Chapter 1. Fiber Carnage

To all intents and purposes, the indigestible fiber in cereals isn‘t any different from the fiber in Metamucil‘s psyllium—fiber is fiber regardless of the source. People who aren‘t accustomed to a high-fiber diet may have identical side effects whether it is Metamucil or high-fiber cereals.

Shocked? Puzzled? Surprised? Bewildered? Here is a brief Q&A which explains why the side effects of various kinds of fiber consumption are identical:

Q. Why does fiber cause bloating?

Because (a) fiber fermentation inside the intestines produces gases, and (b) because the acidity from fermentation causes intestinal inflammation. Since the absorption of gases is the primary function of the intestine, the combined impact of (a) and (b) blocks their absorption, and causes the intestines to expand just like an air balloon.

Q. Why does fiber cause gas?

The intestines are colonized with symbiotic bacteria (normal intestinal flora), which are essential for many health-sustaining functions. Normally, mucin—a component of mucus—provides bacteria with the nutrients they need. But when fiber—soluble as well as insoluble—reaches the lower intestine, the bacteria go wild, ferment everything in sight, and multiply prodigiously. The fermentation is accompanied by lots of gases, just as with yeast-rising dough or aging champagne. If you don‘t experience gas after ingesting fiber, it means that your intestines lack normal bacteria, and you are affected by dysbacteriosis, a serious pathology which is explained in Chapter 4, Dysbacteriosis.

Q. Why does fiber cause “stomach cramps”?

Actually, not stomach cramps, but abdominal cramps. The cramping is a pain sensation in the abdominal region that results from gases, inflammation, acidity, intestinal obstruction, and large stools, or that stems from regular contractions of affected sections of the small and large intestines.

Q. Why does fiber cause nausea  and vomiting?

Once inside the stomach, fiber lumps together and may cause mechanical stimulation of the receptors that activate the vomiting center in the brain. The lumped fiber may also temporarily obstruct the path between the stomach and duodenum, and cause vomiting related to the stomach‘s overload or delayed emptying. If you have gastritis (inflammatory stomach disease) or ulcers, the likelihood of fiber-related nausea and vomiting is even higher because of the fiber‘s contact with extra-sensitive impaired tissues.

Q. Why does fiber cause “unrelieved constipation”?

For the same reason it causes anorectal bleeding. When stools become large from excess fiber, many people, particularly children, seniors, and those affected by hemorrhoidal disease or anal fissures, simply can‘t pass them. If this condition isn‘t quickly resolved, it may lead to fecal impaction. The continuous accumulation of impacted stools may cause diverticular disease (the bulging of the colorectal wall), megacolon (permanent stretching of the colorectal walls), and colorectal perforation (the spilling of intestinal content into the abdominal cavity), which is usually lethal.

Q. Why are there no fiber warnings printed on the boxes of fiber-fortified cereals?

Cigarettes didn‘t have any warnings either for a long, long time. It takes a while to change a belief system.

Q. I am young, fit, and healthy, and I consume lots of fiber. And it causes me no harm. Why?

Fiber is very much like a bomb with a time-delay fuse. For a while, it will not visibly affect you, because young people are still active enough to burn off all excess carbs, their intestines are still supple enough to process fiber, and young anorectal organs are still strong enough to handle large stools. Alas, if you keep consuming lots of fiber, your youthful bliss may soon be over. Just ask your parents and grandparents.

Avoiding dietary fiber in food isn‘t an easy task. It is often hidden behind obscure names such as cellulose, β-glucans, pectin, guar gum, cellulose gum, carrageen, agar-agar, hemicellulose, inulin, lignin, oligofructose, fructooligosaccharides, polydextrose, polylos, psyllium, resistant dextrin, resistant starch, and others.

These ingredients are factory-made from wood pulp, cotton, seaweed, husks, skins, seeds, tubers, and selected high-yield plants that aren‘t suitable for human consumption without extra processing. They are widely used to add texture and volume to ersatz food. For example, guar gum or cellulose gum are added to water and dry milk in order to fake yogurt or sour cream consistency, carrageen gives texture to cheap ice cream, and pectin thickens fruit preserves.

The only reliable way of avoiding hidden sources of fiber is this: read the labels! if you didn‘t learn the name of the ingredient on the product‘s label by the first grade, it doesn‘t belong on your plate or inside your gut.

