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Oesophagus
Original article
Waist belt and central obesity cause partial hiatus hernia and short-segment acid reflux in asymptomatic volunteers
  1. Yeong Yeh Lee1,2,
  2. Angela A Wirz1,
  3. James G H Whiting3,
  4. Elaine V Robertson1,
  5. Donald Smith4,
  6. Alexander Weir4,
  7. Andrew W Kelman1,
  8. Mohammad H Derakhshan1,
  9. Kenneth E L McColl1
  1. 1Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
  2. 2School of Medical Sciences, Universiti Sains Malaysia, Kota Bahru, Kelantan, Malaysia
  3. 3Department of Bioengineering, University of Strathclyde, Glasgow, UK
  4. 4Medical Devices Unit, Department of Clinical Physics, Southern General Hospital, Glasgow, UK
  1. Correspondence to Professor K E L McColl, Institute of Cardiovascular and Medical Sciences, Gardiner Institute, 44 Church Street, Glasgow G11 6NT, UK; Kenneth.mccoll{at}glasgow.ac.uk

Abstract

Objective There is a high incidence of inflammation and metaplasia at the gastro-oesophageal junction (GOJ) in asymptomatic volunteers. Additionally, the majority of patients with GOJ adenocarcinomas have no history of reflux symptoms. We report the effects of waist belt and increased waist circumference (WC) on the physiology of the GOJ in asymptomatic volunteers.

Design 12 subjects with normal and 12 with increased WC, matched for age and gender were examined fasted and following a meal and with waist belts on and off. A magnet was clipped to the squamo-columnar junction (SCJ). Combined assembly of magnet-locator probe, 12-channel pH catheter and 36-channel manometer was passed.

Results The waist belt and increased WC were each associated with proximal displacement of SCJ within the diaphragmatic hiatus (relative to upper border of lower oesophageal sphincter (LOS), peak LOS pressure point and pressure inversion point, and PIP (all p<0.05). The magnitude of proximal migration of SCJ during transient LOS relaxations was reduced by 1.6–2.6 cm with belt on versus off (p=0.01) and in obese versus non-obese (p=0.04), consistent with its resting position being already proximally displaced. The waist belt, but not increased WC, was associated with increased LOS pressure (vs intragastric pressure) and movement of pH transition point closer to SCJ. At 5 cm above upper border LOS, the mean % time pH <4 was <4% in all studied groups. Acid exposure 0.5–1.5 cm above SCJ was increased, with versus without, belt (p=0.02) and was most marked in obese subjects with belt.

Conclusions Our findings indicate that in asymptomatic volunteers, waist belt and central obesity cause partial hiatus herniation and short-segment acid reflux. This provides a plausible explanation for the high incidence of inflammation and metaplasia and occurrence of neoplasia at the GOJ in subjects without a history of reflux symptoms.

  • Gastroesophageal Reflux Disease
  • Gastrointestinal Cancer
  • Gastrointestinal Motility

https://doi.org/10.1136/gutjnl-2013-305803

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    Significance of this study

    What is already known in this subject?

    • In asymptomatic subjects, the cardiac mucosa is inflamed, and its length correlates with age and waist circumference (WC). We have suggested that this may be due to silent short-segment reflux and predispose to adenocarcinoma. We have developed a probe allowing constant and accurate monitoring of location of the squamo-columnar junction (SCJ), and when it is used alongside high-resolution pH and manometry is able to study the functions of the gastro-oesophageal junction in greater detail.

    What are the new findings?

    • The waist belt and increased WC are each associated with proximal displacement of the SCJ within the diaphragmatic hiatus and reduced amplitude of migration of the SCJ during transient LOS relaxations. These findings indicate partial hiatus hernia.

    • There is short-segment acid reflux at 0.5–1.5 cm above the SCJ with waist belt, and it is most marked with the combination of waist belt plus increased WC.

    How might it impact on clinical practice in the foreseeable future?

