Bariatric surgery (BS) effectively treats severe obesity and metabolic diseases [1], but carries a risk of impaired absorption of micronutrients (e.g., vitamins like D, B12, and thiamine, and trace elements like iron, zinc, copper, and calcium) [2] and increased postprandial glucose variability [3]. This is particularly true for BS procedures that involve intestinal bypass such as the widespread Roux-en-Y gastric bypass (RYGB) procedure. Therefore, patients with RYGB surgery are prone to complications such as iron deficiency anemia, insufficiency of vitamin D, B12 or thiamine, and post-bariatric hypoglycemia that often develop years after surgery [4, 5].

These deficiencies can cause a range of nerve dysfunctions [6,7,8], including peripheral neuropathy (PN) characterized by reduced sensation and pain in extremities [9], and autonomic neuropathy affecting the cardiovascular, gastrointestinal, urogenital, and sudomotor systems [10], but also nutrient deficiency specific conditions such as myelopathy (vitamin B12 and copper), Wernicke’s encephalopathy (thiamine), optic neuropathy, and spinocerebellar syndrome (vitamin E) [6]. Increased glycemic variability with hypoglycemic episodes may contribute to neuropathy development [11]. Thus, we hypothesize that BS patients, especially those with intestinal bypass that are prone to micronutrient malabsorption and with a history of longstanding nutritional deficiencies or hypoglycemic events, may be at increased risk of developing PN and autonomic neuropathy. Prior studies lack comprehensive and objective nerve function assessment, as well as long-term follow-up [7, 8, 12, 13]. In this cross-sectional pilot study, we assessed PN and cardiovascular autonomic neuropathy (CAN) in patients who had undergone RYGB more than 5 years ago and had suspected or confirmed nutritional and/or metabolic post-bariatric complications.