Jon Neher, MD

EVIDENCE SUMMARY

A 2012 systematic review of 21 RCTs examined the effect of group-based diabetes education on HbA1c in 2833 adults with T2DM.¹ Intervention groups participated in at least 1 group session lasting an hour led by a health professional or team (eg, physician, nurse, diabetes educator); controls received usual care. Most trials involved 6 to 20 hours of group-based education delivered over 1 to 10 months, although some trials continued the intervention for as long as 24 months. The mean HbA1c at baseline across all patients was 8.23%.

Professional-led group visitsimprove HbA1c

Group education resulted in a significant reduction in HbA1c compared with controls at 6 months (13 trials; 1883 patients; mean difference [MD]=−0.44%; 95% confidence interval [CI], −0.69 to −0.19), 12 months (11 studies; 1503 patients; MD=−0.46%; 95% CI, −0.74 to −0.18), and 24 months (3 studies; 397 patients; MD=−0.87%; 95% CI, −1.25 to −0.49). The trials had high heterogeneity, except for the 3 trials with a 24-month end-point (I² = 0). Most studies had a moderate or high risk of bias.

A larger 2017 meta-analysis enrolling 8533 adults with T2DM came to similar conclusions, although it included a small number of nonrandomized trials (40 RCTs, 3 cluster RCTs, and 4 controlled clinical trials).² Thirteen of the RCTs overlapped with the previously described systematic review.¹ Interventions had to include at least 1 group session with 4 or more adult patients lasting at least 1 hour. In most studies, interventions continued between 4 and 12 months, although some ran 60 months. Controls received usual care. The mean HbA1c at baseline across all patients was 8.3%.

Group-based education compared with controls reduced HbA1c at 6 to 10 months (30 trials, N not given; MD=−0.3%; 95% CI, −0.48 to −0.15), 12 to 14 months (27 trials, N not given; MD=−0.3%; 95% CI, −0.49 to −0.17), and 36 to 48 months (5 trials, N not given; MD=−0.9%; 95% CI, −1.52 to −0.34). In a subgroup analysis, peer-led group visits had no effect (5 trials, 1066 patients; MD=−0.02%; 95% CI, −0.12 to 0.16).

Patients on oral agents alone showed a larger benefit than patients using insulin (38 trials, 5871 patients; −0.81 vs −0.19; P < .0001). Authors of the meta-analysis classified most studies as having a moderate to high risk of bias, with only 4 having low risk.

Duration of intervention: Longer is better for HbA1c values

Another systematic review analyzed 13 RCTs with 4652 patients 16 years and older with T2DM or type 1 diabetes to assess the effect of group visits on HbA1c.³ The review excluded studies that didn’t include a health care provider who could prescribe, diagnose, assess, and refer patients when appropriate.

Group visits led by health professionals or teams improve glycosylated hemoglobin by 0.3% to 0.9% over usual care in patients with type 2 diabetes.

Most interventions ran 3 to 12 months, although one lasted 36 months. (Two RCTs overlapped with the 2012 review, and 2 others with the 2017 review.) Group medical visits resulted in a significant decrease in HbA1c at the end of the intervention period (MD=−0.46%; 95% CI, −0.80 to −0.13) compared with controls. A meta-regression analysis suggested that ongoing treatment (for as long as 3 years) decreased HbA1c more than a shorter treatment duration (by 0.25% per year of treatment), whereas the frequency of treatments didn’t alter the effect. Overall, the trials were heterogenous and most had a high risk of bias.

Continue to: RECOMMENDATIONS

The 2015 National Institute for Health and Care Excellence guideline for the management of T2DM in adults calls group education ­programs “the preferred option” for diabetes education, suggesting that clinicians reserve individual education for patients unable or unwilling to participate in group programs.⁴

The 2017 diabetes self-management education and support policy endorsed by the American Diabetes Association recommends using interprofessional teams and “creative solutions” to increase patient engagement and endorses group meetings as an effective option for patients who choose them.⁵

Editor’s takeaway

Moderate-quality evidence demonstrates that group visits can significantly reduce HbA1c levels. We should consider them for our patients with diabetes who are willing to attend group sessions.

EVIDENCE SUMMARY

A 2012 systematic review of 21 RCTs examined the effect of group-based diabetes education on HbA1c in 2833 adults with T2DM.¹ Intervention groups participated in at least 1 group session lasting an hour led by a health professional or team (eg, physician, nurse, diabetes educator); controls received usual care. Most trials involved 6 to 20 hours of group-based education delivered over 1 to 10 months, although some trials continued the intervention for as long as 24 months. The mean HbA1c at baseline across all patients was 8.23%.

Professional-led group visitsimprove HbA1c

Group education resulted in a significant reduction in HbA1c compared with controls at 6 months (13 trials; 1883 patients; mean difference [MD]=−0.44%; 95% confidence interval [CI], −0.69 to −0.19), 12 months (11 studies; 1503 patients; MD=−0.46%; 95% CI, −0.74 to −0.18), and 24 months (3 studies; 397 patients; MD=−0.87%; 95% CI, −1.25 to −0.49). The trials had high heterogeneity, except for the 3 trials with a 24-month end-point (I² = 0). Most studies had a moderate or high risk of bias.

A larger 2017 meta-analysis enrolling 8533 adults with T2DM came to similar conclusions, although it included a small number of nonrandomized trials (40 RCTs, 3 cluster RCTs, and 4 controlled clinical trials).² Thirteen of the RCTs overlapped with the previously described systematic review.¹ Interventions had to include at least 1 group session with 4 or more adult patients lasting at least 1 hour. In most studies, interventions continued between 4 and 12 months, although some ran 60 months. Controls received usual care. The mean HbA1c at baseline across all patients was 8.3%.

Group-based education compared with controls reduced HbA1c at 6 to 10 months (30 trials, N not given; MD=−0.3%; 95% CI, −0.48 to −0.15), 12 to 14 months (27 trials, N not given; MD=−0.3%; 95% CI, −0.49 to −0.17), and 36 to 48 months (5 trials, N not given; MD=−0.9%; 95% CI, −1.52 to −0.34). In a subgroup analysis, peer-led group visits had no effect (5 trials, 1066 patients; MD=−0.02%; 95% CI, −0.12 to 0.16).

