BIOMECHANICS that determine safe sitting

 Here the bio-mechanical factors and their effects that may determine spinal pathology and lead to backache (Low Back Pain. LBP & further pathology) are discussed.

disc  flexion.

The final common pathway to IV Disc pathology at the joints of the lumbar-sacral junction (L3/4, L4/5, L5/S1) is reduction of the L/S joint angle resulting in posterior movement of the intervertebral disc (IVD) contents and can be seen, on pMRI scan (Smith F 2006).    This retropulsion of disc contents can progress to protrusion and extrusion (see ☛The intervertebral disc→).

Prolonged stretching of the ligaments can lead to laxity, is irreversible and can result in ‘Cumulative Trauma Disorder (CTD). ☛ Ligaments & CTD→


Backward pelvic tilt. Effect of upright sitting.

  • When sitting there is backward tilting (anat; forward rotation) of the pelvis, which reduces or reverses the protective wedge angle of the lower lumbar joints  ☛(See Lumbar & spinal support→).
    • Screen Shot 2016-02-21 at 14.47.24Flexion  The axial loading force comes to lie posterior to the pivot point at the Ischial Tuberosities. A backward turning movement results in backward tilt in of the pelvis.
    • The  backward pelvic  tilt flattens the lumbar lordosis and reduces the protective wedge angle of the lower intervertebral discs.  Resulting in  Posterior translation of the disc contents (NP),, see below→
  • The loss of low lumbar lordosis reduces or even reverses the protective wedge angle of the lower lumbar joints
  • Augmented



terminologic shift



Screen Shot 2016-01-03 at 18.09.442. Axial loading.

With  the currently advocated upright sitting posture there is an increase of compression on the L3 disc is x2.5 above that when lying supine (Nachemson).   This has been questioned by later work and determined by  Wilke (Wilke1999) as 0.10 MPa for standing and  sitting  0.55 MPa.  With  the currently advocated upright sitting posture there is an increase of spinal loading 500% above that of lying supine which is relevant to the 2T reclined mode.   For more detail see ☛ Loading→

  The intra-discal pressure is augmented In the flexed position, largely due to tension of the posterior ligaments,  while the anterior portion of the annulus fibrosis (AF) undergoes compression   In full flexion this can be as much as 100%.   The pressure gradient increases anteriorly,   tending to retropulsion of the nucleus pulposus (NP).

  • Axial compression + flexion. 

  •  Disc prolapse  occurred more frequently when the vertebral segments were wedged to simulate extreme forward bending of the spine (Adams and Hutton, 1982). In this position, the anterior portion of the annulus fibrosis undergoes compression while the posterior portion is under tensile stress. Over 40% of the cadaver discs tested by Adams and Hutton (1982) prolapsed when tested in this hyper flexed posture, and with an average of only 5,400 N of compression force applied. This finding shows that the disc is particularly susceptible to bending stresses. In a later study in which Adams and Hutton (1985) simulated repetitive loading of the disc, previously healthy discs failed at 3,800 N, again mostly through trabecular fractures of the vertebral bodies. Taken together, these studies show that the disc, especially the vertebral endplate, is susceptible to damage when loading is repetitive or when exposed to large compressive forces while in a severely flexed posture.
  • Screen Shot 2016-03-12 at 19.19.39Observed effects :-

Disc narrowing and anterior annular bulge.

End-plate bowing or rupture.

Increased intra-discal pressure

Posterior or poster-lateral prolapse of disc contents   

For remediation to avoid LBP these need to be addressed……    See ☛ Remediation→ 

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Screen Shot 2016-03-19 at 13.15.20pMRI. (Positional MRI)

Confirms and validates assumptions derived from the bio-mechanical studies (above) and clinical observation.  These pMRI scans (Smith FW,2007) show that the reclined mode ensures migration  of IVD nuclear material away from dangerous position near the back of the inter-vertebral joint which occurs with upright (90°) sitting.  It is difficult to refute this evidence.

The mid-upright mode is the worst possible position. How did it happen?   ☛ Why? Mandal explains→

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And is still recommended….Screen Shot 2016-01-14 at 18.19.39 Some of these diagrams suggest that iliac back support is incorporated.  This is a partial solution providing it is correctly configured. See ☛ Lumbar support→

Posterior elements

  • Stretching of the posterior elements (including ligaments) which can become permanent and allow instability. (☛Ligaments & CTD→) & (see ☛ ‘Liagament integrity & creep’)→ 
  • Screen Shot 2013-11-04 at 13.56.25The likely forces that must be resisted by the ilio-lumbar and the supraspinous ligament (shown in blue) when sitting in the usual lumbar support seat, which allows backward tilting of the pelvis, with a bodyweight 40kg (excluding the legs) can be calculated.  Simple moments about the centre of the L5 disk suggests a ligament tension of about 70 kg (700 Newtons).  This is probably a worst-case estimate.   (JD Gorman)

Constrained upright sitting

The adverse effects have been long and variously described    ☛Importance of MOVEMENT→.  There is a recognition that prolonged constrained static postures are uncomfortable and deleterious for both spinal and general health.   Recently there has been interest in continuous small amplitude movement for upright chairs, the chair re-aligning with the users centre of gravity,  and termed  ‘Dynamic Seating’.     Exercise is required to maintain this position. This provides proprioceptive feedback and frequent small amplitude pressure changes which may be comforting for short periods and helps multifidus muscle action. Rani  Lueder  gives a review account (Lueder R 2002) and the referenced evidence→is considerable.

