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Vinegar intake is considered a food item that improves blood glucose in humans. This review aimed to discuss studies that investigated the impact of vinegar intake on the glycemic profile in humans and the putative mechanistic cellular pathways in both human and animal models. A search of literature was performed on the Cochrane, MEDLINE and Web of Science databases for articles published between 1995 and 2018. There is considerable support for vinegar having a positive acute effect on blood glucose levels when combined with carbohydrate-rich meals. Conversely, there are few chronic interventions analyzing the impact of vinegar intake on blood glucose. Based on available evidence, we hypothesize three pathways by which vinegar may improve blood glucose: The inhibition of α-amylase action; increased glucose uptake; and mediation by transcription factors. When evaluating the current body of literature, daily vinegar intake in amounts of ∼10-30 mL (∼2-6 tablespoons) appear to improve the glycemic response to carbohydrate-rich meals; however, there is a paucity of studies investigating chronic effects of vinegar intake.
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Review
Vinegar (acetic acid) intake on glucose metabolism: A narrative
review
Heitor O. Santos
a
,
*
, Wilson M.A.M. de Moraes
b
, Guilherme A.R. da Silva
c
,
Jonato Prestes
b
, Brad J. Schoenfeld
d
a
School of Medicine, Federal University of Uberlandia (UFU), Uberlandia, Minas Gerais, Brazil
b
Graduation Program on Physical Education, Catholic University of Brasilia (UCB), Brasília, Federal District, Brazil
c
Federal University of the State of Rio de Janeiro (UNIRIO), Brazil
d
Department of Health Sciences, CUNY Lehman College, Bronx, NY, USA
article info
Article history:
Received 16 May 2019
Accepted 17 May 2019
summary
Vinegar intake is considered a food item that improves blood glucose in humans. This review aimed to
discuss studies that investigated the impact of vinegar intake on the glycemic prole in humans and the
putative mechanistic cellular pathways in both human and animal models. A search of literature was
performed on the Cochrane, MEDLINE and Web of Science databases for articles published between 1995
and 2018. There is considerable support for vinegar having a positive acute effect on blood glucose levels
when combined with carbohydrate-rich meals. Conversely, there are few chronic interventions analyzing
the impact of vinegar intake on blood glucose. Based on available evidence, we hypothesize three
pathways by which vinegar may improve blood glucose: The inhibition of
a
-amylase action; increased
glucose uptake; and mediation by transcription factors. When evaluating the current body of literature,
daily vinegar intake in amounts of ~10e30 mL (~2e6 tablespoons) appear to improve the glycemic
response to carbohydrate-rich meals; however, there is a paucity of studies investigating chronic effects
of vinegar intake.
©2019 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights
reserved.
1. Introduction
For centuries, vinegar has been widely used as a dietary spice and
natural remedy for various ailments in folk medicine. Moreover, it is
considered a super foodby laypersons, purported to improve
weight loss, digestion and skin quality; so much so that there are
even vinegar diets. The earliest report dates back 2300 years
whereby Hippocrates (c. 420 BC) used vinegar for wound care [1].
Vinegar is a sour-tasting liquid obtained from the anaerobic
conversion of sugars to ethanol by yeasts and aerobic oxidation of
ethanol to acetic acid by bacteria. It may be classied in accordance
with raw materials grain vinegar, such as those obtained from rice
and wheat, or as fruitvinegars, including juices from grape, apple
and coconut [2].
Over the past few decades the prevalence of disorders related to
glucose homeostasissuch as Type 2 diabetes mellitus(T2DM), obesity
and nonalcoholic fatty liver disease has dramatically increased
throughout most of the world [3,4]. Despite many efforts, the current
therapeutic options for the treatment of these disorders remain far
from satisfactory, in part due to serious side effects following phar-
macologic treatment [5].Therefore,newcompoundswithpotential
preventive and therapeutic effects are continually being sought.
A plethora of benets have been proposed for the intake of
vinegar as a non-pharmacological alternative for subjects with
diabetes [1,6,7]. In addition, acetic acid, one of the major compo-
nents of vinegar, is a potential modulator of glucose metabolism in
horses and rodents [8e11]. Hence, the aim of this narrative review
is to provide an overview as to the impact of acute and chronic
vinegar intake on the glycemic prole.
