Dry eyes, laryngopharyngeal reflux, pepsin

Sly Saint

Sly Saint

Senior Member (Voting Rights)
I've not been around much as I developed a big problem with my eyes, and had an ongoing problem with my throat.

I'm cutting to the chase as it has taken me ages to piece things together and finally (have had my eyes tested etc, done a lot of trial and error for relief of both probs).

So I have found I have a condition called LPR also known as silent reflux.
I've also just found out that there is a connection with the dry eyes/sinus/tonsils problems.
Here is one paper:

A new therapeutic approach for the Dry Eye Syndrome in patients with laryngopharyngeal reflux: first data - PMC (nih.gov)

there are several others,
eg
Pepsin is a proteolytic enzyme produced in the stomach alone. Therefore, detecting pepsin in extra-gastric areas is considered a reliable diagnostic biomarker of gastric reflux and a pathogenic mediator of reflux-related damage[11]. Accordingly, pepsin has so far been identified in the larynx, pharynx, sinuses, saliva, and inner ear of subjects with LPR[12]. Thus, it was hypothesized that pepsin could also be present in the eye and play a role in ocular disorders detected in association with LPR. As proof of this concept, pepsin has also been detected in the tears of adults and children with LPR[13]–[14]. It may be imagined that pepsin could arrive at the ocular level by passing through the nasal cavity, the inferior meatus, and the nasolacrimal duct. Supporting this theory, helicobacter pylori has also been detected in the ocular secretions of dyspeptic patients[15]. Consequently, managing patients with LPR and associated ocular disorders represents an urgent challenge for physicians and patients[16]. In this regard, dry eye syndrome (DES) is a common medical condition sometimes associated with LPR[17]. DES is usually characterized by visual disturbances, ocular irritation, ocular pain, photophobia, and excessive tearing, and it significantly affects the quality of life[18]. DES recognizes different causes and pathophysiologic mechanisms. An ocular surface inflammation is a common feature. In this regard, reflux of gastric material (acid and proteolytic) could play an important pathogenetic role.
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A combined treatment for patients with dry eye and associated laryngopharyngeal reflux: a real-life approach - PMC (nih.gov)
also videos re LPR (not to be confused with GERD or basic heartburn).
and the role of pepsin as opposed to stomach acid.

anyway
I'm posting this just in case it helps anyone else.
 
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Found this guy who seems to know what he's talking about and does his research.
LPR Treatment: the Supreme Therapy Guide – Refluxgate

this paper is also informative
Reflux Revisited: Advancing the Role of Pepsin

Reflux Revisited: Advancing the Role of Pepsin - PMC (nih.gov)

this is also interesting
The evidence strongly argues for the following chain of events: inactive pepsin is endocytosed, is activated within the cells, and causes cell damage; this induces oxidative stress and the accumulation of free oxygen radicals which, in turn, damage mitochondria and may lead to cell death. In the experimental system used, the cells were exposed only once to pepsin, thus mimicking what might happen with an isolated episode of LPR. Though damaged, the cells were still viable at 12 hours but with repeated exposure, as would be expected in chronic LPR, the damaged cells may not survive [39].
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Reflux Revisited: Advancing the Role of Pepsin - PMC (nih.gov)
 
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Just in case anyone is further interested in this problem (ie LPR and other issues caused by it) I found this video of an ENT specialist (US) who is very good in explaining all the pros and cons of various treatments on offer. Surprisingly this seems to be an area where the US are playing catch-up. Apparently in Europe the use of alginates is far more common and they are only just coming on the market in the US.
Refreshing tho to hear her say that yes stress might play a role but we all get stressed and it's important to check that nothing else is going on; as she says when you get these nasty symptoms of course you're going to feel anxious, but the stress comes as a result and is not necessarily the cause.
Code: 
https://www.youtube.com/watch?v=zV0a4AYTxTU&t=315s
 
Ash said:
Thanks @Sly Saint, sounds interesting, I can’t open the link though?
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it's not a link; you need to cut and paste it.
obeat said:
I think I may have this condition. How are you treating it?
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hah well that's an ongoing story.
I have been reading loads. I eventually managed to speak to an NHS doctor who also thinks it might be LPR (referred to as silent reflux on NHS) and wanted to put me on PPI's. Suggest anyone does their research on these; can be nasty to come off and play havoc with your digestion/microbiome.
Plus there is a lot of both research evidence and patient evidence that they do not work for LPR.
Dr wasn't happy when I told her that.
I've started with diet/lifestyle modifications which is pretty restrictive(I'm a vegetarian and already have a restricted diet because of kidney stones) and tricky with ME as I have to not lie down.
I'm also going to pay for a pepsin test (not available on NHS).
 
I use a product called Frutin gastro gel for reflux, I can’t tolerate PPIs.

I thought I had asthma for about a year bc reflux was silent to start and made my chest feel v tight. Took lots of steroid inhalers and was really freaked out by it, but once I got the reflux under control (lots of Frutin, no coffee on empty stomach, no spicy foods or v fatty foods, limited desserts and chocolate), tight chest went away.

I also have dry eyes at night.
 
Braganca said:
Frutin gastro gel for reflux
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That's interesting as they don't contain alginate, so they just form a barrier in the stomach. As far as I can find out so far alginates actually inhibit pepsin activity as well as forming the barrier.

