In the Journals

In metabolically healthy obesity, no link between proinflammatory diet, all-cause mortality

Among adults with metabolically healthy obesity, a proinflammatory diet is not associated with increased risk for all-cause and cardiovascular mortality, but this risk persists for those with metabolically unhealthy obesity who adhere to the same diet, according to findings published in Clinical Nutrition.

Yong-Moon Mark Park, MD, PhD, MS, an epidemiologist with the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina, and colleagues analyzed data from 3,733 adults with overweight or obesity without history of previous CVD participating in the 1988-1994 waves of the National Health and Nutrition Examination Survey. Researchers assessed dietary intake via a 24-hour dietary recall, using the findings to calculate dietary inflammatory index (DII) score, a standardized scoring system to assess the influence of diet on inflammation. Researchers also evaluated metabolic parameters, including BMI, blood pressure, serum glucose, serum insulin, triglycerides and HDL cholesterol. Participants were defined as metabolic unhealthy if they had two or more of the following cardiometabolic abnormalities: fasting glucose at least 100 mg/dL or diabetes medication use; BP at least 130/85 mm Hg, triglyceride level at least 150 mg/L, HDL cholesterol level 40 mg/dL or less and high-sensitivity C-reactive protein level greater than the 90th percentile. Researchers used Cox proportional hazard models to estimate HRs for all-cause, CVD and cancer-related mortality.

Within the cohort, 1,918 were considered to have metabolically unhealthy obesity, and 1,815 had metabolic healthy obesity. During a mean follow-up of 18.5 years, 868 participants died, with 622 considered to have metabolically unhealthy obesity.

Researchers observed a markedly increased risk for all-cause mortality and CVD death in adults with the metabolically unhealthy obesity phenotype and a high DII score. For those with the metabolically unhealthy obesity phenotype in the third tertile of DII score, HR for all-cause mortality was 1.44 (95% CI, 1.11-1.86) and HR for CVD mortality was 3.29 (95% CI, 2.01-5.37) vs. those with the same phenotype in the lowest DII tertile, according to researchers. A 1-standard deviation increase in DII score was also positively associated with risk for all-cause (HR = 1.08; 95% CI, 0.99-1.18) and CVD mortality (HR = 1.4; 95% CI, 1.18-1.66).

However, in participants considered to have metabolically healthy obesity, researchers observed no link between DII score, all-cause or CVD mortality. There was no association between DII score and cancer-related mortality for either phenotype, according to researchers.

“Of note is that the positive association between high DII score and mortality was observed only in the [metabolically unhealthy obesity] phenotype, suggesting that proinflammatory diets may aggravate the mortality risk exclusively in overweight or obese individuals with metabolic abnormalities,” the researchers wrote.

The researchers added that adherence to a high-quality diet, defined by Dietary Approaches to Stop Hypertension (DASH)-style prescription and the Healthy Eating Index, was associated with decreased mortality, but only in the metabolically obese normal-weight phenotypes and not in metabolically healthy normal-weight phenotypes.

“These results collectively suggest that certain dietary patterns may have differential effects according to the baseline metabolic phenotype,” the researchers wrote. “This, possibly synergistic, relationship between diet and metabolic phenotype may underscore the need for dietary interventions specified for each metabolic phenotype.” – by Regina Schaffer

Disclosures: The authors report no relevant financial disclosures.

Among adults with metabolically healthy obesity, a proinflammatory diet is not associated with increased risk for all-cause and cardiovascular mortality, but this risk persists for those with metabolically unhealthy obesity who adhere to the same diet, according to findings published in Clinical Nutrition.

Yong-Moon Mark Park, MD, PhD, MS, an epidemiologist with the National Institute of Environmental Health Sciences in Research Triangle Park, North Carolina, and colleagues analyzed data from 3,733 adults with overweight or obesity without history of previous CVD participating in the 1988-1994 waves of the National Health and Nutrition Examination Survey. Researchers assessed dietary intake via a 24-hour dietary recall, using the findings to calculate dietary inflammatory index (DII) score, a standardized scoring system to assess the influence of diet on inflammation. Researchers also evaluated metabolic parameters, including BMI, blood pressure, serum glucose, serum insulin, triglycerides and HDL cholesterol. Participants were defined as metabolic unhealthy if they had two or more of the following cardiometabolic abnormalities: fasting glucose at least 100 mg/dL or diabetes medication use; BP at least 130/85 mm Hg, triglyceride level at least 150 mg/L, HDL cholesterol level 40 mg/dL or less and high-sensitivity C-reactive protein level greater than the 90th percentile. Researchers used Cox proportional hazard models to estimate HRs for all-cause, CVD and cancer-related mortality.

Within the cohort, 1,918 were considered to have metabolically unhealthy obesity, and 1,815 had metabolic healthy obesity. During a mean follow-up of 18.5 years, 868 participants died, with 622 considered to have metabolically unhealthy obesity.

Researchers observed a markedly increased risk for all-cause mortality and CVD death in adults with the metabolically unhealthy obesity phenotype and a high DII score. For those with the metabolically unhealthy obesity phenotype in the third tertile of DII score, HR for all-cause mortality was 1.44 (95% CI, 1.11-1.86) and HR for CVD mortality was 3.29 (95% CI, 2.01-5.37) vs. those with the same phenotype in the lowest DII tertile, according to researchers. A 1-standard deviation increase in DII score was also positively associated with risk for all-cause (HR = 1.08; 95% CI, 0.99-1.18) and CVD mortality (HR = 1.4; 95% CI, 1.18-1.66).

However, in participants considered to have metabolically healthy obesity, researchers observed no link between DII score, all-cause or CVD mortality. There was no association between DII score and cancer-related mortality for either phenotype, according to researchers.

“Of note is that the positive association between high DII score and mortality was observed only in the [metabolically unhealthy obesity] phenotype, suggesting that proinflammatory diets may aggravate the mortality risk exclusively in overweight or obese individuals with metabolic abnormalities,” the researchers wrote.

The researchers added that adherence to a high-quality diet, defined by Dietary Approaches to Stop Hypertension (DASH)-style prescription and the Healthy Eating Index, was associated with decreased mortality, but only in the metabolically obese normal-weight phenotypes and not in metabolically healthy normal-weight phenotypes.

“These results collectively suggest that certain dietary patterns may have differential effects according to the baseline metabolic phenotype,” the researchers wrote. “This, possibly synergistic, relationship between diet and metabolic phenotype may underscore the need for dietary interventions specified for each metabolic phenotype.” – by Regina Schaffer

Disclosures: The authors report no relevant financial disclosures.