Posts

Gallstones: An Ounce Of Prevention Is Worth…

basic-food-groupIf you have some gall, we hope it’s the kind that causes you to exasperate others, and not the kind that hurts in the center of your upper belly, under the ribs, and occasionally spreads to your right upper back or shoulder.  Gallstone disease is the most common and costly of all the digestive conditions in the United States, accounting for nearly a million hospitalizations a year.  It can interfere with breathing and become severe enough to wake you from sleep…if you can get there in the first place.  Sometimes a person will vomit and relieve the pain; at other times he’ll get feverish from an outright blockage of the bile duct that connects the liver and gall bladder to the small intestine.  With a blockage, urine turns dark, stools are clay-colored, and the whites of the eyes may yellow.  We hope it never gets this far.

While allopathic medicine preaches no sure way to prevent gallstones, it allows that there are means to reduce risk.  Staying close to your ideal weight is important.  A real concern with this is that, lately, everybody is jumping onto the “lose weight fast” bandwagon.  It seems that gallstones can form from such a regimen and even from gastric bypass surgery (Shiffman, 1991).   In obesity, bile tends to stand still and cholesterol saturation increases.  Stones can form within a month of severe caloric restriction, as much as twenty-five times more likely than in obese persons who lose weight gradually (Weinsier, 1993).  Once in a while a person gets lucky, and there are no symptoms, despite the fact that most middle-agers probably have small stones.

Whether it was intended to be a mnemonic or not, the association of the “Five F’s” with gallbladder disease has been around for a time.  Female, fair (hair and skin), forty-ish, fertile (gallbladder trouble is associated with high estrogen), and owning too much fat risk gallstones.  But alcohol intake, a high-fat diet (especially fried foods) and sedentary lifestyle are contributing factors.  In an acute gallbladder attack, people will generally go to the ER, where they will get antibiotics and medicine for the pain, which will probably go away.  If an obstruction is noted, surgery will be done.  In a chronic gallbladder condition, surgery, either traditional or laparoscopic, will remove the gallbladder.  In circumstances that can be pinpointed only by a physician, medications called chenodeoxycholic acids or ursodeoxycholic acids can be given to help dissolve the stones.  But this can take as long as two years and the stones often reappear after treatment is stopped.

It is advisable that, if you are prone to gallbladder problems, you eat a low-fat, low-sugar, high fiber diet.  Decreasing fat limits the amount of work the gallbladder has to do every day.  Increasing fiber helps the liver to eliminate toxins faster. Besides, anything that supports liver function also helps it to make more bile.  Alternative treatment of gallbladder disease relies on increased bile production, liquefaction of bile to help get rid of gallbladder sludge, and dissolution of stones so they can be reduced to a size that can pass naturally. Production of bile can be increased with foods that reduce toxic burden on the whole body, including beets, artichokes (Saénz Rodriguez, 2002), greens, and cruciferous vegetables (Tsai, 2006).  Acidulated water also stimulates liver function. Even a shot of unfiltered apple cider vinegar can help.

Since an ounce or prevention is worth more than a ton of cure, take a look at what coffee does for gallbladder disease.  Harvard scientists found that increased intake of caffeinated beverages reduces the risk of symptomatic gallbladder disease in men, while decaf demonstrated no such effect (Leitzmann, 1999).  In a ten-year study of male healthcare professionals, the incidence of gallbladder attacks was significantly lower in those consuming coffee regularly.   A novice coffee drinker might get the jitters and act like Barney Fife charging his cylinder, but the tradeoff is worth it.  Later study by the same researcher discovered a parallel benefit for women (Leitzmann, 2002).  Using ultra-sound to document gallbladder disease, the Third National Health and Nutrition Examination found that, among women, there was a decreased prevalence of previously diagnosed gallbladder disease with increased coffee drinking (Ruhl, 2000).

Primates and guinea pigs are unable to create vitamin C from diet, so supplementation is required.  The enzyme needed to convert glucose into ascorbic acid was lost eons ago.  Without vitamin C, even guinea pigs get gallstones, although we have never seen tiny guinea pig ambulances in our neighborhood.  From the same health and nutrition exam cited earlier, which ran from 1988 to 1994, researchers from the V.A. Center in San Francisco saw an inverse relationship between vitamin C intake and gallstones, strongly so among women, less so among men (Simon, 1998, 2000).  Vitamin C, by the way, affects the catabolism of cholesterol to bile acids.  Using guinea pigs as, well, guinea pigs, Swedish investigators learned that deficiency of vitamin C causes supersaturation of bile and the subsequent formation of cholesterol gallstones.  But they also found an interesting side story in humans.  Increasing ascorbic acid also increases phospholipid concentrations, leading to a strong inverse association with the conditions that lead to stone formation (Gstafsson, 1997).  German scientists came to the same conclusion about ascorbic acid when they found half the incidence of gallstones in a female population that supplemented with vitamin C regularly (Walcher, 2009) (Lammert, 2004).

So far, prevention has addressed measures that are readily available, off the shelf.  An important strategy to prevent stone formation if one is susceptible is to alter the conditions that promote it.  That can be done with phosphatidylcholine (PC), the chief phospholipid from which the cell membrane is made.  Enriching your diet with PC can directly affect cholesterol solubilization and reduce or eliminate the probability of gallstone formation (Kasbo, 2003) (Vakhrushev, 2005) (Lammert, 2004).