    • This asymptomatic short-segment reflux is likely to explain the high prevalence of inflammation, metaplasia and occurrence of neoplasia at the GO junction, and points to potentially reversible lifestyle factors in its aetiology.

    Introduction

    In the Western world, there is a high incidence of adenocarcinoma at the gastro-oesophageal junction (GOJ) and cardia region of the stomach compared to that of the rest of the oesophagus and stomach.1 Adenocarcinoma of the stomach is predominantly the result of Helicobacter pylori infection and that of the oesophagus, the result of reflux-induced columnar metaplasia and dysplasia.2 However, the aetiology of the high incidence of adenocarcinoma focused at the GOJ remains unclear.

    In Japan and other countries where there is a very low incidence of reflux-associated adenocarcinoma, but high incidence of H pylori-associated gastric adenocarcinoma, the incidence of adenocarcinoma at the cardia is only 10% of that of the rest of the stomach.3 By contrast, in the USA and Western Europe where oesophageal adenocarcinoma is more common, the incidence of adenocarcinoma at the cardia is greater than that of the rest of the stomach.4 ,5 This suggests that in the Western world, the vast majority of these cancers of the cardia and GOJ are not due to H pylori gastritis, and probably related to gastro-oesophageal reflux.

    Despite the epidemiological evidence indicating that adenocarcinoma of the GOJ and cardia in the Western world are the result of acid reflux, there is only a weak association between these cancers and reflux symptoms6 This raises the question as to whether the most distal oesophagus may be subject to damage by gastric acid in the absence of reflux symptoms or traditional reflux disease.

    We have recently reported that in healthy volunteers without reflux symptoms, the columnar mucosa at the cardia between oesophageal squamous mucosa and gastric oxyntic mucosa is always inflamed and that its length is positively correlated with age and waist circumference (WC).7 We have also observed that in these asymptomatic subjects, increased WC and associated increased intra-abdominal pressure (IAP) causes gastric acid to penetrate more proximally within the lower oesophageal sphincter (LOS) but without traversing it, and we have termed this intrasphincteric reflux.7 We have suggested that this ingress of acid may be inducing columnar metaplasia of the most distal oesophagus and thus predisposing to progression to adenocarcinoma at this site.

    Adenocarcinoma at the cardia and GOJ is associated with increased body mass index (BMI) and WC, and this persists after correction for reflux symptoms.8 It is also more common in men.9 Men deposit fat within and around the upper abdomen from an early age, whereas females only deposit fat at this site following menopause.10 The earlier expansion of WC in males and its effects on the GOJ might explain the earlier rise in the incidence of these cancers in the former.11

    Another lifestyle factor which might be important in the aetiology of adenocarcinoma of the GOJ and cardia is the use of waist belts.12 Similar to abdominal fat, this also increases IAP. In the current study, we have examined the effects of waist belt as well as WC on the anatomy and physiology of the GOJ, employing a novel probe which allows continuous monitoring of the location of the GOJ. Our study indicates that both factors distort the structure of the GOJ causing partial hiatus hernia and increased acid penetration within the sphincter, and the common combination of increased WC and waist belt has the greatest effect.

    Methods

    Subjects

    Study subjects were healthy volunteers without a history of gastro-oesophageal reflux disease (GORD). Subjects were excluded if they had ever attended primary or secondary care with GORD symptoms, or taken proton-pump inhibitor therapy for GORD symptoms. Subjects were recruited to achieve two groups defined by normal or increased WC and matched for age and gender. Increased WC or ‘obese’ was defined on entry as >102 cm in men and >88 cm in women. Normal WC or ‘non-obese’ was defined as <94 cm in men and <80 cm in women.

