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admin | Bv Homeopathic Treatment | 04.04.2016
This is part 2 of a 2-part series that sheds light on the causes of GERD, Acid Reflux, & Heartburn, and provides new evidence-based solutions that can correct the root causes of these symptoms. In part 1 of this article we reviewed how GERD is often treated in orthodox medicine, as well as how it is often treated in naturopathic practices, and some of the problems associated with those treatments. The evidence is overwhelming that acid reflux, in most common cases, is the result of excess intra-abdominal pressure (IAP) and gas pressing up against the lower esophageal sphincter (see right), causing it to open longer and more often, pushing stomach acid back up into esophagus. There appear to be certain carbohydrates (sugars) that are not well absorbed or broken down by some people.
I personally see too many people who have chronic GERD or Acid Reflux trying to self-treat for years with all sorts of remedies they’ve read about online. Heart Conditions: Cardiovascular symptoms can also mimic symptoms of heartburn, GERD, and Acid Reflux. Lower Esophageal Sphincter Dysfunction and Diverticula: There are other, less common, mechanical causes for reflux, including severe LES dysfunction, or diverticula.
Small-Intestinal Bacterial Overgrowth (SIBO): If you have true SIBO, diagnosed with a  Lactulose Breath Test for Hydrogen and Methane, the following plan will likely give you some success, but it will be limited and temporary.
By self-treating GERD before you have had a proper diagnosis or medical evaluation, you potentially run the risk of making things worse or at best wasting a lot of time and money.
So if you have anything more than very mild symptoms, or you have had this issue for many years, it will almost always help to have a professional who knows what they are doing evaluate you for any of these more serious problems, and can also show you how advanced your symptoms really are.
I am making a big deal out of this, because, well, one of the top physicians specializing in Acid Reflux, Dr. Apart from the 2 dietary changes below, this is the most important step you can take — simply do not eat 3 hours before bed.
You can achieve this by keeping your food intake in a regular 8-12 hour window each day (for example, eating breakfast at 8am, lunch around noon, and a smaller dinner around 6 or 7pm, and bed around 10pm).
In almost every case of GERD, it has been found that lowering the gas from carbohydrates in the digestive tract is the #1 factor in preventing GERD. Double star this one, memorize it, imprint it on your brain if you have GERD, and think about it every time you drink milk or eat dairy. Indigestion of lactose, the sugar found in dairy products, is the top culprit in all this excess gas pressure. This means it spends a lot of time in your gut where bacteria can have a field day creating all kinds of gas that pushes back up into your stomach and esophagus.
In one study, patients were given 30 grams of lactose up their bums (yes, all in the name of science).
It also lowered the threshold by which the esophagus would open, meaning it took less pressure than normal to open it up.5Modulation by colonic fermentation of LES function in humans. While removing dairy completely might be necessary for some, you might be able to get away with cheeses aged more than a month and other dairy products that are very low in lactose. FODMAPs stands for 4 different types of carbohydrates that are known to cause the kind of excess gas in the digestive tract that can lead to GERD.
Here are the most common examples of these carbohydrates I see people eating that may be implicated in GERD and acid reflux.
Polyols (Sugar Alcohols) — sorbitol, mannitol, xylitol, apples, watermelon, peaches, pears, blackberries, cauliflower, and more.
It is almost impossible to give a general recommendation here as some of these will inevitably cause problems for some people and not for others.
In general, the foods listed above are known to be the biggest offenders when it comes to carbohydrates that are poorly absorbed and lead to excess gas.
The reason there tends to be excess gas pushing acid up the esophagus is due to a high level of little critters in the upper GI tract that shouldn’t be there.
This is where things can get very complex, very quickly, and well beyond the scope of this article. If you’ve had GERD for some time, chances are your esophagus is already somewhat inflamed and irritated (esophagitis), and you may have erosion or an ulcer. Since many people with GERD can actually benefit from more stomach acid, it’s important before they attempt to increase the acidity of the stomach that they ensure they first take steps to heal and protect the esophagus.
