Research We’re Reading

NRI scientists are reading latest findings in the field of nutrigenomics to share new information with you.




Studies Explore Mechanisms Behind Obesity-Cancer Link

Original story posted by UNC Lineberger Comprehensive Cancer Center.

May 20, 2019 – New studies led by University of North Carolina Lineberger Comprehensive Cancer Center researchers explore biological mechanisms behind obesity and its link with cancer. Research findings presented at the American Association for Cancer Research Annual Meeting 2019 explore possible reasons for obesity-related resistance to breast cancer treatment and possible strategies to overcome obesity-related immune suppression in cancer.

Here are some of the latest findings presented at the meeting: “I think we’re moving past the question of ‘is obesity an important cancer driver?’ to ‘what do we do about it?’” said UNC Lineberger’s Stephen Hursting, PhD, professor in the UNC Gillings School of Global Public Health Department of Nutrition and the UNC Nutrition Research Institute. Hursting also served as one of the vice chairs of the meeting’s scientific program committee.

  • In preliminary findings from studies in mice presented Tuesday, April 2, Laura Smith, a graduate student inHursting’s lab, reported that obesity at older ages is linked to worse outcomes. Specifically, they found that older, obese mice saw higher tumor growth than younger obese and lean mice and also compared to lean, older mice. Lean, aged and younger obese mice had accelerated growth of the mammary tumors compared to young, obese mice, although to a lesser degree than that of aged, obese mice.

“The worst tumors, the really aggressive, metastatic tumors, were in obese, older mice,” Hursting said. “The least tumorigenic picture was in the young, lean mice.”

The researchers also found increased inflammation in older mice, as well as younger obese mice, leading them to think that there are biological connections that could be driving the links between cancer and both obesity and aging. Researchers plan to continue to evaluate the biological mechanisms that lead to age- and obesity-related breast cancer progression.

Mechanistically, we’ve been digging into this, and there are numerous shared pathways underlying both obesity and aging, and they seem to synergize,” Hursting said.

  • New preliminary findings presented Sunday, March 31 by Laura Bowers, a former postdoctoral fellow in the Hursting lab who is now an assistant professor at Purdue University, provide insight into what may be helping drive obesity-linked resistance to certain breast cancer chemotherapy treatments. Researchers found evidence that leptin, a biological signal released by fat tissue that helps regulate appetite by signaling the “full” feeling in normal conditions, may be involved in resistance.

“Leptin is a product of adipose tissue, and under normal conditions serves as a sensor of energy stores and regulator of appetite” Hursting said. “Leptin levels increase as fat mass increases, and the signals linking appetite with energy stores become dysregulated with obesity. The question is: does all of this circulating leptin in obese conditions have any effect on risk or progression of cancer cells?”

In their preliminary findings from studies of obese mouse models, the researchers found that leptin was linked to increased numbers of tumor-initiating cells. These cells have been shown to contribute to tumor initiation, growth, spread in the body and resistance to chemotherapy treatments.

“These cells have an aggressiveness and resilience to them because of their stem cell-like properties,” Hursting said. “We noticed obesity seems to enrich or increase the number of stem cell-like cells within a tumor, and this study identifies leptin as one of the connections between obesity and tumor-initiating cells.”

  • Preliminary findings point to a potential solution to reverse the immunosuppressive environment around breast cancer tumors driven by obesity.

In preclinical studies led by Shannon McDonell, a medical student at the UNC School of Medicine and graduate student in the Hursting lab, and presented Tuesday, April 2, researchers found that a non-steroidal anti-inflammatory drug, Sulindac, impacted several cell-signaling pathways related to immune function and metastatic potential of breast tumors. They did this by mixing the treatment into diets for obese and non-obese mice, finding that the treatment had a positive impact on controlling immunosuppression and blocking the pro-metastatic effects of obesity. They believe their findings suggest the treatment could be useful to improve outcomes for breast cancer patients.

  • Hursting is also leading multiple sessions at the AACR Annual Meeting, including one focused on metabolism and cancer on Sunday, March 31. Cancer cells often have irregular metabolism, which means they have irregular ways of consuming energy. Hursting said new research has shown there are signals that circulate throughout the body that can influence the metabolism of individual cancer cells.

