"As important as what you eat is how you digest it and what you absorb.”
- when we refer to ulcers, we're talking foregut ulcers. Hindgut 'ulcers' is a completely different thing; for starters they don't exist - they're a myth - because there are no acid-secreting cells in the hindgut. There is, however, hindgut 'acidosis, caused by lactic acid in the hindgut. If you've been given a 'hindgut ulcers' diagnosis or suspicion, see our separate 'Hindgut Ulcers???' Blog post we did in May 2020. (link also at the bottom of the page).
How do ulcers happen? Simple ... no rocket science involved
10-years or so ago, a study on gastric ulcers in horses was published which caused quite a stir in the scientific community.
Up to that point, scientists were more or less sure that ulcers were mainly a Thoroughbred problem; most racehorses had ulcers and the general thinking was that it was genetic, which tends to be the go-to reason when there's a health issue that science doesn't understand 😉
Well guess what - it's not genetic! And this study was the first time that horses other than TBs were looked at, horses with no history of colic or other digestive issues, and - you've guessed it - a huge percentage, up to 80-90% of non-TBs, had gastric ulcers. And around 80% of those horses affected had ulcers in the front section of the foregut, the pars nonglandularis, with 20% of the horses ulcers' in the back section of the foregut, the pars nonglandularis, just before the exit into the small intestine.
The researchers tried many solutions, ranging from different medications to different feeds, and to their utmost surprise they found the best therapy - and preventative - was ... to feed hay. As simple as that. They also found a major cause - not having access to hay for 4-hours or more, including overnight, caused inflammation of the stomach mucosa lining which then developed into gastric ulcers. And when you have inflammation at cellular level, along with red-raw pain, this spreads a whole lot further than just the injurious site, thanks to the nerves in the body which are everywhere, and tell each other everything.
This constant hay-feeding makes perfect evolutionary sense when you look at the normal function of a horses' stomach/foregut, because evolution has made the horse a constant trickle feeder - horses have to have constant access to forage so they can feed 24-hrs/day - it's in their DNA to eat all day and all night. This means the stomach is normally always full of feed, with the horse constantly chewing, constantly creating saliva to buffer the acid pH balance gradient, with it being high at the entrance of the stomach - a pH of around 6-7, dropping down to a more acidic 3-4 before the feed exits into the small intestine.
This gradient isn't meant to change, so we don't get a stronger acid reading in the front section of the foregut, but this is exactly what happens when the horse runs out of hay/roughage for a prolonged period of 4-hours or more. The stomach becomes empty, but the acid-secreting glands in the back section of the foregut keep on producing hydrochloric acid. This is unlike other mammals, i.e. dogs, whose stomachs are used to not eating for long periods, so the acid production shuts down. Not so in horses - the acid continues being produced, and the scientists found really aggressive pH values of 1.3 in the empty stomach compared to a normal 3-4 value.
Under normal circumstances, the horse can cope with these severe levels because the acid section of the stomach has a thick mucosal layer to protect it, so normally, the acid doesn't make direct contact with the epidermal cells of the stomach wall. However, this isn't the case for the front section of the stomach, which only has a very thin mucus layer because being a non-acidic area, a thicker layer isn't needed.
So, back to the stomach now empty, the acid section of the stomach continuing to produce acid at a much stronger pH value, and now - oh-oh - the horse physically moves. The movement cues acid transporting into that unprotected front section of the stomach where it doesn't normally belong, splashing onto the cellular membrane. Result? Remember - its pH level is at a serious 1.3, so we're talking serious burn, destruction of the thin mucus layer straight to the epidermal cells, triggering a major inflammatory response, and finaly, ulceration. And all because of wrong feeding management, letting a horse run out of forage. Empty stomach = stomach front section ulcers.
The simple solution? Feed a horse hay 24/7. The horse chews, this creates saliva which buffers the acid from the bicarb in the saliva, the pH values and gradient rebalance, the mucus layer regenerates and the gastric ulcers heal. Simples.
The other 20% of horses
So now to the other 20% of horses who have ulcers in the acid-producing back area of the stomach, and it took the scientists longer to find out why these occurred. The theory was that this back area has a very thick mucus layer so no matter how aggressive the acid content was, the acid shouldn't penetrate the mucus layer to the cellular tissue underneath. Wrong. Cut to today, and now we know the cause of the why this happens - ongoing, long-term, chronic stress.
Stress is a perfectly normal reaction to a perceived threat - the fight/flight response kicks in and the natural instinct for a horse is to run away. In order to run, fast, the muscles need blood, so cortisol, the stress hormone, shuts down various non-essential parts of the body to divert extra blood to where it's needed to deal with the crisis, i.e. the muscles.