So let‘s stroll along the mouth-to-anus pathway and check out the damage from this fiber orgy.

Fiber‘s effect on the oral cavity: As sticky as glue

The human mouth is primarily intended to cut and chop flesh, not grind indigestible fibers. Unlike humans, cows have so-called hypsodont teeth, which extend very far above the gum line and grow continuously to accommodate a lifetime of wear-and-tear from grinding fibrous grasses.

We aren‘t as lucky—our teeth are brachydont, and aren‘t intended for chewing fiber, otherwise, after a decade or so, you simply wouldn‘t have any teeth left to argue this point with clarity.[8] That‘s why the fiber for human consumption is crushed, milled, or ground first, and requires little or no chewing. But even after processing, it affects the oral cavity with a menacing vengeance:

• Obstruction of the salivary glands. Fiber, especially in dry-roasted cereals, has a tendency to obstruct the salivary glands. When that happens, the tongue senses a polyp-like protrusion. Though unpleasant, this benign problem may, in some instances, cause acute inflammation and require treatment with antibiotics.
• Dental caries (cavities). Powdered (well-milled) fiber of any kind has a natural tendency to lodge itself inside the abrasions both on the chewing surfaces and between the teeth. Once there, it provides perfect feed for normal oral flora. The bacterial fermentation in the mouth produces lactic acids that bind with the minerals that form the enamel mineral matrix. In turn, the weakening of the matrix causes dental caries. That‘s why all kinds of fiber-rich products, especially cereals, are exceptionally destructive for dental health. Not surprisingly, tooth decay is the second most common disease in the United States. The common cold is the first. Weak immunity related to dysbacteriosis happens to be one of the leading causes of most colds as well.
• Periodontal disease (gingivitis, necrotizing ulcerative gingivitis, periodontitis). Pulverized fiber lodges easily inside the gingival sulcus, a pocket that exists between the teeth and the gums (gingiva). The bacterial fermentation inside the sulcus causes inflammation of gingiva, the periodontal ligament, and alveolar bone, and eventual tooth loss. Gingivitis—the initial stage of periodontal disease—is easily recognized by bleeding gums. A receding gum line, even without bleeding, indicates the progression of periodontal disease.

Fiber‘s effect on the esophagus: If not plugged, then burned

The esophagus is the narrow muscular tube that transports chewed food and water from the mouth to the stomach. A chewed mass is called a bolus. The bolus travels the entire length of the esophagus in just a few seconds. This unassuming organ is quite vulnerable to the vagaries of indigestible fiber. The impact is indirect, through the digestive disorders of the stomach, such as heartburn, but the suffering is real—millions of people suffer from dysphagia, the difficulty or inability to swallow food. The other prominent fiber-related complications are:

• Esophageal obstruction. Supplemental fiber may rapidly expand and cause an obstruction when not accompanied by a lot of liquid. It isn‘t likely to happen in healthy adults, but is probable in small children, people with a narrowed esophagus or affected by dysphagia (difficulty swallowing), as well as the mentally disabled, old, and infirm.
• Heartburn is the most common symptom of gastroesophageal reflux disease (GERD)—a spilling over (reflux) of the stomach‘s content back into the esophagus. The burning sensation emanates from the esophageal mucosa, unprotected from digestive juices and enzymes.
• Barrett‘s esophagus (change of mucosa, precursor to cancer), dysphagia (difficulty swallowing), ulceration, bleeding, and esophageal cancer. Indirectly through the GERD, indigestible fiber is a primary causative factor behind these conditions.

Fiber‘s effect on the stomach: The luck stops here

The digestion of protein is the exclusive provenance of the stomach. When gastric digestion commences, the contents of the stomach are churned[9] inside, until it‘s completed (i.e. solid particles of food larger than 2 millimeters, or 0.08,” are no longer detected).

Fiber‘s specific properties—water absorbency, expansion, stickiness (congregation)—interfere with digestion and may cause an array of gastric disorders. Fiber-related problems become more pronounced with age because of the inevitable wear-and-tear on the internal organs. Insoluble fiber affects the stomach particularly hard because it tends to congregate and form lumps, and its rapid expansion fills the stomach with idle bulk.