I’ve personally seen people who took betaine hydrochloride (a supplemental form of stomach acid) make esophageal problems worse since the lining of esophagus has little protection against stomach acid in the first place. These are plants that have been used for millennia for GI problems because when eaten they create a mucilage or mucous that coats and protects the lining of the GI tract.
Generally, here’s my top methods to use before every meal when supporting the esophageal lining. The 2nd class of herbs used for healing an esophagus are the soothing and wound healing herbs. Meadowsweet (Filipendula ulmaria) has already been mentioned, but I’m repeating it because it is not only a wonderful coating herb, it is anti-inflammatory, analgesic, and tones and helps heal the esophagus and stomach. Calendula flower (Calendula officinalis) is perhaps a favorite for soothing and healing an irritated esophagus. Goldenseal is very effective as a tincture, however due to it being an endangered species and that long-term use can be toxic, it should be used with great care and under the supervision of a clinical herbalist or medical professional.
I recommend using it as a tincture, about 15 drops in a little water sipped 3-5 times a day for 2 weeks on and 5 days off, stopping use after 3 months unless guided otherwise by a healthcare professional. Some other common herbs are Gotu Kola (for red or inflamed esophageal tissue) and Turmeric which is powerfully anti-inflammatory. L-Glutamine – the most abundant amino acid in the digestive tract is critical for creating a strong mucosal protective barrier in your digestive tract, from mouth to anus.
Zinc Carnosine – this form of zinc specifically attaches itself to damaged parts of the digestive tract and helps promote tissue healing and reduces inflammation.
In this case, I prefer it as a powder, rather than a capsule, so it can make contact with the esophagus itself.
There are some combination products I have recommended and found useful that contain most or all of these things, including GI Revive from Designs for Health.
Melatonin – Up to 500x the amount of melatonin is made in the digestive tract than in the brain.
Several studies have shown it to be a rather powerful supplement for reducing symptoms of reflux. I personally recommend taking melatonin only in small amounts for short periods of time (1-3mg  2 hours before bed) as it is a powerful hormone your body produces on its own.
Colostrum – I am a huge fan of high quality colostrum for healing the digestive tract from all sorts of inflammatory conditions. You could always have your stomach acid and stomach pH tested to know for sure, and I am almost always a fan of testing, not guessing. Speeds up stomach emptying by creating a more acidic environment, which can lower abdominal pressure.
Kills more bacteria in the stomach and small intestine that can cause excess gas, lowering abdominal pressure. Breaks down carbs faster before they can be fermented and create gas, lowering abdominal pressure. Breaks down proteins more fully, allowing you to absorb more important amino acids from your food.
Likely supports the release of more bile and digestive enzymes, further supporting proper digestion of carbohydrates. Zinc influences carbonic anhydrase (CA), which is used to form acid salts in the stomach and CA deficiency leads to insufficient stomach acid. For this particular situation, I recommend a 75mg capsule of zinc carnosine (which contains 15mg elemental zinc) or GI Revive (see above) for a 2-3 months. After that 15mg a day from food sources is usually enough, though some people need more as lots of things are known to deplete zinc. If there is one thing that is a tonic to the entire digestive process, it is eating bitter foods. It is the bitter taste of foods that really stimulates our entire digestive process from the release of saliva, to stomach acid, to digestive enzymes, and contractions of the digestive tract. If you have a digestive problem, chances are that a good digestive bitter herb will support you. Digestive bitters are best used as tinctures, not as pills, as it is actually the taste that makes them work.

Adding a little whole himalayan (pink) salt also gives you some chloride (which helps in stomach acid production) and almost 100 other critical trace minerals that support your body. My feelings are very mixed about simply taking large amounts of powdered stomach acid in a pill. On the one hand, it can be very effective, and I mean so much so that I have seen people just jump for joy once they started Betaine HCl + Pepsin supplements. Start with around 100-250mg of Betaine HCl with Pepsin & Enzymes after a few bites of your meal, not before or on an empty stomach.
