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Where individuals with no such disorder, under frank reduction of carbohydrate intake would mobilize fat depots leading to ketogenesis, patients affected by these rare disorders would eventually experience hypoglycaemia, coma and ultimately death.104, 105, 106 However, fasting related perioperative ketosis seems not to pose at increased risk of acidosis.53 A recent study reports a VLCKD to be interrupted the day before surgery in 44 prebariatric patients, but no safety outcomes are shown.51 Of note, a recent case report showed that the concomitant use of SGLT‐2 inhibitors and VLCKD consumption in a diabetic patient undergoing surgery led to recurrent intraoperative torsade de pointes.24 Moreover, preoperative VLCD has been shown to induce hypovolaemia possibly increasing the risk of perioperative complications in a study including 28 prebariatric patients.52 However, data relative to the treatment intervention and timing are insufficient to draw conclusions on such outcome. Interestingly, preclinical evidence suggests a protective role played by nutritional ketosis and ketone body β hydroxy‐butyrate (βOHb) infusion on ischaemia induced brain and heart damage.30, 31, 32, 33, 34, 35, 36 The authors suggest that ketone bodies may inhibit excitotoxicity, oxidative stress and apoptosis, avoiding further cellular loss in the penumbra zone around the necrotic core. Lactation ketoacidosis is a well‐described condition in cows, and it occurs as the high demand of glucose leads to fat mobilization, ketosis and ultimately acidosis under certain circumstances. However, it is more and more common to encounter patients affected by both T1D and weight excess, where a change in dietary habits is necessary. To avoid hepatic encephalopathy, it is suggested to privilege vegetable and dairy protein and decrease the amount of animal (meat) protein, with no reduction in total protein intake even when cirrhosis is present, unless directed by a health professional.62 However, with the prevalence of obesity increasing all over the world, and NAFLD being now a common cause of cirrhosis, over 30% of liver transplant recipients are obese, and weight loss is strongly encouraged.63 A case series reports that VLCKD treatment for obesity was well tolerated by two subjects with end stage liver disease (ESLD) effectively reducing weight with no adverse events, and possibly improving liver damage.8 However, ketone bodies are now proven to be signalling, drug‐like, mediators.4 Moreover, the VLCKD is a fairly extreme dietary manipulation possibly leading to serious adverse events when not medically supervised. 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Suppression of LH into the eugonadal range indicates adequate androgen replacement therapy, whereas persistent nonsuppression after the first few months of treatment is an indication of inadequate dose or pattern of testosterone levels. Monitoring of androgen replacement therapy involves, primarily, clinical observations to optimize androgen effects including ensuring the continuation of treatment and surveillance for side effects. It is possible, but unproven, that the risks are dose-dependent although relatively few cases are reported among women using low dose methyl-testosterone (759, 760) while clinical management of children using the alkylated androgen oxandolone often omits liver function tests. Excessive or undesirable androgenic effects may be experienced during androgen therapy due to intrinsic androgenic effects in inappropriate settings (e.g., virilization in women or children). 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