Another session that Hursting co-chaired Sunday, March 31 focused on scientific findings related to a report for the World Cancer Research Fund and the American Institute for Cancer Research on diet, nutrition and physical activity and the prevention of cancer. The report, coauthored by Hursting, “involved the systematic review and meta-analysis of the associations between several hundred dietary factors, as well as exercise, and each of the most common types of cancer”, Hursting said.

“These findings represent important leads on where the field should be going,” Hursting said. “The strong associations identified by this systematic approach provide nutrition and cancer researchers a roadmap for future mechanistic studies.”

Media Contact: Laura Oleniacz, 919-445-4219,

Post: May 20, 2019

Nutrition Decisions in a Conflicting World: Eggs-actly the Issue

by Carol L. Cheatham, Ph.D.
Associate Professor, Psychology and Neuroscience
UNC Nutrition Research Institute

April 18, 2019 – How are we expected to make healthy choices about food when the headlines are so confusing? We all suffer whiplash when we read butter is bad, then butter is good; when red meat is bad, then red meat is good; when red wine is good, and then it is bad….so, what is the headline du jour? Once again, eggs are reported to be bad for you due to their cholesterol content.1 How concerned should we be when we all know the egg has had a tumultuous relationship with science?2

Well, that depends. What other foods do you eat? Is your diet laden with high fat and high sugar foods? Do you have the genetic make-up that means you are sensitive to cholesterol? Many factors go into whether or not you, as an individual, will develop heart disease. Cholesterol is not singularly evil, and actually, it serves many noble purposes in the human body. In fact, if it is not consumed in appropriate quantities, the human body will manufacture it.3 Bottom line – we need cholesterol to live.

So, what is the issue? A recent report in the Journal of the American Medical Association (JAMA), a highly respected scientific journal, sets forth the conclusion that eating eggs increases risk for cardio-vascular disease and in general, death.4 The study is very detailed and involved data from almost 30,000 participants from six different samples. The scientists used all the proper techniques and controls. They even controlled for the diet as a whole. Their conclusion should be solid, right?

Answer this for me – how many times in the past 6 months have you eaten eggs? This question is what you would answer if you completed a food frequency questionnaire (FFQ), which is a method of collecting diet data. Even though FFQs serve an important purpose in nutrition research, the data are subject, as you can imagine, to the fallibility of memory: as humans, our memories are just not that reliable (which is how I have been able to build a career studying memory). In the JAMA report, the answer to this one FFQ question was found to be associated with whether or not one had developed cardio-vascular disease as much as 31 years later. As mentioned, the statistics controlled for other lifestyle factors, but the fact remains, the data are only correlational (which if you remember high school science, does not mean causation) and depend solely on an unreliable memory dump. To contrast, in a similar correlational study published in JAMA in 1999 with data from over 117,000 people, it was reported that healthy people could eat an egg a day without any change in cardio-vascular disease risk.5 Bottom line – correlation provides us clues about what experimental research might be useful, but it does not equal causation.

Okay, so what if we do the experiment and assign people randomly to eat eggs or not to eat eggs? This type of a study (randomized controlled trial or RCT) will allow us to determine causation. Many studies have been completed, and a complete review is beyond the scope of this article; here are the results of a representative study.6 Participants ate 3 eggs a day for four weeks and had their cholesterol assessed. The results showed an improvement in HDL (the “good” cholesterol) function and an improvement in LDL size. As a bonus, plasma antioxidant content was also increased, because the egg contains several nutrients that are amazingly good for the body and brain. As further evidence, another group completed a meta-analysis of the egg research up to that point (2013) and concluded that eggs are not related to an increased risk in cardio-vascular disease, unless the consumer is diabetic.7 Thus, the egg is a great addition to a diet for healthy individuals.

On a personal note, I purposefully ate a dozen eggs a week for 4 weeks to see what effect it would have on my cholesterol in preparation for a study in which I was going to ask women to eat 5 eggs a week.8 This egg experiment only increased my HDL – which is good. My LDL remained stable and my triglycerides decreased. In addition before starting research with the egg in my lab, I researched the egg very carefully and am satisfied that it is a very nutritious and safe food.

So, don’t be too concerned about eating eggs unless you know you are one of the 3 in 1000 people that are sensitive to cholesterol or unless you are unhealthy to start. If you can, buy eggs from a farm that allows the chickens to roam free and eat their natural diet or that feeds them seeds that will increase the fatty acids in the egg (fatty acids are good for your heart). The fatty acids, choline, and lutein found in eggs are phenomenally good for you. In fact, I believe that eggs are the perfect food for brain development and function.


