Received a bachelor’s degree in microbiology and immunology. Worked as a research assistant in a molecular biology laboratory at Stanford University for 6 years. Received a Master’s degree in Nutritional Sciences. Certified as a diabetes educator and worked at the Palo Alto Medical Foundation for 14 years counseling patients. In addition to her clinical experience, Dalia has also been involved in research and teaching. She taught at San Jose State University, and continues to advise students on their theses. She currently works as a research dietitian and study coordinator at Stanford University. She is a reviewer for the Journal of the Academy of Nutrition and Dietetics and was an analyst for the Evidence Analysis Library.
She has spoken in conferences geared to dietitians and physicians.
Current Role at Stanford
•Implements the nutritional component of research protocols, counsels participants, collects and enters food records, develops nutrition education materials, and develops specialized diets for metabolic studies.
•Develops protocols and informed consent forms for IRB submission.
•Collects, compiles, documents, and analyzes clinical research data.
•Recruits and consents subjects.
•Develops and presents curriculum to educate subjects on study diets.
•Implements new techniques to increase adherence to study diets.
•Acts as a liaison between investigators, collaborators, and study participants.
Honors & Awards
Excellence in Clinical Nutrition, Academy of Nutrition and Dietetics (2009)
Education & Certifications
CDE, National Certification Board for Diabetes Educators, Diabetes (2002)
MS, San Jose State University, Nutritional Sciences (1999)
BS, San Jose State University, Medical Microbioology (1985)
work towards BS, Universidad Nacional Autonoma de Mexico, Biomedical Research (1982)
Service, Volunteer and Community Work
Advisor, San Jose State University
Advise graduate students in Nutrition on their theses, including choosing the research project, conducting it, analyzing results and writing the report.
San Jose, California
Reviewer, Journal of the Academy of Nutrition and Dietetics
Review manuscripts submitted for publication.
Evidence Analyst, Academy of Nutrition and Dietetics (8/1/2011 - October 30, 2012)
Evaluate, synthesize, and grade the strength of the evidence to support conclusions that answer a precise series of questions.
Interaction between the host and the microbiome
Substituting poly- and mono-unsaturated fat for dietary carbohydrate reduces hyperinsulinemia in women with polycystic ovary syndrome.
Hyperinsulinemia is a prevalent feature of polycystic ovary syndrome (PCOS), contributing to metabolic and reproductive manifestations of the syndrome. Weight loss reduces hyperinsulinemia but weight regain is the norm, thus preventing long-term benefits. In the absence of weight loss, replacement of dietary carbohydrate (CHO) with mono/polyunsaturated fat reduces ambient insulin concentrations in non-PCOS subjects. The current study evaluated whether this dietary intervention could ameliorate hyperinsulinemia in women with PCOS.Obese women with PCOS (BMI 39 ± 7 kg/m(2)) and insulin resistance completed a crossover study (Stanford University Clinical Research Center) comparing two isocaloric diets, prepared by research dietitians, containing 60% CHO/25% fat versus 40% CHO/45% fat (both 15% protein and ≤7% saturated fat). After 3 weeks on each diet, daylong glucose, insulin, and fasting lipid/lipoproteins were measured.Daylong glucose did not differ according to diet. Daylong insulin concentrations were substantially (30%) and significantly lower on the low CHO/higher fat diet. Beneficial changes in lipid profile were also observed.Replacement of dietary CHO with mono/polyunsaturated fat yields clinically important reductions in daylong insulin concentrations, without adversely affecting lipid profile in obese, insulin-resistant women with PCOS. This simple and safe dietary intervention may constitute an important treatment for PCOS. ClinicalTrials.gov Identifier: NCT00186459.
