Madhusmita Misra, MD, MPH

Fractures, particularly hip and spine fractures, are a major cause of mortality and morbidity among older individuals. The term “osteoporosis” indicates increased porosity of bones resulting in low bone density; increased bone fragility; and an increased risk for fracture, often with minimal trauma.

During the adolescent years, bone accrues at a rapid rate, and optimal bone accrual during this time is essential to attain optimal peak bone mass, typically achieved in the third decade of life. Bone mass then stays stable until the 40s-50s, after which it starts to decline. One’s peak bone mass sets the stage for both immediate and future bone health. Individuals with lower peak bone mass tend to have less optimal bone health throughout their lives, and this becomes particularly problematic in older men and in the postmenopausal years for women.

The best strategy to optimize bone health is to prevent osteoporosis from occurring in the first place. This requires attention to factors that contribute to optimal bone health. One’s genes have a major impact on bone density and are currently not modifiable.

Modifiable factors include mechanical loading of bones through exercise activity, maintaining a normal body weight, and ensuring adequate intake of micronutrients (including calcium and vitamin D) and macronutrients. Medications such as glucocorticoids that have deleterious effects on bones should be limited as far as possible. Endocrine, gastrointestinal, renal, and rheumatologic conditions and others, such as cancer, which are known to be associated with reduced bone density and increased fracture risk, should be managed appropriately.

A deficiency of the gonadal hormones (estrogen and testosterone) and high blood concentrations of cortisol are particularly deleterious to bone. Hormone replacement therapy in those with gonadal hormone deficiency and strategies to reduce cortisol levels in those with hypercortisolemia are essential to prevent osteoporosis and also improve bone density over time. The same applies to management of conditions such as anorexia nervosa, relative energy deficiency in sports, inflammatory bowel disease, celiac disease, cystic fibrosis, chronic kidney disease, and chronic arthritis.

Once osteoporosis has developed, depending on the cause, these strategies may not be sufficient to completely reverse the condition, and pharmacologic therapy may be necessary to improve bone density and reduce fracture risk. This is particularly an issue with postmenopausal women and older men. In these individuals, medications that increase bone formation or reduce bone loss may be necessary.

Medications that reduce bone loss include bisphosphonates and denosumab; these are also called “antiresorptive medications” because they reduce bone resorption by cells called osteoclasts. Bisphosphonates include alendronate, risedronate, ibandronate, pamidronate, and zoledronic acid, and these medications have direct effects on osteoclasts, reducing their activity. Some bisphosphonates, such as alendronate and risedronate, are taken orally (daily, weekly, or monthly, depending on the medication and its strength), whereas others, such as pamidronate and zoledronic acid, are administered intravenously: every 3-4 months for pamidronate and every 6-12 months for zoledronic acid. Ibandronate is available both orally and intravenously.

Denosumab is a medication that inhibits the action of receptor activator of nuclear factor-kappa ligand 1 (RANKL), which otherwise increases osteoclast activity. It is administered as a subcutaneous injection every 6 months to treat osteoporosis. One concern with denosumab is a rapid increase in bone loss after its discontinuation.

Medications that increase bone formation are called bone anabolics and include teriparatide, abaloparatide, and romosozumab. Teriparatide is a synthetic form of parathyroid hormone (recombinant PTH1-34) administered daily for up to 2 years. Abaloparatide is a synthetic analog of parathyroid hormone–related peptide (PTHrP), which is also administered daily as a subcutaneous injection. Romosozumab inhibits sclerostin (a substance that otherwise reduces bone formation and increases bone resorption) and is administered as a subcutaneous injection once a month. Effects of these medications tend to be lost after they are discontinued.

In 2019, the Endocrine Society published guidelines for managing postmenopausal osteoporosis. The guidelines recommend lifestyle modifications, including attention to diet, calcium and vitamin D supplements, and weight-bearing exercise for all postmenopausal women. They also recommend assessing fracture risk using country-specific existing models.

Guidelines vary depending on whether fracture risk is low, moderate, or high. Patients at low risk are followed and reassessed every 2-4 years for fracture risk. Those at moderate risk may be followed similarly or prescribed bisphosphonates. Those at high risk are prescribed an antiresorptive, such as a bisphosphonate or denosumab, or a bone anabolic, such as teriparatide or abaloparatide (for up to 2 years) or romosozumab (for a year), with calcium and vitamin D and are reassessed at defined intervals for fracture risk; subsequent management then depends on the assessed fracture risk.

People who are on a bone anabolic should typically follow this with an antiresorptive medication to maintain the gains achieved with the former after that medication is discontinued. Patients who discontinue denosumab should be switched to bisphosphonates to prevent the increase in bone loss that typically occurs.

In postmenopausal women who are intolerant to or inappropriate for use of these medications, guidelines vary depending on age (younger or older than 60 years) and presence or absence of vasomotor symptoms (such as hot flashes). Options could include the use of calcium and vitamin D supplements; hormone replacement therapy with estrogen with or without a progestin; or selective estrogen receptor modulators (such as raloxifene or bazedoxifene), tibolone, or calcitonin.

It’s important to recognize that all pharmacologic therapy carries the risk for adverse events, and it’s essential to take the necessary steps to prevent, monitor for, and manage any adverse effects that may develop.

Managing osteoporosis in older men could include the use of bone anabolics and/or antiresorptives. In younger individuals, use of pharmacologic therapy is less common but sometimes necessary, particularly when bone density is very low and associated with a problematic fracture history — for example, in those with genetic conditions such as osteogenesis imperfecta. Furthermore, the occurrence of vertebral compression fractures often requires bisphosphonate treatment regardless of bone density, particularly in patients on chronic glucocorticoid therapy.

Preventing osteoporosis is best managed by paying attention to lifestyle; optimizing nutrition and calcium and vitamin D intake; and managing conditions and limiting the use of medications that reduce bone density.

However, in certain patients, these measures are not enough, and pharmacologic therapy with bone anabolics or antiresorptives may be necessary to improve bone density and reduce fracture risk.

Dr. Misra, of the University of Virginia and UVA Health Children’s Hospital, Charlottesville, disclosed ties with AbbVie, Sanofi, and Ipsen.
 

A version of this article appeared on Medscape.com.

Fractures, particularly hip and spine fractures, are a major cause of mortality and morbidity among older individuals. The term “osteoporosis” indicates increased porosity of bones resulting in low bone density; increased bone fragility; and an increased risk for fracture, often with minimal trauma.

During the adolescent years, bone accrues at a rapid rate, and optimal bone accrual during this time is essential to attain optimal peak bone mass, typically achieved in the third decade of life. Bone mass then stays stable until the 40s-50s, after which it starts to decline. One’s peak bone mass sets the stage for both immediate and future bone health. Individuals with lower peak bone mass tend to have less optimal bone health throughout their lives, and this becomes particularly problematic in older men and in the postmenopausal years for women.

The best strategy to optimize bone health is to prevent osteoporosis from occurring in the first place. This requires attention to factors that contribute to optimal bone health. One’s genes have a major impact on bone density and are currently not modifiable.

Modifiable factors include mechanical loading of bones through exercise activity, maintaining a normal body weight, and ensuring adequate intake of micronutrients (including calcium and vitamin D) and macronutrients. Medications such as glucocorticoids that have deleterious effects on bones should be limited as far as possible. Endocrine, gastrointestinal, renal, and rheumatologic conditions and others, such as cancer, which are known to be associated with reduced bone density and increased fracture risk, should be managed appropriately.

A deficiency of the gonadal hormones (estrogen and testosterone) and high blood concentrations of cortisol are particularly deleterious to bone. Hormone replacement therapy in those with gonadal hormone deficiency and strategies to reduce cortisol levels in those with hypercortisolemia are essential to prevent osteoporosis and also improve bone density over time. The same applies to management of conditions such as anorexia nervosa, relative energy deficiency in sports, inflammatory bowel disease, celiac disease, cystic fibrosis, chronic kidney disease, and chronic arthritis.

Once osteoporosis has developed, depending on the cause, these strategies may not be sufficient to completely reverse the condition, and pharmacologic therapy may be necessary to improve bone density and reduce fracture risk. This is particularly an issue with postmenopausal women and older men. In these individuals, medications that increase bone formation or reduce bone loss may be necessary.

Medications that reduce bone loss include bisphosphonates and denosumab; these are also called “antiresorptive medications” because they reduce bone resorption by cells called osteoclasts. Bisphosphonates include alendronate, risedronate, ibandronate, pamidronate, and zoledronic acid, and these medications have direct effects on osteoclasts, reducing their activity. Some bisphosphonates, such as alendronate and risedronate, are taken orally (daily, weekly, or monthly, depending on the medication and its strength), whereas others, such as pamidronate and zoledronic acid, are administered intravenously: every 3-4 months for pamidronate and every 6-12 months for zoledronic acid. Ibandronate is available both orally and intravenously.

Denosumab is a medication that inhibits the action of receptor activator of nuclear factor-kappa ligand 1 (RANKL), which otherwise increases osteoclast activity. It is administered as a subcutaneous injection every 6 months to treat osteoporosis. One concern with denosumab is a rapid increase in bone loss after its discontinuation.

Medications that increase bone formation are called bone anabolics and include teriparatide, abaloparatide, and romosozumab. Teriparatide is a synthetic form of parathyroid hormone (recombinant PTH1-34) administered daily for up to 2 years. Abaloparatide is a synthetic analog of parathyroid hormone–related peptide (PTHrP), which is also administered daily as a subcutaneous injection. Romosozumab inhibits sclerostin (a substance that otherwise reduces bone formation and increases bone resorption) and is administered as a subcutaneous injection once a month. Effects of these medications tend to be lost after they are discontinued.

In 2019, the Endocrine Society published guidelines for managing postmenopausal osteoporosis. The guidelines recommend lifestyle modifications, including attention to diet, calcium and vitamin D supplements, and weight-bearing exercise for all postmenopausal women. They also recommend assessing fracture risk using country-specific existing models.

Guidelines vary depending on whether fracture risk is low, moderate, or high. Patients at low risk are followed and reassessed every 2-4 years for fracture risk. Those at moderate risk may be followed similarly or prescribed bisphosphonates. Those at high risk are prescribed an antiresorptive, such as a bisphosphonate or denosumab, or a bone anabolic, such as teriparatide or abaloparatide (for up to 2 years) or romosozumab (for a year), with calcium and vitamin D and are reassessed at defined intervals for fracture risk; subsequent management then depends on the assessed fracture risk.

People who are on a bone anabolic should typically follow this with an antiresorptive medication to maintain the gains achieved with the former after that medication is discontinued. Patients who discontinue denosumab should be switched to bisphosphonates to prevent the increase in bone loss that typically occurs.

In postmenopausal women who are intolerant to or inappropriate for use of these medications, guidelines vary depending on age (younger or older than 60 years) and presence or absence of vasomotor symptoms (such as hot flashes). Options could include the use of calcium and vitamin D supplements; hormone replacement therapy with estrogen with or without a progestin; or selective estrogen receptor modulators (such as raloxifene or bazedoxifene), tibolone, or calcitonin.

It’s important to recognize that all pharmacologic therapy carries the risk for adverse events, and it’s essential to take the necessary steps to prevent, monitor for, and manage any adverse effects that may develop.

Managing osteoporosis in older men could include the use of bone anabolics and/or antiresorptives. In younger individuals, use of pharmacologic therapy is less common but sometimes necessary, particularly when bone density is very low and associated with a problematic fracture history — for example, in those with genetic conditions such as osteogenesis imperfecta. Furthermore, the occurrence of vertebral compression fractures often requires bisphosphonate treatment regardless of bone density, particularly in patients on chronic glucocorticoid therapy.

Preventing osteoporosis is best managed by paying attention to lifestyle; optimizing nutrition and calcium and vitamin D intake; and managing conditions and limiting the use of medications that reduce bone density.

However, in certain patients, these measures are not enough, and pharmacologic therapy with bone anabolics or antiresorptives may be necessary to improve bone density and reduce fracture risk.

Dr. Misra, of the University of Virginia and UVA Health Children’s Hospital, Charlottesville, disclosed ties with AbbVie, Sanofi, and Ipsen.
 

A version of this article appeared on Medscape.com.

Fractures, particularly hip and spine fractures, are a major cause of mortality and morbidity among older individuals. The term “osteoporosis” indicates increased porosity of bones resulting in low bone density; increased bone fragility; and an increased risk for fracture, often with minimal trauma.

During the adolescent years, bone accrues at a rapid rate, and optimal bone accrual during this time is essential to attain optimal peak bone mass, typically achieved in the third decade of life. Bone mass then stays stable until the 40s-50s, after which it starts to decline. One’s peak bone mass sets the stage for both immediate and future bone health. Individuals with lower peak bone mass tend to have less optimal bone health throughout their lives, and this becomes particularly problematic in older men and in the postmenopausal years for women.

The best strategy to optimize bone health is to prevent osteoporosis from occurring in the first place. This requires attention to factors that contribute to optimal bone health. One’s genes have a major impact on bone density and are currently not modifiable.

Modifiable factors include mechanical loading of bones through exercise activity, maintaining a normal body weight, and ensuring adequate intake of micronutrients (including calcium and vitamin D) and macronutrients. Medications such as glucocorticoids that have deleterious effects on bones should be limited as far as possible. Endocrine, gastrointestinal, renal, and rheumatologic conditions and others, such as cancer, which are known to be associated with reduced bone density and increased fracture risk, should be managed appropriately.

A deficiency of the gonadal hormones (estrogen and testosterone) and high blood concentrations of cortisol are particularly deleterious to bone. Hormone replacement therapy in those with gonadal hormone deficiency and strategies to reduce cortisol levels in those with hypercortisolemia are essential to prevent osteoporosis and also improve bone density over time. The same applies to management of conditions such as anorexia nervosa, relative energy deficiency in sports, inflammatory bowel disease, celiac disease, cystic fibrosis, chronic kidney disease, and chronic arthritis.

Once osteoporosis has developed, depending on the cause, these strategies may not be sufficient to completely reverse the condition, and pharmacologic therapy may be necessary to improve bone density and reduce fracture risk. This is particularly an issue with postmenopausal women and older men. In these individuals, medications that increase bone formation or reduce bone loss may be necessary.