  1. For synopsis of the headlines, see
  2. For review of the egg timeline see
  3. For more information in layman’s terms see
  4. Zhong, V. W., et al. (2019). Associations of dietary cholesterol or egg consumption with incident cardiovascular disease and mortality. JAMA 321(11): 1081-1095.
  5. Hu, F. B., et al. (1999). A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 281(15): 1387-1394.
  6. DiMarco, D. M., et al. (2017). “Intake of up to 3 Eggs per Day Is Associated with Changes in HDL Function and Increased Plasma Antioxidants in Healthy, Young Adults.” J Nutr 147(3): 323-329.
  7. Shin, J. Y., et al. (2013). Egg consumption in relation to risk of cardiovascular disease and diabetes: a systematic review and meta-analysis. Am J Clin Nutr 98(1): 146-159.
  8. For the ICAN study, go to and click on “Projects”

Post: April 18, 2019

Build Stronger Muscles with All Kinds of Protein

Research We’re Reading: From the desks of Martin Kohlmeier, MD, PhD and Robyn Amos-Kroohs, PhD

August 28, 2017 – Protein is an important part of every cell in the body. Protein is also a building block of enzymes, hormones, and other important substances used in body processes. It’s a major component of most body systems, including the immune system, metabolism, and circulatory system. Its importance is why protein is known as a macronutrient, meaning that large amounts are required to help the body function appropriately on a daily basis. And unlike sugar and fats, macronutrients that have acquired bad reputations, protein is recognized as an important part of a healthy diet.

Most of us gather the majority of this vital nutrient from animal sources, such as eggs, meat, and dairy products. Animal protein has the advantage of being a complete protein source, meaning that it supplies all of the 22 amino acids that are required in the body on a daily basis, including nine essential amino acids that the body can’t make on its own. The importance of adequate daily intake cannot be overstated, because your body doesn’t store protein long term the way it does fats and carbohydrates.

For health or personal reasons, however, many people choose to exclude animal protein from their diets. Instead, they source their proteins from vegetables, legumes, and nuts or seeds. Plant proteins don’t always have the full amount of all essential amino acids, but combinations, such as beans and corn, tend to balance each other. Therefore, the key for a healthy plant-based diet is variety and knowing about good plant protein combinations.

Whether sourced from animals or plants, the body uses protein to build new muscle and repair old tissue. There has been some question, however, about whether the source of the protein affects muscle strength and musculoskeletal system health. More and stronger muscles are not just what body builders and athletes want, they also ensure more robust health, important with advancing age. Since everyone can benefit from increased muscle and bone health regardless of their diet preferences, researchers have recently assessed whether animal- or plant-sourced protein makes a difference in muscle strength and health.

In this study, researchers used a validated food frequency questionnaire (FFQ) to assess typical dietary intakes of foods and nutrients. In particular, they calculated how much protein from all food sources participants ate, then analyzed the findings by different types of protein. Participants also completed questionnaires about their levels of physical activity, from being asleep to being very active. The two questionnaires about food and activity, along with body composition and muscle strength, were analyzed to determine relationships between the data. Examination of food patterns and muscle health in these middle-aged men and women found that higher protein intake went with greater muscle mass and strength. The differences were small overall (2-3%) and most of that between the lowest and the next protein intake quartile (medians 0.8 g/kg vs 1.1 g/kg). When participants were clustered by the types of protein sources in their diet, muscle measures were similar. It did not seem to matter whether protein came mainly from plant sources, or from meat, dairy products, or fish. These findings appear to support the notion that adults can sustain healthy and strong muscles with a plant-based diet just as well as with meats, fish, or dairy foods. It’s not important how you get your protein from your diet, but it is important that you get enough of it.

Source: Mangano KM et al. Dietary protein is associated with musculoskeletal health independent of dietary pattern. The Framingham Third Generation Family Study. Am J Clin Nutr 2017 105(3):714-722

Maternal Vitamin D For Preventing Autism

Research We’re Reading: From the desk of Jing Xue, Ph.D

July 27, 2017 – Vitamin D deficiency in pregnant moms is shown to negatively affect fetal growth and children’s health in the long run. Deficient gestational vitamin D status is surprisingly high both globally and in the US. One of the findings that draws attention is the role of vitamin D during pregnancy in children’s chances of developing Autism Spectrum Disorders (ASD). Vitamin D is acquired through sun exposure or food intake. The circulating form of vitamin D can travel through the fetal-placental barrier, thus, developing babies depend solely on their mothers for getting this beneficial nutrient.


