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A. C. Sudlow et al.394
must employ interventions that shift the body fat set point in order to see sustained results.
Bariatric surgery is an effective treatment for obesity which can be in part
attributed to the fact that it treats several of the pathological processes driving obesity, including inducing profound metabolic changes which alter the
homeostatic regulation of our body fat set point. This concept of the set point
is thought to be one of the main contributory factors associated with the critical long-term weight loss maintenance which is responsible for the improvements in cardiovascular risk factors and associated improvement in all-cause
mortality [3, 4].
With our growing understanding of the multisystemic effects of obesity comes
an appreciation that weight is not the sole measure of the efficacy of a treatment
for obesity however it remains a useful and quantifiable measure of the effect of
an intervention. Considering weight loss alone however is an unhelpful metric.
Weight loss in isolation is largely meaningless unless accompanied by a sustained
period of weight loss maintenance which is largely responsible for the physiological changes contributing to control of comorbidity and ultimately, improved mortality. Outcomes from both lifestyle and surgical interventions would suggest that
in evaluating the utility of a treatment, we should perhaps shift our perception to
view weight loss and weight loss maintenance as two distinct entities, governed by
discrete but interrelated homeostatic mechanisms.
2 Set Point Theory
The proposed mechanisms underlying weight regulation have long been dominated by an overly simplistic view that it is governed predominantly by a calculation of energy balance between caloric intake and energy expenditure. The
biological plausibility of this explanation has seen it become near dogma not only
within the wider population but the medical community as well, in spite of mounting evidence to support the fact that mechanisms regulating weight are likely a
complex series of interactions between environmental and biological factors, many
of which remain incompletely understood. Bariatric surgery has proven to be an
effective treatment for obesity in its own right but it has also produced conditions
whereby we can further expand our understanding of the homeostatic mechanisms
regulating weight. Although procedures were initially classified according to the
presumed mechanisms based on anatomical intentions of the operations such as
malabsorptive or volume restrictive, mechanistic studies have demonstrated that
there are a series of changes both centrally and within the gut responsible for not
only weight loss but changes in metabolism and energy balance. While these findings have enlightened our general view of the complex regulatory mechanisms
controlling hunger, satiety and weight regulation, they have also highlighted that
Other Potential Benefits of the Sleeve …
395
it is very likely our current understanding and appreciation of the disease is only
very rudimentary and there are many more unanswered questions. Unlike weight
loss mediated by lifestyle or dietary intervention, patients losing weight following sleeve gastrectomy are able to maintain this weight loss even after they return
to caloric intake similar to their preoperative levels. These findings would suggest
that sleeve gastrectomy produces a sustained changes in central neurohormonal,
metabolic and behavioural processes regulating weight.
One proposed element in the regulation of body weight is thought to be a
centrally determined ‘set point’ which ensures that through various homeostatic
mechanisms there are adjustments in food intake, energy expenditure or a combination of the two in order to maintain a certain inherent body fat mass. From a
basic evolutionary perspective which is supported by the observed trend towards
an increasing prevalence of obesity, this set point appears to be more attuned
to the need of preventing starvation rather than obesity as starvation would
pose a more imminent threat to life. There are a number of different purported
mechanisms by which our bodies ‘defend’ this set amount of fat mass including regulatory feedback from specific body components such as fat mass and/or
neurohormonal signalling. One such theory regarding a set point controlled by
fat mass comes from one of the earliest investigations of the regulation of body
weight, the Minnesota Starvation Experiment [5]. The researchers found following a period of starvation in participants without obesity, the degree of hyperphagia or overeating once the starvation period ended was proportional to the
depletion of fat and muscle mass, suggesting that food intake and appetite may
be in part driven by a homeostatic mechanism to maintain or in this case, restore
lost fat and or muscle mass. This very early work indicated the possible presence
of regulatory mechanisms based on a set point, as hyperphagia persisted only
until the patients returned to the pre-intervention levels of fat and muscle mass.