Anecdotal reports about healing protocols abound.  But some of them are surprisingly supportable.  When a person is hospitalized for gallbladder disease, his food is typically replaced with intravenous fluids.  In a while, the pain goes away, after which time you’re allowed to eat.  It’s believed that some foods invoke an allergic response that is at the root of gallbladder attacks.  In a casual test done in the late 1960’s, Dr. James Breneman, the chair of the Food Allergy Committee of the American College of Allergists, asked 69 people suffering from gallbladder pain to try an elimination diet to determine food allergies.  After the identified foods were taken from their diets, symptoms disappeared.  The offending foods were tagged.  Eggs, pork, onions, chicken and turkey, milk, coffee, and oranges were most bothersome, followed by corn, beans, nuts, spices, peanuts, fish and rye.  In addition to foods, twenty percent of the group had attacks caused by medications (Wright, 2004).

Pain and the fear of surgery will direct a person to the least invasive solution he can find, whether it’s clinically proven or not.  There is at least one such remedy for gallstone dissolution that seems to be popular outside the U.S.—a gallbladder cleanse purportedly designed by a Korean chemist named Dr. Lai Chiu Nan.  It entails drinking four glasses of apple juice (or eating four-five apples) daily for five days.  The juice is supposed to soften the stones.  Maintain a normal diet during this time.  On day six, no dinner is enjoyed.  At 6 PM, a teaspoon of Epsom salts in a glass of warm water is consumed, followed by a second such cocktail two hours later.  Magnesium sulfate opens the gallbladder ducts (Harvey, 1973).  At 10 PM, swallow a half cup of olive oil mixed with a half cup of fresh lemon juice, to lubricate the stones and to ease their passage.  Green stones are supposed to drop into the toilet the next day.  If they don’t, use the olive oil and lemon juice to make vinaigrette.  If they do, a gemologist might make you an offer.  Hey, sometimes folk medicine really works, as in the oatmeal baths for itchy skin or lemon juice and honey for a sore throat.

Bile synthesis has been improved and increased by taking essential fatty acids, most notably fish oil.  In a head-to-head contest with fibrates (drugs used to lower triglycerides and cholesterol), fish oil was found to up the ante on bile acids and to alter their distribution (Jonkers, 2006).  But this wasn’t the first time that fish oil stood in the limelight.  Gall bladder emptying increases with fish oil, as gall bladder motility improves and triglyceride levels drop (Jonkers, 2003).  And it sure works on monkeys (Scobey, 1991).  In prairie dogs, who must be kin to guinea pigs because they are prone to gallstones, menhaden oil (an occasional source of commercial fish oil) increased levels of EPA and DHA and reduced incidence of cholesterol crystals (Booker, 1990).

We normally think of solvents as able to dissolve things, but almost never relate them to the human body except in old Vincent Price movies.  Some scientists might disagree with this neglect because they have learned that gallstones can sometimes be dissolved by plant-sourced solvents, especially a terpene called limonene, common to citrus fruits and recognized as a safe flavoring agent in foods and beverages.  An unsaturated hydrocarbon from plants, limonene has been tried and proven to be a dissolver of cholesterol stones (Sun, 2007), while a welcome side effect is the relief of heartburn and GERD (Ibid.).  In a trial dating back to the 1970’s, a blend of limonene and polysorbate 80 (an emulsifier) was found safe and effective in the lab and the clinic (Igimi, 1976).  Occasionally following gallbladder surgery, stones are retained in the duct.  Injecting a limonene preparation directly to the biliary system was able to dissolve retained stones (Igmini, 1991).  Efficacy was enhanced when limonene was mixed with a medium-chain triglyceride in a Japanese study done toward the end of the last century (Shionogi, 1992).  Besides citrus, a readily available source of such solvent is peppermint oil.  Whether it works orally to dissolve gallstones is under investigation.  It’s doubtful that some of us can wait for the results to be printed.

References

Baranyai T, Terzin V, Vajda A, Wittmann T, Czakó L.
[Acute pancreatitis caused by hypertriglyceridemia].  [Article in Hungarian]
Orv Hetil. 2010 Nov 7;151(45):1869-74.

Booker ML, Scott TE, La Morte WW.
Effects of dietary fish oil on biliary phospholipids and prostaglandin synthesis in the cholesterol-fed prairie dog.
Lipids. 1990 Jan;25(1):27-32.

Doran J, Keighley MR, Bell GD.
Rowachol–a possible treatment for cholesterol gallstones.
Gut. 1979 Apr;20(4):312-7.

Gaby AR.
Nutritional approaches to prevention and treatment of gallstones.
Altern Med Rev. 2009 Sep;14(3):258-67.

Gilat T, Leikin-Frenkel A, Goldiner L, Laufer H, Halpern Z, Konikoff FM.
Arachidyl amido cholanoic acid (Aramchol) is a cholesterol solubilizer and prevents the formation of cholesterol gallstones in inbred mice.
Lipids. 2001 Oct;36(10):1135-40.

Gustafsson U, Wang FH, Axelson M, Kallner A, Sahlin S, Einarsson K.
The effect of vitamin C in high doses on plasma and biliary lipid composition in patients with cholesterol gallstones: prolongation of the nucleation time.
Eur J Clin Invest. 1997 May;27(5):387-91

R. F. HARVEY AND A. E. READ
Effects of oral magnesium sulphate on colonic motility in patients with the irritable bowel syndrome’
Gut, 1973, 14, 983-987

Igimi H, Hisatsugu T, Nishimura M.
The use of d-limonene preparation as a dissolving agent of gallstones
Am J Dig Dis. 1976 Nov;21(11):926-39.

