For more than 2000 years, vinegar has been used to flavor and preserve foods, heal wounds, fight infections, clean surfaces, and manage diabetes. Although vinegar is highly valued as a culinary agent, some varieties costing $100 per bottle, much scrutiny surrounds its medicinal use. Scientific investigations do not support the use of vinegar as an anti-infective agent, either topically or orally. Evidence linking vinegar use to reduced risk for hypertension and cancer is equivocal. However, many recent scientific investigations have documented that vinegar ingestion reduces the glucose response to a carbohydrate load in healthy adults and in individuals with diabetes. There is also some evidence that vinegar ingestion increases short-term satiety. Future investigations are needed to delineate the mechanism by which vinegar alters postprandial glycemia and to determine whether regular vinegar ingestion favorably influences glycemic control as indicated by reductions in hemoglobin A1c. Vinegar is widely available; it is affordable; and, as a remedy, it is appealing. But whether vinegar is a useful adjunct therapy for individuals with diabetes or prediabetes has yet to be determined.
The antiglycemic effect of vinegar was first reported by Ebihara and Nakajima in 1988. In rats, the blood glucose response to a 10% corn starch load was significantly reduced when coadministered with a 2% acetic acid solution. In healthy human subjects, although the glucose response curve was not significantly altered, the area under the insulin response curve following the ingestion of 50 g sucrose was reduced 20% when coadministered with 60 mL strawberry vinegar.Several years later, Brighenti and colleagues demonstrated in normoglycemic subjects that 20 mL white vinegar (5% acetic acid) as a salad dressing ingredient reduced the glycemic response to a mixed meal (lettuce salad and white bread containing 50 g carbohydrate) by over 30% (P < .05). Salad dressings made from neutralized vinegar, formulated by adding 1.5 g sodium bicarbonate to 20 mL white vinegar, or a salt solution (1.5 g sodium chloride in 20 mL water) did not significantly affect the glycemic response to the mixed meal.Separate placebo-controlled trials have corroborated the meal-time, antiglycemic effects of 20 g vinegar in healthy adults.[49–51]
While compiling a glycemic index (GI) table for 32 common Japanese foods, Sugiyama and colleagues documented that the addition of vinegar or pickled foods to rice (eg, sushi) decreased the GI of rice by 20% to 35%. In these trials, healthy fasted subjects ingested the reference and test foods, each containing 50 g carbohydrate, on random days, and the food GI was calculated using the areas under the 2-hour blood glucose response curves. In the vinegar-containing foods, the amount of acetic acid was estimated to be 0.3-2.3 g, an amount similar to that found in 20 g vinegar (approximately 1 g). Ostman and colleagues reported that substitution of a pickled cucumber (1.6 g acetic acid) for a fresh cucumber (0 g acetic acid) in a test meal (bread, butter, and yogurt) reduced meal GI by over 30% in healthy subjects.
Recently, the antiglycemic property of vinegar was demonstrated to extend to individuals with marked insulin resistance or type 2 diabetes. In this crossover trial, individuals with insulin resistance (n = 11, fasting insulin concentrations greater than 20 mU/mL) or with diagnosed type 2 diabetes (n = 10) consumed a vinegar test drink (20 g vinegar, 40 g water, 1 tsp saccharine) or placebo immediately before the consumption of a mixed meal (87 g total carbohydrate). In the insulin-resistant subjects, vinegar ingestion reduced postprandial glycemia 64% as compared with placebo values (P = .014) and improved postprandial insulin sensitivity by 34% (P= .01). In individuals with type 2 diabetes, vinegar ingestion was less effective at reducing mealtime glycemia (−17%, P = .149); however, vinegar ingestion was associated with a slight improvement in postprandial insulin sensitivity in these subjects (+19%, P = .07). The lack of a significant effect of vinegar on mealtime glycemia in the type 2 diabetics may be related to the use of venous blood sampling in this trial. Greater within-subject variation in glucose concentrations are noted for venous blood as compared with capillary blood; moreover, the concentration of glucose in venous blood is lower than that in capillary blood. Thus, capillary blood sampling is preferred for determining the glycemic response to food.