Patients on oral agents alone showed a larger benefit than patients using insulin (38 trials, 5871 patients; −0.81 vs −0.19; P < .0001). Authors of the meta-analysis classified most studies as having a moderate to high risk of bias, with only 4 having low risk.

Duration of intervention: Longer is better for HbA1c values

Another systematic review analyzed 13 RCTs with 4652 patients 16 years and older with T2DM or type 1 diabetes to assess the effect of group visits on HbA1c.³ The review excluded studies that didn’t include a health care provider who could prescribe, diagnose, assess, and refer patients when appropriate.

Group visits led by health professionals or teams improve glycosylated hemoglobin by 0.3% to 0.9% over usual care in patients with type 2 diabetes.

Most interventions ran 3 to 12 months, although one lasted 36 months. (Two RCTs overlapped with the 2012 review, and 2 others with the 2017 review.) Group medical visits resulted in a significant decrease in HbA1c at the end of the intervention period (MD=−0.46%; 95% CI, −0.80 to −0.13) compared with controls. A meta-regression analysis suggested that ongoing treatment (for as long as 3 years) decreased HbA1c more than a shorter treatment duration (by 0.25% per year of treatment), whereas the frequency of treatments didn’t alter the effect. Overall, the trials were heterogenous and most had a high risk of bias.

Continue to: RECOMMENDATIONS

The 2015 National Institute for Health and Care Excellence guideline for the management of T2DM in adults calls group education ­programs “the preferred option” for diabetes education, suggesting that clinicians reserve individual education for patients unable or unwilling to participate in group programs.⁴

The 2017 diabetes self-management education and support policy endorsed by the American Diabetes Association recommends using interprofessional teams and “creative solutions” to increase patient engagement and endorses group meetings as an effective option for patients who choose them.⁵

Editor’s takeaway

Moderate-quality evidence demonstrates that group visits can significantly reduce HbA1c levels. We should consider them for our patients with diabetes who are willing to attend group sessions.

EVIDENCE SUMMARY

A 2012 systematic review of 21 RCTs examined the effect of group-based diabetes education on HbA1c in 2833 adults with T2DM.¹ Intervention groups participated in at least 1 group session lasting an hour led by a health professional or team (eg, physician, nurse, diabetes educator); controls received usual care. Most trials involved 6 to 20 hours of group-based education delivered over 1 to 10 months, although some trials continued the intervention for as long as 24 months. The mean HbA1c at baseline across all patients was 8.23%.

Professional-led group visitsimprove HbA1c

Group education resulted in a significant reduction in HbA1c compared with controls at 6 months (13 trials; 1883 patients; mean difference [MD]=−0.44%; 95% confidence interval [CI], −0.69 to −0.19), 12 months (11 studies; 1503 patients; MD=−0.46%; 95% CI, −0.74 to −0.18), and 24 months (3 studies; 397 patients; MD=−0.87%; 95% CI, −1.25 to −0.49). The trials had high heterogeneity, except for the 3 trials with a 24-month end-point (I² = 0). Most studies had a moderate or high risk of bias.

A larger 2017 meta-analysis enrolling 8533 adults with T2DM came to similar conclusions, although it included a small number of nonrandomized trials (40 RCTs, 3 cluster RCTs, and 4 controlled clinical trials).² Thirteen of the RCTs overlapped with the previously described systematic review.¹ Interventions had to include at least 1 group session with 4 or more adult patients lasting at least 1 hour. In most studies, interventions continued between 4 and 12 months, although some ran 60 months. Controls received usual care. The mean HbA1c at baseline across all patients was 8.3%.

Group-based education compared with controls reduced HbA1c at 6 to 10 months (30 trials, N not given; MD=−0.3%; 95% CI, −0.48 to −0.15), 12 to 14 months (27 trials, N not given; MD=−0.3%; 95% CI, −0.49 to −0.17), and 36 to 48 months (5 trials, N not given; MD=−0.9%; 95% CI, −1.52 to −0.34). In a subgroup analysis, peer-led group visits had no effect (5 trials, 1066 patients; MD=−0.02%; 95% CI, −0.12 to 0.16).

Patients on oral agents alone showed a larger benefit than patients using insulin (38 trials, 5871 patients; −0.81 vs −0.19; P < .0001). Authors of the meta-analysis classified most studies as having a moderate to high risk of bias, with only 4 having low risk.

Duration of intervention: Longer is better for HbA1c values

Another systematic review analyzed 13 RCTs with 4652 patients 16 years and older with T2DM or type 1 diabetes to assess the effect of group visits on HbA1c.³ The review excluded studies that didn’t include a health care provider who could prescribe, diagnose, assess, and refer patients when appropriate.

Group visits led by health professionals or teams improve glycosylated hemoglobin by 0.3% to 0.9% over usual care in patients with type 2 diabetes.

Most interventions ran 3 to 12 months, although one lasted 36 months. (Two RCTs overlapped with the 2012 review, and 2 others with the 2017 review.) Group medical visits resulted in a significant decrease in HbA1c at the end of the intervention period (MD=−0.46%; 95% CI, −0.80 to −0.13) compared with controls. A meta-regression analysis suggested that ongoing treatment (for as long as 3 years) decreased HbA1c more than a shorter treatment duration (by 0.25% per year of treatment), whereas the frequency of treatments didn’t alter the effect. Overall, the trials were heterogenous and most had a high risk of bias.

Continue to: RECOMMENDATIONS

The 2015 National Institute for Health and Care Excellence guideline for the management of T2DM in adults calls group education ­programs “the preferred option” for diabetes education, suggesting that clinicians reserve individual education for patients unable or unwilling to participate in group programs.⁴

The 2017 diabetes self-management education and support policy endorsed by the American Diabetes Association recommends using interprofessional teams and “creative solutions” to increase patient engagement and endorses group meetings as an effective option for patients who choose them.⁵

Editor’s takeaway

Moderate-quality evidence demonstrates that group visits can significantly reduce HbA1c levels. We should consider them for our patients with diabetes who are willing to attend group sessions.