Igimi H, Tamura R, Toraishi K, Yamamoto F, Kataoka A, Ikejiri Y, Hisatsugu T, Shimura H.
Medical dissolution of gallstones. Clinical experience of d-limonene as a simple, safe, and effective solvent.
Dig Dis Sci. 1991 Feb;36(2):200-8.

Igimi H, Watanabe D, Yamamoto F, Asakawa S, Toraishi K, Shimura H.
A useful cholesterol solvent for medical dissolution of gallstones.
Gastroenterol Jpn. 1992 Aug;27(4):536-45.

Jonkers IJ, Smelt AH, Ledeboer M, Hollum ME, Biemond I, Kuipers F, Stellaard F, Boverhof R, Meinders AE, Lamers CH, Masclee AA.
Gall bladder dysmotility: a risk factor for gall stone formation in hypertriglyceridaemia and reversal on triglyceride lowering therapy by bezafibrate and fish oil.
Gut. 2003 Jan;52(1):109-15.

Jonkers IJ, Smelt AH, Princen HM, Kuipers F, Romijn JA, Boverhof R, Masclee AA, Stellaard F.
Fish oil increases bile acid synthesis in male patients with hypertriglyceridemia.
J Nutr. 2006 Apr;136(4):987-91.

Kasbo J, Tuchweber B, Perwaiz S, Bouchard G, Lafont H, Domingo N, Chanussot F, Yousef IM
Phosphatidylcholine-enriched diet prevents gallstone formation in mice susceptible to cholelithiasis.
J Lipid Res. 2003 Dec;44(12):2297-303. Epub 2003 Jul 1.

Kraft K.
Artichoke leaf extract- recent findings reflecting effects on lipid metabolism, liver and gastrointestinal tracts.
Phytomedicine 1997;4:369-78.

Lammert F, Matern S.
Evidence-based prevention of cholecystolithiasis.
Dtsch Med Wochenschr. 2004 Jul 9;129(28-29):1548-50.

Leitzmann MF, Willett WC, Rimm EB, Stampfer MJ, Spiegelman D, Colditz GA, Giovannucci E.
A prospective study of coffee consumption and the risk of symptomatic gallstone disease in men.
JAMA. 1999 Jun 9;281(22):2106-12.

Leitzmann MF, Stampfer MJ, Willett WC, Spiegelman D, Colditz GA, Giovannucci EL.
Coffee intake is associated with lower risk of symptomatic gallstone disease in women.
Gastroenterology. 2002 Dec;123(6):1823-30.

Riber C, Hojgaard L, Madsen JL, Rehfeld JF, Olsen O.
Gallbladder emptying and cholecystokinin response to fish oil and trioleate ingestion.
Digestion. 1996;57(3):161-4.

Ruhl CE, Everhart JE.
Association of coffee consumption with gallbladder disease.
Am J Epidemiol. 2000 Dec 1;152(11):1034-8.

Saénz Rodriguez T, García Giménez D, de la Puerta Vázquez R.
Choleretic activity and biliary elimination of lipids and bile acids induced by an artichoke leaf extract in rats.
Phytomedicine. 2002 Dec;9(8):687-93.

Scobey MW, Johnson FL, Parks JS, Rudel LL.
Dietary fish oil effects on biliary lipid secretion and cholesterol gallstone formation in the African green monkey.
Hepatology. 1991 Oct;14(4 Pt 1):679-84.

Shiffman ML, Sugerman HJ, Kellum JM, Brewer WH, Moore EW.
Gallstone formation after rapid weight loss: a prospective study in patients undergoing gastric bypass surgery for treatment of morbid obesity.
Am J Gastroenterol. 1991 Aug;86(8):1000-5.

Simon JA, Hudes ES.
Serum ascorbic acid and gallbladder disease prevalence among US adults: the Third National Health and Nutrition Examination Survey (NHANES III).
Arch Intern Med. 2000 Apr 10;160(7):931-6.

Simon JA, Hudes ES.
Serum ascorbic acid and other correlates of gallbladder disease among US adults.
Am J Public Health. 1998 Aug;88(8):1208-12.

Sun J.
D-Limonene: safety and clinical applications.
Altern Med Rev. 2007 Sep;12(3):259-64.

Tsai CJ, Leitzmann MF, Willett WC, Giovannucci EL.
Fruit and vegetable consumption and risk of cholecystectomy in women.
Am J Med. 2006 Sep;119(9):760-7.

Vakhrushev IaM, Suchkova EV.
Use of essentiale and cholagogum in prevention of cholelithiasis in fat hepatosis with concomitant cholecystitis 
Ter Arkh. 2005;77(2):18-21.

von Bergmann K, Beck A, Engel C, Leiss O.
Administration of a terpene mixture inhibits cholesterol nucleation in bile from patients with cholesterol gallstones.
Klin Wochenschr. 1987 May 15;65(10):458-62.

Walcher T, Haenle MM, Kron M, Hay B, Mason RA, Walcher D, Steinbach G, Kern P, Piechotowski I, Adler G, Boehm BO, Koenig W, Kratzer W; EMIL study group.
Vitamin C supplement use may protect against gallstones: an observational study on a randomly selected population.
BMC Gastroenterol. 2009 Oct 8;9:74.

Weinsier RL, Ullmann DO.
Gallstone formation and weight loss.
Obes Res. 1993 Jan;1(1):51-6.

