This week guest blogger and esteemed LA colleague, Julie Weibe, PT talks about her conversation the brilliant Lorimer Moseley, Ph.D., B.App.Sc. Her posts sums up one of the reasons Steph and Liz asked Dr. Moseley to write the forward for their book, Pelvic Pain Explained.

Here’s what Julie has to say:

November 17th 2014

Well, we didn’t actually have coffee. But I think I may have been drinking coffee and done a spit-take when I opened my inbox to find that Lorimer Moseley had responded to an insanely long, and question laden email I sent him about a year and a half ago. Tweets had stirred up confusion in my mind over our new understanding of pain developed through the work of he and David Butler. Together, they have guided us into a new world where pain is now understood as a product or output of the brain. The brain is the decision maker as to whether or not a particular signal or input is dangerous enough to warrant a pain response or output. The brain evaluates and estimates the threat based on multiple areas of input: history, emotion, experience, etc., not simply how hard did you fall or how hard were you hit.

Moseley has pioneered the use of motor imagery to address chronic pain states. Providing new inputs through imagery to influence the brains output. In his book, Painful Yarns, he highlighted the story of a man injured in a bread factory accident that had a severe increase in his CRPS (Chronic Regional Pain Syndrome) every Saturday morning. They finally figured out the trigger for his routine Saturday symptom increase was the scent of his neighbor baking bread. Scent input triggered a perceived threat by his brain, which then ramped up and produced the pain output. Chronic pain, not to oversimplify, is an overprotective brain, misinterpreting input and using pain signals as a warning.

I attended a conference in which Lorimer and Paul Hodges team taught these concepts and others regarding the changes in the brain that occur with muscular training. I left with a loose grasp on the concepts, but was still working out the application of it clinically in my primarily non-chronic pain patient population, when the tweets began….

So I wrote Lorimer a note.  Excerpts are below, Lorimer’s responses are bolded:

(JW) At the Fall conference, you talked about output, and Hodges about the influence and changes we see in the brain due to input, it seemed a perfect pairing of information. Input and output intermingled. Creating clinical models around that intermingling in multiple populations is the key and at the heart of why I am writing. So if you have a moment…I have some questions to help me communicate to my patients, and myself how this all gets translated into practice. The messaging in social media and blogs out there is getting a bit confusing, and lack practical steps for application.

People are tweeting stuff like this:

” Pain has never been shown to be caused by the length and strength of muscles. Lets stop telling patients otherwise. #solvePT #PainPT“

So if we follow the logic of this statement, then why do we bother to strengthen? Is that what we should be telling people instead, don’t bother, b/c the evidence shows strength has nothing to do with resolution of your pain? That doesn’t fit with my interpretation of the blend of your work with Hodges work. But perhaps I am missing something, which is why I am writing. In terms of the all important emotional piece, is the capacity to take action in your pain through say exercise an empowering positive emotional input?

(LM) I would say it is, but that does not stand in contradiction to the statement from twitter above.

If for example, the injured tissue involved is say a nail hammered into the back of a patients hand, and the patient hits the hammer over and over again throughout the day….shouldn’t we do something about that, get the patient to stop that? And of course call for a psyche consult. A tongue and cheek way of asking do we run the risk of throwing the baby out with the bath water by not appreciating neuromuscular and mechanical inputs, too (repeated through movement patterning or faulty alignments or bad habits)?

Well, of course we should do something about that. I think you are not thinking of an actual patient here, BUT, you might be thinking of a patient you consider to be continually provoking a nociceptor in the tissues. Then of course you should fix this. The tricky thing is that it can be difficult to demonstrate the nail in the hand effect and many of our tests are not quite as specific as we thought. Still, your argument stands I reckon.

Poor motor control, alignment, shearing forces, weakness, etc all of our previous theories about why we experience pain, do they still hold some merit if essentially they are metaphorically hammering the nail in a little bit deeper each day? If graded motor imagery is a way to change input to the somatosensory cortex to create a change in the brains output, can form, movement, alignment, muscle recruitment strategies, ANS involvement, etc also be inputs to change the brain’s outputs? If not, then why do peripheral treatments seem to improve pain (or reduce the brains interpretation of threat)? Hodges work leads me to believe we can actually change the brain with some of our training ideas.

