Nutrition Frontiers - Spring 2017

Volume 8, Issue 2

Date Posted: 

Wednesday, May 10, 2017

Dear Nutrition Enthusiast,

This issue showcases the calcium/magnesium intake ratio in colorectal adenoma, the role of PPARγ in metabolism and reproduction, and the effects of time-restricted feeding on metabolic parameters. Meet our spotlight investigator, Dr. Maria Cruz-Correa, and her research on gut bacterial genes, diet, and colorectal neoplasia. Learn about matcha, the powdered leaf tea, upcoming announcements and more..


Calcium/Magnesium Intake Ratio Interacts with Polymorphism Associated to Colorectal Neoplasia

A display of food items including milk, nuts, cheese, sardines, and broccoli.The calcium (Ca)/magnesium (Mg) intake ratio may influence the associations of Ca and Mg with risk to colorectal adenoma, recurrence and cancer. Zhu et al investigated gene-nutrient interactions using participants from the Tennessee Colorectal Polyp Study.  In Phase-I, 19 single nucleotide polymorphisms (SNPs) significantly interacting with the Ca/Mg intake ratio in adenoma risk were identified.  In Phase II, one SNP in the parathyroid hormone gene (rs11022858) was replicated.  High Ca/Mg intake ratio tended to be associated with a reduced risk of colorectal adenoma among those with the TT genotype. A high dietary Ca intake (≥ 1000 mg) was significantly associated with 64% reduced adenoma risk only among TT genotype and not associated with risk in other genotypes (CC/TC).  Inversely, Mg intake was not linked to risk among those with the TT genotype while the highest magnesium intake was significantly associated with 27% reduced risk of colorectal adenoma among those with the CC/TC genotype.  Further study on gene-nutrient interactions is needed to develop personalized strategies for colorectal cancer prevention. 


Neuronal PPARγ Involved in Adverse Effects of Diet-Induced Obesity

An image dispalying peroxisome-proliferator activated receptors.Peroxisome-proliferator activated receptor (PPARγ) regulates adipocyte differentiation, lipid and glucose homeostasis, and control of inflammatory responses. The effects of PPARγ in reproduction are less known. In a recent study, Fernandez and colleagues created a deletion of PPARγ in mature neurons (brain-knockout, BKO)  in female mice to investigate the role of neuronal PPARγ in metabolism and reproduction. Although the deletion of PPARγ did not alter the timing of puberty in female mice, fertility was impaired. When the mice were challenged with a 60% high-fat diet, the BKO mice had  the expected alterations in body weight, glucose and insulin tolerance, and leptin levels but were protected from obesity-induced leptin resistance; the BKO mice also were protected from obesity-induced estrous cycle impairment. Further detailed studies using genetic deletions in specific neuronal populations will be necessary to dissect the individual contributions of PPARγ to leptin resistance and reproductive function in obesity.


The Stars in Nutrition and Cancer lecture, Aflatoxin: An Old Carcinogen Teaches Us New Tricks, by John D. Groopman, Ph.D., Johns Hopkins University is now available for viewing here.

Couldn’t make it to the John Milner Nutrition and Cancer Prevention Research Practicum in March, then read one attendee’s testimonial for an in-depth perspective.

Upcoming Events

May 22-25, 2017
Workshop on Nutrigenetics, Nutrigenomics and Precision Nutrition
Kannapolis, NC

May 25-26, 2017
Emerging Role of Branched-Chain Amino Acids in Human Diseases
National Institute of Diabetes and Digestive and Kidney Diseases, NIH
Bethesda, MD

June 13-14, 2017
Workshop on Best Practices for Studies of Diet and the Intestinal Microbiome
NIH Campus and webcast.
In-person registration is full. However, registration to view the meeting via webcast is available. Register by emailing

July 20-24, 2017
Society for Nutrition Education and Behavior 50th Annual Conference
Washington, DC

October 21-25, 2017
Food and Nutrition Conference and Expo
Chicago, IL

December 5-6, 2017
NIH Pathways to Prevention Workshop: Methods for Evaluating Natural Experiments in Obesity
Bethesda, MD

Time-Restricted Feeding Improves Metabolic Parameters in Postmenopausal Obesity Mouse Model

An images with a place setting with a clock on a dinner plate.Time-restricted feeding (TRF) is the practice of restricting the time of calorie intake, rather than the amount of calorie intake, to a specific period in the normal circadian rhythm. TRF is an alternative approach to caloric restriction for metabolic disease and cancer prevention that might have better compliance. Chung and colleagues tested TRF as an intervention in a mouse model of postmenopausal obesity. Ovariectomized mice were fed either normal low fat chow or a high fat diet ad libitum for 9 weeks after which the high fat-fed group was split into ad libitum and TRF high fat-fed groups. Despite having 8-hour access to the same high fat diet as ad libitum-fed mice, TRF mice experienced rapid weight loss followed by weight stabilization, delayed improvement in insulin resistance, amelioration of hepatosteatosis, and beneficial modulation of hepatic gene expression. Further long-term animal studies are being pursued to define the molecular basis for the beneficial effects of TRF on metabolism.


Portrait of Marcia Cruz-Correa,  M.D., Ph.D.Marcia Cruz-Correa, M.D., Ph.D. is a Professor of Medicine and Biochemistry at the University of Puerto Rico (UPR), Adjunct Associate Professor of Medicine at Johns Hopkins University and at the MD Anderson Cancer Center. She also is the Director for Research at the UPR Medical Sciences Campus and the Scientific Director at the UPR Comprehensive Cancer Center. Dr. Cruz-Correa completed her B.S. in biology, her medical degree, and Internal Medicine residency at UPR. She completed a doctoral degree in Clinical Investigation and Genetic Epidemiology at Johns Hopkins School of Public Health. She has a strong focus in cancer genetics, chemoprevention, hereditary cancer and health disparities. She was awarded an R01 for her project Association of Gut Bacterial Genes and Diet to Colorectal Neoplasia.

Read more about Marcia Cruz-Correa

Did You Know?

Matcha:  The Powdered Leaf

A picture of a cup of matcha tea.Matcha, like all teas, comes from the Camellia sinensis plant native to China. Brought to Japan by the renowned Japanese Zen Buddhist Monk Eisai in 1191 A.D., matcha is steam-dried green tea leaves ground into a fine powder.  Given the energy and mental alertness it offered, matcha was valued by monks for thousands of years as medicine. Over time it was discovered that shading tea plants just before harvest creates a smooth, mellow, umami taste in the leaves that allowed matcha to be savored as a delicacy!

Catechins, amino acids, and saponins in matcha contribute to the foaming observed in the mindful ritual of preparing and consuming it in Japanese tea ceremonies.  Whether you try matcha as a replacement to coffee or as a pick-me-up addition to a smoothie — it can be a refreshing culinary addition to all types of foods, including desserts!

Try Traditional Ceremonial Grade Matcha:

  1. Combine 1-3 teaspoon(s) of matcha green tea powder with a small amount of hot water.
  2. Stir or whisk with a chasen, a traditional bamboo whisk, to create a bright emerald green paste.
  3. Add additional hot water and whisk until foam is observed.  Whisking promotes the extraction of the catechins, in particular, epigallocatechin gallate and caffeine.
  4. Savor and sweeten to taste.