    Study protocol

    Study day 1: endoscopy

    Upper endoscopy was performed to exclude hiatus hernia. A small magnet (2×1 mm) attached to an endoclip, was secured to the squamo-columnar junction (SCJ) using a clipping device (Olympus HX-201UR-135; Tokyo, Japan), to allow constant monitoring of its location as previously described.13 Previous studies have indicated that the movement of a mucosal clip during swallowing and transient LOS relaxations (TLOSRs) reflects the movement of the GOJ.14 ,15

    Study days 2 and 3: with and without waist belt

    Subjects reported fasted for two further study days within 2–3 days after endoscopy. On both these study days, a combined assembly of three probes was passed nasally to lie in the oesophagus and proximal stomach (figure 1). The three probes (see details in online supplementary file) consisted of high-resolution 36-channel slim-line manometer (diameter 2.7 mm, Sierra Scientific Instruments, USA), high-definition 12-channel pH catheter (Synmed, UK) and 3-dimensional magnet locator probe which detects the location of the magnet.16–19

    Figure 1
    Figure 1

    A schematic diagram of the combined assembly of 36 channel slimline high-resolution manometer, 3-D gastro-oesophageal junction locator probe and 12-channel pH catheter. The positioning of the assembly within the oesophagus, and the clipped magnet at the squamo-columnar junction are also shown.

    One of the study days was performed without the application of waist belt. Recordings from the inserted assembly were taken fasted for 20–30 min and the subjects seated upright on the bed at 60° angle. They then consumed a test meal (battered fish and French fries) over 15–20 min and were asked to eat until full, but the same amount, for each study day. After the meal, recording was continued for a further 60 min in the similar upright position.

    On the other study day, the above procedure was repeated but with application of waist belt throughout the whole recording period. The waist belt consisted of applying a weight-lifter belt (Nike, USA) and inflating a blood pressure cuff beneath it (constant cuff pressure of 50 mm Hg). The order of study days with and without belt was alternated in a random fashion between obese and non-obese groups. Any upper gastrointestinal (GI) symptoms experienced during the tests were recorded with respect to time, location, duration and character.

    Study day 4: chest X-ray

    All subjects who had a magnet placed in their oesophagus were booked to have a chest X-ray 6–8 weeks later to document the clearance of the magnet.

    The study protocol was approved by West Glasgow Research Ethics Committee, and all subjects gave their written informed consent prior to enrolment.

    Data analysis

    Manometry of the GOJ

    Manometric characteristics were analysed in detail during fasting and after meal, with six end-expiratory points in each period, selected using a custom-made computer programme. Intragastric pressure (IGP) (mm Hg) was defined as the median pressure of the first three sensors immediately distal to the LOS.

    Locations of structural and physiological components within the GOJ

    All measurements (in cm) were determined from the nares. The upper border LOS was defined as the most proximal position where the pressure falls to within 2 mm Hg of intraoesophageal pressure (IOP). The lower border LOS was defined as the most distal position where the pressure rose to >2 mm Hg above gastric baseline. The SCJ was the position of the magnet as detected by the locator probe.

    The location of peak LOS pressure was the position of the maximum pressure within the high-pressure zone (HPZ) of the LOS. The pressure inversion point (PIP) was defined as the transition point from the abdominal pressure compartment (positive wave deflection) into the thoracic pressure compartment (negative wave deflection).

    Acid exposure across the LOS and SCJ

    Acid exposure was examined for mean % of time the pH <4 during fasting and after meal. Location of the pH transition point was defined by the position of the pH sensor recording a drop in mean pH of at least one unit from proximal to distal and corrected for 1.5 cm spacing.

    Statistical analysis

    All data were presented as mean (SE of mean) unless otherwise specified. The effect of ‘central obesity’ was assessed by comparing obese (n=12) versus non-obese (n=12) groups, both without application of belt. The effect of ‘waist belt’ was assessed by comparing the entire group (n=24) with and without belt. The effect of waist belt was also assessed in obese subjects only, with and without belt (n=12). Comparison between groups defined above was tested using related-sample and independent-sample t tests. Significance for all statistical tests was set at p value <0.05.