Last, I would avoid taking HCl with anti-inflammatory drugs like NSAIDs (Ibuprofen, aspirin, etc) or steroids like Prednisone.
The Betaine HCL + Pepsin & Enzymes I use are varied, but I like Digestive Enzymes Ultra from Pure Encapsulations and Digestzymes from Designs for Health which have slightly lower and balanced levels of Betaine HCl. Why Stomach Emptying is Important for Treating GERD: It is well established in medical research that delayed gastric emptying is a major contributor to symptoms of GERD12Delayed Gastric Emptying in Patients with Abnormal Gastroesophageal Reflux. When food sits in the stomach too long it can cause more gas pressure and stretching on the esophagus that may causee the esophageal sphincter to open allowing acid and food to come back up. Stay Well Hydrated: Chronic dehydration will cause the pyloric sphincter not to open as well.
Your physician can test magnesium levels, and you should be at the upper end or even slightly above the standard lab ranges of serum magnesium. Use Pro-Kinetic Herbs — The go-to #1 formula here for speeding up stomach emptying is a 9-herb combination called Iberogast, which has several small but good clinical trials in its favor. Once you have reached this point, this is the time when probiotic bacteria can be most helpful.
However, once you feel like your digestive tract is moving well, as evidenced by reduced bloating and feelings of fullness and regular bowel movements, you might consider probiotics. If you don’t want to take probiotics, there are a few probiotic foods I would recommend. Here is just a rapid-fire list of things that are a mix of things that have been researched as well as good old fashioned advice that people swear by for maintaining their freedom from GERD.
Stop eating 3-4 hours before bed and keep eating with an 10-14 hour window each day (again, see above). As you can see, this is a huge topic, one I’ve tried to address as simply and as straightforward as possible for a general audience.
But I believe you are stronger than you have been led to believe, that your body is more resilient and more able to heal itself, given the right conditions, than you may know.
19 year-old female pacient, born and resident from Belo Horizonte, sought medical attention complaining of a burning sensation in the neck to swallow two weeks ago, related to food intake. Unfortunately there is no english translation available yet for this case.Please refer to the Portuguese version instead or come back later.
There are no prospective studies that have examined for chronic cough in children without lung disease but with gastroesophageal reflux (GER).
Data specific for chronic cough (>4-weeks), symptoms of GER and cough severity were collected. In children without lung disease, the common co-existence of cough with symptoms of GER is independent of the occurrence of esophagitis.
BackgroundAdult data suggest that gastroesophageal reflux (GER) disease (GERD) causes 21–41% of chronic cough [1, 2]. Children aged 0.8–16 years undergoing elective esophago-gastroscopy were invited to participate in the study during the study period (September 2002 till May 2004). Children were categorized as coughers (C+) and non coughers (C-), with reflux esophagitis (E+) and without (E-).
A non-bronchoscopic standardised and repeatable [20] technique was utilised to obtain BAL fluid, as previously described [21]. Quantitative aerobic cultures of bacteria were undertaken on BAL as previously described [22]. Chi square was used to compare categorical variables between groups and odds ratio described. Median and inter-quartile range of BAL cellular profile of all children grouped by cough and reflux esophagitis. DiscussionIn children without an underlying lung problem (other than mild asthma), cough was commonly present in association with gastro-intestinal symptoms suggestive of GERD. ConclusionWe conclude that, in children without lung disease the common co-existence of cough with symptoms of GERD is independent of the occurrence of RE. AcknowledgementsSupport: Study was partially funded by the Royal Children's Hospital Foundation. Competing interestsThe author(s) declare that they have no competing interests.Authors' contributionsAC conceived the idea, designed the study, performed the data analysis and drafted the manuscript. Jonathan Wright, MD often has patients taking 3-4 grams per high protein meal, which is far too much in my opinion than I’ve seen people be able to handle. As with any condition, there are usually unique sets of causes and conditions that bring about symptoms.
