Are consumers benefitting more than they know from recent food and behavior trends?

By: Emma Partridge

American consumers are undoubtedly moving toward natural foods. An analysis by Datassential of consumer foodservice issue concerns may explain some factors in this overall trend; consumers appeared most concerned with antibiotics and steroids in animal proteins and/or dairy products, local food sources and manufacturers surviving, and GMOs, among other issues.1 Fortune magazine calls it “the war on big food” – but are consumers benefitting from more than just those ‘left out’ factors?2 I had the chance to sit down with Dr. Mario Kratz, researcher at the Fred Hutchinson Cancer Research Center, core faculty member of the University of Washington (UW), and Associate Director of the UW Diabetes Research Center, to discuss a few of these food trends and what their intrinsic health benefits might be.

One trend of note is the move toward full-fat dairy products. Whole milk sales rose 11% in the first half of 2015 alongside a 14% fall in skim milk purchases.3 While many speculate this shift is in line with movement toward wholesome, unprocessed foods, there are unrecognized benefits to full-fat dairy beyond its less-processed nature. Full-fat dairy may increase satiety, or lead a person to feel more full than if (s)he ate a low-fat dairy product. In evaluations of 16 dairy fat studies, Dr. Kratz’s team found that, of studies comparing high-fat dairy to low-fat dairy, high-fat dairy intake was actually associated with better weight outcomes, and was not associated with higher weight. Further, 11 of the 16 studies revealed that people who ate more dairy fat or high-fat dairy foods tended to be leaner and/or gain less weight over time than those who ate less dairy fat.4 The results from these analyses make a case for full-fat dairy as a protectant against weight gain, potentially due to increased satiety response. Additionally, there are other fatty acids present in full-fat dairy that can act as hormones, and small amounts of these fatty acids may be beneficial. The scientific reasoning behind the presence of many fatty acids supports full-fat dairy and, on the other side of that coin, there is no data supporting healthful benefits from consuming non-fat, low-fat, or isolated-fat dairy products in which many of the fatty acids have been removed.5

Another food trend of note over the past few years is that of coconut oil. While part of the trend may be attributable to its non-cooking uses, coconut oil is also highly heat resistant, has a long shelf life, and is rich in medium chain saturated fatty acids (MCFAs). The heat-stability of coconut oil is beneficial to reducing intake of harmful free radicals, but MCFAs may be the most significant of coconut oil’s intrinsic health benefits. In a study comparing long chain fatty acids, generally purported to be less-healthy fatty acids, to MCFAs, researchers found MCFA-treated mice exhibited increased energy expenditure, reduced adiposity, and improved insulin sensitivity.6 It is possible, then, that consumers following the coconut oil trend may be reaping such metabolic health benefits.

Perhaps the most significant trend to watch is that of developing healthy, lifestyle-based eating patterns, which is recommended by the 2015 Dietary Guidelines Advisory Committee in the recently-released 2015-2020 Dietary Guidelines for Americans. In a media-driven world of shoulds and should-nots, the Dietary Guidelines Advisory Committee took a different approach with this year’s release: develop patterns of healthy eating and physical activity within the environment around you. Dr. Kratz argues something similar, that pattern matters and a varied eating pattern may allow for small amounts of cravings and diet-breakers, thusly providing a method to control them.5 In short, his “number one” advice point is, “in spite of whatever craze you may be following right now…if you find something new, you should find a way to incorporate it into your overall diverse diet.”

1.Webster M. Changing Consumer Behaviors and Attitudes. Culinary Institute of America; 2015.
2.Kowitt B. Special report: the war on big food. Fortune 2015.
3.O’Connor A. Consumers Are Embracing Full-Fat Foods. The New York Times 2015.
4.bottomlinehealth.com. Why Whole Milk May Be Better Than Skim. Bottom Line Health 2014.
5.Mario Kratz P, MS. In: Emma Partridge MC, ed2016.
6.Montgomery MK, Osborne B, Brown SHJ, et al. Contrasting metabolic effects of medium- versus long-chain fatty acids in skeletal muscle. Journal of Lipid Research. 2013;54(12):3322-3333.

