Deborah Sellmeyer
Clinical Professor, Medicine - Endocrinology, Gerontology, & Metabolism
Web page: http://web.stanford.edu/people/dsellme
Bio
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.
Clinical Focus
- Metabolic Bone Disease
- Endocrinology
- Diabetes and Metabolism
Academic Appointments
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Clinical Professor, Medicine - Endocrinology, Gerontology, & Metabolism
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Member, Stanford Cancer Institute
Professional Education
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Board Certification: American Board of Internal Medicine, Endocrinology, Diabetes and Metabolism (2009)
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Fellowship: UCSF Endocrinology Fellowship (1998) CA
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Residency: Johns Hopkins Hospital Internal Medicine Residency (1994) MD
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Medical Education: Johns Hopkins University School of Medicine (1991) MD
All Publications
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Prebiotic Intervention to Improve Calcium Absorption in Postmenopausal Women After Gastric Bypass: A Randomized Controlled Trial
WILEY. 2022: 307
View details for Web of Science ID 000778074501355
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Skeletal Fluorosis Due to Inhalation Abuse of a Dust Cleaner
WILEY. 2022: 102
View details for Web of Science ID 000778074500299
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Prebiotic to Improve Calcium Absorption in Postmenopausal Women After Gastric Bypass: A Randomized Controlled Trial.
The Journal of clinical endocrinology and metabolism
2021
Abstract
CONTEXT: The adverse skeletal effects of Roux-en-Y gastric bypass (RYGB) are partly caused by intestinal calcium absorption decline. Prebiotics, such as soluble corn fiber (SCF), augment colonic calcium absorption in healthy individuals.OBJECTIVE: We tested the effects of SCF on fractional calcium absorption (FCA), biochemical parameters, and the fecal microbiome in a post-RYGB population. Design, Setting, Participants : Randomized, double-blind, placebo-controlled trial of 20 postmenopausal women with history of RYGB mean 5 years prior.INTERVENTION: 2-month course of 20g/day SCF or maltodextrin placebo orally.MAIN OUTCOMES: Between-group difference in absolute change in FCA (primary outcome) was measured with a gold-standard dual stable isotope method. Other measures included tolerability, adherence, serum calciotropic hormones and bone turnover markers, and fecal microbial composition via 16S rRNA gene sequencing.RESULTS: Mean FCA ±SD at baseline was low at 5.5±5.1%. Comparing SCF to placebo, there was no between-group difference in mean (95% CI) change in FCA (+3.4 [-6.7,+13.6]%), nor in calciotropic hormones or bone turnover markers. The SCF group had a wider variation in FCA change than placebo (SD 13.4% vs. 7.0%). Those with greater change in microbial composition following SCF treatment had greater increase in FCA (r 2=0.72,p=0.05). SCF adherence was high, and GI symptoms similar between groups.CONCLUSIONS: No between-group differences were observed in changes in FCA or calciotropic hormones, but wide confidence intervals suggest a variable impact of SCF that may be due to the degree of gut microbiome alteration. Daily SCF consumption was well-tolerated. Larger and longer-term studies are warranted.
View details for DOI 10.1210/clinem/dgab883
View details for PubMedID 34888663
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Rare Causes of Hypercalcemia: 2021 Update.
The Journal of clinical endocrinology and metabolism
2021
Abstract
CONTEXT: Primary hyperparathyroidism and malignancy are the etiologies in 90% of cases of hypercalcemia. When these entities are not the etiology of hypercalcemia, uncommon conditions need to be considered. In 2005, Jacobs and Bilezikian published a clinical review of rare causes of hypercalcemia, focusing on mechanisms and pathophysiology. This review is an updated synopsis of rare causes of hypercalcemia, extending the observations of the original article.EVIDENCE ACQUISITION: Articles reporting rare associations between hypercalcemia and unusual conditions were identified through a comprehensive extensive PubMed-based search using the search terms "hypercalcemia" and "etiology," as well as examining the references in the identified case reports. We categorized the reports by adults vs. pediatric and further categorized the adult reports based on etiology. Some included reports lacked definitive assessment of etiology and are reported as unknown mechanism with discussion of likely etiology.EVIDENCE SYNTHESIS: There is a growing understanding of the breadth of unusual causes of hypercalcemia. When the cause of hypercalcemia is elusive, a focus on mechanism and review of prior reported cases is key to successful determination of the etiology.CONCLUSIONS: The ever-expanding reports of patients with rare and even unknown mechanisms of hypercalcemia illustrate the need for continued investigation into the complexities of human calcium metabolism.
View details for DOI 10.1210/clinem/dgab504
View details for PubMedID 34240162
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Nutritional Supplements and Skeletal Health.
