, the costs of adherence to these interventions exceed the benefits as time progresses, and patients seem to justify their behavior by re-thinking about the cost/benefit ratio in the long run. How can we then increase the long-term benefits while decrease the costs associated with weight maintenance?

There is a need to understand what factors allow people to successfully maintain a behavior over a long period of time. In recent years, obesity and behavioral scientists have started to explore strategies that involve incorporating ‘mindfulness’ to promote the sustainability of healthy behaviors. Mindfulness is defined as: awareness of the present moment, and paying attention to one’s moment-to-moment experiences non-judgmentally. This attention leads to a clear awareness of one’s own thoughts as well as one’s environment in that one observes what is happening, but instead of reacting, the mind views these thoughts as inconsequential. This does not mean disconnection from life; rather, the mind is actively engaged and flexible. Mindfulness is not a technique but it is a way of being.

You might ask, what does this have to do with obesity and health behaviors? They’re all related. Mindfulness-based interventions (MBIs) have recently become a focus for the treatment of obesity-related eating behaviors. A recent review paper examined the effectiveness of MBIs for changing obesity-related eating behaviors. Of the 21 studies included in the review, 18 studies reported positive results for obesity related eating behavior outcomes. Specifically, mindfulness enhanced self-awareness and self-regulation (i.e. long lasting self-motivation) by improving awareness of emotional and sensory cues, which may be effective for sustaining a behavior in the long term. It’s about acceptance of the moment we’re in and feeling whatever we feel (accepting both positive and negative emotions) without trying to resist, change or control it. Under emotional stress, most of us will try to comfort ourselves by putting something into our mouths, but being aware of the negative emotions, and having greater self-control skills may help us resist the urge to eat large quantities of food or unhealthy food. Thus, greater awareness and self-control skills may help an individual to better monitor and regulate their dietary intake as well as their engagement in physical activity.

When we live to eat, we tend to engage in the act of mindless eating because we tend to see food as a source of reward or entertainment, and we shovel food into our mouths without paying attention to what we’re eating and whether we feel full. However, when we’re more mindful or self-aware (i.e. eating to live), we become more conscious of what goes into our bodies by focusing fully on the act of eating and eating related decisions. The bottom line is mindfulness may help patients identify internal and external eating cues, manage food cravings, and enhance self-regulation and resilience- all factors important to counteract the behavioral fatigue that tends to occur in lifestyle interventions over time. Perhaps, when we’re more mindful, we’ll tune into our bodies instead of our thoughts (i.e., thinking about the costs/benefits), and will start to look at food as nourishment rather than as emotional comfort blanket. It is important to note that research in this area is still preliminary but exploring and understanding the relationship between mindfulness and health behaviors may hold promise for long-term weight management.

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 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 Ann Liu, PhD

Researchers are using carrots to produce a new tracer that will help scientists study vision and brain function. The results of this study were presented in the “Carotenoid and Retinoid Interactive Group: Bioavailability and Metabolism of Carotenoids and Vitamin A” on March 29 by Joshua Smith and John Erdman, PhD, from the University of Illinois at Urbana-Champaign.

Lutein is a carotenoid which accumulates in the retina of the eye and may protect the eyes from damage, especially age-related macular degeneration. It also accumulates in certain areas of the brain and may be beneficial for cognitive performance. However, little is known about how lutein accumulates in tissues such as the brain or how these tissues metabolize it. This led researchers to embark on a mission to develop lutein labeled with a non-radioactive, stable tracer (carbon-13) as a tool to study the metabolism of lutein in tissues.

Enter the colorful carrots. Carrots are a good source of lutein, but the amount of lutein can vary depending on the variety of carrot. Researchers tested seven different carrot cultivars that ranged in color from red to yellow to purple to see which one produced the most lutein. Then they had to culture the carrot cells in flasks and optimize the growing conditions to increase lutein production.

Once they figured out the optimal growing conditions, the carrot cells were fed carbon-13 labeled glucose. The lutein then had to be extracted using reverse-phase high performance liquid chromatography, and incorporation of the carbon-13 tracer was assessed using mass spectrometry. Approximately 58% of the lutein extracted from the carrot cells was uniformly labeled with carbon-13.

So what’s next for this new tracer lutein? The researchers plan to use it to study tissue accumulation of lutein in animal models before embarking on any studies in humans. They will also be going back to the lab bench to see if there are any more changes they can make to further improve their lutein yield.

This research was funded by a grant from Abbott Nutrition through the Center for Nutrition, Learning, and Memory at the University of Illinois.