Beth Livengood, ND - Gastroparesis Case Study (2017 Conference) (LDN, low dose naltrexone)
A case of gastroparesis and how low dose naltrexone helped this patient. Causes, symptoms, diagnostic findings, similar pathologies, demographics, and treatments, including diet, low dose naltrexone, acupuncture, etc; and the mechanisms of action of these treatments.
Linda Elsegood: Welcome to this archived LDN research trust conference presentation. We hope you enjoy it.
Dr Beth Livengood: Hi, I'm Dr Beth Livengood. I'm a naturopathic physician practising in Phoenix, Arizona, and I am a low dose naltrexone prescriber. I learned about it through an integrative residency program that I completed and was privileged to work with a doctor who's already prescribing it successfully for particularly ms and some other autoimmune conditions.
And since then has devoured the literature on it.
So I'd like to present to you today a case of gastroparesis and how low dose naltrexone help this patient with her symptoms? The signs and symptoms are that day and can look like other pathologies as you'll see here, acid reflux and/or regurgitation, early satiety, so a lack of hunger, sometimes an anorexic component, they're due to abdominal pain and bloating and often nausea and vomiting. These don't all have to present. So the picture can be vague. In fact, other pathology such as gastroesophageal reflux disease is a component of gastroparesis, but it can also look like biliary dyskinesia with some gallbladder influence there, or mechanical obstruction, which can be excluded through an endoscopy. So all of those and, and other pathologies need to be looked at when we see any of these signs. So the onset, the aetiology of gastroparesis has several possibilities, but primarily diabetes when there are a nervous component and nervous system component. We know that the nerves are not functioning adequately to have the smooth muscle of the gastrointestinal system function properly. So diabetes is one of the most common causes of gastroparesis. But this occurs within the whole GI tract that we see it, in this case, primarily affecting the stomach.
Surgical complications can occur with any thoracic or abdominal surgeries where the vagus nerve might be accidentally neck, less common than the neuropathy from diabetes. Certain medications can also cause symptoms as gastroparesis. Also less common than the previous two. And then finally, idiopathic gastroparesis, which actually is quite common, and that of course just means we don't know the cause, but we see that this can happen after a viral infection. I've seen a case from a parasitic infection that had a fungal component along with it. Um, and we also are now seeing some research that shows neuronal nitric oxide synthesis is impaired. So this tied back into some of those medications that might impair don't call.
So who was affected? The demographics of atypical gastroparesis patient is four times higher in women than men. And I found this interesting when I drew in the low dose naltrexone component that we see autoimmune disease also affecting women much more frequently than men. So that could possibly tie into the idiopathic component of gastroparesis.
Um, the other reason that women are more frequently affected with this is that the luteal phase of the menstrual cycle, typically slower gastric emptying rates. Anyway, so it could be a cyclical, um, Menzies related pattern. We would want to look at that in our female patients. And then, as I alluded to earlier, gastroesophageal reflux disease, GERD is, um, a correlation in about 40% of adult patients. They will have both of those components, the GERD symptoms as well as. It delayed gastric emptying. Finally, impaired immunity, which may tie in against the autoimmune component, can affect, uh, gastro-aresis. It's part of the risk factors that we see people who are on the medications mentioned previously, people with repeated infections or prolonged stress that has worn down the immune system.
So conventionally, we see prokinetic drugs such as medical bromide used in other countries outside of the United States, Domperidone is recommended, we don't use that in the US, but that has been recommended and that Omeprazole other acid blockers are used for symptom relief, especially when GERD is also involved.
But I want to point out here that by definition there is impaired drug absorption. We are not getting food or drugs into the system adequately through the stomach. So in this case, this is where, um, our liquid or sublingual versions of low dose naltrexone would be more effective and better absorbed. So with that background, our case study today is a 30-year-old female who had all of the symptoms noted above and very, especially the, her most distressing symptom was daily vomiting after every meal. Constant bloating. So over time, she had reduced her student intake to literally nine different foods, which she had found to cause the least trouble. Because of that in the previous six months or so before she came to me, she had lost 30 pounds quite rapidly. So over just a short period of time.
Also, because of the limited food intake, she was at poorly nourished fatigue, and depression had started to set in, and we know fatigue and depression that lack of hope are significant barriers to healing. Healing occurs during rest and during sleep. So with those two comorbidities, if you will, those other symptoms we're actually pretty significant. They were obstacles to her getting well. So her background, which led to diagnosis was that she had several abdominal surgeries, and she was never well since then. So this raised the suspicion of a Vagal nerve nick. She also travelled frequently to Mexico. So we did test her for ova and parasite and other bacteria.
We did a complete thorough stool analysis that was negative. She was negative for diabetes, the medications or the cyclical Nancy's related patterns. So we examined all the different etiologies known etiologies for gastroparesis because she did have the positive test for gastric emptying. It was beyond the typical MTA rate at one, two and four hours.
Her gallbladder was also examined because she did have similar symptoms too, um, the biliary dyskinesia, we mentioned earlier. It wasn't low, but, um, in naturopathic medicine, we have a lot of tools to address—gallbladder ejection fraction. And improves function without just taking the gallbladder out. So that was actually addressed early on and improved.
That was kind of taken out of the picture and reduce the complications of her original diagnosis, which was idiopathic gastroparesis with possible nerve damage and the comorbidity, biliary dyskinesia. So it took care of the latter and then focused on gastroparesis because those symptoms persisted. So among other things, we started low dose naltrexone at three milligrams initially at bedtime.