When a horse is relaxed, roaming outdoors and eating, digestion is well-supported with blood for its energy to digest, but cue a threat and this changes dramatically - who needs digestion when there's a tiger on your tail? So, the non-essential blood vessels dilate, the essential blood vessels expand, and blood is pumped into the muscles to outrun the threat. Once safe, the body rebalances and everything returns to normal, but when a horse is under constant stress, i.e., lack of movement, isolation, stabling, herd stressors, sudden changes, competition, psychological stress of travel and training, breeding and pregnancy, worming, parasites, medications, vaccines, viruses, injury ... you name it! ... that On Button stays switched on, so the blood supply to the all-important foregut function remains disabled.
This disabling occurs just before the entrance into the small intestine, where the thick mucus layer resides, so with a degraded blood supply, this thick mucus layer degrades as well. This is what the study discovered, that the longer a horse was under constant stress, the thinner the mucus layer became, exposing the epidermal cells of the stomach wall membrane to the agressive pH level 1 acids. Again, cue serious burn, serious pain, destruction of the mucus layer, a major inflammatory response, and ulceration.
Gastric ulcers in this back section of the stomach are notoriously harder to treat because the acid is severe - as strong as a car battery - and the pain is chronic, which in itself leads to further stress, so we end up with a vicious - literally - cycle. The stress keeps the cortisol flooding the body, continuing to switch off the body's non-essential functions and diverting the blood to the survival organs, so the protective thick mucus layer can't regenerate. Despite doing all you can to remove the external stressors, this stress is internal.
If the painful fire isn’t put out, the continuing inflammation of a system, especially the digestive system - the system upon which health completely relies on to fuel the very survival of the organism - triggers a cascade of further stressful cellular disruption on the body as a whole, because it’s already trying to work overtime in an attempt to maintain homeostasis, the ability to maintain a relatively stable internal state despite changes in the world outside - aka, balance. All living organisms, from plants to puppies to people, and our horses, need to keep their internal environment regulated to process energy and ultimately survive.
So, while the immune system and other organs are trying to pick up the slack from the non-functioning gut, they themselves become overburdened, exhausted and sluggish, and eventually the whole organism starts to crash. For a healthy balanced body to be firing on all cylinders, we need that gut to be functioning properly - quite simply, life-force depends on it.
Again, hay can be a life-saver here, as chewing relaxes the horse and releases endorphins - happy hormones - a chewing horse is a happy horse! So the more the horse chews, the happier it is, which eventually curtails the production of the stress hormones. However, these particular ulcers also need to be addressed on a therapeutic level.
That stats make for sad reading - this doesn't happen in our wild horses as they're always moving, always eating, and don't have the same stressors as the domesticated horse. These days in our domesticated world, there's a 50% ulcer syndrome showing in regular pet horses; sports horses up to 90%. Even foals are showing up to 80%, so it's a terribly widespread problem. Gastric ulcers can be a reason behind faecal water; why horses don't drink enough water in winter because cold water causes pain on the ulcerative site; horses don't like to be ridden when they have ulcers because of the pain; horses may struggle to eat stemmy hay or go off their feed - all signs that there may be gastric ulcers. They're constantly in pain so always check.
For more information on feeding our horses how they should be fed, see our Why What We Feed Has To Be Right page.
Now to the drug companies
So, we think our horse has got ulcers, and the vet has likely said that there's (allegedly) too much acid going on (but hopefully we've already dispelled that myth), and we need it fixed. Behind the scenes the drug companies are preying upon our GPs and vets, insisting that it's all about too much stomach acid, and that they should write expensive prescriptions for their wonder-drugs for us mortals to either swallow, or something to give to our horses, to quell the acid burn.
Never is there a mention that there might be an actual reason for why there’s acid burn or ulcers; never a suggestion that the curry we ate might have been a bit much, or for our horses, no mention that it's likely to be the lack of constant hay, or the haylage, alfalfa, soya or any of the other poor-quality ingredients, found in our ultra processed feedbags, that are known to cause gut sensitivities and damage the gut environment, and therefore Should Be Avoided.
Truth is, those wonder-drugs not only fail to address the actual causes of acidity and/or ulcers (stressors and/or inappropriate feed) but put us or our horses at further health risks.
If I was to say to you that by feeding acid-stopping drugs to our horses, it might cause ...
- Increased negative bacterial overgrowth
- Impaired digestion causing colic risk
- Significant nutrient malabsorption
- Decreased resistance to infection
- Kidney disease
... what would you say?