Medications that reduce bone loss include bisphosphonates and denosumab; these are also called “antiresorptive medications” because they reduce bone resorption by cells called osteoclasts. Bisphosphonates include alendronate, risedronate, ibandronate, pamidronate, and zoledronic acid, and these medications have direct effects on osteoclasts, reducing their activity. Some bisphosphonates, such as alendronate and risedronate, are taken orally (daily, weekly, or monthly, depending on the medication and its strength), whereas others, such as pamidronate and zoledronic acid, are administered intravenously: every 3-4 months for pamidronate and every 6-12 months for zoledronic acid. Ibandronate is available both orally and intravenously.

Denosumab is a medication that inhibits the action of receptor activator of nuclear factor-kappa ligand 1 (RANKL), which otherwise increases osteoclast activity. It is administered as a subcutaneous injection every 6 months to treat osteoporosis. One concern with denosumab is a rapid increase in bone loss after its discontinuation.

Medications that increase bone formation are called bone anabolics and include teriparatide, abaloparatide, and romosozumab. Teriparatide is a synthetic form of parathyroid hormone (recombinant PTH1-34) administered daily for up to 2 years. Abaloparatide is a synthetic analog of parathyroid hormone–related peptide (PTHrP), which is also administered daily as a subcutaneous injection. Romosozumab inhibits sclerostin (a substance that otherwise reduces bone formation and increases bone resorption) and is administered as a subcutaneous injection once a month. Effects of these medications tend to be lost after they are discontinued.

In 2019, the Endocrine Society published guidelines for managing postmenopausal osteoporosis. The guidelines recommend lifestyle modifications, including attention to diet, calcium and vitamin D supplements, and weight-bearing exercise for all postmenopausal women. They also recommend assessing fracture risk using country-specific existing models.

Guidelines vary depending on whether fracture risk is low, moderate, or high. Patients at low risk are followed and reassessed every 2-4 years for fracture risk. Those at moderate risk may be followed similarly or prescribed bisphosphonates. Those at high risk are prescribed an antiresorptive, such as a bisphosphonate or denosumab, or a bone anabolic, such as teriparatide or abaloparatide (for up to 2 years) or romosozumab (for a year), with calcium and vitamin D and are reassessed at defined intervals for fracture risk; subsequent management then depends on the assessed fracture risk.

People who are on a bone anabolic should typically follow this with an antiresorptive medication to maintain the gains achieved with the former after that medication is discontinued. Patients who discontinue denosumab should be switched to bisphosphonates to prevent the increase in bone loss that typically occurs.

In postmenopausal women who are intolerant to or inappropriate for use of these medications, guidelines vary depending on age (younger or older than 60 years) and presence or absence of vasomotor symptoms (such as hot flashes). Options could include the use of calcium and vitamin D supplements; hormone replacement therapy with estrogen with or without a progestin; or selective estrogen receptor modulators (such as raloxifene or bazedoxifene), tibolone, or calcitonin.

It’s important to recognize that all pharmacologic therapy carries the risk for adverse events, and it’s essential to take the necessary steps to prevent, monitor for, and manage any adverse effects that may develop.

Managing osteoporosis in older men could include the use of bone anabolics and/or antiresorptives. In younger individuals, use of pharmacologic therapy is less common but sometimes necessary, particularly when bone density is very low and associated with a problematic fracture history — for example, in those with genetic conditions such as osteogenesis imperfecta. Furthermore, the occurrence of vertebral compression fractures often requires bisphosphonate treatment regardless of bone density, particularly in patients on chronic glucocorticoid therapy.

Preventing osteoporosis is best managed by paying attention to lifestyle; optimizing nutrition and calcium and vitamin D intake; and managing conditions and limiting the use of medications that reduce bone density.

However, in certain patients, these measures are not enough, and pharmacologic therapy with bone anabolics or antiresorptives may be necessary to improve bone density and reduce fracture risk.

Dr. Misra, of the University of Virginia and UVA Health Children’s Hospital, Charlottesville, disclosed ties with AbbVie, Sanofi, and Ipsen.
 

A version of this article appeared on Medscape.com.

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Misra_Madhusmita_MA_web.jpg

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

A version of this article first appeared on Medscape.com.

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Misra_Madhusmita_MA_web.jpg

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

A version of this article first appeared on Medscape.com.

The actress Sally Field recently described her struggles with postmenopausal osteoporosis – she was given the diagnosis when she was 60 years old despite being physically active and engaging in activities such as biking, hiking, and yoga. As a slim, White woman in her sixth decade of life, she certainly had several risk factors for osteoporosis.

Osteoporosis, a condition associated with weak bones and an increased risk for fracture, is common in women after menopause. It’s defined as a bone mineral density (BMD) T-score of less than or equal to –2.5 on dual-energy x-ray absorptiometry (DXA) scan, occurrence of a spine or hip fracture regardless of BMD, or a BMD T-score between –1 and –2.5, along with a history of certain kinds of fractures or increased fracture risk based on the Fracture Risk Assessment Tool (FRAX).

Misra_Madhusmita_MA_web.jpg

Why increased fracture risk in postmenopausal women?

The primary cause of postmenopausal osteoporosis is the cessation of estrogen production by the ovaries around the menopausal transition. Estrogen is very important for bone health. It reduces bone loss by reducing levels of receptor activator of NF-kappa B ligand (RANKL) and sclerostin, and it probably also increases bone formation through its effects on sclerostin.

Around menopause, the decrease in estrogen levels results in an increase in RANKL and sclerostin, with a consequent increase in bone loss at a pace that exceeds the rate of bone formation, thereby leading to osteoporosis.

Many factors further increase the risk for osteoporosis and fracture in postmenopausal women. These include a sedentary lifestyle, lower body weight, family history of osteoporosis, smoking, and certain medications and diseases. Medications that adversely affect bone health at this age include (but are not limited to) glucocorticoids such as hydrocortisone, prednisone, and dexamethasone; letrozole; excess thyroid hormone; certain drugs used to treat cancer; immunosuppressive drugs; certain antiseizure medications; proton pump inhibitors (such as omeprazole); sodium-glucose cotransporter 2 inhibitors and certain other drugs used to treat type 2 diabetes; and selective serotonin reuptake inhibitors and serotonin and norepinephrine reuptake inhibitors (used to treat anxiety and depression).

Diseases associated with increased osteoporosis risk include certain genetic conditions affecting bone, a history of early ovarian insufficiency, hyperthyroidism, high levels of cortisol, diabetes, hyperparathyroidism, eating disorders, obesity, calcium and vitamin D deficiency, excess urinary excretion of calcium, malabsorption and certain gastrointestinal surgeries, chronic kidney disease, rheumatoid arthritis, certain types of cancer, and frailty.

Furthermore, older age, low bone density, a previous history of fracture, a family history of hip fracture, smoking, and excessive alcohol intake increase the risk for an osteoporotic fracture in a postmenopausal woman.

Bone density assessment using DXA is recommended in postmenopausal women who are at increased risk for low bone density and fracture. Monitoring of bone density is typically initiated about 5 years after the menopausal transition but should be considered earlier in those at high risk for osteoporosis. Women who are aged 70 or older, and those who have had significant height loss, should also get radiography of the spine to look for vertebral fractures.

Optimal nutrition is important for all postmenopausal women. Weight extremes are to be avoided. Although the use of calcium and vitamin D supplementation in postmenopausal women is still debated, the Institute of Medicine recommends that women 51-70 years of age take 1,000-1,200 mg of calcium and 400-600 IU of vitamin D daily, and that those older than 70 years take 1,000-1,200 mg of calcium and 400-800 IU of vitamin D daily.

Women with low vitamin D levels often require higher doses of vitamin D. It’s very important to avoid smoking and excessive alcohol consumption. Optimizing protein intake and exercises that improve muscle strength and improve balance can reduce the risk for falls, a key contributor to osteoporotic fractures.
 

Estrogen to prevent fracture risk

Because estrogen deficiency is a key cause of postmenopausal osteoporosis, estrogen replacement therapy has been used to prevent this condition, particularly early in the menopausal transition (51-60 years). Different formulations of estrogen given via oral or transdermal routes have been demonstrated to prevent osteoporosis; transdermal estrogen is often preferred because of a lower risk for blood clots and stroke. Women who have an intact uterus should also receive a progestin preparation either daily or cyclically, because estrogen alone can increase the risk for uterine cancer in the long run. Estrogen replacement has been associated with a 34% reduction in vertebral, hip, and total fractures in women of this age group.

Sally Field did receive hormone replacement therapy, which was helpful for her bones. However, as typically happens, her bone density dropped again when she discontinued hormone replacement. She also had low vitamin D levels, but vitamin D supplementation was not helpful. She received other medical intervention, with recovery back to good bone health.

Raloxifene is a medication that acts on the estrogen receptor, with beneficial effects on bone, and is approved for prevention and treatment of postmenopausal osteoporosis.

Medications that reduce bone loss (antiresorptive drugs), such as bisphosphonates and denosumab, and those that increase bone formation (osteoanabolic drugs), such as teriparatide, abaloparatide, and romosozumab, are used alone or in combination in women whose osteoporosis doesn’t respond to lifestyle and preventive strategies. The osteoanabolic drugs are typically reserved for women at very high risk for fractures, such as those with a BMD T-score ≤ less than or equal to –3, older women with recent fractures, and those with other risk factors. Treatment is typically lifelong.

Postmenopausal osteoporosis can have far-reaching consequences on one’s quality of life, given the risk for fractures that are often associated with hospitalization, surgery, and long periods of rehabilitation (such as fractures of the spine and hip). It’s important to recognize those at greatest risk for this condition; implement bone health monitoring in a timely fashion; and ensure optimal nutrition, calcium and vitamin D supplementation, and exercises that optimize muscle strength and balance. Hormone replacement therapy is a consideration in many women. Some women will require antiresorptive or osteoanabolic drugs to manage this condition. With optimal treatment, older women can live long and productive lives.

Dr. Misra is Chief, Division of Pediatric Endocrinology, Mass General for Children; Associate Director, Harvard Catalyst Translation and Clinical Research Center; Director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; Professor, department of pediatrics, Harvard Medical School, Boston. She has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AbbVie; Sanofi; Ipsen.

A version of this article first appeared on Medscape.com.

Thach Tran, MD, and colleagues introduced the concept of “skeletal age” in a recently published paper that aims to incorporate the impact of fragility, or low trauma, fractures – which can occur in patients with osteoporosis – on mortality risk.
 

They defined “skeletal age” as the age of the skeleton following a fragility fracture. This is calculated as the chronological age of the individual plus the number of years of “life lost” as a consequence of the specific fracture.

The risk for premature death following fragility fractures is concerning, with 22%-58% of patients with hip fracture dying within a year (Brauer et al.; Rapp et al.). Thus, it’s important to treat osteoporosis in a timely fashion to reduce the risk for such fractures and the excess mortality risk associated with them.

Implementation and uptake of such treatment, however, either before or after a fragility fracture, is far from optimal (Solomon et al). This may be because patients don’t fully understand the consequence of such a fracture, and outcomes measures currently in use (such as relative risk or hazard of mortality) are difficult to communicate to patients.

In the recent paper by Dr. Tran and colleagues, the authors examined the association between fractures and mortality based on sex, age, associated comorbidities, and fracture site. They pooled this information to create a “skeletal age” for each fracture site, using data from the Danish National Hospital Discharge Registry, which documents fractures and related mortality for all Danish people.

They examined mortality over a period of at least 2 years following a fragility fracture in individuals aged 50 or older, and reported that occurrence of any fragility fracture is associated with a 30%-45% increased risk for death, with the highest risk noted for hip and femur fractures (twofold increase). Fractures of the pelvis, vertebrae, humerus, ribs, clavicle, and lower leg were also associated with increased mortality risk, but no increase was seen with fractures of the forearm, knee, ankle, hand, or foot.

The number of years of life lost at any age depending on the fracture site is represented as a linear graph of skeletal age for any chronological age, for specific fracture sites, separated by sex.

For example, the skeletal age of a 50-year-old man who has a hip fracture is 57 years (7 years of life lost as a consequence of the fracture), while that for a 70-year-old man with the same fracture is 75 years (5 years of life lost because of the fracture). Similarly, the skeletal age of a 50-year-old man with a fracture of the pelvis, femur, vertebrae, and humerus is 55 years (5 years of life lost). Fractures of the lower leg, humerus, and clavicle lead to fewer lost years of life.

The authors are to be commended for creating a simple strategy to quantify mortality risk following low-impact or fragility fractures in older individuals; this could enable providers to communicate the importance of osteoporosis treatment more effectively to patients on the basis of their skeletal age, and for patients to better understand this information.

The study design appears reasonably robust as the authors considered many factors that might affect mortality risk, such as sex, age, and comorbidities, and the results are based on information from a very large number of people – 1.6 million.

However, there’s a major issue with the concept of “skeletal age” as proposed by Dr. Tran and colleagues. The term is already in use and defines the maturity of bones in children and adolescents, also called “bone age” (Greulich and Pyle 1959; Skeletal Age, Radiology Key). This is a real oversight and could cause confusion in interpreting “skeletal age.”

Skeletal age as currently defined in children and adolescents is influenced by chronological age, exposure to certain hormones, nutritional deficiencies, and systemic diseases, and is a predictor of adult height based on the skeletal age and current height. This concept is completely different from that being proposed by the authors in this paper. Dr. Tran and colleagues (and the reviewers of this paper) are probably not familiar with the use of the terminology in youth, which is a major oversight; they should consider changing the terminology given this overlap.

Further, fragility fractures can occur from osteoporosis at any age, and this study doesn’t provide information regarding years of life lost from occurrence of fragility fractures at younger ages, or the age at which mortality risk starts to increase (as the study was performed only in those aged 50 or older).

While the study takes into account general comorbidities in developing the model to define years of life lost, it doesn’t account for other factors that can influence fracture risk, such as lifestyle factors, activity level, and genetic risk (family history of osteoporosis, for example). Of note, the impact of additional fractures isn’t considered either and should be factored into future investigations.

Overall, the study is robust and important and provides valuable information regarding mortality risk from a fragility fracture in older people. However, there are some flaws that need to be considered and addressed, the most serious of which is that the term “skeletal age” has been in existence for decades, applied to a much younger age group, and its implications are completely different from those being proposed by the authors here.

A version of this article first appeared on Medscape.com.

Thach Tran, MD, and colleagues introduced the concept of “skeletal age” in a recently published paper that aims to incorporate the impact of fragility, or low trauma, fractures – which can occur in patients with osteoporosis – on mortality risk.
 