A new rationale for breastfeeding – the benefits for the Mom!

By: Mary Scourboutakos

Presently in America breastfeeding rates are sub-par.

While the World Health Organization recommends exclusive breastfeeding for up to six months of age, with continued breastfeeding alongside complementary foods up to two years of age or beyond—in the US 79% of mothers initiate breastfeeding, but only 22% exclusively breastfeed to six months and only 27% are still breastfeeding (non-exclusively) at two years postpartum.1 Meanwhile in countries like Sri Lanka, 83.1% of mothers are still breastfeeding their children two years post-partum.2

So the question is…how do we get women in America to breastfeed longer?
Traditionally, when trying to promote breastfeeding, people have focused on the benefits for infants, such as improved cognitive development,3 fewer childhood infections,4 and decreased risk for obesity and chronic disease later in life.5

But when you consider current rates of breastfeeding (see above!), clearly this approach isn’t working. Nevertheless, there may be a presently unexplored way to promote breastfeeding…

Emerging research suggests that in fact, the benefits of breastfeeding for the mother may surpass the benefits of breastfeeding for the infant.6-8
In fact, research has shown that long-term breastfeeding is associated with decreased maternal risk for breast cancer,9-11 ovarian cancer,12, 13 endometrial cancer,14 diabetes,15 heart disease,16 as well as greater postpartum weight-loss,17, 18 and mental health benefits.19, 20

But how long is long? And by how much does risk decrease? In terms of breast cancer, research from China has shown that women who breastfeed for more than 24 months per child cut their risk for breast cancer in half, compared to women who breastfed for only one to six months.10 Furthermore, dose-response curves for risk of diabetes show an inverse relationship with lifetime duration of breastfeeding, which suggests that the longer you breastfeed for, the lower your risk is.15

So, my unsolicited piece of advice for public health agencies is…if you’re trying to improve rates of breastfeeding, never mind touting the benefits for the baby, maybe try promoting the benefits for the Mom!