I think there is very, very good evidence that we can change the brain by training. Paul’s work adds to a very large body of evidence in this regard. But what has really changed is Paul’s interpretation of that work, which I think is a sensible change, is that the training might be having its main effect in the brain, rather than in the forward shift, by 20ms, of contraction of a particular – not very high impact biomechanically – muscle. The thing that is difficult is interpreting it all – motor control training is not simply that – it is also a conceptual package, graded exposure, cognitive therapy, behavioural therapy. That M1 (Primary Motor Cortex) changes is lovely and interesting, why it changes is PROBABLY due to the contraction, why it changes functionally is very difficult to know, and whether it relates to pain relief is impossible at the moment to work out.

Is there a distinction between how the brain produces “regular” old pain (like a nail driven into your hand) vs phantom pain in that same hand after the nail hammering behavior has stopped? Should their clinical programs be different?

Yes. In the former the clinician should reason honestly and in an informed way and end up removing the nail, but the latter, the clinicians should also reason, there is no nail to remove so the treatment should be different. Both treatments might contain common elements of course.

Isn’t there a way of communicating this so that both inputs and outputs are considered and have some value (input and output intermingled)? Is it just how we are communicating causality? Or am I just lost??

 You are clearly searching and I LOVE this. I hear myself in some of this. The questions that I found most difficult to answer without learning more, and then more etc., etc. (the old the more I know the more I realise I don’t know etc. thing) – are questions like ‘did I ONLY change form? Recruitment? Alignment? Etc? or did I inadvertently do many things.

Again, my questions in part are born out of a lot of the social media trickle down from your work, particularly a lot of statements that I think communicate throwing the baby out with the bath water as we try to create clinical programs. I am not trying to create the message, but came to the source to clarify for those of us in the trenches trying to integrate the info in multiple patient populations. I think (hope?) I am not alone trying to decipher it.

I don’t reckon you would be. I am also trying to work it out. A common misinterpretation of my work is that I think that there is no point thinking about primary nociceptive input in people with pain. I do not think this and I do not think I would ever have said this. What I do think is that there is compelling evidence that the relationship between pain and tissue damage is seldom simple and is sometimes very tenuous indeed.

Thank you for your time, I really appreciate it.

and I yours.

L

Awesome…right?

I was so grateful for all of Lorimer’s insight, and his continued kindness in HOW he delivers his message. Please take note bloggers, and social media users, think WWLD before you tweet or blog. I had some great takeaway’s that have guided my own practice and teaching since this conversation a year and a half ago. First, I really liked that we can earnestly say, that we aren’t really sure why a lot of what we do works, but we are trying to figure it out! And just because we don’t understand the why, it doesn’t negate that our interventions can bring change and help. I can live in that uncomfortable unknown…how about you?

Also, when we change a piece of the puzzle through a peripheral intervention, we likely change multiple inputs at once. It is hard to point to the one thing that ultimately caused the change in pain…that is what our old idea of pain as input promoted and what we can no longer support in the new pain paradigm.

Lorimer’s final point has provided the greatest clarification for me as I slog through the social media pontification and pundits. More importantly as I apply these ideas clinically. “A common misinterpretation of my work is that I think that there is no point thinking about primary nociceptive input in people with pain. I do not think this and I do not think I would ever have said this.”  

And how comforting is it that he is “still trying to work it out”, too.

Thanks again to Lorimer. He is a great communicator and teacher, moving us all forward!

To learn more about the new pain science paradigm, check out:  Lorimer’s Ted Talk Explain Pain and Painful Yarns.

And if you haven’t already, SUBSCRIBE to this blog (up top, to the right, under Stephanie’s photo!), so you can get the weekly blog update in your email inbox, and follow us on Facebook and Twitter where the conversation on pelvic health is ongoing!