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The pMRI evidence

An investigation using Whole-body Positional MRI (pMRI), by FW. Smith, Bashir W (2007) who found that the upright position, at 90°, caused disc contents to move the most, while the relaxed position (135°/45° reclined) caused disc contents to move the least. This confirms that the upright position is the worst for the back, while the relaxed position is the best.

The above effect has been shown incontrovertibly to occur by pMRI scans (Smith FE 2006).  From  which the following pictures are derived (arrows, etc, are added).  This confirms the bio-mechanical evidence.

Screen Shot 2016-02-12 at 15.16.18pMRI scan in reclined, relaxed, sitting mode shows the NP in a safe mid-position.  The hip angle is at 135°.    the NP is in the safe  mid-position.   This is practical and preferable and is advocated for the 2Tilt principle in the reclined mode.


Screen Shot 2016-02-12 at 15.18.49pMRI scan in an upright sitting mode shows the NP has translated posteriorly which can culminate in protrusion.   Hips are at an angle of 90° with the seat-pan horizontal.

This is visual confirmation of the bio-mechanical evidence.

Activation of   nociceptors (pain receptors) in the posterior layers of the disc (annulus fibrosis, AF) and adjoining structures (ligaments, dura mater and emerging nerve roots) produce back pain (LBP) and sciatica.

It can be said that as bipedalism and upright (orthograde) posture evolved, the hominin spine was developed in an active orthograde group with a lifespan of about 30 years.   ☛ ‘Paleo-anthropology’→.    After adopting a sedentary lifestyle a wrongly shaped seating artefacts were adopted in historically recent times.   A paradigm change  is now required if these adverse effects are to be corrected.  ☛Remediation→    ☛A Full Solution→

Bio-mechanical factors only have been considered.  The aetiology of LBP is much more complicated.

LBP. Cause (Aetiology).

The causes of LBP are multifactorial  and ill understood.    It is suggested (Adam et al.2002)  that  there is a need to integrate the evidence from genetics, biomechanics, biochemistry, cell biology and psychology to construct a comprehensive model.

Twin studies suggest that only 70% of the UK population is liable to LBP (Spector 1999). Other twin studies strongly emphasise the genetic factor in the aetiology of LBP  (Battie et al., 2002).   Genetics are not a cause of LBP but a risk factor acting through, possibly, spinal configuration or components of the disc composition.

Psycho-social factors, regarded as an important in the large increase in the last 20 years (Waddell 1996), is  more a response rather than a cause, resulting increases reporting.     Anecdotal evidence from patients with chronic LBP should not be ignored.  Although usually unaware of any causative incident, they are fully aware of what makes their symptoms better or worse.

The prevalence and incidence of LBP in populations that do not use Western style upright chairs but other ‘natural’ styles of sitting. which are culturally determined, is very low or nil, suggesting an adverse effect of the use of Western style upright chairs.    In Japan, this increases as elements of the population adopt Western chairs (Schlemper 1987).

Nutrition, environment and lifestyle may all play a part in the aetiology of LBP, but the only new factors that might account for the present epidemic is lack of exercise and a sedentary Western lifestyle.    Driving, office work, computers and TV,  the modern worker spends an increasing amount of time in a chair.

Epidemiological studies of  backache prevalence.

The literature on epidemiological evidence is extensive but, in relation to aetiology, confusing due to uncertainties and imprecision in describing reliably the condition that is under review.  Low back ‘trouble’ extends from LBP of psycho-genic origin to a midline IVD protrusion causing a corda equina syndrome, which is a surgical emergency.  Meta-analysis of systematic reviews, useful for evidence based therapeutics, have to be viewed with caution in extrapolating to clinical conditions. (Furfan et al 2001).  I have often seen wrong conclusions in my own field.

A study by the US Department of Health and Human Resources (NIOSH 1997) reviewed a number of factors and the general conclusions seem to suggest that the evidence was contradictory and confusing. There was an emphasis on non-physical psycho-social factors and heavy load handling.   Much of the research into the causation of spinal breakdown has concentrated on violent or inappropriate spinal usage afflicting manual workers today and hominins in prehistory (See Origins of lumbar vulnerability→).

In a Swedish review (Linton, van Tulder.2001) of controlled trials of preventive interventions for back pain problems only exercise gave evidence of relatively moderate significance perhaps suggesting that sitting has no influence on LBP.   The divergence of the  clinical and other evidence from that of some epidemiological studies suggests that the methodology of the latter should be reassessed rather than an immediate conclusion that seating plays no part in the symptomatology of LBP.

Invisibility is possibly due to  the universality of the upright sitting posture on chairs becoming  a part of the human condition in Western orientated populations, so that it fails to become apparent to recognition in systematic reviews.  This impacts on research, where musculo-skeletal funding is minuscule, in spite of the economic, which is about £13billion annually in the UK, and personal cost .

Next ☛Effects on the upright seated posture.