How Gut Dysbiosis Impacts Digestion And Appetite
Today I want to cover how gut pathogens can negatively impact the ability to digest food and regulate appetite. Here is an illustration of what should be, but oftentimes isn’t, absorbed in the digestive tract:
Your ability to absorb nutrition is reliant on a healthy small intestine. If any part of the small intestine–duodenum, jejunum or ileum–is diseased, health and proper weight regulation are close to impossible.
Mouth and Esophagus
Once food is placed in the mouth and chewing begins, digestion starts. In the mouth, chewed food mixes with saliva secreted by the salivary glands. Saliva contains amylase, an enzyme that begins the breakdown of carbohydrate starches. A second enzyme called lingual lipase is released from glands in the tongue and back of the mouth. This enzyme begins the breakdown of fat. This mass of newly chewed food mixed with saliva is called a bolus.
Please note that any oral pathogens that may be present in the mouth will hitch a ride on this bolus as it’s swallowed. So too any other pathogens that populate your respiratory tract and happen to be in your mouth or throat at the time.
The bolus passes the pharynx and enters the esophagus. At the end of the esophagus, lies the lower esophageal sphincter.
Sphincters and various other muscles exist throughout your digestive tract, and their primary function is to allow swallowed food and its remnants to pass from one section of your intestinal tract to another. Ideally, partially digested food should continue in one direction. However, sometimes this process malfunctions.
For example, gastroesophageal reflux disease or GERD is caused when partially digested food mixed with gastric juice reenters the esophagus. I covered this disorder here. Be aware that pathogens and their toxic bacterial byproducts are quite capable of interfering with the normal function of these circular muscles.
Once past the lower esophageal sphincter, the swallowed bolus enters the stomach. Here it mixes with gastric juice to form a semiliquid substance called chyme. The stomach is lined with cells that contain millions of gastric glands producing this gastric juice, which is composed of water, electrolytes, hydrochloric acid, enzymes, mucus and intrinsic factor.
Hydrochloric acid has a very low pH of about 2, which is about the same pH as lemon juice. Hydrochloric acid has some extremely important functions:
- It activates pepsinogen to pepsin. Pepsin is a protease enzyme that splits apart or hydrolyzes proteins into their amino acid building blocks.
- It denatures protein. Proteins are quite complex structures so denaturing unfolds these structures allowing pepsin and other proteases secreted by the pancreas to begin the process of breaking them apart.
- It releases nutrients from various organic complexes.
- It is an important bactericidal substance meaning it kills bacteria ingested with food. All food contains bacteria, and as I just mentioned, any bacteria found in the mouth or throat will also be swallowed with it. The less acidic your stomach acid, the more likely your chances of developing a gastrointestinal infection.
Apart from pepsin, two other enzymes exist in gastric juice: amylase that was swallowed with the bolus and gastric lipase, an enzyme produced by cells of the stomach. Gastric lipase hydrolyzes short- and medium-chain fatty acids and is responsible for up to 20% of fat digestion in humans.
Intrinsic factor is also secreted by the same cells that secrete hydrochloric acid and is absolutely vital for the proper absorption of vitamin B12, also known as cobalamin.
Inhibiting the release of hydrochloric acid and intrinsic factor, either by binge drinking of alcohol or by taking proton-pump inhibitors like Prilosec®, Nexium®, or Prevacid® will inevitably lead to a number of negative health outcomes:
- It will lead to the inability to properly digest protein which in turn causes protein deficiency. Undigested protein is now more likely to reach the colon where it will contribute to dysbiosis of the colon.
- It will cause impaired digestion of up to 20% of fat. This will result in deficiencies in fat-soluble vitamins and minerals. Undigested fat that reaches the colon will also lead to colonic dysbiosis, further compromising the health of this part of the digestive tract.
- It will sooner or later cause small intestinal bacterial overgrowth. This will displace beneficial lactobacillus species and inevitably cause leaky gut in the small intestine.
- It will lead to B12 deficiencies. B12 deficiencies in turn cause:
- skin pallor
- shortness of breath
- tingling and numbness in extremities
- abnormal gait
- loss of concentration
- memory loss
- swelling of nerve fibers
If this list of symptoms reminds you of those confused old people clogging the aisle of your local grocery store, this isn’t your imagination. Many of the elderly suffer from B12 deficiencies.
Unfortunately, due to their habit of eating gluten grains and high-fiber foods, many people, including the elderly, suffer from GERD and pop antacids and proton-pump inhibitors like Gummi Bears® at a movie matinée. The results are infection of the small intestine and B12 deficiencies.
At the bottom of the stomach lies the pyloric sphincter where it opens every so often to allow chyme to enter the first part of the small intestine or the duodenum. Here again is an illustration of what the absorptive structures of the small intestine looks like:
You see that area labeled the brush border? This is where beneficial gut bacteria live and is also the site of most digestion. If this brush border is damaged, digestion will be compromised. And impaired digestion is just another way of saying nutrient deficiency and ill health. This is the area of the small intestine damaged by the autoimmune disorder known as celiac disease.