EVIDENCE SUMMARY

A 2016 Cochrane systematic review identified 2 double-blind RCTs that evaluated statins for preventing cognitive decline and dementia in patients with either risk factors or a history of vascular disease.¹ The authors couldn’t perform a meta-analysis because of heterogeneity.

Statins don’t prevent dementia

The first RCT found that 5804 patients (70-82 years old with pre-existing vascular disease or increased risk because of smoking, hypertension, or diabetes) manifested equivalent cognitive decline at 3.5 years after random assignment to pravastatin 40 mg/d or placebo.² Investigators measured cognition with the Mini-Mental State Exam (MMSE), which scores cognitive function on a scale of 0 to 30, with higher numbers indicating better function (mean difference [MD] at follow-up=0.06 points; 95% confidence interval [CI], −0.04 to 0.16).

A second RCT evaluated simvastatin 40 mg/d or placebo for as long as 5 years in 20,536 patients 40 to 80 years of age with a history of coronary artery disease or diabetes.³ The study excluded patients with dementia at baseline. The odds of developing dementia didn’t differ between groups (odds ratio=1.0; 95% CI, 0.61-1.65).

Both studies were originally designed to measure cardiovascular outcomes. The authors rated both as high quality with a low risk of bias.

A contrast to earlier, lower-quality studies

These results contrast with an earlier meta-analysis based on one of the previously described RCTs and lower-quality evidence (16 cohort studies and 3 case-control studies) that found using statins to be associated with lower relative risk (RR) of dementia than not using a statin (all-type dementia RR=0.82; 95% CI, 0.69-0.97; Alzheimer’s disease RR=0.70; 95% CI, 0.60-0.83).^3,4

The total patient population was more than 2 million and varied widely. Duration of statin use and type of statin (simvastatin, atorvastatin, fluvastatin, pravastatin, rosuvastatin) also varied. The authors noted potential bias in results for 2 reasons: Cross-sectional studies included patients with impaired cognition who were less likely to be prescribed statins, and statin use was determined by patient self-report.

Statins don’t treat dementia

A Cochrane review that included 4 RCTs with 1154 patients, 50 to 90 years old, assessed the effect of ≥6 months of statin therapy (atorvastatin 80 mg/d or simvastatin 40-80 mg/d) on the course of Alzheimer’s disease and vascular dementia.⁵ Most patients had mild to moderate dementia and most were also taking an anticholinesterase inhibitor.

Continue to: All studies reported...

All studies reported outcomes using the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), scored 0 to 70, with lower numbers indicating better function, and the MMSE. Results of statin use were equivalent to placebo (ADAS-Cog MD= −0.26; 95% CI, −1.05 to 0.52; MMSE MD= −0.32; 95% CI, −0.71 to 0.06).

But do they slow its progression?

In contrast, a case-control study of 6431 patients with mild-to-moderate Alzheimer’s disease concluded that statin use was associated with slower progression of AD.⁶ Using cholinesterase inhibitor discontinuation as a proxy for worsening dementia, researchers noted that patients with early statin exposure (719 patients) had a lower rate of cholinesterase discontinuation than patients who didn’t receive early statin therapy (RR=0.85; 95% CI, 0.76-0.95).

A 2016 systematic review attempted to identify randomized clinical trials evaluating the effects of statin withdrawal in dementia.⁷ None were found.

RECOMMENDATIONS

Based primarily on post-marketing surveillance data, the US Food and Drug Administration (FDA) has warned that memory loss and confusion are occasionally associated with statin use from within one day to several years of initiation.⁸ The FDA indicated that such symptoms are rare, not associated with dementia or clinically significant cognitive decline, and resolve with discontinuation of the medication.

EVIDENCE SUMMARY

A 2016 Cochrane systematic review identified 2 double-blind RCTs that evaluated statins for preventing cognitive decline and dementia in patients with either risk factors or a history of vascular disease.¹ The authors couldn’t perform a meta-analysis because of heterogeneity.

Statins don’t prevent dementia

The first RCT found that 5804 patients (70-82 years old with pre-existing vascular disease or increased risk because of smoking, hypertension, or diabetes) manifested equivalent cognitive decline at 3.5 years after random assignment to pravastatin 40 mg/d or placebo.² Investigators measured cognition with the Mini-Mental State Exam (MMSE), which scores cognitive function on a scale of 0 to 30, with higher numbers indicating better function (mean difference [MD] at follow-up=0.06 points; 95% confidence interval [CI], −0.04 to 0.16).

A second RCT evaluated simvastatin 40 mg/d or placebo for as long as 5 years in 20,536 patients 40 to 80 years of age with a history of coronary artery disease or diabetes.³ The study excluded patients with dementia at baseline. The odds of developing dementia didn’t differ between groups (odds ratio=1.0; 95% CI, 0.61-1.65).

Both studies were originally designed to measure cardiovascular outcomes. The authors rated both as high quality with a low risk of bias.

A contrast to earlier, lower-quality studies

These results contrast with an earlier meta-analysis based on one of the previously described RCTs and lower-quality evidence (16 cohort studies and 3 case-control studies) that found using statins to be associated with lower relative risk (RR) of dementia than not using a statin (all-type dementia RR=0.82; 95% CI, 0.69-0.97; Alzheimer’s disease RR=0.70; 95% CI, 0.60-0.83).^3,4

The total patient population was more than 2 million and varied widely. Duration of statin use and type of statin (simvastatin, atorvastatin, fluvastatin, pravastatin, rosuvastatin) also varied. The authors noted potential bias in results for 2 reasons: Cross-sectional studies included patients with impaired cognition who were less likely to be prescribed statins, and statin use was determined by patient self-report.

Statins don’t treat dementia

A Cochrane review that included 4 RCTs with 1154 patients, 50 to 90 years old, assessed the effect of ≥6 months of statin therapy (atorvastatin 80 mg/d or simvastatin 40-80 mg/d) on the course of Alzheimer’s disease and vascular dementia.⁵ Most patients had mild to moderate dementia and most were also taking an anticholinesterase inhibitor.

Continue to: All studies reported...

