Vinegar is promoted as a natural appetite suppressant, based on previous reports that vinegar ingestion significantly increases subsequent satiety. However there are concerns about the appropriateness and safety of this advice, and it is unclear if poor product palatability may explain previously published effects on appetite.
To investigate if vinegar palatability and tolerability have a role in suppressing appetite and food intake in two sequential and related acute human feeding studies.
Subjects and methods:
Healthy, young, normal weight unrestrained eaters were recruited to Study 1 (n=16), an acute feeding study supplying vinegar within both palatable and unpalatable drinks alongside a mixed breakfast in comparison to a non-vinegar control; and to Study 2 (n=14), a modified sham feeding study (taste only without ingestion) comparing vinegar to a non-vinegar control following a milkshake preload. Both studies were a randomized crossover balanced design for the assessment of appetite, energy intake and glycaemic response.
In Study 1, ingestion of vinegar significantly reduced quantitative and subjective measures of appetite, which were accompanied by significantly higher nausea ratings, with unpalatable treatment having the greatest effect. Significant correlations between palatability ratings and appetite measures were found. In Study 2, orosensory stimulation with vinegar did not influence subsequent subjective or quantitative measures of appetite compared with control.
These studies indicate that vinegar ingestion enhances satiety whereas orosensory stimulation alone does not, and that these effects are largely due to poor tolerability following ingestion invoking feelings of nausea. On this basis the promotion of vinegar as a natural appetite suppressant does not seem appropriate.
The provision of vinegar as a source of oral acetate, the two carbon short-chain fatty acid, has been reported to significantly increase subsequent satiety in acute conditions1, 2, 3 and to significantly lower body mass index in chronic conditions4 (reviewed by Darzi et al.5).
Vinegar is therefore being promoted as a natural appetite suppressant in the popular press, resulting in the perception that vinegar is a healthy addition to the diet to aid weight loss,6 and giving rise to the marketing of weight loss capsules that contain apple cider vinegar. However, this raises concerns about the appropriateness and safety of this advice, as ingestion of vinegar products have been reported to be linked with oesophageal injury,7, 8 biochemical disturbances,9 dental erosion10 and acute pancreatitis11 and symptoms such as acid reflux, burping/flatulence and changes in bowel habit.12 It could further be argued that the scientific evidence currently available is not sufficient to warrant such health claims.
It is unclear if previously reported effects of vinegar ingestion on satiety arose from a physiological effect of short-chain fatty acid ingestion, possibly mediated via activation of the free fatty acid receptors FFA2 (previously GPR43) and FFA3 (previously GPR41),13, 14, 15, 16 or if poor product tolerability may explain the effects. In appetite investigations, palatability, tolerability and acceptability pose large confounding influences. A strong linear relationship between rated palatability and differences in food intake following such manipulation (for example by adding citric acid to soup17 or cumin to a yogurt drink18) has been demonstrated.19 This provides a rationale that the palatability of oral acetate may explain effects on appetite and satiety.
The validity of results from previous studies investigating acute effects of vinegar ingestion on subsequent satiety are also uncertain as quantitative effects on appetite were not investigated, and subjective effects on appetite were investigated with the use of a single-rating bipolar scale,1, 2 or point scale3 rather than a variety of appetite-related visual analogue scale (VAS) questionnaires. VAS are considered the most appropriate questionnaire to subjectively assess appetite and their use has been previously validated.20
Vinegar ingestion has also been shown to blunt postprandial glycaemia and insulinaemia both in healthy individuals2, 21, 22, 23, 24, 25 and in individuals with insulin resistance and type 2 diabetes mellitus.26 Product tolerability may also explain these findings. A higher cephalic-phase insulin release is reported to occur following exposure to foods rated as highly palatable in comparison with foods with lower palatability ratings,27, 28 although this is not a consistent finding.29 Furthermore, sham feeding with unappetizing foods has been shown to significantly delay gastric emptying30 and reduce cephalic-phase vagal stimulation31 in comparison with more appetizing foods, which would in turn suggest a role for product tolerability in metabolic effects.
