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Advanced Topics: A Guide to Gallstones

Guide to Gallstones

migraine Gallstones are an odd phenomenon. Despite being exceptionally common, affecting between 10-15% of the U.S. population, pinpointing the causes of gallstones has been elusive. Older age, being female and overweight/obese increase the likelihood of developing gallstones, a process that develops over several years but can, under some circumstances such as rapid weight loss, develop over weeks.


Because most gallstones are composed largely of cholesterol, doctors have blamed high cholesterol as the cause for gallstone formation, but that notion is proving---as with all other issues surrounding cholesterol---to be an oversimplification. This, in addition to the fact that fat consumption, while it does not cause gallstone formation, can unmask their presence, since fat digestion requires bile and a stone that becomes lodged in the bile duct causes acute gallbladder pain to develop, has unfortunately caused many doctors to conflate the two phenomena and advise people with gallstones to consume a low-fat, low-cholesterol diet. This awful advice remains common today despite several studies demonstrating that reducing fat or calories actually causes gallstone formation.

Part of the widespread confusion over how gallstones develop is due to a proliferation of poor quality studies that have led to many false or premature conclusions about gallstone disease, such as:
  • There is weak evidence suggesting that increased consumption of vegetables and fruits is associated with reduced potential for gallstones. These data are epidemiological and therefore unreliable.

  • Likewise, there is weak evidence linking alcohol consumption, coffee consumption, physical activity, dietary magnesium intake, nut consumption and a vegetarian diet with reduced potential for gallstones, while additional weak evidence suggests an association between higher trimethylamine oxide (TMAO) levels and greater risk for gallstones.

Such conclusions are potentially true, but the majority of observational associations are eventually disproven by real prospective clinical studies. Some conclusions reached via observation are laughable, such as one study that suggested that obtain vocational work training caused gallbladder disease.

In other words, low-quality observational studies have led to a mix of conflicting conclusions, much as they have in the broader world of nutrition. Low quality observational data are conducted, rather than real prospective clinical studies, due to the difficulties of conducting a real clinical study. Such a study would involve randomizing participants to a specific dietary program versus control diet and tracking, in this case, gallbladder ultrasound, an effort that would require years and thousands of participants in the hopes that a difference in gallstone occurrence develops. Such a study will likely never be performed.

We are therefore left with trying to construct a rational approach to preventing gallstone development based on relatively limited observations.

Better evidence, however, suggests that:
  • Greater dietary fat intake is associated with reduced risk for gallstone development. Ingestion of dietary fat provokes vigorous, often near-total, gallbladder contraction and emptying of bile contents, while decreased fat intake provokes little to no gallbladder contraction that, in turn, leads to bile stasis and stone formation.

  • Weight loss achieved via calorie restriction or limiting dietary fat results in a high incidence of gallstone formation, as high as 54%, even in the initial 4-8 weeks. (The risk is so great that people who undergo gastric bypass surgery often have their gallbladders removed at the same time.) Not restricting dietary fat intake, however, abolishes or dramatically reduces this risk. The difference lies in taking in dietary fat such that the gallbladder continues to contract to expel bile and thereby preventing bile stasis that promotes stone formation. While we do not, of course, limit intake of fats and oils in the Undoctored lifestyle, it may require as little as 20 grams per day of fat intake to avert development of gallstones during weight loss.

  • Higher blood insulin levels and insulin resistance promote gallstone formation. Although the evidence is observational, the effect is large (260% increased likelihood) and thereby one of the situations in which cause-effect associations suggested by observational evidence can actually be true.
  • Omega-3 fatty acids may provide some protection from gallstone formation during weight loss.

  • If further protection from gallstone formation during weight loss is desired, or a there is need to dissolve existing stones not responsible for acute symptoms, ursodeoxycholic acid, 600-1200 mg per day (typically divided into two doses per day) reduced likelihood of stone formation to near zero during weight loss.

