Misconception presented:

“Doctors do not know exactly why some people get gallstones and others don’t”

Truthabout what cause gallstones is never disclosed to patients by New Zealand surgeons when conducting a diagnosis and alternative treatment options: 

Most of this information is never disclosed to clients, intentionally blocking patients from receiving sufficient relevant information to make an informed decision about alternative treatment options.

Top ten lie: ‘We don’t know why gallstones or gallbladder problems occur, so you have no option but surgery’ 

There are three types of gallstones [20] (i) Pure cholesterol stones, which contain at least 90% cholesterol, (ii) pigment stones either brown or black, which contain at least 90% bilirubin and (iii) mixed composition stones, which contain varying proportions of cholesterol, bilirubin and other substances such as calcium carbonate, calcium phosphate and calcium palmitate. Causes are due to:


  •          Gallstones are 4-10 times more frequent in older than younger subjects
  •          About a quarter of women over 60 years will develop them [13]


  •          Women during their fertile years are almost twice as likely as men
  •          Increased levels of the hormone oestrogen, as a result of pregnancy or hormone therapy, or the use of combined (oestrogen-containing) forms of hormonal contraception, may increase cholesterol levels in bile and also decrease gallbladder movement, resulting in gallstone formation [60]


  •          People with diabetes generally have high levels of fatty acids called triglycerides. These fatty acids may increase the risk of gallstones.
  •          Gallbladder function is impaired in the presence of diabetic neuropathy, and regulation of hyperglycaemia with insulin seems to raise the lithogenic index [24]


  •          Cholesterol gallstone prevalence varies widely, from extremely low (<5%) in Asian and African populations, to intermediate (10-30%) in European and Northern American populations, and to extremely high (30-70%) in populations of Native American ancestry (Pima Indians in Arizona, Mapuche Indians in Chile) [53]

Obesity and body fat distribution

Rapid weight loss

  •          Rapid weight loss is associated with occurrence of sludge and gallstones in 10-25% of patients in a few weeks of initiating the slimming procedures [61]

Post pregnancy


  •          Nutritional exposure to western diet, i.e., increase intake of fat, refined carbohydrates and decrease in fibre content is a potent risk factor for development of gallstones [65,66]
  •          The biliary calcium concentration plays a part in bilirubin precipitation and gallstone calcification [40,41] Many patients with gallstones have increased biliary calcium, with supersaturation of calcium carbonate [42]
  •          Calcium intake seems to be inversely associated with gallstone prevalence [67] Dietary calcium decreases cholesterol saturation of gallbladder bile by preventing the reabsorption of secondary bile acids in the colon.
  •          Vitamin C influences 7α hydroxylase activity in the bile and it was shown that ascorbic acid might reduce lithogenic risk in adults. [68]
  •          Coffee consumption seems to be inversely correlated with gallstone prevalence, due to an increased enterohepatic circulation of bile acids. Coffee components stimulate cholecystokinin release, [69] enhance gallbladder motility, inhibit gallbladder fluid absorption, decrease cholesterol crystallization in bile [70] and perhaps increase intestinal motility. [71,72]

Physical activity (lack of)

  •          Sedentary behaviour is positively associated with the risk of cholecystectomy. [17]

Drugs (PPI’s, Opioids, Contraception)

  •          The lithogenic role of ceftriaxone [36,37] can also precipitate in the gallbladder as sludge [38]
  •          Use of the somatostatin analogue octreotide, has been cited as another contributing factor in the development of gallstones. [43]
  •          All fibric acid derivatives increase biliary cholesterol saturation while lowering serum cholesterol.
  •          Clofibrate is a potent inhibitor of hepatic acyl-CoA cholesterol acyltransferase (ACAT).
  •          ACAT inhibition leads to an increased availability of free or unesterified cholesterol for secretion into bile, favouring gallstone formation. [24]
  •          Prolonged use of proton pump inhibitors has been shown to decrease gallbladder function, potentially leading to gallstone formation. [73]
  •          Oestrogen treatment also reduces the synthesis of bile acid in women


  •          Cholesterol supersaturation for in obese persons
  •          Defective conversion of cholesterol to bile acids in the non-obese
  •          Interruption of the enterohepatic circulation of bile acids during overnight fasting
  •          Fasting in the short term increases the cholesterol saturation of gallbladder bile and in the longer term, causes gallbladder stasis which can lead to sludge, and eventually gallstone formation. Younger women with gallstones were shown to be more prone to skip breakfast than controls. [63] A shorter overnight fasting is protective against gallstones in both sexes. [64]
  •          Pigment stones occur when red blood cells are being destroyed, leading to excessive bilirubin in the bile.
  •          Black pigment stones are more common in patients with cirrhosis or chronic hemolytic conditions such as the thalassemias, hereditary spherocytosis, and sickle cell disease, in which bilirubin excretion is increased. [28,29]
  •          Primary bile-duct stones are associated with infection
  •          Primary brown pigment stones of the bile ducts often occur in Asians, associated with decreased biliary ecretory Immunogloblin A (IgA.)[30]
  •          Prolonged total parenteral nutrition, [35] starvation, or rapid weight loss. [36,37]
  •          Impaired motility of the gallbladder as seen in patient with high spinal cord injury [43]

Njeze, G. E. (2013). GallstonesNigerian Journal of Surgery : Official Publication of the Nigerian Surgical Research Society19(2), 49–55. http://doi.org/10.4103/1117-6806.119236

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