This basic concept appears to be supported by later research suggesting it was
not necessarily signals from fat per se as the determining factor rather, neurohormones responding to variation in fat mass which were major contributors to
our homeostatic control of body weight. The adipocyte derived hormone, leptin
appears to play a potentially critical role in this regulatory pathway, serving as
signal to the hypothalamus regarding nutritional status, energy balance and body
weight. Although leptin mediates its activity via both orexigenic and anorectic
neurons in the hypothalamus, leptin activity appears to be more closely related
to preservation of body weight rather than prevention of obesity. In weight loss
where it appears to have its greatest effect, as leptin levels fall with decreasing
body weight and overall fat mass, there is a rise in NPY levels [6]. NPY is produced in the arcuate nucleus and is one of the most potent orexigenic hormones,
mediating increased appetite and food intake. Similarly, changes in leptin receptor sensitivity, receptor mutations or resistance could also potentiate these effects
with preserved leptin levels. It has been proposed that conditions which alter the
A. C. Sudlow et al.396
leptin concentrations at which the hypothalamus perceives as a state of energy
imbalance may change the intrinsic ‘set point’ however it is unclear how this is
mediated [7].
3 Weight Regulation and Weight Loss Maintenance
The emergence of bariatric surgery as a treatment for obesity has deepened our
understanding of the metabolic and homeostatic mechanisms involved in obesity and specifically how weight is regulated. The ability to produce significant
weight loss which is sustained in the long term, unlike that seen with any lifestyle intervention has led to further development of the “set point” theory to
describe how weight is maintained in both healthy weight patients and in those
with obesity. The set point theory evolved from the idea that individuals possess an intrinsic mechanism for weight regulation by which their body appears
to have a baseline weight around which there is little variation once they have
reached adulthood. Without sustained and major changes in diet or lifestyle/activity levels, most individuals will maintain their weight around this set point which
appears to have at least in part a genetic basis. This concept may serve to explain
why without intervention such as bariatric surgery, the majority of patients may
be able to lose weight with lifestyle measures initially but will struggle to maintain this in the long term.
4 Weight Loss and Weight Loss Maintenance Following
Sleeve Gastrectomy
Given the relative late adoption of sleeve gastrectomy in comparison to other
procedures, there is not as much long term data regarding weight loss compared to RYGB although evidence from studies with short to mid-term follow
up would support that it produces roughly equivalent weight loss and similar levels of improvement or resolution of many obesity related comorbidities [8–10].
Although there is some variation in the individual pattern of weight loss, following
sleeve gastrectomy the majority of patients will follow a similar trajectory with a
period of rapid weight loss over the first year to 18 months followed by a period of
weight loss plateau and eventual gradual regain. Longer term studies with follow
up > 5 years would suggest %EWL in the range of 50–60% [11, 12]. Although it is
recognised that following SG, some patients will regain some of the initial weight
lost however, the critical element to recognise is that most weight loss is durable
and is maintained around what appears to be a new “settling point”. Looking at
the natural pattern of weight gain over the course of an individual’s life, there is a
general and gradual trend towards increasing weight. Patients following SG follow
this same pattern however now starting from a new, lower baseline weight and following a parallel trajectory.
Other Potential Benefits of the Sleeve …
Bariatric surgery was initially viewed as a treatment governed by the fundamental principles of volume restriction and malabsorption to produce weight loss.
Our early understanding at the time of its effects with regards to the metabolic
changes it evoked as well as the mechanisms by which it acted were incomplete.
Although the procedures since then have also changed as evidenced by the widespread adoption of sleeve gastrectomy, perhaps the most critical shift in the field of
bariatric surgery has been our greater appreciation of the complexity of obesity as
a disease as well as the mechanisms of weight regulation and how this is affected
by surgery. Mechanistic and behavioural studies have demonstrated that number
of interrelated mechanisms including alterations in appetite and satiety, neurohormonal signalling as well as bile acid metabolism are key mediators of the effects
of SG with regards to weight loss and improvements in metabolic dysfunction
[13–15].