A healthy brush border produces appropriate levels of gut hormones. Conversely, an unhealthy brush border will produce fewer of these hormones. There are many hormones produced by a healthy small intestine. I could write a book on this subject but for today’s post, I want to concentrate on those most directly involved in proper digestion and satiety.
Secretin is produced by S-cells in the duodenum in the presence of chyme. This hormone tells the pancreas to release pancreatic juice rich in digestive enzymes to complete the breakdown of carbohydrate, protein and fat. Without these enzymes, there isn’t much hope for proper digestion.
Pancreatic juice also contains electrolytes that include sodium, potassium and calcium. Finally, it has bicarbonate, which is important because it raises the pH of the very acidic chyme entering the duodenum from the stomach. While low pH is what you want in the stomach, it is not what you want in the small intestine. Raising the pH of chyme is essential for the correct functioning of digestive enzymes released from the pancreas. S-cells damaged from pathogens or diet are not likely to release appropriate amounts of secretin to signal the pancreas to release its juice.
If pancreatic juice is not released, not only is digestion impeded and important electrolytes not secreted, but the small intestine and colon will experience inflammation from highly acidic chyme as it irritates the gastrointestinal mucosa and destroys beneficial bacterial populations in both locations. Many experience burning diarrhea as a result. This will encourage the growth of pathogenic bacterial species that thrive in inflamed conditions. A pancreas that does not release pancreatic juice is one that will become inflamed leading to pancreatitis, and in extreme cases, pancreatic cancer.
Cholecystokinin or CCK is a hormone secreted by L-cells in the duodenum that is also responsible for stimulating pancreatic secretion of digestive enzymes. It is also essential for proper gallbladder contraction and the release of bile into the small intestine. Bile, pancreatic lipase, and pancreatic colipase are responsible for 80% to 90% of proper fat digestion. If L-cells are not secreting CCK, or releasing it in insufficient quantities, the gallbladder will not contract as it should. Bile in a gallbladder that isn’t regularly expelled is going to harden into stones. Fat in stool or steatorrhea is a telltale sign that fat malabsorption is occurring.
The gallbladder is also an important route for bound toxins to be excreted from the liver and into the intestine for eventual elimination in feces. Therefore, if the cells that produce CCK are damaged from diet or dysbiosis, this very important detox pathway is not working properly. A liver that can’t dispose of toxins through proper bile excretion is a diseased liver; and a diseased liver means a diseased human.
Gallbladder disease is especially common in gluten-consuming societies and was one of the first manifestations of Western-type diseases when flour was introduced to the diet of cultures that had never eaten wheat. It is a very common finding in celiacs and gluten-sensitive people. (1) Knowing what you know about gluten’s promotion of intestinal inflammation and gut dysbiosis this should surprise none of you.
The inability to properly digest fat means improper digestion of fat-soluble vitamins A, D, E and K. And since many minerals also rely on these vitamins and proper fat absorption for transport across the gut wall, deficiencies in magnesium, zinc, calcium and other minerals are all but assured. As I wrote in the last post, deficiencies lead to food cravings.
CCK delays stomach emptying causing a feeling of fullness that curbs appetite. CCK receptors are abundant throughout the central nervous system, including the hypothalamus, site of weight control. CCK reduces appetite and food intake in both rodents and humans. (2) (3) So less secretion of CCK will lessen satiety signals sent to the brain and cause overeating.
Finally, in rodents CCK has been shown to trigger a gut-brain-liver neuronal circuit that directly reduces the production of glucose in the liver. (4) Type 2 diabetes is characterized by uncontrolled synthesis of glucose suggesting that dysregulation of CCK plays an important role in the development of this disorder.
Motilin is secreted by M-cells of the duodenum and jejunum. It stimulates stomach and small intestinal movement, pancreatic secretions, and like CCK, gallbladder contractions. Proper intestinal movement guards against small intestinal bacterial overgrowth so impairment of motilin secretion would increase the odds of gut infection.
Glucagon-like peptides (GLPs) are also released by healthy L-cells of the small intestine and colon, and the alpha cells of the pancreas. These hormones influence insulin and glucagon secretion and their dysregulation may be a contributing factor in insulin resistance. These hormones reduce appetite and the rate of stomach emptying making you feel full. So again, any damage to L-cells will impede the release of these insulin-regulating and satiety-enhancing hormones.
This hormone is secreted by cells in the ileum and is the focus of quite a bit of research for its appetite-suppressing effect in rodents, primates and humans. (5) (6) (7) Supplementation of probiotics and prebiotics in rats has been shown to increase levels of this hormone. (8)
Small intestinal bacterial overgrowth due to impaired intestinal peristalsis affects the ileum first and would have the most profound adverse impact on this hormone’s production. Speaking from my experience, nothing has suppressed my intake of food more than clearing up my intestinal dysbiosis and supplementing with prebiotics and probiotics. I believe it’s due to increases in peptide YY and reduction in endotoxemia which will be the subject of the next post.