All studies reported outcomes using the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), scored 0 to 70, with lower numbers indicating better function, and the MMSE. Results of statin use were equivalent to placebo (ADAS-Cog MD= −0.26; 95% CI, −1.05 to 0.52; MMSE MD= −0.32; 95% CI, −0.71 to 0.06).

But do they slow its progression?

In contrast, a case-control study of 6431 patients with mild-to-moderate Alzheimer’s disease concluded that statin use was associated with slower progression of AD.⁶ Using cholinesterase inhibitor discontinuation as a proxy for worsening dementia, researchers noted that patients with early statin exposure (719 patients) had a lower rate of cholinesterase discontinuation than patients who didn’t receive early statin therapy (RR=0.85; 95% CI, 0.76-0.95).

A 2016 systematic review attempted to identify randomized clinical trials evaluating the effects of statin withdrawal in dementia.⁷ None were found.

RECOMMENDATIONS

Based primarily on post-marketing surveillance data, the US Food and Drug Administration (FDA) has warned that memory loss and confusion are occasionally associated with statin use from within one day to several years of initiation.⁸ The FDA indicated that such symptoms are rare, not associated with dementia or clinically significant cognitive decline, and resolve with discontinuation of the medication.

EVIDENCE SUMMARY

A 2016 Cochrane systematic review identified 2 double-blind RCTs that evaluated statins for preventing cognitive decline and dementia in patients with either risk factors or a history of vascular disease.¹ The authors couldn’t perform a meta-analysis because of heterogeneity.

Statins don’t prevent dementia

The first RCT found that 5804 patients (70-82 years old with pre-existing vascular disease or increased risk because of smoking, hypertension, or diabetes) manifested equivalent cognitive decline at 3.5 years after random assignment to pravastatin 40 mg/d or placebo.² Investigators measured cognition with the Mini-Mental State Exam (MMSE), which scores cognitive function on a scale of 0 to 30, with higher numbers indicating better function (mean difference [MD] at follow-up=0.06 points; 95% confidence interval [CI], −0.04 to 0.16).

A second RCT evaluated simvastatin 40 mg/d or placebo for as long as 5 years in 20,536 patients 40 to 80 years of age with a history of coronary artery disease or diabetes.³ The study excluded patients with dementia at baseline. The odds of developing dementia didn’t differ between groups (odds ratio=1.0; 95% CI, 0.61-1.65).

Both studies were originally designed to measure cardiovascular outcomes. The authors rated both as high quality with a low risk of bias.

A contrast to earlier, lower-quality studies

These results contrast with an earlier meta-analysis based on one of the previously described RCTs and lower-quality evidence (16 cohort studies and 3 case-control studies) that found using statins to be associated with lower relative risk (RR) of dementia than not using a statin (all-type dementia RR=0.82; 95% CI, 0.69-0.97; Alzheimer’s disease RR=0.70; 95% CI, 0.60-0.83).^3,4

The total patient population was more than 2 million and varied widely. Duration of statin use and type of statin (simvastatin, atorvastatin, fluvastatin, pravastatin, rosuvastatin) also varied. The authors noted potential bias in results for 2 reasons: Cross-sectional studies included patients with impaired cognition who were less likely to be prescribed statins, and statin use was determined by patient self-report.

Statins don’t treat dementia

A Cochrane review that included 4 RCTs with 1154 patients, 50 to 90 years old, assessed the effect of ≥6 months of statin therapy (atorvastatin 80 mg/d or simvastatin 40-80 mg/d) on the course of Alzheimer’s disease and vascular dementia.⁵ Most patients had mild to moderate dementia and most were also taking an anticholinesterase inhibitor.

Continue to: All studies reported...

All studies reported outcomes using the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), scored 0 to 70, with lower numbers indicating better function, and the MMSE. Results of statin use were equivalent to placebo (ADAS-Cog MD= −0.26; 95% CI, −1.05 to 0.52; MMSE MD= −0.32; 95% CI, −0.71 to 0.06).

But do they slow its progression?

In contrast, a case-control study of 6431 patients with mild-to-moderate Alzheimer’s disease concluded that statin use was associated with slower progression of AD.⁶ Using cholinesterase inhibitor discontinuation as a proxy for worsening dementia, researchers noted that patients with early statin exposure (719 patients) had a lower rate of cholinesterase discontinuation than patients who didn’t receive early statin therapy (RR=0.85; 95% CI, 0.76-0.95).

A 2016 systematic review attempted to identify randomized clinical trials evaluating the effects of statin withdrawal in dementia.⁷ None were found.

RECOMMENDATIONS

Based primarily on post-marketing surveillance data, the US Food and Drug Administration (FDA) has warned that memory loss and confusion are occasionally associated with statin use from within one day to several years of initiation.⁸ The FDA indicated that such symptoms are rare, not associated with dementia or clinically significant cognitive decline, and resolve with discontinuation of the medication.

EVIDENCE SUMMARY

A systematic review and meta-analysis of prospective cohort studies evaluating infant risk factors for childhood obesity found that breastfeeding was associated with a lower risk of obesity.¹ The authors identified 10 trials (primarily from the United States and Europe) with more than 76,000 infants that compared the effect of some breastfeeding in the first year to no breastfeeding. Follow-up ranged from 2 to 14 years (median 6 years).

Having ever breastfed decreased the odds of future overweight (BMI >85th percentile) or obesity (BMI >95th percentile) by 15% (adjusted odds ratio [AOR]=0.85; 95% confidence interval [CI], 0.74-0.99).

Subsequent studies suggest increased risk with formula feeding

Three large, prospective, longitudinal cohort studies have been published since the meta-analysis. One, which followed 43,367 term infants in Japan, found that formula feeding before 6 months was associated with increased risk of obesity compared with continuous breastfeeding for 6 months.² Researchers evaluated weight at 7 years and adjusted for child and maternal factors associated with weight gain (AOR for obesity, formula-fed infants=1.8; 95% CI, 1.3-2.6).

A similar prospective longitudinal cohort study of 2868 infants in Australia analyzed maternal breastfeeding diaries and followed children’s weight to age 20 years.³ Introducing a milk other than breast milk before 6 months of age was linked to increased risk of obesity at age 20 (odds ratio [OR]=1.5; 95% CI, 1.1-1.9).