 

educator :: advocate :: clinician

 

 

 

By guest blogger Jordan Hoffman 

Stephanie here: In the late summer and early fall of last year I began experiencing increasingly painful periods. I was bleeding very heavily, taking up to 12 Advil per day without relief, and was very concerned about what was happening in my reproductive tract. Our LA clinic opened in May and therefore I didn’t have a gynecologist here. I knew if I did they would suggest that I take oral contraceptives, which I do not tolerate, or get an IUD, which I did not want. One of my patients told me Jordan Hoffman, an LA-based acupuncturist, and this weeks guest blogger, helped her resolve recurrent yeast and urinary tract infections. I set up an appointment and expected to receive acupuncture treatments for my symptoms. Instead, we discovered some interesting things that correlated with my gynecological demise.

Our LA clinic became very busy very fast. I was eating on the run and in between patients. My diet changed in that I started eating easy, low prep things like packaged string cheese, cottage cheese, salads with cheese, yogurt, etc. I was exhausted and drinking triple the amount of coffee I used to. I was also eating chicken sausage, chicken in salad, chicken everything because it was easy.

Jordan told me I needed to take out dairy and chicken, replace coffee with tea (caffeine is okay, coffee is not) and take an individualized herbal supplement that he made for me. My first thought was that he was definitely trying to make me miserable. I love cheese, and I am from New Jersey, I have been a coffee drinker my entire life.  However, I was uncomfortable enough that I would  take this experiment on for a month and time would tell.

It worked. The next month I had NO cramps. I did not even know my period was coming. I have now been through four cycles successfully, even though I do drink one cup of coffee a day now (sorry Jordan!). This experience taught me that diet can have a profound influence on our bodies. Dietary modifications are  low-risk with possible significant therapeutic benefit. In this week’s blog Jordan will tell us why.

Okay, take it away Jordan!

Thanks Steph! Simply put: cow milk is for cows, goat milk is for goats, and human milk is for humans. Every species produces milk specific to its own species’ needs and digestive capabilities. And every species stops drinking its own milk after infancy.

Except humans.

Not only do we drink other animals’ milk but we are lead to believe from an early age: “Milk—It does a Body Good!” And yet, every day I see patients with profound and wide-ranging ill effects from consuming any and all dairy products in any quantity whatsoever. As such, ZERO dairy is the only amount of dairy that is fit for human consumption. Almond, soy and rice milks are very good substitutes.

This article is going to focus on dairy and its role in various medical conditions that may lead to or worsen pelvic pain. No matter the origin, chronic musculo-skeletal imbalances can lead to organ dysfunction and chronic organ dysfunction can certainly lead to musculo-skeletal imbalances.

Irritable Bowel Syndrome– Chronic Constipation

Irritable Bowel Syndrome (IBS) is a common catch-all diagnosis for alternating bouts of constipation and diarrhea with accompanying cramping and pain. Stress is often the default cause given to IBS. But while it can definitely play a role, stress does not cause problems alone. Rather, it exacerbates pre-existing ones. Stress plus the pathogens introduced to the gut from dairy can lead to IBS.

Dairy is a known allergen that can cause constipation, especially in children (1). You can easily do an Immunoglobulin E (IgE) blood test to check for food allergies, like to dairy. Yet, in many instances, patients have brought me their allergy tests showing no IgE response to dairy. Puzzled, I did some more research. IgE is the most likely or common immune response from our body to an allergen. But it is by no means the only response. In fact, an allergy to cow milk showing up as constipation may not even be mediated by IgE (2), revealing a less than complete picture painted by those tests.

Sixty percent of the protein content in dairy is casein, which when introduced to our digestive system becomes Beta-Casomorphine (BCM). Casein is used to make glue. Ever wonder why the logo used for Elmer’s Glue is a cow? Casein. Now notice the second part to that word: “morphine.” Just like opiate drugs, BCM can exert a numbing and paralyzing effect on our intestinal motility (3), and an analgesic and addictive response in our brain and nervous system compelling us to want more. Casein can also trigger a histamine response (4) in our intestines leading to more inflammation and irritation which can lead to more constipation.