Role of wheat and grains

It is likely that wheat and related grains are a contributor to gallstone formation via several routes. Recall that cholecystokinin, or CCK, is a hormone released by the duodenum when fat is ingested that, in turn, provokes gallbladder contraction. CCK levels with fat ingestion can be 100% or higher after ingestion of a high-fat meal compared to a low-fat meal. The lectin, wheat germ agglutinin, is known to block CCK. When ingested food contacts the duodenum, CCK is released that, in turn, provokes the gallbladder to contract and expel bile through the bile duct to emulsify fats and provokes the pancreas to release pancreatic enzymes to digest fats, proteins, and carbohydrates. When wheat germ agglutinin is in the vicinity, from, say, a sandwich, bagel, or breakfast cereal, CCK is blocked. One consequence is inadequate release of bile from the gallbladder, and thereby bile stasis, i.e., bile that accumulates in the gallbladder and encourages crystal formation that leads to gallstones, a phenomenon that is clearly observed in people with celiac disease although it also occurs in people without celiac disease since it is mediated via wheat germ agglutinin, not gluten. Wheat germ agglutinin, by the way, is found in wheat, rye, barley, and rice, all with identical structures. There may be other means by which wheat and related grains cultivate gallstone formation, but that remains speculative, factors such as direct intestinal inflammation caused by wheat germ agglutinin and changes in bowel flora due to impaired digestion from lack of adequate bile and pancreatic enzymes.

A role for SIBO?

There is also growing appreciation that gallstones contain multiple species of bacteria and may therefore represent yet another manifestation of dysbiosis, disrupted bowel flora. The microorganisms recovered from people with acute gallbladder attacks and cholecystitis (and even from gallstones themselves, even in the absence of overt infection) are typically Escherichia coli, Klebsiella, Enterobacter, Pseudomonas, Citrobacter---i.e., the Gram-negative Enterobacteriaceae species that dominate in small intestinal bacterial overgrowth, SIBO. And, because the bile duct empties into the duodenum, the uppermost portion of the small intestine, it suggests that dysbiosis that cultivates gallstone formation must be in the form of SIBO in which the entire length of gastrointestinal tract is overpopulated with pathogenic bacterial species. If dysbiosis were confined to the colon, it likely would not reach the duodenum. It therefore stands to reason that a full-length dysbiosis must be present in order to reach the duodenum.

A recent analysis demonstrated that the bacterial composition of stool from people with gallstones is different from healthy people without gallstones, specifically enriched in Enterobacteriaceae, and that the bacterial composition of both gallstones and bile in people with stones is unique, with an even greater proportion of Enterobacteriaceae as well as Ruminococcaceae, Bacteroidales, and Clostridiales. Some have therefore speculated that the change in bacterial composition in the gallbladder and biliary tree leads to supersaturation of bile with cholesterol crystals, promoting stone formation. It is not yet possible to declare that dysbiosis/SIBO causes or contributes to gallstone formation or whether it is a consequence, but growing evidence is pointing towards SIBO as an important contributor. Indeed, observational evidence has suggested that people with gallstones have greater likelihood of SIBO, both hydrogen- and methane-positive.


It is a tangle, no doubt, but one that is gradually becoming untangled. We await better answers, but until then, we can still derive a few take-home messages. If you have gallstones or wish to never develop them, you should:
  • Banish all wheat and grains, i.e., sources of wheat germ agglutinin that blocks gallbladder contraction and cultivates bile stasis, as well as intestinal inflammation and dysbiosis. Of course, if you do not yet have gallstones, removing all wheat and grains from the diet yields enormous health benefits, including not blocking CCK and impaired digestion.

  • Never limit dietary fat and thereby encourage full and frequent gallbladder emptying that prevents bile stasis. We do not limit fat in the Undoctored lifestyle but enjoy fatty cuts of meat as well as butter, ghee, coconut oil, olive oil, and avocado oil. This remains true even if you have had your gallbladder removed. If any fat intolerance is encountered after gallbladder removal, e.g., diarrhea or abdominal discomfort with fat ingestion, first think SIBO, not lack of bile. The bacterial species of SIBO impair fat digestion. (The only people who can benefit by limiting fat are those with active gallbladder disease in whom fat digestion can provoke gallbladder attacks.) Limiting dietary fat can reduce symptoms once gallstones develop, but does not address the cause, not to mention raises triglycerides that lead to heart disease, cultivates fatty liver, raises blood sugar and pushes you closer to type 2 diabetes. Limiting dietary fat is a very destructive practice and yields no benefits for gallbladder or bile health. Nor do the majority of people without a gallbladder need to supplement bile or pancreatic enzymes if SIBO is addressed.

  • Explore the question of SIBO--which has become enormously easier with availability of the AIRE device for H2 breath detection. (See the Undoctored Protocol for SIBO that details how to use the AIRE device.) The ability to measure breath hydrogen gas is a game-changer for intestinal health. You can also appreciate that, if SIBO was the cause for gallstones, removing the gallbladder does nothing to address the cause. Uncorrected SIBO carries considerable long-term consequences such as autoimmune diseases, diverticular disease, and colon cancer. Addressing SIBO therefore adds an entirely new collection of health benefits to your life.

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