They defined “skeletal age” as the age of the skeleton following a fragility fracture. This is calculated as the chronological age of the individual plus the number of years of “life lost” as a consequence of the specific fracture.

The risk for premature death following fragility fractures is concerning, with 22%-58% of patients with hip fracture dying within a year (Brauer et al.; Rapp et al.). Thus, it’s important to treat osteoporosis in a timely fashion to reduce the risk for such fractures and the excess mortality risk associated with them.

Implementation and uptake of such treatment, however, either before or after a fragility fracture, is far from optimal (Solomon et al). This may be because patients don’t fully understand the consequence of such a fracture, and outcomes measures currently in use (such as relative risk or hazard of mortality) are difficult to communicate to patients.

In the recent paper by Dr. Tran and colleagues, the authors examined the association between fractures and mortality based on sex, age, associated comorbidities, and fracture site. They pooled this information to create a “skeletal age” for each fracture site, using data from the Danish National Hospital Discharge Registry, which documents fractures and related mortality for all Danish people.

They examined mortality over a period of at least 2 years following a fragility fracture in individuals aged 50 or older, and reported that occurrence of any fragility fracture is associated with a 30%-45% increased risk for death, with the highest risk noted for hip and femur fractures (twofold increase). Fractures of the pelvis, vertebrae, humerus, ribs, clavicle, and lower leg were also associated with increased mortality risk, but no increase was seen with fractures of the forearm, knee, ankle, hand, or foot.

The number of years of life lost at any age depending on the fracture site is represented as a linear graph of skeletal age for any chronological age, for specific fracture sites, separated by sex.

For example, the skeletal age of a 50-year-old man who has a hip fracture is 57 years (7 years of life lost as a consequence of the fracture), while that for a 70-year-old man with the same fracture is 75 years (5 years of life lost because of the fracture). Similarly, the skeletal age of a 50-year-old man with a fracture of the pelvis, femur, vertebrae, and humerus is 55 years (5 years of life lost). Fractures of the lower leg, humerus, and clavicle lead to fewer lost years of life.

The authors are to be commended for creating a simple strategy to quantify mortality risk following low-impact or fragility fractures in older individuals; this could enable providers to communicate the importance of osteoporosis treatment more effectively to patients on the basis of their skeletal age, and for patients to better understand this information.

The study design appears reasonably robust as the authors considered many factors that might affect mortality risk, such as sex, age, and comorbidities, and the results are based on information from a very large number of people – 1.6 million.

However, there’s a major issue with the concept of “skeletal age” as proposed by Dr. Tran and colleagues. The term is already in use and defines the maturity of bones in children and adolescents, also called “bone age” (Greulich and Pyle 1959; Skeletal Age, Radiology Key). This is a real oversight and could cause confusion in interpreting “skeletal age.”

Skeletal age as currently defined in children and adolescents is influenced by chronological age, exposure to certain hormones, nutritional deficiencies, and systemic diseases, and is a predictor of adult height based on the skeletal age and current height. This concept is completely different from that being proposed by the authors in this paper. Dr. Tran and colleagues (and the reviewers of this paper) are probably not familiar with the use of the terminology in youth, which is a major oversight; they should consider changing the terminology given this overlap.

Further, fragility fractures can occur from osteoporosis at any age, and this study doesn’t provide information regarding years of life lost from occurrence of fragility fractures at younger ages, or the age at which mortality risk starts to increase (as the study was performed only in those aged 50 or older).

While the study takes into account general comorbidities in developing the model to define years of life lost, it doesn’t account for other factors that can influence fracture risk, such as lifestyle factors, activity level, and genetic risk (family history of osteoporosis, for example). Of note, the impact of additional fractures isn’t considered either and should be factored into future investigations.

Overall, the study is robust and important and provides valuable information regarding mortality risk from a fragility fracture in older people. However, there are some flaws that need to be considered and addressed, the most serious of which is that the term “skeletal age” has been in existence for decades, applied to a much younger age group, and its implications are completely different from those being proposed by the authors here.

A version of this article first appeared on Medscape.com.

Thach Tran, MD, and colleagues introduced the concept of “skeletal age” in a recently published paper that aims to incorporate the impact of fragility, or low trauma, fractures – which can occur in patients with osteoporosis – on mortality risk.
 

They defined “skeletal age” as the age of the skeleton following a fragility fracture. This is calculated as the chronological age of the individual plus the number of years of “life lost” as a consequence of the specific fracture.

The risk for premature death following fragility fractures is concerning, with 22%-58% of patients with hip fracture dying within a year (Brauer et al.; Rapp et al.). Thus, it’s important to treat osteoporosis in a timely fashion to reduce the risk for such fractures and the excess mortality risk associated with them.

Implementation and uptake of such treatment, however, either before or after a fragility fracture, is far from optimal (Solomon et al). This may be because patients don’t fully understand the consequence of such a fracture, and outcomes measures currently in use (such as relative risk or hazard of mortality) are difficult to communicate to patients.

In the recent paper by Dr. Tran and colleagues, the authors examined the association between fractures and mortality based on sex, age, associated comorbidities, and fracture site. They pooled this information to create a “skeletal age” for each fracture site, using data from the Danish National Hospital Discharge Registry, which documents fractures and related mortality for all Danish people.

They examined mortality over a period of at least 2 years following a fragility fracture in individuals aged 50 or older, and reported that occurrence of any fragility fracture is associated with a 30%-45% increased risk for death, with the highest risk noted for hip and femur fractures (twofold increase). Fractures of the pelvis, vertebrae, humerus, ribs, clavicle, and lower leg were also associated with increased mortality risk, but no increase was seen with fractures of the forearm, knee, ankle, hand, or foot.

The number of years of life lost at any age depending on the fracture site is represented as a linear graph of skeletal age for any chronological age, for specific fracture sites, separated by sex.

For example, the skeletal age of a 50-year-old man who has a hip fracture is 57 years (7 years of life lost as a consequence of the fracture), while that for a 70-year-old man with the same fracture is 75 years (5 years of life lost because of the fracture). Similarly, the skeletal age of a 50-year-old man with a fracture of the pelvis, femur, vertebrae, and humerus is 55 years (5 years of life lost). Fractures of the lower leg, humerus, and clavicle lead to fewer lost years of life.

The authors are to be commended for creating a simple strategy to quantify mortality risk following low-impact or fragility fractures in older individuals; this could enable providers to communicate the importance of osteoporosis treatment more effectively to patients on the basis of their skeletal age, and for patients to better understand this information.

The study design appears reasonably robust as the authors considered many factors that might affect mortality risk, such as sex, age, and comorbidities, and the results are based on information from a very large number of people – 1.6 million.

However, there’s a major issue with the concept of “skeletal age” as proposed by Dr. Tran and colleagues. The term is already in use and defines the maturity of bones in children and adolescents, also called “bone age” (Greulich and Pyle 1959; Skeletal Age, Radiology Key). This is a real oversight and could cause confusion in interpreting “skeletal age.”

Skeletal age as currently defined in children and adolescents is influenced by chronological age, exposure to certain hormones, nutritional deficiencies, and systemic diseases, and is a predictor of adult height based on the skeletal age and current height. This concept is completely different from that being proposed by the authors in this paper. Dr. Tran and colleagues (and the reviewers of this paper) are probably not familiar with the use of the terminology in youth, which is a major oversight; they should consider changing the terminology given this overlap.

Further, fragility fractures can occur from osteoporosis at any age, and this study doesn’t provide information regarding years of life lost from occurrence of fragility fractures at younger ages, or the age at which mortality risk starts to increase (as the study was performed only in those aged 50 or older).

While the study takes into account general comorbidities in developing the model to define years of life lost, it doesn’t account for other factors that can influence fracture risk, such as lifestyle factors, activity level, and genetic risk (family history of osteoporosis, for example). Of note, the impact of additional fractures isn’t considered either and should be factored into future investigations.

Overall, the study is robust and important and provides valuable information regarding mortality risk from a fragility fracture in older people. However, there are some flaws that need to be considered and addressed, the most serious of which is that the term “skeletal age” has been in existence for decades, applied to a much younger age group, and its implications are completely different from those being proposed by the authors here.

A version of this article first appeared on Medscape.com.

Although weight loss surgery offers many benefits for people with obesity, it can have deleterious effects on bone health in both teenagers and adults and increase the risk for fracture.

Currently, the two most common types of weight loss surgery performed include sleeve gastrectomy and Roux-en-Y gastric bypass (RYGB). Sleeve gastrectomy involves removing a large portion of the stomach so that its capacity is significantly decreased (to about 20%), reducing the ability to consume large quantities of food. Also, the procedure leads to marked reductions in ghrelin (an appetite-stimulating hormone), and some studies have reported increases in glucagon-like peptide 1 (GLP-1) and peptide YY (PYY), hormones that induce satiety. Gastric bypass involves creating a small stomach pouch and rerouting the small intestine so that it bypasses much of the stomach and also the upper portion of the small intestine. This reduces the amount of food that can be consumed at any time, increases levels of GLP-1 and PYY, and reduces absorption of nutrients with resultant weight loss. Less common bariatric surgeries include gastric banding and biliopancreatic diversion with duodenal switch (BPD-DS). Gastric banding involves placing a ring in the upper portion of the stomach, and the size of the pouch created can be altered by injecting more or less saline through a port inserted under the skin. BPD-DS includes sleeve gastrectomy, resection of a large section of the small intestine, and diversion of the pancreatic and biliary duct to a point below the junction of the ends of the resected gut.

Weight loss surgery is currently recommended for people who have a body mass index greater than or equal to 35 regardless of obesity-related complication and may be considered for those with a BMI greater than or equal to 30. BMI is calculated by dividing the weight (in kilograms) by the height (in meters). In children and adolescents, weight loss surgery should be considered in those with a BMI greater than 120% of the 95th percentile and with a major comorbidity or in those with a BMI greater than 140% of the 95th percentile.
 

What impact does weight loss surgery have on bone?

Multiple studies in both adults and teenagers have demonstrated that sleeve gastrectomy, RYGB, and BPD-DS (but not gastric banding) are associated with a decrease in bone density, impaired bone structure, and reduced strength estimates over time (Beavers et al;  Gagnon, Schafer; Misra, Bredella). The relative risk for fracture after RYGB and BPD-DS is reported to be 1.2-2.3 (that is, 20%-130% more than normal), whereas fracture risk after sleeve gastrectomy is still under study with some conflicting results. Fracture risk starts to increase 2-3 years after surgery and peaks at 5-plus years after surgery. Most of the data for fractures come from studies in adults. With the rising use of weight loss surgery, particularly sleeve gastrectomy, in teenagers, studies are needed to determine fracture risk in this younger age group, who also seem to experience marked reductions in bone density, altered bone structure, and reduced bone strength after bariatric surgery.

What contributes to impaired bone health after weight loss surgery?

The deleterious effect of weight loss surgery on bone appears to be caused by various factors, including the massive and rapid weight loss that occurs after surgery, because body weight has a mechanical loading effect on bone and otherwise promotes bone formation. Weight loss results in mechanical unloading and thus a decrease in bone density. Further, when weight loss occurs, there is loss of both muscle and fat mass, and the reduction in muscle mass is deleterious to bone.

Other possible causes of bone density reduction include reduced absorption of certain nutrients, such as calcium and vitamin D critical for bone mineralization, and alterations in certain hormones that impact bone health. These include increases in parathyroid hormone, which increases bone loss when secreted in excess; increases in PYY (a hormone that reduces bone formation); decreases in ghrelin (a hormone that typically increases bone formation), particularly after sleeve gastrectomy; and decreases in estrone (a kind of estrogen that like other estrogens prevents bone loss). Further, age and gender may modify the bone consequences of surgery as outcomes in postmenopausal women appear to be worse than in younger women and men.
 

Preventing bone density loss

Given the many benefits of weight loss surgery, what can we do to prevent this decrease in bone density after surgery? It’s important for people undergoing weight loss surgery to be cognizant of this potentially negative outcome and to take appropriate precautions to mitigate this concern.

We should monitor bone density after surgery with the help of dual energy x-ray absorptiometry, starting a few years after surgery, particularly in those who are at greatest risk for fracture, so that we can be proactive about addressing any severe bone loss that warrants pharmacologic intervention.

More general recommendations include optimizing intake of calcium (1,200-1,500 mg/d), vitamin D (2,000-3,000 IUs/d), and protein (60-75 g/d) via diet and/or as supplements and engaging in weight-bearing physical activity because this exerts mechanical loading effects on the skeleton leading to increased bone formation and also increases muscle mass over time, which is beneficial to bone. A progressive resistance training program has been demonstrated to have beneficial effects on bone, and measures should be taken to reduce the risk for falls, which increases after certain kinds of weight loss surgery, such as gastric bypass.

Meeting with a dietitian can help determine any other nutrients that need to be optimized.

Though many hormonal changes after surgery have been linked to reductions in bone density, there are still no recommended hormonal therapies at this time, and more work is required to determine whether specific pharmacologic therapies might help improve bone outcomes after surgery.

Dr. Misra is chief of the division of pediatric endocrinology, Mass General for Children; associate director, Harvard Catalyst Translation and Clinical Research Center; director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; and professor, department of pediatrics, Harvard Medical School, Boston.

A version of this article originally appeared on Medscape.com.

Although weight loss surgery offers many benefits for people with obesity, it can have deleterious effects on bone health in both teenagers and adults and increase the risk for fracture.

Currently, the two most common types of weight loss surgery performed include sleeve gastrectomy and Roux-en-Y gastric bypass (RYGB). Sleeve gastrectomy involves removing a large portion of the stomach so that its capacity is significantly decreased (to about 20%), reducing the ability to consume large quantities of food. Also, the procedure leads to marked reductions in ghrelin (an appetite-stimulating hormone), and some studies have reported increases in glucagon-like peptide 1 (GLP-1) and peptide YY (PYY), hormones that induce satiety. Gastric bypass involves creating a small stomach pouch and rerouting the small intestine so that it bypasses much of the stomach and also the upper portion of the small intestine. This reduces the amount of food that can be consumed at any time, increases levels of GLP-1 and PYY, and reduces absorption of nutrients with resultant weight loss. Less common bariatric surgeries include gastric banding and biliopancreatic diversion with duodenal switch (BPD-DS). Gastric banding involves placing a ring in the upper portion of the stomach, and the size of the pouch created can be altered by injecting more or less saline through a port inserted under the skin. BPD-DS includes sleeve gastrectomy, resection of a large section of the small intestine, and diversion of the pancreatic and biliary duct to a point below the junction of the ends of the resected gut.