Another aspect of dairy that can lead to chronic constipation is in its bacteria load. Pasteurization occurs at 162 degrees Fahrenheit for 15 seconds. Yet, to sterilize water we are advised to boil it at 212 degrees Fahrenheit for several minutes. There are bacteria that can survive pasteurization. In fact, the United States allows for a somatic cell count (SCC) of up to 750,000 per ml (5). Whether those cells are active pathogens like Mycobacterium Avium Subspecies Paratuberculosis (MAP) (6) or E. Coli (7), or non-active due to effective pasteurization, our immune system still recognizes them as foreign and kicks in to gear with an inflammatory response.

Inflammatory Bowel Disease

The Standard American Diet (S.A.D.) has historically placed the main focus of each meal on animal protein, and doesn’t even take into account the glass of milk on the side, the cheese along with the protein, or the ice cream for dessert. Severe inflammatory bowel diseases like Ulcerative Colitis and Crohn’s Disease are linked to the over-consumption of animal fats and the under-consumption of fiber (8), which is absent in all forms of animal protein but abundantly present in beans, peas and lentils—superior sources clean protein. Such diets can even compromise our intestinal clearance of bacteria, mentioned earlier, leading to further inflammation (9).

Hormone Dysregulation

One of the simplest ways to link food choice and the pelvis is that everything flows downhill, especially when it comes to hormones, urogenital and reproductive health. While many of our environmental pollutants can exert an adverse effect higher up the endocrine system chain at the pituitary level, the first place I tend to look for culprits is diet.

Cows are fed and bred to lactate throughout their pregnancy with particular elevated milk production in the latter half of gestation. As such, even regardless of whether they are injected with exogenous hormones, the cows’ own hormones can show up in its milk. Dairy products you consume account for 60-70% of all dietary sources of estrogen (10) with at least 6 different hormones also being found in milk, including progesterone, and testosterone (11). One way we excrete hormones from the body is through stool. Studies show that there is a direct correlation between fecal weight and fecal estrogen content (12). And with the constipating effect of dairy, we now can see yet another link between chronic digestion dysfunction and hormone dysregulation.

For men, this undue influence on their endocrine function can show up as erectile dysfunction (also an indication of atherosclerosis aided by the cholesterol in dairy), low sperm counts and ejaculatory volume (13), and testicular and prostate cancers (14). For women, this can show up as irregular and painful periods, endometriosis (15), Polycystic Ovarian Syndrome (16), and breast and ovarian cancer (17).

Where to begin

Accepting the truth about dairy flies in the face of American identity and all we have been conditioned to believe since we were kids about this primary food in the SAD. But don’t believe me and the research I have done or the results I have seen with patients. Believe yourself. Come off dairy, all forms completely. Read labels. Ask questions in restaurants. Go dairy-free for at least 4 weeks and then if you are still curious, introduce it and only it in a meal and see how you feel the next couple of days. Most of my patients will immediately feel poorly—stomach aches, sinus congestion, knee pain, etc. For some, it may only clog the arteries of their heart or disrupt their menstrual cycle, both of which take time to reveal themselves. Let the decision to cut out dairy come from your own personal experience guided by critical thinking and a willingness to experiment with self-awareness and truth.

Cheers,

Jordan

Jordan Hoffman is a California Licensed Acupuncturist, a Diplomate in Oriental Medicine and Nationally Board Certified in Chinese Herbology, specializing in Addiction, Internal Medicine, Pain Management and Nutritional and Lifestyle Counseling.  He maintains his acupuncture practice in West LA and Canoga Park, CA.  For more information, please visit http://www.JordanHoffmanAcupuncture.com.