We therefore carried out two related human investigations with the aim of determining if vinegar influences appetite when validated methodology is used (appetite VAS ratings, energy intake (EI) at subsequent ad libitum meal and 24 h intake), and further to investigate if the palatability and tolerability of vinegar-containing products have a role in influencing appetite. Effects on postprandial glycaemia (Studies 1 and 2) and insulinaemia (Study 2 only) were also investigated. In Study 1, we investigated the acute effects of vinegar ingestion provided when the palatability had been manipulated but the ingested dose of acetate (25 mmol) was identical; in Study 2, we investigated acute effects of orosensory stimulation with vinegar, without ingestion of the acetate, using the modified sham feeding (MSF) technique, on appetite and metabolic response, allowing the separation between the physiological effects of ingestion/absorption and those of taste.
Subjects and Methods
This paper reports the results from two studies:
In Study 1, acute postprandial effects on appetite and blood glucose in response to a standard breakfast preload served alongside either an unpalatable (Unpal) or more palatable (Pal) vinegar-containing drink or control (CON) drink were investigated.
In Study 2, acute postprandial effects on appetite and plasma glucose and insulin in response to a standard milkshake preload followed by an MSF phase with either a vinegar-containing (VIN) or CON drink were investigated.
Both studies were conducted at the University of Surrey Clinical Investigation Unit (CIU) and were approved by the University of Surrey Ethics Committee and conducted in accordance with the guidelines laid down in the Declaration of Helsinki. All subjects provided written, informed consent prior to commencing the studies. Figure 1 gives an overview of the study day protocols.
Sixteen healthy subjects (3 male, 13 female) aged 21–33 years (Study 1) and fourteen healthy subjects (6 male, 8 female) aged 20–42 years (Study 2) were recruited from the student population at the University of Surrey (Table 1). Inclusion criteria were a body mass index 19–27 kg m−2, age <45 years, fasting blood glucose 6.0 mmol/l, weight stable for at least 3 months and not following a weight-reducing diet, a score <3.5 on the Dutch Eating Behaviour Questionnaire restraint scale,32 absence of gastrointestinal, endocrine or cardiovascular disorders, no history of depression, eating disorders or substance abuse, not pregnant or lactating, not taking regular medication (except birth control medication), non-smoker and reported habitual alcohol intake 20 units. All recruited subjects completed the studies.
Both studies were a randomized crossover design. Subjects attended study mornings at the CIU separated by at least 2 days (for washout) and were assigned to the experimental condition (Pal, Unpal or CON in Study 1; VIN or CON in Study 2) in a counterbalanced randomly assigned order (using http://www.randomizer.org/). For both studies, subjects completed 24 h food diaries and refrained from unaccustomed exercise and alcohol consumption during the 24 h proceeding each study morning. A standard, commercially prepared low-fibre meal (<5 g fibre) was consumed for the evening meal before the test day. On each study morning, subjects arrived following an overnight fast of at least 12 h. Due to the nature of the studies it was not possible to blind participants or investigators to the experimental conditions.
Study 1 protocol (influence of vinegar palatability following ingestion)
Subjects attended study mornings at the CIU on three occasions. Upon arrival, two initial fasting capillary whole blood samples were taken 30 and 5 min before the test preload. Two initial VAS to subjectively assess appetite and nausea were completed following each blood sample. Subjects were then served a standard breakfast of jam sandwiches (8 g Olivio spread and 16 g Tesco strawberry jam per 38 g slice Kingsmill Everyday Soft Bread) cut into quarters alongside the test drink they were randomized to on that occasion. On the first study morning, subjects were provided seven quarters of a jam sandwich (2543 kJ, 12.3 g protein, 95.4 g carbohydrate, 21.7 g fat), equivalent to three and a half slices bread, and were instructed to consume a minimum of four full quarters (1454 kJ, 6.9 g protein, 54.5 g carbohydrate, 12.4 g fat), equivalent to two slices bread. On subsequent study mornings, subjects were provided the same number of quarters ingested on the first study occasion. This procedure has been previously reported33 and used in our group.34 Subjects were instructed to consume the breakfast and drinks within 15 min. The test drinks all had a total mass of 350 g divided between two glasses, supplied 24 kJ and 25 mmol acetic acid, and were prepared as follows:
CON drink: 75 g sugar-free squash+275 g water divided across two drinks
Unpal drink: 25 g vinegar+25 g sugar-free squash+100 g water in one drink that was consumed first, followed by 50 g sugar-free squash+100 g water in a second drink
Pal drink: 25 g vinegar+75 g sugar-free squash+250 g water divided across two drinks
The vinegar used was Tesco White Wine Vinegar, which contains 6% acetic acid. The first drink for the Unpal treatment was less palatable than the Pal treatment, as the vinegar was more concentrated and the drink less sweet, due to less squash being added. After breakfast subjects completed VAS rating questionnaires asking ‘How pleasant was the taste of the drink?’ and ‘How palatable was the breakfast?’. Blood samples were collected at 15, 30, 45, 60, 90, 120 and 180 min postprandially and VAS to assess appetite and nausea were completed after blood samples at 30, 60, 90, 120 and 180 min postprandially. At 180 min, subjects were served an ad libitum test meal.
