Hypogonadism and sub-fertility can be frequently associated to obesity and metabolic syndrome. Hypogonadal state has demonstrated to induce a worsening of co-morbidities such as cardiovascular disorders and type II diabetes [17]. In particular the correlation between testosterone low level and peripheral insulin resistance could lead to presume an important role of testosterone on the glycaemic metabolic improvement after bariatric surgery [18, 19]. As recently reported in literature, alterations in sex hormones, testosterone in male obese patients, can improve drastically after weight [15, 18, 20, 21]. Obviously, treatment of impaired fertility and poor sexual life in obese patients will result in implementation of overall health and quality of life.

In a recent meta-analysis, it has been demonstrated that body weight loss significantly increases testosterone levels in obese patients. Moreover, testosterone recovery seems to be directly correlated with the weight loss. Testosterone rise induced by lifestyle interventions was only modest, probably reflecting the relatively modest results of the targeted diet and physical activity on body weight loss. The testosterone increase would be more important after surgical-induced weight loss (9.8 % with diet vs. 32 % with surgery) [20].

As a matter of fact, male hypogonadism could represent a new co-morbidity to consider when evaluating patients for bariatric surgery, and so it could become a new possible criterion for patients with BMI ≥35 [19].

More studies, based on randomised trials, are needed to confirm the role of testosterone of glycaemic metabolic control after bariatric surgery.

Morbid obesity is strongly associated with nonalcoholic fatty liver disease (NAFLD), which is one of the most common causes of chronic liver disease worldwide [22].

NAFLD includes a broad spectrum of liver tissue alterations, which range from steatosis (pure fatty liver) through nonalcoholic steatohepatitis (NASH) to fibrosis, cirrhosis and liver failure. In the severely obese, the fatty liver and its stages often have progressed to NASH or cirrhosis even before contemplating therapy [23].

Weight loss should be a primary therapy for NAFLD. However, evidence supporting intentional weight loss as a therapy for NAFLD is limited [24].

Since insulin resistance causes abnormal deposition of triglycerides in the liver, the link between metabolic syndrome and NALFD is clear. By the way bariatric surgery could improve NALFD, ameliorating also other factors like weight loss, inflammation, dyslipidaemia and intestinal hormones. These are the reasons bariatric surgery has to be considered a potential treatment of NALFD [22, 25].

The NAFLD guideline does not formally recommend bariatric surgery for the treatment of NASH because beyond potential benefits, there is an important lack of scientific evidence that could demonstrate any recommendation to support or reject bariatric surgery to treat NASH patients [26, 27].

On the other hand, it is important to note that bariatric surgery is not contraindicated in NASH patients without cirrhosis [28, 29].

The promising results in literature about metabolic surgical treatment of liver steatosis should encourage to design new randomised clinical trials in order to assess the therapeutic effect of bariatric surgery with long follow-up periods.

Class I obesity (BMI >30 < 35 kg/m²) has been demonstrated to have a co-morbidity burden, in particular type II diabetes, similar than class II or III obesity; even class I obesity is associated with lower mortality rate than higher obesity class [30].

In the Consensus Conference Statement on Bariatric Surgery for morbid obesity published 10 years ago, Buchwald already proposed the possibility in extending the benefits of bariatric surgery to patients with class I obesity who have a condition that can be cured or markedly improved by substantial and sustained weight loss [31]. Since 2004 a considerable number of trials, meta-analysis and observational studies have been published about possible extension of the NIH recommendation of 1991 [1, 32–34].

In 2009 the American Diabetes Association considered the current evidence insufficient to recommend surgery to BMI >30 with type II diabetes. Recently the International Diabetes Federation suggested that patients with type II diabetes with class I obesity could be candidate to surgery if they fall in the same metabolic and clinical conditions warranting prioritisation in the 35–40 BMI class [4].

Recently ASMBS stated that the BMI alone is a poor index of adiposity and risk. Underlining the limitation of the 35 BMI cut-off, the ASMBS concluded that bariatric surgery shouldn’t be denied to patient with BMI >30 < 35 kg/m² or >27.5 kg/m² for at-risk ethnicities who do not achieve substantial and durable weight and co-morbidity improvement [35, 36].