You don‘t even need to consume that much fiber to feel its punch. For example, TV commercials for antacids are commonly shot inside Mexican restaurants because beans—a main staple of Mexican cuisine—commonly cause heartburn, even though a 100 g (0.22 lb) serving of beans contains a paltry 4 to 5 g of fiber. Just imagine the cumulative impact on the aging stomach of 30 to 40 grams of fiber consumed daily. Here are the most prominent problems:

• Nausea and vomiting. The congregated lumps of fiber may cause mechanical stimulation of the receptors that activate the vomiting center in the brain. That much, as you recall, is stated in the side effect section of common fiber supplements.
• Obstruction (Gastric outlet obstruction, Duodenal obstruction). The lumps of expanded fiber, primarily from supplements, may temporarily obstruct the path between the stomach and duodenum. If there are no other pathologies, the situation resolves itself with nausea and vomiting.
• Gastroparesis (delayed stomach emptying). The stomach‘s peristalsis and digestion are completed when specialized receptors no longer detect undigested components over 2 mm. The undigested lumps of fiber may considerably extend the duration of the gastric phase of digestion because the stomach can‘t distinguish between an undigested chunk of meat and a lump of fiber. This problem is particularly acute among older individuals, who may have weak peristaltic contractions of the stomach. The digestion can extend from the customary 4–6 hours to 10, 12, and beyond. The extended exposure of the stomach lining to digestive juices and enzymes, particularly while laying down, may cause inflammation and ulceration of the esophagus and upper stomach regions (cardia and fundus), that aren‘t as well-protected as its lower regions (antrum and pylorus). [The original meaning of gastroparesis is the paralysis (paresis) of the stomach‘s peristalsis related to nerve damage from trauma, diabetes, surgery, medication, and other causes. Today this term is broadly used as delayed stomach emptying irrespective of nerve damage – ed.]
• Gastroesophageal Reflux Disease (GERD). Simply speaking, GERD results from two primary factors: overloading the stomach with food and liquids, and delayed digestion (indigestion). Because indigestible fiber expands four to five times its size, it is the largest contributor to the stomach‘s overload. Absence of indigestion, heartburn, and reflux is one of the most immediate and pronounced benefits of low- or fiber-free diets.
• Dyspepsia. A general term that describes non-specific pain and discomfort that emanates from the stomach (upper middle abdominal region). The sensation of pain may result from conditions described above and below. The pain may become more pronounced after a meal. Meals heavy in all kinds of fiber cause more pain because of the volume and the extended duration of digestion. Some medical writers refer to dyspepsia as “indigestion.” Well, guess what substance doesn‘t digest in the stomach?
• Gastritis. All of the above conditions, related to fiber interfering with or extending gastric digestion, are the primary causes of gastritis—an inflammation of the stomach‘s mucosa, caused by the inability of the stomach‘s lining to withstand its own aggressive environment. The risk of gastritis goes up exponentially if you‘re under a great deal of stress (it inhibits digestion); consume alcohol (in small amounts it stimulates digestion, but inhibits in large); drink coffee, chew gum, or smoke (all three stimulate digestion); regularly take aspirin and other NSAIDs drugs; or are infected with H.pylori bacteria. The fiber adds to this mix far more than the proverbial two cents. Please note that there is nothing wrong with stimulating digestion when appropriate. The problems develop when the digestion is stimulated inappropriately—between meals, before going to bed, while experiencing reflux, dyspepsia, and similar circumstances.
• Gastric Ulcer (Peptic ulcer disease). A perforation of the stomach‘s mucosa causes ulcers. Gastritis commonly precedes ulceration and bleeding. All of the causative factors behind gastritis apply to ulcers as well. Fiber extends digestion. The longer the digestion lasts, the more difficult, if not outright impossible, for the ulcers to heal. That‘s why people who are admitted to a hospital with a bleeding ulcer are placed on a liquids-only diet. If a zero-fiber diet helps ulcers to heal, a low-fiber one isn‘t as likely to cause them.
• Hiatal (Hiatus) Hernia. The diaphragm (midriff) is a muscular membrane that separates the heart and lungs (thoracic cavity) from the digestive organs (abdominal cavity). The esophagus connects with the stomach through the esophageal hiatus—an opening in the diaphragm. A pathological protrusion (herniation) of the stomach‘s upper wall above the diaphragm through that opening is called hiatal hernia. This condition affects over 40% of the population[10] in the United States. When the stomach capacity is exceeded by food and fluids, the upward pressure created by peristalsis (at the bottom of the stomach) causes its upper walls to prolapse into the opening. Fiber is the only food that expands four to five times its original size once inside the stomach. This expansion creates strong volumetric pressure long after the meal has already been consumed. Neither proteins, nor fats, nor soluble carbohydrates can expand beyond their initial volume. A horizontal position (i.e. while lying down) is likely to contribute to herniation. You may have heard that herniation contributes to heartburn, dyspepsia, gastritis, and peptic ulcers. It isn‘t so—the hiatal hernia simply mirrors the state of the affected stomach, and these conditions are already present there, regardless of the hernia. Unless patients stop recklessly stuffing their stomachs with fiber, the majority of surgeries to remove hiatal hernias are also useless.