Study 2 protocol (orosensory effects of vinegar)
Subjects attended study mornings at the CIU on two occasions. Upon arrival, two initial fasting capillary whole blood samples were taken 30 and 5 min before the test preload. Two baseline VAS to subjectively assess appetite and nausea were completed following each blood sample. Subjects were then provided Nurishment milkshake (420 g, 1804 kJ, 21.0 g protein, 60.0 g CHO and 12.6 g fat) at time=0 min that they were asked to consume within 5 min. At time=6 min, an MSF phase was commenced comprising either:
CON drink: 180 g tap water
VIN drink: 30 g Tesco White Wine Vinegar (containing 6% acetic acid)+150 g water
The VIN drink contained added vinegar at a level of 16.7 g vinegar per 100 g total volume (equivalent to 167 mmol/l acetic acid), which is the same concentration as the Unpal drink used in Study 1. The MSF drinks were divided equally between 10 small taster cups. Subjects were asked to sip from one cup at a time and to hold the drink in their mouth for 25 s without swallowing. They then expectorated the drink into a pre-weighed receptacle and 5 s later were asked to sip from the next cup. This sequence continued for all 10 cups, which took approximately 5 min. The pre-weighed receptacle was then re-weighed in order to determine the recovery following the MSF sequence. Subjects completed VAS asking ‘How pleasant was the taste of the sham fed drink?’ and ‘How palatable was the milkshake?’. Blood samples were collected at 15, 30, 45, 60, 90, 120 and 180 min postprandially and VAS to assess appetite and nausea were completed after blood samples at 30, 60, 90, 120 and 180 min postprandially. Subjects were then served an ad libitum test meal.
Qualitative and quantitative appetite assessment
Appetite sensations were subjectively assessed using 100 mm VAS for fullness, hunger, prospective food consumption and desire to eat sweet/savoury/salty/fatty as previously described.20, 35 A question regarding nausea was also included. Additional questions unrelated to appetite (for example calmness, tiredness and anxiety) were asked to mask the purpose of the study. Subjects were not informed that the studies were investigating effects on appetite. Appetite was assessed quantitatively by providing an ad libitum test meal at 180 min comprising a homogenous pasta dish served in a quantity exceeding usual portion sizes as previously used by our group.34, 36 The dish supplied 9750 kJ, 81.5 g protein, 339.1 g carbohydrate, 70.0 g fat and 15.9 g fibre. Subjects were served in confined individual booths free from distractions and instructed to eat until they were ‘comfortably full’. Subjects were then free to leave and completed a diet diary for the remainder of the day for determination of 24 h EI. Dietary analysis was performed using WinDiets Professional Version 2005 (Robert Gordan University, Aberdeen, UK).
Blood sample processing and analysis
In Study 1, whole blood capillary samples were immediately analysed for blood glucose concentrations using the HemoCue 201 Plus (HemoCue, Sheffield, UK). The first drop of capillary blood drawn following fingerprick was wiped away and the next drop was loaded onto a HemoCue microcuvette for analysis. In Study 2, capillary blood samples were collected into fluoride microvette tubes (Starstedt, Beaumont, Leicester, UK) and centrifuged at 1750 g for 10 min. Plasma glucose concentrations were analysed on the day of collection using the YSI 2300 Stat Plus Glucose Analyzer (YSI Incorporated, Yellow Springs, OH, USA), which had an intra- and inter-assay CV of <2% and 1.2%, respectively. The remaining plasma was stored at −20 °C until analysed for insulin concentrations using an immunochemiluminometric ELISA kit (Invitron, Monmouth, UK), which had an intra- and inter-assay CV of 5.8 and 12.5%, respectively. Samples from the same subjects were analysed on the same plate.