I had originally intended to cover the How&Why of all these side-effect issues here, but as I started to write I realised it would take way too long. So I’ll just go with what I feel is the most important for us horse owners, specifically impaired digestion, impaired gut flora syndrome, and impaired nutrient absorption, because let's face it - these alone mean one very sick horse.
So, with so much new research coming out about the damaging side-effects of acid-stopping drugs, let's just dive straight in and talk Omeprazole, aka a PPI (Proton Pump Inhibitor), an acid-production blocker - a vet's go-to drug of choice for equine ulcers.
Proton Pump Inhibitors
When it comes to our horses, the acid-blocking drug of choice is generically known as a PPI, aka a Proton Pump Inhibitor, i.e. Omeprazole (and plenty of others ending in ‘zole’). It's also probably useful to understand what a proton pump is, so here we go with a quick explanation. A proton pump is a natural part of every body out there, an integral membrane protein essential for cellular energy production; their vital function is literally to 'pump' an electrical instruction across a biological membrane, to trigger an essential function for balanced homeostasis to exist. Hope that wasn't too science-y.
Now to the equine foregut, and its own proton pump's instruction is to produce digestive acid, so an inhibitor of the proton pump reduces the production of acid. It does this by blocking the enzyme in the wall of the stomach that produces acid. Hence the name, Proton Pump Inhibitor, aka PPI.
Let's delve a little deeper
... and what they do to the body. PPIs are a group of drugs whose main action is a significant, and long-lasting, reduction of stomach acid production; they are the most potent inhibitors of acid secretion available. Vets prescribe them for equine ulcers because on the surface, they provide fairly quick relief and you can't argue with that. Your horse has ulcers, and half a ton of p****d-off horse in pain is no joke. So the powerful chemicals in the ‘zoles’ switch off the proton pump which secretes the stomach acid. Hence, in theory, by turning the acid off, there’s no more burn, and ultimately that's the goal, to stop the pain, and make your horse safe to be around again.
Sounds simple enough, so what's not to love? Here's the reality - behind the scenes PPIs drastically mess with the biochemisty, which I’ll get to further on. (I'll quickly confess now that I'm not a fan of PPIs, in case you hadn't guessed. At all.)
Although generally assumed to be safe, studies as far back as 2010 have shown that PPIs have numerous side effects, including causing a further altered gut environment and impaired nutrient absorption, to an increased risk for kidney disease and neurological impairment. And here’s the irony – this is a biggie so it deserves bold type – remember, those ulcers are there because the gut environment is already altered. As said above, it's usually due to either some form of stress or inappropriate feeding, or inappropriate feeding which causes stress, which then destroys the rest of the gut function etc etc.
These clever, natural, proton pumps in the body are a highly complex, essential part of the mammalian physiology, and ... they’re not just limited to the stomach. They’re present in just about every cell in the whole body, so let's quickly talk cells for a moment. Other than red blood cells, all of the body’s cells have a mitochondria (probably my favourite M-word which I use a lot on this website), which is the energy-producing furnace in the middle of every cell. Imagine the coal fire on a steam train being constantly fed coal to create the heat to generate steam, which produces the energy that makes the train move. That coal fire is the train’s ‘mitochondria’.
So, the body’s cellullar mitochondria metabolise (burn) carbs, fat, chemicals, minerals – you name it, the mitochondria burn them, to produce specific energies to make the body’s various systems operate and do what they're meant to. And how do they do this? They trigger this thing called a proton - a source of electric instruction which is pumped across a membrane that’s specifically harnessed to form ATP, the body’s main storage form of energy.
Now here’s the rub - without an efficiently functioning proton-pumping system pumping their message, the body must rely on anaerobic systems for energy production, which will lead to rapid fatigue.
So, back to the proton pump in the stomach, the pump to make the acid-secreting cells secrete the acid, aka the parietal cells. The chewed food mixed with saliva (bolus), travels down the oesophagus towards the stomach, collecting beneficial bacteria - and a few digestive enzymes - on the way. This very action triggers the foregut’s proton pump to stand by, ready to release the stomach acid to start the digestion process.
Remember as we said much earlier, when the food bolus arrives in the stomach, it’s immediately mixed with the protein-digesting enzyme, pepsinase, the precursor to pepsin. I say precursor, because pepsinase needs to be converted to pepsin in order to work, and the converter is ... you’ve guessed it - stomach acid.
