Beth Auten, MA, MSLIS, AHIP

Evidence summary

Bicarbonate therapy demonstrates benefit in 2 meta-analyses

Two recent meta-analyses evaluated studies of bicarbonate therapy in patients with CKD, and both found benefit.^1,2

A 2020 meta-analysis included 15 RCTs (N = 2445) of adults (mean age, 61 years; range, 40.5-73.9 years) with CKD.¹ Most trials enrolled patients with an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m²; however, 1 study (N = 80) enrolled patients who had an eGFR of 60 to 90 mL/min/1.73 m² and albuminuria, and another (N = 74) enrolled patients with an eGFR of 15 to 89 mL/min/1.73 m². Four studies included patients with normal baseline bicarbonate levels, while the rest enrolled patients with metabolic acidosis. The primary outcome was CKD progression at study conclusion, which ranged from 3 to 60 months (median, 12 months).

Compared to placebo or no therapy, sodium bicarbonate (variously dosed) resulted in a small reduction in the rate of loss of kidney function (defined by eGFR or creatinine clearance) from baseline to trial completion (14 trials, N = 2073; standardized mean difference [SMD] = 0.26; 95% CI, 0.13-0.40; P = .018; I² = 50%).¹Sodium bicarbonate therapy also resulted in a moderate reduction in the risk of end-stage renal disease (7 trials, N = 1526; risk ratio [RR] = 0.53; 95% CI, 0.30-0.89; P = .011; I² = 69%; number needed to treat [NNT] = 14).¹ There was no difference in hospitalizations for heart failure, risk of worsening blood pressure, or all-cause mortality between the sodium bicarbonate and control groups.

Subgroup analysis by follow-up time found a significant preservation of eGFR only in studies with follow-up > 12 months (4 trials, N = 392; weighted mean difference = 3.71 mL/min/1.73 m²; 95% CI, 0.18-7.24; P = .042; I² = 63%).¹ Duration of therapy did not affect initiation of dialysis. Another subgroup analysis found that low- and moderate-quality studies were more likely than high-quality studies to find a change in the primary outcome. Overall, there was significant heterogeneity among the trials (control intervention, follow-up duration, methods of assessment of kidney function, dosage of sodium bicarbonate), as well as underrepresentation of female, pediatric, and elderly patients.

Another meta-analysis, published in 2019 by a different research group, analyzed 7 RCTs (N = 815) that comprised a subset of those in the newer analysis.² The 2019 analysis similarly found that, compared to placebo or usual care, oral bicarbonate therapy resulted in statistically significantly higher eGFRs at 3 to 60 months’ follow-up (mean difference = 3.1 mL/min/1.73 m²; 95% CI, 1.3-4.9).² The authors noted that the protective effect on eGFR was not seen in studies reporting outcomes at 1 year. Progression to end-stage renal disease or initiation of dialysis were not used as outcomes.

Significant outcomes seen in 1 large study

The largest study (N = 740) included in the 2020 meta-analysis (and discussed separately due to its size and duration) was a multicenter, unblinded, pragmatic trial investigating bicarbonate therapy in CKD.³ Patients were adults (mean age, 67.8 years) with CKD stages 3 to 5 and metabolic acidosis (serum bicarbonate level of 18-24 mmol/L); mean serum creatinine was 2.3 mg/dL, and mean serum bicarbonate was 21.5 mmol/L. Patients with severe heart failure or uncontrolled hypertension were excluded.

Compared to placebo or no therapy, sodium bicarbonate (variously dosed) resulted in a small reduction in the rate of loss of kidney function.

Researchers randomized patients to oral sodium bicarbonate (titrated to a target serum concentration of 24-28 mmol/L) or standard care for a median duration of 30 months. The primary endpoint was time to doubling of serum creatinine, and secondary endpoints included all-cause mortality, time to initiation of dialysis, hospitalization rate, and hospital length of stay.

Continue to: Patients treated with...

