New goals for Podiatric Biomechanics

Dave I think low stress zone is a better term, since we can't say no stress. If you read the paper which Kevin and I published in JAPMA this month we actually describe this concept therein.

"Any abnormal movements or abnormal temporal movement patterns of the subtalar joint axis during dynamic function are likely to increase the mechanical stress on the tissues that limit subtalar joint motion, and this may, in turn, result in musculoskeletal pathology. Because the magnitude of stress in tissues that restrain a joint at the ends of its range of motion is increased when the joint approaches that end range of motion, the magnitude of tissue stress in these restraining structures will necessarily decrease when the joint is functioning in its midrange position. With this in mind, any treatment approach that tends to limit the extreme excursions of the subtalar joint rotational position and the subtalar joint axis spatial location, and that attempts to normalise their temporal movement patterns, should be capable of reducing tissue stress around the joint, thus improving symptoms caused by increased magnitudes of tissue stress."

Spooner S.K., Kirby K.A.: The subtalar joint axis locator. JAPMA Vol 96, No.3 May/June 20006 p.212-219

Although we were talking about the STJ here, clearly the concept is applicable to all synovial joints.

Thanks for you input Dave.

 

Simon

Totally agree!

What about this though, Sound bites are not literally translated. So 'A stress free life' tends to mean free of stress that causes us distress and grief.
In the same way the 'stress free zone ' can mean the zone where we are free of pathological stress. I really think this is a term that could replace the 'Neutral position' as the biomechanical objective which, is still foremost in most podiatrists phsyce when considering how to reduce pathology.
If you and Kevin (as you are both sticklers for accuracy, fair play!) prefer you could modify this to the PSF Zone - Pathological Stress Free Zone.

Just a thought. (Hey I'm off to my stress free zone now, the Judo Club)

Cheers Dave

 

Gosh, you're making my head hurt with all those big words, Simon and Kevin. It was sure a lot easier when I thought that orthotics worked by making the subtalar joint function in the neutral position!!!

 

Hi all,

On low stress zone of joints. Should the knee function in the middle of its range of motion? When the knee is in the middle of its range of motion, weight bearing, there must be a significant amount of stress on the joint because the tension required in the quadriceps tendon to hold the joint in this position. Perhaps position of the joint is not that important for explaining stress on a joint. In the STJ you can have injury from being pronated to the end of range of motion (Sinus Tarsi syndrome) and you can be injured with too much supination of the STJ (ankle sprains) You can function with sinus tarsi syndrome, but it is very difficult to function with a severely sprained ankle. Perhaps, this is the reason for the vast majority of people functioning near maximal pronation and very few people function around neutral position.

On why Mert Root thought the foot should function around neutral position. (It may have been John Weed who wrote this) One of them theorized that neutral was a position of stability. Here is an explanation of the theory. Body weight is applied from above through the talus to the calcaneus. Ground reactive force acts upward on the calcaneus. When ground reactive force is directly in line with body weight, (They are two different forces) this is a position of "stability", because these forces will not tend to cause the calcaneus to rotate relative to the talus. If the calcaneus were to evert a little bit, the position of ground reactive force, relative to the force from the talus would be offset and would create a force couple that would cause the calcaneus to evert. (They did not use the term force couple, but it is a force couple.) This is also where the notion that once the calcaneus everts out of neutral it will continue to evert until it reaches its end of range of motion.

Problems with this idea: This describes a very unstable position. Any external perturbation would make the STJ move either toward maximal supination or maximal pronation. Although the major that the above theory should be discarded is that it ignores the forefoot. This was the major flaw in Root et, al thinking is that they examined the rearfoot independent of the forefoot. (Forefoot varus, Rearfoot varus).