Calculations and statistical analysis
The primary outcome for both studies was EI of the ad libitum test meal served 3 h postprandially. Assuming a s.d. for EI of 494 kJ from data previously reported by our group,34 a post priori power calculation determined that there was an 80% probability of detecting a 370 kJ difference in EI with 16 volunteers for Study 1 (three-way crossover) and of detecting a 401 kJ difference in EI with 14 volunteers for Study 2 (two-way crossover) at a significance level of 0.05. All statistical analyses were conducted using SPSS for Windows 16.0. Data was tested for normality using the Kolmogorov–Smirnov test. Differences between treatments for palatability VAS scores, 3 h ad libitum EI and 24 h EI were assessed by one-way repeated measures ANOVA with post hoc Holm–Bonferroni test if normally distributed, and by Friedman’s ANOVA with post hoc Wilcoxon signed-rank test if not normally distributed in Study 1 and by paired samples t-test if normally distributed, and by Wilcoxon signed-rank test if not normally distributed in Study 2. Postprandial subjective VAS ratings and glycemic and insulinemic response were assessed by two-way (vinegar treatment × time) repeated measures ANOVA in both studies. The area under curve (AUC) for postprandial plasma metabolites and subjective appetite and nausea ratings were calculated by the trapezoidal rule. Data from Study 1 was pooled from all study days to examine the relationship of palatability VAS ratings and nausea AUC with subjective appetite AUC, 3 h ad libitum EI and 24 h EI by correlation analysis (two-tailed Pearson’s product moment (parametric) and Spearman’s rho (non-parametric) as appropriate). Differences were considered to be significant at a level of P0.05. Post hoc differences in Study 1 were considered significant at a level of P0.0167 (=0.05/3), P0.025 (=0.05/2) and P0.05 (=0.05/1) for the lowest, second lowest and highest P value respectively, with sequential rejection, as specified by Holm37 for parametric data, and at a level of P0.0167 (=0.05/3) for the Wilcoxon signed-rank test for non-parametric data. All data are displayed as mean±s.d.
Study 1: Influence of ingested vinegar palatability
Pleasantness and palatability ratings
Vinegar treatment significantly decreased the rated pleasantness of taste of the test drinks (Figure 2a) and palatability of breakfast (Table 2). Mean ratings increased in the order Unpal, Pal and CON, with post hoc analysis finding significant differences between all comparisons.
Postprandial nausea ratings
Postprandial nausea ratings were significantly influenced by vinegar treatment (Table 2, Figure 2b). Post hoc analysis found nausea ratings were significantly higher following both Pal and Unpal treatment in comparison with CON, and were higher following Unpal treatment than Pal, although this difference was not significant.
Qualitative appetite assessment
Vinegar treatment significantly influenced postprandial VAS appetite ratings for fullness, hunger and prospective food consumption, and the desire to eat something sweet was influenced with a trend approaching significance when analysed by two-way (treatment*time) repeated measures ANOVA (Table 2). No significant effects for the desire to eat something savoury, salty and fatty were found. Post hoc analysis found fullness was significantly higher for both Pal and Unpal treatment compared with CON.
Quantitative appetite assessment
Vinegar treatment significantly reduced 3 h ad libitum EI and 24 h EI. Mean intake increased in the order Unpal, Pal and CON. Differences between Unpal and CON approached significance and were significant for 3 h ad libitum EI and 24 h EI, respectively (Table 2). Analysis of ad libitum EI was carried out on 15 subjects following removal of an outlier with an intake value >3 s.d. over the mean intake during Unpal treatment. Data from two subjects was excluded due to incomplete 24 h intake dietary records, therefore analyses on 24 h intake were carried out on the remaining 14 subjects.
Postprandial glucose response
Vinegar treatment significantly reduced postprandial glycaemia, with vinegar ingestion resulting in a lower and later glucose peak than CON (Table 2), which was to a significant level between Pal treatment and CON.
Correlation of appetite parameters with nausea and palatability ratings
Appetite VAS ratings AUC were significantly and positively correlated with pleasantness of drink taste ratings and breakfast palatability ratings, whereas correlations with nausea VAS ratings AUC were weak, negative and non-significant, except for prospective consumption (Table 3). Ad libitum EI was significantly and positively correlated with drink pleasantness taste ratings and breakfast palatability ratings, and was significantly and negatively correlated with nausea ratings AUC. Twenty-four hour EI was significantly correlated with drink pleasantness ratings. Selected correlations are displayed in Figure 3.