Finally, in a prospective cohort of 568 children in India, 17% of children who breastfed for fewer than 6 months were above the 90th percentile for weight at age 5 years, compared with 10% of children who were breastfed for at least 18 months.⁴ The result didn’t reach statistical significance, however (P=.08).

Interventions that increase breastfeeding don’t seem to have an impact

An RCT of an intervention to promote breastfeeding didn’t find any effect on subsequent obesity rates. Researchers in Belarus randomized 17,046 mother-infant pairs to breastfeeding promotion, modeled on the UNICEF Baby-Friendly Hospital Initiative, or usual care. The intervention increased the prevalence of exclusive breastfeeding (at 3 months, 43% vs 6%; at 6 months, 7% vs 0.6%; P values not given).

When researchers evaluated 13,879 children at 11 or 12 years by intention-to-treat analysis, however, they found no difference in mean BMI between the children whose mothers received the intervention and those whose mothers didn’t (BMI difference=0.16; 95% CI, -0.02 to 0.35).⁵

Introduction of solid foods: Later is better

A systematic review investigated the association between the timing of introducing complementary (solid) foods and childhood obesity in 23 primarily cross-sectional and cohort studies (17 from the United States, Canada, and Europe) with more than 33,000 patients. Follow-up ranged from 4 to 19 years.

Eight of the 21 studies that used BMI as an outcome found that early introduction of complementary foods was associated with a higher childhood BMI. In the largest study (a cohort of 17,561 infants), introducing complementary foods before 3 months was associated with higher risk of obesity at age 5 years than introducing them thereafter (OR=1.3; 95% CI, 1.1-1.6).⁶ Introduction of solids after 4 months was not associated with childhood obesity.

A systematic review of 10 primarily cross-sectional and cohort studies with more than 3000 infants evaluated associations between the types of complementary foods given and the development of childhood obesity.⁷ Six of the 10 studies were from Europe and none were from the United States. Follow-up ages ranged from 4 to 11 years.

Scheduled feeding was associated with rapid weight gain at a higher rate than feeding on demand.Outcomes were heterogeneous, and no meta-analysis could be performed. The authors cited 3 studies (total 1174 infants) that found various positive associations between total caloric intake during complementary feeding and childhood obesity. No consistent evidence pointed to increased risk from specific foods or food groups.

Scheduled feeding is linked to rapid infant weight gain

A cohort study evaluated the baseline data of an Australian RCT (on an intervention to promote proper nutrition) in 612 infants, mean age 4.3 months.⁸ Researchers looked at the relationship between feeding on demand vs scheduled feeding (assessed by parental report) and weight gain in infancy. “Rapid weight gain” was defined as >0.67 change in weight-for-age Z-score between birth and enrollment.

Scheduled feeding was associated with rapid weight gain at a higher rate than feeding on demand (OR=2.3; 95% CI, 1.1-4.6). This study didn’t use childhood obesity as an outcome.

EVIDENCE SUMMARY

A systematic review and meta-analysis of prospective cohort studies evaluating infant risk factors for childhood obesity found that breastfeeding was associated with a lower risk of obesity.¹ The authors identified 10 trials (primarily from the United States and Europe) with more than 76,000 infants that compared the effect of some breastfeeding in the first year to no breastfeeding. Follow-up ranged from 2 to 14 years (median 6 years).

Having ever breastfed decreased the odds of future overweight (BMI >85th percentile) or obesity (BMI >95th percentile) by 15% (adjusted odds ratio [AOR]=0.85; 95% confidence interval [CI], 0.74-0.99).

Subsequent studies suggest increased risk with formula feeding

Three large, prospective, longitudinal cohort studies have been published since the meta-analysis. One, which followed 43,367 term infants in Japan, found that formula feeding before 6 months was associated with increased risk of obesity compared with continuous breastfeeding for 6 months.² Researchers evaluated weight at 7 years and adjusted for child and maternal factors associated with weight gain (AOR for obesity, formula-fed infants=1.8; 95% CI, 1.3-2.6).

A similar prospective longitudinal cohort study of 2868 infants in Australia analyzed maternal breastfeeding diaries and followed children’s weight to age 20 years.³ Introducing a milk other than breast milk before 6 months of age was linked to increased risk of obesity at age 20 (odds ratio [OR]=1.5; 95% CI, 1.1-1.9).

Finally, in a prospective cohort of 568 children in India, 17% of children who breastfed for fewer than 6 months were above the 90th percentile for weight at age 5 years, compared with 10% of children who were breastfed for at least 18 months.⁴ The result didn’t reach statistical significance, however (P=.08).

Interventions that increase breastfeeding don’t seem to have an impact

An RCT of an intervention to promote breastfeeding didn’t find any effect on subsequent obesity rates. Researchers in Belarus randomized 17,046 mother-infant pairs to breastfeeding promotion, modeled on the UNICEF Baby-Friendly Hospital Initiative, or usual care. The intervention increased the prevalence of exclusive breastfeeding (at 3 months, 43% vs 6%; at 6 months, 7% vs 0.6%; P values not given).

When researchers evaluated 13,879 children at 11 or 12 years by intention-to-treat analysis, however, they found no difference in mean BMI between the children whose mothers received the intervention and those whose mothers didn’t (BMI difference=0.16; 95% CI, -0.02 to 0.35).⁵

Introduction of solid foods: Later is better

A systematic review investigated the association between the timing of introducing complementary (solid) foods and childhood obesity in 23 primarily cross-sectional and cohort studies (17 from the United States, Canada, and Europe) with more than 33,000 patients. Follow-up ranged from 4 to 19 years.

Eight of the 21 studies that used BMI as an outcome found that early introduction of complementary foods was associated with a higher childhood BMI. In the largest study (a cohort of 17,561 infants), introducing complementary foods before 3 months was associated with higher risk of obesity at age 5 years than introducing them thereafter (OR=1.3; 95% CI, 1.1-1.6).⁶ Introduction of solids after 4 months was not associated with childhood obesity.