What determines whether the ground will attempt to move the STJ is the position of the center of pressure under the entire foot relative to the STJ axis. When I first started criticising Neutral position theory, people kept saying that I did not understand the thoery. I hope the above shows that I understand the theory and that the criticism of the theory is valid. I just wish that we could reach a point where my knowledge of the Root paradigm will just be of historical interest for people studying paradigm change rather than having to refute the continued use of the paradigm. Don't get me wrong. Root, Orien and Weed made some very valuable observations and contributions and all in all they advanced the field of podiatric biomechanics. We just have to take the good and discard the bad. The idea that the foot should function around neutral position should be discarded.

Cheers,

Eric

 

Kevin, Simon, Eric.

Eureka!! So thats it then, after a long debate, the definition we've (at least me anyway) been searching for the (Kirby Fuller Spooner) KFS Low stress Zone. A whole concept, encapsulated in a catch phrase, which is easily communicated and understandable on many levels.
Which can be expanded to accurately and reliably explain pathology and useful methods for treatment in all subjects, situations and activities.

Importantly, I think, it also lets go the idea of Neutral position as the goal but can still explain why using that technique can result in succesful treatment.

The reason I say Kirby Fuller Spooner, is that they have worked on research and presented papers which encompass all this ie STJ axis locator, SJT equilibriu and SALRE, Tissue stress theory. These three have pushed podiatry, kicking and screaming, into a new era of rational and reliable thinking, theory and practice in the field of applied clinical biomechanics.

Any seconders?

Cheers Dave Smith

 

In all seriousness, I am a stickler for good terminology since good terminology allows efficient and unambiguous communication to occur so that ideas and concepts can be transferred with minimum confusion and with maximum understanding and comprehension. If good terminology is created and used by those communicating ideas, then overall greater knowledge will be transferred from one individual to another.

Because of my desire for good terminology, I don't like either "low stress zone" or "no stress zone" as terminology to describe where the structures that make up a joint complex, such as the subtalar joint (STJ), may be at their least stress. I suspect that using a joint complex, rather than a specific structure, may be problematic, however it could still be useful.

For example, if the STJ is in neutral position, this may be a position of medium tensile stress in the talo-calcaneal interosseous ligament, may be a position of medium compression stress at the middle facet of the talo-calcaneal joint, and may be a position of lowest compression stress at the posterior facet of the talo-calcaneal joint. In other words, we must be very careful as to which specific anatomical structure of that joint we are talking about, what type of stress we are talking about (i.e. compression, tension, shearing), what type of activity we are talking about (i.e. weightbearing or non-weightbearing), before we jump to a conclusion as to whether a rotational position of a joint is a "low stress zone" or not.

Further, we must also realize that for a biological tissue to have no stress or too low of a stress over a period of time is also harmful to these tissues. Too little stress on muscles, tendons, ligaments, and bone will make them atrophy and negatively affect many of their mechanical characteristics. All of these negative internal structural effects that occur within these structural components of the body can be attributed to insufficient loading of the tissues over a period of time, such as the huge problems associated with prolonged immobilization or prolonged bedrest in the everyday person or with prolonged weightlessness in astronauts.

Therefore, instead of only considering the potential high-stress events that may cause traumatic or overuse injuries to the structural components of the foot and lower extremity by proposing terms such as "no stress zone" or "low stress zone", we should also consider the long term negative effects of having a joint in a "no stress" or "low stress" position. Because of the aforementioned reasons, I propose that we use a term such as "optimal stress zone", defined as follows:

Optimal stress zone: That range of rotational positions of a joint where the tissues which comprise the joint are subjected to stress levels that are not only low enough to best avoid tissue injury but also high enough to best promote long-term tissue health.

I also propose that in most individuals, the optimal stress zone for the subtalar joint is the rotational position from 3 degrees from the maximally pronated position to the neutral position.

 

Kevin

I like 'Optimal stress zone'.
I don't like to define the or confine the parameters of such a zone by stating that most will be in the range of 3dgs from max pronation-to neutral.
Two reasons.
Lets leave behind the term 'Neutral position' except as a position of reference.
Neutral position in ingrained in the minds of everyone who has attended podiatry schools and is a difficult concept to discard. To continually refer to it will only make it more difficult to let go of.
Perhaps we could refer to this position as the 'position of reference' such as we do for the saggital plane position of the ankle at 90 dgs to the shank or the knee position of reference is 180dgs of extention from the femur.