2. Method
A search of literature was performed on the Cochrane, MEDLINE
and Web of Science databases for articles published between 1995
and 2018 using the following combinations of keywords: acetic
*Corresponding author. Federal University of Uberlandia, Av. Para, nº1720 Bloco
2U Campus Umuarama, 38400-902, Uberlandia, Minas Gerais, Brazil.
E-mail address: heitoroliveirasantos@gmail.com (H.O. Santos).
Contents lists available at ScienceDirect
Clinical Nutrition ESPEN
journal homepage: http://www.clinicalnutritionespen.com
https://doi.org/10.1016/j.clnesp.2019.05.008
2405-4577/©2019 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.
Clinical Nutrition ESPEN xxx (xxxx) xxx
Please cite this article as: Santos HO et al., Vinegar (acetic acid) intake on glucose metabolism: A narrative review, Clinical Nutrition ESPEN,
https://doi.org/10.1016/j.clnesp.2019.05.008
acid blood glucose,apple cider vinegar,apple cider vinegar
health,vinegar blood glucose,vinegar blood insulin,vinegar
diabetes. Human interventions that performed glycemic
analyses with vinegar ingestion were included. Moreover, animal
studies were included to help elucidate potential mechanisms
of action.
3. Mechanism of actions in animal studies
Nakao et al. [12] submitted rats to a protocol of exhaustive
swimming and observed that immediate post-exercise provision of
a combination of acetic acid plus glucose resulted in higher liver
glycogen stores than either glucose or acetic acid alone within 2 h
after exercise. This nding suggests that consumption of oral acetic
acid with glucose can facilitate liver glycogen restoration during the
early period of recovery. It should be noted that effects of acetic acid
on glycogen repletion were only apparent when simultaneously
consumed with glucose, a precursor of glycogen synthesis. Simi-
larly, Fushimi et al. [8] pre-conditioned rats to 7 days of swimming
exercise and then, after an overnight fast, submitted them to a 2-h
swimming bout. Following the bout, the rodents were fed glucose
with or without provision of acetic acid. Results indicated that
acetic acid led to a greater preservation of soleus and gastrocne-
mius glycogen content, and this effect was dependent on the acti-
vation of glycogen synthase.
Research by Fushimi et al. [8e10] found that acetic acid de-
creases the synthesis of the enzymes xylulose-5-phosphate and
fructose-2,6-biphosphatase in the liver, and also the ratio of fruc-
tose-1,6-bisphosphate to fructose-6-phosphate in skeletal muscle.
It hence decreases the activity of phosphofructokinase-1 and he-
patic malonyl-CoA (Fig. 1). Furthermore, since malonyl-CoA allo-
sterically inhibits carnitine palmitoyl-transferase, its inhibition
provides an increase in the action of carnitine palmitoyl-transferase
and consequently in
b
-oxidation. This increase of hepatic
b
-oxida-
tion is a possible mechanism that corroborates the results of Kondo
et al. [13], who reported a decrease in visceral fat in patients sub-
mitted to vinegar intake.
Pan et al. [14] demonstrated that oral administration of acetic
acid (10 mL/kg body weight once daily) in mice subjected to 8
weeks of treadmill exercise promoted a greater expression of AMP-
activated protein kinase (AMPK), phosphorylated AMPK (pAMPK),
peroxisome proliferator-activated receptor delta (PPAR
d
) mRNA,
and peroxisome proliferator-activated receptor gamma coactivator
1-alpha (PGC-1
a
) levels in the soleus muscle. Moreover, acetic acid
increased myosin heavy chain (MHC) oxidative type I and mixed
oxidative-glycolytic type IIa expression, while increasing the IIb
isoforms; results indicative of an enhanced endurance exercise
capacity. Taken together these ndings suggest that both acute and
chronic acetic acid ingestion can optimize the restoration of muscle
glycogen and increase fatty acid oxidation. The proposed mecha-
nisms are illustrated in Fig. 2.
4. Mechanism of actions in human studies
Mitrou et al. [15,16] showed that enhanced stimulation of
glucose uptake caused by apple cider vinegar consumption may, at
least partly, reduce the need for insulin secretion. To investigate
these mechanistic actions, eleven insulin-resistant individuals
were randomized to receive either 30 mL of apple cider vinegar or
placebo before a test meal consisting of bread, cheese, ham, orange
juice, butter and a cereal bar (equivalent to 75 g of carbohydrates).