    Results

    Out of 27 healthy subjects, 24 (mean age 34.6 years) completed the study and were analysed. Of these two groups, 12 subjects were obese (mean WC=104 cm) and 12 non-obese (mean WC=75.5 cm), and they had similar mean age (35.8 vs 33.4 years) and gender (7 vs 7 men). The mean (SEM) height of recruited subjects was similar in non-obese versus obese subjects (174.6±3.0 vs 173.8±2.6 cm). None of the study subjects reported any upper GI symptoms with or without application of the waist belt throughout the entire recording period. All subjects who had chest X-ray after 6–8 weeks were cleared from the magnet initially clipped to the SCJ.

    Waist belt and the GOJ

    The effect of the waist belt was examined by comparing its effect in the entire group of 24 subjects (ie, combining 12 obese and 12 non-obese).

    GOJ pressures (expiratory)

    IGP was greater in subjects with versus without belt during fasting (18.7 vs 13.5 mm Hg, p=0.005) and after meal (20.5 vs 15.7 mm Hg, p<0.001) (table 1). An increase in IOP was seen with belt during fasting (4.3 vs −2.0 mm Hg, p<0.001) and after meal (5.7 vs −0.3 mm Hg, p<0.001). There was no difference in gastro-oesophageal pressure gradient (GOPG) with belt, either fasted or after meal, a result of equivalence in absolute pressure rise of IGP and IOP. The peak LOS pressure relative to atmospheric pressure was greater with belt during fasting (35.8 vs 30.1 mm Hg, p=0.01) and after meal (39.4 vs 30.8 mm Hg, p<0.001). The peak LOS pressure relative to IGP was higher in belt-on versus belt-off after meal (18.9 vs 15.1 mm Hg, p=0.04).

    View this table:
    Table 1

    Effect of waist belt and central obesity on expiratory gastro-oesophageal junction pressure

    Location of SCJ and its position within HPZ

    After the meal, the upper and lower border of the LOS and the diaphragm as reflected by the PIP and peak LOS were all displaced proximally with belt-on versus belt-off towards nares by mean distances of between 0.7 and 2.3 cm (p<0.002 for each) (table 2, figure 2). The LOS length did not differ significantly in belt-on versus belt-off, fasted or after meal.

    View this table:
    Table 2

    Effect of waist belt and central obesity on relative locations of anatomical structures of the gastro-oesophageal junction

    Figure 2
    Figure 2

    Changes in locations of squamo-columnar junction (SCJ) and pH transition point within the high pressure zone relative to the peak lower oesophageal sphincter (LOS) pressure point (peak LOS) associated with central obesity and waist belt. Gastric acidity is the shaded area with its proximal margin, the pH transition point. The pH transition point was moved closer to the SCJ with the application of belt but not obesity.

    The SCJ was located closer to the nares with belt-on versus belt-off during fasting (43.2 vs 45.0 cm, p<0.001) and also after meal (41.4 vs 44.0 cm, p<0.001). The SCJ was also displaced proximally within the HPZ. After the meal, the SCJ was located more proximally with respect to peak LOS with belt-on versus belt-off (1.7 cm above vs 0.2 cm below, p=0.01), as well as to the PIP (0.9 cm above vs 0.6 cm below, p=0.001), and was closer to the upper border of the LOS during fasting (3.3 cm below vs 4.8 cm below, p=0.01) and after meal (2.6 cm below vs 3.7 cm below, p=0.04). The magnitude of the migration of the SCJ during TLOSRs was less in with versus without belt (3.9 vs 5.5 cm, p=0.005) (table 2). The reduced proximal movement of the SCJ during TLOSRs is consistent with its resting position being already proximally displaced.