397
5 Behavioural Change Following SG Contributing to a
Shift in the Set Point and Long Term Weight Loss
Although there are well recognised behavioural changes following SG which may
play an important role in weight loss maintenance, the concept that it is solely the
result of a decreased volume in food intake has been consistently demonstrated
to be incorrect. In both human and rodent models, it is recognised that there is
decreased food intake during the early postoperative period however weight loss
persists after this transient change disappears [16, 17]. There are however recognised changes in eating behaviours which are more likely to be contributory factors in maintaining weight loss. In one study looking at rats undergoing bariatric
surgery, there was a clear change in food preferences following SG and RYGB
with a decrease in the intake of dietary fat as well as a preference for less calorie dense foods. Interestingly, only the rats undergoing SG subsequently displayed
an avoidance after intragastric oil administration whereas the RYGB rats did not,
suggesting that the development of food avoidance in the SG model may contribute to altered food choices [18]. These findings were supported by a further study
which demonstrated a reduced preference for high fat containing foods as well
as an alteration in nutrient sensing which lowered the satiety threshold, resulting
in smaller meal size following SG [19]. In human studies, these changes in food
preferences are more controversial. One study observed patients following SG and
showed a 68% reduction in caloric intake not only a result of decreased volume
but due to a preference for less calorie dense foods up to two years postoperatively
[20]. These findings have been supported by further studies demonstrating changes
in food preferences with patients post SG reporting sensing an increased intensity
of sweet and fatty flavours which was accompanied by decreased enjoyment and
desire for these same food groups [21]. Other studies showed no changes in food
selection when more direct measures of behaviour were employed [22].
A. C. Sudlow et al.398
6 Neurohormonal Regulation of the Body Set Point
Given the observed changes in food preferences, appetite and eating behaviour,
there has been an increasing focus on gut derived neurohormonal signalling which
may underlie or potentiate these changes and how they contribute to weight loss
maintenance. In the period following SG, there may be an adjustment of the
pre-existing set point at which the body perceives there to be an energy deficit.
Lowering this threshold would alter the point at which the normal homeostatic
mechanisms normally preventing excessive weight loss would become active.
The role of leptin has been extensively investigated with suggestions that there
is the possibility of increased leptin receptor sensitivity or receptor upregulation
which would counteract the normal hypothalamic response to falling leptin levels
due to fat loss however, this has not been borne out by data from rat models [16].
Looking specifically at RYGB, there are studies which have served to support the
role of leptin, demonstrating that leptin deficient mice lost less weight following
bypass surgery. This finding would suggest that intact leptin signalling pathways
are required to demonstrate the beneficial response to bariatric surgery however,
its exact role in SG has yet to be elucidated [23]. Other potential neurohormonal
mediators which have been proposed to have an important role in postoperative
weight loss maintenance include PYY and GLP-1 which are both secreted by the
L cells primarily found in the distal ileum. PYY is a key hypothalamic regulator of satiety mediated though its effects of delayed gastric emptying and reduced
gastric acid secretion and is thought to potentially counteract the orexigenic effects
of falling leptin levels in the postoperative period. Like PYY, GLP-1 has important
and similar regulatory effects with regards to appetite but as an incretin hormone
is also thought to potentiate many of the metabolic improvements in glycaemic
control following SG. Both PYY and GLP-1 levels rise post sleeve gastrectomy
which appears to be related to increased appetite suppression and improved weight
loss [15, 24–26]. Resection of the gastric fundus in SG differentiates it from other
commonly performed procedures such as RYGB or LAGB which is an important
consideration when it comes to the neurohormonal changes it imparts as this is
the primary location for the production of ghrelin which plays an important role
in regulating hunger. A meta-analysis of 25 studies including two randomised
controlled trials demonstrated decreased levels of ghrelin following SG however the implications for postoperative weight loss, weight loss maintenance and
the metabolic implications are less clear [14, 15, 27]. Outcomes with RYGB are
similar with regards to all of the aforementioned parameters despite the fact that
it has been associated with maintained or increased ghrelin levels. Furthermore,
studies in ghrelin deficient mice have demonstrated comparable outcomes following SG to wild type mice with regards to weight loss, food intake and dietary
preferences, suggesting the effects of SG are ghrelin independent [28]. While
these studies have not definitively demonstrated a causal role in weight loss
following bariatric surgery, it is likely that neurohormonal changes related to ghrelin are part of a complex interaction of numerous factors in postoperative weight
regulation.