Williams CA, Goldstone F, Greenham J.
Flavonoids, cinnamic acids and coumarins from the different tissues and medicinal preparations of Taraxacum officinale.
Phytochemistry. 1996 May;42(1):121-7.

Wright, Jonathan V.
The 99.9 percent effective technique for eliminating gallbladder attacks forever
Nutrition and Healing. 2004; 11(9):1

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

What Is A Hiatal – Or Hiatus – Hernia?

intestineThere is an oval shaped opening in the diaphragm through which the esophagus passes on its way to the stomach.  The esophagus is regulated by a sphincter muscle that opens when we swallow to let food into the stomach.  Once the food gets there, the sphincter is supposed to close in order to prevent stomach acid from flowing backward.  After we swallow, the esophagus contracts (peristalsis) both longitudinally and circularly.  This action pulls the stomach upward into the hiatus a little, after which it is then relaxed.  If the top of the stomach slides or rolls into the hiatus and stays there, a hiatus hernia occurs.  This activity can cause chest pains that mirror cardiac episodes, complete with shortness of breath, which is why hiatal hernia is sometimes called the “great mimic.”

What Causes A Hiatal Hernia?

Sometimes the diaphragmatic muscle tissue surrounding the juncture of the esophagus and stomach is weak, allowing a portion of the stomach to peek through the hiatus. This can also happen from an injury to the area, as when an athlete gets the wind knocked out of him from the shock of being tackled, punched or kicked. It’s possible to be born with an unusually large hiatus, too. Then, there’s the intense pressure from coughing, vomiting, heavy lifting, or straining during bowel movement (Kakarlapudi, 2002) (Puri, 2004).

Heredity is an infrequent factor in hiatal hernia, but obesity (Pandolfino, 2006) and smoking may play a more significant role, particularly in the reflux that accompanies it  (Lee, 2001) (Sontag, 1991), where smoking was found to increase pressure upon the sphincter and obesity upon the diaphragm.

Will It Ever Go Away?

There is some evidence that the presence of hiatus hernia contributes to abnormal acid reflux (Dunne, 2000), and that the reverse may also be true.  It is believed that acute acid injury can shorten the esophagus and pull the stomach upward, through the hiatus.  How’s that for circular reasoning: the acid causes the hernia; the hernia causes the acid?  If this is so, avoidance of exacerbating foods might be in order.  High-fat and fried foods aggravate reflux by delaying stomach emptying.  Fat sits in the stomach longer than other macronutrients and requires more acid to be digested.  But you also need to pay attention to spicy foods, creamed foods (including soups), fast foods and even chocolate and milk.  Despite being healthy and nutritious, citrus fruits and juices can trigger acid reflux. Tomatoes, caffeinated beverages and alcohol contribute to the misery.  Eating smaller meals reduces pressure on the sphincter and the diaphragm. Because surgery fails to solve the problem due to frequent recurrence, it is generally not recommended, although using a mesh of some kind to narrow the hiatus has met a modicum of success (Puri, 2004). Losing weight (if you need to) relieves pressure on the diaphragm and eliminates a significant risk factor for associated esophagitis (Wilson, 1999).  One of the non-traditional techniques for easing a hiatal hernia is to drink warm water first thing in the morning, and then stand on your toes and suddenly drop onto your heels, the idea being that the weight of the water will pull the stomach down and out of the hiatus.  Who knows?

The frequency of hiatal hernia increases with age, from about 10% in people less than 40 years old to almost 70% in those above 70.  Some researchers attribute causation to low-fiber diet, since less-developed societies incur practically no hiatus involvement (Burkitt, 1971, 1981).  Others suggest that using chairs and toilets, instead of merely squatting for social encounters and personal needs, contributes to hiatal hernias (Sontag, 1999).  Inasmuch as we’re conditioned to the position of our carriages, we might as well increase the fiber and keep the chairs.  The Institute of Medicine suggests that we consume 14 grams of fiber for every 1000 calories we take in.  Odds are that most Americans fall short.  But we know that you don’t.

Are There Supplements?

Because protrusion of the stomach above the diaphragm is a mechanical/structural issue that requires a mechanical/structural fix, we need to focus on reflux sequestration.  After you’ve gone through all the antacids on the shelf, starting with Rolaids and working up to proton pump inhibitors like Prilosec OTC, you might explore the alternatives, especially since drugs tend to deplete the body of certain nutrients.  In light of that, you may be interested in a licorice preparation called deglycyrrhizinated licorice (DGL), a supplement that has the glycyrrhizin take out because it could raise blood pressure in some people.  Licorice enhances mucus production, which is protective against acid (Kolarski, 1987).  That’s a good thing.  Its derivative, carbenoxolone (Reed, 1978) (Young, 1986), likewise enhances mucus, but has the potential to increase sodium and water retention and to decrease potassium levels in susceptible persons.

Prostaglandins, derived from fatty acids, are hormone-like substances that control various body processes, including the manufacture of protective mucus in the esophagus.  Melatonin is a supplement that appears ready and willing to stimulate the formation of prostaglandin E2 and tone down acid reflux via that mechanism (Konturek, 2007).  (You might be familiar with melatonin as a supplement to encourage restful sleep.)  In the realm of herbal preparations is STW 5, marketed as Iberogast, a blend of licorice root, caraway, lemon balm, German chamomile and other herbs.  Double-blind, randomized, placebo-controlled tests found this combination product to be an effective treatment for disturbed digestion (Madisch, 2004) (Meltzer, 2004) without nasty side effects.   If you are so inclined to try them, the separate ingredients in this preparation may help to tame heartburn.

