Dr. Sellmeyer is an internationally recognized expert in Metabolic Bone Disease. She is a renowned clinician who joined the Stanford faculty in 2018 as a Professor of Medicine. She has been recognized for her clinical excellence with induction into the Miller Coulson Academy of Clinical Excellence while she was at Johns Hopkins. In addition to her clinical expertise, Dr. Sellmeyer maintains a research program that centers on the effect of nutrition and environmental factors on skeletal metabolism which she has investigated through both smaller CRC-based trials and large multi-center trials. Studies she has conducted have investigated the role of dietary sodium chloride, source of dietary protein (animal, vegetable, dairy, soy), role of dietary potassium and alkaline potassium salts, targeted thoracic exercises on kyphosis, whether structured exercise can prevent bone loss in premenopausal women treated for breast cancer, and studies validating nutritional assessment questionnaires. Her expertise as a clinical researcher has enabled development of a multi-disciplinary translational research team including basic scientists in the orthopedic department, junior faculty members with K grant funding, and basic scientists in the endocrine division to develop translational projects studying the effects of osteoporosis medications on basic elements of skeletal biology utilizing bone biopsies from treated individuals as well as clinical trials of novel therapies for rare bone disorders. Dr. Sellmeyer also is a esteemed educator, having received multiple teaching awards.
- Metabolic Bone Disease
- Diabetes and Metabolism
Clinical Professor, Medicine - Endocrinology, Gerontology, & Metabolism
Member, Stanford Cancer Institute
Board Certification: American Board of Internal Medicine, Endocrinology, Diabetes and Metabolism (1998)
Fellowship: UCSF Endocrinology Fellowship (1998) CA
Residency: Johns Hopkins Hospital Internal Medicine Residency (1994) MD
Medical Education: Johns Hopkins University School of Medicine (1991) MD
- Now That You Can Get What You Want, Can You Keep What You Need? Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 2019
Glycemic control and changes in hip bone mineral density in men and women with type 2 diabetes: The Health, Aging and Body Composition Study
WILEY. 2019: 162
View details for Web of Science ID 000508614700474
A Unique Cause of Hypercalcemia
WILEY. 2019: 76
View details for Web of Science ID 000508614700214
Proteinuria is Associated with Increased Risk of Fragility Fracture in Men With or at Risk for HIV infection Proteinuria and Fracture Risk Association.
Journal of acquired immune deficiency syndromes (1999)
Proteinuria has been associated with bone loss and fractures in general population but data in HIV-infected population is lacking.Prospective, multicenter cohort study of men with or at risk for HIV infection.Between 2006 and 2015, urine protein measurements and bone fracture histories were ascertained semi-annually in 947 HIV-infected (HIV+) and 969 HIV-uninfected (HIV-) men ≥ age 40. Proteinuria was defined as protein-to-creatinine ratio ≥ 200 mg/g at ≥ 2 consecutive visits.1) all fractures (excluding fractures of skull, face, digits) 2) fragility fractures (fractures of vertebral column, femur, wrist, humerus). Multivariable Cox proportional hazards models assessed the association between proteinuria and fracture after adjusting for additional risk factors.The overall period prevalence of proteinuria was higher among HIV+ than HIV- (29% vs 6%, p<0.001). Men with proteinuria had a significantly higher risk of fragility fracture compared to men without proteinuria (aHR=2.29 [1.12-4.66]), and did not differ by HIV-serostatus (p-interaction=0.83). The risk of all fractures was not statistically different between men with or without proteinuria (aHR=1.31 [0.84-2.05]). Among HIV+ men, the association between confirmed proteinuria and fragility fracture was attenuated (aHR=2.12 [0.95-4.73]) after additional adjustment for CD4 T cell count/mm, history of AIDS, the presence of detectable plasma HIV-1 RNA, and cumulative exposure to tenofovir disoproxil fumarate.Proteinuria was more common in HIV+ than HIV- men and was a strong independent risk factor for fragility fracture regardless of HIV serostatus. Proteinuria should prompt consideration of a thorough evaluation for bone disease among HIV+ persons.
View details for DOI 10.1097/QAI.0000000000002039
View details for PubMedID 30939529
A Randomized Controlled Trial of Exercise to Prevent Bone Loss in Premenopausal Women with Breast Cancer.