A group of researchers from Australia and the Netherlands recently showed that mothers with vitamin D deficiency during mid-gestation are more than twice as likely to give birth to an autistic child. The study was carried out on a group of 4334 pregnant women from different ethnic backgrounds. In the group, 16.5% of the subjects were deficient in vitamin D during mid-gestation, while 25.9% had higher vitamin D levels although not reaching the optimum levels. Compared with mothers with optimum levels of vitamin D during pregnancy, those with deficient levels were 2.42 times as likely to have their children diagnosed with ASD later in life.

A Swedish group of researchers conducted a population-based study where they looked into the health records of more than half a million Swedish-born children and similarly found that maternal vitamin D deficiency status is a potential contributing factor for ASD, especially for children with intellectual disability. The approach taken by this group is less direct, as they extrapolated vitamin D status during pregnancy by using secondary care records from the mothers. However, a wide variety of confounding factors were taken into consideration so that their result still warranted further investigation of the causal relation between maternal vitamin D and ASD.

Taking a different approach, researchers looked into 58 pairs of siblings from various ethnic groups. One sibling in each pair was diagnosed with ASD and the other not. Vitamin D levels were measured from blood that had been collected immediately after birth. The results show that children with ASD have significantly lower vitamin D levels at birth than their paired siblings. Because fetal vitamin D status is directly determined by the mothers, these results indicate that vitamin D status among pregnant women is closely linked to ASD risks for babies as they grow.


The current dietary recommendation for vitamin D is 600 international units (IU) per day according to the US Institute of Medicine. Unfortunately, the recommendation is sufficient only to maintain optimum bone health, while evidence for a proper level of vitamin D to maintain extra-skeleton functions is lacking. Thus, it is urgent that more efforts are made to further study the causality between vitamin D and many health outcomes, such as immune function, neurological development, birth outcomes, and reproduction.

Saraf R, et al. Global summary of maternal and newborn vitamin D status – a systematic review. Matern Child Nutr. 2016 Oct;12(4):647-68. doi: 10.1111/mcn.12210. Epub 2015 Sep 15. PMID: 26373311

Vinkhuyzen AAE, et al. Gestational vitamin D deficiency and autism spectrum disorder. BJPsych Open. 2017 Apr 10;3(2):85-90. doi: 10.1192/bjpo.bp.116.004077. eCollection 2017 Mar. PMID: 28446959 PMCID: PMC5385921

Magnusson C, et al. BJPsych Open. Maternal vitamin D deficiency and the risk of autism spectrum disorders: population-based study. 2016 Apr 7;2(2):170-172. eCollection 2016 Mar. PMID: 27703770 PMCID: PMC4998950

Fernell E, et al. Autism spectrum disorder and low vitamin D at birth: a sibling control study. Mol Autism. 2015 Jan 14;6:3. doi: 10.1186/2040-2392-6-3. eCollection 2015.

Effects of Inadequate Hydration on Kidney Disease

From the desk of: Saroja Voruganti, Ph.D.

While drinking at least eight glasses of water a day may not be necessary under normal conditions, maintaining adequate hydration, especially during physical exertion in warm weather, is essential for optimal health.

A recent article published in the American Journal of Kidney Disease suggests that exercise and dehydration contribute to development of chronic kidney disease, particularly the type that is related to heat stress. Heat stress-related kidney disease is increasingly observed in farmers, fishermen, miners, and transportation and construction workers. This type of kidney disease is also called Mesoamerican nephropathy since it was first observed in sugarcane workers in Latin America. Even though they drank a lot of water, these workers suffered high rates of chronic kidney disease.

The authors noted decreased sodium levels and increased uric acid levels after heavy exertion. Uric acid is a breakdown product of DNA and can become elevated with muscle damage. Thus, exercising or working under hot conditions results not only in water loss, but also sodium loss and low-grade muscle injury, which ultimately affect kidney function. Muscle injury and dehydration also cause uric acid to increase, which again results in kidney injury. Kidney injury intensifies with continuous exposure to heat, exercise and dehydration and finally develops into chronic kidney disease. Therefore, maintaining an adequate level of hydration by drinking water with electrolytes at frequent intervals seems to prevent the increase in uric acid levels that occur with heat and exercise.