A systematic review of 10 primarily cross-sectional and cohort studies with more than 3000 infants evaluated associations between the types of complementary foods given and the development of childhood obesity.⁷ Six of the 10 studies were from Europe and none were from the United States. Follow-up ages ranged from 4 to 11 years.

Scheduled feeding was associated with rapid weight gain at a higher rate than feeding on demand.Outcomes were heterogeneous, and no meta-analysis could be performed. The authors cited 3 studies (total 1174 infants) that found various positive associations between total caloric intake during complementary feeding and childhood obesity. No consistent evidence pointed to increased risk from specific foods or food groups.

Scheduled feeding is linked to rapid infant weight gain

A cohort study evaluated the baseline data of an Australian RCT (on an intervention to promote proper nutrition) in 612 infants, mean age 4.3 months.⁸ Researchers looked at the relationship between feeding on demand vs scheduled feeding (assessed by parental report) and weight gain in infancy. “Rapid weight gain” was defined as >0.67 change in weight-for-age Z-score between birth and enrollment.

Scheduled feeding was associated with rapid weight gain at a higher rate than feeding on demand (OR=2.3; 95% CI, 1.1-4.6). This study didn’t use childhood obesity as an outcome.

EVIDENCE SUMMARY

A systematic review and meta-analysis of prospective cohort studies evaluating infant risk factors for childhood obesity found that breastfeeding was associated with a lower risk of obesity.¹ The authors identified 10 trials (primarily from the United States and Europe) with more than 76,000 infants that compared the effect of some breastfeeding in the first year to no breastfeeding. Follow-up ranged from 2 to 14 years (median 6 years).

Having ever breastfed decreased the odds of future overweight (BMI >85th percentile) or obesity (BMI >95th percentile) by 15% (adjusted odds ratio [AOR]=0.85; 95% confidence interval [CI], 0.74-0.99).

Subsequent studies suggest increased risk with formula feeding

Three large, prospective, longitudinal cohort studies have been published since the meta-analysis. One, which followed 43,367 term infants in Japan, found that formula feeding before 6 months was associated with increased risk of obesity compared with continuous breastfeeding for 6 months.² Researchers evaluated weight at 7 years and adjusted for child and maternal factors associated with weight gain (AOR for obesity, formula-fed infants=1.8; 95% CI, 1.3-2.6).

A similar prospective longitudinal cohort study of 2868 infants in Australia analyzed maternal breastfeeding diaries and followed children’s weight to age 20 years.³ Introducing a milk other than breast milk before 6 months of age was linked to increased risk of obesity at age 20 (odds ratio [OR]=1.5; 95% CI, 1.1-1.9).

Finally, in a prospective cohort of 568 children in India, 17% of children who breastfed for fewer than 6 months were above the 90th percentile for weight at age 5 years, compared with 10% of children who were breastfed for at least 18 months.⁴ The result didn’t reach statistical significance, however (P=.08).

Interventions that increase breastfeeding don’t seem to have an impact

An RCT of an intervention to promote breastfeeding didn’t find any effect on subsequent obesity rates. Researchers in Belarus randomized 17,046 mother-infant pairs to breastfeeding promotion, modeled on the UNICEF Baby-Friendly Hospital Initiative, or usual care. The intervention increased the prevalence of exclusive breastfeeding (at 3 months, 43% vs 6%; at 6 months, 7% vs 0.6%; P values not given).

When researchers evaluated 13,879 children at 11 or 12 years by intention-to-treat analysis, however, they found no difference in mean BMI between the children whose mothers received the intervention and those whose mothers didn’t (BMI difference=0.16; 95% CI, -0.02 to 0.35).⁵

Introduction of solid foods: Later is better

A systematic review investigated the association between the timing of introducing complementary (solid) foods and childhood obesity in 23 primarily cross-sectional and cohort studies (17 from the United States, Canada, and Europe) with more than 33,000 patients. Follow-up ranged from 4 to 19 years.

Eight of the 21 studies that used BMI as an outcome found that early introduction of complementary foods was associated with a higher childhood BMI. In the largest study (a cohort of 17,561 infants), introducing complementary foods before 3 months was associated with higher risk of obesity at age 5 years than introducing them thereafter (OR=1.3; 95% CI, 1.1-1.6).⁶ Introduction of solids after 4 months was not associated with childhood obesity.

A systematic review of 10 primarily cross-sectional and cohort studies with more than 3000 infants evaluated associations between the types of complementary foods given and the development of childhood obesity.⁷ Six of the 10 studies were from Europe and none were from the United States. Follow-up ages ranged from 4 to 11 years.

Scheduled feeding was associated with rapid weight gain at a higher rate than feeding on demand.Outcomes were heterogeneous, and no meta-analysis could be performed. The authors cited 3 studies (total 1174 infants) that found various positive associations between total caloric intake during complementary feeding and childhood obesity. No consistent evidence pointed to increased risk from specific foods or food groups.

Scheduled feeding is linked to rapid infant weight gain

A cohort study evaluated the baseline data of an Australian RCT (on an intervention to promote proper nutrition) in 612 infants, mean age 4.3 months.⁸ Researchers looked at the relationship between feeding on demand vs scheduled feeding (assessed by parental report) and weight gain in infancy. “Rapid weight gain” was defined as >0.67 change in weight-for-age Z-score between birth and enrollment.

Scheduled feeding was associated with rapid weight gain at a higher rate than feeding on demand (OR=2.3; 95% CI, 1.1-4.6). This study didn’t use childhood obesity as an outcome.

EVIDENCE SUMMARY

Red-yeast rice is a Chinese dietary and medicinal product of yeast (Monascus purpureus) grown on rice. It contains a wide range of biologically active compounds, including lovastatin (monacolin K). The FDA has banned the sale of red-yeast rice products with more than trace amounts of lovastatin.¹

Red-yeast rice beats placebo, similar to statins

A systematic review of 22 RCTs (N=6520), primarily conducted in China using 600 to 2400 mg red-yeast rice extract daily (lovastatin content 5-20 mg), assessed outcomes in patients with known CHD and dyslipidemia.² In one trial of 4870 patients, users of red-yeast rice had significant reductions in CHD mortality (relative risk [RR]=0.69; 95% confidence interval [CI], 0.54-0.89), incidence of MI (RR=0.39; 95% CI, 0.28-0.55), and revascularization (RR=0.67; 95% CI, 0.50-0.89) compared with placebo users.

