In musculoskeletal therapy today, I like to say that we have two main groups. We have the anti-structuralists, those who (often solely) believe in the psychosocial model of pain, and we have the pro-structuralists, who believe in the importance of addressing and correcting structure, i.e posture.
If you’ve read some of my work before, you know that I pretty much belong to the pro-structural division. However, at the same time, I disagree with many popular notions that my fellow structuralists are supporting. A huge portion of this, is the view on pelvic alignment; the dreaded anterior pelvic tilt, which I consider to be a harmful, misleading myth. Another massive deception is the “relax the shoulders” cue, that I’ve written about it in my thoracic outlet syndrome article, that you can check out if you’re feeling exceptionally curious.
While writing this article, I knew I had to go hard or not at all, as the myth of anterior pelvic tilt is so deeply rooted. So please bear with my bluntness, and try to see the reason behind the points being made.
I too, though, used to believe that anterior pelvic tilt was a major problem of high prevalence. Because I am not unique, nor special, nor more intelligent or more knowledgeable than you. Hopefully not more rational, either! So please keep on reading to learn why I had no other choice but to renegade from this utter myth and harmful belief. Learn why this belief is not rooted in biomechanical understanding, it’s not rooted in science, it’s not rooted in common sense, nor does the approach bear therapeutic fruits of improvement. I am appealing to your healthy sense of judgement, in order to help our suffering patients.
Fig. 1 – Wrong, and wrong. They’re both WRONG!
Now, to be fair, there is no widely accepted consensus with regards to pelvic alignment, and this is why I somewhat understand the frustration uttered by the anti-structural side. Of course, I don’t agree that the solution is to tie the hands up and do nothing, other than addressing the patient’s stress and social life. But much criticism directed toward the structural division within MSK therapy is a well directed one.
In fact, and this is an indicator on both groups’ lack of effectiveness, the current protocols for dealing with lower back pain are so poor, that the world health organization claim that up to 85% of all LBP occurrences are of unknown cause, and has no specific treatment!
Low back pain, the most common spinal disorder, affects over 80% of persons at some point in their life, and from 4–33% of a population at any one time. Spinal Disorders include trauma, mechanical injury, spinal cord injury, inflammation, infection, and tumour. About 80–85% of back pain episodes have no known cause. – World Health Organization
Based on the heterogeneity of the populations, interventions, and comparison groups, we conclude that there are insufficient data to draw firm conclusion on the clinical effect of back schools, low-level laser therapy, patient education, massage, traction, superficial heat/cold, and lumbar supports for chronic LBP. – Middelkoop et al., 2011
It is often claimed that up to 90% of low back pain (LBP) episodes resolve spontaneously within 1 month. However, the literature in this area is confusing due to considerable variations regarding the exact definitions of LBP as well as recovery. The results of the review show that, despite the methodological variations and the lack of comparable definitions, the overall picture is that LBP does not resolve itself when ignored. – Hestbaek et al., 2003
Low back pain (LBP), a highly prevalent problem in society, is often a recurrent condition. – Freeman et al., 2010
“We don’t know the cause of lower back pain” – Eyal Lederman
There is indeed a great need for a paradigm shift. Are we able to get there by connecting common sense, the evidence and clinical experience? Let me kindly propose a way out from the comfort zone.
- 1 Why anterior pelvic tilt is NOT a valid pathology
- 2 The problem with established measurements
- 3 Changing pelvic posture is simple, but not easy
- 4 In conclusion
Why anterior pelvic tilt is NOT a valid pathology
So why am I making these bold claims? Is it just to make even fewer friends that I were before? A true desire to become the black sheep of MSK therapy? Although it may seem that way, the answer is no.
I truly believe that the anterior pelvic tilt fallacy is harming a lot of patients, unknowingly. Almost everyone believe in it; both patients and therapists (that is, those who accept the notion of structural importance). Therefore, it is now my mission to do all that I can to proclaim what I consider to be the true facts of pelvic alignment and correctives.