1.National Center for Chronic Disease Prevention and Health Promotion. Breastfeeding – Report Card. 2014; Available at:http://www.cdc.gov/breastfeeding/pdf/2014breastfeedingreportcard.pdf(Accessed: 7 February 2016).
2.Ministry of Health Care and Nutrition. Sri Lanka – Demographic and Health Survey. 2006; Available at: http://www.statistics.gov.lk/social/DHS%20200607%20FinalReport.pdf (Accessed: 2016 February).
3.Quigley MA, Hockley C, Carson C, Kelly Y, Renfrew MJ, and Sacker A. Breastfeeding is associated with improved child cognitive development: a population-based cohort study. J Pediatr, 2012. 160(1):25-32.
4.Li R, Dee D, Li CM, Hoffman HJ, and Grummer-Strawn LM. Breastfeeding and risk of infections at 6 years. Pediatrics, 2014. 134 Suppl 1:S13-20.
5.Yan J, Liu L, Zhu Y, Huang G, and Wang PP. The association between breastfeeding and childhood obesity: a meta-analysis. BMC Public Health, 2014. 14:1267.
6.Schwarz EB. Infant feeding in America: enough to break a mother’s heart? Breastfeed Med, 2013. 8(5):454-7.
7.Bartick MC, Stuebe AM, Schwarz EB, Luongo C, Reinhold AG, and Foster EM. Cost analysis of maternal disease associated with suboptimal breastfeeding. Obstet Gynecol, 2013. 122(1):111-9.
8.Bartick M and Reinhold A. The burden of suboptimal breastfeeding in the United States: a pediatric cost analysis. Pediatrics, 2010. 125(5):e1048-56.
9.Zhou Y, Chen J, Li Q, Huang W, Lan H, and Jiang H. Association between breastfeeding and breast cancer risk: evidence from a meta-analysis. Breastfeed Med, 2015. 10(3):175-82.
10.Zheng T, Duan L, Liu Y, Zhang B, Wang Y, Chen Y, et al. Lactation reduces breast cancer risk in Shandong Province, China. Am J Epidemiol, 2000. 152(12):1129-35.
11.De Silva M, Senarath U, Gunatilake M, and Lokuhetty D. Prolonged breastfeeding reduces risk of breast cancer in Sri Lankan women: a case-control study. Cancer Epidemiol, 2010. 34(3):267-73.
12.Luan NN, Wu QJ, Gong TT, Vogtmann E, Wang YL, and Lin B. Breastfeeding and ovarian cancer risk: a meta-analysis of epidemiologic studies. Am J Clin Nutr, 2013. 98(4):1020-31.
13.Li DP, Du C, Zhang ZM, Li GX, Yu ZF, Wang X, et al. Breastfeeding and ovarian cancer risk: a systematic review and meta-analysis of 40 epidemiological studies. Asian Pac J Cancer Prev, 2014. 15(12):4829-37.
14.Jordan SJ, Cushing-Haugen KL, Wicklund KG, Doherty JA, and Rossing MA. Breast-feeding and risk of epithelial ovarian cancer. Cancer Causes Control, 2012. 23(6):919-27.
15.Aune D, Norat T, Romundstad P, and Vatten LJ. Breastfeeding and the maternal risk of type 2 diabetes: a systematic review and dose-response meta-analysis of cohort studies. Nutr Metab Cardiovasc Dis, 2014. 24(2):107-15.
16.Schwarz EB, Ray RM, Stuebe AM, Allison MA, Ness RB, Freiberg MS, et al. Duration of lactation and risk factors for maternal cardiovascular disease. Obstet Gynecol, 2009. 113(5):974-82.
17.Jarlenski MP, Bennett WL, Bleich SN, Barry CL, and Stuart EA. Effects of breastfeeding on postpartum weight loss among U.S. women. Prev Med, 2014. 69:146-50.
18.Baker JL, Gamborg M, Heitmann BL, Lissner L, Sorensen TI, and Rasmussen KM. Breastfeeding reduces postpartum weight retention. Am J Clin Nutr, 2008. 88(6):1543-51.
19.Groer MW. Differences between exclusive breastfeeders, formula-feeders, and controls: a study of stress, mood, and endocrine variables. Biol Res Nurs, 2005. 7(2):106-17.
20.Groer MW and Davis MW. Cytokines, infections, stress, and dysphoric moods in breastfeeders and formula feeders. J Obstet Gynecol Neonatal Nurs, 2006. 35(5):599-607.

Obesity is Not a Disease of Sloth and Gluttony

By Caitlin Dow, PhD

The most recent data from the CDC indicates that approximately 35% of American adults have obesity (1). In order to reduce obesity prevalence, a popular notion is that people with obesity just need to “eat less and move more.” Indeed, many public health programs use this concept as their primary approach for combating obesity. While eating less and moving more may help prevent obesity or result in successful, sustained weight loss in individuals who are simply overweight (but not yet obese), ongoing research indicates that these simple lifestyle changes will do very little in the face of prolonged obesity (2).

If you look at any weight loss study, you will most assuredly find the same results, regardless of study design. The first six months are generally characterized by substantial weight loss, followed by sustained weight regain, resulting in a final weight that is negligibly lower and potentially higher than the starting weight . This “checkmark effect” or weight loss recidivism that has been reported nearly ubiquitously across diet and exercise-based weight loss trials (3) indicates that lifestyle interventions are generally not successful modalities for treating obesity.