The Bottom Line

Lose extra pounds, avoid foods that trigger heartburn, make your last meal of the day two or more hours before bedtime, don’t lie down right after lunch, stop smoking, have smaller meals throughout the day, elevate the head of the bed six inches and try a supplement.  Cutting back on sugar and simple carbs might help.  And if, like some of us, you have no pride, go ahead and jump up and down on your heels.  But put on some rhythmic music first, else all suspicion will be gone.

References

Burkitt DP, James PA.
Low-residue diets and hiatus hernia.
Lancet. 1973 Jul 21;2(7821):128-30.

Burkitt DP.
Hiatus hernia: is it preventable?
Am J Clin Nutr. 1981 Mar;34(3):428-31.

Alan J Cameron, M.D
Barrett’s esophagus: prevalence and size of hiatal hernia
The American Journal of Gastroenterology.  Vol 94, Iss 8, Aug 1999, Pp. 2054–2059

Dent J, El-Serag HB, Wallander MA, Johansson S.
Epidemiology of gastro-oesophageal reflux disease: a systematic review.
Gut. 2005 May;54(5):710-7.

Dunne DP, Paterson WG.
Acid-induced esophageal shortening in humans: a cause of hiatus hernia?
Can J Gastroenterol. 2000 Nov;14(10):847-50.

Kahrilas PJ.
The role of hiatus hernia in GERD.
Yale J Biol Med. 1999 Mar-Jun;72(2-3):101-11.

Kakarlapudi GV, Awad ZT, Haynatzki G, Sampson T, Stroup G, Filipi CJ.
The effect of diaphragmatic stressors on recurrent hiatal hernia.
Hernia. 2002 Dec;6(4):163-6. Epub 2002 Sep 17.

Kolarski V, Petrova-Shopova K, Vasileva E, Petrova D, Nikolov S.
Erosive gastritis and gastroduodenitis–clinical, diagnostic and therapeutic studies.
Vutr Boles. 1987;26(3):56-9.

Konturek SJ, Konturek PC, Brzozowski T, Bubenik GA.
Role of melatonin in upper gastrointestinal tract.
J Physiol Pharmacol. 2007 Dec;58 Suppl 6:23-52.

Lee SJ, Song CW, Jeen YT, Chun HJ, Lee HS, Um SH, Lee SW, Choi JH, Kim CD, Ryu HS, Hyun JH.
Prevalence of endoscopic reflux esophagitis among Koreans.
J Gastroenterol Hepatol. 2001 Apr;16(4):373-6.

Madisch A, Holtmann G, Mayr G, Vinson B, Hotz J.
Treatment of functional dyspepsia with a herbal preparation. A double-blind, randomized, placebo-controlled, multicenter trial.
Digestion. 2004;69(1):45-52. Epub 2004 Jan 30.

Mogica Martínez MD, Paredes Cruz E, Tenorio Pastrana MA, Rodríguez Castellón J, Molina Ortiz C, del Rosario Canseco Raymundo M, López Durán JL, Becerril Angeles M.
Prevalence of hiatal hernia and chronic esophagitis in adult asthmatic patients.

Rev Alerg Mex. 2001 Sep-Oct;48(5):145-50.

Melzer J, Rösch W, Reichling J, Brignoli R, Saller R.
Meta-analysis: phytotherapy of functional dyspepsia with the herbal drug preparation STW 5 (Iberogast).
Aliment Pharmacol Ther. 2004 Dec;20(11-12):1279-87.

John E. Pandolfino, Hashem B. El–Serag, Qing Zhang, Nimeesh Shah, Sudip K. Ghosh, Peter J. Kahrilas
Obesity: A Challenge to Esophagogastric Junction Integrity
Gastroenterology.  Volume 130, Issue 3 , Pages 639-649, March 2006

Petersen H, Johannessen T, Sandvik AK, Kleveland PM, Brenna E, Waldum H, Dybdahl JD.
Relationship between endoscopic hiatus hernia and gastroesophageal reflux symptoms.
Scand J Gastroenterol. 1991 Sep;26(9):921-6.

Pettersson GB, Bombeck CT, Nyhus LM.
Influence of hiatal hernia on lower esophageal sphincter function.
Ann Surg. 1981 Feb;193(2):214-20.

V. Puri, G. V. Kakarlapudi, Z. T. Awad and C. J. Filipi
Hiatal hernia recurrence: 2004
Hernia. Volume 8, Number 4 (2004), 311-317

Reed PI, Davies WA.
Controlled trial of a carbenoxolone/alginate antacid combination in reflux oesophagitis.
Curr Med Res Opin. 1978;5(8):637-44.

Skinner DB.
Pathophysiology of gastroesophageal reflux.
Ann Surg. 1985 Nov;202(5):546-56.

Sontag SJ, Schnell TG, Miller TQ, Nemchausky B, Serlovsky R, O’Connell S, Chejfec G, Seidel UJ, Brand L.
The importance of hiatal hernia in reflux esophagitis compared with lower esophageal sphincter pressure or smoking.
J Clin Gastroenterol. 1991 Dec;13(6):628-43.

Sontag SJ.
Defining GERD.
Yale J Biol Med. 1999 Mar-Jun;72(2-3):69-80.