First, let’s look at why the notion of anterior pelvic tilt most likely became popular in the first place. And yes, the most accurate term is “popular”, because ATP is not supported by anything other than popularity. Its correction do not produce results, it is not based on science, nor common sense, nor biomechanical facts. And yes, I am repeating myself. And ripping my hair out. And crying. All due of the fallacy of ATP and its dangerous application to poor suffering patients.
The mythological origin of APT
Pelvic alignment is a paradox in several ways, and this is why so many misinterpret its position, often leading to malcorrectives, and exacerbated injury. The first obvious reason why most people think their back is too arched, is simply because they look in the mirror or at their patient and see a huge arch. Secondly, if they extend their lower back, it hurts. Obviously extension must be the problem, right? Absolutely, utterly false. This is the paradox.
The reason for these issues are that …
- The perceived excessive arch of the spine is coming from the mid-back / upper-lumbar levels, not from the lower lumbar levels, where the injuries are virtually always occurring.
- Spinal flexion causes shearing and damage to the backside of the spinal disc, and extension presses on – but is not the cause of – this wound on the disc. This is why extension (harmlessly) hurts when you have been wounded by habitual, continuous flexion.
Fig. 2 – Extension hurts, but is the cure. Flexion feels better, but is the CAUSE!
People like to believe in what they see. But what we see, and the mechanism we theorize, should go hand in hand with clinical outcomes and at least a moderate amount of evidence. Don’t you agree? If they do not, should we keep looking for an answer that correlates with reality?
I hear a lot of talk about “neutral spine” all the time, and the therapist is often pointing to straight backs, claiming it to be in perfect neutrality. But, my friends, the spine isn’t straight; it has specific curvature. The point is that there is no consensus with regards to what neutral spine really is, nor what it looks like, nor how to measure it. It is based on popular misconceptions of “hyperlordosis” (even though the evidence doesn’t support that), and pain upon extension.
Once again, if you live in flexion, the disc ultimately perforates posteriorly, i.e the disc herniates backward. Flexion is causing this, not extension. But when we assume an extended pelvic posture, there will be imposed compression onto the wounded posterior region of the disc, causing pain. And often fear. However, with logic and reasoning we can understand why this pain occurs, why it’s not dangerous but rather irrelevant. Irrelevant because it is caused by continuous, habitual flexion, which we have now removed. And once again, the paradox is that flexion will make the pain go away as you remove pressure from the posteriorly wounded disc, but will ultimately cause exacerbation of the same injury. No wonder people are confused!
Yes, the mechanism of the cause and sensation of back pain is a paradox. We are thus required to use logic and thorough examinations rather than bias & emotions when treating these issues.
What does the common sense say?
I touched on some common sense above, but let’s carry on. There is more.
Virtually all lumbar disc herniations are protruding posteriorly, meaning that they are generally directed backward (Gerald L. Burke, «Backache: From occiput to coccyx»). Science has shown again and again that this occurrence is associated with spinal flexion, which is bending of the spine. Many experiments have shown that they can predict the disc hernia’s direction with relatively high accuracy, based on the compressive angles imposed on the subject.
If almost all disc herniations are protruding on the back-side , how can possibly extension be the cause? Extension would cause an anterior protrusion, as sometimes seen in the upper cervicals, where the joint is exposed to continuous habitual hyperextension. This is rarely, if ever, seen in the lumbosacral region.
Furthermore, almost all disc herniations are occurring in the two low-most segments of the lumbar spine, between the L4-L5, and the L5-S1 vertebrae (95% – Moore et al., 2007). Because it is occurring so close to the pelvis, and not further up in the lumbar levels, it’s a safe bet that the pelvic alignment is the most important factor contributing to these injuries. But, because the herniations are directed backwards, this can impossibly mean that pelvic extension is causing it. It must be pelvic flexion; a lack of sacral extension. And, supporting this notion, we also see atrophy (degeneration) of the spinal extensor muscles in the patients with chronic lower back pain.