In conclusion, as clearly stated in the recent position statement of IFSO, the access to bariatric surgery should not be denied to patient with class I obesity associated with significant obesity-related co-morbidities simply on the basis of BMI level [37].

Gastroesophageal reflux disease (GERD) is one most common disease worldwide. Obesity has demonstrated to increase the severity and the incidence of GERD due to several factors such as augmented intra-abdominal pressure, increased hiatal hernia incidence, oesophageal dismotility disorders and lower oesophageal sphincter decreased pressure [38, 39]. Roux-en-Y gastric bypass (RYGB) is considered an anti-reflux system, and there is accordance in literature about GERD remission after RYGB. In fact RYGB has been proposed by many authors as a good choice for redo surgery in case of failed anti-reflux operations [40–42].

Studies in literature are inconsisted regarding the possible effect of laparoscopic adjustable gastric banding (LAGB) or laparoscopic sleeve gastrectomy (LSG) on patients with preoperative existing GERD. There is not a clear evidence of worsening of GERD after LAGB because of the difficulty of distinguishing recurrent GERD and symptoms indicating a complication of the banding [43, 44].

Some series demonstrated an initial GERD remission after surgery probably due to the weight loss, reduced intra-gastric pressure and reduced number of transient lower oesophageal relaxation (TLESR) after LAGB. However, a significant worsening of reflux symptoms and de novo esophagitis has been demonstrated during long-term follow-up [38, 45]. Outcomes in terms of GERD after LSG are contradictory [46].

Symptomatic GERD complicates sleeve gastrectomy up to 25 % of cases according to the literature [47, 48].

In fact despite the initial high incidence of de novo GERD symptoms or worsening of GERD after LSG, many studies demonstrate a decrease of GERD on long-term follow-up. Possible causes are the weight loss and the “Angle of His” restorations [38, 49, 50].

Some technical precautions could avoid the worsening of GERD or creation of de novo GERD symptoms after LSG: avoiding large pouch, strictures that could decreased the acid clearance, the lesion of lower oesophageal sphincter and antrum narrowing [38, 49, 50].

The presence of GERD symptoms could be actually considered only a relative contraindication to sleeve gastrectomy and gastric banding in morbidly obese patients [51, 52].

Even in the absence of large RCT, RYGBP could be the procedure of choice in case of symptomatic GERD [14, 43] As suggested by many authors, a preoperative oesophageal manometry and pH-metry should be performed in patients candidate to LSG [38, 39].

Further prospective studies are needed to clarify the role of GERD in the selection for bariatric operations.

Several studies demonstrate a significant worsening of bone density after bariatric surgery, in particular in postmenopausal women.

As calcium absorption happens in the duodenum and proximal jejunum, performing procedures with the bypass of duodenum or with a malabsorptive component in patients with pre-existing osteoporosis could not be recommended [53, 54].

In these cases, preoperative endoscopy is mandatory. In case of direct familiarity with upper GI cancer, procedures that consist of the exclusion of part of the stomach are not recommended. If LAGB or SG is not suitable for a patient with upper GI cancer familiarity, it is possible to perform RYGBP with subtotal gastrectomy [55, 56].

In case of high suspicion of low adherence to the follow-up after bariatric surgery, a SG should be recommended, avoiding the procedures that can require a strict follow-up (malabsorptive or LAGB) [14, 57, 58]. However, the exclusion of these patients from bariatric surgery programmes should be evaluated.

When a morbid obese patient is affected by systemic diseases, it should be recommended to perform a pure restrictive procedure [3, 59, 60].

There isn’t too much literature about obesity surgery and type I diabetes. After bariatric surgery, patients with type I diabetes demonstrate a significant improvement in terms of quality of life, with an improvement of glycaemic control and reduction of overall doses of insulin.

In case of malabsorptive procedure, there are risks of impaired or inadequate drugs absorption; this is why a restrictive procedure should be performed. On the other hand, it should be considered that the bypass of duodenum and proximal part of jejunum represents weight-independent factor of insulin sensibilisation [14, 61, 62].