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The answer is no. “Blood thinner” is somewhat of a misnomer as it does not change the viscosity or concentration of any component of the blood, but prevents the coagulation cascade at some point depending on the agent used. Beta blockers do reduce cardiac output, but not close to any degree that would compromise flow to an organ system like the GI tract. Not to mention that the stomach, although vascular like you mentioned, does not really perform a lot of absorption of nutrients. This occurs mostly in the small intestine where the blood supply is essential to take nutrients to the portal system.

Blood thinners do not thin the blood. They prevent the blood from clotting too easily.

In nearly all cases this does not actually improve blood flow/mechanics at all. Because blood is to flow properly in the first place.

However blood pressure medication can obviously improve blood flow to different parts of the body and thus improve blood flow to the stomach; or more importantly the small intestine, and thus do change speed of digestion.

However you give beta blockers to normalize blood pressure and heart rate. So at best you‘d just get regular digestion going?

Though the psychological effects of beta blockers would have a much more massive effect on digestion anyway: parasympathetic signaling would increases do to feeling more relaxed because of no palpitations.

Are beta blockers more like “fiber” but for the heart system?

Insults of low blood flow to the gut can ultimately lead to digestion issues, but not commonly from medication use like you are asking about. Certain medications affect the digestive system by limiting blood flow as a side effect, although not typical blood thinners like heparin or warfarin or riveroxiban. NSAIDs such as aspirin and ibuprofen (which do have mild "blood thinning" effect-although unrelated) do constrict gastric blood flow and lead to increased risk of gastric ulcers and are recommended to be taken with food. If blood pressure does get too low (usually in the case of shock), certain areas of the large intestine can die and bleed from lack of blood flow causing digestive issues. In addition, sometimes people with really bad vascular disease like atherosclerosis or high cholesterol can get stomach pain after they eat because the digestive system is demanding more blood flow than their arteries can give them. As other commenters have already mentioned, "blood thinners" are anticoagulants, meaning they make it harder for your blood to clot. Beta blockers work by slowing down the heart and allowing veins to dilate. Neither of these mechanisms directly affect blood flow to your digestive system.

Maybe more like lower octane gas for a car?

Something no one else has mentioned so far is that the effects of diet on certain blood thinners is in regards to warfarin which is metabolized in the liver and certain foods can change the enzymes in your liver which will break down warfarin faster or slower. This could mean blood clots more or less than the desired effect so diet is monitored with that medication. With other newer meds this is not an issue and regular dosing can be used.

Yeah people don’t realize how much clotting has already been done almost as soon as blood is exposed to open air, so when patients on anticoagulation have a bleed, it definitely looks a lot thinner

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No, not really.

Per my gastroenterologist and people I’ve know who study this stuff… Fiber kind fills the nooks and crannies of your intestines and provides a food for the bacteria in your gut. The “good” bacteria in your gut happen to thrive on fiber.

Beta blockers work by blocking receptors in your heart muscle that sense certain hormones (namely adrenaline) in your blood, thus making your heart less sensitive to them. The hormones being blocked make your heart pump harder and faster. Because they are blocked, your heart beats slower and less hard.

In the case of beta blockers, your body being less sensitive to adrenaline has the effect of relieving physical signs of stress. This can to a calming effect for some people.

Edit: made this comment shorty after waking up, fixed a major typo.

Dumb question, based largely on what is probably an over-simplified understanding of cardiac output. I thought beta blockers improved cardiac output?

I always thought of it more in terms of the contractility improvement than anything, although I know a beta blocker alters other things included in CO, but with that basis of understanding in mind, maybe I'm missing the fact that some other factor outweighs the contractility thing?

I think you have it reversed.

Beta receptors are receptors for epinephrine (adrenaline). Activation of the receptors among other effects, increases heart rate and force of contraction, and constricts blood vessels (these raise blood pressure). It can also make you more alert to the point of jitteryness. Beta2 receptors are found in the airway can cause the bronchioles to open improving breathing. So commonly used puffers for asthma etc probably contain the B2 activator.