    Location of pH transition point and its position within HPZ

    As shown in table 3, the pH transition point indicated the change from oesophageal to gastric pH. The pH transition point was located more proximal to nares with belt-on versus belt-off during fasting (44.5 vs 47.2 cm, p<0.001) and after meal (42.7 vs 45.8 cm, p<0.001) (table 2). The pH transition point was also located more proximally with respect to the peak LOS pressure (figure 2). During fasting, the pH transition point was 2.2 cm below peak LOS without belt but was only 0.7 cm below peak LOS with belt (p=0.002). After meal, the pH transition point was 2.0 cm below peak LOS without belt but was 0.4 cm above peak LOS with belt (p=0.004). The pH transition point during fasting was 2.2 cm distal to the SCJ without belt, but with belt was significantly closer at 1.2 cm (p=0.04). After meal, the pH transition point was 1.8 cm distal to the SCJ without belt, but with belt 1.3 cm distal to it (p=0.04).

    View this table:
    Table 3

    Acid exposure in distal oesophagus during fasting and after meal in obese and non-obese subjects and with and without belt

    Acid exposure across the LOS and SCJ

    At 5 cm above upper border LOS (traditional site) and 1–2 cm proximal to upper border LOS, the mean % of time pH <4 was minimal (<4%) with or without belt, before or after meal (table 3). However, acid reflux 1.3 cm above the SCJ 30–60 min after meal was greater with belt-on at 6.1% vs 1.6% with belt-off (p=0.02). The % of TLOSRs with acid reflux at 1.3 cm above the SCJ was greater with belt-on versus belt-off (46.4% vs 18.5%, p=0.001). The acid clearance time following episodes of reflux at 1.3 cm above the SCJ was significantly longer with belt-on versus belt-off (49.5 s vs 14.0 s, p=0.001) (table 4). Likewise, the number of swallows needed to clear the acid after reflux at 1.3 cm above the SCJ was greater with belt-on versus belt-off (2.2/TLOSR vs 0.7/TLOSR, p<0.001).

    View this table:
    Table 4

    Mechanism of acid exposure across the LOS and SCJ

    Central obesity and the GOJ

    Studies of obesity and the GOJ were performed by comparing the 12 obese and 12 non-obese subjects without waist belt.

    GOJ pressures (expiratory)

    IGP was higher in obese versus non-obese subjects during fasting (16.1 vs 10.9 mm Hg, p<0.001) and after meal (18.5 vs 12.9 mm Hg, p<0.001) (table 1). GOPG was also higher in the obese subjects during fasting (17.6 vs 13.3 mm Hg, p=0.003) and after meal (17.8 vs 14.2 mm Hg, p=0.01). IOP was higher in the obese subjects only after meal (0.7 vs −1.3 mm Hg, p<0.001). No significant difference in peak LOS pressure relative to atmospheric pressure or IGP was observed in obese versus non-obese subjects during fasting. The peak LOS relative to IGP was trended lower in obese versus non-obese after meal (12.9 vs 17.2 mm Hg, p=0.08).

    Location of SCJ and its position within HPZ

    The lower border of the LOS was more proximal relative to nares in obese versus non-obese subjects after meal (44.5 vs 47.5 cm, p=0.001) (table 2). However, the position of the upper border and total length of the LOS were similar in obese versus non-obese subjects, fasted or after meal (figure 2). The location of the crural diaphragm was also similar in obese versus non-obese subjects as reflected by the similar distances of PIP and peak LOS from nares, fasted or after meal (table 2).

    The SCJ was located closer to the nares in obese versus non-obese subjects, during fasting (43.0 vs 47.0 cm, p<0.001) and after meal (41.1 vs 46.4 cm, p<0.001) (table 2). The SCJ was also located more proximally within the HPZ (figure 2). During fasting, the SCJ was 1.7 cm below the peak LOS in non-obese, but 1.8 cm above the peak LOS in obese (p<0.001) and after meal, 1.0 cm below vs 2.9 cm above, p=0.03. The SCJ was also located more proximally with respect to the PIP in obese versus non-obese subjects during fasting (1.2 cm above vs 1.3 cm below, p=0.03) and after meal (1.6 cm above vs 1.8 cm below, p=0.01). The SCJ was also closer to the upper border LOS after the meal in obese versus non-obese (1.3 cm below vs 4.6 cm below, p=0.004). The magnitude of the proximal migration of the SCJ during TLOSRs was less in obese versus non-obese subjects (4.2 vs 6.8 cm, p=0.04).