Other Potential Benefits of the Sleeve …
399
7 Bile Acids and Long-Term Fat Mass Set Point
Regulation
Changes in bile acid metabolism have also been identified as potential targets
for inducing long term weight loss following SG. Studies have demonstrated an
increase in serum bile acids following SG in rats which are thought to play an
important role in metabolic regulation via their interaction with the nuclear receptor, farnesoid X receptor (FXR) [29]. FXR is a bile acid receptor and a key regulator in bile acid synthesis which also plays an important role in lipid and glucose
metabolism [30]. This may be a key mediator, linking the alterations in bile acids
following surgery to changes in glucose metabolism and plays a critical role in
the postoperative remission of T2DM. The presence of this link was demonstrated
when mice with a genetic disruption of FXR and diet induced obesity had attenuated weight loss and glycaemic control after a sleeve gastrectomy, suggesting the
potential role of this pathway in mediating the effects of surgery [31]. Increased
levels of bile acids may also contribute to an overall negative energy balance in the
postoperative period via their effect on the bile acid receptor, TGR5 which results
in increased oxygen consumption and energy expenditure. In rodent models following sleeve gastrectomy, increases in bile acids result in upregulation of TGR5
activity, mediating an increase in brown adipose tissue (BAT) thermogenesis [32].
BAT is involved in postprandial increases in thermogenesis and is thought to play
a protective role against obesity. Overall energy expenditure has not been demonstrated to rise following SG however this increase in BAT thermogenesis may
be sufficient to counteract the drop in total energy expenditure that is commonly
observed following weight loss, thereby contributing to the maintenance of a new,
lower weight set point. Experimental studies looking at non-invasive methods of
measuring thermogenesis have supported this observation in human studies with
patients following SG demonstrating increased BAT thermogenesis when measured with infrared thermography whereas there was no change evident following RYGB [33]. Although only preliminary, this data would support the possible
role of SG in inducing changes in BAT activation and postoperative alterations in
energy expenditure.
8 Conclusions
Sleeve gastrectomy has proven to be an effective method of inducing clinically
significant weight loss, improving obesity related complications and cardiometabolic risk factors for mortality. Of critical importance in the success of SG as a
procedure has been its ability to produce these changes which are sustained in
the long-term however the mechanisms by which this occurs are incompletely
understood. Long-term follow up data would suggest that these changes are in
part the result of a re-setting of the intrinsic ‘set point’. Studies using both rodent
and human data indicate that this new, lower set point may cause the changes
in eating behaviours, hunger and satiety. This may be mediated by complex
A. C. Sudlow et al.400
interactions of neurohormonal and bile acid signalling both within the gut and
centrally. An understanding of the regulatory pathways involved in the ‘set point’
may help identify means of improving surgical outcomes. This may also explain
why patients immediately after surgery have profound reductions in hunger and
increases in satiety, because they find themselves 25–30% above their new set
point. As they reach their new set point their hunger and satiety may return to normal to allow them to maintain themselves at this new set point. This is therefore
not a failure of the operation of its mechanisms but rather explains clinical observations. Clinicians can thus use the explanation of the body fat set point changes
after sleeve gastrectomy to inform patients to help them achieve optimal long term
health benefits.
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401
Quality of Life and Bariatric Surgery
Rawan El-Abd and Salman Al-Sabah
Quality of life includes mental, physical, and social well-being. Besides increased
morbidity and mortality, obesity is also associated with reduced quality of life as
reported by studies assessing Health-Related Quality of Life (HRQL) in patients
with obesity, which report BMI to be associated with fatigue, chronic pain, and physical limitations, ultimately resulting in poor patient health perception and reduced
quality of life (QOL) [1–7] that is more prominent in the female population [8].