As you can see, the relationship between the stomach and the fiber is awkward at best, ruinous at worse. Well, what else would you expect when matching a primary digestive organ with an indigestible substance?

Fiber‘s effect on the small intestine: Not welcome at any price

The journey of food from the plate to the large intestine—that is, through the mouth, esophagus, stomach, and small intestine—normally takes about 24 hours, depending on what was on that plate.

The small intestine is long and thin—about 7 meters (23‘) of coiled tubing laid out in a tight serpentine shape (3.5 to 4 cm wide in adults), which is about the width of a half-a-dollar coin.

The more insoluble fiber there is in the meal, the longer the trip, because of the bottlenecks in the small intestine, which is an organ nature intended for moving along liquid chyme, not lumps of heavy fiber. If you doubt this, just visualize the following experiment:

• To replicate the chewing action, use a fork to crush a serving of high-fiber cereal in a bowl;
• To reproduce the stomach‘s churning, add water or milk to the bowl, mix thoroughly, and let the crushed cereal soak in the liquid;
• To imitate the small intestine, cut a piece of garden hose, about 7 meters long, and lay it down into a serpentine shape—a good approximation of the small intestine‘s architecture;
• To simulate the propulsion of food through the small intestine, keep adding the “digested” cereals through a funnel on top until it appears at the other end of the hose. Or will it appear?

It‘s highly unlikely. The more fiber in the cereal, the faster this dense, thick, semi-liquid mass will clog the hose (intestine) at the bottom of its very first bend, and there are quite a few more bends left to go. To propel the cereal to the end of the hose, you‘d need to keep adding more of the mixture from the top, in order to push out the jam in the middle—a process strikingly similar to pressure-stuffing homemade sausages with ground meat.

Unlike the clumps of cereal, any liquid poured through the funnel, no matter how thick, will soon reach the end thanks to the inscape-able laws of gravitation. As long as the exit is located below the en-trance, no clogging occurs, even if the hose is old and worn out.

If you chew your food thoroughly, and your stomach digests it well, it‘s transformed to chyme—a thick liquid without any solids. And the first organ to greet chyme is the duodenum.

Duodenum. Literally twelve fingers‘ breadths, the duodenum is the first and the shortest (18–25 cm) section of the small intestine. The pyloric valve (sphincter) separates the stomach from the duodenum. When the gastric phase of digestion is completed, this valve controls the transfer of chyme into the duodenum. Once inside, the chyme is neutralized with bicarbonate, mixed with bile and pancreatic juices, and the intestinal phase of digestion begins.

Fiber is particularly hard on the duodenum, because, unlike the stomach, the duodenum isn‘t expandable, but a small, narrow, and easy-to-clog circular tube shaped like the letter C. That‘s why duodenitis (a condition identical to gastritis) and duodenal ulcer (a condition identical to gastric ulcer) strike their victims in their early twenties, twenty to thirty years ahead of the peak occurrences of gastritis and gastric ulcer.

It‘s a well-known fact among military doctors that duodenitis and duodenal ulcers are quite common among recent recruits. No surprise there—beans, legumes, whole grain cereals, whole wheat pasta, and bread make up the largest share of military rations, and young soldiers are particularly prodigious eaters after the daily grind of military life.

The duodenum possesses a few specifics that make it particularly vulnerable to obstruction with fiber. The ducts from the liver, gallbladder, and pancreas congregate into the common bile duct and terminate inside the duodenum. They supply a prodigious amount of bile (400 to 800 ml daily) and pancreatic juice (up to 1500 to 3000 ml daily). It doesn‘t take long to cause considerable damage to the liver, gallbladder, and pancreas by blocking, even partially, a considerable outflow of these fluids.

