Another study shows chiropractic is much less expensive and more effective for lower back problems

I came across a study that was in the December 2010 issue of JMPT (journal of manipulative therapeutics) that shows after adjusting for risk adjustment ( a fancy way of saying severity), the cost of chiropractic intervention was markedly less than going the traditional medical route (http://www.dynamicchiropractic.com/mpacms/dc/article.php?id=55052)

One of the major cost drivers we experience in our office is when our patient decides to go to the emergency room for care.  Typically, they are given pain killers or a shot of toradol for the pain which does nothing for the problem.

In many managed care plans, the medical doctor must give the referral.  To their credit, many tell their patients that they can only offer medication and then refer them to someone like me for further intervention.  Others, find themselves being sent from specialist (often orthopedics) to rehab, without having the problem that created the back issue ever resolved.  I treat many patients who tell me they are fine as long as they do the exercises and then get ready in bed to be able to move.  This tells me their problem is now subacute and have never been resolved. This causes periodic exacerbations, spinal, hip and knee degeneration and of course, they become less active and avoid painful activities.

In our office, we look for the cause and use tests that show the mechanical faults leading to back pain. Through active evaluation (a process of treat, test and treat), we get to the root of the back problem and other problems such as the hip, foot and knee improve as well, since these are merely symptoms of the gait issue that created them.  Perhaps, the greater level of understanding chiropractors have avoids costly MRI and other tests that come with increasing severity.

Many studies really need to compare not just the episode, but with chiropractic care, do people have far fewer episodes of back pain.  Also, foot orthotics are quite helpful as well as myofascial treatment to the region, which is becoming a larger part of many more progressive chiropractic practices as they move away from the less effective and more expensive model of heat, ultrasound and passive care and move toward the model of exercise, myofascial and active modes of care.

What do you think?  As always, I value your opinion.

Dead Butt Syndromes and other fairy tales affecting those who run

A few weeks ago, I read an article that was posted on the NY Times web site regarding something called Dead Butt Syndrome (http://well.blogs.nytimes.com/2010/12/21/when-the-diagnosis-is-dead-butt-syndrome/).  Apparently, this is a problem with the gluteus medius (one of the larger muscles in the butt) which as this person. The person who wrote this article is a veteran runner and as she said “For people who have persistent pain, it’s healing gone wrong,” Dr. Bright said. “That gluteus medius isn’t firing the way it’s supposed to. You’re getting an inhibition of the muscle fibers. It’s kind of dead.” 


The problem with this all encompassing diagnosis of Dead Butt Syndrome is the same with many of the attempts to globally diagnose and then come up with a cure without fully understanding the mechanisms involved.  


Over the past year, I have been reading and reviewing Thomas Meyers book on Anatomy Trains (available through Amazon.com) which shows the myofascia actually controls motion, not the muscles making this diagnosis a part of the problem rather than the solution. 

 As many of our patients know, I diagnose through active evaluation, treat the fascial restrictions and then retest the firing patterns involved.  Sometimes my first impressions are right on but I do a number of maneuvers until I figure out how to restore a more normal firing pattern.  Often, tight hip capsules (fibrous tissue surrounding the hip) can cause this problem, as well as foot overpronation and gait asymmetry.  It does not just happen to nice people like this author.  The Fascia surrounding the muscles tighten, cause the gluteus medius to recruit in other muscles such as the obliques , hamstrings, other gluteal muscles, erector spinae and even affect the upper back as the problem worsens.  

My concern is the piecemeal type of diagnosis this is, only addresses the symptom, which is really a gait issue.  This person was over and under striding (one leg is tight in back, the other tight in front causing a short stride one one side and a longer stride on the other) way before the symptoms appeared and likely ran and stretched through it.  Like most things mechanical, you can run it until it dies or fix it so it wont. The net effect is it torques the pelvis, causing a loss of leverage and your legs tighten.  Your stride shortens, you pull muscles, have problems in the calves and you mechanically have some real issues.  To fix this, you need to understand that this diagnosis of dead butt is just a symptom, rather than the problem.  You cannot, as many our runners know after visiting many practitioners who were not effective enough, fix this with a quick itis or osis diagnosis which sounds medically intelligent but hardly will lead to a solution, because of the lack of understanding of the gait mechanism that created it.  Enough said.


There is no such thing as a dead butt.  There is a thing called foot overpronation or supination or asymmetric gait which will cause this type of a problem. For those looking for a solution, you can email me directly at backfixer@aol.com.  I would be most happy to give you cost effective guidance on problems like this.


What do you think?  As always, I value your opinion

It Takes a Community to Treat an Epidemic

Women and their children wait to receive maternal child health services at a health center in Tanzania. Photography by Nathan Golon.

It was a long trip from Dar es Salaam, due north then west, first on paved roads and then on dusty country paths that meandered through the fields. Few fields were planted with corn or bananas while large tracts of land were open fields with little evidence of agriculture. Clusters of thatched huts passed by quickly as we made our way to the health center. In small villages along the way, women assiduously swept the earth in front of their households as children ran around pushing a ball or playing with small sticks. Men, some old, some young, sat around in circles on low stools or tree trunks in animated conversations.

It was late in the afternoon when we finally arrived at the health center. A jubilant clinical officer came out to meet us followed by two dozen peer educators, all singing and dancing in a heartfelt welcome. I was proudly informed that this small health center had already engaged close to 300 persons with HIV in care and had close to 200 already started on HIV medicines. These are just a few of the millions who have benefited from the HIV scale-up, a historic public health achievement. While only about 100,000 individuals with HIV in low and middle income countries were able to access treatment in 2002, by the end of 2009 this number has skyrocketed to close to 4 million. Most remarkably, sub Saharan Africa is the region that has had the most dramatic increase.