Wilson LJ, Ma W, Hirschowitz BI.
Association of obesity with hiatal hernia and esophagitis.
Am J Gastroenterol. 1999 Oct;94(10):2840-4.

Young GP, Nagy GS, Myren J, Kronborg IJ, Logan KR, Reed PI, Hopper JL.
Treatment of reflux oesophagitis with a carbenoxolone/antacid/alginate preparation. A double-blind controlled trial.
Scand J Gastroenterol. 1986 Nov;21(9):1098-104.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.

Gastroesophageal Reflux Is Not For The Faint Of Heart

Where Does It Come From?

antacidsIf you’re among the more than sixty million American adults who have heartburn at least once a month, odds are you’ll pick an OTC medication rather than see your doctor. With what you hear on TV and what you see in magazines, you know there’s a slew of remedies to pick from. The one you buy, though, is the one with the most valuable coupon from the Sunday inserts, right?  Right. Heartburn is related to gastroesophageal reflux disease (GERD), but is not exactly the same thing. Heartburn is a sensation of tightness, pain or discomfort that follows an occurrence of acid reflux. Reflux first, heartburn (cardialgia in scientific terms) next. Sometimes there is no discomfort with reflux. Therefore, you can have reflux without heartburn, but you can’t have heartburn without reflux. Reflux is the fire; heartburn is the smoke. The pain is an indication that your esophagus is being damaged by stomach acid. If this happens often, you have GERD.

The exact cause of GERD is not well-defined, but there is awareness that a few factors might be involved, including hiatal hernia (when the stomach pushes up through a hole in the diaphragm), abnormally weak contraction of the lower esophageal sphincter muscle (a ring of muscles where the esophagus meets the stomach to keep food from going backward), and abnormal emptying of the stomach. A welcome announcement is that some of this can be temporary. The management of GERD should be individualized, depending on its seriousness. Mild occasional symptoms can often be controlled with conservative measures, among them diet. Some foods can trigger a GERD episode. Examples include fatty foods, fried foods, alcohol, caffeine, citrus fruits and juices, spicy foods, tomatoes and tomato products, chocolate, carbonated beverages, onions, garlic and dairy. Some foods may be particular to you.

Besides foods, contributors to the agony of reflux include obesity, an epidemic of which is sweeping not only the United States, but also the developed world. Body mass index (BMI) portends the occurrence of GERD (Hajar, 2012), and not just in adults. An increase of a child’s waist circumference, even if normal-weight, elevates risk of reflux disease (Quitadamo, 2012). Some medications can share the blame, too. Calcium channel blockers, theophylline (a bronchial dilator used to treat asthma), nitrates (used to relax blood vessels), and antihistamines are on the list. Smoking, by the way, weakens the lower esophageal sphincter.

How About My Baby?

The causes of infant reflux are easy to understand. The sphincter is insufficiently developed to do its job, so, until it matures, stomach contents creep backward, up and out. It also could be a case of eating too much too fast. Thankfully, this is a self-limiting process that usually resolves by six to twelve months of age (Jung, 2001). In infants, actual GERD is rare, albeit a more serious pathology that warrants medical diagnosis and intervention. Complaints of regurgitation are common during the first year of life, peaking at 4 months (Nelson, 1997).

Here, food intolerance, and especially that of cow’s milk, cannot be discounted, despite what Grandma says about the family history of milk intake. No one can explain why, notwithstanding its use for years, cow’s milk is suddenly a culprit in juvenile gastric complaints of this nature (Semeniuk, 2006). Elimination-challenge studies done in Denmark have demonstrated that cow’s milk hypersensitivity is a real issue (Nielsen, 2004). Inconsolable crying, failure to gain weight, refusing food, bad breath, and burping and hiccups are common symptoms. If the baby vomits, good. Otherwise the pain is doubled as the acid goes back down and multiplies the damage to the esophagus.

What To Do?

If you’ve used all the antacids on the market and have decided to move up to something more potent, the next step is histamine 2 receptor blockers, a.k.a. Pepcid, Tagamet, or Zantac. These drugs can heal the esophagus 50% of the time by blocking the early stages of acid production. No acid, no hurt. But insufficient stomach acid interferes with food digestion, especially of protein. Constipation, dizziness, skin rash, hallucinations, and confusion are side effects. But H2 inhibitors start to work in less than an hour. Yay. Next up the ladder are proton pump inhibitors, the most potent of GERD medications. These include Prilosec, Prevacid and Nexium. They last longer in the body than H2 blockers, but take longer to get started. These have even neater side effects, like tremors, palpitations, muscle spasms, and yellowing eyes. But none of these happen to all people, and some never happen to anybody you know.

How about a natural approach?  Stop eating three hours before bedtime and don’t go supine right after a meal. Elevate the head of your bed six inches to work with gravity. Stop eating when you’re satisfied, not when you’re so filled you can’t get up from the table. Lose that gut.

Is There Something I Can Take?

Mucus is the protective barrier between acid and the gastric lining. The amount of mucus in the esophagus is negligible, but may be just enough to protect against the damage and discomfort caused by refluxed acid (Dixon, 2001). Because it is known to improve the secretion of mucus, licorice extract (deglycyrrhizinated licorice), either singly or as part of an herbal complex, demonstrated capability to attenuate acid reflux symptoms (Larkworthy, 1975) by improving the gastric environment (vanMarle, 1981). Carbenoxolone, a synthesized licorice preparation, exhibited effectiveness comparable to drug therapy (Bickel 1981) at increasing mucus thickness.