A person who has a genu valgum gait may be excessively supinated and have corresponding trauma to the lateral tissues. This may be relieved by posting the foot in a less supinated position but still inverted in relation to the position of reference. The defined optimal position may be a few degrees of pronation but to acheive this may be unreasonable in terms of the magnitude of posting required. So this persons undefined optimal stress zone would be a few degrees supinated.
Therefore the 'Optimal stress zone' should be left up to the to the clinician to decide on for each patient.

Cheers Dave

 

Not all individuals would have their "optimal stress zone" for the STJ from 3 degrees from maximally pronated to STJ neutral. However, in the thousands of feet I have examined and treated, I would say that this range of rotational positions of the STJ seems to be where the STJ has the least chance of occuring injury. It is rare to see a person who functions around a STJ supinated position that doesn't suffer inversion ankle sprains.

 

You're such a wordsmith Kirby. If I practice long and hard and stay up all night, will I see pigs too?

In all seriousness, this is a great definition, but I was so close to being immortilised for ever as the inventor of the low stress zone and then Prof. Kirby comes along and bursts that bubble. I suppose now everyone will call it the Kirby optimal stress zone or the Kirby OSZ, he's already got skives, what more does he want.... I just want some of that fame

 

What about Zone of optimal stress, then the acronym can be ZOOS. Spooner's Zoos, wow it sounds so good. Please, please, please say we can call it Zoos Uncle Kevin. Can we Uncle Kevin? Can we?

 

Simon:

Excellent idea for an improved acronym, Simon. To give it more appeal with the famous god of Greek mythology (and honoring therefore Tony Achilles' contributions), it should be pronounced as "Zeus" to rhyme with "noose" not "Zewz" to rhyme with "news".

Zone of Optimal Stress (ZOOS): That range of rotational positions of a joint where the tissues which comprise the joint are subjected to stress levels that are not only low enough to best avoid tissue injury but also high enough to best promote long-term tissue health.

 

Very good boys.

Alternatively:

ZOOS: Zone of Obfuscated Sh!t@: An undefined range of positions within a joint where nothing of much significance occurs.

 

Before making Simon Spooner happy. Could you explain us your definition from maximally pronated position and neutral position? and How do you evaluate these 3 degrees? (Do we return to perform degrees measurings?)

Regards,

 

Definitions:

Subtalar joint maximally pronated position: The rotational position of the subtalar joint (STJ) where no further pronation motion of the STJ is available.

Subtalar joint neutral position: The midrange rotational position of the STJ where there is approximately twice as much supination range of motion as pronation range of motion but which may be alternatively determined to be at different midrange rotational positions of the STJ depending on the determination method used by the examiner.

Three degrees is the approximate amount of eversion that the calcaneus should be able to rotate within the frontal plane during relaxed bipedal stance to reach the maximally pronated STJ position when the STJ is at the pronation limit of the zone of optimal stress (ZOOS).

BTW Javier, I have seen Dr. Spooner quite happy sometimes....he is second from the right with a few of us biomechanics types at the PFOLA conference in Boston 2004.

 

How about this?

Spooners, Kirby-Achilles Zone Of Optimum Stress

AKA Spooners KAZOOS.

Is that agreed then?

 

How do you measure it?

Regards,

 

With the maximum pronation test and a tractograph (i.e. goniometer).

 

Thank you Kevin, for your acknowledgement regarding the 'greek' input.
Pythagoras and Socrates would be happy to see their ancestors holding up their end!!!!

 

Am I ever grumpy? More to the point is Bartold really that small? He makes "Dan the man" look like a giant in that photo. Or am I having that perspective problem again?

Beautiful Day here in Devon

 

Maybe not grumpy.....just a little testy at times. Glad I never get that way.

That is quite a photo.....podiatrists/biomechanists from land of OZ, US, UK and Belgium all posing as if anxoiusly waiting for World Cup 2006. Sorry, Dr. Spooner, I know that your sport is rugby.