This next bit's really important. Without the acid, pepsinase doesn’t become pepsin - depressed acid levels means depressed pepsin levels, so this means that proteins won’t get broken down into their crucial-building-blocks-for-the-body amino acids and peptides. Which means a deficiency of those essential amino acids, which creates its own significant side-effects, i.e. depressive stress, anxiety and exhaustion. Already we can see the first negative side-effect of giving our horses a PPI; inhibiting the release of stomach acid from the parietal cells impairs the onset of protein digestion.
Let's move on to further effects of PPIs (and we haven’t even got to what else happens in the digestion process). Research shows that – more bold type needed - PPI’s also bind to the many other proton pumps in the body (https://www.ncbi.nlm.nih.gov/pubmed/1647821). This really is significant. This binding to the body's other proton pumps is essentially irreversible - PPIs continue to inhibit all the other proton pumps until the body’s own master antioxidant, glutathione, which can only be made by the body, has to step in to facilitate disassociation. This means that stopping feeding PPIs won’t stop their damaging effects immediately, meaning that weaning the body off PPIs is much more complex than we think.
However, getting back to digestion, the Big Issue for me with the PPIs/Omeprazoles of the world is that the foregut needs its acid to perform digestion, and feeding PPIs stops this essential function.
A bit more about digestion
As explained earlier, the foregut is all about pre-digestion, as in kick-starting the digestion process off - it provides the environment, and the muscle, to churn that bolus from solid chunks to a soup-y liquid (chyme) of broken down food, saliva, acid and pepsin, to enable a smooth passing of the chyme digesta into the small intestine where it meets more digestive enzymes. A bit like a pre-wash programme on our washing machine before the main cycle kicks in. Without acid, this pre-wash won’t happen. A quick reminder - the stomach acid works with digestive enzymes at the pre-digestion process to start the breakdown of the food. If the acid’s switched off at the beginning, the digestion process is impaired from the get-go.
The perfect world of digestion
Let’s break the foregut digestion down into easy stages – the full gory details of how a perfectly functioning digestive system works, from the second food goes into our horse’s mouth:
- Food is chewed, causing three pairs of salivary glands to release saliva. The acid-buffering agent in saliva, bicarbonate, buffers and protects the mix of chewed food and saliva (bolus). Saliva also contains small amounts of amylase, the first of many crucial digestive enzymes, which starts pre-digesting carbs.
- Once the bolus is swallowed, it travels down the oesophagus where various beneficial flora reside, ready to jump into the mix to start their own important digestive role.
- The bolus arrives in the foregut, where it meets lactic acid bacteria which starts to pre-digest starch, and pepsinase which is converted to pepsin when it meets the stomach acid.
- The muscular wall of the foregut is now churning, mixing the digesta thoroughly with the stomach acid and pepsin. Together they initiate the process of digestion and degradation of starches and proteins (amino acids).
- Once the foregut has done what it needs to, the pepsin and acid digesta mix is now a soupy mix called chyme, and is pushed through the exit valve into the small intestine, where a team of other digestive organs get involved. First up, the duodenum signals the liver to release bile to break down the fats. Next, the pancreas secretes further digestive enzymes to continue the process of enzymatic breakdown of the proteins, fats, starches and sugars. The pancreatic juices also contain some alkali and further bicarbs to provide more buffering of any acid that left the stomach, to help maintain an optimal environment in the intestine for those important digestive enzymes to function.
- It’s only now that the serious business of digestive processes starts taking place, as the small intestine also has its own digestive enzymes – as well as more beneficial bacteria - to continue the breakdown of those proteins, fats, starches and sugars.
- Finally, much further down the small intestine, when everything’s now broken down and assimilated, the nutrients are finally absorbed through the intestinal wall and carried off by the blood stream to whatever cells need the nutrients. This generally takes 3-4 hours, usually moving at a rate of approximately 30cm per minute.
Imagine how much longer digestion will take with the PPI effect; worse, they amplify the burden by overloading the digestive tract with undigested digesta, which greatly increases the risk of colic, laminitis and acidosis. Introduce PPIs and you can see how, by switching off the acid secretion:
- the acid level declines
- the pH of the stomach increases
- the structure of the digesta is impaired
- enzymatic digestion is limited
- nutrient absorption is impaired which drastically impairs health, wellness, and staying sound and active.
We might think we feed our horses well, but without the acid influence, they’ll end up under-nourished. We can feed the most nutritious diet imaginable, packed with vitamins, minerals and other essential nutrients, but if they’re not absorbing those nutrients that you’ve paid good money to provide, they won’t benefit from them.