I tried the uk version of Gaviscon (main ingredient sodium alginate) for a few nights but it gave me very dry mouth (possibly due to the calcium carbonate in it) so I stopped using it.
 
A very good source of info:
Dr. Jamie Koufman is an award-winning, pioneering physician & surgeon, researcher, author, and one of the world’s leading authorities on acid reflux. With 45 years experience practicing medicine, Kings, Presidents, Rock Stars, Opera Singers, Broadway and TV Personalities have all trusted their Voices and Vocal Cord Surgeries to Dr. Koufman.

In addition to being a New York Times best-selling author, Dr. Koufman has been seen on Dr. Oz, Good Morning America, CBS News, and lectured at Harvard, Hopkins, Mayo Clinic, and UCLA, to name a few. She coined the terms laryngopharyngeal reflux (LPR) and silent reflux, and it is her seminal scientific work that put LPR on the map. In addition, she was the first to connect the three words reflux, diet and cure in her book Dropping Acid.
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Dr. Jamie Koufman - LPR, Acid Reflux, Chronic Cough & GERD Specialist
 
PPIs are the standard therapy for patients with suspected LPR. In open-label studies, PPIs have been shown to be beneficial for decreasing LPR symptoms (71,72). However, there is growing evidence from randomized placebo-controlled trials that PPI treatment is not effective for the treatment of LPR. For instance, in contrast to these open-label uncontrolled studies, a placebo-controlled multicenter study showed that esomeprazole 40 mg (twice a day) was comparable to placebo in regard to the symptomatic response in suspected LPR patients (73). Similarly, in a more recent meta-analysis of controlled studies, PPI therapy was found to be ineffective for LPR (74)
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Alginates: From the ocean to gastroesophageal reflux disease treatment (turkjgastroenterol.org)
 
I got my results back from the pepsin test; both positive. So at least I know now and have an indication of how bad it is.
So will read the info provided with the results and try and follow what they advise. They also have provided me with a letter for my GP which also includes research paper references; useful particularly where prescription of PPIs is concerned.
 
I have a very long history of LPR and live in New York. So I have seen three of the top experts on LPR - the ENT Jamie Koufman, the ENT Jonathan Aviv, and the gastroenterologist Philip Katz. They all attribute the rise in the incidence of esophageal cancer to LPR.

The mainstay of their treatment approaches is lifestyle modification. All of them recommend raising the head of one’s bed by at least 3 inches, if not more, so that you sleep at an angle, allowing gravity to reduce the severity of nighttime episodes of silent reflux.

But aside from that, the lifestyle changes are fairly extreme. For example, Koufman recommends that patients drink nothing but highly alkaline bottled water, eat only alkaline foods, remain upright for 4 hours after eating, and consume no food after 7:30PM because, in her view, the digestive system “slows down” at night. In other words, enormous self-discipline, and the ability to spend most of the day upright, is necessary. If that fails, she regularly refers patients to surgeons for Nissan fundoplication or other newer, unproven surgeries.

Aviv has a similar treatment approach but one that is a bit easier to implement - remain upright for 3 hours after eating, avoid all late night snacking, consume acidic foods that are high in antioxidants (e.g. blueberries) mixed with alkaline foods so the overall pH is not acidic.

In my case, Koufman recommended fundoplication. Aviv was against it, saying it often turns people with autonomic issues into “swallowing cripples” who can’t get food down from their mouths into their stomachs. I went to Phil Katz for a third opinion. He ran a number of tests and said I wasn’t actually refluxing food or liquid at night. He said the mechanism that causes pepsin to move into the upper airways is not really understood, and suggested that it may be aerosolized. He was against surgery in my case and basically said there’s a lot more speculation than hard science into the causes of LPR.

My personal view is that virtually everyone with ME/CFS has some degree of dysautonomia as a result of small fiber neuropathy and/or vagus nerve dysfunction, slowing down peristalsis and in some cases resulting in gastroparesis. There are tests that check for this type of dysfunction - gastric emptying studies, a newer test called the Smart Pill, even upper endoscopy, which sometimes finds food in the stomach 12+ hours after eating. Unfortunately, the few medications that treat gastroparesis either have serious neurological side effects or are antibiotics like erythromycin that affect the microbiome, have potential cardiac side effects, and are not recommended for long-term use. Again, this leaves lifestyle changes as the mainstay of treatment. Of course, one lifestyle approach that none of these experts recommend but that isn’t terribly hard to implement is to eat small meals more frequently instead of large meals less frequently.
 
Sly Saint said:
That's interesting as they don't contain alginate, so they just form a barrier in the stomach. As far as I can find out so far alginates actually inhibit pepsin activity as well as forming the barrier.

I tried the uk version of Gaviscon (main ingredient sodium alginate) for a few nights but it gave me very dry mouth (possibly due to the calcium carbonate in it) so I stopped using it.
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see this thread
https://www.s4me.info/threads/using...ed-to-higher-migraine-risk-study-warns.38258/
 
Sean said:
I get dry mouth and eyes, and serious reflux (GERD). I have been on PPIs for years (Omeprazole, 20mg), and use a fair bit of oral moisturising gel, mainly at night.
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Forgot to mention that during the day I use small sips of olive oil and gargle it to keep the mouth from drying out. Effective, cheap, and safe.
 
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