Based on a rudimentary understanding of metabolism, the calories in/out approach should work for weight loss and weight loss maintenance. So why doesn’t it work for so many people? The answer lies in the complex network linking the environment, genetic predisposition to obesity, as well as metabolic and physiological changes. A large body of literature indicates that the brain’s reward systems are significantly dysregulated in individuals with obesity (4). In an environment that supports ease of access to highly palatable foods, the pleasurable effects of consuming said foods can override homeostatic control of intake. While some people are able to regulate intake despite the high palatability of these foods, a number of genetic mutations in the brain’s reward systems may result in overeating and obesity in many people. Furthermore, the hypersensitive reward systems that often lead to obesity can become insensitive once a state of obesity is attained. In effect, this leads to overeating to receive the same pleasure from the same foods. These dysregulated reward systems are coupled with preadipocyte expansion into mature adipocytes, allowing for increased fat storage. While this isn’t the entire story, this should shed some light on the complex interactions of dysregulated internal systems that foster the metabolic abnormalities that result in obesity. Importantly though, these impairments are typically only demonstrated once obesity has been introduced and sustained (3).

As for weight loss, when caloric restriction is initiated, the body triggers a number of systems to prevent starvation. From an evolutionary perspective, this makes sense as food sources were often unpredictable and the body adapted to conserve energy – the “feast and famine” principle. However, for most of us living in industrialized nations, famine is rare and feast is common, limiting the need for this once very necessary adaptation (though the body has not evolved to recognize the abundance of calories in our modern food supply). When we try to induce weight loss via caloric restriction, the body will reduce its resting metabolic rate to counter these advances (5). This supports the “set point theory” – the idea that the body will defend its highest-sustained weight. In fact, as weight loss increases, the drive to restore the highest bodyweight only increases (6). It’s like when you’re pulling on your dog’s leash to get him into the vet and he plants his feet firmly and resists with all his might. Ultimately his strength pulls him out of his collar and sends him running in the opposite direction. Except here we’re talking about the human body and it’s not nearly as comical.

All of these biological adaptations that introduce, sustain, and defend obesity explain why weight loss and its maintenance is so exhaustingly difficult for so many people. As Ochner and colleagues suggest, most individuals who had obesity but lost weight simply have “obesity in remission and are biologically very different from individuals of the same age, sex, and body weight who never had obesity.” As a hypothetical scenario, imagine you are comparing two people: they weigh the same, but person A had obesity and has lost weight whereas person B has never lost weight. Person A will have to burn up to 300 calories more (or consume 300 calories fewer) than person B to maintain that weight (2). This underscores the idea that weight regain is not simply an issue of willpower and weakness.

What we need more of are studies evaluating multiple approaches to weight loss (surgeries, medications, likely in combination with lifestyle changes). What we need less of is bias from people without obesity, the media, and even healthcare providers. Indeed, “the mere recommendation to avoid calorically dense foods might be no more effective for the typical patient seeking weight reduction than would be a recommendation to avoid sharp objects for someone bleeding profusely” (2). We also need better obesity prevention approaches because, clearly, it’s biologically more feasible to prevent weight gain than to lose weight and keep it off.


1.Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adults obesity in the United States, 2011-2012. JAMA. 2014;311(8):806-814. doi:10.1001/jama.2014.732.

2.Ochner CN, Tsai AG, Kushner RF, Wadden TA. Treating obesity seriously: when recommendations for lifestyle change confront biological adaptations. Lancet Diabetes Endocrinol. 2015:

3.Ochner CN, Barrios DM, Lee CD, Pi-Sunyer FX. Biological mechanisms that promote weight regain following weight loss in obese humans. Physiol Behav. 2013:120:106-13. doi: 10.1016/j.physbeh.2013.07.009.