How was this achieved in a region plagued with weak health systems and a multitude of health crises? Shortage of skilled health care workers, lack of continuity model of healthcare for a chronic condition like HIV, dilapidated facilities, inadequate laboratories, entrenched stigma, and poverty are just some of the challenges that faced the HIV response. As I walked around the health center, I kept pondering the question, “how was this accomplished and what does it teach us?” I visited the cramped room where the clinical officer saw all her patients, where the 44 charts of the ones she had seen that day lay on the rickety table. I opened one chart and saw the neatly filled rows of information. I followed her to the pharmacy, a tiny room where the precious medications are kept under lock and key, then passed by the laboratory where a technician proudly showed me his new equipment and his impeccably organized registers.

Dr. Wafaa El-Sadr (second from left) with ICAP Tanzania staff.

The answer to my question dawned on me when I finally sat down to talk with the staff and the peer educators, themselves living with HIV. The answer lay in the fact that they were one, one team that worked together hand in hand. No hierarchy was evident, no sense of the provider as the source of wisdom and the patient as the passive recipient. The staff described the needs of the community, the gaps in services and the innovations they had come up with to cope with impediments. The peer educators astutely asked about nutrition and poverty. They shared their need for new bicycles to be able to make home visits to check on the patients assigned to them. All were passionate about their community, all were adamant on achieving high quality of care, all were cognizant of their individual value as well as their collective power.

Many years into the future, when the history of the HIV response is written, some will credit the billions of dollars of resources for the achievements. Yet, a most important factor might be overlooked. The secret of this remarkable success may lie in the partnership that I witnessed between passionate and committed staff members with knowledgeable and empowered patients.

Wafaa El-Sadr, MD, MPH, is director of ICAP at Columbia University and director of the Center for Infectious Disease Epidemiologic Research (CIDER) at Columbia University’s Mailman School of Public Health. Dr. El-Sadr also is professor of clinical medicine and epidemiology at Columbia University.

Paleolithic Diet Clinical Trials, Part V

Dr. Staffan Lindeberg's group has published a new paleolithic diet paper in the journal Nutrition and Metabolism, titled "A Paleolithic Diet is More Satiating per Calorie than a Mediterranean-like Diet in Individuals with Ischemic Heart Disease" (1).

The data in this paper are from the same intervention as his group's 2007 paper in Diabetologia (2). To review the results of this paper, 12 weeks of a Paleolithic-style diet caused impressive fat loss and improvement in glucose tolerance, compared to 12 weeks of a Mediterranean-style diet, in volunteers with pre-diabetes or diabetes and ischemic heart disease. Participants who started off with diabetes ended up without it. A Paleolithic diet excludes grains, dairy, legumes and any other category of food that was not a major human food source prior to agriculture. I commented on this study a while back (3, 4).

One of the most intriguing findings in his 2007 study was the low calorie intake of the Paleolithic group. Despite receiving no instruction to reduce calorie intake, the Paleolithic group only ate 1,388 calories per day, compared to 1,823 calories per day for the Mediterranean group*. That's a remarkably low ad libitum calorie intake in the former (and a fairly low intake in the latter as well).

With such a low calorie intake over 12 weeks, you might think the Paleolithic group was starving. Fortunately, the authors had the foresight to measure satiety, or fullness, in both groups during the intervention. They found that satiety was almost identical in the two groups, despite the 24% lower calorie intake of the Paleolithic group. In other words, the Paleolithic group was just as full as the Mediterranean group, despite a considerably lower intake of calories. This implies to me that the body fat "set point" decreased, allowing a reduced calorie intake while body fat stores were burned to make up the calorie deficit. I suspect it also decreased somewhat in the Mediterranean group, although we can't know for sure because we don't have baseline satiety data for comparison.

There are a few possible explanations for this result. The first is that the Paleolithic group was eating more protein, a highly satiating macronutrient. However, given the fact that absolute protein intake was scarcely different between groups, I think this is unlikely to explain the reduced calorie intake.

A second possibility is that certain potentially damaging Neolithic foods (e.g., wheat and refined sugar) interfere with leptin signaling**, and removing them lowers fat mass by allowing leptin to function correctly. Dr. Lindeberg and colleagues authored a hypothesis paper on this topic in 2005 (5).

A third possibility is that a major dietary change of any kind lowers the body fat setpoint and reduces calorie intake for a certain period of time. In support of this hypothesis, both low-carbohydrate and low-fat diet trials show that overweight people spontaneously eat fewer calories when instructed to modify their diets in either direction (6, 7). More extreme changes may cause a larger decrease in calorie intake and fat mass, as evidenced by the results of low-fat vegan diet trials (8, 9). Chris Voigt's potato diet also falls into this category (10, 11). I think there may be something about changing food-related sensory cues that alters the defended level of fat mass. A similar idea is the basis of Seth Roberts' book The Shangri-La Diet.

If I had to guess, I would think the second and third possibilities contributed to the finding that Paleolithic dieters lost more fat without feeling hungry over the 12 week diet period.


*Intakes were determined using 4-day weighed food records.

**Leptin is a hormone produced by body fat that reduces food intake and increases energy expenditure by acting in the brain. The more fat a person carries, the more leptin they produce, and hypothetically this should keep body fat in a narrow window by this form of "negative feedback". Clearly, that's not the whole story, otherwise obesity wouldn't exist. A leading hypothesis is that resistance to the hormone leptin causes this feedback loop to defend a higher level of fat mass.