Study 2: Orosensory effects of vinegar
Pleasantness and palatability ratings
The VIN drink was rated as significantly less pleasant than CON, whereas palatability ratings for the milkshake did not differ between treatments (Table 2).
Postprandial nausea ratings
Postprandial nausea ratings did not differ between treatments (Table 2).
Qualitative appetite assessment
None of the postprandial appetite ratings differed between treatments (Table 2).
Quantitative appetite assessment
Mean intake of the ad libitum test meal provided 3 h postprandially and 24 h EI did not differ between treatments (Table 2).
Postprandial glucose and insulin response
No influence of VIN treatment on postprandial glycaemia (Table 2) or insulinaemia (data not shown) was found.
Recovery of MSF drink following sham feeding
Recovery of the VIN drink when expectorated following sham feeding was significantly higher than CON recovery (Table 2), suggestive that vinegar stimulated saliva production.
Our findings from the present studies suggest that vinegar ingestion influences appetite when investigated using validated methodology, and also influences postprandial glycaemia. The tolerability of VIN products appears to have a role in observed effects on appetite and glycaemia, possibly arising from induced nausea following ingestion.
In Study 1, it was found that vinegar ingestion (supplying 25 mmol acetic acid) significantly influenced quantitative and subjective appetite measures and glycaemia, suggesting that vinegar treatment is associated with a significantly reduced appetite, in agreement with previous studies,1, 2, 3 which used similar dosages of acetic acid (28 mmol). Vinegar treatment was also associated with a reduced glycaemic response, in common with previous studies.2, 21, 22, 23 By contrast, in Study 2 orosensory stimulation with a drink containing vinegar (of the same concentration as the Unpal drink in Study 1) did not influence appetite when assessed subjectively or quantitatively, nor did it influence glycaemic and insulinaemic responses.
Vinegar ingestion invoked significant increases in rated nausea in Study 1, which increased with decreasing product palatability, suggesting poor tolerability, with Unpal being the least well tolerated. Palatability and nausea appeared to have an influence on appetite, with appetite tending to decrease and nausea tending to increase in the order CON, Pal and Unpal. This provides support for the hypothesis that the palatability and tolerability of vinegar had an influence on subsequent appetite. However, in Study 2, the mere taste of vinegar in the absence of ingestion did not induce nausea and did not influence the rated palatability of the milkshake, although the VIN drink in Study 2 was rated as significantly less pleasant than CON and stimulated enhanced salivary production. This suggests the influence of the palatability of the VIN drink is short-lived when only tasted and not ingested. The results from Study 1 and Study 2 together imply that it is the interaction between ingestion and palatability that is important, and the orosensory properties alone of vinegar-containing products are not sufficient to influence appetite and the metabolic response. This is suggestive of a role for the poor tolerability rather than palatability of vinegar giving rise to feelings of nausea following ingestion, thereby reducing subsequent appetite and glycaemia.
Medium to strong significant correlations were found between palatability VAS ratings and all appetite VAS (positive for hunger, prospective consumption and desire to eat sweet/fatty/salty, and negative for fullness), ad libitum test meal and 24 h EI in Study 1. Although correlations do not imply causality, these findings support our hypothesis that the palatability or tolerability of the vinegar-containing test products had a role in decreasing appetite/increasing satiety.
The influence of palatability on appetite has been investigated by a number of researchers. Yeomans (2007) re-analysed data from 11 different studies that measured ad libitum intake of an unpalatable food in comparison with a control food; for example cumin banana colada vs control banana colada18 and stale vs fresh popcorn.38 A strong, linear relationship was found between differences in palatability ratings and ad libitum intakes of those foods (R=0.85, P<0.0001),19 thereby supplying evidence of a role for palatability in satiation. These findings fit in with the findings from the present study of a more transient and short-term influence of palatability on appetite regulation. Effects of palatability on subsequent satiety have not been extensively investigated. De Graaf and colleagues (1999) reported that food palatability influenced satiation (intra-meal satiety), but not subsequent satiety. A dose–response reduction in ad libitum intake of the soup was found with decreasing palatability; however, there were no effects on subsequent satiety, hunger ratings or ad libitum test meal intake regardless of intermeal duration.17 Unfortunately, effects on nausea were not assessed, so it is difficult to directly relate the postprandial findings from that study to the present study.