Current osteoporosis reports
2021
Abstract
PURPOSE OF REVIEW: Nutrition influences skeletal health throughout the lifespan, from the impact of maternal intakes during development, through the development of peak bone mass, to the rate of bone loss during aging. However, there are limited data available on the effects of nutritional supplements on bone density, let alone fracture risk. This review will assess the current literature, focusing on human studies, and emphasizing nutrients where bone density or fracture data are available.RECENT FINDINGS: Calcium and vitamin D supplements, in combination, reduce fracture risk, particularly in populations with low intakes. Extensive recent analyses have supported the safety of these interventions at recommended intakes. There is growing evidence that specific isoflavones may improve bone density although fracture data are lacking. Multiple other nutrient supplements may benefit skeletal health, but data are limited. The effect size of nutrient interventions are relatively small, requiring large sample sizes for trials with bone outcomes, may be difficult to blind, and the impact of supplementation may depend on baseline intake. However, nutrition is the only intervention that can be implemented life long and on a population wide basis. Further investigation is needed into the potential benefits of nutritional supplements to determine in which settings supplements may add benefit in addition to dietary intakes.
View details for DOI 10.1007/s11914-020-00651-x
View details for PubMedID 33420633
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Bone tissue composition in post-menopausal women varies with glycemic control from normal glucose tolerance to type 2 diabetes mellitus.
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
2020
Abstract
The risk of fragility fracture increases for people with type 2 diabetes mellitus (T2DM), even after controlling for bone mineral density, body mass index, visual impairment, and falls. We hypothesize that progressive glycemic derangement alters micro-scale bone tissue composition. We used Fourier-transform infrared (FTIR) imaging to analyze the composition of iliac crest biopsies from cohorts of post-menopausal women characterized by oral glucose tolerance testing: normal glucose tolerance (NGT; n=35, age=65±7, HbA1c=5.8±0.3%), impaired glucose tolerance (IGT; n=26, age=64±5, HbA1c=6.0±0.4%), and overt T2DM on insulin (n=25, age=64±6, HbA1c=9.13±0.6). The distributions of cortical bone mineral content had greater mean values (+7%) and were narrower (-10%) in T2DM vs. NGT groups (p<0.05). The distributions of acid phosphate, an indicator of new mineral, were narrower in cortical T2DM vs. NGT and IGT groups (-14% and -14%, respectively) and in trabecular NGT and IGT vs. T2DM groups (-11% and -10%, respectively) (all p<0.05). The distributions of crystallinity were wider in cortical NGT vs. T2DM groups (+16%) and in trabecular NGT vs. T2DM groups (+14%) (all p<0.05). Additionally, bone turnover was lower in T2DM vs. NGT groups (P1NP: -25%, CTx: -30%, ucOC: -24%). Serum pentosidine was similar across groups. The FTIR compositional and biochemical marker values of the IGT group typically fell between the NGT and T2DM group values, though the differences were not always statistically significant. In summary, worsening glycemic control was associated with greater mineral content and narrower distributions of acid phosphate, an indicator of new mineral, which together are consistent with observations of lower turnover; however, wider distributions of mineral crystallinity were also observed. A more mineralized, less heterogeneous tissue may affect tissue-level mechanical properties, and in turn degrade macroscale skeletal integrity. In conclusion, these data are the first evidence of progressive alteration of bone tissue composition with worsening glycemic control in humans.
View details for DOI 10.1002/jbmr.4186
View details for PubMedID 32970898
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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
View details for DOI 10.1002/jbmr.3914
View details for PubMedID 31845376
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A Unique Cause of Hypercalcemia
WILEY. 2019: 76
View details for Web of Science ID 000508614700214
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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 000508356602107
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A Unique Cause of Hypercalcemia
WILEY. 2019: 76
View details for Web of Science ID 000508356601043
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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
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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)
2019
Abstract
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
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A Randomized Controlled Trial of Exercise to Prevent Bone Loss in Premenopausal Women with Breast Cancer.
Journal of women's health (2002)
2018
Abstract
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
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National Institutes of Health Consensus Development Conference: Lactose Intolerance and Health
ANNALS OF INTERNAL MEDICINE
2010; 152 (12): 792-?
View details for Web of Science ID 000278827700005
View details for PubMedID 20404261
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A proposed method for assessing plasma hypertonicity in vivo
EUROPEAN JOURNAL OF CLINICAL NUTRITION
2007; 61 (1): 143-146
Abstract
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
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Effect of alendronate on bone mineral density and biochemical markers of bone turnover in type 2 diabetic women - The fracture intervention trial
DIABETES CARE
2004; 27 (7): 1547-1553
Abstract
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
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Older women with diabetes have an increased risk of fracture: A prospective study
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
2001; 86 (1): 32-38
Abstract
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