Maintaining adequate hydration in conditions of heat and exercise is important to minimize risk of kidney injury, but chronic heat and physical exertion stress kidney function and can cause kidney damage even when water is consumed. Under these conditions, it is important to stay extra hydrated to avoid increased uric acid levels and muscle damage, which also contribute to the risk of long-term kidney damage.

Reference: American Journal of Kidney Diseases 2015; Oct 5. pii: S0272-6386(15)01156-7. doi: 10.1053/j.ajkd.2015.08.021


Preventing Fetal Alcohol Spectrum Disorders (FASD)

From the desk of: David Horita, Ph.D.

In a recently published paper1, NRI investigator Phil May and colleagues showed that the prevalence of fetal alcohol syndrome (FAS) and partial fetal alcohol syndrome (PFAS) is two to three times higher than previously estimated.

Curious babyDr. May’s study differs from most FAS prevalence studies in its use of active case ascertainment testing methods to estimate prevalence. This technique includes developmental testing of the child and detailed one-on-one interviews of the mother. The interview questions covered alcohol use during pregnancy, but also asked questions related to secondary factors, such as overall drinking history, marital status; socioeconomic status, and diet/nutrition. This approach is much more labor-intensive than the more common survey approach that relies on self-reported alcohol use information. However, it is also more accurate: self-reported alcohol usage surveys often underestimate FAS because of the stigma of drinking during pregnancy.

This study estimated prevalence of FAS as 3-8 per 1,000 and PFAS as 8-18 per 1000 children in the community. This suggests that up to 2.5 % of children in the US have some degree of FAS. These numbers are significantly higher than previous estimates2 of less than 1 %. In concordance with other studies, May and colleagues found correlations between maternal drinking and child physiology – children with FAS and PFAS were shorter, had lower weight and distinct facial characteristics. Additionally, FAS and PFAS children scored lower on IQ tests and in reading, spelling, and arithmetic ability, and they exhibited more communication, socialization, and behavior disorders than non-FAS children.

Knowing the prevalence of FAS and PFAS guides prioritizing prevention and intervention efforts. Numerous studies have placed the economic cost of FAS and associated disorders at over $1 million per case per lifetime3. These costs include increased medical treatments, increased educational costs, decreased worker productivity, and increased societal costs (youths with FAS are estimated to be nineteen times more likely to be in prison than youths without FAS4). Across the US, the difference in prevalence of 1 vs 2.5 % translates to a difference of several billion dollars per year in real costs. Dr. May’s research clarifies the social and economic value of FAS prevention efforts.

There is no cure for FAS. The finding that 2-3 times more children in the US show FAS symptoms than previously estimated underscores the importance of FAS research that could lead to treatments. For instance, other ongoing NRI studies are investigating the potential of nutritional supplements to ameliorate symptoms in young children with FAS5.


David Horita joined the NRI in 2013 as a grant writer. He assists faculty by identifying funding opportunities and writing/editing research proposals. David developed research and writing experience in metabolism and cell signaling during his 13 years as a faculty member in Biochemistry at Wake Forest University School of Medicine. He did postdoctoral work at the NCI/NIH and obtained a Ph.D. in physical chemistry from the University of Wisconsin and a B.A. in chemistry from Carleton College.



1May PA, Keaster C, Bozeman R, Goodover J, Blankenship J, Kalberg WO, Buckley D, Brooks M, Hasken J, Gossage JP, Robinson LK, Manning M, Hoyme HE (2015). Prevalence and characteristics of fetal alcohol syndrome and partial fetal alcohol syndrome in a Rocky Mountain Region City. Drug Alcohol Depend 155:118-2


3Popova S, Stade B, Lange S, Bekmuradov D, Rehm J (2012). Economic impact of fetal alcohol syndrome (FAS) and fetal alcohol spectrum disorders (FASD). Public Health Agency of Canada. Ottawa, Ontario, CA

4Popova S, Stade B, Lange S, Rehm J (2012). A model for estimating the economic impact of fetal alcohol spectrum disorder. J Popul Ther Clin Pharmacol 191:e51-e65

5Wozniak JR, Fuglestad AJ, Eckerle JK, Fink BA, Hoecker HL, Boys CJ, Radke JP, Kroupina MG, Miller NC, Brearley AM, Zeisel SH, Georgieff MK (2015). Choline supplementation in children with fetal alcohol spectrum disorders: a randomized, double-blind, placebo-controlled trial. Am J Clin Nutr (in press)

Is Life Expectancy a Good Measure of Health?