Weight loss surgery is currently recommended for people who have a body mass index greater than or equal to 35 regardless of obesity-related complication and may be considered for those with a BMI greater than or equal to 30. BMI is calculated by dividing the weight (in kilograms) by the height (in meters). In children and adolescents, weight loss surgery should be considered in those with a BMI greater than 120% of the 95th percentile and with a major comorbidity or in those with a BMI greater than 140% of the 95th percentile.
 

What impact does weight loss surgery have on bone?

Multiple studies in both adults and teenagers have demonstrated that sleeve gastrectomy, RYGB, and BPD-DS (but not gastric banding) are associated with a decrease in bone density, impaired bone structure, and reduced strength estimates over time (Beavers et al;  Gagnon, Schafer; Misra, Bredella). The relative risk for fracture after RYGB and BPD-DS is reported to be 1.2-2.3 (that is, 20%-130% more than normal), whereas fracture risk after sleeve gastrectomy is still under study with some conflicting results. Fracture risk starts to increase 2-3 years after surgery and peaks at 5-plus years after surgery. Most of the data for fractures come from studies in adults. With the rising use of weight loss surgery, particularly sleeve gastrectomy, in teenagers, studies are needed to determine fracture risk in this younger age group, who also seem to experience marked reductions in bone density, altered bone structure, and reduced bone strength after bariatric surgery.

What contributes to impaired bone health after weight loss surgery?

The deleterious effect of weight loss surgery on bone appears to be caused by various factors, including the massive and rapid weight loss that occurs after surgery, because body weight has a mechanical loading effect on bone and otherwise promotes bone formation. Weight loss results in mechanical unloading and thus a decrease in bone density. Further, when weight loss occurs, there is loss of both muscle and fat mass, and the reduction in muscle mass is deleterious to bone.

Other possible causes of bone density reduction include reduced absorption of certain nutrients, such as calcium and vitamin D critical for bone mineralization, and alterations in certain hormones that impact bone health. These include increases in parathyroid hormone, which increases bone loss when secreted in excess; increases in PYY (a hormone that reduces bone formation); decreases in ghrelin (a hormone that typically increases bone formation), particularly after sleeve gastrectomy; and decreases in estrone (a kind of estrogen that like other estrogens prevents bone loss). Further, age and gender may modify the bone consequences of surgery as outcomes in postmenopausal women appear to be worse than in younger women and men.
 

Preventing bone density loss

Given the many benefits of weight loss surgery, what can we do to prevent this decrease in bone density after surgery? It’s important for people undergoing weight loss surgery to be cognizant of this potentially negative outcome and to take appropriate precautions to mitigate this concern.

We should monitor bone density after surgery with the help of dual energy x-ray absorptiometry, starting a few years after surgery, particularly in those who are at greatest risk for fracture, so that we can be proactive about addressing any severe bone loss that warrants pharmacologic intervention.

More general recommendations include optimizing intake of calcium (1,200-1,500 mg/d), vitamin D (2,000-3,000 IUs/d), and protein (60-75 g/d) via diet and/or as supplements and engaging in weight-bearing physical activity because this exerts mechanical loading effects on the skeleton leading to increased bone formation and also increases muscle mass over time, which is beneficial to bone. A progressive resistance training program has been demonstrated to have beneficial effects on bone, and measures should be taken to reduce the risk for falls, which increases after certain kinds of weight loss surgery, such as gastric bypass.

Meeting with a dietitian can help determine any other nutrients that need to be optimized.

Though many hormonal changes after surgery have been linked to reductions in bone density, there are still no recommended hormonal therapies at this time, and more work is required to determine whether specific pharmacologic therapies might help improve bone outcomes after surgery.

Dr. Misra is chief of the division of pediatric endocrinology, Mass General for Children; associate director, Harvard Catalyst Translation and Clinical Research Center; director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; and professor, department of pediatrics, Harvard Medical School, Boston.

A version of this article originally appeared on Medscape.com.

Although weight loss surgery offers many benefits for people with obesity, it can have deleterious effects on bone health in both teenagers and adults and increase the risk for fracture.

Currently, the two most common types of weight loss surgery performed include sleeve gastrectomy and Roux-en-Y gastric bypass (RYGB). Sleeve gastrectomy involves removing a large portion of the stomach so that its capacity is significantly decreased (to about 20%), reducing the ability to consume large quantities of food. Also, the procedure leads to marked reductions in ghrelin (an appetite-stimulating hormone), and some studies have reported increases in glucagon-like peptide 1 (GLP-1) and peptide YY (PYY), hormones that induce satiety. Gastric bypass involves creating a small stomach pouch and rerouting the small intestine so that it bypasses much of the stomach and also the upper portion of the small intestine. This reduces the amount of food that can be consumed at any time, increases levels of GLP-1 and PYY, and reduces absorption of nutrients with resultant weight loss. Less common bariatric surgeries include gastric banding and biliopancreatic diversion with duodenal switch (BPD-DS). Gastric banding involves placing a ring in the upper portion of the stomach, and the size of the pouch created can be altered by injecting more or less saline through a port inserted under the skin. BPD-DS includes sleeve gastrectomy, resection of a large section of the small intestine, and diversion of the pancreatic and biliary duct to a point below the junction of the ends of the resected gut.

Weight loss surgery is currently recommended for people who have a body mass index greater than or equal to 35 regardless of obesity-related complication and may be considered for those with a BMI greater than or equal to 30. BMI is calculated by dividing the weight (in kilograms) by the height (in meters). In children and adolescents, weight loss surgery should be considered in those with a BMI greater than 120% of the 95th percentile and with a major comorbidity or in those with a BMI greater than 140% of the 95th percentile.
 

What impact does weight loss surgery have on bone?

Multiple studies in both adults and teenagers have demonstrated that sleeve gastrectomy, RYGB, and BPD-DS (but not gastric banding) are associated with a decrease in bone density, impaired bone structure, and reduced strength estimates over time (Beavers et al;  Gagnon, Schafer; Misra, Bredella). The relative risk for fracture after RYGB and BPD-DS is reported to be 1.2-2.3 (that is, 20%-130% more than normal), whereas fracture risk after sleeve gastrectomy is still under study with some conflicting results. Fracture risk starts to increase 2-3 years after surgery and peaks at 5-plus years after surgery. Most of the data for fractures come from studies in adults. With the rising use of weight loss surgery, particularly sleeve gastrectomy, in teenagers, studies are needed to determine fracture risk in this younger age group, who also seem to experience marked reductions in bone density, altered bone structure, and reduced bone strength after bariatric surgery.

What contributes to impaired bone health after weight loss surgery?

The deleterious effect of weight loss surgery on bone appears to be caused by various factors, including the massive and rapid weight loss that occurs after surgery, because body weight has a mechanical loading effect on bone and otherwise promotes bone formation. Weight loss results in mechanical unloading and thus a decrease in bone density. Further, when weight loss occurs, there is loss of both muscle and fat mass, and the reduction in muscle mass is deleterious to bone.

Other possible causes of bone density reduction include reduced absorption of certain nutrients, such as calcium and vitamin D critical for bone mineralization, and alterations in certain hormones that impact bone health. These include increases in parathyroid hormone, which increases bone loss when secreted in excess; increases in PYY (a hormone that reduces bone formation); decreases in ghrelin (a hormone that typically increases bone formation), particularly after sleeve gastrectomy; and decreases in estrone (a kind of estrogen that like other estrogens prevents bone loss). Further, age and gender may modify the bone consequences of surgery as outcomes in postmenopausal women appear to be worse than in younger women and men.
 

Preventing bone density loss

Given the many benefits of weight loss surgery, what can we do to prevent this decrease in bone density after surgery? It’s important for people undergoing weight loss surgery to be cognizant of this potentially negative outcome and to take appropriate precautions to mitigate this concern.

We should monitor bone density after surgery with the help of dual energy x-ray absorptiometry, starting a few years after surgery, particularly in those who are at greatest risk for fracture, so that we can be proactive about addressing any severe bone loss that warrants pharmacologic intervention.

More general recommendations include optimizing intake of calcium (1,200-1,500 mg/d), vitamin D (2,000-3,000 IUs/d), and protein (60-75 g/d) via diet and/or as supplements and engaging in weight-bearing physical activity because this exerts mechanical loading effects on the skeleton leading to increased bone formation and also increases muscle mass over time, which is beneficial to bone. A progressive resistance training program has been demonstrated to have beneficial effects on bone, and measures should be taken to reduce the risk for falls, which increases after certain kinds of weight loss surgery, such as gastric bypass.

Meeting with a dietitian can help determine any other nutrients that need to be optimized.

Though many hormonal changes after surgery have been linked to reductions in bone density, there are still no recommended hormonal therapies at this time, and more work is required to determine whether specific pharmacologic therapies might help improve bone outcomes after surgery.

Dr. Misra is chief of the division of pediatric endocrinology, Mass General for Children; associate director, Harvard Catalyst Translation and Clinical Research Center; director, Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital; and professor, department of pediatrics, Harvard Medical School, Boston.

A version of this article originally appeared on Medscape.com.

Many years ago, at the conclusion of a talk I gave on bone health in teens with anorexia nervosa, I was approached by a colleague, Ann Neumeyer, MD, medical director of the Lurie Center for Autism at Massachusetts General Hospital, Boston, who asked about bone health in children with autism spectrum disorder (ASD).

When I explained that there was little information about bone health in this patient population, she suggested that we learn and investigate together. Ann explained that she had observed that some of her patients with ASD had suffered fractures with minimal trauma, raising her concern about their bone health.

This was the beginning of a partnership that led us down the path of many grant submissions, some of which were funded and others that were not, to explore and investigate bone outcomes in children with ASD.

Over the years it has become very clear that these patients are at high risk for low bone density at multiple sites. This applies to prepubertal children as well as older children and adolescents. One study showed that 28% and 33% of children with ASD 8-14 years old had very low bone density (z scores of ≤ –2) at the spine and hip, respectively, compared with 0% of typically developing controls.

Studies that have used sophisticated imaging techniques to determine bone strength have shown that it is lower at the forearm and lower leg in children with ASD versus neurotypical children.

These findings are of particular concern during the childhood and teenage years when bone is typically accrued at a rapid rate. A normal rate of bone accrual at this time of life is essential for optimal bone health in later life. While children with ASD gain bone mass at a similar rate as neurotypical controls, they start at a deficit and seem unable to “catch up.”

Further, people with ASD are more prone to certain kinds of fracture than those without the condition. For example, both children and adults with ASD have a high risk for hip fracture, while adult women with ASD have a higher risk for forearm and spine fractures. There is some protection against forearm fractures in children and adult men, probably because of markedly lower levels of physical activity, which would reduce fall risk.

Many of Ann’s patients with ASD had unusual or restricted diets, low levels of physical activity, and were on multiple medications. We have since learned that some factors that contribute to low bone density in ASD include lower levels of weight-bearing physical activity; lower muscle mass; low muscle tone; suboptimal dietary calcium and vitamin D intake; lower vitamin D levels; higher levels of the hormone cortisol, which has deleterious effects on bone; and use of medications that can lower bone density.

In order to mitigate the risk for low bone density and fractures, it is important to optimize physical activity while considering the child’s ability to safely engage in weight-bearing sports.

High-impact sports like gymnastics and jumping, or cross-impact sports like soccer, basketball, field hockey, and lacrosse, are particularly useful in this context, but many patients with ASD are not able to easily engage in typical team sports.

For such children, a prescribed amount of time spent walking, as well as weight and resistance training, could be helpful. The latter would also help increase muscle mass, a key modulator of bone health.

Other strategies include ensuring sufficient intake of calcium and vitamin D through diet and supplements. This can be a particular challenge for children with ASD on specialized diets, such as a gluten-free or dairy-free diet, which are deficient in calcium and vitamin D. Health care providers should check for intake of dairy and dairy products, as well as serum vitamin D levels, and prescribe supplements as needed.

All children should get at least 600 IUs of vitamin D and 1,000-1,300 mg of elemental calcium daily. That said, many with ASD need much higher quantities of vitamin D (1,000-4,000 IUs or more) to maintain levels in the normal range. This is particularly true for dark-skinned children and children with obesity, as well as those who have medical disorders that cause malabsorption.

Higher cortisol levels in the ASD patient population are harder to manage. Efforts to ease anxiety and depression may help reduce cortisol levels. Medications such as protein pump inhibitors and glucocorticosteroids can compromise bone health.

In addition, certain antipsychotics can cause marked elevations in prolactin which, in turn, can lower levels of estrogen and testosterone, which are very important for bone health. In such cases, the clinician should consider switching patients to a different, less detrimental medication or adjust the current medication so that patients receive the lowest possible effective dose.

Obesity is associated with increased fracture risk and with suboptimal bone accrual during childhood, so ensuring a healthy diet is important. This includes avoiding sugary beverages and reducing intake of processed food and juice.

Sometimes, particularly when a child has low bone density and a history of several low-trauma fractures, medications such as bisphosphonates should be considered to increase bone density.

Above all, as physicians who manage ASD, it is essential that we raise awareness about bone health among our colleagues, patients, and their families to help mitigate fracture risk.

Madhusmita Misra, MD, MPH, is chief of the Division of Pediatric Endocrinology at Mass General for Children, Boston.

A version of this article first appeared on Medscape.com.

Many years ago, at the conclusion of a talk I gave on bone health in teens with anorexia nervosa, I was approached by a colleague, Ann Neumeyer, MD, medical director of the Lurie Center for Autism at Massachusetts General Hospital, Boston, who asked about bone health in children with autism spectrum disorder (ASD).

When I explained that there was little information about bone health in this patient population, she suggested that we learn and investigate together. Ann explained that she had observed that some of her patients with ASD had suffered fractures with minimal trauma, raising her concern about their bone health.

This was the beginning of a partnership that led us down the path of many grant submissions, some of which were funded and others that were not, to explore and investigate bone outcomes in children with ASD.

Over the years it has become very clear that these patients are at high risk for low bone density at multiple sites. This applies to prepubertal children as well as older children and adolescents. One study showed that 28% and 33% of children with ASD 8-14 years old had very low bone density (z scores of ≤ –2) at the spine and hip, respectively, compared with 0% of typically developing controls.