Coupled pelvic and hip, flexion and extension have a key role in establishing lordosis and kyphosis in the lower spine. Because fascial, ligamentous and muscular tissue span (non)-adjacent vertebrae and sacrum, movement between sacrum and adjacent vertebrae, or movement resulting in external pelvic (tilt) motion, can affect each other. Considerable forces are exerted in the area of the caudal intervertebral discs. – (Vleeming & Stoeckart, 2007)
Is it just a coincidence that 95+% of lumbar disc herniations are protruding posteriorly? Is it another coincidence that the two low-most levels, the ones that are most affected by pelvic position, are by far the most prevalently affected levels of injury? Is it a coincidence that we see muscular atrophy in the muscles that cause lumbosacral extension in chronic LBP-sufferers? I don’t even have to answer that.
Furthermore, and a slight digression with regards to the excessive curvature – the hinge – in the thoracolumbar junction. Is it dangerous? Well, it’s probably not optimal, but research has shown that only 0-4% of disc injuries occur in the thoracic spine (Moore et al., 2007). Personally, I am not that worried about extension, but I do tell my patients to stop hinging! Especially at the upper cervical levels, but also by not allowing the thorax to hang behind the pelvis.
What does the research show?
I’ve touched on this already, but let me back up what I just said. You see, the cause of lower back pain, it all points to lumbosacral flexion as the root problem, NOT to hyperlordosis (read my study, Larsen 2018a). In other words, nothing validates the notion of anterior pelvic tilt being the main contributor and cause of common lower back pain, as far as I can see.
The evidence shows that flexion causes posteriorly directed disc herniations, as mentioned above, which is highly prevalent in virtually all chronic sufferers. It shows atrophy of the muscles that contribute to lumbosacral extension, not flexion. It shows a prevalence of reduced lumbosacral curvature, i.e a flattened lower back and reduced extension in the sacrum.
I reiterate; the evidence, common sense, mechanics, nor results support “anterior pelvic tilt” as a common driver of lower back pain. It does, however, support the notion of habitual flexion as a prevalent cause of lower back pain. I strongly encourage you to stop allowing yourself to be deceived by the lordotic curvature often seen in the thoracolumbar junction, as it is rarely the cause of chronic lower back pain.
Direction and mechanism of disc injuries
Spine loads associated with lifting a 9-kg weight were estimated at three torso flexion angles (0 degrees, 22.5 degrees, and 45 degrees)… The degree of torso flexion had a dramatic impact on cycles to failure. Motion segments experiencing the 0 degrees torso flexion condition averaged 8,253 cycles to failure (+/-2,895), while the 22.5 degrees torso flexion angle averaged 3,257 (+/-4,443) cycles to failure, and motion segments at the 45 degrees torso flexion angle lasted only 263 cycles (+/-646), on average. Fatigue failure of spinal tissues can occur rapidly when the torso is fully flexed during occupational lifting tasks; however, many thousands of cycles can be tolerated in a neutral posture. – S. Gallagher et al., 2005
If the spine is exposed to greater levels of load, in the presence of repetitive flexion, it is more likely to experience vertebral fracture. However, if the spine is exposed to many cycles of low peak loads, injury is more likely to occur to the intervertebral disc than to the vertebral bone or endplate. – Parkinson & Callaghan, 2009
Repetitive flexion motion alone encouraged posterior or posterolateral nucleus tracking through the annulus. Marshall & McGill, 2010
Flexion places the anulus at risk by facilitating nuclear flow, limiting circumferential disruption while promoting radial rupture, and rendering the endplate/vertebra junction vulnerable to failure. – Veres et al., 2009
Fiber angles of longissimus thoracis and iliocostalis lumborum were documented with high resolution ultrasound at L3, with the spine in neutral curvature and fully flexed. Full lumbar flexion changes the line of action of these muscle compromising their role to support anterior shear forces on the spine – anterior shear forces have been recently documented to be highly related to the risk of reporting a back injury. – McGill et al., 2000