In otherwise healthy children undergoing flexible upper gastrointestinal endoscopy (esophago-gastroscopy), the aims of the study were to (1) define the frequency of cough in relation to symptoms of GER, (2) examine if children with cough and reflux esophagitis (RE) have different airway cellularity and microbiology in bronchoalveolar lavage (BAL) when compared to those without.
Children aged <16-years (n = 150) were defined as 'coughers' (C+) if a history of cough in association with their GER symptoms was elicited before BAL were obtained during elective esophago-gastroscopy. Median neutrophil percentage in BAL was significantly different between groups; highest in C+E- (7, IQR 28) and lowest in C-E+ (5, IQR 6).
Airway neutrophilia when present in these children is more likely to be related to airway bacterial infection and not to esophagitis.
All children undergoing esophago-gastroscopy had seen a consultant paediatric gastroenterologist and the procedure performed under general anaesthesia including endotracheal intubation. GERD was considered present if histology of oesophageal biopsy showed reflux esophagitis (basal cell hyperplasia and mucosal inflammatory neutrophilic infiltrate, with ?5 eosinophils per high power field) as determined by pathologists blinded to the child's respiratory history [17]. Briefly, with the child's head turned to the left, an 8F catheter was passed through the endotracheal tube, beyond the carina. However cough was just as likely to be present in children with and without RE and, none of the common symptoms of GERD with cough was associated with the presence of RE. Airway neutrophilia when present in these children were more likely to be related to airway bacterial infection and not to RE. ABC is supported by the National Health and Medical Research Council and the Royal Children's Hospital Foundation.
My go-to formula for this is first to try GI-MicrobX from Designs for Health, or Parabotanic from Moss Nutrition for 30-45 days.  These should be used at the right doses and under supervision of a healthcare professional. Presence of esophagitis on esophageal biopsies was considered reflux esophagitis positive (E+).
In children with underlying respiratory problems, chronic cough and airway neutrophilia has been reported to occur with GERD [4]. The primary indication(s) for the esophago-gastroscopy were recorded by the consultant gastroenterologist performing the esophago-gastroscopy. Children were defined as 'coughers' (C+) if the parents or consultant (gastroenterologist or respiratory paediatrician) had elicited a history of chronic cough (>4-weeks) [18, 19] with any GERD symptoms (table 1) and scored ?2 on the cough visual analog scale [16].
Two specimens were obtained; the first used for microbiology examination and the 2nd collection utilised for cytology.
Viral studies were also performed on BAL; direct immunofluorescence antigen (DFA) was used to detect RSV, adenovirus, parainfluenza viruses 1,2,3 and influenza A and B. Airway neutrophilia was highest in children with cough and without RE (C+E-) and, lowest in children without cough and with RE (C-E+). Further objective and in-depth studies are required to evaluate the common subjective occurrence of cough in children with GER symptoms. Acknowledgment: We are grateful to Mary DaSilva and the nurses of the Department of Gastroenterology, Royal Children's Hospital as well as the anaesthetists in particular Drs A Newton, I Webb, D Hill, M Pabari and D Ho, without whom this project would not be possible. Allison Siebecker, ND, has developed some wonderful protocols on her site for you to learn more about testing for SIBO and reducing bacterial overgrowth and bloating from both a dietary, antibiotic, and herbal medicine perspectives here. However, there are no prospective studies that have examined the specific relationship between cough and objectively defined GERD in children without an underlying lung disease, and paediatric cough differs significantly from adult cough [5].

Children who had cough on the day of the esophago-gastroscopy were defined as current coughers, which consisted of children with chronic cough and those with a recent (?4-weeks) history of cough. Cell count was performed on the cell suspension, cytocentrifuge slides were prepared and stained (modified Wright's stain) for cell differential profile; additional slides were prepared for lipid laden macrophage index (LLMI) using Oil Red O stain where 100 macrophages counted and scored 0–4. When DFA was negative, polymerase chain reaction (PCR) tests [25] were undertaken for all the above viruses. Furthermore, cough may exacerbate GER, these common symptoms may simply co-exists and, cause and effect is far from proven [6, 7]. Children were enrolled for the study on the morning of their elective procedure and were opportunistically enrolled i.e. Written consent was obtained and the study approved by our institution's human ethics committee. Only 17 children had tobacco smoke exposure and as numbers were small, comparisons were not made.Sixty nine (46%) children had chronic cough (C+).