Patients treated with bicarbonate therapy had a 64% lower risk of doubling their serum creatinine compared to those treated with standard care (hazard ratio [HR] = 0.36; 95% CI, 0.22-0.58; P < .001; NNT = 9.6).³ Bicarbonate therapy also significantly reduced the risk of dialysis (HR = 0.5; 95% CI, 0.31-0.81; P = .005; NNT = 19); all-cause mortality (HR = 0.43; 95% CI, 0.22-0.87; P = .01; NNT = 27); hospitalization rates (34.6% vs 14.2% by end of study in standard care and bicarbonate groups, respectively; P < .001); and hospital length of stay (1160 total d/y vs 400 total d/y; P < .0001).³ Inspection of Kaplan Meier curves shows outcomes beginning to diverge after 1 to 2 years of treatment. This trial was limited by the lack of blinding, placebo control, and standardization of care protocols.

Recommendations from others

The National Kidney Foundation’s 2012 Kidney Disease Outcomes Quality Initiative guidelines for the management of CKD recommend oral bicarbonate therapy for patients with CKD and serum bicarbonate concentrations < 22 mmol/L.⁴ The guidelines state that serum bicarbonate levels < 22 mmol/L correlate with an increased risk of CKD progression and death, whereas high bicarbonate levels (> 32 mmol/L) correlate with increased risk of death independent of level of kidney function. These guidelines cite small studies of alkali therapy slowing progression of CKD, although it was noted that the evidence base was not strong.

Editor’s takeaway

The evidence shows a small but consistent effect of bicarbonate therapy on CKD progression. For patients with CKD stages 3 to 5 and metabolic acidosis (defined by serum bicarbonate levels < 22 mmol/L), the use of supplemental oral sodium bicarbonate, which is inexpensive and safe, can delay or prevent progression of serious disease.

Evidence summary

Bicarbonate therapy demonstrates benefit in 2 meta-analyses

Two recent meta-analyses evaluated studies of bicarbonate therapy in patients with CKD, and both found benefit.^1,2

A 2020 meta-analysis included 15 RCTs (N = 2445) of adults (mean age, 61 years; range, 40.5-73.9 years) with CKD.¹ Most trials enrolled patients with an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m²; however, 1 study (N = 80) enrolled patients who had an eGFR of 60 to 90 mL/min/1.73 m² and albuminuria, and another (N = 74) enrolled patients with an eGFR of 15 to 89 mL/min/1.73 m². Four studies included patients with normal baseline bicarbonate levels, while the rest enrolled patients with metabolic acidosis. The primary outcome was CKD progression at study conclusion, which ranged from 3 to 60 months (median, 12 months).

Compared to placebo or no therapy, sodium bicarbonate (variously dosed) resulted in a small reduction in the rate of loss of kidney function (defined by eGFR or creatinine clearance) from baseline to trial completion (14 trials, N = 2073; standardized mean difference [SMD] = 0.26; 95% CI, 0.13-0.40; P = .018; I² = 50%).¹Sodium bicarbonate therapy also resulted in a moderate reduction in the risk of end-stage renal disease (7 trials, N = 1526; risk ratio [RR] = 0.53; 95% CI, 0.30-0.89; P = .011; I² = 69%; number needed to treat [NNT] = 14).¹ There was no difference in hospitalizations for heart failure, risk of worsening blood pressure, or all-cause mortality between the sodium bicarbonate and control groups.

Subgroup analysis by follow-up time found a significant preservation of eGFR only in studies with follow-up > 12 months (4 trials, N = 392; weighted mean difference = 3.71 mL/min/1.73 m²; 95% CI, 0.18-7.24; P = .042; I² = 63%).¹ Duration of therapy did not affect initiation of dialysis. Another subgroup analysis found that low- and moderate-quality studies were more likely than high-quality studies to find a change in the primary outcome. Overall, there was significant heterogeneity among the trials (control intervention, follow-up duration, methods of assessment of kidney function, dosage of sodium bicarbonate), as well as underrepresentation of female, pediatric, and elderly patients.

Another meta-analysis, published in 2019 by a different research group, analyzed 7 RCTs (N = 815) that comprised a subset of those in the newer analysis.² The 2019 analysis similarly found that, compared to placebo or usual care, oral bicarbonate therapy resulted in statistically significantly higher eGFRs at 3 to 60 months’ follow-up (mean difference = 3.1 mL/min/1.73 m²; 95% CI, 1.3-4.9).² The authors noted that the protective effect on eGFR was not seen in studies reporting outcomes at 1 year. Progression to end-stage renal disease or initiation of dialysis were not used as outcomes.