Compared with placebo, results showed that vinegar intake
decreased insulinemia, while increasing blood ow and glucose
uptake [15]. Several studies corroborate the ndings of Mitrou
et al., lending support to the hypothesis that the glycemic benets
of vinegar may be attributed to an improvement in glucose uptake
[8e10]. Waller et al. (2009) provided horses with a hypertonic so-
dium acetate-acetic acid solution via nasogastric gavage followed
by a typical hay-grain meal (acetate treatment) or a hay-grain meal
alone (control treatment) after exhaustive exercise [11]. Acetate
supplementation resulted in an enhanced rate of muscle glycogen
resynthesis in skeletal muscle during the initial 4 h of the recovery
period.
Fig. 1. Blood glucose improvement hypothesis through acetic acid action in the
musculoskeletal system and liver. Rats fed acetic acid, which is a substance found in
vinegars that improves glucose metabolism, exhibit lower glycolysis in the liver and
musculoskeletal system, thus improving the glycogen restoration [8e10]. The known
glycolysis inhibition by acetic acid in rats is represented by an X symbol.
Fig. 2. Exercise training, coupled with vinegar intake, may improve glucose uptake
and increase expression of genes involved in mitochondrial respiration and fatty acid
oxidation [14]. Acetic acid across vinegar may promote fatty acid oxidation, sparing of
muscle and liver glycogen utilization during exercise by AMPK stimulation, which
optimizes muscle glycogen replacement and enhances glucose uptake after exercise.
AMPK phosphorylation/activation results in GLUT4 translocation from intracellular
storage depots to the plasma membrane (1) and activation of PGC-1
a
and its trans-
location to the mitochondria (2) and nucleus (3). In the mitochondria, PGC-1
a
activates
additional transcription factors, which thereby increases the expression of key mito-
chondrial proteins involved with mitochondrial biogenesis, potentially culminating in
improved endurance capacity. Among lipid pathways, elevated free fatty acids activate
the nuclear transcription factor PPAR-
d
(4), whereas increased expression of the CPT1,
HSL and UCPs proteins, as well as inhibition of muscle ACC2, mediate reduction in the
lipogenesis (5). AMPK, AMP-activated protein kinase; HSL, hormone-sensitive lipase;
mtDNA, mitochondrial DNA; nDNA, nuclear DNA; pAMPK, phosphorylated AMPK;
PGC-1
a
, peroxisome proliferator-activated receptor gamma coactivator 1-alpha; PPAR-
d
Peroxisome proliferator-activated receptor delta; UCP, uncoupling protein.
H.O. Santos et al. / Clinical Nutrition ESPEN xxx (xxxx) xxx2
Please cite this article as: Santos HO et al., Vinegar (acetic acid) intake on glucose metabolism: A narrative review, Clinical Nutrition ESPEN,
https://doi.org/10.1016/j.clnesp.2019.05.008
5. Vinegar action during carbohydrate digestion
Given that an alkaline condition is required for optimal carbo-
hydrate digestion [17], the acid properties of vinegar can result in
hindered absorption when consumed with a carbohydrate-rich
meal (Fig. 3). This is supported by in vitro data showing that a
decrease in pH below 4.0 inactivates
a
-amylase [18]. However, a
recent in vivo study found that
a
-amylase hydrolyzed up to 80% of
bread starch in the rst 30 min of gastric digestion [19]. Therefore,
given that the pH of commercially marketed vinegars is about 2e3
[1,20], its consumption may inactivate the salivary
a
-amylase ac-
tion and decrease its release until nutrients reach the small intes-
tine, whose passage is responsible for 30e40% of complex
carbohydrate digestion [17]. Furthermore, vinegar acid does not
appear to damage the stomach lining, since its pH is less acidic than
gastric juice and common acidic beverages (e.g. lemon Juice and
Coca-Cola®Classic) (Table 1).
6. Acute impact of vinegar intake following carbohydrate-
rich meals
Johnston et al. [24] sought to test the hypothesis that vinegar
intake decreases the postprandial glycemic response only in meals
composed of complex carbohydrates. Employing a crossover
design, diabetics (n ¼9) and non-diabetics (n ¼29) received 10 g of
apple cider vinegar added to the test meal of a bagel and orange
juice or dextrose and orange juice. Compared to placebo (without
vinegar), glycemia was 20% lower in the area under the curve
120 min after the meal, whilst the consumption of vinegar with
dextrose did not show any glycemic improvement [24].