In our cohort of children presenting to gastroenterologists for evaluation of GER as opposed to children selected from respiratory clinics, children with RE were as likely as children without RE to have a history of cough. Cough is indeed the most common symptom presenting to general practitioners [8, 9] and in children, the aetiology of chronic cough is heterogenous [5].
All LLMI and cellular examinations were performed by cytologists blinded to the children's medical history.
Of the 31 children with positive bacterial culture in their BAL, 23 had current cough, and 19 were in C+ group. Studies based on children from respiratory clinics have shown a high frequency of GERD [26–29].
Some studies on children with chronic cough have described airway neutrophilia [10, 11] that is possibly related to persistent airways infection [10].GERD is defined as symptoms or complications of GER [12].
Medical history was obtained from a parent on a standardised proforma for all children and spirometry (Kit, Cosmed, Italy) was performed on those aged ?6 years. The spectrum of GERD includes reflux esophagitis (RE) and the presence of non-acid reflux, in association with appropriate symptoms [12, 13]. We hypothesised that in children without an underlying lung disease, cough is more likely to be present in children with RE than those without RE and, are more likely to have airway neutrophilia. Positive BAL cultures was more likely to be present in children with current cough than in children without current cough but there was no significant difference between C+ and C- groups, and between E+ and E- groups (table 3). Cohort studies on highly selected patients almost invariably show a positive association between GER and respiratory symptoms. Investigations used to confirm and elucidate the diagnosis of GERD includes, histological examination of esophageal biopsies, pHmetry, esophageal manometry and intraluminal impedance monitoring [14]; each modality has its strengths and weaknesses [12, 14].
Parent(s) also scored their child's current cough on a validated cough visual analog scale of 1 (no cough) to 10 (most severe cough) [16]. Histological confirmation of RE is a specific way of confirming GERD even though the majority of children with clinical symptoms and complications suggestive of GERD have normal biopsies [12].
To determine repeatability of the questions relating cough to GERD (table 1) symptoms, parent(s) of 10 children answered the same questions again within 2–3 weeks. When grouped by presence of cough and GERD, there was a small (table 2) but significant difference in BAL neutrophils % between groups (figure 1, p = 0.008), with the highest values in C+E- group and the lowest in C-E+ group. In contrast, systematic reviews especially in evidence based treatment effects on GERD and respiratory symptoms has shown that the evidence for the linkage is significantly weaker than published cohort studies [31]. Exclusion criteria were children with; neuro-developmental abnormalities, clinical history of primary aspiration and known underlying cardiorespiratory disease other then mild asthma (no exacerbations in the last 12 months). Indeed, using Cochrane methodology we found a low effect of GERD treatment on cough [32] which is in contrast to non-controlled trials where the cough improvement rates by non-surgical intervention was as high as 86–100% [33, 34].The coexistence of symptoms do not imply causation [6, 7]. Until intraluminal impedance become more widely available and normal values are known for children, flexible gastrointestinal endoscopy and oesophageal biopsy gives the most precise indication that GER has caused disease (GERD). Like asthma and GER, cough and GER are also common and thus "would be expected to coexist, purely on the basis of chance" [7]. Flexible upper gastrointestinal endoscopy (esophago-gastroscopy) is the most commonly used investigation for this purpose in some institutions like ours.
In 2 group comparisons however, BAL neutrophil % (figure 2) was significantly higher in the C+E- group (n = 21, median 7, IQR 4) compared to C-E+ (n = 38, median 4, IQR 5) groups and C-E- groups (n = 31, median 6, IQR 5.2). None of the studies that showed an association between GERD and respiratory symptoms in children with an underlying respiratory problem had adequate controls and cough itself could lead to reflux events [35, 36].