Significant outcomes seen in 1 large study

The largest study (N = 740) included in the 2020 meta-analysis (and discussed separately due to its size and duration) was a multicenter, unblinded, pragmatic trial investigating bicarbonate therapy in CKD.³ Patients were adults (mean age, 67.8 years) with CKD stages 3 to 5 and metabolic acidosis (serum bicarbonate level of 18-24 mmol/L); mean serum creatinine was 2.3 mg/dL, and mean serum bicarbonate was 21.5 mmol/L. Patients with severe heart failure or uncontrolled hypertension were excluded.

Compared to placebo or no therapy, sodium bicarbonate (variously dosed) resulted in a small reduction in the rate of loss of kidney function.

Researchers randomized patients to oral sodium bicarbonate (titrated to a target serum concentration of 24-28 mmol/L) or standard care for a median duration of 30 months. The primary endpoint was time to doubling of serum creatinine, and secondary endpoints included all-cause mortality, time to initiation of dialysis, hospitalization rate, and hospital length of stay.

Continue to: Patients treated with...

Patients treated with bicarbonate therapy had a 64% lower risk of doubling their serum creatinine compared to those treated with standard care (hazard ratio [HR] = 0.36; 95% CI, 0.22-0.58; P < .001; NNT = 9.6).³ Bicarbonate therapy also significantly reduced the risk of dialysis (HR = 0.5; 95% CI, 0.31-0.81; P = .005; NNT = 19); all-cause mortality (HR = 0.43; 95% CI, 0.22-0.87; P = .01; NNT = 27); hospitalization rates (34.6% vs 14.2% by end of study in standard care and bicarbonate groups, respectively; P < .001); and hospital length of stay (1160 total d/y vs 400 total d/y; P < .0001).³ Inspection of Kaplan Meier curves shows outcomes beginning to diverge after 1 to 2 years of treatment. This trial was limited by the lack of blinding, placebo control, and standardization of care protocols.

Recommendations from others

The National Kidney Foundation’s 2012 Kidney Disease Outcomes Quality Initiative guidelines for the management of CKD recommend oral bicarbonate therapy for patients with CKD and serum bicarbonate concentrations < 22 mmol/L.⁴ The guidelines state that serum bicarbonate levels < 22 mmol/L correlate with an increased risk of CKD progression and death, whereas high bicarbonate levels (> 32 mmol/L) correlate with increased risk of death independent of level of kidney function. These guidelines cite small studies of alkali therapy slowing progression of CKD, although it was noted that the evidence base was not strong.

Editor’s takeaway

The evidence shows a small but consistent effect of bicarbonate therapy on CKD progression. For patients with CKD stages 3 to 5 and metabolic acidosis (defined by serum bicarbonate levels < 22 mmol/L), the use of supplemental oral sodium bicarbonate, which is inexpensive and safe, can delay or prevent progression of serious disease.

Evidence summary

Bicarbonate therapy demonstrates benefit in 2 meta-analyses

Two recent meta-analyses evaluated studies of bicarbonate therapy in patients with CKD, and both found benefit.^1,2

A 2020 meta-analysis included 15 RCTs (N = 2445) of adults (mean age, 61 years; range, 40.5-73.9 years) with CKD.¹ Most trials enrolled patients with an estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m²; however, 1 study (N = 80) enrolled patients who had an eGFR of 60 to 90 mL/min/1.73 m² and albuminuria, and another (N = 74) enrolled patients with an eGFR of 15 to 89 mL/min/1.73 m². Four studies included patients with normal baseline bicarbonate levels, while the rest enrolled patients with metabolic acidosis. The primary outcome was CKD progression at study conclusion, which ranged from 3 to 60 months (median, 12 months).

Compared to placebo or no therapy, sodium bicarbonate (variously dosed) resulted in a small reduction in the rate of loss of kidney function (defined by eGFR or creatinine clearance) from baseline to trial completion (14 trials, N = 2073; standardized mean difference [SMD] = 0.26; 95% CI, 0.13-0.40; P = .018; I² = 50%).¹Sodium bicarbonate therapy also resulted in a moderate reduction in the risk of end-stage renal disease (7 trials, N = 1526; risk ratio [RR] = 0.53; 95% CI, 0.30-0.89; P = .011; I² = 69%; number needed to treat [NNT] = 14).¹ There was no difference in hospitalizations for heart failure, risk of worsening blood pressure, or all-cause mortality between the sodium bicarbonate and control groups.

