The present data suggest that dietary acetic acid may help lower fasting blood glucose in people with diabetes, and lower triglycerides in people with overweight and obesity, as well as with type 2 diabetes. However, in the two studies in healthy, non-overweight or obese participants included in this systematic review, no benefits were detected. The intervention also had no effect on BMI or body fat, regardless of which group it was studied in. Overall, people with type 2 diabetes or with overweight or obesity are the most likely to see benefit on cardiometabolic risk factors from acetic acid supplementation.
These data are supported by previous meta-analyses that examined the effects of acetic acid supplementation on both postprandial glucose levels as well as fasting glucose levels. One of these meta-analyses, which focused on the acute effects of vinegar ingestion, found that the consumption of acetic acid in the form of vinegar with a meal lowered both postprandial glucose and insulin levels. Another meta-analysis that focused on trials performed in participants with type 2 diabetes found that consuming acetic acid in the form of vinegar led to lower fasting blood glucose. However, unlike the current study, this study found that acetic acid also lowered HbA1c. Also unlike the meta-analysis at hand, the authors observed reductions in body weight and fat mass. Preclinical studies performed in mice also support these findings, as acetic acid and vinegar improved serum lipids in diet-induced obese mice.
Even if statistically significant benefits are established to exist, the question of clinical relevance regarding the achieved glucose and lipid improvements remains. One way to determine clinical relevance is to compare the effects seen in this study to pharmaceutical effects. The present study found that in people with diabetes, acetic acid supplementation lowered fasting blood glucose by about 35 mg/dL, while metformin lowers blood glucose by about 20 mg/dL at lower doses and about 80 mg/dL at higher doses. Furthermore, the present study did not find any statistically significant reduction in HbA1c, which is a measure of longer-term glycemic control, whereas metformin has shown reductions in HbA1c of about 1–2%, depending on the dosage used. While the present study did not find it to be statistically significant, there may indeed be a benefit on HbA1c, given the confidence intervals (CI: -2.95–0.16). Acetic acid lowered fasting triglycerides by about 21 mg/dL, while the fibrate class of drugs used for lowering blood lipids in people with diabetes showed reductions between 50mg/dL and 180 mg/dL, with reductions of up to 50% seen in some trials.
Figure 2: How the effects of acetic acid compare to select drugs
Garber et al. Am J Med. 1997 Dec.
Damci et al. Eur J Intern Med. 2003 Oct.
There are several proposed mechanisms by which acetic acid might improve cardiometabolic risk factors in people with diabetes, metabolic syndrome, or obesity. In rodent studies and in vitro studies, acetic acid has been shown to activate a protein called AMP-activated protein kinase (AMPK) which stimulates glucose uptake and lipid oxidation (AMPK is one of the targets of the drug metformin). Additionally, studies in diet-induced obese mice found that acetic acid increases the expression of genes regulating fatty acid oxidation in the liver and attenuates body fat accumulation in mice. In a previous study in humans with type 2 diabetes, acute acetic acid consumption improved glucose kinetics without substantially altering lipid metabolism, suggesting an acute increase in insulin sensitivity, possibly through AMPK. There are also some hints from animal research suggesting that the gut microbiome may play a role in vinegar’s mechanism of action.
The study under review has some limitations that should be considered when interpreting the results. First, there was a relatively high risk of bias, with about 63% (10/16) of the studies showing a “high risk” of bias, and only about 13% (2/16) showing a “low risk” of bias. Second, there was no standardization of the form of acetic acid consumed across trials, nor was there any real control for dosing, either experimentally or statistically, which may be important, given the previous dose-response experiments. Third, there were relatively few trials among different populations, which limits the power of the analysis and the ability to draw conclusions. Finally, the present study did not examine the effect of the length of the intervention, as the duration of included studies ranged from 4 to about 13 weeks.
Previous meta-analyses are consistent with the current findings of reduced fasting blood glucose levels as a result of acetic acid supplementation, and previous randomized trials and preclinical data provide evidence to support the reduction in triglycerides seen in people with type 2 diabetes. However, the overall quantity and quality of the evidence is low. In this context, the overall high risk of bias, various potentially outcome-relevant methodological differences between the input studies, and subgroup analyses based on few, or in one case only two, studies, should be kept in mind.