    Location of pH transition and its position within HPZ

    The pH transition point relative to nares was more proximal in obese versus non-obese subjects, during fasting (45.1 vs 48.4 cm, p<0.001) and after meal (43.4 vs 47.3 cm, p=0.04) (table 2). The fasting pH transition point was 3.0 cm distal to position of peak LOS pressure in non-obese subjects, but only 0.3 cm distal in obese subjects (p<0.001). Likewise, after meal, the pH transition point was 1.8 cm below peak LOS pressure in non-obese subjects but 0.7 cm above it in obese subjects (p=0.03). The pH transition point was at a similar distance distal to SCJ in obese versus non-obese subjects during fasting (2.1 vs 1.4 cm, p=0.7) and after meal (2.2 vs 0.9, p=0.1).

    Acid exposure across the LOS and SCJ

    At 5 cm above upper border LOS (traditional site) and 1–2 cm proximal to upper border LOS, the mean % of time pH <4 was minimal (<4%) in obese and non-obese subjects, before or after meal (table 3). Acid reflux at 0.5 cm above the SCJ 30–60 min after meal in obese versus non-obese subjects was not significantly different at 3.0% and 0.7%, respectively, p=0.1). The frequency of TLOSRs was similar between groups, and despite not having any significant acid above the SCJ, the % of TLOSRs carrying acid was greater in obese versus non-obese subjects (32.8% vs 4.2%, p=0.04) (table 4).

    Short-segment reflux in obese subjects with belt-on versus other groups

    There was no acid reflux at traditional site and 1–2 cm proximal to upper border LOS in obese subjects with belt-on, before or after meal (table 3). However, acid reflux at 0.5 cm above the SCJ 30–60 min after meal was 9.7% in obese subjects with belt-on compared with 3.0% in obese subjects without belt (p=0.02, vs obese belt-on) and 0.7% in non-obese subjects without belt (p=0.04, vs obese belt-on) (figure 3). There were more TLOSRs (7.3/h vs 5.0/h, p=0.001) and % of TLOSRs with acid reflux at 0.5 cm above the SCJ (56.4% vs 32.8%, p=0.04) in obese belt-on versus belt-off (table 4). Likewise, following acid reflux at 0.5 cm above the SCJ, the acid clearance time was longer (72.3 s vs 23.4 s, p=0.01) and a greater number of swallows were needed to clear acid (3.2/TLOSR vs 1.1/TLOSR, p<0.001) in obese subjects with belt-on versus belt-off (table 4).

    Figure 3
    Figure 3

    Acid exposure (mean % time pH <4) at 0.5 cm above the squamo-columnar junction in obese subjects with belt-on versus other groups (obese belt-off and non-obese belt-off), *p<0.05.

    Discussion

    Using novel technology we were able to perform detailed studies of the effect of increased WC and a waist belt on the GOJ in asymptomatic volunteers. Both produced abnormalities with a common effect being proximal displacement of the GOJ within the diaphragmatic hiatus. Though neither increased WC nor the waist belt increased acid exposure at the conventional site 5 cm above the upper border LOS, there was evidence of short-segment acid reflux at 0.5–1.5 cm above SCJ with the waist belt and this was most marked in those with increased WC.