The blockage of biliary and pancreatic ducts can be purely mechanical or caused by duodenitis, an inflammation that affects the lining of the duodenum and the common duct itself. Again, the prolonged contact of a fibrous, acidified mass with the duodenal mucosa is the most likely cause of both inflammation and blockage. The conditions that follow are quite common:

• Pancreatitis (inflammation of the pancreas). Besides fiber there isn‘t any other substance in human nutrition that enters the duodenum not only as is, but also expanded many times its original size. Lo and behold, the recent (17th edition) of The Merck Manual of Diagnosis and Therapy confirms this fact: “recent data indicate that obstruction of the pancreatic duct in the absence of biliary reflux can produce pancreatitis.”[11] Acute pancreatitis is quite common in toddlers, who are placed on solid food, which means loads of fiber from cereals, bread, pasta, fruits, and vegetables. The condition itself often remains undiagnosed, while its most prominent symptom—the onset of juvenile diabetes (type I), a failure to produce insulin because of acute inflammation—manifests itself almost immediately. Here is yet another ruinous aspect of fiber that strikes so early in life.
• Cholecystitis (Inflammation of the gallbladder). Gallstones are the primary (90%) cause of acute (sudden, severe) and chronic cholecystitis. Gallstones are formed from concentrated bile salts when the outflow of bile from the gallbladder is blocked. The gallstones cause inflammation either by irritating the gallbladder mucosa or by obstructing the duct that connects it to the duodenum. The gallstones are the secondary factor, because before they can form, something else must first obstruct the biliary ducts. Just like with pancreatitis, that “something” is either inflammatory disease or obstruction caused by fiber.

Women are affected by gallstones far more than men, because they are more likely to maintain a “healthy” diet, which nowadays means a diet that is low in fat and high in fiber. Since the gallbladder concentrates bile pending a fatty meal, no fat in the meal means no release of bile. The longer concentrated bile remains in the gallbladder, the higher the chance for gallstones to form.

Upper (jejunum) and lower (ileum) small intestine. The duodenum transitions into the jejunum, which comprises the upper two-fifths of the small intestine. It‘s distinguished from the ileum by its larger width and thickness, slightly more pronounced mucosa structure, and deeper color, because it embodies more blood vessels.

It‘s somewhat ironic that the name jejunum is derived from the Latin fasting, because during dissection this particular segment of the small intestine was always found empty. Apparently, the fathers of anatomy, who named the internal organs, hadn‘t yet been confronted with the scourge of indigestible fiber; otherwise this particular section of the small intestine would be called intestinum repletus (filled intestine).

The final three-fifths of the small intestine are called the ileum (from Latin‘s groin, meaning near groin). The ileum is narrower (3.5–3.75 cm), has thinner walls, and is not as vascular. At the very end, the ileocal valve terminates the small intestine and prevents the content of cecum (the first section of large intestine) from spilling back into the small intestine.

One look at the small intestine, laid out inside the abdominal cavity like a tangled, convoluted garden hose, makes it apparent that this organ was designed to move fluids only, and that it‘s remarkably easy to jam with solid, undigested stuff. There is only one substance that can get down there undigested and expanded many times its size—indigestible fiber. And when that happens, here are the possible outcomes (a partial list):