From the desk of: Mirko Hennig, Ph.D.

“Wishing you a long, happy and healthy life” is what we repeatedly say as we get older. A recent, global study published in The Lancet (2015; 386, p.743-800) clearly emphasizes the importance of the latter referring to our quality of life. According to the Global Burden of Disease (GBD) study, worldwide life expectancy at birth rose by 6.2 years between 1990 and 2013. However, these additional years come at a price as healthy life expectancy at birth increased by only 5.4 years over the same 13 year time span. The massive, country-specific assessment utilized age-specific mortalities and data accumulated for 306 diseases in 188 countries between 1990 and 2013. While the study highlights the need for more and better data about disabilities to estimate healthy life expectancies in a more reliable manner, several consistent trends emerge:

Implications of this study
Living longer but suffering more? While life expectancy in 1990 in the US averaged 71.9 and 78.8 years for male and female population, respectively, it increased significantly reaching averages of 76.3 and 81.4 years in 2013. However, the years of life expectancy gained are not necessarily lived healthily. On average, 9.2 (8% of life expectancy) and 11.9 (15%) years of male and female lives born in 1990 are associated with disability. This burden of disease increases to 10.5 (14%) and 12.8 (16%) years for male and female population born in 2013. Thus, the data suggests a widening gap between longer and healthy lives.

senior woman and doctor with tablet pc at hospitalNeglected, age-related diseases. The reason for an increased disease burden over our longer life spans can at least partially be attributed to a rising prevalence of age-related conditions. While the GBD team shows that health loss due to cardiovascular and circulatory diseases and cancer stagnated or even decreased over the period 1990-2013, the drivers of the difference between longer and healthy life expectancies are musculoskeletal disorders, mental and substance use disorders, neurological disorders, and diabetes, accompanied by vision and hearing loss.

While the leading cause of increased disease burden in the US in 2013 continues to be ischemic heart disease, it is now followed by back and neck pain. Chronic obstructive pulmonary disease ranks third. Tracheal, bronchus and lung cancer, depression, diabetes, Alzheimer’s, other musculoskeletal disorders, stroke and sense organ disorder round out the 2013 top ten in the US.

Take-home message
Research and development investments by the National Institutes of Health (NIH) and the pharmaceutical industries have traditionally focused on cardiovascular diseases, endocrine disorders and cancer. As a consequence, sustained gains have been made against the majority of the leading causes of death worldwide. On the other hand, few age-related diseases such as musculoskeletal disorders, neurological disorders, diabetes and hearing and vision loss receive the attention they deserve in public policy discussions and health research priorities. A balanced diet rich in antioxidants and anti-inflammatories plays an important role to forestall the onset of age-related disorders. Therefore, researchers at the Nutrition research Institute (NRI) in Kannapolis including Drs. Cheatham, Surzenko and Zeisel investigate the interplay of nutrition and cognitive function. However, more investment and research has to shift towards diseases that debilitate, rather than kill in order to maintain health progress in ageing populations.

Go With Your Gut: How a community of trillions affects your individual health

From the desk of: Katie Meyer, Ph.D.

Everyday we learn more about how the gut microbiome may influence health. Our gut microbial community—a super-organism, with trillions of members—has been associated with obesity, diabetes, cancer, heart disease, and immune disorders, and even moods. These findings have generated enormous enthusiasm among researchers and the lay public, as they suggest a largely untapped area for health-promoting interventions. One mechanism through which the gut microbiome may affect health is through the metabolism of food and nutrients. We know that the production of some bioactive metabolites is dependent on the genetic machinery of gut microbes. We also know that individuals differ in the production of bioactive metabolites following nutrient ingestion. A critical next step is delineating the gut microbiome-specific pathways from food consumption to metabolite production to health status. This is an area of active research at the NRI, and the focus of a new scientific publication.

bef6d795-dcaa-4705-a6f3-5b7536df7b06THE STUDY
A group at the Fred Hutchinson Cancer Research Center recently characterized individuals with respect to their blood levels of plant food metabolites and their gut microbial community. The researchers focused on enterolignans, metabolites of polyphenolic compounds (micronutrients) called lignans, found in plants. The intake of lignans, such as through the consumption of seeds and whole grains, has been associated with decreased colon and breast cancer risk. Enterolignans are some of the bioactive metabolites that may directly contribute to the health benefits of plant food-rich diets.