Since publication of the seminal study by Brighenti et al. (1995),
in which vinegar in the form of salad dressing signicantly altered
the glycemic response to a mixed meal [25], a number of studies
have endeavored to further investigate this topic in healthy sub-
jects (Table 2) and in those with glucose disturbances (Table 3). As
noted in these tables, most of the studies supporting a role for
vinegar as a glucose-lowering nutraceutical are based on acute tests
on its interaction with carbohydrate-rich meals. The usual studied
dose is 20 g of vinegar per meal [25e30], which is equivalent to 1 g
of acetic acid [26]. Converting to homemade measures, 20 g of
vinegar corresponds to approximately 4 tablespoons [26].
7. Impact of vinegar intake based on chronic interventions
Chronic interventions show that vinegar can improve glycemic
and lipid proles in those with type 2 diabetes (T2DM) and dysli-
pidemia [37,38]. Mahmoodi et al. divided 60 patients with T2DM
into two groups: 15 mL intake of apple cider vinegar per day or
control [37]. After one month, subjects who ingested vinegar
decreased glycemia and glycated hemoglobin (HbA1c) from
175 mg/dL to 156 mg/dL and from 7.56% to 7.03%, respectively. In
another study, hyperlipidemic subjects (14 men and 5 women
subjects) who consumed 30 mL of apple cider vinegar twice daily
for 8 weeks decreased serum concentrations of total cholesterol
(45 in men and 51 mg/dL in women), triglycerides (105 in men
and 109 mg/dL in women) and LDL (39 in men and 20 mg/dL in
women) from baseline, whereas HDL levels did not change [39].
Alternatively, a parallel, randomized, double-blind, placebo-
controlled study of 97 participants found that daily consumption of
Fig. 3. Blood glucose improvement hypothesis through vinegar action in the
a
-amylase inhibition. When vinegar is ingested alongside carbohydrates-rich meals, a blood glucose
improvement is believed to occur due to the
a
-amylase inhibition. Hence, there should be lower carbohydrate digestion until the nutrients reach the stomach,which results in lower
blood glucose levels.
Table 1
pH of common vinegar types and other substances Adapted from Reddy et al.,
2016; Tawo et al., 2009; Zandim et al., 2004 [21e23].
Common food items and substances pH
Hydrochloric Acid (1 mol/L) <1.0
Gastric Juice 1e3
Lemon Juice 2.3
Coca-Cola®Classic 2.4
Rice Vinegar 2.5
White Wine 2.5
Apple Vinegar 2.7
Ethanol 2.8
Teas 2.9e5.2
Pineapple 3.3
Balsamic Vinegar 3.4
Orange 3.6
Tomato 4.2
Coffee 5.1
Urine 6.0
Distilled Water 5.9
Pure Water 7.0
Blood 7.4
Baking Soda Solution 8.4
Toothpaste 9.9
Milk of Magnesia 10.5
Sodium Hydroxide (1 mol/L) 14.0
H.O. Santos et al. / Clinical Nutrition ESPEN xxx (xxxx) xxx 3
Please cite this article as: Santos HO et al., Vinegar (acetic acid) intake on glucose metabolism: A narrative review, Clinical Nutrition ESPEN,
https://doi.org/10.1016/j.clnesp.2019.05.008
30 mL of apple cider vinegar for two months did not improve lipid
and HbA1c levels; however, the subjects were non-diabetics with
normal lipid concentrations [38].
The longest study analyzing vinegar intake lasted twelve weeks
[13]. Overweight Japanese patients were divided into one of three
groups: 15 mL of apple cider vinegar (n ¼51), 30 mL of apple cider
vinegar (n ¼54), or placebo (n ¼50). In contrast to most of the
acute studies and short-term studies, glycemic prole did not
change (glycemia remained ~90 mg/dL, insulinemia ~10
m
IU/mL
and HbA1c ~5.3%). However, there was a reduction of serum tri-
glycerides and visceral fat in the groups that ingested vinegar.