Subgroup analysis by follow-up time found a significant preservation of eGFR only in studies with follow-up > 12 months (4 trials, N = 392; weighted mean difference = 3.71 mL/min/1.73 m²; 95% CI, 0.18-7.24; P = .042; I² = 63%).¹ Duration of therapy did not affect initiation of dialysis. Another subgroup analysis found that low- and moderate-quality studies were more likely than high-quality studies to find a change in the primary outcome. Overall, there was significant heterogeneity among the trials (control intervention, follow-up duration, methods of assessment of kidney function, dosage of sodium bicarbonate), as well as underrepresentation of female, pediatric, and elderly patients.

Another meta-analysis, published in 2019 by a different research group, analyzed 7 RCTs (N = 815) that comprised a subset of those in the newer analysis.² The 2019 analysis similarly found that, compared to placebo or usual care, oral bicarbonate therapy resulted in statistically significantly higher eGFRs at 3 to 60 months’ follow-up (mean difference = 3.1 mL/min/1.73 m²; 95% CI, 1.3-4.9).² The authors noted that the protective effect on eGFR was not seen in studies reporting outcomes at 1 year. Progression to end-stage renal disease or initiation of dialysis were not used as outcomes.

Significant outcomes seen in 1 large study

The largest study (N = 740) included in the 2020 meta-analysis (and discussed separately due to its size and duration) was a multicenter, unblinded, pragmatic trial investigating bicarbonate therapy in CKD.³ Patients were adults (mean age, 67.8 years) with CKD stages 3 to 5 and metabolic acidosis (serum bicarbonate level of 18-24 mmol/L); mean serum creatinine was 2.3 mg/dL, and mean serum bicarbonate was 21.5 mmol/L. Patients with severe heart failure or uncontrolled hypertension were excluded.

Compared to placebo or no therapy, sodium bicarbonate (variously dosed) resulted in a small reduction in the rate of loss of kidney function.

Researchers randomized patients to oral sodium bicarbonate (titrated to a target serum concentration of 24-28 mmol/L) or standard care for a median duration of 30 months. The primary endpoint was time to doubling of serum creatinine, and secondary endpoints included all-cause mortality, time to initiation of dialysis, hospitalization rate, and hospital length of stay.

Continue to: Patients treated with...

Patients treated with bicarbonate therapy had a 64% lower risk of doubling their serum creatinine compared to those treated with standard care (hazard ratio [HR] = 0.36; 95% CI, 0.22-0.58; P < .001; NNT = 9.6).³ Bicarbonate therapy also significantly reduced the risk of dialysis (HR = 0.5; 95% CI, 0.31-0.81; P = .005; NNT = 19); all-cause mortality (HR = 0.43; 95% CI, 0.22-0.87; P = .01; NNT = 27); hospitalization rates (34.6% vs 14.2% by end of study in standard care and bicarbonate groups, respectively; P < .001); and hospital length of stay (1160 total d/y vs 400 total d/y; P < .0001).³ Inspection of Kaplan Meier curves shows outcomes beginning to diverge after 1 to 2 years of treatment. This trial was limited by the lack of blinding, placebo control, and standardization of care protocols.

Recommendations from others

The National Kidney Foundation’s 2012 Kidney Disease Outcomes Quality Initiative guidelines for the management of CKD recommend oral bicarbonate therapy for patients with CKD and serum bicarbonate concentrations < 22 mmol/L.⁴ The guidelines state that serum bicarbonate levels < 22 mmol/L correlate with an increased risk of CKD progression and death, whereas high bicarbonate levels (> 32 mmol/L) correlate with increased risk of death independent of level of kidney function. These guidelines cite small studies of alkali therapy slowing progression of CKD, although it was noted that the evidence base was not strong.

Editor’s takeaway

The evidence shows a small but consistent effect of bicarbonate therapy on CKD progression. For patients with CKD stages 3 to 5 and metabolic acidosis (defined by serum bicarbonate levels < 22 mmol/L), the use of supplemental oral sodium bicarbonate, which is inexpensive and safe, can delay or prevent progression of serious disease.

Evidence summary

Multiple analyses suggest short sleep increases obesity risk

Three recent, large systematic reviews of prospective cohort studies with meta-analyses in infants, children, and adolescents all found associations between short sleep at intake and later excessive weight.