4.Kenny JP. Reward mechanisms in obesity: new insights and future directions. Neuron. 2011:69(4):664-79. doi:10.1016/j.neuron.2011.02.016

5.Grattan BJ, Connolly-Schoonen J. Addressing Weight Loss Recidivism: A Clinical Focus on Metabolic Rate and the Psychological Aspects of Obesity. ISNR Obesity. 2012. doi:10.5402/2012/567530

6.Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J Obes.2010:34:S47-55. doi:10.1038/ijo.2010.184


Soda Politics: A Discussion with Dr. Marion Nestle

By Chris Radlicz

Marion Nestle, PhD, MPH is Paulette Goddard Professor in the Department of Nutrition, Food Studies, and Public Health at New York University, which she has chaired from 1988-2003. Additionally, she is Professor of Sociology at NYU and Visiting Professor of Nutritional Sciences at Cornell. Dr. Nestle earned her PhD in molecular biology and MPH from University of California, Berkeley. Her research examines scientific and socioeconomic influences on food choice, obesity, and food safety, with an emphasis on the role of food marketing. She is the author of several prize-winning books, and in her latest, Soda Politics: Taking on Big Soda (and Winning), Dr. Nestle provides insight on the soda industries tactics to gain consumers and addresses what is now working in the fight against ‘Big Soda’. I recently had the opportunity to ask Dr. Nestle some questions relevant to her newest book.

1. How has your background in molecular biology lead you to your career interest in public health, and particularly food politics?

The direct story is that I was teaching undergraduate molecular and cell biology in the Biology Department at Brandeis University and was assigned a nutrition course to teach. Undergraduate biology majors wanted a course in human biology and it was my turn to take one on. From the first day I started preparing that course, it was like falling in love. I’ve never looked back. Politics was in the course from day one. It’s not possible to understand how people eat without understanding the social, economic, and political environment of food marketing and food choice.

2. What lead you to write your newest book, “Soda Politics: Taking on Big Soda (and Winning)”?

I’ve been writing about soda marketing since the late 1990s when I learned about “pouring rights” contracts–soda company arrangements with educational institutions for exclusive sale of their brand. These started with colleges but had just gotten to elementary schools when I learned about them.  Since then, I’ve followed Coke and Pepsi marketing with great interest.  I teach food politics and food advocacy at NYU and was well aware of all the advocacy groups working to reduce soda intake as a public health measure.  When my agent suggested that I ought to write a book about sodas, it seemed like a terrific idea to encourage readers to engage in advocacy for healthier food systems.  Sodas are a good example of how to do this.

3. The title is provocative. Why do you say that those taking on ‘Big Soda’ are in fact ‘winning’?

That’s the best part.  Soda sales are way down in the United States. The soda industry thinks public health advocacy is responsible, and who am I to argue?

4. What has influenced the slow but successful decline in soda consumption seen today?

Excellent public health advocacy. Think of New York City’s poster campaigns over the last four or five years. These illustrated the amount of sugar in sodas and how far you would have to walk to work off the calories in one vending machine soda

5. The Coca-Cola funded non-profit, “Global Energy Balance Network”, recently shut its doors. Do you think this is evidence of gaining momentum?

Reporters from the New York Times and the Associated Press were shocked to discover that Coca-Cola was funding university research to demonstrate that physical activity is more effective than eating healthfully in preventing weight gain.  This idea is patently false. Investigations revealed that the researchers worked closely with Coca-Cola executives to craft the research, conduct it, interpret it, publish it, and present it at meetings. This too seemed shocking. Now Coca-Cola is scrutinizing who it supports and many organizations know they need to be more careful to avoid such conflicts of interest.

6. In what ways do you see parallels in tactics used by ‘Big Soda’ and those previously used by cigarette companies in defending their respective products?

Soda is not tobacco but the tactics sure look similar. The soda industry follows the tobacco industry’s playbook to the letter. It too attacks inconvenient science, buys loyalty, funds front groups, lobbies behind the scenes to get what it wants, and spends fortunes to oppose public health measure that might reduce soda intake.

7. Where can people follow your current work and get involved in this fight against ‘Big Soda’?

I write an (almost) daily blog at www.foodpolitics.com where I cover such issues. Soda Politics has an Appendix that lists the principal advocacy groups working on soda issues and provides links to their websites.  It’s easy to get involved in food advocacy and well worth the time.