The direction of bending motion affected the tracking pattern of the nucleus through the annular fibres in a predictable pattern. Specifically, bending the motion segments at an angle of 30° to the left of the sagittal plane flexion axis biased the movement of the nucleus toward the posterior right side of the disc in 15 of the 16 specimens. Based on this animal model, shown to have similar biomechanical behaviour to humans, the direction that the nucleus tracks through the annular fibres appears to be dependent upon the direction of bending motion. – Aultman et al., 2004
The nuclear material was pressed through this cleft to create a fluid-filled, delaminated pocket between collagen fibers within a lamellar bundle in an anular layer. This was the first stage of damage and disc herniation production at a microscopic level. In full anular herniation, this process is repeated until the nucleus pulposus had tracked completely through the annulus. – Tampier et al., 2007
The study provides evidence that the BMI above 25 kg/m(2) increases the risk of lumbar disc degeneration. Overweight at young age seems to be particularly detrimental. – Liuke et al., 2005
Disc wall failure in healthy motion segments requires both flexion and an elevated rate of compression. Damage is initiated in the mid-then-outer annular fibers, this a likely consequence of the higher strain burden in these same fibers arising from endplate curvature – Wade et al., 2014
Although the compression forces on the L4-5 intervertebral disc were fairly insensitive to the interplay between the recruitment of muscle and ligament, the shear force was significantly higher with a greater degree of lumbar flexion. The risk of injury may be influenced more by the degree of lumbar flexion than the choice of stoop or squat technique. – Potvin et al., 1991
This meta-analysis demonstrates a strong relationship between LBP and decreased LLC, especially when compared to age-matched healthy controls. Among specific diseases, LBP by disc herniation or degeneration was shown to be substantially associated with the loss of LLC. – Chun, 2017
As pelvic incidence, sacral slope, and lumbar lordosis indicating the parameters of lumbosacral sagittal alignments get smaller, the numbers of lumbar disc degenerations and herniated intervertebral discs increase. When pelvic incidence is below 45.6 degrees, it is more likely for degenerative changes of lumbar disc to affect more than three segments. – Lee et al., 2012
We concluded that Lumbar lordotic Cobb’s angle and age can be predictors of the level of lumbar disc herniation. This did not differ among men and women. – Skaf et al., 2011
In the disc hernia group the patients had a relatively straight spine in the sagittal plane. The sacrum was more vertical, and the value of the lumbar lordosis was lower, as was the amplitude of the spinal curvatures, when compared with those of the healthy group. This results in a higher gravitational compressive force which may, in turn, lead to progressive degeneration of the discs. – Rajnics et al., 2002
The degree and risk of intervertebral disc degeneration and herniation increases in parallel to the decrease in sacral kyphosis and lumbar lordosis, and to the increase in sacral surface angle. A statistically significant difference with regard to the angles of lumbar lordosis, sacral kyphosis, and sacral table was determined between individuals with and without intervertebral disc degeneration. In addition, a statistically significant difference with regard to the angles of lumbar lordosis, sacral kyphosis, and sacral table was determined between individuals with and without intervertebral disc herniation – Ergün et al., 2010
Measurements of the curvature of the lumbar spine are useful in the investigations of low back pain. It is unclear whether the degree of lumbar lordosis, sacral inclination and lumbosacral angulation are the same for all normal adults. Sacral inclination appeared to be a more important determinant of the degree of lumbar lordosis. – Amonoo-Kuofi, 1992
In the patient group, significant reduction in the cross-section area of the psoas major was observed at the level and the site of the disc herniation. A significant correlation between cross-section area of the psoas major and ipsilateral continuous sciatica was found. – Dangaria et al., 1998