 

Hi Simon,
I only have low level genetics and dim memories...but I thought (apart from mutation) that "evolution" was about the change in frequency of allelles in a given population that were then displayed as phenotype...and that these shifts are driven by segements of a population failing to pass on genes by being removed before breeding by some sort of selection pressure...which apart from "drink driving" the human gene pool does not seem to have any more.
regards Phill

 

Phill,

Think of a condition that causes either a. premature death prior to breeding age or b. sterility.

Most human traits are polygenic. Now think what happens if one or more of the genes that codes for either a or b above, also codes for an aspect of foot morphology?

Here's a great and true expression I heard once:

"If you want to win the Olympic 100m final, you need to pick your parents."

Any chance of answering my questions now please Phill?

 

oK Simon....I did not claim evolution has ended....just asked you to explain your claim that the human foot is still evolving. My memories (dim as stated) come from the secondary and tertiary places I have attended. If my very simple understanding of frequency of allelles in the gene pool and the change in their frequency is wrong I'd be happy to have it explained in words of two syllables or less and then some other people reading might learn something too....I'm happy to state publicly that you must know more about everything than I do if that would help your style become a bit more educational and a little less obtuse. If you are trying to tell me that you don't know and that no one knows that's fine too.
regards Phill Carter

 

Phill,

You don't need to state publicly that I know anymore than anyone else. As I have repeatedly stated, I am not an expert on this. I do not wish to appear obtuse, but I have provided answers to your assertions. I have tried to avoid entering into a long, boring discussion of quantitative genetics theory on this biomechanics forum, but since you insist:

So Phill, what you are describing his basically Hardy-Weinberg equilibrium which states that in a large random-mating population with no selection, mutation or migration, the gene frequencies and the genotype frequencies are constant from one generation to the next; and, furtheremore there is a simple relationship between the gene frequencies and the genotype frequencies. Right?

Unfortunately, the assumptions stated above do not hold true to our case in point. The genetic properties of a population are influenced in the process of transmission of genes from one generation to the next by a number of agencies. These factors in themselves form whole chapters of contemporary textbooks on the subject, but i'll try to explain as briefly and as simply as I can:

Population size.
The genes passed from one generation to the next are a sample of the genes in the parent generation. Therefore the gene frequencies are subject to sampling variation between successive generations, and the smaller the number of parents the greater the sampling variation. This is less of a problem when dealing with large populations of individuals, but when dealing with isolated pockets such on small island groups we observe larger sampling variation.

Differences of fertility and viability.
The phenotypic effects of genes on fertility and viability cannot be ignored because these influence the genetic constitution of the succeeding generation. The different genotypes among the parents may have different fertilities, and if they do they will contribute unequally to the gametes out of which the next generation is formed. In this way the gene frequency may be changed in the transmission. Furthermore, the genotypes among the newly formed zygotes may have different survival rates, and so the gene frequencies in the new generation may be changed by the time the individuals are adult and themselves become parents. These processes are what we call selection.

Migration and mutation.
The gene frequencies in the population may also be changed by immigration of individuals from another population, and by gene mutation.

Mating system.
The genotypes in the progeny are determined by the union of the gametes in pairs to form zygotes, and the union of the gametes is influenced by the mating of the parents. So the genotype frequencies in the offspring generation are influenced by the genotypes of the pairs that mate in the parent generation. Random mating means that any individual has an equal chance of mating with any other individual in the population. Unfortunately humans do not mate randomly. If a population covers a large geographic area, individuals inhabiting the same locality are more likely to mate than individuals inhabiting different localities, and so the mated pairs tend to be related by ancestory.

I hope that this provides the answers you were looking for without being obtuse. If you wish to learn more about any of the above, I'll try and respond, but I really don't think this forum is the right place for this discussion.

