I am an endocrinologist with particular interests in reproductive and bone health.

I enjoy treating patients with menstrual disorders, menopause, fractures, osteoporosis, parathyroid imbalance, and calcium imbalance.

As a certified menopause practitioner (North American Menopause Society), I help women fine-tune their health at the mid-life transition. Some women transition through menopause with ease, while others experience challenging symptoms like hot flashes, slowed metabolism, and mood changes. This transition period provides a good opportunity to create a "game plan" for preserving future health. It also marks the beginning of natural bone loss, leaving one more susceptible to fragility fractures.

I provide individualized treatment plans for bone health to men and women of all ages, including for those with specific challenges such as chronic steroid use. As a certified clinical densitometrist (International Society for Clinical Densitometry), I personally review all my patients' bone density scan images. Thus, please bring any non-Stanford bone density scan images to your appointment with me.

Appointments with me are available on Stanford's main campus (300 Pastuer Drive) and at the Stanford Medicine Outpatient Center (450 Broadway, Redwood City).

Clinical Focus

  • Osteoporosis
  • Bone Diseases
  • Parathyroid Diseases
  • Calcium Metabolism Disorders
  • Reproductive Health
  • Menopause
  • Amenorrhea
  • Polycystic Ovary Syndrome
  • Thyroid Gland
  • Adrenal Glands
  • Primary Ovarian Insufficiency
  • Osteoporotic Fractures
  • Stress Fracture
  • Primary Hyperparathyroidism
  • Hypoparathyroidism
  • Hormone Replacement Therapy
  • Female Athlete Triad Syndrome
  • Diabetes and Metabolism
  • Endocrinology

Academic Appointments

Administrative Appointments

  • Associate Program Director, Endocrinology Fellowship Training Program, Stanford (2015 - Present)

Professional Education

  • Fellowship: New York Presbyterian Hospital (2009) NY
  • Board Certification: American Board of Internal Medicine, Endocrinology, Diabetes and Metabolism (2008)
  • Residency: Brigham and Women's Hospital Harvard Medical School (2006) MA
  • Internship: Brigham and Women's Hospital Harvard Medical School (2004) MA
  • Medical Education: Harvard Medical School (2003) MA
  • Fellowship, Columbia University Medical Center, New York, NY, endocrinology, diabetes & metabolism (2009)

All Publications

  • Declining Rates of Inpatient Parathyroidectomy for Primary Hyperparathyroidism in the US. PloS one Kim, S. M., Shu, A. D., Long, J., Montez-Rath, M. E., Leonard, M. B., Norton, J. A., Chertow, G. M. 2016; 11 (8)


    Parathyroidectomy is the only curative therapy for patients with primary hyperparathyroidism. However, the incidence, correlates and consequences of parathyroidectomy for primary hyperparathyroidism across the entire US population are unknown. We evaluated temporal trends in rates of inpatient parathyroidectomy for primary hyperparathyroidism, and associated in-hospital mortality, length of stay, and costs. We used the Healthcare Cost and Utilization Project Nationwide Inpatient Sample (NIS) from 2002-2011. Parathyroidectomies for primary hyperparathyroidism were identified using International Classification of Diseases, Ninth Revision codes. Unadjusted and age- and sex- adjusted rates of inpatient parathyroidectomy for primary hyperparathyroidism were derived from the NIS and the annual US Census. We estimated 109,583 parathyroidectomies for primary hyperparathyroidism between 2002 and 2011. More than half (55.4%) of patients were younger than age 65, and more than three-quarters (76.8%) were female. The overall rate of inpatient parathyroidectomy was 32.3 cases per million person-years. The adjusted rate decreased from 2004 (48.3 cases/million person-years) to 2007 (31.7 cases/million person-years) and was sustained thereafter. Although inpatient parathyroidectomy rates declined over time across all geographic regions, a steeper decline was observed in the South compared to other regions. Overall in-hospital mortality rates were 0.08%: 0.02% in patients younger than 65 years and 0.14% in patients 65 years and older. Inpatient parathyroidectomy rates for primary hyperparathyroidism have declined in recent years.