However, when compared with statin therapy, red-yeast rice didn’t yield statistically significant differences in CHD mortality (2 trials, N=220; RR=0.26; 95% CI, 0.06-1.21), incidence of MI (1 trial, N=84; RR=0.95; 95% CI, 0.30-3.05) or revascularization (1 trial, N=84; RR=1.14; 95% CI, 0.38-3.46).

Red-yeast rice outperforms placebo in CHD and MI—but not stroke

A secondary analysis of an RCT evaluated the impact of red-yeast rice extract (600 mg twice a day) for 4.5 years on cardiovascular events and mortality in 1530 Chinese patients 60 years of age and older with hypertension and a previous MI.³ The lovastatin content of the red-yeast rice was 5 to 6.4 mg/d.

Compared with placebo, red-yeast rice was associated with a lower incidence of CHD events (RR=0.63; 95% CI, 0.36-0.83), nonfatal MI (RR=0.48; 95% CI, 0.37-0.71), and all-cause mortality (RR=0.65; 95% CI, 0.49-0.83) but not with a statistically significant difference in stroke (RR=0.63; 95% CI, 0.47-1.09) or cardiac revascularization (RR=0.68; 95% CI, 0.52-1.19).

Total adverse events in this study were similar for red-yeast rice and placebo (2.1% vs 1.2%, respectively; P>.05). They included gastrointestinal discomfort, allergic reactions, myalgias, edema, erectile dysfunction, and neuropsychological symptoms.

Red-yeast rice is similar to placebo or another statin in statin-induced myalgia

In patients with known coronary artery disease and dyslipidemia, therapy with red-yeast rice extract is linked to reductions in CHD mortality and myocardial infarction similar to statins. In a small community-based trial of 62 adults with dyslipidemia and a history of statin-induced myalgia, investigators randomized patients to receive either red-yeast rice extract at 1800 mg (with 3.1 mg lovastatin) or placebo twice daily for 24 weeks.⁴ Patients’ weekly self-reports of pain (on a 10-point scale) were skewed at baseline (1.4 in the red-yeast rice group vs 2.6 in the placebo group; P=.026) but similar at 12 weeks (1.4 with red-yeast rice vs 1.9 with placebo; P=.30) and 24 weeks (1.2 with red-yeast rice vs 2.0 with placebo; P=.120).

An RCT of 43 adults with dyslipidemia and history of statin intolerance compared red-yeast rice extract (2400 mg, with 10 mg lovastatin) with pravastatin (20 mg) dosed twice a day.⁵ At the end of 12 weeks, mean self-reported pain scores (on a 10-point scale) were similar (1.4 with red-yeast rice vs 1.1 with pravastatin; P=.82), as were discontinuation rates because of myalgia (5% with red-yeast rice vs 9% with pravastatin; P=.99).

RECOMMENDATIONS

A narrative review of alternative therapies for heart failure and hypercholesterolemia states that red yeast rice may be a cost-saving option for hypercholesterolemia in patients who can’t afford other medications (purchased mostly online, cost $8-$20/month for a dosage equivalent to lovastatin 20 mg/d).⁶

A ConsumerLab review of red yeast rice products available since the FDA ban in 2011 tested products marketed in the United States and found variable amounts of lovastatin.^1,7 The group determined that labeling was a poor guide to lovastatin content, which ranged from 0 to 20 mg per daily dose, and that the products may not have been standardized. The group concluded that therapeutic effects weren’t predictable.

EVIDENCE SUMMARY

Red-yeast rice is a Chinese dietary and medicinal product of yeast (Monascus purpureus) grown on rice. It contains a wide range of biologically active compounds, including lovastatin (monacolin K). The FDA has banned the sale of red-yeast rice products with more than trace amounts of lovastatin.¹

Red-yeast rice beats placebo, similar to statins

A systematic review of 22 RCTs (N=6520), primarily conducted in China using 600 to 2400 mg red-yeast rice extract daily (lovastatin content 5-20 mg), assessed outcomes in patients with known CHD and dyslipidemia.² In one trial of 4870 patients, users of red-yeast rice had significant reductions in CHD mortality (relative risk [RR]=0.69; 95% confidence interval [CI], 0.54-0.89), incidence of MI (RR=0.39; 95% CI, 0.28-0.55), and revascularization (RR=0.67; 95% CI, 0.50-0.89) compared with placebo users.

However, when compared with statin therapy, red-yeast rice didn’t yield statistically significant differences in CHD mortality (2 trials, N=220; RR=0.26; 95% CI, 0.06-1.21), incidence of MI (1 trial, N=84; RR=0.95; 95% CI, 0.30-3.05) or revascularization (1 trial, N=84; RR=1.14; 95% CI, 0.38-3.46).

Red-yeast rice outperforms placebo in CHD and MI—but not stroke

A secondary analysis of an RCT evaluated the impact of red-yeast rice extract (600 mg twice a day) for 4.5 years on cardiovascular events and mortality in 1530 Chinese patients 60 years of age and older with hypertension and a previous MI.³ The lovastatin content of the red-yeast rice was 5 to 6.4 mg/d.

Compared with placebo, red-yeast rice was associated with a lower incidence of CHD events (RR=0.63; 95% CI, 0.36-0.83), nonfatal MI (RR=0.48; 95% CI, 0.37-0.71), and all-cause mortality (RR=0.65; 95% CI, 0.49-0.83) but not with a statistically significant difference in stroke (RR=0.63; 95% CI, 0.47-1.09) or cardiac revascularization (RR=0.68; 95% CI, 0.52-1.19).

Total adverse events in this study were similar for red-yeast rice and placebo (2.1% vs 1.2%, respectively; P>.05). They included gastrointestinal discomfort, allergic reactions, myalgias, edema, erectile dysfunction, and neuropsychological symptoms.