A B-blocker blocks these responses from happening. So they block increases cardiac output associated with excitement or stress, and keep your heart and breathing at baseline.

And that is why B blockers are banned in precision sports such as snooker or target shooting. B2 Activators such as those asthma puffers are banned in cardio heavy sports because they improve the ability to pull oxygen through the airway.

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Beta blockers don't improve cardiac output (in fact they can worsen it in some cases). They block adrenaline receptors: adrenaline makes your heart beat faster and more vigorously, so with this drugs you have the opposite effect (slower heart rate, less powerful contractions). So the cardiac output decreases (or at least doesn't improve despite adrenaline stimulation). Cardiac output in fact depends mainly on: heart rate, blood volume and contraction

Warfarin is in a sense a vitamin k poison. However, when you eat vitamin k containing foods such as leafy green vegetables, it has zero effect on the metabolism of warfarin. Instead the vitamin K acts as an antidote by replacing the vitamin K that warfarin blocked. There are other drugs that can affect the metabolism of warfarin however.

If they are used correctly they can improve cardiac output.

When you need to go on beta blockers you can have some problems with your heart not pumping correctly. High BP does not correlate to high cardiac output.

Not to be pedantic but if someone is take a beta blocker for atrial fibrillation it will increase cardiac output despite the reduction in heart rate. Actually most people who take a beta blocker probably have an increase in CO due to higher stroke volume. Only for those who take it for sinus tachycardia would have a deceased in CO.

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Okay, thanks for the clarification; I know it's used in musical performance, so I could've followed that case back to its correct line of explanation if I'd thought about it. And that's really interesting about the precision sports - I wouldn't have thought of the advantage of a beta blocker in sports like that but it makes perfect sense.

For some reason, I could never keep the adrenergic receptors straight. I think part of the difficulty for me, personally, is that I've taken a beta blocker and felt like it was easier to "breathe" which is obviously nonsensical from a bronchiole standpoint, so I probably keep transposing the effect in my head to make sense of that.

Thanks for the chance to revisit some of this!

CO = EF x HR so what you’re discussing is that they will increase EF with increased end diastolic pressures but decreased HR will ultimately shift the equation to a lower cardiac output

CO = Stroke volume x hr. It's a fine balance. If someone is in af with fvr then stroke volume will be low because of decreased preload (as there won't be as much time for ventricles to fill) therefore slowing hr will allow more filling and increased sv and ultimately co.

No CO = SV x HR. EF = (SV/EDV)/100. Please tell me more about how CHF patients take beta blockers to decrease the CO though /s

In addition to all the great answers here I wanted it mention some medications that can affect absorption from the GI tract.

As all the other comments mentioned, beta blockers and other agents that decrease heart rate and blood pressure do not affect absorption from the GI tract. However, there are some agents with the opposite effect that do.

Many agents we refer to as vasopressors can have this affect, some common ones would be norepinephrine, epinephrine, and phenylephrine. These agents act on act on alpha-1 receptors as well as others. Their action causes peripheral vasoconstriction, which increases and maintains blood pressure, often in critically ill patients. This action maintains adequate perfusion of the heart and brain, but can cause less blood flow to other areas due to vasoconstriction. This can include the GI tract, which may cause decreased absorption of medications and nutrients from the GI tract.

This is a very simplified explanation, but it’s the first thing to came to mind.

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Beta blockers produce a pronounced fall in heart rate they do not increase it

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That being said, one does run a higher risk of a GI bleed while on anticoagulants based on various risk factors.

Beta blockers work a bit too systemically to cause a specific issue in the gut, though nadolol does have a niche in treating portal hypertension.

Hello. Gastroenterologist here. As with all health questions, the answer is nuanced and complicated. I’ll highlight a few relevant points here that I didn’t see addressed in some of the other responses.

1. The digestion process is multistep and the stomach involvement is one of the earlier steps. Most of the absorptive surface area is in the small intestines. The stomach provides mechanical mixing in an acidic environment in addition to the mechanical breakdown started by the chewing process in some of the digestive enzymes found in saliva. Other key enzymes, including those made by the exocrine pancreas are mixed with the food stuffs starting in the second portion of the duodenum via biliary system through bile excretion.