Studies that have used sophisticated imaging techniques to determine bone strength have shown that it is lower at the forearm and lower leg in children with ASD versus neurotypical children.

These findings are of particular concern during the childhood and teenage years when bone is typically accrued at a rapid rate. A normal rate of bone accrual at this time of life is essential for optimal bone health in later life. While children with ASD gain bone mass at a similar rate as neurotypical controls, they start at a deficit and seem unable to “catch up.”

Further, people with ASD are more prone to certain kinds of fracture than those without the condition. For example, both children and adults with ASD have a high risk for hip fracture, while adult women with ASD have a higher risk for forearm and spine fractures. There is some protection against forearm fractures in children and adult men, probably because of markedly lower levels of physical activity, which would reduce fall risk.

Many of Ann’s patients with ASD had unusual or restricted diets, low levels of physical activity, and were on multiple medications. We have since learned that some factors that contribute to low bone density in ASD include lower levels of weight-bearing physical activity; lower muscle mass; low muscle tone; suboptimal dietary calcium and vitamin D intake; lower vitamin D levels; higher levels of the hormone cortisol, which has deleterious effects on bone; and use of medications that can lower bone density.

In order to mitigate the risk for low bone density and fractures, it is important to optimize physical activity while considering the child’s ability to safely engage in weight-bearing sports.

High-impact sports like gymnastics and jumping, or cross-impact sports like soccer, basketball, field hockey, and lacrosse, are particularly useful in this context, but many patients with ASD are not able to easily engage in typical team sports.

For such children, a prescribed amount of time spent walking, as well as weight and resistance training, could be helpful. The latter would also help increase muscle mass, a key modulator of bone health.

Other strategies include ensuring sufficient intake of calcium and vitamin D through diet and supplements. This can be a particular challenge for children with ASD on specialized diets, such as a gluten-free or dairy-free diet, which are deficient in calcium and vitamin D. Health care providers should check for intake of dairy and dairy products, as well as serum vitamin D levels, and prescribe supplements as needed.

All children should get at least 600 IUs of vitamin D and 1,000-1,300 mg of elemental calcium daily. That said, many with ASD need much higher quantities of vitamin D (1,000-4,000 IUs or more) to maintain levels in the normal range. This is particularly true for dark-skinned children and children with obesity, as well as those who have medical disorders that cause malabsorption.

Higher cortisol levels in the ASD patient population are harder to manage. Efforts to ease anxiety and depression may help reduce cortisol levels. Medications such as protein pump inhibitors and glucocorticosteroids can compromise bone health.

In addition, certain antipsychotics can cause marked elevations in prolactin which, in turn, can lower levels of estrogen and testosterone, which are very important for bone health. In such cases, the clinician should consider switching patients to a different, less detrimental medication or adjust the current medication so that patients receive the lowest possible effective dose.

Obesity is associated with increased fracture risk and with suboptimal bone accrual during childhood, so ensuring a healthy diet is important. This includes avoiding sugary beverages and reducing intake of processed food and juice.

Sometimes, particularly when a child has low bone density and a history of several low-trauma fractures, medications such as bisphosphonates should be considered to increase bone density.

Above all, as physicians who manage ASD, it is essential that we raise awareness about bone health among our colleagues, patients, and their families to help mitigate fracture risk.

Madhusmita Misra, MD, MPH, is chief of the Division of Pediatric Endocrinology at Mass General for Children, Boston.

A version of this article first appeared on Medscape.com.

Many years ago, at the conclusion of a talk I gave on bone health in teens with anorexia nervosa, I was approached by a colleague, Ann Neumeyer, MD, medical director of the Lurie Center for Autism at Massachusetts General Hospital, Boston, who asked about bone health in children with autism spectrum disorder (ASD).

When I explained that there was little information about bone health in this patient population, she suggested that we learn and investigate together. Ann explained that she had observed that some of her patients with ASD had suffered fractures with minimal trauma, raising her concern about their bone health.

This was the beginning of a partnership that led us down the path of many grant submissions, some of which were funded and others that were not, to explore and investigate bone outcomes in children with ASD.

Over the years it has become very clear that these patients are at high risk for low bone density at multiple sites. This applies to prepubertal children as well as older children and adolescents. One study showed that 28% and 33% of children with ASD 8-14 years old had very low bone density (z scores of ≤ –2) at the spine and hip, respectively, compared with 0% of typically developing controls.

Studies that have used sophisticated imaging techniques to determine bone strength have shown that it is lower at the forearm and lower leg in children with ASD versus neurotypical children.

These findings are of particular concern during the childhood and teenage years when bone is typically accrued at a rapid rate. A normal rate of bone accrual at this time of life is essential for optimal bone health in later life. While children with ASD gain bone mass at a similar rate as neurotypical controls, they start at a deficit and seem unable to “catch up.”

Further, people with ASD are more prone to certain kinds of fracture than those without the condition. For example, both children and adults with ASD have a high risk for hip fracture, while adult women with ASD have a higher risk for forearm and spine fractures. There is some protection against forearm fractures in children and adult men, probably because of markedly lower levels of physical activity, which would reduce fall risk.

Many of Ann’s patients with ASD had unusual or restricted diets, low levels of physical activity, and were on multiple medications. We have since learned that some factors that contribute to low bone density in ASD include lower levels of weight-bearing physical activity; lower muscle mass; low muscle tone; suboptimal dietary calcium and vitamin D intake; lower vitamin D levels; higher levels of the hormone cortisol, which has deleterious effects on bone; and use of medications that can lower bone density.

In order to mitigate the risk for low bone density and fractures, it is important to optimize physical activity while considering the child’s ability to safely engage in weight-bearing sports.

High-impact sports like gymnastics and jumping, or cross-impact sports like soccer, basketball, field hockey, and lacrosse, are particularly useful in this context, but many patients with ASD are not able to easily engage in typical team sports.

For such children, a prescribed amount of time spent walking, as well as weight and resistance training, could be helpful. The latter would also help increase muscle mass, a key modulator of bone health.

Other strategies include ensuring sufficient intake of calcium and vitamin D through diet and supplements. This can be a particular challenge for children with ASD on specialized diets, such as a gluten-free or dairy-free diet, which are deficient in calcium and vitamin D. Health care providers should check for intake of dairy and dairy products, as well as serum vitamin D levels, and prescribe supplements as needed.

All children should get at least 600 IUs of vitamin D and 1,000-1,300 mg of elemental calcium daily. That said, many with ASD need much higher quantities of vitamin D (1,000-4,000 IUs or more) to maintain levels in the normal range. This is particularly true for dark-skinned children and children with obesity, as well as those who have medical disorders that cause malabsorption.

Higher cortisol levels in the ASD patient population are harder to manage. Efforts to ease anxiety and depression may help reduce cortisol levels. Medications such as protein pump inhibitors and glucocorticosteroids can compromise bone health.

In addition, certain antipsychotics can cause marked elevations in prolactin which, in turn, can lower levels of estrogen and testosterone, which are very important for bone health. In such cases, the clinician should consider switching patients to a different, less detrimental medication or adjust the current medication so that patients receive the lowest possible effective dose.

Obesity is associated with increased fracture risk and with suboptimal bone accrual during childhood, so ensuring a healthy diet is important. This includes avoiding sugary beverages and reducing intake of processed food and juice.

Sometimes, particularly when a child has low bone density and a history of several low-trauma fractures, medications such as bisphosphonates should be considered to increase bone density.

Above all, as physicians who manage ASD, it is essential that we raise awareness about bone health among our colleagues, patients, and their families to help mitigate fracture risk.

Madhusmita Misra, MD, MPH, is chief of the Division of Pediatric Endocrinology at Mass General for Children, Boston.

A version of this article first appeared on Medscape.com.

We have long recognized that our environment has a significant impact on our general health. Air pollution is known to contribute to respiratory conditions, poor cardiovascular outcomes, and certain kinds of cancer. Less well-known (or studied) is the potential impact of such fumes on bone health.

It’s increasingly important to identify factors that might contribute to suboptimal bone density and associated fracture risk in the population as a whole, and particularly in older adults. Aging is associated with a higher risk for osteoporosis and fractures, with their attendant morbidity, but individuals differ in their extent of bone loss and risk for fractures.

Known factors affecting bone health include genetics, age, sex, nutrition, physical activity, and hormonal factors. Certain medications, diseases, and lifestyle choices – such as smoking and alcohol intake – can also have deleterious effects on bone.

More recently, researchers have started examining the impact of air pollution on bone health.

As we know, the degree of pollution varies greatly from one region to another and can potentially significantly affect life in many parts of the world. In fact, the World Health Organization indicates that 99% of the world’s population breathes air exceeding the WHO guideline limits for pollutants.

Air pollutants include particulate matter (PM) as well as gases, such as nitric oxide, nitrogen dioxide, ammonia, carbon monoxide, sulfur dioxide, ozone, and certain volatile organic compounds. Particulate pollutants include a variety of substances produced from mostly human activities (such as vehicle emissions, biofuel combustion, mining, agriculture, and manufacturing, and also forest fires). They are classified not by their composition, but by their size (for example, PM1.0, PM2.5, and PM10 indicate PM with a diameter < 1.0, 2.5, and 10 microns, respectively). The finer the particle, the more likely it is to cross into the systemic circulation from the respiratory tract, with the potential to induce oxidative, inflammatory, and other changes in the body.

Many studies report that air pollution is a risk factor for osteoporosis. Some have found associations of lower bone density, osteoporosis, and fracture risk with higher concentrations of PM1.0, PM2.5, or PM10, even after controlling for other factors that could affect bone health. Some researchers have reported that although they didn’t find a significant association between PM and bone health, they did find an association between distance from the freeway and bone health – thus, exposure to polycyclic aromatic hydrocarbons and black carbon from vehicle emissions needs to be studied as a contributor to fracture risk.

Importantly, a prospective, observational study from the Women’s Health Initiative (which included more than 9,000 ethnically diverse women from three sites in the United States) reported a significant negative impact of PM10, nitric oxide, nitrogen dioxide, and sulfur dioxide over 1, 3, and 5 years on bone density at multiple sites, and particularly at the lumbar spine, in both cross-sectional and longitudinal analyses after controlling for demographic and socioeconomic factors. This study reported that nitrogen dioxide exposure may be a key determinant of bone density at the lumbar spine and in the whole body. Similarly, other studies have reported associations between atmospheric nitrogen dioxide or sulfur dioxide and risk for osteoporotic fractures.
 

Why the impact on bones?

The potential negative impact of pollution on bone has been attributed to many factors. PM induces systemic inflammation and an increase in cytokines that stimulate bone cells (osteoclasts) that cause bone loss. Other pollutants (gases and metal compounds) can cause oxidative damage to bone cells, whereas others act as endocrine disrupters and affect the functioning of these cells.

Pollution might also affect the synthesis and metabolism of vitamin D, which is necessary for absorption of calcium from the gut. High rates of pollution can reduce the amount of ultraviolet radiation reaching the earth which is important because certain wavelengths of ultraviolet radiation are necessary for vitamin D synthesis in our skin. Reduced vitamin D synthesis in skin can lead to poorly mineralized bone unless there is sufficient intake of vitamin D in diet or as supplements. Also, the conversion of vitamin D to its active form happens in the kidneys, and PM can be harmful to renal function. PM is also believed to cause increased breakdown of vitamin D into its inactive form.

Conversely, some studies have reported no association between pollution and bone density or osteoporosis risk, and two meta-analyses indicated that the association between the two is inconsistent. Some factors explaining variances in results include the number of individuals included in the study (larger studies are generally considered to be more reproducible), the fact that most studies are cross-sectional and not prospective, many do not control for other factors that might be deleterious to bone, and prediction models for the extent of PM or other exposure may not be completely accurate.

However, another recent meta-analysis reported an increased risk for lower total-body bone density and hip fracture after exposure to air pollution, particularly PM2.5 and nitrogen dioxide, but not to PM10, nitric oxide, or ozone. More studies are needed to confirm, or refute, the association between air pollution and impaired bone health. But accumulating evidence suggests that air pollution very likely has a deleterious effect on bone.

When feasible, it’s important to avoid living or working in areas with poor air quality and high pollution rates. However, this isn’t always possible based on one’s occupation, geography, circumstances, or economic status. Therefore, attention to a cleaner environment is critical at both the individual and the macro level.

As an example of the latter, the city of London extended its ultralow emission zone (ULEZ) farther out of the city in October 2021, and a further expansion is planned to include all of the city’s boroughs in August 2023.

We can do our bit by driving less and walking, biking, or using public transportation more often. We can also turn off the car engine when it’s not running, maintain our vehicles, switch to electric or hand-powered yard equipment, and not burn household garbage and limit backyard fires. We can also switch from gas to solar energy or wind, use efficient appliances and heating, and avoid unnecessary energy use. And we can choose sustainable products when possible.

For optimal bone health, we should remind patients to eat a healthy diet with the requisite amount of protein, calcium, and vitamin D. Vitamin D and calcium supplementation may be necessary for people whose intake of dairy and dairy products is low. Other important strategies to optimize bone health include engaging in healthy physical activity; avoiding smoking or excessive alcohol intake; and treating underlying gastrointestinal, endocrine, or other conditions that can reduce bone density.

Madhusmita Misra, MD, MPH, is the chief of the division of pediatric endocrinology, Mass General for Children; the associate director of the Harvard Catalyst Translation and Clinical Research Center; and the director of the Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital, Boston.

A version of this article first appeared on Medscape.com.

We have long recognized that our environment has a significant impact on our general health. Air pollution is known to contribute to respiratory conditions, poor cardiovascular outcomes, and certain kinds of cancer. Less well-known (or studied) is the potential impact of such fumes on bone health.

It’s increasingly important to identify factors that might contribute to suboptimal bone density and associated fracture risk in the population as a whole, and particularly in older adults. Aging is associated with a higher risk for osteoporosis and fractures, with their attendant morbidity, but individuals differ in their extent of bone loss and risk for fractures.

Known factors affecting bone health include genetics, age, sex, nutrition, physical activity, and hormonal factors. Certain medications, diseases, and lifestyle choices – such as smoking and alcohol intake – can also have deleterious effects on bone.

More recently, researchers have started examining the impact of air pollution on bone health.