There is also evidence that food palatability and/or tolerability may influence the metabolic response, which may explain the observed effects of vinegar ingestion on postprandial glycaemia in Study 1. However, findings are not equivocal. In comparison with a ‘palatable test meal’, ingestion of a ‘non-palatable meal’ (the same meal blended and freeze-dried into a desiccated biscuit) resulted in significantly lower postprandial glycaemia39 and insulinaemia.40 It is, however, possible that the meal form and texture may have influenced the metabolic effects rather than the product palatability. A role for palatability in cephalic-phase metabolic responses has also been tested. Bellisle and colleagues27, 28 reported a significantly lower cephalic-phase insulin release amplitude with ingestion of a ‘low palatability meal’ in comparison to a ‘high palatability meal’, although these early studies did have low participant numbers. However, Teff and Engelman29 found no difference between cephalic-phase insulin release amplitude following MSF with ‘palatable’ and ‘unpalatable’ foods. This suggests that ingestion of the unpalatable product is necessary to induce differential effects on cephalic-phase responses, which offers similarities to findings reported in the present paper, where vinegar ingestion invoked effects on appetite and glycaemia (Study 1) whereas merely tasting vinegar did not (Study 2).
Gastric motility may also be influenced by food palatability and taste, which in turn may influence appetite and the metabolic response. The rate of gastric emptying has been shown to be significantly delayed when an oral liquid test meal is preceded by a MSF bitter tasting meal replacement bar in comparison with a non-bitter control.30 As would be expected, the influence of taste appears to occur during the cephalic phase of digestion as demonstrated by intragastric infusion of a bitter solution having no influence on the gastric emptying rate in comparison to water.41 These findings supply a rationale for the observed effects in Study 1 in the present paper, but not for Study 2. The gastric emptying rate is reported to be delayed following ingestion of both acetate provided as vinegar23, 42 and propionate added to bread24, 43 and a pasta meal44 with the exception of one study that found no effect on the gastric emptying rate following an acute challenge with vinegar.1 Delayed gastric emptying has been linked to nausea and early satiety in patients suffering from gastroparesis.45, 46 Thus, delayed gastric emptying may also provide an explanation for short-chain fatty acid ingestion invoking feelings of nausea, in addition to the unpleasant taste.
An alternate possible explanation is that the vinegar may be ‘tasted’ further down the GIT when ingested. There is evidence that taste molecules are expressed in the GIT47, 48 and that taste-signalling proteins are expressed on enteroendocrine L cells in the small intestine, the same cells that express the appetite regulatory gut peptides glucagon-like peptide 1 (GLP-1) and peptide YY (PYY).47, 49 This suggests taste sensing in the GIT may have a role in modulating appetite and may provide an explanation for observed effects in the present studies, with vinegar ingestion influencing appetite and glycaemia (Study 1), but orosensory stimulation not (Study 2). This provides further rationale for a role for an interaction between ingestion and tolerability in influencing appetite, in part due to induced nausea.
A limitation of the present studies is that effects on gut hormones were not assessed, effects on satiation were not investigated and the gastric emptying rate was not measured. Furthermore, in Study 2, it may have been of benefit to use a solid mixed meal rather than a liquid milkshake preload to allow closer comparison with Study 1. The use of a liquid preload may provide some explanation for the shorter-lived influence of vinegar treatment on appetite compared with Study 1. We chose to use a milkshake in Study 2, as it can be consumed much quicker than a solid meal, thus allowing the MSF phase of the protocol to commence at the earlier phase of digestion and absorption of the preload.
In conclusion, results from these studies indicate that vinegar ingestion reduces appetite when investigated using validated appetite assessment methods and suppresses postprandial glycaemia. These effects appear to be largely due to poor product tolerability following ingestion invoking feelings of nausea, whereas orosensory stimulation alone did not induce any effects. On this basis, the promotion of vinegar as a natural appetite suppressant does not seem appropriate, particularly in view of the potential health risks.7, 8, 9, 10, 11 Further work is warranted to investigate effects of chronic supplementation with apple cider vinegar capsules in overweight and obese subjects on appetite control, body weight and adverse symptoms, to investigate if marketing these capsules as a weight loss aid is appropriate and safe.
We are grateful to the volunteers who participated in the study and also to Chloe Cooke, Leanne Johnson, Vicky Martins and Jennifer Pickard for their assistance in conducting the studies. JD was supported by an educational fellowship from Premier Foods.