Data analysis compared the CSA (cross-section area) between the symptomatic and asymptomatic sides. There was a positive correlation between the percentage decrease in CSA of psoas on the affected side and with the rating of pain (rho = 0.608, P < 0.01), reported nerve root compression (rho = 0.812, P < 0.01), and the duration of symptoms (rho = 0.886, P < 0.01). There was an association between decrease in the CSA of multifidus and duration of symptoms. – Barker et al., 2004
At the L4 endplate level, cross-sectional areas of the multifidus and paravertebral muscles in the patient group were smaller than in the control group, and the difference was statistically significant (P = 0.001, P = 0.010, respectively). We did not find any significant difference between the patient and the control groups in gluteus maximus cross-sectional area. Chronic low back pain caused atrophy of the paraspinal, isolated multifidus, quadratus lumborum, psoas, and the gluteus maximus muscles to varying degrees, which was most prominent in the multifidus – Kamaz et al., 2007
In patients with long-standing unilateral back pain due to monosegmental degenerative disc disease, selective multifidus, erector spinae, quadratus lumborum and psoas atrophy develops on the symptomatic side. – Ploumis et al., 2011
Because training of the lumbar muscles is a commonly recommended intervention in low back pain (LBP), it is important to clarify whether lumbar muscle atrophy is related to LBP. Fat infiltration seems to be a late stage of muscular degeneration, and can be measured in a non-invasive manner using magnetic resonance imaging. The purpose of this study was to investigate if fat infiltration in the lumbar multifidus muscles (LMM) is associated with LBP in adults and adolescents. Fat infiltration was noted in 81% of the adults but only 14% of the adolescents. In the adults, severe fat infiltration was strongly associated with ever having had LBP – Kjaer et al., 2007
Recent advances in the understanding of the biomechanics of LBP have highlighted the importance of muscular stabilization of the «neutral zone» range of motion in the low back. The lumbar multifidus muscles (LMM) are important stabilizers of this neutral zone, and dysfunction in these muscles is strongly associated with LBP. The dysfunction is a result of pain inhibition from the spine, and it tends to continue even after the pain has resolved, likely contributing to the high recurrence rate of LBP. – Freeman et al., 2010
MF (multifidus) muscle atrophy was present in 80% of the patients with LBP. – Kader et al., 2000
Since body weight correlated significantly with L4 CSA this dimension was used as an ‘internal standard’ and further inter-individual comparisons were made using paraspinal: L4 and psoas: L4 (i.e. muscle to bone) CSA ratios. Muscle assessments made in this ‘relative’ fashion revealed significant reductions in paraspinal and psoas dimensions in patients with chronic compared to recent onset LBP. – Cooper et al., 1992
Disc degeneration was more frequently seen in the patients than in the healthy volunteers. The psoas and back muscles (erector spinae and multifidus) of the patients were smaller than those of the volunteers. Patients had also more fat deposits in the back muscles than controls. – Parkkola et al., 1993
Distinguishing between “anterior pelvic tilt” and swayback posture
As touched upon, one of the biggest misconceptions regarding excessive spinal curvature, is mistaking a thoracolumbar hinge for being excessive lumbar lordosis. In reality, what these patients do is tucking the pelvis and hanging back with the thorax, making it appear to be lumbar lordosis, when it is in fact low lumbar flexion(!) and thoracolumbar hyperextension (Evan Osar, 2012 – “Corrective exercise solutions to common hip and shoulder dysfunction“).
Notice how the butt is pointing downward, not up. The lumbosacral angle is reduced, and excessive anterior compression will be forced upon the discs in that area. The thorax is hanging posterior to the pelvis, and the hip joint is hyperextended. These are all epitome signs of swayback posture with posterior pelvic tilt. Correcting such a person’s pelvis further into flexion may cause serious consequences down the line.
I’ll repeat that. The indicators of swayback posture:
- Butt pointing down (pubic symphysis anterior to ASIS)
- Thorax posterior to the pelvis
- Hip hyperextended
- Knees fully extended
If you want to learn how I treat swayback posture, I’ve written about that in my lower back article.