The success of a bariatric intervention does not only relate to weight loss, but
is also determined by its effect on QOL, behaviors of eating disorders, food tolerance, and resolution of co-morbidities. It is expected that after bariatric surgery quality of life improves due to weight loss, better function, and resolution
of co-morbidities, however, the occurrence of side effects may hinder that. Such
side effects include recurrent vomiting, regurgitation, or poor postoperative nutrient absorption [9, 10].
In fact, the great majority of studies in the literature conclude that HRQL
improves drastically within months after bariatric surgery with maintained effect
up to 10 years post-operatively in some patients [11–16]. If assessed before and
after undergoing a bariatric procedure, patients score better post-operatively and
can even score better than the “normal” general population, making bariatric surgery an intervention of great impact on QOL [11, 12]. The changes in HRQL after
bariatric surgery are not absolute but rather they largely reflect periods of weight
loss, weight regain, and weight stability. HRQOL greatly improves with a weight
loss of 30% after bariatric surgery [17] and starts deteriorating as a patient regains
weight [16]. Peak improvement is seen in the short-term (6–12 months) but tends
to slowly decrease with time (1 to 6 years post operatively), which is greatly
R. El-Abd (*) · S. Al-Sabah
Faculty of Medicine, Health Sciences Centre, Kuwait University, Jabriya, Kuwait
e-mail: rawanela@gmail.com
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer
Nature Switzerland AG 2021
S. Al-Sabah et al. (eds.), Laparoscopic Sleeve Gastrectomy,
https://doi.org/10.1007/978-3-030-57373-7_39
403
404
influenced by the total weight loss and side-effects of specific procedures [14,
18]. In extended follow-up studies, it was reported that the periods between 6 and
10 years postoperatively show stability in both body weight and HRQL scores [16]
and that a maintained total weight loss of only 10% is sufficient for a positive long
term outcome on HRQL. In fact, if assessed after 10 years, patients who underwent bariatric surgery show better outcomes on health perception, social interaction psychosocial functioning and depression than those who did not undergo an
intervention [16].
Food tolerance, gastrointestinal health, and quality of life are different between
surgeries. Sleeve Gastrectomy (SG) and Roux-en-Y Gastric Bypass (RYGB) show
better effect on HRQL as compared to Gastric Banding (GB) with a significant
relation to weight loss after each surgery [19, 20]. SG also results in better food
tolerance, eating behavior, and gastrointestinal quality of life than RYGB and GB,
which contribute to its favorable outcome on HRQL [9, 21]. Gastrointestinal quality of life is strongly correlated with food tolerance after surgery [19].
To assess the QOL of patients, different tools are available, the most studied
are:
R. El-Abd and S. Al-Sabah
1 Medical Outcomes Survey Short Form 36S (SF-36)
This is a questionnaire of 36 items around 8 areas: physical functioning, social
functioning, physical problems, emotional problems, mental health, energy, pain,
and general perception of health. Results are reported into 2 categories: physical
health and mental health. It is scored from 0 to 100 for each area [22–24].
2 Bariatric Analysis and Reporting Outcome System
(BAROS) Score [25]
This score is done after a bariatric intervention and assess its effectiveness
through examining 3 domains: weight loss, changes in co-morbidities, and quality of life. Each domain can have up to 3 points, with points deducted for complications or reoperations. It finally divides patients into 5 groups and determines
the success or failure of the intervention. This score can be used to compare outcomes of different operations or surgeons and serve as a uniform assessment of
outcomes.
3 The Bariatric Quality of Life Index (BQL)
This tool combines medical data of a patient with a questionnaire of 13 questions
and 65 points. It measures a patient’s QOL before and after a bariatric intervention. It was reported to be superior to other questionnaires (e.g., BAROS) [26, 27].
A study conducted to validate this questionnaire reported BQL to show a strong