2. the stomach is sensitive to vascular considerations similar to all tissues in the body. The minimal amount of blood delivery for oxygenation and energy delivery for a tissue to function will vary depending on the tissue. The cardiac output necessary for functions at rest are generally much lower than the maximum cardiac output that the heart can achieve. While cases of insufficient blood delivery to the G.I. tract can occur, this would be unusual to come from just the medications mentioned here at intended doses unless there were some other extenuating circumstance. Gut ischemia can occur with severe disruption of blood flow such as vascular blockage of specific systems (such as a clot) or global hypoperfusion from significant decreases in cardiac output, like that found in shock physiology.

Please excuse any typos as this response was done on my phone via voice recognition.

Stiff hearts due to cardiac remodelling get improved CO with a reduction in HF due to incresed end-diastolic volumes as described by the Frank-Starling equation.

The simple equation for CO doesn't always hold, especially in pathological physiology. There are many exceptions in clinical medicine.

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No, these drugs do not affect digestion in any clinically sigificant way assuming therapeutic serum concentrations. Blood thinners do not "thin" the blood in the way that one would think of it (e.g. they do not cause hemodilution and are not colloid/crystaloid volume expanders like NS, Hartmans solution, or Ringger's lactate, certain lipid emulsions, etc.), but rather posess antiplatelet properties- e.g. they prevent platelets from sticking together usually by inhibiting a clotting factor. The ditary restriction flow from the fact that certain vitamins are chemical precursors to clotting factors- particularly vitamin A and Vitamin K. In fact these vitamins are used to reverse the effects of some blood thinners, such as sodium warfin in cases of poisoning.

Betablockers act on CNS beta receptors and supress the effects of adreniline/epinephrine causing vassodialation and decreased heart rate. However, they have no effect on the production of HCl in the stomach. Most substances cannot be absorbed through the stomach, Ethanol is the rare exception, such that these drugs have no effect on digestion at the level of the stomach.

However, some beta blockers (metoprolol and propranolol were studied) do speed up GI motility (increased parastalsis) in dose-dependent fashion at the level of the esophogus sigmoid colon, but the effects were marginal at therapeutic serum concentrations, and other beta blockers were shown to have opposite effect.

Yes this is seen with a bit of frequency in the hospital. Usually anticoagulants are stopped for a short time and bleeds in GI tract explored and then clipped. Sometimes people undergo a secondary procedure to stop their need for a blood thinner (like an ablation) or they resume it on a short time after discharge.

Is there any kind of drug that does "change the viscosity or concentration of any component of blood"?

In the strictest terms, yes. For example, Hydroxyurea decreases cell production in the bone marrow and can rapidly decrease a population of white cells called myeloid cells in the case of leukemia where the count can exceed 100,000. This is to prevent leukostasis which is where the cancerous cells thicken the blood and cause it to sludge causing respiratory failure or stroke.

Yeah, where I went wrong in particular was in misremembering the relationship with contractility. I thought a beta blocker was a positive inotrope, not a negative one. But I also have pretty atrocious memory and recall, so I figured I was missing something, somewhere.

This is not as clear as some have made it out to be here if you broaden the definition of blood thinner. For warfarin/etc, likely no. But...

This is a really good question and interesting to think about. Blood thinner is a very broad generalization. To increase diffusion digestion, just "thinner" blood is unlikely to make a difference, unless micro thrombotic events are happening that interfere, which might actually be the case in severe diabetics, smokers + other conditions, or those with metastatic cancer. But I don't think there'd be any clinical relevancy here, nor has it been looked into; these parties are not suffering from relevant malabsorption otherwise, and if they were, you'd look into less dangerous avenues to increase it.

Interesting though, some "blood thinners" like pentoxyfylline actually increase the lumen of vessels, the malleability of blood cells and vessels, and even increase growth of new vessels. I haven't gone down a pub med deep dive, but I wouldn't be surprised to learn that pentoxyfylline might aid here and even hold some therapeutic value. If it hasn't been looked into, someone should!

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