The largest meta-analysis included 42 prospective studies with 75,499 patients ranging in age from infancy to adolescence and with follow-up ranging from 1 to 27 years. In a pooled analysis, short sleep—variously defined across trials and mostly assessed by parental report—was associated with an increased risk of obesity or overweight (relative risk [RR] = 1.58; 95% CI, 1.35-1.85; I²= 92%), compared to normal and long sleep. When the authors adjusted for suspected publication bias using a “trim and fill” method, short sleep remained associated with later overweight or obesity (RR = 1.42; 95% CI, 1.12-1.81). Short sleep was associated with later unhealthy weight status in all age groups: 0 to < 3 years (RR = 1.4; 95% CI, 1.19-1.65); 3 to < 9 years (RR = 1.57; 95% CI, 1.4-1.76);9 to < 12 years (RR = 2.23; 95% CI, 2.18-2.27); and 12 to 18 years (RR = 1.3; 95% CI, 1.11-1.53). In addition to high heterogeneity, limitations of the review included variability in the definition of short sleep, use of parent- or self-reported sleep duration, and variability in classification of overweight and obesity in primary studies.¹

A second systematic review and meta-analysis included 25 longitudinal studies (20 of which overlapped with the previously discussed meta-analysis) of children and adolescents (N = 56,584). Patients ranged in age from infancy to 16 years, and follow-up ranged from 6 months to 10 years (mean, 3.4 years). Children and adolescents with the shortest sleep duration were more likely to be overweight or obese at follow-up (pooled odds ratio [OR] = 1.76; 95% CI, 1.39-2.23; I² = 70.5%) than those with the longest sleep duration. Due to the overlap in studies, the limitations of this analysis were similar to those already mentioned. Lack of a linear association between sleep duration and weight was cited as evidence of possible publication bias; the authors did not attempt to correct for it.²

Three large systematic reviews all found associations between short sleep at intake and later excessive weight.

The third systematic review and meta-analysis included 22 longitudinal studies (18 overlapped with first meta-analysis and 17 with the second) of children and adolescents (N = 24,821) ages 6 months to 18 years. Follow-up ranged from 1 to 27 years. This meta-analysis standardized the categories of sleep duration using recommendations from the Sleep Health Foundation. Patients with short sleep duration had an increased risk of overweight or obesity compared with patients sleeping “normal” or “longer than normal” durations (pooled OR = 2.15; 95% CI, 1.64-2.81; I² = 67%). The authors indicated that their analysis could have been more robust if information about daytime sleep (ie, napping) had been available, but it was not collected in many of the included studies.³

Accelerometer data quantify the sleep/obesity association

A subsequent cohort study (N = 202) sought to better examine the association between sleep characteristics and adiposity by measuring sleep duration using accelerometers. Toddlers (ages 12 to 26 months) without previous medical history were recruited from early childhood education centers. Patients wore accelerometers for 7 consecutive days and then returned to the clinic after 12 months for collection of biometric information. Researchers measured body morphology with the BMI z-score (ie, the number of standard deviations from the mean). Every additional hour of total sleep time was associated with a 0.12-unit lower BMI z-score (95% CI, –0.23 to –0.01) at 1 year. However, every hour increase in nap duration was associated with a 0.41-unit higher BMI z-score (95% CI, 0.14-0.68).⁴

Recommendations from others

In 2016, the American Academy of Sleep Medicine (AASM) recommended the following sleep durations (per 24 hours): infants ages 4 to 12 months, 12-16 hours; children 1 to 2 years, 11-14 hours; children 3 to 5 years, 10-13 hours; children 6 to 12 years, 9-12 hours; and teenagers 13 to 18 years, 8-10 hours. The AASM further stated that sleeping the recommended number of hours was associated with better health outcomes, and that sleeping too few hours increased the risk of various health conditions, including obesity.⁵ In 2015, the American Academy of Pediatrics Committee on Nutrition acknowledged the association between obesity and short sleep duration and recommended that health care professionals counsel parents about age-appropriate sleep guidelines.⁶

Editor’s takeaway

Studies demonstrate that short sleep duration in pediatric patients is associated with later weight gain. However, associations do not prove a causal link, and other factors may contribute to both weight gain and poor sleep.

Evidence summary

Multiple analyses suggest short sleep increases obesity risk

Three recent, large systematic reviews of prospective cohort studies with meta-analyses in infants, children, and adolescents all found associations between short sleep at intake and later excessive weight.