“Anterior pelvic tilt”, a thoracic stability problem
If you analyze “real” examples of so-called anterior pelvic tilt closely, you’ll see that the excessive arching appearance is usually coming from the middle back, like with swayback posture. However, in opposition with the above, the person in figure x is lacking hip extension, the butt is pointing upward, and the thorax is anterior to the pelvis.
In the picture below, notice that the curvature of the lower lumbosacral area – the area where most injuries appear – is not looking abnormal at all. It’s nice and straight, slightly extended, as it should be. The lumbosacral spine isn’t overly arched at all, it is rather properly aligned. The upper lumbar, however, is very arched and the thorax is hinging backward. So, is the pelvis the problem, or is the thorax the problem? It is a thoracic stability problem.
Rarely does a case like this appear in my office, as most people are in swayback posture with posterior pelvic tilt. However, when they occur, it’s important to know that this is a thoracic and hip joint stability problem and not a pelvic alignment problem. When thoracic stability is reintroduced by no longer allowing the thorax to hinge backward, and being “long through the neck”, the hip flexor problem and lacking hip extension will usually resolve on its own. They tighten because the thoracic spine is not stabilized properly, as is evident from the thoracolumbar hinge. Malcorrecting such a patient by setting the pelvis further into flexion will often lead to LBP and injury down the line, in my experience. I’ve seen it several times. Thus, I reiterate; it is not a pelvic alignment problem.
Some claim that about 75% of the general patient group are in posterior tilt, and 25% in anterior tilt (Osar, 2012). Personally, I find that the great majority of people are in swayback posture with posterior pelvic tilt, in various degrees.
These are the signs of “true” hyperlordosis (of the TL-junction, not the pelvis!). It’s important to be able to distinguish between this postural strategy, and swayback posture with posterior pelvic tilt.
- Butt pointing up
- Thorax anterior to the pelvis
- Hip flexion
- Knees rarely locked
The problem with established measurements
There are several common approaches used to measure pelvic alignment, but because there’s no consensus with regards to what proper pelvic alignment really is, one may wonder what they are indeed based on. My view; popularity. Surely, they are not resolving chronic LBP.
Two common and popular measuring protocols are as following
- Measuring and aligning the PSIS and ASIS on a horizontal line
- Measuring lumbar lordosis by examining whether or not the T12 vertebrae is posterior to the sacral base.
There are several problems with these approaches. I’ll start with the first one.
Measuring and aligning the ASIS to PSIS horizontally, is not based on true natural spinal curvature. It is based on popularity and guessing. Aligning the PSIS and ASIS will cause a flattening of the lumbosacral lordosis. The pubic symphysis will be anterior to the ASIS (they should be vertically aligned, more on this soon), and the spinal extensors will disengage in posture. In the illustration above, we can see that the butt is pointing down and that the hip is hyperextended, even when the ASIS is slightly inferior to the PSIS!
If you use the above method, can you truthfully claim that it has ever permanently resolved LBP? We’ve all tried it, and it does not work. How could it, when based on false pretences?
Secondly, the T12-S1 measuring do not at all evaluate sacral angle. So, while it may be a somewhat reliable indicator of lumbar lordosis, it tells us absolutely nothing about the pelvic position and thus neither about the lumbosacral level, the L5-S1. Many hinge at the L5-S1 junction by tucking the pelvis in posture, greatly exposing the intervertebral disc to continuous, uneven malcompressive forces. This will not be detected by this protocol. Furthermore, it doesn’t reveal whether or not this lordosis is caused by swayback posture, or pelvic tilt. It is not a very useful measurement, in my opinion.
The image above shows a decent pelvic alignment. However, by measuring the PSIS to ASIS landmarks and correcting the pelvis in accordance with these, it’ll take the pelvis from a position of proper alignment and into habitual flexion, potentially creating many a malady. So many therapists do this, sadly.
How to measure and align the pelvis properly
To reliably assess and align the pelvis, we need to assess pelvic landmarks. Now, ASIS to PSIS are pelvic landmarks, but are not horizontal when the lower back and pelvis are in proper extension. The ASIS and pubic symphysis, however, are perfect landmarks for this measurement.