As we know, the degree of pollution varies greatly from one region to another and can potentially significantly affect life in many parts of the world. In fact, the World Health Organization indicates that 99% of the world’s population breathes air exceeding the WHO guideline limits for pollutants.

Air pollutants include particulate matter (PM) as well as gases, such as nitric oxide, nitrogen dioxide, ammonia, carbon monoxide, sulfur dioxide, ozone, and certain volatile organic compounds. Particulate pollutants include a variety of substances produced from mostly human activities (such as vehicle emissions, biofuel combustion, mining, agriculture, and manufacturing, and also forest fires). They are classified not by their composition, but by their size (for example, PM1.0, PM2.5, and PM10 indicate PM with a diameter < 1.0, 2.5, and 10 microns, respectively). The finer the particle, the more likely it is to cross into the systemic circulation from the respiratory tract, with the potential to induce oxidative, inflammatory, and other changes in the body.

Many studies report that air pollution is a risk factor for osteoporosis. Some have found associations of lower bone density, osteoporosis, and fracture risk with higher concentrations of PM1.0, PM2.5, or PM10, even after controlling for other factors that could affect bone health. Some researchers have reported that although they didn’t find a significant association between PM and bone health, they did find an association between distance from the freeway and bone health – thus, exposure to polycyclic aromatic hydrocarbons and black carbon from vehicle emissions needs to be studied as a contributor to fracture risk.

Importantly, a prospective, observational study from the Women’s Health Initiative (which included more than 9,000 ethnically diverse women from three sites in the United States) reported a significant negative impact of PM10, nitric oxide, nitrogen dioxide, and sulfur dioxide over 1, 3, and 5 years on bone density at multiple sites, and particularly at the lumbar spine, in both cross-sectional and longitudinal analyses after controlling for demographic and socioeconomic factors. This study reported that nitrogen dioxide exposure may be a key determinant of bone density at the lumbar spine and in the whole body. Similarly, other studies have reported associations between atmospheric nitrogen dioxide or sulfur dioxide and risk for osteoporotic fractures.
 

Why the impact on bones?

The potential negative impact of pollution on bone has been attributed to many factors. PM induces systemic inflammation and an increase in cytokines that stimulate bone cells (osteoclasts) that cause bone loss. Other pollutants (gases and metal compounds) can cause oxidative damage to bone cells, whereas others act as endocrine disrupters and affect the functioning of these cells.

Pollution might also affect the synthesis and metabolism of vitamin D, which is necessary for absorption of calcium from the gut. High rates of pollution can reduce the amount of ultraviolet radiation reaching the earth which is important because certain wavelengths of ultraviolet radiation are necessary for vitamin D synthesis in our skin. Reduced vitamin D synthesis in skin can lead to poorly mineralized bone unless there is sufficient intake of vitamin D in diet or as supplements. Also, the conversion of vitamin D to its active form happens in the kidneys, and PM can be harmful to renal function. PM is also believed to cause increased breakdown of vitamin D into its inactive form.

Conversely, some studies have reported no association between pollution and bone density or osteoporosis risk, and two meta-analyses indicated that the association between the two is inconsistent. Some factors explaining variances in results include the number of individuals included in the study (larger studies are generally considered to be more reproducible), the fact that most studies are cross-sectional and not prospective, many do not control for other factors that might be deleterious to bone, and prediction models for the extent of PM or other exposure may not be completely accurate.

However, another recent meta-analysis reported an increased risk for lower total-body bone density and hip fracture after exposure to air pollution, particularly PM2.5 and nitrogen dioxide, but not to PM10, nitric oxide, or ozone. More studies are needed to confirm, or refute, the association between air pollution and impaired bone health. But accumulating evidence suggests that air pollution very likely has a deleterious effect on bone.

When feasible, it’s important to avoid living or working in areas with poor air quality and high pollution rates. However, this isn’t always possible based on one’s occupation, geography, circumstances, or economic status. Therefore, attention to a cleaner environment is critical at both the individual and the macro level.

As an example of the latter, the city of London extended its ultralow emission zone (ULEZ) farther out of the city in October 2021, and a further expansion is planned to include all of the city’s boroughs in August 2023.

We can do our bit by driving less and walking, biking, or using public transportation more often. We can also turn off the car engine when it’s not running, maintain our vehicles, switch to electric or hand-powered yard equipment, and not burn household garbage and limit backyard fires. We can also switch from gas to solar energy or wind, use efficient appliances and heating, and avoid unnecessary energy use. And we can choose sustainable products when possible.

For optimal bone health, we should remind patients to eat a healthy diet with the requisite amount of protein, calcium, and vitamin D. Vitamin D and calcium supplementation may be necessary for people whose intake of dairy and dairy products is low. Other important strategies to optimize bone health include engaging in healthy physical activity; avoiding smoking or excessive alcohol intake; and treating underlying gastrointestinal, endocrine, or other conditions that can reduce bone density.

Madhusmita Misra, MD, MPH, is the chief of the division of pediatric endocrinology, Mass General for Children; the associate director of the Harvard Catalyst Translation and Clinical Research Center; and the director of the Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital, Boston.

A version of this article first appeared on Medscape.com.

We have long recognized that our environment has a significant impact on our general health. Air pollution is known to contribute to respiratory conditions, poor cardiovascular outcomes, and certain kinds of cancer. Less well-known (or studied) is the potential impact of such fumes on bone health.

It’s increasingly important to identify factors that might contribute to suboptimal bone density and associated fracture risk in the population as a whole, and particularly in older adults. Aging is associated with a higher risk for osteoporosis and fractures, with their attendant morbidity, but individuals differ in their extent of bone loss and risk for fractures.

Known factors affecting bone health include genetics, age, sex, nutrition, physical activity, and hormonal factors. Certain medications, diseases, and lifestyle choices – such as smoking and alcohol intake – can also have deleterious effects on bone.

More recently, researchers have started examining the impact of air pollution on bone health.

As we know, the degree of pollution varies greatly from one region to another and can potentially significantly affect life in many parts of the world. In fact, the World Health Organization indicates that 99% of the world’s population breathes air exceeding the WHO guideline limits for pollutants.

Air pollutants include particulate matter (PM) as well as gases, such as nitric oxide, nitrogen dioxide, ammonia, carbon monoxide, sulfur dioxide, ozone, and certain volatile organic compounds. Particulate pollutants include a variety of substances produced from mostly human activities (such as vehicle emissions, biofuel combustion, mining, agriculture, and manufacturing, and also forest fires). They are classified not by their composition, but by their size (for example, PM1.0, PM2.5, and PM10 indicate PM with a diameter < 1.0, 2.5, and 10 microns, respectively). The finer the particle, the more likely it is to cross into the systemic circulation from the respiratory tract, with the potential to induce oxidative, inflammatory, and other changes in the body.

Many studies report that air pollution is a risk factor for osteoporosis. Some have found associations of lower bone density, osteoporosis, and fracture risk with higher concentrations of PM1.0, PM2.5, or PM10, even after controlling for other factors that could affect bone health. Some researchers have reported that although they didn’t find a significant association between PM and bone health, they did find an association between distance from the freeway and bone health – thus, exposure to polycyclic aromatic hydrocarbons and black carbon from vehicle emissions needs to be studied as a contributor to fracture risk.

Importantly, a prospective, observational study from the Women’s Health Initiative (which included more than 9,000 ethnically diverse women from three sites in the United States) reported a significant negative impact of PM10, nitric oxide, nitrogen dioxide, and sulfur dioxide over 1, 3, and 5 years on bone density at multiple sites, and particularly at the lumbar spine, in both cross-sectional and longitudinal analyses after controlling for demographic and socioeconomic factors. This study reported that nitrogen dioxide exposure may be a key determinant of bone density at the lumbar spine and in the whole body. Similarly, other studies have reported associations between atmospheric nitrogen dioxide or sulfur dioxide and risk for osteoporotic fractures.
 

Why the impact on bones?

The potential negative impact of pollution on bone has been attributed to many factors. PM induces systemic inflammation and an increase in cytokines that stimulate bone cells (osteoclasts) that cause bone loss. Other pollutants (gases and metal compounds) can cause oxidative damage to bone cells, whereas others act as endocrine disrupters and affect the functioning of these cells.

Pollution might also affect the synthesis and metabolism of vitamin D, which is necessary for absorption of calcium from the gut. High rates of pollution can reduce the amount of ultraviolet radiation reaching the earth which is important because certain wavelengths of ultraviolet radiation are necessary for vitamin D synthesis in our skin. Reduced vitamin D synthesis in skin can lead to poorly mineralized bone unless there is sufficient intake of vitamin D in diet or as supplements. Also, the conversion of vitamin D to its active form happens in the kidneys, and PM can be harmful to renal function. PM is also believed to cause increased breakdown of vitamin D into its inactive form.

Conversely, some studies have reported no association between pollution and bone density or osteoporosis risk, and two meta-analyses indicated that the association between the two is inconsistent. Some factors explaining variances in results include the number of individuals included in the study (larger studies are generally considered to be more reproducible), the fact that most studies are cross-sectional and not prospective, many do not control for other factors that might be deleterious to bone, and prediction models for the extent of PM or other exposure may not be completely accurate.

However, another recent meta-analysis reported an increased risk for lower total-body bone density and hip fracture after exposure to air pollution, particularly PM2.5 and nitrogen dioxide, but not to PM10, nitric oxide, or ozone. More studies are needed to confirm, or refute, the association between air pollution and impaired bone health. But accumulating evidence suggests that air pollution very likely has a deleterious effect on bone.

When feasible, it’s important to avoid living or working in areas with poor air quality and high pollution rates. However, this isn’t always possible based on one’s occupation, geography, circumstances, or economic status. Therefore, attention to a cleaner environment is critical at both the individual and the macro level.

As an example of the latter, the city of London extended its ultralow emission zone (ULEZ) farther out of the city in October 2021, and a further expansion is planned to include all of the city’s boroughs in August 2023.

We can do our bit by driving less and walking, biking, or using public transportation more often. We can also turn off the car engine when it’s not running, maintain our vehicles, switch to electric or hand-powered yard equipment, and not burn household garbage and limit backyard fires. We can also switch from gas to solar energy or wind, use efficient appliances and heating, and avoid unnecessary energy use. And we can choose sustainable products when possible.

For optimal bone health, we should remind patients to eat a healthy diet with the requisite amount of protein, calcium, and vitamin D. Vitamin D and calcium supplementation may be necessary for people whose intake of dairy and dairy products is low. Other important strategies to optimize bone health include engaging in healthy physical activity; avoiding smoking or excessive alcohol intake; and treating underlying gastrointestinal, endocrine, or other conditions that can reduce bone density.

Madhusmita Misra, MD, MPH, is the chief of the division of pediatric endocrinology, Mass General for Children; the associate director of the Harvard Catalyst Translation and Clinical Research Center; and the director of the Pediatric Endocrine-Sports Endocrine-Neuroendocrine Lab, Mass General Hospital, Boston.

A version of this article first appeared on Medscape.com.

I am often asked about the impact of dietary nutrients on bone health, particularly as many patients with low bone density, many with a history of multiple fractures, are referred to me. Many factors affect bone density, an important predictor of fracture risk, including genetics, body weight and muscle mass, bone loading exercise, menstrual status, other hormonal factors, nutritional status, optimal absorption of dietary nutrients, and medication use.

Dietary nutrients include macronutrients (carbohydrates, proteins, fat, and fiber) and micronutrients (such as dietary minerals and vitamins). The importance of micronutrients such as calcium, phosphorus, magnesium, and vitamins C, D, and K in optimizing bone mineralization and bone formation has been well documented.

The impact of protein intake on bone health is slightly more controversial, with some studies suggesting that increased protein intake may be deleterious to bone by increasing acid load, which in turn, increases calcium loss in urine. Overall data analysis from multiple studies support the finding that a higher protein intake is modestly beneficial for bone at certain sites, such as the spine.

Though data regarding the impact of dietary carbohydrates on bone are not as robust, it’s important to understand these effects given the increasing knowledge of the deleterious impact of processed carbohydrates on weight and cardiometabolic outcomes. This leads to the growing recommendations to limit carbohydrates in diet.
 

Quality and quantity of carbs affect bone health

Available studies suggest that both the quality and quantity of carbohydrates that are in a diet as well as the glycemic index of food may affect bone outcomes. Glycemic index refers to the extent of blood glucose elevation that occurs after the intake of any specific food. Foods with a higher glycemic index cause a rapid increase in blood glucose, whereas those with a low glycemic index result in a slower and more gradual increase. Examples of high–glycemic index food include processed and baked foods (such as breakfast cereals [unless whole grain], pretzels, cookies, doughnuts, pastries, cake, white bread, bagels, croissants, and corn chips), sugar-sweetened beverages, white rice, fast food (such as pizza and burgers), and potatoes. Examples of low glycemic index foods include vegetables, fruits, legumes, dairy and dairy products (without added sugar), whole-grain foods (such as oat porridge), and nuts.

A high–glycemic index diet has been associated with a greater risk for obesity and cardiovascular disease, and with lower bone density, an increased risk for fracture. This has been attributed to acute increases in glucose and insulin levels after consumption of high–glycemic index food, which causes increased oxidative stress and secretion of inflammatory cytokines, such as interleukin 6 and tumor necrosis factor alpha, that activate cells in bone that increase bone loss.

Higher blood glucose concentrations induced by a higher dietary glycemic index can have deleterious effects on osteoblasts, the cells important for bone formation, and increase bone loss through production of advanced glycation end products that affect the cross linking of collagen in bone (important for bone strength), as well as calcium loss in urine. This was recently reported in a study by Garcia-Gavilan and others, in which the authors showed that high dietary glycemic index and dietary glucose load are associated with a higher risk for osteoporosis-related fractures in an older Mediterranean population who are at high risk for cardiovascular events. Similar data were reported by Nouri and coauthors in a study from Iran.

The quantity and quality of dietary carbohydrates may also have an impact on bone. The quality of carbohydrates has been assessed using the carbohydrate quality index (CQI) and the low carbohydrate diet score (LCDS). The CQI takes into account dietary fiber intake, glycemic index, intake of processed vs. whole grain, and solid vs. total carbohydrates in diet. A higher CQI diet is associated with reduced cardiovascular risk. Higher LCDS reflects lower carbohydrate and higher fat and protein intake.