Journal of women's health (2002)
Background/Introduction/Objective: Premenopausal women treated for breast cancer are at high risk for bone loss. This trial examined the effects of a 1-year combined aerobic and resistance exercise program on bone mineral density (BMD) in women treated for premenopausal breast cancer.MATERIALS AND METHODS: Premenopausal women (n=206) age ≤55 years at cancer diagnosis who were within two years of receiving adjuvant chemotherapy were randomized to a 12-month exercise program or a control group. BMD was measured by dual-energy X-ray absorptiometry at baseline and after 1 year; blood was drawn for skeletal markers. Change from baseline to end of study was compared within and between treatment groups using paired and unpaired t-tests.RESULTS: Lumbar spine BMD declined in both treatment groups with no significant difference between treatment groups (-0.008±0.003g/cm2 exercise vs. -0.014±0.003g/cm2 control, p=0.24). However, among the women who did not lose lean mass during the study (n=100, 54 control, 46 exercise), the exercise intervention prevented lumbar spine bone loss (0.001±0.005g/cm2 treatment group vs. -0.014±0.005g/cm2 control group, p=0.03). Bone turnover markers decreased significantly in both groups with no differences between groups.CONCLUSIONS: Among women who maintained lean mass, our exercise intervention prevented bone loss; however, our intervention did not prevent bone loss among women who lost muscle mass. Additional investigation into exercise regimens that can prevent both bone and muscle loss may help prevent long-term consequences of premenopausal breast cancer treatment.
View details for PubMedID 30312118
- National Institutes of Health Consensus Development Conference: Lactose Intolerance and Health ANNALS OF INTERNAL MEDICINE 2010; 152 (12): 792-?
A proposed method for assessing plasma hypertonicity in vivo
EUROPEAN JOURNAL OF CLINICAL NUTRITION
2007; 61 (1): 143-146
Indices of plasma hypertonicity, elevated plasma concentrations of solutes that draw fluid out of cells by osmosis, are needed to pursue hypertonicity as a possible risk factor for obesity and chronic disease. This paper proposes a new index that may be more sensitive to mild hypertonicity in vivo at a point in time than traditional measures. The index compares mean corpuscular volume (MCV) estimates from diluted (in solution by automated cell counter) and nondiluted blood (calculated from manual hematocrit, MCV=Hct/RBC*10(6)). A larger Auto vs Manual MCV (>2 fl) in vitro indicates hypertonicity in vivo if the cell counter diluent is isotonic with the threshold for plasma vasopressin (PVP) release and PVP is detectable in plasma (>0.5 pg/ml). To evaluate this principle of concept, hypertonicity was induced by 24-h fluid restriction after a 20 ml/kg water load in four healthy men (20-46 years). Unlike serum and urine indices, the MCV difference-&-PVP index detected hypertonicity in all participants.
View details for DOI 10.1038/sj.ejcn.1602481
View details for Web of Science ID 000242830700022
View details for PubMedID 16855542
Effect of alendronate on bone mineral density and biochemical markers of bone turnover in type 2 diabetic women - The fracture intervention trial
2004; 27 (7): 1547-1553
Alendronate sodium (ALN) increases bone mineral density (BMD) in heterogeneous populations of postmenopausal women, but its effect is unknown in women with type 2 diabetes. The objective of this project was to compare changes in BMD during 3 years of ALN treatment versus placebo in diabetic women.We used data from the Fracture Intervention Trial, a randomized blinded placebo-controlled trial conducted at 11 centers in which 6458 women aged 54-81 years with a femoral neck BMD of
or=200 mg/dl.In diabetic women, 3 years of ALN treatment was associated with increased BMD at all sites studied, including 6.6% at the lumbar spine and 2.4% at the hip, whereas women in the placebo group experienced a decrease in BMD at all sites except the lumbar spine. The safety/tolerability of ALN was similar to placebo, except for abdominal pain, which was more likely in the ALN group.ALN increased BMD relative to placebo in older women with type 2 diabetes and was generally well tolerated as a treatment for osteoporosis. Increases in BMD with ALN therapy compared with placebo were similar between women with and without diabetes.
View details for Web of Science ID 000222397100004
View details for PubMedID 15220226
Older women with diabetes have an increased risk of fracture: A prospective study
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
2001; 86 (1): 32-38
To determine whether type 2 diabetes is associated with fracture in older women, we analyzed data from 9654 women, age 65 yr or older, in the Study of Osteoporotic Fractures. Diabetes with age at onset 40 yr or older was reported by 657 women, of whom 106 used insulin. A total of 2624 women experienced at least one nonvertebral fracture during an average follow-up of 9.4 yr, and 388 had at least one vertebral fracture during an average interval of 3.7 yr. Although diabetes was associated with higher bone mineral density, it was also associated with a higher risk of specific fractures. Compared with nondiabetics, women with diabetes who were not using insulin had an increased risk of hip [relative risk (RR), 1.82; 95% confidence interval (CI), 1.24-2.69] and proximal humerus (RR, 1.94; 95% CI, 1.24-3.02) fractures in multivariate models controlling for age, body mass index, bone density, and other factors associated with fractures and diabetes. Insulin-treated diabetics had more than double the risk of foot (multivariate adjusted RR, 2.66; 95% CI, 1.18-6.02) fractures compared with nondiabetics. This study indicates that diabetes is a risk factor for hip, proximal humerus, and foot fractures among older women, suggesting that fracture prevention efforts should be a consideration in the treatment of diabetes.
View details for Web of Science ID 000166580100007
View details for PubMedID 11231974