The production of enterolignans has large individual variability, which may reflect individual differences in the gut microbiome. To test this, the researchers compared the gut microbial community in people with different levels of enterolignans, controlling for differences in diet and other lifestyle factors. Their results revealed significant differences between features of the gut microbiome—including in the diversity of microbiota and taxonomic composition—and blood levels of one enterolignan, enterolactone, showing that enterolignan production is defined, at least in part, by an individual’s gut microbiome. These results connect differences in the gut microbial community and the presence of beneficial metabolites, illustrating the potential for the gut microbiome to influence health through the production of health-related bioactive compounds.

This study is an example of how we will move towards a detailed understanding of the gut microbiome’s role in health status through dietary metabolites and individual differences in the health effects of diet. Ultimately, we aim to identify the specific gut microbial features related to the production of beneficial metabolites so that we can design personalized diets to optimize health and intervene at the microbiome level.


Reference: Huller MAJ, Lancaster SM, Li F, et al. Enterolignan-producing phenotypes are associated with increased gut microbial diversity and altered composition in premenopausal women in the United States. Cancer Epidemiol Biomarkers Prev 2015;24:546-554.


Eat More Produce, Reduce Cancer

From the desk of: Jessica Sisneros, M.S., R.D., L.D.N.

ThinkstockPhotos-179077332It’s spring! Farmers markets are opening and these are great places to find a variety of local, seasonal produce, which flourishes now. Making room for these powerhouses in your everyday food choices is important for your health. A 2012 peer-reviewed analysis in Food and Chemical Toxicology states that approximately 20,000 cancer cases could be prevented every year if one-half of Americans were to increase their serving of fruits and vegetables by one serving per day. The recommended serving size for one serving of vegetables is equal to 1 cup of raw leafy vegetables, ½ cup of other vegetables or 1/2 cup of vegetable juice. The recommended serving size for one serving of fruit is 1 medium fruit (medium is defined as the size of a baseball), ½ cup chopped, cooked or canned fruit or ½ cup juice.

There are several reasons to take advantage of the fruits and vegetables at your local farmers market. This produce is the freshest and tastiest available. Fruits are allowed to ripen in the field and are brought directly to you—no long-distance shipping, no gassing to interrupt the ripening process, no sitting in storage for weeks. This is as real as it gets—fresh food from the garden.

One of the first delicacies of spring is fresh asparagus. In the southeast asparagus is in season from February to June. Fresh asparagus is usually bright green, although some markets may also sell purple or white varieties. The tips should be firm and tight, not mushy. When choosing your asparagus the stalk size is not an indicator of tenderness.

Eating asparagus is an excellent way to protect yourself against heart disease, as it contains folate, as well vitamins E, A, and C. In addition to helping your heart, folate helps cells regenerate; vitamin E provides antioxidant protection; and vitamins A and C prevent cancer. Asparagus also contains potassium, which helps to lower blood pressure. Asparagus is an excellent low-calorie, high-fiber vegetable to add to your meals this spring. Other seasonal produce that can be found at the farmers market in May includes arugula, artichoke, beets, cabbage, garlic, green beans, peppers, onions, kale, lettuce, spinach and strawberries. Enjoy this bounty of fresh produce and stay well!



Roasted Asparagus from the Produce Lady 

1 lb. asparagus
2 tbsp. olive oil
1 cup crumbled blue cheese, Parmesan or other cheese (optional)

Preheat oven to 350 degrees F. In a large bowl, toss the asparagus and olive oil. Pour asparagus and oil into a nonstick pan, top with cheese. Bake 15 to 20 minutes. Serves 4.