Interestingly, participants who consumed 30 mL of apple cider
vinegar showed a 41 mg/dL (157e116 mg/dL) reduction in serum
triglycerides, but levels returned to baseline four weeks after of the
end of intervention. Serum cholesterol levels also decreased in the
group consuming a higher vinegar intake (220e207 mg/dL), while
HDL and LDL levels did not change. Body weight decreased by two
kilograms (from 73 to 71 kg) in the group ingesting 30 mL of vin-
egar per day, while the group that ingested 15 mL/day lost one kg
(from 74 to 73 kg). Alternatively, the placebo group presented a
slight body weight increase (200 g). Notwithstanding, this study
had a number of controls that enhanced validity, including equating
caloric intake between groups (~1800 calories/d), limiting alcohol
intake, avoiding functional foods, and prohibiting vinegar con-
sumption other than that provided in the study. Thus, given the
greater fat loss reported in the vinegar groups compared to con-
trols, vinegar can be considered more effective than many ther-
mogenic supplements touted as fat burners [40,41].
Vinegar use shows promise for the treatment of polycystic ovary
syndrome (PCOS). Wu et al. [42] demonstrated that consumption of
a beverage containing 15 mL of apple cider vinegar for 90e110 d
resulted in decreased markers of insulin resistance in six of the
seven subjects and reduced the luteinizing hormone/follicle-
stimulating hormone ratio in ve of the subjects. Moreover,
ovulatory menstruation was restored within 40 days in four of the
subjects. While these ndings are intriguing, the study was limited
by a small sample size and lack of a control group.
8. Side-effects
Chronic intake of excessive amounts of vinegar can cause
serious health problems. A large administration of apple cider
vinegar regularly for 6 years was associated with high urinary
excretion of potassium, sodium and bicarbonate and stimulated
plasma renin activity in a 28-year-old patient admitted to the
hospital because of muscle cramps and hypokalemia. The patient
ingested ~250 mL of vinegar (i.e. 12.5 g of acetic acid) per day
diluted in water and as salad dressing [43]. Moreover, acute vinegar
intake was implicated as a causal factor of ulcerative injury to the
oropharynx and oesophagus in a case report of a 39-year-old
woman who drank one tablespoon of white vinegar to softencrab
shell stuck in her throat [44].
Unsubstantiated statements by the media may unduly inuence
the lay public to incorrectly administer vinegar therapeutically. For
example, a 72-year-old Caucasian man with history of dyslipidemia,
gastroesophageal reux disease and mild obesity added 2 table-
spoons daily of acetic acid (household vinegar) to his diet after
reading an article in a health magazine that claimed vinegar helps
to decrease food intake (by promoting satiety) and lowers choles-
terol. Nine days later, the individual was admitted to the hospital
with intractable singultus (hiccups), associated with anorexia and
epigastric pain [45]. In another instance, a 14-year-old girl received
chemical burns after following an Internet-based protocol for nevi
removal using apple cider vinegar [46]. Vinegar also caused
chemical burns to the face in an 8-year-old girl after her aunt
applied a vinegar-containing solution in an effort to alleviate
pediculosis capitis [47]. Topical incidents associated with vinegar
have been reported in adults, as well. A home-made poultice
Table 2
Acute effects of vinegar intake on glycemic parameters of health subjects.
Author and year n Study design Intervention meal Outcomes
Brighenti et al., 1995
[25]
5 Crossover, placebo-
controlled
100 g of chopped lettuce with olive oil, or olive oil
plus 1 g of acetic acid in vinegar form or vinegar
neutralized through sodium bicarbonate. After
ingestion of the seasoned lettuce, 50 g of white
bread was consumed
Blood glucose, analyzed before, and up to 95 min
after meals, was 31% lower when they ingested
lettuce salad with the dressing containing vinegar
than the other tested meals
Liljeberg and Bj
orck,
1998 [28]
10 Crossover, placebo-
controlled
On the rst day patients received 122 g of white
bread, 8 g of olive oil and 23 g of cheese; on the
second day they received the same meal with 20 g
of vinegar
When individuals ingested the sandwich with
vinegar, compared to that without vinegar, the
blood glucose and postprandial insulinemia were
reduced within 30e60 min
Johnston and Buller,
2005 [27]
11 Randomized, crossover,
placebo-controlled
20 g of apple cider vinegar added in test meals
composed of bread and orange juice (glycemic
load ¼81). Additionally a lower glycemic load meal
(glycemic load ¼48) was analyzed, which
contained 200 g of rice and 50 g of chicken breast,
both cooked