Diets that are rich in refined or processed carbohydrates with added sugar are proinflammatory and increase oxidative stress, which may lead to increased bone loss, low bone density, and increased fracture risk. These foods also have a high glycemic index.

In contrast, diets that are rich in whole grains, legumes, fruits, vegetables, nuts, and olive oil have a lower glycemic index and are beneficial to bone. These diets have a higher CQI and LCDS (as reported by Nouri and coauthors) and provide a rich source of antioxidants, vitamins, minerals, and other nutrients (such as calcium, magnesium, and vitamins B, C, and K), which are all beneficial to bone. Gao and others have reported that implementing a low glycemic index pulse-based diet (lentils, peas, beans) is superior to a regular hospital diet in preventing the increase in bone loss that typically occurs during hospitalization with enforced bed rest.

Most reports of the impact of carbohydrates on bone health are from observational studies. In an interventional study, Dalskov and coauthors randomly assigned children aged 5-18 years who had parents with overweight to one of five diets (high protein/low glycemic index, high protein/high glycemic index, low protein/low glycemic index, low protein/high glycemic index, or regular) for 6 months.

Contrasting with our understanding that protein intake is overall good for bone, this study found that among patients receiving a high–glycemic index diet, those who were on a high-protein diet had greater reductions in a bone formation marker than did those on a low-protein diet, with no major changes observed with the other diets. This suggests the influence of associated dietary nutrients on bone outcomes and that protein intake may modify the effects of dietary carbohydrates on bone formation. Similarly, the fat content of food can alter the glycemic index and thus may modify the impact of dietary carbohydrates on bone.

In summary, available data suggest that the quantity and quality of carbohydrates, including the glycemic index of food, may affect bone health and that it is important to exercise moderation in the consumption of such foods. However, there are only a few studies that have examined these associations, and more studies are necessary to further clarify the impact of dietary carbohydrates on bone as well as any modifications of these effects by other associated food groups. These studies will allow us to refine our recommendations to our patients as we advance our understanding of the impact of the combined effects of various dietary nutrients on bone.

Madhusmita Misra, MD, MPH, is chief of the division of pediatric endocrinology, Mass General for Children, Boston, and serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for AbbVie, Sanofi, and Ipsen.

A version of this article first appeared on Medscape.com.

I am often asked about the impact of dietary nutrients on bone health, particularly as many patients with low bone density, many with a history of multiple fractures, are referred to me. Many factors affect bone density, an important predictor of fracture risk, including genetics, body weight and muscle mass, bone loading exercise, menstrual status, other hormonal factors, nutritional status, optimal absorption of dietary nutrients, and medication use.

Dietary nutrients include macronutrients (carbohydrates, proteins, fat, and fiber) and micronutrients (such as dietary minerals and vitamins). The importance of micronutrients such as calcium, phosphorus, magnesium, and vitamins C, D, and K in optimizing bone mineralization and bone formation has been well documented.

The impact of protein intake on bone health is slightly more controversial, with some studies suggesting that increased protein intake may be deleterious to bone by increasing acid load, which in turn, increases calcium loss in urine. Overall data analysis from multiple studies support the finding that a higher protein intake is modestly beneficial for bone at certain sites, such as the spine.

Though data regarding the impact of dietary carbohydrates on bone are not as robust, it’s important to understand these effects given the increasing knowledge of the deleterious impact of processed carbohydrates on weight and cardiometabolic outcomes. This leads to the growing recommendations to limit carbohydrates in diet.
 

Quality and quantity of carbs affect bone health

Available studies suggest that both the quality and quantity of carbohydrates that are in a diet as well as the glycemic index of food may affect bone outcomes. Glycemic index refers to the extent of blood glucose elevation that occurs after the intake of any specific food. Foods with a higher glycemic index cause a rapid increase in blood glucose, whereas those with a low glycemic index result in a slower and more gradual increase. Examples of high–glycemic index food include processed and baked foods (such as breakfast cereals [unless whole grain], pretzels, cookies, doughnuts, pastries, cake, white bread, bagels, croissants, and corn chips), sugar-sweetened beverages, white rice, fast food (such as pizza and burgers), and potatoes. Examples of low glycemic index foods include vegetables, fruits, legumes, dairy and dairy products (without added sugar), whole-grain foods (such as oat porridge), and nuts.

A high–glycemic index diet has been associated with a greater risk for obesity and cardiovascular disease, and with lower bone density, an increased risk for fracture. This has been attributed to acute increases in glucose and insulin levels after consumption of high–glycemic index food, which causes increased oxidative stress and secretion of inflammatory cytokines, such as interleukin 6 and tumor necrosis factor alpha, that activate cells in bone that increase bone loss.

Higher blood glucose concentrations induced by a higher dietary glycemic index can have deleterious effects on osteoblasts, the cells important for bone formation, and increase bone loss through production of advanced glycation end products that affect the cross linking of collagen in bone (important for bone strength), as well as calcium loss in urine. This was recently reported in a study by Garcia-Gavilan and others, in which the authors showed that high dietary glycemic index and dietary glucose load are associated with a higher risk for osteoporosis-related fractures in an older Mediterranean population who are at high risk for cardiovascular events. Similar data were reported by Nouri and coauthors in a study from Iran.

The quantity and quality of dietary carbohydrates may also have an impact on bone. The quality of carbohydrates has been assessed using the carbohydrate quality index (CQI) and the low carbohydrate diet score (LCDS). The CQI takes into account dietary fiber intake, glycemic index, intake of processed vs. whole grain, and solid vs. total carbohydrates in diet. A higher CQI diet is associated with reduced cardiovascular risk. Higher LCDS reflects lower carbohydrate and higher fat and protein intake.

Diets that are rich in refined or processed carbohydrates with added sugar are proinflammatory and increase oxidative stress, which may lead to increased bone loss, low bone density, and increased fracture risk. These foods also have a high glycemic index.

In contrast, diets that are rich in whole grains, legumes, fruits, vegetables, nuts, and olive oil have a lower glycemic index and are beneficial to bone. These diets have a higher CQI and LCDS (as reported by Nouri and coauthors) and provide a rich source of antioxidants, vitamins, minerals, and other nutrients (such as calcium, magnesium, and vitamins B, C, and K), which are all beneficial to bone. Gao and others have reported that implementing a low glycemic index pulse-based diet (lentils, peas, beans) is superior to a regular hospital diet in preventing the increase in bone loss that typically occurs during hospitalization with enforced bed rest.

Most reports of the impact of carbohydrates on bone health are from observational studies. In an interventional study, Dalskov and coauthors randomly assigned children aged 5-18 years who had parents with overweight to one of five diets (high protein/low glycemic index, high protein/high glycemic index, low protein/low glycemic index, low protein/high glycemic index, or regular) for 6 months.

Contrasting with our understanding that protein intake is overall good for bone, this study found that among patients receiving a high–glycemic index diet, those who were on a high-protein diet had greater reductions in a bone formation marker than did those on a low-protein diet, with no major changes observed with the other diets. This suggests the influence of associated dietary nutrients on bone outcomes and that protein intake may modify the effects of dietary carbohydrates on bone formation. Similarly, the fat content of food can alter the glycemic index and thus may modify the impact of dietary carbohydrates on bone.

In summary, available data suggest that the quantity and quality of carbohydrates, including the glycemic index of food, may affect bone health and that it is important to exercise moderation in the consumption of such foods. However, there are only a few studies that have examined these associations, and more studies are necessary to further clarify the impact of dietary carbohydrates on bone as well as any modifications of these effects by other associated food groups. These studies will allow us to refine our recommendations to our patients as we advance our understanding of the impact of the combined effects of various dietary nutrients on bone.

Madhusmita Misra, MD, MPH, is chief of the division of pediatric endocrinology, Mass General for Children, Boston, and serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for AbbVie, Sanofi, and Ipsen.

A version of this article first appeared on Medscape.com.

I am often asked about the impact of dietary nutrients on bone health, particularly as many patients with low bone density, many with a history of multiple fractures, are referred to me. Many factors affect bone density, an important predictor of fracture risk, including genetics, body weight and muscle mass, bone loading exercise, menstrual status, other hormonal factors, nutritional status, optimal absorption of dietary nutrients, and medication use.

Dietary nutrients include macronutrients (carbohydrates, proteins, fat, and fiber) and micronutrients (such as dietary minerals and vitamins). The importance of micronutrients such as calcium, phosphorus, magnesium, and vitamins C, D, and K in optimizing bone mineralization and bone formation has been well documented.

The impact of protein intake on bone health is slightly more controversial, with some studies suggesting that increased protein intake may be deleterious to bone by increasing acid load, which in turn, increases calcium loss in urine. Overall data analysis from multiple studies support the finding that a higher protein intake is modestly beneficial for bone at certain sites, such as the spine.

Though data regarding the impact of dietary carbohydrates on bone are not as robust, it’s important to understand these effects given the increasing knowledge of the deleterious impact of processed carbohydrates on weight and cardiometabolic outcomes. This leads to the growing recommendations to limit carbohydrates in diet.
 

Quality and quantity of carbs affect bone health

Available studies suggest that both the quality and quantity of carbohydrates that are in a diet as well as the glycemic index of food may affect bone outcomes. Glycemic index refers to the extent of blood glucose elevation that occurs after the intake of any specific food. Foods with a higher glycemic index cause a rapid increase in blood glucose, whereas those with a low glycemic index result in a slower and more gradual increase. Examples of high–glycemic index food include processed and baked foods (such as breakfast cereals [unless whole grain], pretzels, cookies, doughnuts, pastries, cake, white bread, bagels, croissants, and corn chips), sugar-sweetened beverages, white rice, fast food (such as pizza and burgers), and potatoes. Examples of low glycemic index foods include vegetables, fruits, legumes, dairy and dairy products (without added sugar), whole-grain foods (such as oat porridge), and nuts.

A high–glycemic index diet has been associated with a greater risk for obesity and cardiovascular disease, and with lower bone density, an increased risk for fracture. This has been attributed to acute increases in glucose and insulin levels after consumption of high–glycemic index food, which causes increased oxidative stress and secretion of inflammatory cytokines, such as interleukin 6 and tumor necrosis factor alpha, that activate cells in bone that increase bone loss.

Higher blood glucose concentrations induced by a higher dietary glycemic index can have deleterious effects on osteoblasts, the cells important for bone formation, and increase bone loss through production of advanced glycation end products that affect the cross linking of collagen in bone (important for bone strength), as well as calcium loss in urine. This was recently reported in a study by Garcia-Gavilan and others, in which the authors showed that high dietary glycemic index and dietary glucose load are associated with a higher risk for osteoporosis-related fractures in an older Mediterranean population who are at high risk for cardiovascular events. Similar data were reported by Nouri and coauthors in a study from Iran.

The quantity and quality of dietary carbohydrates may also have an impact on bone. The quality of carbohydrates has been assessed using the carbohydrate quality index (CQI) and the low carbohydrate diet score (LCDS). The CQI takes into account dietary fiber intake, glycemic index, intake of processed vs. whole grain, and solid vs. total carbohydrates in diet. A higher CQI diet is associated with reduced cardiovascular risk. Higher LCDS reflects lower carbohydrate and higher fat and protein intake.

Diets that are rich in refined or processed carbohydrates with added sugar are proinflammatory and increase oxidative stress, which may lead to increased bone loss, low bone density, and increased fracture risk. These foods also have a high glycemic index.

In contrast, diets that are rich in whole grains, legumes, fruits, vegetables, nuts, and olive oil have a lower glycemic index and are beneficial to bone. These diets have a higher CQI and LCDS (as reported by Nouri and coauthors) and provide a rich source of antioxidants, vitamins, minerals, and other nutrients (such as calcium, magnesium, and vitamins B, C, and K), which are all beneficial to bone. Gao and others have reported that implementing a low glycemic index pulse-based diet (lentils, peas, beans) is superior to a regular hospital diet in preventing the increase in bone loss that typically occurs during hospitalization with enforced bed rest.

Most reports of the impact of carbohydrates on bone health are from observational studies. In an interventional study, Dalskov and coauthors randomly assigned children aged 5-18 years who had parents with overweight to one of five diets (high protein/low glycemic index, high protein/high glycemic index, low protein/low glycemic index, low protein/high glycemic index, or regular) for 6 months.

Contrasting with our understanding that protein intake is overall good for bone, this study found that among patients receiving a high–glycemic index diet, those who were on a high-protein diet had greater reductions in a bone formation marker than did those on a low-protein diet, with no major changes observed with the other diets. This suggests the influence of associated dietary nutrients on bone outcomes and that protein intake may modify the effects of dietary carbohydrates on bone formation. Similarly, the fat content of food can alter the glycemic index and thus may modify the impact of dietary carbohydrates on bone.

In summary, available data suggest that the quantity and quality of carbohydrates, including the glycemic index of food, may affect bone health and that it is important to exercise moderation in the consumption of such foods. However, there are only a few studies that have examined these associations, and more studies are necessary to further clarify the impact of dietary carbohydrates on bone as well as any modifications of these effects by other associated food groups. These studies will allow us to refine our recommendations to our patients as we advance our understanding of the impact of the combined effects of various dietary nutrients on bone.

Madhusmita Misra, MD, MPH, is chief of the division of pediatric endocrinology, Mass General for Children, Boston, and serves or has served as a director, officer, partner, employee, advisor, consultant, or trustee for AbbVie, Sanofi, and Ipsen.

A version of this article first appeared on Medscape.com.

An 18-year-old woman with Crohn’s disease (diagnosed 3 years ago) came to my office for advice regarding management of osteoporosis. Her bone density was low for her age, and she had three low-impact fractures of her long bones in the preceding 4 years.

Loss of weight after the onset of Crohn’s disease, subsequent loss of periods, inflammation associated with her underlying diagnosis, and early treatment with glucocorticoids (known to have deleterious effects on bone) were believed to have caused osteoporosis in this young woman.

A few months previously, she was switched to a medication that doesn’t impair bone health and glucocorticoids were discontinued; her weight began to improve, and her Crohn’s disease was now in remission. Her menses had resumed about 3 months before her visit to my clinic after a prolonged period without periods. She was on calcium and vitamin D supplements, with normal levels of vitamin D.

After reading that exercise was good for bones, she asked me about it. Were there specific types of exercise that would help optimize her chances of improving her bone health?

Many factors determine bone health including (but not limited to) genetics, nutritional status, exercise activity (with mechanical loading of bones), macro- and micronutrient intake, hormonal status, chronic inflammation and other disease states, and medication use.