A combination product called STW5, containing chamomile, clown’s mustard, angelica root, caraway, milk thistle, celandine and licorice root proved to be as effective as cimetidine (Tagamet) in protecting against acid-induced ulcerations (Khayyal, 2001)
and was identified as a valid therapeutic option for those who prefer phytotherapy to drugs (Melzer, 2004) (Madisch, 2001).

Melatonin is a supplemental hormone produced by the pineal gland that people use to help them sleep. In the gut it’s been identified as an important signaling molecule, where it seems to have a local effect on esophageal mucosa, stimulating the production of prostaglandin E2, which is protective of that mucus layer (Konturek, June, 2007). Additionally, melatonin inhibits gastric acid secretion while enhancing gastrin release, thus stimulating the sphincter to contract and limit esophagus contact with acid (Konturek, Dec, 2007). Even though melatonin trials are limited, results are significant.

Studies that examine alternative approaches to GERD treatment are in the works. While it is such that proton pump inhibitors (PPI’s), often the first line treatment, are effective for non-erosive GERD, their applicability to other GERD patients is under question. An odd thing about PPI’s is they are often used to diagnose GERD based on a person’s response to the drug. A favorable response indicates that GERD has been effectively addressed. That, however, does not necessarily indicate healing of the underlying pathology, which is almost always a problem with the lower esophageal sphincter. A low-carb diet and weight loss might just be the best bet.

References

Achem SR, Robinson M.
A prokinetic approach to treatment of gastroesophageal reflux disease.
Dig Dis. 1998 Jan-Feb;16(1):38-46.

Altman KW, Stephens RM, Lyttle CS, Weiss KB.
Changing impact of gastroesophageal reflux in medical and otolaryngology practice.
Laryngoscope. 2005 Jul;115(7):1145-53.

Bickel M, Kauffman GL Jr.
Gastric gel mucus thickness: effect of distention, 16,16-dimethyl prostaglandin e2, and carbenoxolone.
Gastroenterology. 1981 Apr;80(4):770-5.

Champion MC.
Prokinetic therapy in gastroesophageal reflux disease.
Can J Gastroenterol. 1997 Sep;11 Suppl B:55B-65B.

J Dixon PhD, V Strugala PhD, S M Griffin MD, P W Dettmar PhD, A Allen DPhil and J P Pearson PhD
Esophageal mucin: an adherent mucus gel barrier is absent in the normal esophagus but present in columnar-lined Barrett’s esophagus
The American Journal of Gastroenterology (2001) 96, 2575–2583

Guslandi M, Cambielli M, Bierti L, Tittobello A.
Effect of carbenoxolone and cimetidine on gastric mucin.
Clin Ther. 1980;3(1):40-2.

Hajar N, Castell DO, Ghomrawi H, Rackett R, Hila A.
Impedance pH Confirms the Relationship Between GERD and BMI.
Dig Dis Sci. 2012 Mar 27. [Epub ahead of print]

Jung AD.
Gastroesophageal reflux in infants and children.
Am Fam Physician. 2001 Dec 1;64(11):1853-60.

Khan M, Santana J, Donnellan C, Preston C, Moayyedi P.
Medical treatments in the short term management of reflux oesophagitis
Cochrane Database Syst Rev. 2007 Apr 18;(2):CD003244.

Khayyal MT, el-Ghazaly MA, Kenawy SA, Seif-el-Nasr M, Mahran LG, Kafafi YA, Okpanyi SN.
Antiulcerogenic effect of some gastrointestinally acting plant extracts and their combination.
Arzneimittelforschung. 2001;51(7):545-53.

Kim DC, Kim SH, Choi BH, Baek NI, Kim D, Kim MJ, Kim KT.
Curcuma longa extract protects against gastric ulcers by blocking H2 histamine receptors.
Biol Pharm Bull. 2005 Dec;28(12):2220-4.

Kolarski V, Petrova-Shopova K, Vasileva E, Petrova D, Nikolov S.
Erosive gastritis and gastroduodenitis–clinical, diagnostic and therapeutic studies.
Vutr Boles. 1987;26(3):56-9.

Konturek SJ, Konturek PC, Brzozowski T, Bubenik GA.
Role of melatonin in upper gastrointestinal tract.
J Physiol Pharmacol. 2007 Dec;58 Suppl 6:23-52.

Konturek SJ, Zayachkivska O, Havryluk XO, Brzozowski T, Sliwowski Z, Pawlik M, Konturek PC, Cześnikiewicz-Guzik M, Gzhegotsky MR, Pawlik WW.
Protective influence of melatonin against acute esophageal lesions involves prostaglandins, nitric oxide and sensory nerves.
J Physiol Pharmacol. 2007 Jun;58(2):361-77.

Larkworthy W, Holgate PF.
Deglycyrrhizinized liquorice in the treatment of chronic duodenal ulcer. A retrospective endoscopic survey of 32 patients.
Practitioner. 1975 Dec;215(1290):787-92.

Lieberman D.
Treatment approaches to reflux oesophagitis.
Drugs. 1990 May;39(5):674-80.

Madisch A, Melderis H, Mayr G, Sassin I, Hotz J.
A plant extract and its modified preparation in functional dyspepsia. Results of a double-blind placebo controlled comparative study.
Z Gastroenterol. 2001 Jul;39(7):511-7.

Madisch A, Holtmann G, Mayr G, Vinson B, Hotz J.
Treatment of functional dyspepsia with a herbal preparation. A double-blind, randomized, placebo-controlled, multicenter trial.
Digestion. 2004;69(1):45-52. Epub 2004 Jan 30.

Maton PN, Burton ME.
Antacids revisited: a review of their clinical pharmacology and recommended therapeutic use.
Drugs. 1999 Jun;57(6):855-70.

 Meletis, Chris D. and Zabriski, Nieski. “Clinical Natural Medicine Handbook.” New Rochelle, NY: Mary Ann Liebert, Inc., 2008. Pp. 208-220

Melzer J, Rösch W, Reichling J, Brignoli R, Saller R.
Meta-analysis: phytotherapy of functional dyspepsia with the herbal drug preparation STW 5 (Iberogast).
Aliment Pharmacol Ther. 2004 Dec;20(11-12):1279-87.

Nelson SP, Chen EH, Syniar GM, Christoffel KK.
Prevalence of symptoms of gastroesophageal reflux during infancy. A pediatric practice-based survey.
Arch Pediatr Adolesc Med. 1997 Jun;151(6):569-72.

Nielsen RG, Bindslev-Jensen C, Kruse-Andersen S, Husby S.
Severe gastroesophageal reflux disease and cow milk hypersensitivity in infants and children: disease association and evaluation of a new challenge procedure.
J Pediatr Gastroenterol Nutr. 2004 Oct;39(4):383-91.

Niemcryk SJ, Joshua-Gotlib S, Levine DS.
Outpatient experience of patients with GERD in the United States: analysis of the 1998-2001 National Ambulatory Medical Care Survey.
Dig Dis Sci. 2005 Oct;50(10):1904-8.

Ness-Jensen E, Lindam A, Lagergren J, Hveem K.
Changes in prevalence, incidence and spontaneous loss of gastro-oesophageal reflux symptoms: a prospective population-based cohort study, the HUNT study.
Gut. 2011 Dec 21. [Epub ahead of print]

NIH Publication No. 07–0882
May 2007
National Digestive Diseases Information Clearinghouse
Heartburn, Gastroesophageal Reflux (GER), and Gastroesophageal Reflux Disease (GERD)
http://digestive.niddk.nih.gov/ddiseases/pubs/gerd/index.aspx

O’Mahony R, Al-Khtheeri H, Weerasekera D, Fernando N, Vaira D, Holton J, Basset C.
Bactericidal and anti-adhesive properties of culinary and medicinal plants against Helicobacter pylori.
World J Gastroenterol. 2005 Dec 21;11(47):7499-507.

Lyn Patrick, ND
Gastroesophageal Reflux Disease (GERD): A Review of Conventional and Alternative
Treatments

Altern Med Rev 2011;16(2):116-133

Quitadamo P, Buonavolontà R, Miele E, Masi P, Coccorullo P, Staiano A.
Total and Abdominal Obesity are Risk Factors for Gastroesophageal Reflux Symptoms in Children.
J Pediatr Gastroenterol Nutr. 2012 Mar 20. [Epub ahead of print]

Rees WD, Rhodes J, Wright JE, Stamford LF, Bennett A.
Effect of deglycyrrhizinated liquorice on gastric mucosal damage by aspirin.
Scand J Gastroenterol. 1979;14(5):605-7.

Richter JE, Bradley LC.
Psychophysiological interactions in esophageal diseases.
Semin Gastrointest Dis. 1996 Oct;7(4):169-84.

Salim AS.
Sulfhydryl-containing agents in the treatment of gastric bleeding induced by nonsteroidal anti-inflammatory drugs.
Can J Surg. 1993 Feb;36(1):53-8.

Semeniuk J, Kaczmarski M.
Gastroesophageal reflux (GER) in children and adolescents with regard to food intolerance.
Adv Med Sci. 2006;51:321-6.

Sontag SJ.
The medical management of reflux esophagitis. Role of antacids and acid inhibition.
Gastroenterol Clin North Am. 1990 Sep;19(3):683-712.

van der Pol R, Smite M, Benninga MA, van Wijk MP.
Non-pharmacological therapies for GERD in infants and children.
J Pediatr Gastroenterol Nutr. 2011 Dec;53 Suppl 2:S6-8.

van Marle J, Aarsen PN, Lind A, van Weeren-Kramer J.
Deglycyrrhizinised liquorice (DGL) and the renewal of rat stomach epithelium.
Eur J Pharmacol. 1981 Jun 19;72(2-3):219-25.

Vologzhanina LG, Vladimirskiĭ EV.
Efficacy of the drinking magnesium-calcium sulfate mineral water in the combined treatment of duodenal ulcer comorbid with gastroesophageal reflux.      
Vopr Kurortol Fizioter Lech Fiz Kult. 2005 Nov-Dec;(6):17-9.

WebMD Health News. Dec. 22, 2011
Study: Acid Reflux on the Rise
Obesity Increase Likely to Blame, Researchers Say
Salynn Boyles;  Reviewed by Louise Chang, MD
http://www.webmd.com/heartburn-gerd/news/20111222/study-acid-reflux-prevalence-increasing

Wiener GJ, Morgan TM, Copper JB, Wu WC, Castell DO, Sinclair JW, Richter JE.
Ambulatory 24-hour esophageal pH monitoring. Reproducibility and variability of pH parameters.
Dig Dis Sci. 1988 Sep;33(9):1127-33.

*These statements have not been evaluated by the FDA.
These products are not intended to treat, diagnose, cure, or prevent any disease.