• Mechanical obstruction. The medical term for an undigested mass that forms inside the stomach or intestines and gets stuck there is bezoar (pronounced bee-zawr). Indigestible fiber is the only consumable substance that doesn‘t digest, and has the potential to form bezoars, which cause mechanical obstruction of the small intestine. When bezoars are lodged beyond the reach of the endoscope, abdominal surgery is the only option available to remove the obstruction. Bezoars are rare among healthy adults, but more common among children (whose intestines are comparatively tiny and underdeveloped). Old and infirm individuals, whose intestines lack the muscular tone needed to propel anything but fluids, are also vulnerable. That‘s why indigestible fiber should be taboo for children, or very old, infirm, and bed-ridden patients.
• Enteritis (inflammation of the small intestine). The insides of the small intestine are covered with a pinkish mucosal membrane, superficially similar to the insides of one‘s mouth or vagina. The assimilation of digested nutrients into the bloodstream is the sole function of the intestinal mucosa. It can only assimilate nutrients dissolved in liquid chyme. It isn‘t intended to transport anything other than mildly acidic chyme (pH 6.0 to 6.5). Once inside the stomach, undigested fiber soaks up acid and enzymes like a sponge. When expanded fiber enters the small intestine, the permanent contact with the delicate mucosa causes mechanical and chemical damage, which in turn causes mucosal inflammation (enteritis). Once inflamed, the mucosa can no longer absorb the nutrients and gases formed during digestion, and the intestines expand, causing bloating and cramping, which is often accompanied by severe pain.
• Crohn‘s disease. If left unchecked long enough, enteritis progresses into Crohn‘s disease. The mucosal inflammation gets so severe that it may cause intestinal obstruction—a condition similar to a stuffy nose during a cold, flu, or allergy attack, all of which cause acute inflammation of the nasal mucosa. The inflammation may happen at any point along the length of the small and large intestines, but it‘s most commonly localized in the bottom section of the ileum—the place where clogging with undigested fiber, bacterial fermentation, and fecal reflux is likeliest to occur. According to The Merck Manual of Diagnosis and Therapy: “Over the past few decades, the incidence of Crohn‘s disease has increased in the Western populations of Northern European and Anglo-Saxon ethnic derivation, third-world populations, blacks, and Latin Americans.”[12] What else happened during “the past few decades?” A substantial increase in the consumption of indigestible fiber, of course.
• Hernia. When intestines protrude through the abdominal wall or inside the scrotum, they cause hernias. About 5 million Americans suffer from this unpleasant, potentially lethal condition. Coughing, straining, or lifting weights isn‘t generally enough to push the intestines so hard that they pierce the abdominal muscles or squeeze down into the scrotum (inguinal hernia). Intestinal bloating from inflammatory diseases caused by indigestible fiber is the primary force capable of expanding the intestines so much that they don‘t have enough room inside the abdominal cavity, and may ripple through the abdominal wall. The physical exertion that causes the actual herniation is a secondary force. Straining to move large stools (caused by fiber) is one of the major causes of hernia as well.
• Malnutrition, and vitamin and mineral deficiencies. All the hard work that the body did breaking food down into basic nutrients—simple sugars, amino acids, fatty acids, vitamins, and minerals—is wasted unless they get assimilated into the blood-stream to become energy, electrolytes, hormones, enzymes, neurotransmitters, tissues, and other substances that keep our bodies functional and healthy. This final act of digestion takes place throughout the entire length of the small intestine, unless it‘s affected by inflammation. In this case, the essential nutrients will not digest, even if your diet contains plenty of them. Since indigestible fiber is the major source of intestinal inflammation, it is also a major cause of malnutrition and mineral and vitamin deficiencies. Pernicious anemia, which is a chronic shortage of dietary iron, folic acid, and vitamin B12, related to gastric and intestinal inflammation, is one of the most common forms of such a deficiency. It‘s also the most difficult to overcome, because regular oral supplements won‘t digest, no matter what the dose, unless the fiber is completely withdrawn and the stomach and intestines permitted to heal.

Fiber‘s effect on the large intestine: Demolition completed

The large intestine (a.k.a. gut, colon, bowel, entrails, and viscera) is a bona fide digestive organ. Its time is primarily taken up with the fermentation of undigested carbohydrates and assimilation of nutrients, water, and electrolytes. In the process, the large intestine converts the remnants of liquid chyme into stools and expels them. The more undigested fiber there is in the chyme, the larger and harder the stools become.

The adjective “large” next to the word “intestine” is misleading—the large intestine isn‘t that large vis-à-vis the small intestine, but wide. In Russian, for example, the intestines aren‘t small or large, but, respectively (and correctly), thin for small and thick for large. Length-wise, the large intestine is under 1.5 meters (5‘); width-wise, it‘s 6 to 9 cm (2.3–3.5”) at the base, narrowing down at the end.

The large intestine is made up of four functional sections that encircle the small intestine. It starts with a sac at the bottom that metamorphoses into a tube that looks like the letter “U” upside down. At the opposite end of the tube, another sac, terminated by a tight sphincter, completes the U-turn. Respectively, these are the cecum, colon, rectum, and anal canal.