This hormone is secreted along with GLPs and peptide YY by healthy intestinal L-cells. In both rodents and humans it reduces food intake. (9) (10) Like the other satiety hormones, its production will be enhanced by the presence of healthy gut flora but inhibited in the presence of gut dysbiosis.
Ghrelin does not suppress appetite. On the contrary, it is termed the “hunger hormone” because it acts on the arcuate nucleas (ARC) region of the hypothalamus to increase food intake. It is synthesized mainly in the stomach. Ghrelin acts in opposition to peptide YY, oxyntomodulin, glucagon-like peptides, CCK and other satiety hormones. As it is produced in the stomach, it is the least likely of the appetite-regulatory hormones to be impacted by small gut dysbiosis.
Other gut hormones that depend on a healthy, non-damaged gut, are glucose-dependant insulinotropic peptide (GIP), enterogastrone, amylin, somatostatin, and substance P. Proper digestion and appropriate short-term hunger-suppressing signals are all reliant on a healthy small intestine. A healthy small intestine, in turn, is reliant on healthy gut flora. You can’t have the one without the other.
After transiting the last section of the small intestine or ileum, chyme empties through the ileocecal valve into the right-hand side of the colon known as the cecum. Here, contractions mix the mainly liquid contents of undigested food so that sodium, chloride and water are absorbed. Approximately 90% to 95% of the water and sodium entering the colon daily are absorbed here.
The colon contains the most gut bacteria of any part of the digestive tract. It is here that any undigested food is typically fermented by bacteria. However, in the case of small intestinal bacterial overgrowth, some food will also be fermented there.
In the colon, soluble fiber is fermented by friendly bifidobacteria into short-chain saturated fatty acids that are transported to the liver and other cells. However, bifidobacteria-produced butyrate serves as “food” for the cells lining the colon. Butyrate strengthens these cells and makes the colon wall impervious to translocating gram-negative endotoxins and their highly inflammatory lipopolysaccharide cell-wall remnants. In other words, if you want to reduce endotoxemia from the colon, you want plenty of butyrate.
While colonic bacteria mainly ferment carbohydrates (fiber and undigested starches), other substrates that can feed bacteria in a healthy colon are glycoproteins (mainly from mucin), sugar alcohols (sorbitol and xylitol), fructose, pectins, gums and some proteins and amino acids. If you have trouble digesting milk sugar or lactose, it will end up in the colon where bacteria will produce plenty of gas as they ferment it.
However, large quantities of undigested carbohydrate, fat or protein should never reach the colon. If they do, something is amiss in the small intestine. You can rest assured that this will cause bacterial blooms in the colon that specialize in fermenting these substrates, many of them pathogenic.
These bacterial species will crowd out friendly species like bifidobacteria. The entry of highly acidic chyme that was not properly neutralized by pancreatic juice in the duodenum will also affect beneficial species for the worse.
Excess fermentation in the colon will cause lots of gas and discomfort. This will cause the colon to expand like a balloon which can lead to diverticulitis as pouches form along the colonic wall with some becoming infected as bacteria and undigested food become trapped within them. And yes, this also includes indigestible fiber that everyone keeps telling you is great for your health. For more on the destructive role of indigestible fiber on GI health, I again refer you to Fiber Menace: The Truth About the Leading Role of Fiber in Diet Failure, Constipation, Hemorrhoids, Irritable Bowel Syndrome, Ulcerative Colitis, Crohn’s Disease, and Colon Cancer.
A colon is only as healthy as the digestive tract that precedes it. If the stomach or small intestine is not functioning properly or diseased, the colon will reflect that, always. Any treatment that concentrates solely on the health of the colon risks being short-lived if low stomach acid or small gut dysbiosis is not also resolved.
To recap, gut dysbiosis will interfere with proper digestion and appetite control by:
- inhibiting the release of brush-border hormones necessary for proper pancreatic and gallbladder function.
- impair the proper digestion and absorption of fat and fat-soluble vitamins and minerals.
- impair the proper digestion of protein.
- impair the proper digestion of carbohydrate.
- inhibit the pH neutralization of acidic chyme from the stomach.
- inhibit secretion of hormones that regulate intestinal motility.
- inhibit secretion of hormones that play a leading role in short-term appetite control.
- inhibit secretion of hormones that play a role in regulating insulin and blood glucose levels.
- increase inflammation throughout the gastrointestinal tract and the occurrence of endotoxemia.
- displace beneficial bacteria in the small intestine and colon that would otherwise keep these areas of your digestive tract and you healthy.
In the next post, I’ll detail how gastrointestinal dysbiosis, endotoxemia and inflammation impacts metabolism for the worse.
Gropper, S. R., Smith, J. L., Groff, J. L. (2009). Advanced Nutrition and Human Metabolism. Belmont, CA: Wadsworth Cengage Learning.