    Increased WC and waist belt increased mean IGP by a similar amount of 5.2 mm Hg each at the beginning of study during fasting. In both cases, this was accompanied by the SCJ being displaced proximally after meal with respect to the diaphragmatic hiatus as reflected by the peak LOS pressure and PIP. Whereas the SCJ was an average of 1.0 cm below the position of the peak LOS pressure point in those with smaller WC, it was 2.9 cm above it in those with larger WC. Similarly with waist belt, the SCJ was an average of 0.2 cm below the peak LOS pressure in those with belt-off, whereas, it was 1.7 cm above it in those with belt-on. Likewise, the pH transition point representing the position where pH changes from oesophageal to gastric pH was also displaced proximally within the diaphragmatic hiatus with increased WC and waist belt.

    During TLOSRs, there is marked proximal migration of the SCJ of up to 6.8 cm. Increased WC and waist belt substantially reduced the amplitude of this proximal migration during TLOSRs. This may be explained by the GOJ being already proximally displaced and, thus, the magnitude of the proximal migration occurring with the contraction of the longitudinal muscle during TLOSRs being reduced.

    We are only aware of two previous studies which have investigated the effect of compression by waist belt on the position of the SCJ within the diaphragmatic hiatus in asymptomatic volunteers.20 ,21 In these studies by Kahrilas et al21, no differential movement of the SCJ relative to the diaphragm was observed. The differences between these studies and our current study is likely to be due to the fact that the earlier studies relied on X-ray imaging of a clip and the underside of the diaphragm, whereas in our study, we have employed the newer and more sensitive technologies of intraluminal high-resolution manometry, high-resolution pH and intraluminal detection of magnetic clip with the latter having an accuracy of±0.2 cm.13

    What is the explanation for the proximal displacement of the SCJ and pH transition point within the LOS? These changes could be explained by the increased IAP associated with central obesity or waist belt producing partial hiatus hernia. The HPZ is normally composed of the superimposed pressures exerted by the intrinsic LOS and the extrinsic LOS, that is, diaphragmatic crura. In our subjects, the GOJ and its intrinsic sphincter appear to be displaced proximally within the HPZ of the crura, but not sufficiently to form identifiable double pressure peaks. A full hiatus hernia occurs when the GOJ is displaced sufficiently proximally to cause clear separation of the intrinsic LOS and extrinsic diaphragmatic crura to produce separation of pressure peaks with an area of lower pressure between them representing the hernial sac.20 This is thought to be due to weakening of the crura and also weakening or rupture of the phreno-oesophageal ligament.22 Bredenoord et al23 also described the phenomenon of intermittent hiatus hernia where high-resolution manometry demonstrated intermittent double peaks. In patients being investigated for reflux symptoms, increased WC has been associated with separation of the GOJ components.24 Our current study involves asymptomatic volunteers with no endoscopic evidence of hiatus hernia and no high-resolution manometry evidence of double peaks. The more proximal positioning of the GOJ within the diaphragmatic hiatus in our asymptomatic subjects without evidence of double peaks suggests that this may be early or partial hiatus hernia, and may represent the early stages of its development. The proximal displacement of the GOJ within the diaphragmatic hiatus without overall lengthening of the HPZ could be explained by the proximal and distal borders of the intrinsic sphincter normally lying slightly distal relative to those of the extrinsic crural diaphragm.

    An additional mechanism might explain the more proximal location of the SCJ and more proximal extension of gastric acidity within the LOS in those with increased WC. The chronic increased IAP, partial hiatus hernia, and shortening of the distal segment of the LOS may allow gastric acid to impinge upon the most distal oesophageal squamous mucosa causing it to undergo columnar metaplasia and, thus, proximal migration of the SCJ. We have previously reported proximal extension of the gastric cardia mucosa associated with increased WC in asymptomatic volunteers.7

    With the waist belt there was evidence of proximal displacement of the diaphragmatic hiatus itself represented by the location of the upper and lower borders of the LOS and peak LOS pressure relative to nares, but this was not observed with increased WC. It is possible that the absence of displacement associated with increased WC was due to it being more difficult to detect between the two groups of subjects with differing WC than between the same subjects with or without belt. However, in our previous larger study of 27 subjects with increased WC and 24 with normal WC, proximal displacement of the diaphragmatic hiatus was still not apparent.7 The lack of proximal displacement of the diaphragmatic hiatus with obesity might be due to adaptive changes to diaphragmatic strength associated with chronic elevation of IAP, as has been observed with peritoneal dialysis.25