The pubic symphysis and ASIS should be vertically aligned (Osar, 2012). The pubic symphysis should never be anterior to the ASIS, but I’ll personally allow it to be somewhat posterior to it, under some circumstances. When these landmarks are aligned, the lumbosacral spinal erectors should be mildly palpably active in posture, and a nice and smooth arch of the lowmost spinal segments should be visible.
It does not tell us whether or not the sacrum is counternutated, but the sacroiliac joint is believed to move so little (Vleeming et al.,) that it shouldn’t matter significantly. Anyway, lumbosacral extension also promotes sacral nutation (meaning sacral extension in relation to the ilium), so it should all be covered.
Let me post Lee et al., one more time, as it’s very relevant to this topic.
As pelvic incidence, sacral slope, and lumbar lordosis indicating the parameters of lumbosacral sagittal alignments get smaller, the numbers of lumbar disc degenerations and herniated intervertebral discs increase. When pelvic incidence is below 45.6 degrees, it is more likely for degenerative changes of lumbar disc to affect more than three segments.
In practice, stand on the side of the patient and have them put their index finger at the pubic bone. But your finger at the ASIS and measure vertically whether or not the pubis is anterior or posterior to the ASIS. If it is anterior to it, simply pull their pelvis back and up, into extension, and re-measure. If it has been corrected, teach them to stay there. They’ll need to learn how to stand, walk, run, and train in that position. More on this in my lower back article, posted further up.
Most postural “experts” lack attention to detail
Let’s have a look at Figure 1 again, in case you wondered why I wrote that it was misrepresenting correct posture. Sadly, people like this is why the psychosocial proponents are rightfully mocking postural work. It is based completely on popular (mis)perception, not on real biomechanical understanding and functionality.
In the BAD model, we see good pelvic alignment, hyperlordotic thoracolumbar junction and a deficit of hip extension. The typical “real anterior pelvic tilt” that I wrote about earlier. The problem is, once again, that this is caused by thoracic instability and not the fallacious anterior pelvic tilt! This person would need to pull the ribcage gently down while maintaining lumbosacral tensegrity and positioning. The neck and shoulders need to gently elevate, being “long through the neck” (Osar, 2012).
In the “GOOD” model, we see posterior pelvic tilt (notice that the butt is pointing down, and the visible fold between the butt and the thigh – no, it’s NOT fat, it is the sign of dysfunction!), flattened lumbosacral lordosis and hyperextension of the hip joint. Further more, we see forward head and shoulder posture, and an overly extended mid-thoracic region. The pelvis needs to come back and up into extension and posterior from mid-foot, the ribcage needs to be pulled slightly down and forward, and the neck and shoulders must gently elevate. Again, the “long neck” cue is useful.
Detailed postural corrective strategies are not really within the scope of this article, but it is important to show why many of these postural “gurus” are making it hard for both patients and therapists alike to find valuable, accurate information. Please use common sense, and if something doesn’t work after years of trying, do something else. Postural work is not just “straightening out”, it is a detailed work that requires relatively intricate knowledge of biomechanical function and its assessments.
Changing pelvic posture is simple, but not easy
With the desire of instant gratification. Many patients, and therapists wish that some simple exercises and movement training will resolve lower back pain. I believe this to be false. I’ve tried it, and it does not work. In fact, my view is that exercises alone can never change posture. It can never change habits. The only way to change habits, is to be aware of proper structure, assuming it, and staying there. I.e changing our habits.
Now, I am not saying that exercises are irrelevant. But let’s be reasonable; will a birddog exercise for the multifidus or similar be able to reverse continuous, habitual tucking of the pelvis? Of course not. How could 2 minutes of spinal extensive exercises reverse the remaining 23 hours of pelvic tucking? Surely, we want our habits and our exercises to support – and not oppose – each other.