She had an initial and quick response that just reduced her stress. She coded here as, um, got a pause between her fight or flight instincts and her actions. So she was constantly on the sympathetic ready to go, No waiting for the next bad thing to happen and that went away. Her overall wellbeing was improved; her stress was reduced.
And her sleep. Initially, it was actually very heavy, and she had some of the morning grogginess. She didn't complain of the vivid dream that we often hear about, but just unrestful sleep really too heavy. So what we did for that was moot the naltrexone dosing a little earlier, so it wasn't as close to bedtime, and that seemed to help with the grogginess.
She was satisfied with that. So in the following month, month two through six, we maintain the dose at three milligrams because we saw, besides the overall wellbeing improved when we saw others' symptoms begin to reduce. Her food tolerance improved. So previously, she was able to tolerate only nine different foods, and by month six, she was eating dozens of foods.
In fact, I had to remind her how far she's come because there were still some foods that she couldn't tolerate, but it was vastly improved. Um, from a naturopathic standpoint, food intolerance, we call them sensitivities can also have an autoimmune component or an allergic atopic component, um, which LDN we know could be very useful in addressing those types of things and overactive immune response.
And that's very common for food intolerances. So we found that improved because of that, her symptoms reduced. She had less bloating, less nausea, and rarely, if ever, vomiting. So the overall, her lifestyle was dramatically improved within six months. Her version of this, her quote of how that felt was that she had increased nerves in patients in an otherwise paralyzed the guts.
So those are her words. She was referring to again, a sense of hunger. She actually felt hungry and wanted to eat. She had the urge to defecate, whereas before everything just sat in her GI tract. So it really made improvements that way. So as I mentioned, this was part of a larger protocol. We started very early on with acupuncture that helped the gallbladder function.
And then in her words. She said that the acupuncture seemed to help with acute issues and flare up, whereas the LDN seemed to be systemically, always helping. Uh, well, she also received some visceral massage, which we've seen in research is recommended and found to be helpful for gastroparesis gentle abdominal type massage brings improved nerves function and circulation to the organs.
Right. And we know if she had any kind of nerve damage from the surgery, this would be important. We eliminated the food sensitivities, which we already talked about, and she also had a medical marijuana certification, which in Arizona, we have a quite a thorough program to certify for medical marijuana.
And again, in the patient's words, she said that this seemed to bridge the gap between what the LDN was able to take care of, versus what she could manage on her own. So the medical marijuana, she self dosed and I believe that's what she referred to as managing on her own wasn't adequate. And so the LDN seemed to bridge the gap.
So how does this work? A couple of proposed mechanism of action. The first one here has been well elucidated in the literature, which is the opioid antagonistic action that actually promotes our endogenous endorphins to be made a little more effectively. So one aspect of low dose naltrexone that particularly interests me is that it works synergistically with other medications.
And in this case, with medical marijuana, the two LDN and cannabis act on different opioid receptors. So the cannabinoids bind to CB one, the LDN binding to the new Delta and Kappa opioid receptors. Uh, overtime in the last 13 years or so, we have confirmed through the literature that there are no contraindications between two.
There are no symptoms of withdrawal if you're taking both of those. And in 2012 there was a study that actually showed that cannabis augments the analgesic effects of opioids, and that could include our own endogenous opioids without significantly altering plasma opioid levels. So this is good because um, it kind of confirming the 2006 study you see here where the THC intoxication component, which is basically a side effect, unwanted for most of them.
That's actually blunted when you add the LDN. So we're increasing the opioid effects while blunting the intoxication effects of medical cannabis. Pretty cool. So for her, that worked well. We also see the anti-anxiety effect augmented that caution there, and the 2010 study showed that the cardiovascular effects were also augmented, which meant a little increase in heart rate for people who had that effect from cannabis. Interesting side note, the high dose of naltrexone at 50 milligrams is nonspecific. So yes, it affects some of those opioid receptors, but also Gabba and possibly a bunch of other receptors.
So not as specific as are targeted low dose naltrexone. And then the second mechanism of action I wanted to point out with the inhibition on TLR four receptors. These are some of the initial promoters of the inflammation process within the nervous system. Um, inflammation, of course, coming from reflux, that extra acid from food sensitivities, inflammation from prior surgeries or illness, all of these, um will trigger the TLR for cascade. They found that throughout the body, but especially interestingly on the glial cells in the brain. So we can speculate right away how this might impact the pathophysiology of multiple sclerosis and how LDN might work on that. Why is it so effective on the ms? Well, anyway, it could be the same reason it's effective on other inflammatory disorders.
The sedimentation rates that we sometimes take as an inflammatory marker in the blood, it can be reduced with low dose naltrexone. So that's the response that we would hope to see as inflammation comes down in conditions such as rheumatoid arthritis, lupus, any inflammatory condition, including gastroparesis.
So we would look for ESR to come down as inflammation comes down. So an interesting, I think a little bit newer area of research in how LDN might affect the inflammation process. In conclusion, um, we see that LDN is working not only on our opioid receptors and promoting our own endogenous endorphin production, but it's also affecting the inflammation cascade directly and reducing inflammation.
LDN works synergistically with many medications, and we've highlighted, in this case, how it may augment medical cannabis. These synergistic effects are seeing it through initially, and I've seen this most often, the initial reaction is an improved sense of wellbeing. This translates into an improved tolerance to the health condition one is working through reduced stress, reduce anxiety, and then along comes the reduction in pain and reduction information, which we're now learning is how that works to the TLR four, the glial cells and the immune system throughout the body. We see reduced inflammation—so good success with that gastroparesis case, and more to come.
Linda Elsegood: Thank you for listening to this presentation. All past conference presentations can be found on our website, www.ldnresearchtrust.org.