 

 

 

 

References:

1. J Pediatr. 1995 Jan;126(1):34-9. Chronic constipation as a symptom of cow milk allergy. Iacono G, Carroccio A, Cavataio F, Montalto G, Cantarero MD, Notarbartolo A.
2. J Pediatr Gastroenterol Nutr.2010 Aug;51(2):171-6. doi: 10.1097/MPG.0b013e3181cd2653. Cow’s-milk-free diet as a therapeutic option in childhood chronic constipation. Irastorza I, Ibañez B, Delgado-Sanzonetti L, Maruri N, Vitoria JC.
3. 2000 Jun-Aug;34(3-4):181-6. Effect of opioid active therapeutics on the ascending reflex pathway in the rat ileum. Allescher HD, Storr M, Piller C, Brantl V, Schusdziarra V..
4. Int Arch Allergy Immunol.1992;97(2):115-20. A naturally occurring opioid peptide from cow’s milk, beta-casomorphine-7, is a direct histamine releaser in man. Kurek M, Przybilla B, Hermann K, Ring J.
5. Determining U.S. Milk Quality Using Bulk-tank Somatic Cell Counts, 2010. United States Department of Agriculture Animal and Plant Health Inspection Service. http://www.aphis.usda.gov/animal_health/nahms/dairy/downloads/dairy_monitoring/BTSCC_2010infosheet.pdf
6. J Food Prot.2010 Jul;73(7):1357-97. Assessment of food as a source of exposure to Mycobacterium avium subspecies paratuberculosis (MAP). National Advisory Committee on Microbiological Criteria for Foods.
7. What Is the Current Milk Quality in the U.S.? Scott J. Wells, Stephen L. Ott. Centers for Epidemiology and Animal Health, USDA-APHIS-VS. file:///C:/Users/Jordan/Documents/Research/Current%20Milk%20Quality%20in%20the%20U.S..html
8. Am J Gastroenterol.2011 Apr;106(4):563-73. doi: 10.1038/ajg.2011.44. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Hou JK, Abraham B, El-Serag H.
9. Dig Dis.2014;32(4):389-94. doi: 10.1159/000358143. Epub 2014 Jun 23. Dietary clues to the pathogenesis of Crohn’s disease. Pfeffer-Gik T, Levine A.
10. Med Hypotheses.2001 Oct;57(4):510-4. Is milk responsible for male reproductive disorders? Ganmaa D, Wang PY, Qin LQ, Hoshi K, Sato A.
11. Food Addit Contam Part A Chem Anal Control Expo Risk Assess.2012;29(5):770-9. doi: 10.1080/19440049.2011.653989. Epub 2012 Feb 14. Development of an LC-MS/MS method to quantify sex hormones in bovine milk and influence of pregnancy in their levels. Regal P, Cepeda A, Fente C.
12. N Engl J Med.1982 Dec 16;307(25):1542-7. Estrogen excretion patterns and plasma levels in vegetarian and omnivorous women. Goldin BR, Adlercreutz H, Gorbach SL, Warram JH, Dwyer JT, Swenson L, Woods MN.
13. Am J Clin Nutr.2013 Feb;97(2):411-8. doi: 10.3945/ajcn.112.042432. Epub 2012 Dec 26. High dietary intake of saturated fat is associated with reduced semen quality among 701 young Danish men from the general population. Jensen TK, Heitmann BL, Jensen MB, Halldorsson TI, Andersson AM, Skakkebæk NE, Joensen UN, Lauritsen MP, Christiansen P, Dalgård C, Lassen TH,Jørgensen N.
14. Med Hypotheses.2003 May;60(5):724-30. The experience of Japan as a clue to the etiology of testicular and prostatic cancers. Ganmaa D, Li XM, Qin LQ, Wang PY, Takeda M, Sato A.
15. Reprod Sci.2014 Oct 29. pii: 1933719114556487. [Epub ahead of print] 17β-Estradiol and Lipopolysaccharide Additively Promote Pelvic Inflammation and Growth of Endometriosis. Khan KN, Kitajima M, Inoue T, Fujishita A, Nakashima M, Masuzaki H.
16. Turk J Med Sci.2014;44(5):781-6. Insulin-like growth factor 1, liver enzymes, and insulin resistance in patients with PCOS and hirsutism. Çakir E, Topaloğlu O, Çolak Bozkurt N, Karbek Bayraktar B, Güngüneş A, Sayki Arslan M, Öztürk Ünsal İ, Tutal E, Uçan B, Delıbaşi T.
17. Med Hypotheses.2003 Feb;60(2):268-75. The experience of Japan as a clue to the etiology of breast and ovarian cancers: relationship between death from both malignancies and dietary practices. Li XM, Ganmaa D, Sato A.