Higher glycemic load meals ingested with vinegar
resulted in postprandial glycemia 55% lower than
meals without vinegar. There was no glycemia
improvement when vinegar was ingested along
with the lower glycemic load meal
Ostman et al., 2005
[31]
12 Randomized, crossover 18, 23 and 28 g of vinegar with a white bread
serving (50 g of carbohydrates) after overnight
fasting
Postprandial glycemia response at 30 and 45 min,
and the insulinemia at 15 and 30 min, were
signicantly reduced after ingesting 28 g of vinegar,
in comparison with lower doses and the control
meal (without vinegar)
Salbe et al., 2009 [29] 5 Randomized, crossover,
placebo-controlled
Individuals randomly received placebo and 20 mL of
apple vinegar followed by mashed potatoes (0.75 g
of carbohydrate/kg body weight). Oral octreotide
was given for insulin suppression along with the
meals
Glycemia levels, measured every 20 min along
180 min of testing, were signicantly higher after
vinegar ingestion when compared with placebo
Ishak et al., 2018 [32] 10 Randomized, cross-
over intervention
Intervention encompassed 4 trials: control, mixture
only, exercise only, and exercise þmixture. The
mixture consisted of 20 mL of garlic, ginger and
lemon juices honey and apple cider vinegar based
on a ratio of 1: 1: 1: 1: 1
Postprandial glucose response calculated as area
under curve for 120 min were 8%, 13% and 15%
lower than control in mixture only, exercise alone
and exercise þmixture, respectively
H.O. Santos et al. / Clinical Nutrition ESPEN xxx (xxxx) xxx4
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containing 4.5% acetic acid applied to the dorsum of the left foot
under occlusion with gauze in a 59-year-old woman resulted in a
deeply ulcerated lesion [48].
9. Perspectives and clinical view
The majority of studies to date have used apple cider vinegar
[13,15,16,24,27,29,30,37]. To the best of our knowledge, there are no
studies that used garlic vinegar in a human intervention. Given
evidence that garlic consumption improves lipid proles and in-
hibits production of advanced glycation end products (AGEs)
[49,50], future research should seek to determine if additional
benets are achieved through the consumption of garlic vinegar.
Interestingly, cooking meat marinated in vinegar to 150
C for
15 min per 1 h reduced the production of AGEs compared to
cooking the meat without marinating [51].
In vitro data showed vinegar to be a good dietary source of
antioxidants [52]. It should be noted however that the present re-
view did not address this issue as apple cider is the more studied
vinegar in human studies and its antioxidant effect is negligible.
Despite claims that vinegar is a good antioxidant source, various
fruits (e.g. orange, mango, cherry and banana) have an antioxidant
activity between 8- and 40-fold higher than apple cider vinegar
[53]. Thus, ingestion of fruits is a better alternative for attaining
antioxidants than vinegar.
Regarding glucose disturbances, the majority of research covers
the benets of vinegar ingestion in subjects with T2DM, whereas
only one study investigated its effects in subjects with T1DM.
Further research is therefore warranted to better understand the
relationship between vinegar intake and T1DM.
In addition to its use as a remedy for dysregulated glycemia,
vinegar also shows promise in ameliorating non-alcoholic fatty
liver disease, PCOS and weight loss. However, chronic interventions
Table 3
Acute effects of vinegar intake on glycemic parameters of subjects with glucose disturbances.
Author and year Subjects Study design Intervention meal Outcomes
Johnston et al., 2004
[26]
8 individuals without
diabetes, 11 with
prediabetes and 10 with
type 2 diabetes
Crossover, placebo- controlled Patients were randomized to intake
20 g of apple cider vinegar along with
40 g of water or placebo drink, followed
by a test meal consisting of white bread,
butter and orange juice
After 30 and 60 min postprandial, the
glycemic response was lower only in
those subjects with prediabetes
White and Johnston,
2007 [30]
11 type-2 diabetics
non-insulin users
Randomized, crossover,
placebo-controlled
Subjects were submitted to a
standardized dietary plan for two days,
which included adding 2 tablespoons of
apple cider vinegar to the supper along
with one slice of cheese (~30 g)
The fasting blood glucose level was
signicantly lower on the vinegar day,
but biologically it was a very low value,
in which glycemia decreased in only
5 mg/dL
Johnston et al., 2010
[24]
9 diabetics and 29
non-diabetics subjects
Double-blind, randomized,
crossover, placebo- controlled
2 g, 10 g, or 20 g of apple cider or red
raspberry vinegars were consumed
2 min or 5 h before the meal test, or
vinegar pill(sodium acetate)
administrated 2 min before the meal.