View details for PubMedID 27910718
Adipose Cell Size and Regional Fat Deposition as Predictors of Metabolic Response to Overfeeding in Insulin-Resistant and Insulin-Sensitive Humans
2016; 65 (5): 1245-1254
Obesity is associated with insulin resistance (IR), but significant variability exists between similarly-obese individuals, pointing to qualitative characteristics of body fat as potential mediators. To test the hypothesis that obese, insulin-sensitive (IS) individuals possess adaptive adipose cell/tissue responses, we measured subcutaneous adipose cell size, insulin-suppression-of lipolysis, and regional fat responses to short-term overfeeding in BMI-matched overweight/obese individuals classified as IS or IR. At baseline, IR subjects exhibited significantly-greater visceral adipose tissue(VAT), intrahepatic lipid(IHL), plasma FFAs , adipose cell diameter, and %small adipose cells. With weight gain (3.1+1.4 kg), IR subjects demonstrated no significant change in adipose cell size, VAT, or insulin-suppression-of lipolysis, and only 8% worsening of insulin-mediated glucose uptake (IMGU).Alternatively, IS subjects demonstrated significant adipose cell enlargement, decrease in %small adipose cells, increase in VAT, IHL, lipolysis, 45% worsening of IMGU, and decreased expression of lipid metabolism genes. Smaller baseline adipose cell size and greater enlargement with weight gain predicted decline in IMGU, as did increase in IHL, VAT, and decrease in insulin-suppression-of lipolysis. Weight gain in IS humans causes maladaptive changes in adipose cells, regional fat distribution, and insulin resistance. The correlation between worsening insulin resistance and changes in adipose cell size, VAT, IHL, and insulin-suppression-of lipolysis highlight these factors as potential mediators between obesity and insulin resistance.
View details for DOI 10.2337/db15-1213
View details for Web of Science ID 000375028000015
View details for PubMedID 26884438
5-Lipoxygenase Metabolite 4-HDHA Is a Mediator of the Antiangiogenic Effect of omega-3 Polyunsaturated Fatty Acids
SCIENCE TRANSLATIONAL MEDICINE
2011; 3 (69)
Lipid signaling is dysregulated in many diseases with vascular pathology, including cancer, diabetic retinopathy, retinopathy of prematurity, and age-related macular degeneration. We have previously demonstrated that diets enriched in ω-3 polyunsaturated fatty acids (PUFAs) effectively reduce pathological retinal neovascularization in a mouse model of oxygen-induced retinopathy, in part through metabolic products that suppress microglial-derived tumor necrosis factor-α. To better understand the protective effects of ω-3 PUFAs, we examined the relative importance of major lipid metabolic pathways and their products in contributing to this effect. ω-3 PUFA diets were fed to four lines of mice deficient in each key lipid-processing enzyme (cyclooxygenase 1 or 2, or lipoxygenase 5 or 12/15), retinopathy was induced by oxygen exposure; only loss of 5-lipoxygenase (5-LOX) abrogated the protection against retinopathy of dietary ω-3 PUFAs. This protective effect was due to 5-LOX oxidation of the ω-3 PUFA lipid docosahexaenoic acid to 4-hydroxy-docosahexaenoic acid (4-HDHA). 4-HDHA directly inhibited endothelial cell proliferation and sprouting angiogenesis via peroxisome proliferator-activated receptor γ (PPARγ), independent of 4-HDHA's anti-inflammatory effects. Our study suggests that ω-3 PUFAs may be profitably used as an alternative or supplement to current anti-vascular endothelial growth factor (VEGF) treatment for proliferative retinopathy and points to the therapeutic potential of ω-3 PUFAs and metabolites in other diseases of vasoproliferation. It also suggests that cyclooxygenase inhibitors such as aspirin and ibuprofen (but not lipoxygenase inhibitors such as zileuton) might be used without losing the beneficial effect of dietary ω-3 PUFA.
View details for DOI 10.1126/scitranslmed.3001571
View details for Web of Science ID 000292971100004
View details for PubMedID 21307302
Effect of omega-3 fatty acid supplementation on indicators of membrane fluidity
FEDERATION AMER SOC EXP BIOL. 2010
View details for Web of Science ID 000208675504417