Cecum. The cecum is a large pouch at the bottom of the ascending colon, also known as the blind gut. It is called blind because it only has one exit, just like a blind alley. The cecum is located at the lower-right-hand side of the abdomen. It collects chyme from the ileum, which is the final segment of the small intestine.

The cecum can hold up to 1.5 liters (1.58 quarts) of chyme. A sphincter (ileocecal valve) prevents chyme from spilling back into the small intestine whenever you lie down, bend down, or stand on your head.

As water, electrolytes, and micronutrients get absorbed into the bloodstream, the chyme is slowly propelled up the ascending colon. By this stage, it begins transformation into what we call stools or feces.

The cecum‘s most famous sibling—the appendix—is attached to the cecum‘s inside wall, further to the left, just under the intersection with the small intestine. Despite what you may have seen in pictures, the appendix is pointed upwards, not downwards, and its orifice faces sideways, not down.

Colon. The terms colon and large intestine are often used interchangeably, although technically this isn‘t correct. Actually, the colon is the tubing between the cecum and rectum, and it is divided into four parts: the first three are named for their direction: ascending, transverse, descending, and the fourth—sigmoid—for its sigma-like shape.

This is why medical professionals use the term colorectal in connection with such words as cancer, exam, surgery, x-ray, etc., because saying “an exam of the large intestine” is cumbersome, while “colon exam” is incorrect: doctors must pass and examine the rectum before reaching the colon, hence the term “colorectal exam.”

The word colon gave birth to numerous related terms, none of them particularly pleasant, such as colic (abdominal pain emanating from the colon), colitis (inflammation of the large intestine), colonoscopy (examination with an optical scope), colonics (a type of generous two-way enema), and colonic (specific to the large intestine, as in colonic bacteria).

The fecal mass goes up through the ascending colon, makes a sharp left, passes the transverse colon, turns down into the descending colon, and then makes a slight right into the sigmoid colon—the ramp leading into the rectum, and the last stop before being dumped. The mucus secretion (binding factor), water removal (drying factor), and bacterial action (volumetric factor) solidify the remnants of liquid chyme into solid stools before they reach the descending colon. The descending and sigmoid colon essentially perform a storage function for ready-to-be eliminated stools.

Rectum. The rectum is a stretchable, muscular sac, 10 to 15 cm (4”–6”) long, situated at the end of the sigmoid colon. It‘s right above the anus, and it shares a central space inside one‘s pelvis with the reproductive organs. Not romantic, but it works. The term rectal ampoule is often applied to the rectum‘s shape, because it‘s narrow at the bottom and dilates further up to form an ampoule-like appearance.

Anal Canal. This is the least appreciated organ, and usually the first to get into trouble because it‘s so tiny. The anal canal‘s maximum aperture is tight and narrow—3.5 cm (1.37”). The anal canal itself is about 3 cm (1.18”) long, and is encircled with two taut muscular sphincters—internal and external. Both sphincters perform in concert to keep the stools safely inside the rectum. We can consciously control only the external sphincter, while the internal is controlled autonomously, by the body itself.

The elimination of stools is the final act of digestion. Technically, it should be as easy as eating—the first act of digestion. When everything works just right, it is, but when it doesn‘t, it becomes a long and awful ordeal, first because of large stools caused by undigested fiber, second because of all the damage caused by large stools.

As with everything else in life, timing is everything with digestion: the mouth is busy chewing an average meal for 15–20 minutes; the healthy stomach digests an average mixed meal in 5 to 7 hours; the small intestine takes about 24 hours to transport chyme down to the large intestine; and the large intestine processes stools in about 72 hours.

In young, healthy people, indigestible fiber slows down stomach digestion and the transport time in the small intestine, but considerably speeds up the transport time (motility) in the large intestine, sometimes down to 24 hours. When this happens, the person may experiences diarrhea and cramping, which are usually “diagnosed” as irritable bowel syndrome. The word “diagnosed” is in quotes, because what‘s happening isn‘t a disease, but the natural reaction of a healthy colon to an unhealthy content. If caught early, the “syndrome” disappears a few days after the fiber is removed from the diet.

When a person is no longer young, or the digestive organs aren‘t in perfect shape, everything takes longer—the digestion in the stomach, the transport of chyme through the small intestine, and colonic motility. And when fiber is added, it takes even longer: