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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.

Infant Acid Reflux

baby-scratching-his-noseIt’s a sad commentary on current events when you notice that every other infant you meet seems to have GERD, gastroesophageal reflux disease. You know the scene by now. Almost everything the baby swallows gets regurgitated, which, by the way, is not quite the same as vomited. In the former, the material often goes back down; in the latter, it comes out. The acid burns on the way up, and it burns on the way back down.  The agony of it all! The apparent high incidence of GERD makes you wonder if there really are more cases, or is it merely over-diagnosed and mistaken for simple reflux?

What It Is
There is confusion between GER and GERD. Reflux is just that—stomach contents back up into the esophagus and sometimes come out the mouth or nose as spit-up or vomit. Reflux is common to about half of all infants under three months of age, but commonly decreases to less than 1% by one year (Hrabovsky, 1986). The prevalence of GER peaks between one and four months and often resolves at six months.   Physiologically, normal reflux is characterized by spitting up with burps, but the child continues to feed well and thrive without respiratory or other systemic involvement.

When additional symptoms appear, such as extreme irritability, blood loss, respiratory problems, chronic cough, disturbed sleep, apnea and cyanosis in wheezing, and poor growth, GERD may be suspected. Vomiting may occur more than twice a day and  continue longer than a few weeks. At this point, the infant may arch his back during or immediately after eating. Refusal to feed is common. It’s important to call the doctor if vomiting is projectile, is green or yellow, or looks like coffee grounds.

The Cause
The cause of GERD has not been pinpointed, but it’s safe to assume that the lower esophageal sphincter (LES), the muscle that closes the esophagus after swallowing and allowing food into the stomach, is not mature enough to do its job. It’s also possible that the section of the diaphragm through which the esophagus passes is poorly developed. If a baby is born with respiratory problems, xanthine drugs, such as theophylline or even caffeine, may be given to stimulate breathing. These increase gastric acid secretion and decrease LES pressure, resulting in reflux (Vandenplas, 1986).

The Diagnosis
You would think that, by this point in medical history, a pediatrician would know the difference between GER and GERD, yet according to a study performed at the Pediatric Specialty Center in New Orleans, it seems that doctors are overprescribing anti-reflux medications because they think they are treating GERD when the patient may only have GER (Khoshoo, 2007). British researchers also objurgated overuse of drugs in a declaration made in their Drugs and Therapeutics Bulletin in 2009. Part of the reason for this rise in medicating is parent expectations, so blame does not sit only on the physician. Some parents don’t feel as if they’ve visited a doctor unless they leave with a prescription. It was interesting to find in the Khoshoo study that some things under the parents’ control could account for GER symptoms, including thickness of the formula, changes in formula, the amounts fed, and the position of the baby.

If GERD is suspected, anatomic abnormalities may be detected by an upper GI exam, the kind that requires a barium swallow and x-ray. Being non-invasive, this is a relatively simple procedure. However, barium is physiologically inert and cannot be used to evaluate rates of gastric emptying. Extended monitoring of esophageal pH, however, is deemed the gold standard of GERD diagnosis, and may be accomplished using specially designed electrodes just for babies (Gille, 1982) (Koch, 1981). New devices are portable and 100% sensitive, looking for a drop in pH to less than 4.0, lasting for at least eight to fifteen seconds (Mohan, 2002). In severe cases, endoscopy and/or esophageal biopsy may be employed where esophagitis is suspected, both requiring sedation and invasion, something no parent wants for his child.

Treatment
Transient LES relaxation is considered the main mechanism behind infant reflux and probably has little or no effect on gastric emptying (Omari, 2002). If that is the case, thickening of formula is part of the therapeutic approach, and may be done so with a variety of food elements, including carob bean gum (Wenzl, 2003) or a tablespoon of rice cereal in two ounces of formula, reducing reflux by a considerable margin. Holding the baby more vertical while feeding is another useful approach (Cosgrove, 1998), and keeping him in that position for thirty minutes afterward offers substantial benefit.  Some studies report that cereal-thickened formula is more effective than posturing (Chao, 2007) (Vandenplas, 1998), but both are the preferred first line treatment (Baudon, 2009).

The use of pacifiers to keep a baby calm is ubiquitous. Some babies are happiest when they are sucking on something, although dependence on a pacifier might interfere with breast feeding and lead to dental problems later on. This non-nutritive sucking may increase the frequency of reflux if the baby is lying down, but generally not if sitting up (Orenstein, 1988). In some countries, pacifiers are rarely used to calm an infant. In the UAR, for example, mothers prefer to calm their offspring with soothing herbs, the commonest being anise. Fennel, gripe water (a blend of bicarbonate, ginger, dill, fennel and chamomile, sometimes containing alcohol), cumin, chamomile tea, mint, or fenugreek tea are other options (Abdulrazzaq, 2009). FYI, gripe water is regulated by the FDA in the United States, and the alcohol is out of the equation.  You can check it out here:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1297971/pdf/10844880.pdf
(Blumenthal, 2000). Colic Calm is one approved version available, although others may be out there.

If a child is so sensitized, cow’s milk will exacerbate GERD by inducing gastric dysrhythmia and delayed gastric emptying (Ravelli, 2001) (Nielsen, 2004). Allergy or sensitivity to cow’s milk protein cannot be determined by a single test, and neither should it be diagnosed only by clinical symptoms. Elimination-and-challenge procedures might tell all the story a parent needs. With frequency put at 3%, this is an area worth exploring with your physician (Høst, 1995, 2002), especially if your baby shows signs of distress (Ewing, 2005).

There is a hierarchy of infant reflux treatment, starting with formula thickening and postural changes and ending with drugs, the mildest of which are the H2-blockers such as Tagamet and Pepcid. The more potent proton pump inhibitors (PPIs), such as Prilosec and Prevacid, are of questionable efficacy in infants, and are presented with conflicting evidence (Higginbotham, 2010). It is suggested to save the drugs as the last resort, but to try them even before allowing your baby to be invaded by an endoscope.  H2 blockers will suppress the manufacture of stomach acid, as will PPIs, but not without side effects. With many drugs there is no dose low enough to be safe, especially in infants.  Because there is no simple tool a pediatrician can use to diagnose GERD in an infant, the Rx pad is often the first weapon. A parent’s anxiety only reassures the physician that he’s doing what’s best. Of course, marketing by the pharmaceutical companies makes it even easier to write a prescription, but that also makes it harder to distinguish between GER and GERD.

References

Abdulrazzaq YM, Al Kendi A, Nagelkerke N.
Soothing methods used to calm a baby in an Arab country.
Acta Paediatr. 2009 Feb;98(2):392-6.


Baudon JJ.
Gastroesophageal reflux in infants: myths and realities. 
Arch Pediatr. 2009 May;16(5):468-73. Epub 2009 Mar 19.


I Blumenthal
The gripe water story.
J R Soc Med. 2000 April; 93(4): 172–174.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1297971/pdf/10844880.pdf


Chao HC, Vandenplas Y.
Effect of cereal-thickened formula and upright positioning on regurgitation, gastric emptying, and weight gain in infants with regurgitation.
Nutrition. 2007 Jan;23(1):23-8.


Cosgrove M, Dodge J.
Gastro-oesophageal reflux in children.
Eur J Gastroenterol Hepatol. 1998 Jul;10(7):547-8.


Drug and Therapeutics Bulletin (dtb.bmj.com).  2009; 47(12): 134-137
Managing gastro-oesophageal reflux in infants
Relevant BNF section: 1.1,1.2,1.3, Appendix 2


Ewing WM, Allen PJ.
The diagnosis and management of cow milk protein intolerance in the primary care setting.
Pediatr Nurs. 2005 Nov-Dec;31(6):486-93.


Gille P, Aubert D, Cingotti M, François JY, Prihnenko N, Spiroux M, Jouan M.
Infant esophageal pH monitoring
Chir Pediatr. 1982 Mar-Apr;23(2):69-72.


Grant L, Cochran D.
Can pH monitoring reliably detect gastro-oesophageal reflux in preterm infants?
Arch Dis Child Fetal Neonatal Ed. 2001 Nov;85(3):F155-7; discussion F157-8.


Higginbotham,  Tanner W, PharmD
Effectiveness and Safety of Proton Pump Inhibitors in Infantile Gastroesophageal Reflux Disease
Ann Pharmacother March 2010 vol. 44 no. 3: 572-576


Høst A, Jacobsen HP, Halken S, Holmenlund D.
The natural history of cow’s milk protein allergy/intolerance.
Eur J Clin Nutr. 1995 Sep;49 Suppl 1:S13-8.


Høst A.
Frequency of cow’s milk allergy in childhood.
Ann Allergy Asthma Immunol. 2002 Dec;89(6 Suppl 1):33-7.


Hrabovsky EE, Mullett MD.
Gastroesophageal reflux and the premature infant.
J Pediatr Surg. 1986 Jul;21(7):583-7.


Iacono G, Carroccio A, Cavataio F, Montalto G, Kazmierska I, Lorello D, Soresi M, Notarbartolo A.
Gastroesophageal reflux and cow’s milk allergy in infants: a prospective study.
J Allergy Clin Immunol. 1996 Mar;97(3):822-7.


Khoshoo V, Edell D, Thompson A, Rubin M.
Are we overprescribing antireflux medications for infants with regurgitation?
Pediatrics. 2007 Nov;120(5):946-9.


A. Koch, R. Gass
Continuous 20–24 hr esophagealpH-monitoring in infancy *
Journal of Pediatric Surgery. Volume 16, Issue 2, April 1981, Pages 109–113


Mohan N and Soni A
Gastro-esophageal reflux in neonates.
Journal of Neonatology. 2002; 16(3):  257-266


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.


Omari TI, Barnett CP, Benninga MA, Lontis R, Goodchild L, Haslam RR, Dent J, Davidson GP.
Mechanisms of gastro-oesophageal reflux in preterm and term infants with reflux disease.
Gut. 2002 Oct;51(4):475-9.


Orenstein SR.
Effect of nonnutritive sucking on infant gastroesophageal reflux.
Pediatr Res. 1988 Jul;24(1):38-40.


Ravelli AM, Tobanelli P, Volpi S, Ugazio AG.
Vomiting and gastric motility in infants with cow’s milk allergy.
J Pediatr Gastroenterol Nutr. 2001 Jan;32(1):59-64.


M P Tighe, R M Beattie
Perspective
Managing gastro-oesophageal reflux in infancy
Arch Dis Child 2010;95:243-244 doi:10.1136/adc.2009.170407


Yvan Vandenplas, D. De Wolf, L. Sacre
Influence of Xanthines on Gastroesophageal Reflux in Infants at Risk for Sudden Infant Death Syndrome
Pediatrics Vol. 77 No. 6 June 1, 1986: pp. 807 -810


Vandenplas Y.
A critical appraisal of current management practices for infant regurgitation.
Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1997 May-Jun;38(3):187-202.


Yvan Vandenplas, MD, Jere Ziffer Lifshitz, MS, Susan Orenstein, MD, et al
Nutritional Management of Regurgitation in Infants
J Am Coll Nutr. August 1998; vol. 17 no. 4: 308-316


Van Howe RS, Storms MR.
Gastroesophageal reflux symptoms in infants in a rural population: longitudinal data over the first six months.
BMC Pediatr. 2010 Feb 11;10:7.


Wenzl TG, Schneider S, Scheele F, Silny J, Heimann G, Skopnik H.
Effects of thickened feeding on gastroesophageal reflux in infants: a placebo-controlled crossover study using intraluminal impedance.
Pediatrics. 2003 Apr;111(4 Pt 1):e355-9.

*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.
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