    View details for DOI 10.1371/journal.pone.0161192

    View details for PubMedID 27529699

  • Quality of life and hypertension after hormone therapy withdrawal in New York City MENOPAUSE-THE JOURNAL OF THE NORTH AMERICAN MENOPAUSE SOCIETY Warren, M. P., Richardson, O., Chaudhry, S., Shu, A. D., Swica, Y., Sims, V. R., Sloan, N. L. 2013; 20 (12): 1255-1263


    Many women stopped hormone therapy (HT) or estrogen therapy (ET) after the Women's Health Initiative results were published in 2002. This study assessed the incidence of hypertension, weight gain, and dyslipidemia; conditions that predispose to chronic diseases; medication use; and quality of life in women who used HT/ET for at least 5 years and subsequently stopped its use compared with those who continued its use.A retrospective study was conducted. All consenting eligible women (aged 56-73 y) in physicians' offices were interviewed, and measurements of weight, height, waist-to-hip ratio, and body fat were performed. Standardized quality-of-life and menopausal and medical questionnaires were administered. Three groups were compared: group 1, women who have remained on HT/ET; group 2, women who have resumed HT/ET after stopping for at least 6 months; and group 3, women who have stopped HT/ET and have not resumed.One hundred fifty-nine women were enrolled in group 1, 43 women were enrolled in group 2, and 108 women were enrolled in group 3. Women's characteristics were similar, except that group 3 was 1.5 (0.5) years older and had 4.4 (0.7) years less HT/ET use than groups 1 and 2. Utian Quality of Life scores were significantly lower in group 3 (83.4 [12.5]) than in groups 1 and 2 (87.6 [13.3], P < 0.02), particularly in the occupational satisfaction scale. About 16.6% and 16.3% of women in groups 1 and 2 were on antihypertensive medication, respectively, compared with 27.4% in group 3 (P < 0.04).Discontinuation of HT/ET may predispose some women to the risk of hypertension and may affect their quality of life.

    View details for DOI 10.1097/gme.0b013e31828cfd3b

    View details for Web of Science ID 000330465700007

    View details for PubMedID 23571529

  • Trabecular and Cortical Microarchitecture in Postmenopausal HIV-Infected Women CALCIFIED TISSUE INTERNATIONAL Yin, M. T., Shu, A., Zhang, C. A., Boutroy, S., McMahon, D. J., Ferris, D. C., Colon, I., Shane, E. 2013; 92 (6): 557-565


    Our objective was to assess the effects of HIV infection and antiretroviral therapy on trabecular and cortical microarchitecture in postmenopausal minority women. A subgroup of 106 (46 HIV-infected, 60 uninfected) postmenopausal Hispanic and African American women from an established cohort had areal bone mineral density (aBMD) measured by dual-energy X-ray absorptiometry and trabecular and cortical volumetric BMD (vBMD) and microarchitecture measured by high-resolution peripheral quantitative computed tomography (HRpQCT) at the radius and tibia. HIV-infected women were slightly younger (58 ± 1 vs. 61 ± 1 years, p = 0.08), and had lower body mass index (BMI; 28 ± 1 vs. 32 ± 1 kg/m(2), p < 0.01). BMI-adjusted aBMD Z scores were lower in HIV-infected women at the lumbar spine, total hip, and ultradistal radius. Serum N-telopeptide and C-telopeptide levels were also higher in HIV-infected women. Trabecular and cortical vBMD were similar at the radius, but cortical area (105.5 ± 2.4 vs. 120.6 ± 2.0 mm(2), p < 0.01) and thickness (956 ± 33 vs. 1,075 ± 28 μm, p < 0.01) at the tibia were approximately 11-12 % lower in HIV-infected women. Differences remained significant after adjusting for age, BMI, and race/ethnicity. In contrast, cortical porosity was similar in the two groups. Although HIV-infected postmenopausal women had lower aBMD at the spine, total hip, and ultradistal radius and higher levels of bone resorption markers, the only differences detected by HRpQCT were lower cortical thickness and area at the tibia.

