The date of fracture was determined from hospital admission data. Date of death was determined from death certificates held by the National Health Service NHS Information Centre for participants from England and Wales, and the NHS Central Register Scotland for participants from Scotland [ 18 ].

In the current analysis, hospital admission data were available until March 31, , and mortality data were available until February 14, Therefore, we censored follow-up on March 31, , or the date of first fracture or death, whichever occurred first. In total, , participants without baseline fractures were included in the analysis Fig.

Flow diagram of study design. Baseline touchscreen questionnaires were used to assess several potential confounding variables, including age, household income, smoking status, alcohol consumption, physical activity, dietary supplements, overall health rating, medical history including the histories of type 2 diabetes T2D , cardiovascular disease CVD , or cancer diagnosed by a doctor, and menopausal status and hormone replacement therapy women only.

Lean mass and body weight were measured with the Tanita BC MA body composition analyzer Tanita Corporation of America, IL. Standing height was measured using the Seca device SECA, Hamburg, Germany. BMI was calculated as weight in kilograms divided by height in meters squared.

The proportional hazards assumption of Cox models was tested based on the Schoenfeld residuals and almost no evidence of violation was observed Additional file 1 : Table S9. We tested for potential nonlinearity by using a likelihood ratio test comparing the model with only a linear term against the model with linear and cubic spline terms [ 23 , 24 ].

To minimize the potential confounding effects and reverse causality brought by diabetes, CVD, and cancer [ 25 , 26 , 27 , 28 , 29 ], we also conducted additional sensitivity analyses by excluding participants who had self-reported physician-diagnosed T2D, CVD, or cancer at baseline.

All analyses were performed using R version 3. In the main analyses, we performed two-sample MR analyses Fig. The random-effect inverse-variance weighted IVW method was applied as the primary analysis [ 32 ]. We also performed MR Egger [ 33 ], weighted median [ 34 ], and mode-based regressions as sensitivity analyses.

The current study included , men Furthermore, the baseline characteristics by sex are presented in Additional file 1 : Table S2. Consistently, we observed similar results when stratified by BMI Table 2 and Additional file 1 : Table S4.

The results Additional file 1 : Table S6 were highly consistent with the main results. All models were adjusted for age, household income, lean mass, standing height, smoking status, alcohol consumption, physical activity, calcium supplement use, vitamin D supplement use, overall health rating, diabetes, cardiovascular disease, cancer, and for women, menopausal status and use of hormone replacement therapy.

During approximately 2,, person-years of follow-up median [IQR] follow-up, 8. S4 in men only. To reduce potential collider bias, we also presented the results of the age-adjusted model and another minimally-adjusted model Table S7. In sensitivity analyses, consistent results were observed from weighted median, MR-Egger, and mode-based methods Table 4.

IVW odds ratio OR were 1. In addition, no horizontal pleiotropy was detected for all MR analyses Additional file 1 : Table S Subgroup analyses suggested that these associations were likely to be modulated by adiposity status especially in men. Observational studies have reported controversial findings on the associations of VAT with skeletal outcomes [ 14 , 36 , 37 , 38 , 39 ].

We also tried to adjust for BMI or bodyweight instead of lean mass and got consistent results. However, studies from Chinese adults reported that there was no correlation between VAT and BMD [ 39 ].

Though adjustment for potential confounding factors, the above cross-sectional analysis between VAT and BMD limited the causal inference. Congruent with our results, a previous case-cohort study with a total of fracture cases and non-cases found there was no significant relationship between VAT and incident fractures [ 37 ].

However, previous studies did not explore the nonlinear relationship between VAT and skeletal outcomes [ 14 , 36 , 40 , 41 ]. In summary, the relationship between VAT and skeletal outcomes was complex, and further studies in different populations are needed to validate our findings.

These sex-dependent associations can be attributed to the differences in the sex hormone levels in men and women [ 42 ]. Sex hormones play a major role in the growth and maintenance of the skeletal system [ 43 ], and have pronounced effects on adipose tissue [ 44 ].

Although the causal association between VAT and BMD remains unclear, previous studies suggested that adipose tissue could increase bone mass due to physical weight-bearing, while also imposing an adverse effect on BMD through the production of hormones and adipokines by adipocytes [ 45 , 46 ].

From this perspective, it appears biologically plausible that the association between VAT and BMD may vary according to the amounts of VAT or by different adiposity statuses.

We were not aware of any previous MR study directly assessing the association between VAT and skeletal outcomes. Consistent with our findings, an MR study found that BMI-adjusted waist circumference a proxy for central fat distribution was not correlated with BMD, suggesting that the effect of fat distribution might be neutral [ 47 ].

Similarly, Ma et al. recently conducted MR analyses and reported that BMI was causally associated with BMD but not associated with fracture. Moreover, they also found that the waist-to-hip ratio adjusted for BMI, hip circumference adjusted for BMI and waist circumference adjusted for BMI were not related to BMD or fracture occurrence [ 5 ].

In summary, these results did not support a causal relationship between VAT and skeletal outcomes, although further evidence is warranted to verify the reliability of our findings. There were several strengths of our study. The large sample size and the detailed information enabled us to conduct comprehensive statistical adjustments in the observational analyses.

Besides, this was the first study to directly explore the potential causal association of VAT with DXA-derived BMD and fracture by MR analysis. Up to now, there only existed a few studies using surrogate-VAT e. Several potential limitations should be acknowledged. Secondly, the participants were White British from UK Biobank in our study.

Therefore, the generalization of the study findings to other populations should be exercised with caution. Thirdly, for the MR analysis, we should acknowledge the slight sample overlap between the exposure and outcome GWAS datasets.