 

Hi Simon,
Thank you for the very educational response, I think this still all kind of fits in with the over all concept of what I had said, it just redefines what constitutes selection pressures etc but I think it fails to indicate how you think what is going on now is altering the mix of what constitues the genes for human feet.....is this unable to be defined or understood at the moment....just looking for the basis of your claim that evolution of the human foot is still occurring...other than by mutation possibilities of course.
regards Phill

 

Phill,

I've explained the basis of this claim several times now. If you don't understand what I have written I'm sorry, but I'm struggling to simplify it any more. I don't understand why you can accept how mutation can influence this but fail to recognise the other concepts involved in the processes of genetic change in populations. Moreover, I'm struggling to understand how you can accept mutation, but then still call black white and white black?

So OK Phill, your right the only way the foot is evolving is by mutation, this is not true, but i'm tired, bored of this conversation and just found out that my father has been taken into hospital. So forgive if i don't respond to any more of this.

 

Phill,

Sorry for that somewhat grumpy response, but I'm sure you'll appreciate how a phone call in the middle of writing it telling me my father had been taken into hospital after long-term illness may have had a detrimental effect on my mood.

Perhaps Phill, I might be in a better position to respond if you could define for me what you think constitutes evolution? And how this process works?

Once again, sorry for the grumpy response.

 

Phill,

One further after thought. Perhaps you could explain to me why you think the processes I have described with exception of mutation don't contribute to evolution?

Many thanks.

 

Hi Simon,
Sorry to hear about your Dad. And thanks for your input...to clarify what I'm thinking...it's not that I think the human foot is not evolving...I just wanted to understand better why you think it is, I accept that the things you outlined will influence the frequency of allelles in the resulting gene pool and as a result of that will cause a shift in genotypes over time...I just wondered and still wonder what direct links if any you can make to the human foot from your theoretical understanding of these issues or if it is just theorising. I do believe as I said up front that "our" foot now lives well outside the environment in which it evolved and that it is being asked to last much longer than the previously typical usage life......do we have any concrete basis for thinking our foot is adapting to the changes in it's environment . I keep mentioning mutation as a kind of "special case" because even in closed gene pools of a static nature mutation could still theoretically occur and cause change, even when no selection pressures were at work.
regards Phill Carter

 

The difficulty in studying genetic change is in isolating the genetic components from the environmental components of the phenotype. So for example, it is obvious that shoe size is increasing with time, such that our feet today are as an average larger than in previous generations. Is the foot evolving to become larger? Or is it purely down to improved diets? Perhaps a combination of the two?

The best way to study heritability is using mz twins seperated at birth. Unfortunatley these are like gold dust. I am not aware of any large scale heritability studies which have focused on foot based phenotypes other than my own (Spooner S.K. Predictors of hallux valgus: A study of heritability. PhD Thesis, University of Leicester 1998) Even so I'm still not sure how you could design a study which would provide a "concrete basis for thinking the foot was adapting to changes in its environment". I guess you would need a number of mz's, seperated at birth, half of whom had grown up in the jungle and the other half in the city. I don't think you're going to find too many of them around.

However, several workers have written on the racial/ ethnic differences that exist in the foot. Perhaps these are an indicator of the foots adaptation? It is interesting that in my relatively limited exposure to black/ afro-carribean feet that there appears to be a propensity for (asymptomatic) pes planus. I don't think I've ever seen a black afro-carribean with a cavus foot???? If the "out of Africa" theory is correct then perhaps some of the differences observed between black African origin feet and white European origin feet are indicators of adaptation. I'm certain that other racial differences could also be ascribed to adaption.

I'm interested in your statement that:

Since previously you had written:

If you believe that foot is evolving as you stated, then the assertion that "our foot lives well outside the environment in which it evolved" by definition cannot ever be true.

Just playing with you on this last bit Phill, I know what your saying really.

 

BTW the biggest environmental influence on the foot is likely to be the shoe.

 

Possibly...
The following is from the literature review of my PhD Thesis:

Barnicott and Hardy (1955) used footprinting to measure the angle of 1st MPJ abduction in a barefooted Nigerian population. Comparisons were made with results obtained from age-matched Nigerian soldiers who wore army issue boots and a group of university students and nurses of mixed gender with clinically normal feet. They reported a statistically significant difference between the Nigerian females and European females, but no significant difference between the shod and unshod Nigerians (males and females).