Vinegar doses were added to the test
meal of white bagel, 20 g butter and
200 g juice (3 trials) or dextrose
solution (1 trial). Placebo drinks were
prepared in an identical manner but
minus the vinegar
Compared to the placebo test, the
intake of 10 g of apple vinegar lower
20% the area under the curve 120 min
for glycemia after the meal, whilst the
consumption of vinegar with dextrose
did not show any glycemic
improvement
Mitrou et al., 2010 [33] 10 patients with type 1
diabetes
Crossover, placebo-controlled The subjects were randomly assigned to
consume 30 mL vinegar þ20 mL water
or placebo (50 mL water) 5 min before a
meal composed of bread, cheese, turkey
ham, orange juice, butter, and a cereal
bar
Compared to the placebo test, the meal
with vinegar lower by almost 20% the
area under the curve 240 min for
postprandial glycemia
Liatis et al., 2010 [34] 16 type-2 diabetic
individuals
Crossover, placebo-controlled In the rst group was given a high-
glycemic index meal 50 g (mashed
potatoes and 250 mL low-fat milk) on
two different days, with and without
the addition of 20 g wine vinegar. In the
second group, patients were given an
isocaloric meal with the same nutrient
composition, but low-glycemic index
(100 g whole grain bread, 55 g lettuce
and 20 g low-fat cheese)
Incremental area under the curve of
glucose for 120 min was lower after the
addition of vinegar in the high-glycemic
index meal, but not into low-glycemic
index
Kuzeyli kahraman,
2011 [35]
16 type-2 diabetic
patients who had been
treated with metformin
only
Crossover, placebo-controlled 275 g baked beans, 195 g rice,
106 g salad plus 50 g of grape vinegar
on the rst day, but not with vinegar on
the second day
Postprandial blood glucose and insulin
measurements were not different in the
vinegar group when compared with the
reference group
van Dijk et al., 2012
[36]
12 type well-controlled
2 diabetic patients
Randomized, crossover After an overnight fast, subjects
ingested either 75 g glucose beverage
with 25 g white vinegar or without
vinegar
Vinegar co-ingestion did not attenuate
the postprandial rise in plasma glucose
or insulin
Panayota Mitrou et al.,
2015 [15]
11 insulin-resistant
individuals
Randomized crossover study 30 mL of apple vinegar or placebo
before a test meal, which consisted of
bread, cheese, ham, orange juice, butter
and a cereal bar (equivalent to 75 g of
carbohydrates)
Compared with placebo, the vinegar
intake decreased the serum insulin and
triglycerides, and increased the
musculoskeletal glucose uptake
performed through the arteriovenous
difference method during 300 min
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with more controlled diet are needed to draw better conclusions as
to its efcacy.
Ultimately, since high intake of acidic foodstuffs such as vinegar
can irritate mucous membranes, such as the mouth, it is important
to monitor any symptoms that may occur. Caution is required in
people with stomach disorders. Importantly, gastric problems are
often encountered in patients with diabetes mellitus [54], and there
is no support with respect to vinegar intake and stomach safety.
The recommendation of vinegar consumption in clinical practice
should be considered in line with individual preferences, e.g. taste
tolerance.
10. Conclusion
Acute and short-term studies show that vinegar intake has a
benecial effect on the glycemic prole, with apple cider the most
studied type of vinegar. Evidence suggests that chronic intake may
improve glycemia as well, especially in T2DM individuals. However,
while a considerable number of studies have acutely analyzed the
effects of vinegar intake co-ingested with meals rich in carbohy-
drate, only a few interventions have included relevant follow-ups
and diet control. Taken together, consumption of 10e30 mL
(~2e6 tablespoons) of vinegar as a dressing or diluted in beverages
appears to be adequate to acutely alter glycemic prole. In contrast,
this dose can be infeasible if used habitually.
Author's contributions
H.O.S. and W.M.A.M.M. conducted the literature search and
drafted and revised the manuscript. G.A.R.S., JP and B.J.S. critically
reviewed and revised the manuscript.
Funding/sponsorship
None.
Declaration of interest
The authors have no interests to declare.
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https://doi.org/10.1016/j.clnesp.2019.05.008
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