However, we used powerful instruments to estimate the associations [ 48 ] between the exposures and the outcomes. Therefore, any sample overlap should not significantly bias our findings. The UK Biobank data are available from the UK Biobank on application www.

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We thank BD Biosciences for donating blood collection kits and Abbott Australasia Pty Ltd for donating assay kits for OH Vitamin D.

The Busselton Healthy Ageing Study is supported by grants from the Government of Western Australia Office of Science, Department of Health and the City of Busselton and from private donations to the Busselton Population Medical Research Institute. None of the funding agencies had any role in the conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review, or approval of the manuscript.

Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, Western Australia, , Australia. Medical School, University of Western Australia, Crawley, Western Australia, Australia.

Busselton Population Medical Research Institute, Busselton, Western Australia, Australia. School of Population and Global Health, University of Western Australia, Crawley, Western Australia, Australia. Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia.

Department of Clinical Biochemistry, PathWest Laboratory Medicine, Queen Elizabeth II Medical Centre, Nedlands, Western Australia, Australia.

Department of Clinical Biochemistry, PathWest Laboratory Medicine, Fiona Stanley Hospital, Murdoch, Western Australia, Australia. You can also search for this author in PubMed Google Scholar. Correspondence to K. Written informed consent was obtained from participants.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Reprints and permissions. Zhu, K. et al. Relationship between visceral adipose tissue and bone mineral density in Australian baby boomers. Osteoporos Int 31 , — Download citation.

Received : 19 March Accepted : 21 July Published : 27 July Issue Date : December Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative. Abstract Summary Adiposity has a complex relationship with bone health.

Introduction Increased body mass is associated with higher bone mineral density BMD , but higher visceral adipose tissue VAT may have a negative impact on bone health. Methods VAT mass and BMD of whole body, total hip, femoral neck and lumbar spine were measured using DXA.

Results The mean age was Conclusion In middle-aged Australians, after covariate adjustment, higher DXA-derived VAT mass is associated with reduced bone density, suggesting that excess visceral fat may be deleterious to bone, especially in males.

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What is a tongue-tie? The inclusion of the sedentary lifestyle was also important because there is a positive relationship between increased habitual physical activity and BMD [ 18 ].

Gender is an important variable related to skeletal formation. Male adolescents, more than girls, are affected by biological processes that accelerate bone development [ 2 ].

In the final stages of adolescence, boys are taller and have a higher bone mineral density [ 2 ]. Through childhood and adolescence, when compared to the female gender, boys have an increased likelihood of practicing sports [ 8 , 9 ], which are related to bone development. Moreover, during adulthood, hormonal characteristics of male obesity may exert deleterious effects on bone microarchitecture [ 19 ].

Therefore, the inclusion of gender as a potential confounder constitutes a methodological strength, because it indicates that IAAT is inversely related to BMD independent of this important confounder. Indeed, obese subjects, from an early age, have increased bone density, mainly due to the stress occasioned by the increased weight on bone tissue that causes deformation and, hence, leads to bone remodeling [ 2 ].

It is noteworthy that although obesity is positively related to BMD, more recent findings suggest that bone quality is compromised in obese subjects [ 21 ]. On the other hand, our findings point out that body fatness distribution should be considered as a potential confounder in this relationship, because increased IAAT was inversely related to BMD, independent of general obesity.

Previous studies involving anthropometric waist-to-hip ratio [ 20 ] and DXA variables abdominal fatness in kg [ 7 ] identified similar relationship patterns in children and adults, respectively. The inverse relationship between IAAT and BMD could be based on the action of adipokines produced by adipose tissue over growth mediators related to bone development.

Nemet et al. Similarly, the adipose tissue located in the abdominal region mainly the visceral one has a special role in the release of adipokines into the bloodstream [ 23 ].

Therefore, it is possible to believe that IAAT could be a risk factor related to a harmful effect in bone remodeling and in turn to a risk factor of osteoporosis in adulthood.

Visceral adipose tissue is related to insulin resistance and insulin plays a role in the proliferation of osteoblasts. Thus, decreased insulin action may be one of the possible mechanisms by which obesity affects bone mass. In agreement, in a recent study, increased insulin concentration and HOMA-IR were considered negative predictors of bone mineral density in adolescents [ 24 ].

However, this is a recent finding that needs further top research focusing on the understanding of the physiological common mechanisms behind this association. On the other hand, limitations should be recognized: i the cross-sectional design absence of causality statements , ii an absence of measurements relating to the intake of calcium and vitamin D and iii an absence of pro-inflammatory adipokines.

Moreover, there were correlations of low magnitude between BMD and IAAT, indicating that other variables are important in this relationship and, therefore, further studies are necessary to identify them. In summary, our findings indicate that abdominal obesity negatively affects the bone density of obese children and adolescents, indicating that abdominal obesity could be a determinate in the development of osteoporosis in adulthood.

Further studies should analyze whether this negative effect also occurs in non-obese youth. National Osteoporosis Foundation: Strong voices for strong bones.

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Arq Bras Endocrinol Metabol. The imaging revealed that women with more visceral fat had increased bone marrow fat and decreased bone mineral density. However, there was no significant correlation between either subcutaneous fat or total fat and bone marrow fat or bone mineral density.

Bredella said. According to the National Women's Health Information Center, 10 million Americans have osteoporosis and 18 million more have low bone mass, placing them at risk for the disease.

While bone loss is more common in women, the research team is currently conducting a study to determine whether belly fat is also a risk factor for bone loss in men. Coauthors are Martin Torriani, M. Note: Copies of RSNA news releases and electronic images will be available online at RSNA.

RSNA is an association of more than 46, radiologists, radiation oncologists, medical physicists and related scientists committed to excellence in patient care through education and research. The Society is based in Oak Brook, Ill.