In practice, it is simple. Pull the pelvis back and up, so that the butt is pointing slightly upward and the spinal lumbosacral erectors are palpably active in posture. Hard work, following a simple protocol. I’ve written about this process in the article mentioned earlier, and thus won’t go into unnecessary detail about this here. The main point in this article, as you’ve probably seen already, is to raise awareness to what I consider to be the real factors and keys to understanding and resolving lower back pain.
Although I realize that this article is very bold, I must emphasize that the point here is to obliterate the notion of anterior pelvic tilt and its involvement in common LBP, to help patients improve their health, and definitely not to criticize therapists that have been deceived by this fallacious myth. I do whole heartedly believe that most therapists are doing their best, and want to help their patients. But with all the conflicting advice and data out there, this may be proving to be increasingly more difficult.
We live in a time where instant gratification is sought desperately. Pain and therapeutic approaches are no exception. Clearly, in my eyes, there is no sensible reason why we would treat anterior pelvic tilt as means for lower back pain, so why are these groundless ideas still being employed world wide?
Fig. 13 – Cognitive dissonance
I believe that the reason for this, is fear. Because as we know, there’s no lack of education nor experience out there; yet we have a great lack of results with regards to certain issues, such as chronic low back pain. We have lots of people with both 20 years of education and experience, who are not able to resolve these issues. So, it’s not an intelligence problem, it’s not a knowledge problem, and it’s not an experience problem. It is in my perception, a fear problem.
Fear of making the patient worse. Fear of pain. Fear of failure. Fear of being wrong. Fear of standing out from the crowd. Fear of leaving conformity. So much fear, in fact, that it blinds “us” to common sense of simple mechanics and evidence. Yes, as you’ve seen above, the mechanics are indeed simple.
The cause of chronic lower back pain is continuous, habitual lumbosacral flexion. The biggest obstacle we need to surpass to solve chronic lower back pain, is the current misleading belief system. It is naive to believe that psychosocial aspects are solely responsible for CLBP. It is ignorant to believe that lumbosacral extension, i.e anterior pelvic tilt, is responsible for the great prevalence of LBP, when considering the relevant evidence as well as the great lack of predictable results and improvement from employing current approaches.
I hope that in time, the importance of lumbopelvic extension will be embraced. I did not discover this principle myself, I learned it from the biomechanical pioneer Dr. Evan Osar (buy his book “Corrective exercise solution to common hip and shoulder dysfunction”, it is a game changer). And I must say that ever since applying these principles of increasing postural lumbosacral extension, my results when treating lower back maladies have skyrocketed.
I also like to be able to know why my work works. I don’t like mystical nonsense. The notion of increasing lumbopelvic extension makes sense, it’s supported by science and by biomechanical reasoning. It is also supported anecdotally by great in-clinic results treating LBP. At least 90% of my clients with LBP who really do an effort to do this change, resolve their back pain permanently. Again, a very bold claim. You may decide for yourself whether or not you think I am “full of it”, or if this may in fact be real. Remember, though, that there can only be one truth. And most issues do have a solution. Dare we look for it persistently? Dare we challenge the norm? Dare we relinquish conformity?
This article is probably the most controversial one I have written so far. I truly believe that the notion of “anterior pelvic tilt” is doing much more harm than good, and that it must be abolished. It is harming patients. It is confusing therapists. It is not based on common sense, nor research, nor biomechanical reasoning, and certainly not on clinical results.
Lastly, the conclusion by points.
- ATP is not causing lumbar disc herniations
- ATP is rarely, if ever, causing LBP
- ATP as primary cause of CLBP is not supported by the evidence
- Swayback posture is usually misinterpreted as ATP
- True anterior pelvic tilt is rare
- Malcorrecting ATP will hurt your patient
- The common measuring protocols for the pelvis do not work
- The right, and useful way to measure the pelvic landmarks are ASIS to pubic symphysis, vertically
- There is massive lack of consensus in all aspects of biomechanical interpretation