The marked antiglycemic effect of vinegar in insulin-resistant subjects is noteworthy and may have important implications. Multicenter trials have demonstrated that treatment with antiglycemic pharmaceuticals (metformin or acarbose) slowed the progression to diabetes in high-risk individuals; moreover, because these drugs improved insulin sensitivity, the probability that individuals with impaired glucose tolerance would revert to a normal, glucose-tolerant state over time was increased.
In healthy subjects, Ostman and colleagues demonstrated that acetic acid had a dose-response effect on postprandial glycemia and insulinemia. Subjects consumed white bread (50 g carbohydrate) alone or with 3 portions of vinegar containing 1.1, 1.4, or 1.7 g acetic acid. At 30 minutes post-meal, blood glucose concentrations were significantly reduced by all concentrations of acetic acid as compared with the control value, and a negative linear relationship was calculated between blood glucose concentrations and the acetic acid content of the meal (r = −0.47, P = .001). Subjects were also asked to rate feelings of hunger/satiety on a scale ranging from extreme hunger (−10) to extreme satiety (+10) before meal consumption and at 15-minute intervals after the meal. Bread consumption alone scored the lowest rating of satiety (calculated as area under the curve from time 0-120 minutes). Feelings of satiety increased when vinegar was ingested with the bread, and a linear relationship was observed between satiety and the acetic acid content of the test meals (r = 0.41, P = .004).
In a separate trial, healthy adult women consumed fewer total calories on days that vinegar was ingested at the morning meal. In this trial, which used a blinded, randomized, placebo-controlled, crossover design, fasting participants consumed a test drink (placebo or vinegar) followed by the test meal composed of a buttered bagel and orange juice (87 g carbohydrate). Blood samples were collected for 1 hour after the meal. At the end of testing, participants were allowed to follow their normal activities and eating patterns the remainder of the day, but they were instructed to record food and beverage consumption until bedtime. Vinegar ingestion, as compared with placebo, reduced the 60-minute glucose response to the test meal (−54%, P < .05) and weakly affected later energy consumption (−200 kilocalories, P = .111). Regression analyses indicated that 60-minute glucose responses to test meals explained 11% to 16% of the variance in later energy consumption (P < .05).Thus, vinegar may affect satiety by reducing the meal-time glycemic load. Of 20 studies published between 1977 and 1999, 16 demonstrated that low-glycemic index foods promoted postmeal satiety and/or reduced subsequent hunger.
It is not known how vinegar alters meal-induced glycemia, but several mechanisms have been proposed. Ogawa and colleagues examined the effects of acetic acid and other organic acids on disaccharidase activity in Caco-2 cells.Acetic acid (5 mmol/L) suppressed sucrase, lactase, and maltase activities in concentration- and time-dependent manners as compared with control values, but the other organic acids (eg, citric, succinic, L-maric, and L-lactic acids) did not suppress enzyme activities. Because acetic acid treatment did not affect the de-novo synthesis of the sucrase-isomaltase complex at either the transcriptional or translational levels, the investigators concluded that the suppressive effect of acetic acid likely occurs during the posttranslational processing of the enzyme complex. Of note, the lay literature has long proclaimed that vinegar interferes with starch digestion and should be avoided at meal times.
Several investigations examined whether delayed gastric emptying contributed to the antiglycemic effect of vinegar. Using noninvasive ultrasonography, Brighenti and colleagues did not observe a difference in gastric emptying rates in healthy subjects consuming bread (50 g carbohydrate) in association with acetic acid (ie, vinegar) vs sodium acetate (ie, vinegar neutralized by the addition of sodium bicarbonate); however, a significant difference in post-meal glycemia was noted between treatments with the acetic acid treatment lowering glycemia by 31.4%. In a later study, Liljeberg and Bjorck added paracetamol to the bread test meal to permit indirect measurement of the gastric emptying rate. Compared with reference values, postmeal serum glucose and paracetamol concentrations were reduced significantly when the test meal was consumed with vinegar. The results of this study should be carefully considered, however, because paracetamol levels in blood may be affected by food factors and other gastrointestinal events. In rats fed experimental diets containing the indigestible marker polyethylenglycol and varying concentrations of acetic acid (0, 4, 8, 16 g acetic acid/100 g diet), dietary acetic acid did not alter gastric emptying, the rate of food intake, or glucose absorption.
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