Using multichannel intra-luminal impedance monitoring in adults, Sifrim and colleagues recently showed that cough leading to reflux occurred in half of the episodes (as opposed to reflux leading to cough) [36].Chronic cough in children is heterogenous [5, 19]. Some paediatric cohort studies have shown that GERD is rarely (3–8%) [37, 38] the cause of cough. We found that bacteria bronchitis (based on positive BAL culture) associated with neutrophilia was common and significantly more likely to be present in children with cough [39]. Similarly, Fitch et al described that airway neutrophilia was common in children with non-specific chronic cough and speculated that it was likely related to persistent airways infection [10]. However, the diagnostic threshold for quantitative culture on BAL for bronchitis in children (as opposed to pneumonia) is unknown and caution is needed in the interpretation of BAL microbiology [40].This study was neither a controlled trial nor one designed to define the aetiology of cough. In the context of the methodological problems in studying cough in children that includes the relative unreliable subjective reporting of cough (when compared to objectively measured cough [16, 41] and large placebo and time period (natural resolution with time) effects [32, 42], attributing cough to an aetiology in a non controlled study is fraught with errors. We cannot be definitive, but our findings of high occurrence of significant bacteria culture also suggest that chronic cough in children are unlikely caused by RE alone.Postulated mechanisms between cough and GERD include aspiration and sensory nerve stimulation [43]. We have previously shown that E+ (called G+ in previous paper) group had the lowest airway neutrophils [21] as also described in a small (n = 11) study in adults with GERD and cough [44]. Our findings showing airway neutrophilia highest in the C+E- group suggests that although cough was identified in association with GERD symptoms, the aetiologies of the cough, in most children is unlikely to be related to RE alone. As we had described that airway microbiology do not reflect gastric aspirates in these children, aspiration of gastric contents is very unlikely cause of the airway neutrophilia [21]. In contrast, Sacco et al described increased airway neutrophilia and LLMI in children with GERD and respiratory symptoms [4]. They however diagnosed GERD based on pHmetry, enrolled children from a different setting to ours as they selected children from respiratory clinics and, did not examine microbiology of the airways [4]. Bacterial airway infections causes airway neutrophilia and this is likely the main reason why neutrophilia was highest in the C+ group. Other causes or contributors to airway neutrophilia are however possible and this cannot be addressed in our study. Adult studies on chronic cough have found a significant number of patients with airway eosinophilia [3] but our study like other paediatric studies [10, 45, 46] demonstrated that airway eosinophilia is a very infrequent finding in children with chronic cough without an underlying pulmonary disease.Our data cannot be extrapolated to other definitions of GERD and it is possible that other definitions of GERD may yield different findings.
Thus while the discussions have so far emphasised that the symptom of cough in children with GER symptoms is either poorly related to RE, it is also possible that esophago-gastroscopy is less useful investigatory tool for paediatric cough. We used esophageal biopsy as the definition for practical reasons and it is also a common method of diagnosing GERD in Australian children. Assertions that cough is related to acid GERD can occur with unique pHmetry indices (eg reflux index of 0% required to be cough free) and that cough can take a prolonged time (a year) to settle post GERD intervention [48] are difficult to prove or disprove in the context of the difficulties with using cough as the primary outcome measure in studies and the feasibility of the required studies. The controversy of extra-esophageal manifestations of GERD [49] such as laryngopharyngeal reflux also is beyond the scope of this article.
Review articles and guidelines [12, 49] are available; in the North American Society for Pediatric Gastroenterology and Nutrition guidelines for paediatric GER article, the section on upper airway symptoms included a discussion on cough and GER.
The good repeatability found was however consistent with existing data; questions on cough combined with another symptom has good repeatability [42, 50, 51]. Furthermore, we did not use a standardised research based questionnaire for infant or child detection of GER such as those devised by Orenstein [52] because of its non feasibility in the context of the study.
However this method is widely used [53] for practical reasons and the cellularity values in our C-E- group were similar to published data on bronchoscopically obtained BAL [40].

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