Bariatric surgery was originally developed for weight reducing purposes. Today we know that these gastrointestinal interferences also markedly reduces the risk for cardiovascular disease as shown by an estimated 40% reduction in 10 y Framingham risk score
[5]. Furthermore, Heneghan et al showed that bariatric surgery is associated with a 68% resolution/reduction of obesity associated hypertension
[5]. However, the mean follow up time of this analysis was only 34 months and studies over longer periods (
ie. 8 to 10 y) are few and usually uncontrolled
[5],
[6]. The present investigation, being an
ad hoc-analysis based on the controlled prospective SOS study
[4],
[15], provides the first longterm direct comparison between conventionally treated (
ie. dietary advice, life style changes, pharmacology etc) obese patients and those treated surgically with either GBP or VBG/B. Previously published meta-analyses have shown that a pharmacological reduction of diastolic pressure by 5 mm Hg considerably reduces the risks of stroke and ischemic heart disease
[7]. Interestingly, a blood pressure reduction of this order of magnitude was in the present study recorded only in the GBP cohort at the 10 y follow-up and despite a relatively low usage of antihypertensives. It is well known that weight reduction
per se is associated with a decrease in blood pressure mainly due to the improvement of renal sodium retention that is commonly associated to obesity
[16],
[17]. Increased exercise and a diet with low sodium and calorie contents can reduce blood pressure in a weight dependent fashion
[13],
[18]. However, the long-term compliance with these types of life style changes is low and there is eventually a relapse to overweight and increased blood pressure. Bariatric surgery is currently the only evidence-based treatment for maintaining a reduction in body weight
[3].
Indeed, at the 2 y follow-up in the present study, the two bariatric surgery cohorts exhibited reduced BMI and a reduced arterial blood pressure compared to the non-operated controls. However, at the 10 y follow-up in VBG/B patients, blood pressure had returned near to preoperative levels despite a reduction in body weight. One explanation may be that an increased inclination for social interaction following weight reduction creates iterated situations with a psychosocial stimulation of the sympathetic nervous system, in turn increasing blood pressure
[17]. Another possibility is that restrictive bariatric surgery induces a dietary pattern promoting hypertension
[19].
In contrast to restrictive bariatric surgery, GBP was followed by a marked decrease in blood pressure also at the 10 y follow-up. This finding suggests that GBP interferes with blood pressure control via at least 2 principles: an initial transient blood pressure reduction related to weight loss
per se (similar as after VBG/B), and a more long term mechanism unrelated to weight loss. This interpretation is supported by the present observation that arterial blood pressure was markedly more depressed after GBP than after VBG/B, already after a period of only 2 y. Actually, a weight-independent blood pressure reducing effect of GBP has previously been reported as early as week one postoperatively, thus before any significant weight loss
[20]. Based on these observations it is plausible to assume that the exclusion of the gastroduodenum, or the direct loading of undigested food into the jejunum, added or removed a blood pressure regulating factor acting in parallel with the depressor effect of weight loss (Supporting information
Figure S2).
In analysing diurnal urinary volumes, we found that the GBP patients excreted more urine per day than weight-matched patients treated with restrictive bariatric surgery. Furthermore, regression analysis demonstrated that changes in urinary output were linearly associated with blood pressure changes only in the GBP cohort (Supporting information
Figure S3), indicating that blood pressure reduction following gastric bypass can be attributed to a diuretic action. It can perhaps be questioned whether a chronic enhancement of diuresis by only 100 to 200 mL per day explains the lowered blood pressure in the GBP cohort. Interestingly, the users of diuretics compared to non-users in the non-operated cohort had a similar difference in urinary output as the one observed between GBP and VBG/B (Supporting information
Table S1). These results indicate that the GBP-associated diuretic action is of clinical relevance with regard to blood pressure control.
The mechanisms behind the diuretic action following GBP are obscure. Bueter
et al. recently demonstrated that an oral salt load in rats operated with GBP was followed by an increased urine output and natriuresis as well as increased water intake. However, these authors could not distinguish between if the increased diuresis was a primary mechanism, or if it was secondary to blood volume expansion following drinking
[21]. In the present study, 24 h natriuresis was higher after GBP, whereas potassium excretion was more or less constant, suggesting a primary natriuretic effect. The finding that the serum sodium concentration was elevated in the GBP group speaks, however, against such an action ()
[22].
We found that the calculated salt intake was more than +1 g higher per day after GBP compared to salt intake in the patients treated with restrictive bariatric surgery. Intuitively, high salt intake should increase blood pressure
[12]–
[14]. However, this was not the case in the present study indicating that GBP patients lower their blood pressure despite an increased consumption of salty foods. It may be speculated that GBP increases both salt appetite and natriuresis explaining the slightly increased serum sodium concentrations observed in the present study. By use of surveys, Tichansky
et al. showed that GBP patients were more likely to develop an increased taste/affinity for salty foods than gastric banding patients who where more likely to develop an increased taste/affinity for sweet foods
[23]. Hence, our findings support the existence of a sodium sensor in the human upper gut
[24]–
[26], that normally inhibits salt appetite and influence natriuresis, being “bypassed” following GBP. The involved gastrointestinal signalling mechanisms remains to be clearified.
The present study has some obvious limitations: The cohort analysis was performed
ad hoc and interpretations must be made with caution because the SOS study was originally designed to compare bariatric surgery
per se with conventionally treated obese patients and the study power was determined using mortality as the primary outcome variable
[15]. Another potential source of error in the present study is the 24 h sampling of urine. As the urine was collected by the study participants themselves, sampling errors related to over- or under-collections must be considered. However, there is little reason to believe that any of the surgery groups would be more likely to provide over- or under-collections. In addition, the differences in diurnal urine output and sodium excretion between GBP- and VBG/B subjects remained significant after adjusting these analyses for 24 h urinary excretion of creatinine (data not shown). Another potential limitation of the study is that the cohort representing ‘restrictive’ bariatric surgery consists of two types of surgical procedures: VBG (n

=

1189 and n

=

843 at the 2 y and 10 y visit, respectively) and gastric banding (n

=

328 and n

=

202). These two operations have some obvious technical differences that might have influenced the primary outcome variables (BMI, arterial pressure, use of antihypertensives/diuretics, diurnal urinary volume, estimated salt intake). However, when a subgroup comparison was performed only one significant difference appeared: the diastolic pressure had decreased more after gastric banding at the 2 y visit (Supporting information
Table S2). As this difference (≈1,2 mmHg) is of minor clinical relevance the merger of the two operations into a single cohort seems to be justified.
In conclusion: Gastric bypass is associated with a longstanding reduction in both systolic and diastolic blood pressures and an increased diuresis not related to weight loss. Despite a greater blood pressure reduction, the daily salt consumption is higher after GBP than after restrictive bariatric surgery.