For the past six months, Stephanie and Liz have been busily working on writing a book titled Pelvic Pain Explained: Everything you Need to know to Help you Navigate the Complex Terrain of Pelvic Pain. The book will be published by Rowman & Littlefield. (We don’t have the publication date yet, so stay tuned for that info!) As we’ve watched them hustle to get the manuscript together, we couldn’t help but wonder what it was that made them decide to take on the task, so we asked them!

Q. What was the impetus for your writing a book on pelvic pain?

A. Stephanie: “Very little was known about pelvic pain when I started in the field 15 years ago. Many of the patients that I saw in the early years had been suffering for at least ten years, had seen more than 20 providers, and were often on disability and opiates.

At that time I was working with a physician and we specialized solely in treating pelvic pain disorders. For this reason, my experience as a pelvic floor physical and occupational therapists was different than most. Rather than taking a continuing education course, as many aspiring pelvic floor PTs do, I was working with a pelvic pain pioneer in an interdisciplinary setting. So I found myself at medical conferences arguing that the pelvic floor muscles can be a source of pelvic pain.

Sometimes I won the argument, most of the time I lost. During this time, I also developed manual therapy skills, knowledge about medications, procedures, and surgeries. We started to figure out what would and would not work for different types of patients. Being exposed to a high volume of people with pelvic pain very quickly taught me that despite similar symptoms or the same diagnosis,  every patient was different and I had to individualize treatment plans to get them to to work.

More importantly, however, I developed clinical reasoning skills to re-work the treatment when patients either stopped responding or could not tolerate treatment. And this happened all the time. As I was developing these skills, research started to emerge and the technology boom made this information available to anyone who wanted it.

Information does not equal knowledge, however, and I had to figure out what do with patient confusion from chat rooms, being criticized by other professionals in chat rooms, and how to incorporate new diagnoses and treatment options into clinical practice. Today, it’s widely accepted that the pelvic floor muscles can be a source of pelvic pain, though many medical professionals and sufferers still do not know it.

Furthermore, we know pelvic pain encompasses much more than the pelvic floor muscles, and treatment needs to be devised with this in mind. I wanted to write this book to acknowledge the struggles patients and providers encounter, and provide knowledge to streamline the current diagnosis and treatment strategies, even in the face of a broken healthcare system. My hope is that by sharing our knowledge we will provide a platform for more effective and efficient management of pelvic pain.

A: Liz: “For years our colleagues and patients asked, ‘When are you guys going to write a book?’ I guess we finally succomed to the pressure! We’ve been teaching, lecturing, writing in professional journals for years. This was just the next logical step.

But more to the point, there are so few resources out there with good, accurate information for people suffering from pelvic pain as well as providers who treat pelvic pain. And at the same time, there is a real knowledge deficit, even among providers who should know something about pelvic pain. The number of questions we get from people from all over the world on the phone, via email, via our blog, via our website really spoke to this. We believe their needs to be one resource for people to get all of these answers. Our hope is that having this book be that resource will serve to promote awareness to the public and professional community about pelvic pain and help people get better faster.

Q: How has this blog played into your decision to write a book?

A: Stephanie: “The blog has shown me that people need reliable information on pelvic pain and made me realize that sharing our clinical knowledge allows us to help people globally. Through the comments I have learned that people are getting appropriate care but just as many are not. We need to change this and do better!

A: Liz: “We get so many follow up questions and comments with every post. Plus, we receive a  tremendous amount of positive feedback from other providers as well as patients about this blog, so for me, that reconfirmed the need for good info about pelvic pain.

Thank you Stephanie and Liz for stoking our curiosity! The next four weeks will be pretty busy as we all pitch in to get the manuscript ready to turn into the publisher, SO a handful of friends of PHRC have generously agreed to pitch in with a month’s worth of fantastic guest blog posts!

Look for them in the coming weeks!

If you have any further questions about Stephanie and Liz’s upcoming book, please do not hesitate to leave them in the comment section below.

All our best,

The PHRC Team