Nutrition Information Per Serving

75.1 Calories, Total Fat 6.9 g, Cholesterol 0.0 mg, Sodium 1.3 mg, Total Carbohydrates 3.0 g, Dietary Fiber 1.4 g, Protein 1.5 g



Shop Local

Farmers markets are found throughout the country depending on growing seasons. To find a farmer’s market close to you, click here


Reference: Estimation of cancer risk and benefits associated with a potential increased consumption of fruits and vegetables (Food and Chemical Toxicology. 2012 December; V50: 4421-4427)

Understanding Nutrigenomics

Why “good” and “bad” are irrelevant when talking about genes and nutrition

From the desk of: Mihai Niculescu, M.D., Ph.D.

…“How to override your bad genes with food.” “Can Exercise Override Bad Genes?” “Good Nutrition Can Overcome Bad Genes”…

woman drawing dnaWe are bombarded by media with these kinds of messages. The main theme, of course, is that many of us may have “bad” genes that would put us at risk of a certain poor health outcome unless we eat less of “this” and more of “that.” Knowing myself as a bearer of several such genetic variations, I almost feel, at times, guilty that I am harboring such “bad” genes, albeit without my consent.

Here is why such thinking is wrong, and why the paper I have read recently is a good example of how the public should understand what nutrigenomics is, and why there are no such things as “bad” or “good” genes when it comes to nutrition (except for very few documented cases). And here I am talking about those genetic variations (changes in our genetic code) that are quite frequent (being present in up to 50 percent of us).

First, let’s establish a couple of things. 1: Genetic variations that are at high frequency in a population are the result of Darwinian selection. If such genes are (still) frequent in the human population, all this means is that individuals who carry them had no troubles in reproducing and in disseminating their genes through their offspring. This only tells us that those individuals were okay in the environment (including nutrition) they used to live in. 2: Scientists discovered that, in many cases, genetic variations across one or more genes are not randomly combined, but rather they exist in only several combinations (called haplotypes). These combinations of genetic variations are inherited by descendants.

The study by Ameur and colleagues (see link below) looked at how these haplotypes, or combinations of genetic variations, evolved during human evolution for those genes responsible for processing omega-3 and -6 fatty acids acquired from vegetable oils. When comparing the present European populations with archaic hominins and distant primates, they concluded that a certain combination of such variations (called Haplotype D), appeared after the split from Neanderthals (around 500,000 years ago). Moreover, this means that the Haplotype D, being enriched in more recent populations (Africa, Middle East, Asia and Europe), while quite rare in the Americas, indicates that the Haplotype D shows positive selection (its frequency increases in more recent populations), meaning that it brought some type of survival advantage in the environment from Africa, Asia, and Europe, but not in the Americas.

Interestingly, the researchers also measured how Haplotype D influences the omega-3 and -6 metabolism, and they concluded that the Haplotype D accelerates the conversion of omega-3 and -6 fats from vegetable sources, into molecular species that are found mainly in fish oil (DHA and EPA), and also into arachidonic acid (main omega-6 component). Note: DHA and EPA have many health benefits, while arachidonic acid is a pro-inflammatory molecule. So, by all means, Haplotype D carriers were at an advantage during the development of the human race in the Afro-Eurasia continental mass. Is this, then, a “good” haplotype? “Definitely,” would answer the proponents of the “good” and “bad” genes concept.

But here is the catch! The same Haplotype D (so beneficial during our evolution) proved to be a problem when it comes to our modern lifestyle and nutrition habits. It turns out that the Haplotype D actually increases the risk of having coronary artery disease, but only because we eat more omega-6 oils than we should (and not enough omega-3 oils). Because Haplotype D carriers are so efficient in converting omega-6 precursors to arachidonic acid, they have an increased inflammation status, which contributes in turn to the coronary artery disease. This is “bad,” isn’t it?

So how should we interpret these findings, and how do we know what we should eat? This study is a good example of how we can tackle individualized nutrition. It suggests that those people who have the Haplotype D should increase their intake of omega-3, and decrease the omega-6 intake.

“Good” and “bad” genes? Hardly. Rather, we should focus on how fit our environment (nutrition included) is for our genes. This is a much more productive approach, allowing us to reshape our lifestyle to what each of us needs.


Reference: Genetic Adaptation of Fatty-Acid Metabolism: A Human-Specific Haplotype Increasing the Biosynthesis of Long-Chain Omega-3 and Omega-6 Fatty Acids (Am J Hum Genet. 2012 May 4; 90(5): 809-820)