As an example, let’s have a quick look at how this affects the important micronutrients. Decades of research have confirmed that low stomach acid reduces absorption of several key nutrients such as iron, B12, folate, calcium and zinc, with many reduced micronutrient levels also dependant on each other being absorbed.
- Iron deficiency is a well-known consequence of stomach acid reduction. It causes chronic anemia, which means that the body’s tissues are literally starving for oxygen.
- Absorbing B12 relies entirely upon stomach acid. The most complex of our vitamins, B12 enters the body bound to food proteins, and as per the protein process above, the vitamin molecules must first be separated from these proteins with the help of – you guessed it – stomach acid and pepsin. Interestingly, B12 deficiency is not usually from lack of intake, but rather from lack of absorption. And … insufficient B12 absorption leads to a deficiency in the production of red blood cells, aka pernicious anemia.
- Folate – again, low stomach acid levels interferes with folate (folic acid) absorption. Human studies show that when folate is given to achlorydric patients (with no stomach acid) along with an HCL (hydrochloric acid) supplement, absorption of the vitamin increased by 54%. Here's the study link if you want a read: https://books.google.co.uk/books?id=4XvjIrpw5r8C&pg=PA157&lpg=PA157&dq=pedrosa+folate+b12+absorption+atrophic+gastritis+russell&source=bl&ots=5YanuTOOfd&sig=-jXC0OP0TwR9NHgJ53wFOWVBv60&hl=en&ei=2e7AS5r5EIrangeA_tiJCg&sa=X&oi=book_result&ct=result&redir_esc=y#v=onepage&q=pedrosa%20folate%20b12%20absorption%20atrophic%20gastritis%20russell&f=false
- Calcium – again, the importance of stomach acid in calcium absorption has been known since the 1960s, when one human study showed ulcer patients were barely absorbing any calcium at all (just 2%) due to low gastric pH (6.5) and very little stomach acid.
- Zinc - in another controlled trial, another acid reducer treatment reduced zinc absorption by around 50% - http://americancollegeofnutrition.org/content/the-journal/cgi/content/abstract/10/4/372
Increased bacterial overgrowth (SIBO)
Acid is also the microbial contaminant disinfectant - switching the acid off causes pro-inflammatory bacterial overgrowth in the small intestine, which in itself creates a knock-on effect:
- Over population of bad bacteria v. good bacteria causes mal-digestion of carbohydrates.
- This in turn produces gas.
- This gas increases the pressure in the foregut, causing the lower esophageal sphincter (LES) to malfunction.
- The malfunction of the LES allows acid from the stomach to enter the oesophagus, thus producing the symptoms of acid burn. So when your vet says your horse has acid in the ‘upper digestive tract’ (oesophagus), this is what’s going on.
Bacterial overgrowth has a number of other undesirable effects, including inflammation, and as before, reducing nutrient absorption. Studies have confirmed that by suppressing stomach acid, PPIs profoundly alter the gastrointestinal bacterial population. Researchers in Italy have shown increased incidence of SIBO (small intestinal bacterial overgrowth) in 50% of patients using PPIs, compared to only 6% of healthy control subjects. https://www.ncbi.nlm.nih.gov/pubmed/20060064
To summarise the PPI effect
They drastically impair digestion and nutrient absorption. It’s a product I simply cannot endorse. There is another way, and it’s healthy, and natural – it’s all about lifestyle factors, removing stressors and/or tweaking the diet.
10.10.20 - Edited to add:
Acid production is needed to absorb magnesium, calcium and vitamin D, so feeding a PPI can impact this very important nutrient absorption function, a factor to consider if you're feeding a mineral balancer.
14.4.21 - Update
"Recently more importance has been placed on the co-administration of NSAIDs and the inhibitors of gastric acid secretion, such as proton pump inhibitors and histamine H2 receptor antagonists, in determining a significant alteration of intestinal microbiota composition and exacerbating NSAIDs enteropathy [21,66]. PPIs determine hypochloremia causing abnormal growth of bacteria that can colonise the small intestine causing SIBO (Small Intestinal Bacterial Overgrowth) with increased bacterial translocation [67,68]. Wallace et al in fact reported that PPIs, in particular omeprazole resulted in significant dysbiosis, with both a substantial increase in Gram-negative bacteria and a significant reduction in the proportion of Actinobacteria (mainly Bifidobacter ssp.) in the jejunum."
Read the full report here: Utzeri E, Usai P. Role of non-steroidal anti-inflammatory drugs on intestinal permeability and nonalcoholic fatty liver disease. World J Gastroenterol 2017; 23(22): 3954-3963 [PMID: 28652650 DOI: 10.3748/wjg.v23.i22.3954]