    View details for DOI 10.1007/s00223-013-9716-8

    View details for Web of Science ID 000319021400008

    View details for PubMedID 23460340

    View details for PubMedCentralID PMC3656136

  • Bone structure and turnover in type 2 diabetes mellitus OSTEOPOROSIS INTERNATIONAL Shu, A., Yin, M. T., Stein, E., Cremers, S., Dworakowski, E., Ives, R., Rubin, M. R. 2012; 23 (2): 635-641


    We compared skeletal parameters in type 2 diabetic (T2DM) and non-diabetic postmenopausal women. Bone structure by dual energy x-ray absorptiometry (DXA) and HR-pQCT was not different, although procollagen type 1 amino-terminal propeptide (P1NP) and osteocalcin levels were lower in T2DM.T2DM is associated with increased fracture risk, but, paradoxically, with higher cross-sectional bone density (BMD) as measured by DXA. We sought explanations to this puzzle by investigating detailed structural and biochemical skeletal parameters in T2DM.Cross-sectional comparison of 25 postmenopausal T2DM women and 25 matched controls using DXA, high-resolution peripheral quantitative computed tomography (HR-pQCT) and biochemical bone turnover markers.BMD by DXA did not differ between T2DM and controls. HR-pQCT assessment also did not differ, with the exception of cortical area at the tibia, which tended to be lower in the diabetics (difference of 12 ± 6 [mean ± SD] mm, p = 0.06). P1NP and osteocalcin levels were lower in T2DM as compared to controls (P1NP, 34.3 ± 16 vs. 57.3 ± 28 ng/ml; p = 0.005; osteocalcin, 4.5 ± 2 vs. 6.2 ± 2 nmol/L; p = 0.001).Postmenopausal women with T2DM had lower levels of bone formation markers as compared to controls. Aside from a possible decrease in cortical bone area at a weight-bearing site, bone structure was not altered in T2DM. Lower bone turnover may be a skeletal parameter that is present in T2DM.

    View details for DOI 10.1007/s00198-011-1595-0

    View details for Web of Science ID 000299306300024

    View details for PubMedID 21424265

  • Vitamin D deficiency in HIV-infected postmenopausal Hispanic and African-American women OSTEOPOROSIS INTERNATIONAL Stein, E. M., Yin, M. T., McMahon, D. J., Shu, A., Zhang, C. A., Ferris, D. C., Colon, I., Dobkin, J. F., Hammer, S. M., Shane, E. 2011; 22 (2): 477-487


    We evaluated vitamin D status in HIV+ and HIV- postmenopausal African-American (AA) and Hispanic women. Most women (74-78%) had insufficient 25-hydroxyvitamin D (25OHD) levels, regardless of HIV status. 25OHD was lower in AA women and women lacking supplement use, providing support for screening and supplementation. Among HIV+ women, 25OHD was associated with current CD4 but not type of antiretroviral therapy.To evaluate vitamin D status and factors associated with vitamin D deficiency and insufficiency in HIV-infected (HIV+) postmenopausal minority women.In this cross-sectional study, 89 HIV+ and 95 HIV- postmenopausal women (33% AA and 67% Hispanic) underwent assessment of 25OHD, 1,25-dihydroxyvitamin D, parathyroid hormone, markers of bone turnover and bone mineral density by dual energy X-ray absorptiometry.The prevalence of low 25OHD did not differ by HIV status; the majority of both HIV+ and HIV- women (74-78%) had insufficient levels (<30 ng/ml). Regardless of HIV status, 25OHD was significantly lower in AA subjects, and higher in subjects who used both calcium and multivitamins. In HIV+ women on antiretroviral therapy (ART), 25OHD was directly associated with current CD4 count (r=0.32; p<0.01) independent of age, ethnicity, BMI, or history of AIDS-defining illness. No association was observed between 1,25(OH)(2)D and CD4 count or between serum 25OHD, 1,25(OH)(2)D or PTH and type of ART.In postmenopausal minority women, vitamin D deficiency was highly prevalent and associated with AA race and lack of supplement use, as well as lower current CD4 cell count. These results provide support for screening and repletion of vitamin D in HIV+ patients.