The greater deviation of the hallux observed in the European females when compared to the European males was believed to be due to constrictive female footwear. The smaller difference between genders in the Nigerian population supported this conclusion. However, no details of the type of shoes worn by the females, or the length of time for which the army boots had been worn were provided. Since little differences existed in the results obtained from the shod and unshod Nigerian populations, racial factors may have been significant. No test of the methodologies repeatability wwas presented.

Sim-Fook and Hodgson (1958) concluded that the wearing of shoes led to the development of hallux valgus following their comparative study of 107 barefooted Chinese and 118 Chinese who wore either canvasslip on shoes or wooden soled sandals. results of clinical and radiological examinations revealed a 33% prevalence of hallux valgus among the shod and a prevalence of only 2% among the unshod. Interestingly, metatarsus primus varus, a component of the hallux valgus deformity, and a suspected aetiological factor in hallux valgus, was present in only 6% of the shod, as compared to 24% of the unshod. However, since no diagnostic criteria were presented for these deformities, the results of this study must be considered with caution.

Kilmartin and Wallace (1993) argued that the populations studied by Sim-Fook and Hodgson (1958) were poorly matched: the unshod population were selected from a fishing community, who used their feet to hold fishing lines taut, leaving their hands free to work. Clinical examination of this population revealed "a remarkable degree of prehensile strength" within the hallux. Kilmartin and Wallace (1993) postulated that this may be considered as a form of exercise therapy that could prevent the deformity. Indeed, Groiso (1992) demonstrated the beneficial effects of exercise therapy in the treatment of hallux valgus.

Shine (1965) studied the islanders of St. Helena of whom 1,400 went barefoot, and 1,606 wore shoes. A linear relationship between the prevalence of hallux valgus and the length of time for which shoes had been worn was reported. However, the effect of increasing age on the condition may have obscured these results if this effect is seperate from the effect of longterm shoe-wearing. The shod populations were all grouped together. Some of the subjects had been using shoes for more than 60 years while other had only been shod for one year. The authors present a diagnostic criteria for the condition. However, they did not test the assessment techniques' repeatability or validity.

Maclennan (1966) studied 1,256 barefooted subjects in New Guinea (665 males, 591 females). The auther reports a prevalence of hallux valgus of the order of 1% in males and 4% in females. Clearly this prevalence is lower than has commonly been reported for shod populations. However, shoe could have played no role in the development of the deformity within this population and cannot, therefore, explain the gender differences in the prevalence of hallux valgus within this population.

Meyer (1979) compared the foot skeletons of 50 unshod Pecos indians with 50 medieval Yogoslavian peasents who hard worn some type of leather footwear. Unshod and shod population displayed mean 1st MPJ angles of 6.5 degrees and 14 degrees respectively. The accuracy of these measurements made from skeletons is questionable. The relationship between the hallux and its metatarsal is dependent upon the supporting soft tissue structures that encompass the 1st MPJ. The decomposition of gthese structures, which must have occured, would clearly have influenced the observed bony relationships. Moreover, no influences of racial or social factors were considered. Furthermore, the small sample group cannot be considered as representative and so the general conclusions that can be drawn from this study are limited.

Gottshalk et al. (1981) reported that hallux valgus occured among both urban and rural, black, South African women, but with less frequency than in white women. All subjects were over fifty years old and shod. There was a significant difference between the black and white groups (p<0.01), but not between the two black groups. They concluded that hallux valgus was due not to the wearing of shoes, but to some basic abnormallity of the foot.

