Guest guest Posted May 9, 2011 Report Share Posted May 9, 2011 Rajpura wrote: > <http://www.acidrefluxwise.com/page/3/?tag=diet>Recent studies suggest > that acupressure applied to the acupoint P6 reduces relaxations of the > lower esophageal sphincter. These relaxations are the major cause of > acid reflux. > Thanks for the link. Because some of us have acid reflux this may seem like a logical thing to try but is it? Most of us have had treatments to permanently relax the the LES a bit. Those that don't have a problem with reflux definitely don't need to reduce relaxations. In achalasia the relaxation of the LES when swallowing is usually either nonexistent or dysfunctional. The relaxation of the LES after a swallow is not the relaxation that is the problem with GERD though. In GERD the problem is that the LES relaxes too much or too often at other times when it shouldn't be relaxing so much. Achalasia and GERD are kind of opposites, but not exactly. The LES could be lacking the complete functionality for the relaxation it needs when swallowing and also be relaxing too often at other times. That would be very untypical of achalasia though, except post treatment where the LES is permanently a bit relaxed. That post treatment effect is due to cut or broken muscle fibers and not because of a neurological change that can be tampered with. What neurology that remains of the muscle function, dysfunctional as it is, may be tampered with but it is limited by the ability of the modified muscles to respond because of the surgical or dilatation treatments and also because of the nerve damage from the achalasia. That nerve damage because of achalasia also means that what may reduce LES pressure in normal subjects may increase LES pressure in those with achalasia. In fact that is one way to diagnose achalasia. There is a drug, not often used this way, that in normal subjects causes the LES to relax but in achalasia it causes the LES to increase pressure. Would acupressure work the same in people with achalasia? You would have study it in achalasia to know and there are some studies about that. More on that below. How good is the evidence that it worked at all in those studies? The articles in the links did not give much information on what was actually in the studies. Here is one such study: The American Physiological Society AJP Gastrointestinal and Liver Physiology Inhibition of transient lower esophageal sphincter relaxations by electrical acupoint stimulation http://ajpgi.physiology.org/content/289/2/G197.full This study did not study achalasia but it does discuss it. One of the problems with this study is that it is small. Another problem is that what they want to measure, Transient LES relaxations (TLESRs), is something that changes in one person from one time to another. You can't just measure one person under two sessions and know if the change is just chance or something you did different in those sessions, such as the methods. You have to measure a group of people and show that the change for the group was more than expected by chance. That is what they try to do with this study but the group is small. The number of people in the main protocol is just 14. You can see the problem with the number of TLESRs randomly changing even in their own study. First look at Fig. 2: http://ajpgi.physiology.org/content/289/2/G197/F2.small.gif Each circle or black dot is a subject. The baseline, neiguan and sham columns are three different test. The lines that connect the circles and dots indicate the subject by connecting the count of each subject's TLESRs from one test to the next. The short black bar is a type of median, and is the main measure they are interested in. On Fig. 2 the median for neiguan (acupoint P6) is lower than for the baseline (untreated) and sham (same treatment but on the wrong part of the body). The lines connecting the dots tend to slope up, but not all, from neiguan to the other tests. The lower neiguan medians and the upward slope of the lines is what you would expect for their conclusion to be true. But notice that many of the subjects moved up or down from baseline to sham even though the medians of the two tests are the same. It shows that the numbers can change up or down for a subject because of things other than the test's purpose. Now take a look at Fig. 3: http://ajpgi.physiology.org/content/289/2/G197/F3.small.gif Notice the two sets of circles for sham. Each set is by the same group of people but taken a week apart. The scores have changed and so have the medians. These should be just changes by chance. Now look at the two neiquan sets. Again these are for the same group of people as the sham sets. Notice that the neiguan set on the right has a higher median than the sham set next to it. If that had happened in the first protocol there wouldn't be a claim that this treatment lowered TLESRs, but this is in protocol 2 so that is not what they are trying to prove here, but it should still raise questions about whether the result in protocol 1 is valid. We have seen that the number of TLESRs for a subject or the median for a group of subjects can change just by chance. They calculate that the result of protocol one is statistically significant. Maybe it is, but I see reason to wonder about conclusion. But what about for achalasia. This study was just in normal subjects not achalasia subjects. In the discussion section they mention that stimulation at Hukou has been shown in two other studies to decrease basal LES pressure and increase swallow-induced LES relaxation in achalasia subjects, but that another study found that it did not change esophageal motility in patients with achalasia. So, this study claims to reduce relaxations, two others claim to increase relaxation, while another claims no change is found. Hukou and neiguan are close but not the same, one on the hand the other on the wrist. Even so, I think better studies are going to have to be produced to prove these claims and show that it helps for achalasia. notan Quote Link to comment Share on other sites More sharing options...
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