The largest meta-analysis included 42 prospective studies with 75,499 patients ranging in age from infancy to adolescence and with follow-up ranging from 1 to 27 years. In a pooled analysis, short sleep—variously defined across trials and mostly assessed by parental report—was associated with an increased risk of obesity or overweight (relative risk [RR] = 1.58; 95% CI, 1.35-1.85; I²= 92%), compared to normal and long sleep. When the authors adjusted for suspected publication bias using a “trim and fill” method, short sleep remained associated with later overweight or obesity (RR = 1.42; 95% CI, 1.12-1.81). Short sleep was associated with later unhealthy weight status in all age groups: 0 to < 3 years (RR = 1.4; 95% CI, 1.19-1.65); 3 to < 9 years (RR = 1.57; 95% CI, 1.4-1.76);9 to < 12 years (RR = 2.23; 95% CI, 2.18-2.27); and 12 to 18 years (RR = 1.3; 95% CI, 1.11-1.53). In addition to high heterogeneity, limitations of the review included variability in the definition of short sleep, use of parent- or self-reported sleep duration, and variability in classification of overweight and obesity in primary studies.¹

A second systematic review and meta-analysis included 25 longitudinal studies (20 of which overlapped with the previously discussed meta-analysis) of children and adolescents (N = 56,584). Patients ranged in age from infancy to 16 years, and follow-up ranged from 6 months to 10 years (mean, 3.4 years). Children and adolescents with the shortest sleep duration were more likely to be overweight or obese at follow-up (pooled odds ratio [OR] = 1.76; 95% CI, 1.39-2.23; I² = 70.5%) than those with the longest sleep duration. Due to the overlap in studies, the limitations of this analysis were similar to those already mentioned. Lack of a linear association between sleep duration and weight was cited as evidence of possible publication bias; the authors did not attempt to correct for it.²

Three large systematic reviews all found associations between short sleep at intake and later excessive weight.

The third systematic review and meta-analysis included 22 longitudinal studies (18 overlapped with first meta-analysis and 17 with the second) of children and adolescents (N = 24,821) ages 6 months to 18 years. Follow-up ranged from 1 to 27 years. This meta-analysis standardized the categories of sleep duration using recommendations from the Sleep Health Foundation. Patients with short sleep duration had an increased risk of overweight or obesity compared with patients sleeping “normal” or “longer than normal” durations (pooled OR = 2.15; 95% CI, 1.64-2.81; I² = 67%). The authors indicated that their analysis could have been more robust if information about daytime sleep (ie, napping) had been available, but it was not collected in many of the included studies.³

Accelerometer data quantify the sleep/obesity association

A subsequent cohort study (N = 202) sought to better examine the association between sleep characteristics and adiposity by measuring sleep duration using accelerometers. Toddlers (ages 12 to 26 months) without previous medical history were recruited from early childhood education centers. Patients wore accelerometers for 7 consecutive days and then returned to the clinic after 12 months for collection of biometric information. Researchers measured body morphology with the BMI z-score (ie, the number of standard deviations from the mean). Every additional hour of total sleep time was associated with a 0.12-unit lower BMI z-score (95% CI, –0.23 to –0.01) at 1 year. However, every hour increase in nap duration was associated with a 0.41-unit higher BMI z-score (95% CI, 0.14-0.68).⁴

Recommendations from others

In 2016, the American Academy of Sleep Medicine (AASM) recommended the following sleep durations (per 24 hours): infants ages 4 to 12 months, 12-16 hours; children 1 to 2 years, 11-14 hours; children 3 to 5 years, 10-13 hours; children 6 to 12 years, 9-12 hours; and teenagers 13 to 18 years, 8-10 hours. The AASM further stated that sleeping the recommended number of hours was associated with better health outcomes, and that sleeping too few hours increased the risk of various health conditions, including obesity.⁵ In 2015, the American Academy of Pediatrics Committee on Nutrition acknowledged the association between obesity and short sleep duration and recommended that health care professionals counsel parents about age-appropriate sleep guidelines.⁶

Editor’s takeaway

Studies demonstrate that short sleep duration in pediatric patients is associated with later weight gain. However, associations do not prove a causal link, and other factors may contribute to both weight gain and poor sleep.