Red-yeast rice is similar to placebo or another statin in statin-induced myalgia

In patients with known coronary artery disease and dyslipidemia, therapy with red-yeast rice extract is linked to reductions in CHD mortality and myocardial infarction similar to statins. In a small community-based trial of 62 adults with dyslipidemia and a history of statin-induced myalgia, investigators randomized patients to receive either red-yeast rice extract at 1800 mg (with 3.1 mg lovastatin) or placebo twice daily for 24 weeks.⁴ Patients’ weekly self-reports of pain (on a 10-point scale) were skewed at baseline (1.4 in the red-yeast rice group vs 2.6 in the placebo group; P=.026) but similar at 12 weeks (1.4 with red-yeast rice vs 1.9 with placebo; P=.30) and 24 weeks (1.2 with red-yeast rice vs 2.0 with placebo; P=.120).

An RCT of 43 adults with dyslipidemia and history of statin intolerance compared red-yeast rice extract (2400 mg, with 10 mg lovastatin) with pravastatin (20 mg) dosed twice a day.⁵ At the end of 12 weeks, mean self-reported pain scores (on a 10-point scale) were similar (1.4 with red-yeast rice vs 1.1 with pravastatin; P=.82), as were discontinuation rates because of myalgia (5% with red-yeast rice vs 9% with pravastatin; P=.99).

RECOMMENDATIONS

A narrative review of alternative therapies for heart failure and hypercholesterolemia states that red yeast rice may be a cost-saving option for hypercholesterolemia in patients who can’t afford other medications (purchased mostly online, cost $8-$20/month for a dosage equivalent to lovastatin 20 mg/d).⁶

A ConsumerLab review of red yeast rice products available since the FDA ban in 2011 tested products marketed in the United States and found variable amounts of lovastatin.^1,7 The group determined that labeling was a poor guide to lovastatin content, which ranged from 0 to 20 mg per daily dose, and that the products may not have been standardized. The group concluded that therapeutic effects weren’t predictable.

EVIDENCE SUMMARY

Red-yeast rice is a Chinese dietary and medicinal product of yeast (Monascus purpureus) grown on rice. It contains a wide range of biologically active compounds, including lovastatin (monacolin K). The FDA has banned the sale of red-yeast rice products with more than trace amounts of lovastatin.¹

Red-yeast rice beats placebo, similar to statins

A systematic review of 22 RCTs (N=6520), primarily conducted in China using 600 to 2400 mg red-yeast rice extract daily (lovastatin content 5-20 mg), assessed outcomes in patients with known CHD and dyslipidemia.² In one trial of 4870 patients, users of red-yeast rice had significant reductions in CHD mortality (relative risk [RR]=0.69; 95% confidence interval [CI], 0.54-0.89), incidence of MI (RR=0.39; 95% CI, 0.28-0.55), and revascularization (RR=0.67; 95% CI, 0.50-0.89) compared with placebo users.

However, when compared with statin therapy, red-yeast rice didn’t yield statistically significant differences in CHD mortality (2 trials, N=220; RR=0.26; 95% CI, 0.06-1.21), incidence of MI (1 trial, N=84; RR=0.95; 95% CI, 0.30-3.05) or revascularization (1 trial, N=84; RR=1.14; 95% CI, 0.38-3.46).

Red-yeast rice outperforms placebo in CHD and MI—but not stroke

A secondary analysis of an RCT evaluated the impact of red-yeast rice extract (600 mg twice a day) for 4.5 years on cardiovascular events and mortality in 1530 Chinese patients 60 years of age and older with hypertension and a previous MI.³ The lovastatin content of the red-yeast rice was 5 to 6.4 mg/d.

Compared with placebo, red-yeast rice was associated with a lower incidence of CHD events (RR=0.63; 95% CI, 0.36-0.83), nonfatal MI (RR=0.48; 95% CI, 0.37-0.71), and all-cause mortality (RR=0.65; 95% CI, 0.49-0.83) but not with a statistically significant difference in stroke (RR=0.63; 95% CI, 0.47-1.09) or cardiac revascularization (RR=0.68; 95% CI, 0.52-1.19).

Total adverse events in this study were similar for red-yeast rice and placebo (2.1% vs 1.2%, respectively; P>.05). They included gastrointestinal discomfort, allergic reactions, myalgias, edema, erectile dysfunction, and neuropsychological symptoms.

Red-yeast rice is similar to placebo or another statin in statin-induced myalgia

In patients with known coronary artery disease and dyslipidemia, therapy with red-yeast rice extract is linked to reductions in CHD mortality and myocardial infarction similar to statins. In a small community-based trial of 62 adults with dyslipidemia and a history of statin-induced myalgia, investigators randomized patients to receive either red-yeast rice extract at 1800 mg (with 3.1 mg lovastatin) or placebo twice daily for 24 weeks.⁴ Patients’ weekly self-reports of pain (on a 10-point scale) were skewed at baseline (1.4 in the red-yeast rice group vs 2.6 in the placebo group; P=.026) but similar at 12 weeks (1.4 with red-yeast rice vs 1.9 with placebo; P=.30) and 24 weeks (1.2 with red-yeast rice vs 2.0 with placebo; P=.120).

An RCT of 43 adults with dyslipidemia and history of statin intolerance compared red-yeast rice extract (2400 mg, with 10 mg lovastatin) with pravastatin (20 mg) dosed twice a day.⁵ At the end of 12 weeks, mean self-reported pain scores (on a 10-point scale) were similar (1.4 with red-yeast rice vs 1.1 with pravastatin; P=.82), as were discontinuation rates because of myalgia (5% with red-yeast rice vs 9% with pravastatin; P=.99).

RECOMMENDATIONS

A narrative review of alternative therapies for heart failure and hypercholesterolemia states that red yeast rice may be a cost-saving option for hypercholesterolemia in patients who can’t afford other medications (purchased mostly online, cost $8-$20/month for a dosage equivalent to lovastatin 20 mg/d).⁶

A ConsumerLab review of red yeast rice products available since the FDA ban in 2011 tested products marketed in the United States and found variable amounts of lovastatin.^1,7 The group determined that labeling was a poor guide to lovastatin content, which ranged from 0 to 20 mg per daily dose, and that the products may not have been standardized. The group concluded that therapeutic effects weren’t predictable.