    View details for DOI 10.1007/s00198-010-1299-x

    View details for Web of Science ID 000286207800008

    View details for PubMedID 20585939

  • Low Bone Mass and High Bone Turnover in Postmenopausal Human Immunodeficiency Virus-Infected Women JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM Yin, M. T., McMahon, D. J., Ferris, D. C., Zhang, C. A., Shu, A., Staron, R., Colon, I., Laurence, J., Dobkin, J. F., Hammer, S. M., Shane, E. 2010; 95 (2): 620-629


    Low bone mineral density (BMD) is commonly reported in young men and women with HIV infection, and fracture rates may be higher. With effective antiretroviral therapy (ART), the HIV population is aging. However, little is known about the skeletal status of postmenopausal women.We aimed to assess the effects of HIV infection and ART on BMD and bone turnover in postmenopausal minority women.A prospective cohort study was performed in 92 HIV+ and 95 HIV- postmenopausal Hispanic and African-American women.We measured BMD by dual-energy x-ray absorptiometry, fracture prevalence, serum levels of inflammatory cytokines (TNFalpha, IL-6), bone turnover markers, calciotropic hormones, and estrone.HIV+ women were younger (56 +/- 1 vs. 60 +/- 1 yr; P < 0.01) and had lower BMI (28 +/- 1 vs. 30 +/- 1 kg/m(2); P < 0.01) and estrone levels. Prevalence of T scores below -1.0 was greater in HIV+ women at the spine (78 vs. 64%; P < 0.05), total hip (45 vs. 29%; P < 0.05), and femoral neck (64 vs. 46%; P < 0.05), and Z scores adjusted for BMI were lower in HIV+ women at the same sites. Serum TNFalpha, N-telopeptide, and C-telopeptide were significantly higher in HIV+ than HIV- women, particularly those receiving ART. HIV+ status was independently and negatively associated with spine and hip BMD after adjustment for age, ethnicity, BMI, and alcohol.The lower BMD, higher prevalence of low BMD, and higher levels of bone turnover markers detected in HIV+ postmenopausal minority women could place them at high risk for future fractures.

    View details for DOI 10.1210/jc.2009-0708

    View details for Web of Science ID 000274298200022

    View details for PubMedID 19965927

    View details for PubMedCentralID PMC2840861

  • Adherence to Osteoporosis Medications After Patient and Physician Brief Education: Post Hoc Analysis of a Randomized Controlled Trial AMERICAN JOURNAL OF MANAGED CARE Shu, A. D., Stedman, M. R., Polinski, J. M., Jan, S. A., Patel, M., Truppo, C., Breiner, L., Chen, Y., Weiss, T. W., Solomon, D. H. 2009; 15 (7): 417-424


    To examine whether adherence to osteoporosis medications can be improved by educational interventions targeted at primary care physicians (PCPs) and patients.Post hoc analysis of data collected as part of a prospective randomized controlled trial to improve initiation of osteoporosis management such as bone mineral density testing or osteoporosis drug initiation.The trial was conducted among patients at risk for osteoporosis enrolled in Horizon Blue Cross Blue Shield of New Jersey. For a 3-month period, randomly selected PCPs and their patients received education about osteoporosis diagnosis and treatment. The PCPs received face-to-face education by trained pharmacists, while patients received letters and automated telephone calls. The control group received no education. We assessed medication adherence during 10 months following the start of the intervention using the medication possession ratio (MPR), the ratio of available medication to the total number of days studied.These analyses included 1867 patients (972 randomized to the intervention group and 875 to the control group) and their 436 PCPs. During 10 months following the intervention, the median MPRs were 74% (interquartile range [IQR], 19%-93%) for the intervention group and 73% (IQR, 0%-93%) for the control group (P = .18). The median times until medication discontinuation after the intervention were 85 days (IQR, 58-174 days) for the intervention group and 79 days (IQR, 31-158 days) for the control group.The educational intervention did not significantly improve medication compliance or persistence with osteoporosis drugs.

    View details for Web of Science ID 000268159100002

    View details for PubMedID 19589009

    View details for PubMedCentralID PMC2885859