    The changes in LOS pressure also differed with increased WC versus belt. Unlike increased WC, the waist belt caused a rise in the peak LOS pressure relative to atmospheric pressure, and a less marked rise relative to IGP reflecting IAP. Any increase in IAP will cause a rise in pressure of the intra-abdominal segment of the LOS due to the abdominal pressure acting on it.26 ,27 The rise in LOS pressure relative to IGP, as well as atmospheric pressure, may be explained by reflex contraction of the crural diaphragm which has been previously observed with increased IAP caused by abdominal constriction by belt or leg-raising.28 ,29 The lack of increase in LOS pressure with increased WC may be due to the reflex not responding to the more chronic elevation or the IAP. Alternatively, it may represent weakness of the crura and phreno-oesophageal ligament in those with chronic elevation of IAP due to increased WC. We have previously reported that LOS pressure, relative to IGP, is reduced in those with increased WC, but not with application of waist belt.30

    The waist belt was associated with increased acid exposure of the most distal oesophagus. In the whole group the acid exposure 1.3 cm above the SCJ in those with belt-on was 6.1% compared with 1.6% in those with belt-off (p=0.02). It was not possible to achieve the exact location of the pH electrode between the groups, but acid exposure is known to increase with proximity to the SCJ and, thus, the minor difference in location will have minimal rather than any exaggerated difference. Likewise, in obese subjects with belt-on, the acid exposure was 9.7% at 0.5 cm above SCJ versus 3% at 0.5 cm above SCJ in obese subjects without belt (p=0.02) and versus 0.7% at 0.5 cm in non-obese subjects without belt (p=0.04). The acid exposure of the distal intrasphincteric segment of the oesophagus was the greatest in obese with belt and least in non-obese without belt.

    Our ability to accurately monitor the location of the SCJ throughout the TLOSRs and measurement of local acidity allowed examination of the mechanism of reflux associated with increased WC and waist belt. The predominant mechanism of the acid exposure was increased reflux occurring during TLOSRs and reduced clearance of the acid. It is known that full hiatus hernia increases acid reflux during TLOSRs and its subsequent clearance. It therefore seems like the similar reflux noted with waist belt and increased WC are related to the proximal displacement of the GOJ within the diaphragmatic hiatus exerting similar effects. The reason for the acid reflux only involving the most distal intrasphincteric segment of the oesophagus is unclear, but might be related to the partial nature of the hiatus hernia and the fact that the waist belt did not increase the GOPG.

    In summary, our studies demonstrate that in asymptomatic volunteers, waist belt and central obesity are associated with proximal displacement of the SCJ within the diaphragmatic hiatus, and that the combination is associated with short-segment acid reflux. The latter might explain the high incidence of inflammation and metaplasia, as well as occurrence of adenocarcinoma observed at the GOJ in asymptomatic subjects.

    Acknowledgments

    We would like to thank all volunteers who have taken part in our studies.

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    Supplementary materials

    • Supplementary Data

      This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.

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    Footnotes

    • Contributors YYL: Data acquisition, analysis and interpretation of data, drafting of manuscript, statistical analysis, intellectual contribution. AAW: data acquisition, intellectual contribution. JGHW: design of probe, intellectual contribution. EVR: intellectual contribution. MHD: analysis support, intellectual contribution. DS: design of probe, technical support. AW: software design, technical support. AWK: software design, technical support. KELMcC: study concept and design, drafting of manuscript, critical revision of manuscript for intellectual content, study supervision.

    • Competing interests None.

    • Patient consent Obtained.

    • Ethics approval West Glasgow Research Ethics Committee.

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