Much Cut:

Rao and Joseph (1992) compared arch height indices (AHI) in children who habitually wore shoes and children who had never worn footwear (1555 shod, 745 unshod). Static footprints were obtained using inked rubber mats. 154 children (6.7%) were diagnosed as flat-footed. A significantly higher prevalence of pes planus existed in children who wore shoes (8.6%) than among the unshod (2.8%) (p<0.001). This result supports the contentions of didia and Nyenwe (1988) who believed shoewearing influenced the development of the medial longitudinal arch. Interestingly, Rao and joseph (1992) also reported that 710 children displayed ligamentous laxity. The ratio of flat foot in children with ligamentous laxity was 14.4% compared with 3.35% in those who had no ligamentous laxity. The preponderance of flat foot also varied with the type of footwear worn. Rao and Joseph (1992) concluded that shoes which encased the toes were more detrimental to arch development than open-toed sandals or slippers and that the detrimental effects of closed-toe shoes were enhanced in the presence of ligamentous laxitiy....

 

Brain not engaged, this is not true, lots of work been done on club-foot. Sorry to mislead.

 

Too many postings from me already today- I guess this is what happens when you wake up at 5.30am on a Saturday morning- Sorry.

Reading back over my old PhD thesis has reminded me of something I failed to mention a couple of weeks ago in my discussion with david h on why his hard flat surface theory was flawed.

If you look at many of the studies comparing shod versus unshod populations they demonstrate differences in the prevalence of foot problems. In the majority of cases the populations being compared are inhabiting the same terrain. Thus the differences in prevalence of pathology cannot be ascribed to terrain alone, but to the major environmental influence on the foot that is footwear.

 

Thanks for that. Were you able to determine a ratio and for what conditions?

 

Yes, but ..... the non-shoe wearing population still do develop foot pathology (eg HAV) .... but its way less in prevalance... IMPLICATION: Footwear is a risk factor AND NOT a causal factor.

 

Craig,
You said:
"Yes, but ..... the non-shoe wearing population still do develop foot pathology (eg HAV) .... but its way less in prevalance... IMPLICATION: Footwear is a risk factor AND NOT a causal factor."

Which I go along with. I was asked by Kevin Kirby some while back in this thread if I thought that hard, flat surfaces were the only etiological factor in foot dysfunction and pathology, and I replied that other factors obviously must be taken into account.
Certainly footwear plays a part, as does ageing, repetitive motion or positioning (think tailors bunion), and systemic disease.

I haven't looked at the studies mentioned by Simon, so cannot really comment.
But I stand by my guns on the hard and flat surfaces being a causative factor in much of the foot pathology we see, and in particular musculoskeletal problems like metatarsalgia and plantar fasciitis.
Regards,
davidh

 

Agreed. Because hallux valgus is multifactorial so:

Hallux valgus= m X1 + X2 + ....Xn + C

As a simple additive linear model. The problem is we don't know that is simple linear and moreover, we don't know what all the independents are either.

Suffice to say HV certainly has a large genetic component, which in my study population at that time was greater than the environmentall component. Yielding heritability estimates of approx. 0.61 +/- 0.08 and 0.78 +/- 0.08 for males and females respectively.

Heres a nice poser for students to think about: what is the difference between a risk factor and a causative factor? If the shod indivduals in the studies had remained barefoot some of them would have still got the condition anyway, but given the greater prev. in the shod population, some of these if they had remained barefoot may not have developed the condition right? So in these individuals did the shoe-wearing cause the condition? If so is it not then a causative factor?

 

I think we have to get away from talking about causes and think of the mindset of "risk factors". Hard surfaces do not necessarily cause anything (most people who function on hard surfaces do not develop problems); footwear does not necessarily cause anything (most people who wear footwear do not get problems); pronated feet does not necessarily cause anything (look at all those people who pronate excessivley who do not get problems); etc etc .... what footwear, pronated feet, hard surfaces, etc do is increase the risk for problems .... being a "risk factor" and a "cause" are different things.

You never hear a cardiolgist talk about high LDL's causing heart disease --- they all say high LDL's increase the risk for heart disease (...substantially) ... why are we still stuck in the mindset of "causes" ... its epidemiology 101.

 

Too lazy, but if you read the snip from my lit review above you can calculate them for yourself.

I only looked at HV.