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Clinical care/Education/Nutrition
Effects of carbohydrate quality and amount on plasma lactate: results from the OmniCarb trial
  1. Jiun-Ruey Hu1,
  2. Yingfei Wu2,
  3. Frank M Sacks3,
  4. Lawrence J Appel2,
  5. Edgar R Miller III2,
  6. J Hunter Young2,
  7. Stephen P Juraschek4
  1. 1Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA
  2. 2Welch Center for Epidemiology, Prevention, and Clinical Research, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, USA
  3. 3Department of Nutrition, Harvard University T H Chan School of Public Health, Boston, Massachusetts, USA
  4. 4Division of General Medicine and Primary Care, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
  1. Correspondence to Dr Stephen P Juraschek; sjurasch{at}bidmc.harvard.edu

Abstract

Introduction Plasma lactate is a marker of non-oxidative glucose metabolism associated with progression to diabetes. We examined the effect of carbohydrate quality (glycemic index (GI)) and amount (%kcal) on plasma lactate. We hypothesized that low GI (≤45 (g)) versus high (≥65 (G)) and low %kcal from carbohydrate (40% kcal (c)) versus high (58% kcal (C)) each would reduce lactate levels.

Research design and methods We measured lactate in OmniCarb, a randomized, cross-over trial of four diets in overweight/obese adults without diabetes or cardiovascular disease (N=163). The four diets were high carbohydrate+high GI (CG, reference), high carbohydrate+low GI (Cg), low carbohydrate+high GI (cG), and low carbohydrate+low GI (cg). Participants (N=163) consumed each of the four diets over a 5-week period, separated by 2-week washout periods. Plasma lactate levels were measured at baseline, during which the participants consumed their own diets, and after each 5-week period.

Results Baseline plasma lactate was 1.2 mmol/L. In the setting of high carbohydrate amount, reducing GI lowered plasma lactate non-significantly by 0.08 mmol/L (Cg vs CG: 95% CI −0.16 to 0.00; p=0.06). In the setting of high GI, reducing carbohydrate amount lowered plasma lactate by 0.10 mmol/L (cG vs CG: 95% CI −0.19 to −0.02; p=0.02). The combined effect of reducing GI and carbohydrate proportion in the diet (cg vs CG) was similar (cg vs CG: −0.08; 95% CI −0.16 to 0.00; p=0.04). All four diets reduced plasma lactate compared with baseline.

Conclusions Compared with a diet with high GI and high carbohydrate amount, diets with low GI and/or low carbohydrate amount reduced plasma lactate. Whether this change in lactate leads to long-term change in glucose metabolism needs to be examined.

Trial registration number NCT00608049.

  • lactic acidosis
  • carbohydrates
  • diet
  • insulin resistance
http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/bmjdrc-2020-001457

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    Footnotes

    • Twitter @ruey_hu, @LarryAppel, @ermiller14, @spjuraschek

    • Presented at This project was presented as a poster at the 2019 Scientific Sessions of the American Heart Association (AHA) in Philadelphia, Pennsylvania on November 16, 2019.

    • Contributors SPJ designed the study, conducted data collection, performed primary data analyses, and critically reviewed the manuscript. J-RH interpreted the data and wrote the paper. YW performed secondary data analysis. FMS, LJA, and JHY provided critical reading of the manuscript and comments. ERM designed the study and provided critical reading of the manuscript and comments. All coauthors provided final approval of the article. SPJ takes final responsibility for the final content.

    • Funding The OmniCarb study was supported by NIH grants HL-084568 and HL-084568. SPJ’s work was supported by K23HL135273 and R21HL144876. J-RH was supported by the Linda Kao Memorial Fund.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Ethics approval The study protocol was approved by the institutional review boards at Johns Hopkins University (IRB# NA_00014138) and the Harvard School of Public Health (IRB# 2007 P-001351).

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data availability statement Data are available upon reasonable request.