Despite promises of good health (because we all “know” that weight loss cures everything), Weight Loss Surgery (WLS) survivors are at risk of a plethora of health issues:
Gastric surgery is associated with numerous nutritional disorders, including pernicious anemia, iron deficiency anemia, bone mineral disease, postvagotomy syndrome, early and late dumping syndromes, hyperinsulinemic hypoglycemia, malnutrition, malabsorption, and functional pancreatic exocrine insufficiency. Deficiencies of fat-soluble vitamins (A, D, E, K) and water-soluble vitamins (B group, C) can be related to inadequate intakes, aversion to particular foods, diarrhea, small intestinal bacterial overgrowth, or malabsorption. Malabsorption of iron, copper, zinc, magnesium, or calcium can be caused by postgastrectomy achlorhydria, decreased solubility of dietary salts or trace elements, or inadequate contact of minerals with the absorptive surface of the duodenum after bypass surgery. Peripheral neuropathy after gastric surgery can result from deficiency in vitamin B1 (thiamine), vitamin B2 (riboflavin), vitamin B6 (pyridoxine), vitamin B12 (cobalamin), folate, zinc, copper, or vitamin E (α-tocopherol). Deficiencies of multiple B group vitamins may coexist after gastric surgery and can contribute to nutritional polyneuropathy, which manifests with numbness, paresthesia, neuritic pain, sensory loss, gait disturbance, muscle weakness, muscle wasting, or loss of reflexes.
https://doi.org/10.1093/nutrit/nuaa004
And now we can add a new (or rather, very old) problem to the mix – Beriberi.
That’s right fucking beriberi.
How’s that for a blast from the past?
https://doi.org/10.1093/nutrit/nuaa004
Beriberi is caused by thiamine deficiency.
Thiamine deficiency leads to:
It includes neuropathic symptoms, clinical progression, cranial nerve palsy, urinary retention, anorexia, dysphagia, severe constipation, ileus, orthostatic hypotension, cardiac arrhythmia and coexistence of heart failure and Wernicke encephalopathy. A symmetric polyneuropathy with more marked involvement of the lower limbs than the upper limbs is typical. Nerve conduction studies typically show markedly decreased amplitude of compound motor action potentials and sensory nerve action potentials, especially in the lower limbs. Sural nerve biopsies show axonal degeneration, loss of myelinated fiber density, and subperineural edema with minimal demyelination.
The place where your body absorbs most of its thiamine is the duodenum and proximal jejunum – making Roux-en-Y gastric bypass, Billroth II partial gastrectomy or total gastrectomy survivors most at risk of developing thiamine deficiency. But beriberi has also developed after restrictive procedures like laparoscopic sleeve gastrectomy, gastroplasty and laparoscopic adjustable gastric banding.
And this can develop any time after WLS. Even years and years later.
It can develop in WLS survivors who “appear well-nourished” (I interpret that to mean still fat.)
It’s not easy to spot and face it, what doctor in this day and age is going to be looking for beriberi?
The thing is, the human digestive system is a spectacularly intricate system – some of which we still don’t fully understand – and this is the kind of thing that happens when you tinker with that system. It is not something anyone should consider lightly.
The medical world is still discovering what havoc WLS can wreak on a human body.
And losing weight is not a cure-all.
How much pain and suffering could we avoid if we could just learn to accept our bodies?
Thoughts from a Fat Old Lady 
BeriBeri was reported after the original gastric bypass from the 1970’s. I mentioned it in my 1982 report to NAAFA. This disease had been eradicated until WLS became popular.