Exercise certainly has beneficial effects on bone. Bone-loading activities increase bone formation through the activation of certain cells in bone called osteocytes, which serve as mechanosensors and sense bone loading. Osteocytes make a hormone called sclerostin, which typically inhibits bone formation. When osteocytes sense bone-loading activities, sclerostin secretion reduces, allowing for increased bone formation.

Consistent with this, investigators in Canada have demonstrated greater increases in bone density and strength in schoolchildren who engage in moderate to vigorous physical activity, particularly bone-loading exercise, during the school day, compared with those who don’t (J Bone Miner Res. 2007 Mar;22[3]:434-46; J Bone Miner Res. 2017 Jul;32[7]:1525-36). In females, normal levels of estrogen seem necessary for osteocytes to bring about these effects after bone-loading activities. This is probably one of several reasons why athletes who lose their periods (indicative of low estrogen levels) and develop low bone density with an increased risk for fracture even when they are still at a normal weight (J Clin Endocrinol Metab. 2018 Jun 1;103[6]:2392-402; Med Sci Sports Exerc. 2015 Aug;47[8]:1577-86).

One concern around prescribing bone-loading activity or exercise to persons with osteoporosis is whether it would increase the risk for fracture from the impact on fragile bone. The extent of bone loading safe for fragile bone can be difficult to determine. Furthermore, excessive exercise may worsen bone health by causing weight loss or loss of periods in women. Very careful monitoring may be necessary to ensure that energy balance is maintained. Therefore, the nature and volume of exercise should be discussed with one’s doctor or physical therapist as well as a dietitian (if the patient is seeing one).

In patients with osteoporosis, high-impact activities such as jumping; repetitive impact activities such as running or jogging; and bending and twisting activities such as touching one’s toes, golf, tennis, and bowling aren’t recommended because they increase the risk for fracture. Even yoga poses should be discussed, because some may increase the risk for compression fractures of the vertebrae in the spine.

Strength and resistance training are generally believed to be good for bones. Strength training involves activities that build muscle strength and mass. Resistance training builds muscle strength, mass, and endurance by making muscles work against some form of resistance. Such activities include weight training with free weights or weight machines, use of resistance bands, and use of one’s own body to strengthen major muscle groups (such as through push-ups, squats, lunges, and gluteus maximus extension).

Some amount of weight-bearing aerobic training is also recommended, including walking, low-impact aerobics, the elliptical, and stair-climbing. Non–weight-bearing activities, such as swimming and cycling, typically don’t contribute to improving bone density.

In older individuals with osteoporosis, agility exercises are particularly useful to reduce the fall risk (J Am Geriatr Soc. 2004 May;52[5]:657-65; CMAJ. 2002 Oct 29;167[9]:997-1004). These can be structured to improve hand-eye coordination, foot-eye coordination, static and dynamic balance, and reaction time. Agility exercises with resistance training help improve bone density in older women.

An optimal exercise regimen includes a combination of strength and resistance training; weight-bearing aerobic training; and exercises that build flexibility, stability, and balance. A doctor, physical therapist, or trainer with expertise in the right combination of exercises should be consulted to ensure optimal effects on bone and general health.

In those at risk for overexercising to the point that they start to lose weight or lose their periods, and certainly in all women with disordered eating patterns, a dietitian should be part of the decision team to ensure that energy balance is maintained. In this group, particularly in very-low-weight women with eating disorders, exercise activity is often limited until they reach a healthier weight, and ideally after their menses resume.

For my patient with Crohn’s disease, I recommended that she see a physical therapist and a dietitian for guidance about a graded increase in exercise activity and an exercise regimen that would work best for her. I assess her bone density annually using dual-energy x-ray absorptiometry. Her bone density has gradually improved with the combination of weight gain, resumption of menses, medications for Crohn’s disease that do not affect bone deleteriously, remission of Crohn’s disease, and her exercise regimen.

Dr. Misra is chief of the division of pediatric endocrinology at Mass General Hospital for Children and professor in the department of pediatrics at Harvard Medical School, both in Boston. She reported conflicts of interest with AbbVie, Sanofi, and Ipsen.

A version of this article first appeared on Medscape.com.

An 18-year-old woman with Crohn’s disease (diagnosed 3 years ago) came to my office for advice regarding management of osteoporosis. Her bone density was low for her age, and she had three low-impact fractures of her long bones in the preceding 4 years.

Loss of weight after the onset of Crohn’s disease, subsequent loss of periods, inflammation associated with her underlying diagnosis, and early treatment with glucocorticoids (known to have deleterious effects on bone) were believed to have caused osteoporosis in this young woman.

A few months previously, she was switched to a medication that doesn’t impair bone health and glucocorticoids were discontinued; her weight began to improve, and her Crohn’s disease was now in remission. Her menses had resumed about 3 months before her visit to my clinic after a prolonged period without periods. She was on calcium and vitamin D supplements, with normal levels of vitamin D.

After reading that exercise was good for bones, she asked me about it. Were there specific types of exercise that would help optimize her chances of improving her bone health?

Many factors determine bone health including (but not limited to) genetics, nutritional status, exercise activity (with mechanical loading of bones), macro- and micronutrient intake, hormonal status, chronic inflammation and other disease states, and medication use.

Exercise certainly has beneficial effects on bone. Bone-loading activities increase bone formation through the activation of certain cells in bone called osteocytes, which serve as mechanosensors and sense bone loading. Osteocytes make a hormone called sclerostin, which typically inhibits bone formation. When osteocytes sense bone-loading activities, sclerostin secretion reduces, allowing for increased bone formation.

Consistent with this, investigators in Canada have demonstrated greater increases in bone density and strength in schoolchildren who engage in moderate to vigorous physical activity, particularly bone-loading exercise, during the school day, compared with those who don’t (J Bone Miner Res. 2007 Mar;22[3]:434-46; J Bone Miner Res. 2017 Jul;32[7]:1525-36). In females, normal levels of estrogen seem necessary for osteocytes to bring about these effects after bone-loading activities. This is probably one of several reasons why athletes who lose their periods (indicative of low estrogen levels) and develop low bone density with an increased risk for fracture even when they are still at a normal weight (J Clin Endocrinol Metab. 2018 Jun 1;103[6]:2392-402; Med Sci Sports Exerc. 2015 Aug;47[8]:1577-86).

One concern around prescribing bone-loading activity or exercise to persons with osteoporosis is whether it would increase the risk for fracture from the impact on fragile bone. The extent of bone loading safe for fragile bone can be difficult to determine. Furthermore, excessive exercise may worsen bone health by causing weight loss or loss of periods in women. Very careful monitoring may be necessary to ensure that energy balance is maintained. Therefore, the nature and volume of exercise should be discussed with one’s doctor or physical therapist as well as a dietitian (if the patient is seeing one).

In patients with osteoporosis, high-impact activities such as jumping; repetitive impact activities such as running or jogging; and bending and twisting activities such as touching one’s toes, golf, tennis, and bowling aren’t recommended because they increase the risk for fracture. Even yoga poses should be discussed, because some may increase the risk for compression fractures of the vertebrae in the spine.

Strength and resistance training are generally believed to be good for bones. Strength training involves activities that build muscle strength and mass. Resistance training builds muscle strength, mass, and endurance by making muscles work against some form of resistance. Such activities include weight training with free weights or weight machines, use of resistance bands, and use of one’s own body to strengthen major muscle groups (such as through push-ups, squats, lunges, and gluteus maximus extension).

Some amount of weight-bearing aerobic training is also recommended, including walking, low-impact aerobics, the elliptical, and stair-climbing. Non–weight-bearing activities, such as swimming and cycling, typically don’t contribute to improving bone density.

In older individuals with osteoporosis, agility exercises are particularly useful to reduce the fall risk (J Am Geriatr Soc. 2004 May;52[5]:657-65; CMAJ. 2002 Oct 29;167[9]:997-1004). These can be structured to improve hand-eye coordination, foot-eye coordination, static and dynamic balance, and reaction time. Agility exercises with resistance training help improve bone density in older women.

An optimal exercise regimen includes a combination of strength and resistance training; weight-bearing aerobic training; and exercises that build flexibility, stability, and balance. A doctor, physical therapist, or trainer with expertise in the right combination of exercises should be consulted to ensure optimal effects on bone and general health.

In those at risk for overexercising to the point that they start to lose weight or lose their periods, and certainly in all women with disordered eating patterns, a dietitian should be part of the decision team to ensure that energy balance is maintained. In this group, particularly in very-low-weight women with eating disorders, exercise activity is often limited until they reach a healthier weight, and ideally after their menses resume.

For my patient with Crohn’s disease, I recommended that she see a physical therapist and a dietitian for guidance about a graded increase in exercise activity and an exercise regimen that would work best for her. I assess her bone density annually using dual-energy x-ray absorptiometry. Her bone density has gradually improved with the combination of weight gain, resumption of menses, medications for Crohn’s disease that do not affect bone deleteriously, remission of Crohn’s disease, and her exercise regimen.

Dr. Misra is chief of the division of pediatric endocrinology at Mass General Hospital for Children and professor in the department of pediatrics at Harvard Medical School, both in Boston. She reported conflicts of interest with AbbVie, Sanofi, and Ipsen.

A version of this article first appeared on Medscape.com.

An 18-year-old woman with Crohn’s disease (diagnosed 3 years ago) came to my office for advice regarding management of osteoporosis. Her bone density was low for her age, and she had three low-impact fractures of her long bones in the preceding 4 years.

Loss of weight after the onset of Crohn’s disease, subsequent loss of periods, inflammation associated with her underlying diagnosis, and early treatment with glucocorticoids (known to have deleterious effects on bone) were believed to have caused osteoporosis in this young woman.

A few months previously, she was switched to a medication that doesn’t impair bone health and glucocorticoids were discontinued; her weight began to improve, and her Crohn’s disease was now in remission. Her menses had resumed about 3 months before her visit to my clinic after a prolonged period without periods. She was on calcium and vitamin D supplements, with normal levels of vitamin D.

After reading that exercise was good for bones, she asked me about it. Were there specific types of exercise that would help optimize her chances of improving her bone health?

Many factors determine bone health including (but not limited to) genetics, nutritional status, exercise activity (with mechanical loading of bones), macro- and micronutrient intake, hormonal status, chronic inflammation and other disease states, and medication use.

Exercise certainly has beneficial effects on bone. Bone-loading activities increase bone formation through the activation of certain cells in bone called osteocytes, which serve as mechanosensors and sense bone loading. Osteocytes make a hormone called sclerostin, which typically inhibits bone formation. When osteocytes sense bone-loading activities, sclerostin secretion reduces, allowing for increased bone formation.

Consistent with this, investigators in Canada have demonstrated greater increases in bone density and strength in schoolchildren who engage in moderate to vigorous physical activity, particularly bone-loading exercise, during the school day, compared with those who don’t (J Bone Miner Res. 2007 Mar;22[3]:434-46; J Bone Miner Res. 2017 Jul;32[7]:1525-36). In females, normal levels of estrogen seem necessary for osteocytes to bring about these effects after bone-loading activities. This is probably one of several reasons why athletes who lose their periods (indicative of low estrogen levels) and develop low bone density with an increased risk for fracture even when they are still at a normal weight (J Clin Endocrinol Metab. 2018 Jun 1;103[6]:2392-402; Med Sci Sports Exerc. 2015 Aug;47[8]:1577-86).

One concern around prescribing bone-loading activity or exercise to persons with osteoporosis is whether it would increase the risk for fracture from the impact on fragile bone. The extent of bone loading safe for fragile bone can be difficult to determine. Furthermore, excessive exercise may worsen bone health by causing weight loss or loss of periods in women. Very careful monitoring may be necessary to ensure that energy balance is maintained. Therefore, the nature and volume of exercise should be discussed with one’s doctor or physical therapist as well as a dietitian (if the patient is seeing one).

In patients with osteoporosis, high-impact activities such as jumping; repetitive impact activities such as running or jogging; and bending and twisting activities such as touching one’s toes, golf, tennis, and bowling aren’t recommended because they increase the risk for fracture. Even yoga poses should be discussed, because some may increase the risk for compression fractures of the vertebrae in the spine.

Strength and resistance training are generally believed to be good for bones. Strength training involves activities that build muscle strength and mass. Resistance training builds muscle strength, mass, and endurance by making muscles work against some form of resistance. Such activities include weight training with free weights or weight machines, use of resistance bands, and use of one’s own body to strengthen major muscle groups (such as through push-ups, squats, lunges, and gluteus maximus extension).

Some amount of weight-bearing aerobic training is also recommended, including walking, low-impact aerobics, the elliptical, and stair-climbing. Non–weight-bearing activities, such as swimming and cycling, typically don’t contribute to improving bone density.

In older individuals with osteoporosis, agility exercises are particularly useful to reduce the fall risk (J Am Geriatr Soc. 2004 May;52[5]:657-65; CMAJ. 2002 Oct 29;167[9]:997-1004). These can be structured to improve hand-eye coordination, foot-eye coordination, static and dynamic balance, and reaction time. Agility exercises with resistance training help improve bone density in older women.

An optimal exercise regimen includes a combination of strength and resistance training; weight-bearing aerobic training; and exercises that build flexibility, stability, and balance. A doctor, physical therapist, or trainer with expertise in the right combination of exercises should be consulted to ensure optimal effects on bone and general health.

In those at risk for overexercising to the point that they start to lose weight or lose their periods, and certainly in all women with disordered eating patterns, a dietitian should be part of the decision team to ensure that energy balance is maintained. In this group, particularly in very-low-weight women with eating disorders, exercise activity is often limited until they reach a healthier weight, and ideally after their menses resume.

For my patient with Crohn’s disease, I recommended that she see a physical therapist and a dietitian for guidance about a graded increase in exercise activity and an exercise regimen that would work best for her. I assess her bone density annually using dual-energy x-ray absorptiometry. Her bone density has gradually improved with the combination of weight gain, resumption of menses, medications for Crohn’s disease that do not affect bone deleteriously, remission of Crohn’s disease, and her exercise regimen.

Dr. Misra is chief of the division of pediatric endocrinology at Mass General Hospital for Children and professor in the department of pediatrics at Harvard Medical School, both in Boston. She reported conflicts of interest with AbbVie, Sanofi, and Ipsen.

A version of this article first appeared on Medscape.com.