Evidence summary

Multiple analyses suggest short sleep increases obesity risk

Three recent, large systematic reviews of prospective cohort studies with meta-analyses in infants, children, and adolescents all found associations between short sleep at intake and later excessive weight.

The largest meta-analysis included 42 prospective studies with 75,499 patients ranging in age from infancy to adolescence and with follow-up ranging from 1 to 27 years. In a pooled analysis, short sleep—variously defined across trials and mostly assessed by parental report—was associated with an increased risk of obesity or overweight (relative risk [RR] = 1.58; 95% CI, 1.35-1.85; I²= 92%), compared to normal and long sleep. When the authors adjusted for suspected publication bias using a “trim and fill” method, short sleep remained associated with later overweight or obesity (RR = 1.42; 95% CI, 1.12-1.81). Short sleep was associated with later unhealthy weight status in all age groups: 0 to < 3 years (RR = 1.4; 95% CI, 1.19-1.65); 3 to < 9 years (RR = 1.57; 95% CI, 1.4-1.76);9 to < 12 years (RR = 2.23; 95% CI, 2.18-2.27); and 12 to 18 years (RR = 1.3; 95% CI, 1.11-1.53). In addition to high heterogeneity, limitations of the review included variability in the definition of short sleep, use of parent- or self-reported sleep duration, and variability in classification of overweight and obesity in primary studies.¹

A second systematic review and meta-analysis included 25 longitudinal studies (20 of which overlapped with the previously discussed meta-analysis) of children and adolescents (N = 56,584). Patients ranged in age from infancy to 16 years, and follow-up ranged from 6 months to 10 years (mean, 3.4 years). Children and adolescents with the shortest sleep duration were more likely to be overweight or obese at follow-up (pooled odds ratio [OR] = 1.76; 95% CI, 1.39-2.23; I² = 70.5%) than those with the longest sleep duration. Due to the overlap in studies, the limitations of this analysis were similar to those already mentioned. Lack of a linear association between sleep duration and weight was cited as evidence of possible publication bias; the authors did not attempt to correct for it.²

Three large systematic reviews all found associations between short sleep at intake and later excessive weight.

The third systematic review and meta-analysis included 22 longitudinal studies (18 overlapped with first meta-analysis and 17 with the second) of children and adolescents (N = 24,821) ages 6 months to 18 years. Follow-up ranged from 1 to 27 years. This meta-analysis standardized the categories of sleep duration using recommendations from the Sleep Health Foundation. Patients with short sleep duration had an increased risk of overweight or obesity compared with patients sleeping “normal” or “longer than normal” durations (pooled OR = 2.15; 95% CI, 1.64-2.81; I² = 67%). The authors indicated that their analysis could have been more robust if information about daytime sleep (ie, napping) had been available, but it was not collected in many of the included studies.³

Accelerometer data quantify the sleep/obesity association

A subsequent cohort study (N = 202) sought to better examine the association between sleep characteristics and adiposity by measuring sleep duration using accelerometers. Toddlers (ages 12 to 26 months) without previous medical history were recruited from early childhood education centers. Patients wore accelerometers for 7 consecutive days and then returned to the clinic after 12 months for collection of biometric information. Researchers measured body morphology with the BMI z-score (ie, the number of standard deviations from the mean). Every additional hour of total sleep time was associated with a 0.12-unit lower BMI z-score (95% CI, –0.23 to –0.01) at 1 year. However, every hour increase in nap duration was associated with a 0.41-unit higher BMI z-score (95% CI, 0.14-0.68).⁴

Recommendations from others

In 2016, the American Academy of Sleep Medicine (AASM) recommended the following sleep durations (per 24 hours): infants ages 4 to 12 months, 12-16 hours; children 1 to 2 years, 11-14 hours; children 3 to 5 years, 10-13 hours; children 6 to 12 years, 9-12 hours; and teenagers 13 to 18 years, 8-10 hours. The AASM further stated that sleeping the recommended number of hours was associated with better health outcomes, and that sleeping too few hours increased the risk of various health conditions, including obesity.⁵ In 2015, the American Academy of Pediatrics Committee on Nutrition acknowledged the association between obesity and short sleep duration and recommended that health care professionals counsel parents about age-appropriate sleep guidelines.⁶

Editor’s takeaway

Studies demonstrate that short sleep duration in pediatric patients is associated with later weight gain. However, associations do not prove a causal link, and other factors may contribute to both weight gain and poor sleep.