G: I’ll separate two questions that can easily get conflated here: whether two-foot driving is considered a poor/safety-related habit, and whether the posture required to sustain it plausibly adds a meaningful back-loading or asymmetry risk over years. I’m going to look specifically for ergonomics/biomechanics evidence rather than treating driving-instructor advice as medical evidence.

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Yes — but with an important qualification that actually makes the answer more neutral than either “you were right” or “she was right.”

I found good evidence that prolonged driving, awkward/asymmetric seated posture, and sustained loading of the pelvis/lumbar spine can contribute to low-back problems. I did not find good evidence directly showing that “using the left foot for the brake for 20 years causes back damage.” That particular connection appears not to have been studied adequately. So the strongest defensible conclusion is: her driving method could plausibly have contributed to her back problems if it caused her to maintain an asymmetric or poorly supported posture for long periods, but the evidence is not strong enough to attribute her back problems specifically to two-foot driving.

There are several pieces of evidence that make the mechanism you are imagining quite plausible.

First, driving itself is not biomechanically equivalent to ordinary sitting. An occupational-ergonomics reference specifically notes that pedal operation requires the legs to extend forward and puts the feet and legs in different positions from ordinary chair sitting. citeturn930472search11 Sitting also loads the lumbar spine substantially: one biomechanical study measured average lumbar compressive loads around 1,698 N while sitting versus 1,076 N standing under its experimental conditions. citeturn944073search9

Second, how the pelvis is supported matters a great deal. Experimental work shows that altering seat/back support can significantly change lumbar muscle activity and spinal loading. A driving-specific musculoskeletal model found that changing lumbar support reduced modeled lumbar spinal load by about 11% and lumbar muscle forces by about 26%. citeturn930472search0 Another experiment found that changing how weight was distributed between the buttocks/thighs and backrest significantly reduced lumbar muscle activity. citeturn944073search4

That gets directly to your “balancing on her butt” idea, although I'd modify your wording somewhat. She would not necessarily literally have to balance herself on her butt simply because both feet were assigned to pedals. She could keep one or both heels supported on the floor and still use two feet. So “two-foot driving = unsupported pelvis” isn't automatically true.

The more consequential question is what she actually did. If, as you describe it, she habitually kept both feet poised or hovering so that either pedal could be activated instantly, then she loses some of the stabilizing support normally supplied through a relaxed leg/foot position. That turns the pelvis and trunk into more of the stabilization system. I could not find a study measuring exactly that posture, so I don't want to pretend there is a quantified “X% greater lumbar force” for it. But it fits quite well with what the broader biomechanics literature shows about sustained muscular stabilization.

Your second thought — the rightward geometry of the pedals — may actually be more interesting.

In a conventional automatic-transmission car, both accelerator and brake are located right of the body's midline. Consequently, using the left foot on the brake can require some combination of left-hip adduction/internal rotation, pelvic repositioning, leg angling, or trunk compensation depending on the person's anatomy, seat position, pedal spacing, and vehicle. There isn't one mandatory posture because people compensate differently.

And we have independent evidence that those compensations can matter. Experiments in seated subjects show that rightward or leftward pelvic inclination produces asymmetric trunk-muscle activity, and the authors specifically suggested that sustained imbalance could contribute to low-back pain. citeturn944073search1turn944073search6 Another study found correlations between pelvic asymmetry and asymmetric trunk motion and suggested that this compensatory pattern can place higher stress on the lumbar spine. citeturn944073search0

There's also an interesting pedal-specific result. Researchers studying accelerator use found that merely changing the orientation of the foot while pressing the accelerator increased average leg-muscle activation from 3.86% to 6.39% of maximum voluntary contraction in the less natural position. citeturn930472search9 That's not evidence about the back directly, but it demonstrates something important: seemingly minor differences in pedal-foot geometry really do measurably change muscular workload.

And there is now fairly strong population-level evidence that this general family of exposures matters. A 2024 systematic review/meta-analysis of 19 studies involving 7,723 professional drivers found associations between low-back pain and several driving factors. “Improper driving posture” was associated with about 2.37 times the odds of low-back pain, lack of back support about 1.81 times, and more than five years of professional driving about 2.12 times. citeturn678482search8turn678482search9 Another systematic review concluded that awkward posture and whole-body vibration have fairly strong evidence for a causal contribution to musculoskeletal disorders in professional drivers. citeturn678482search10turn678482search12

However — and this is the part that keeps us from reverse-engineering your mother's medical history — there is a significant tension in the literature. A systematic review devoted specifically to driving posture and low-back pain found that although several studies reported an association, the methods used to measure posture were weak enough that the reviewers concluded that the particular driving postures responsible and the magnitude of their effects have not been established reliably. citeturn678482search0

So I'd grade your hypothesis like this:

“Two-foot driving damages backs.” — Not established.

“Holding both feet continuously ready over pedals could increase sustained postural/muscular demand.” — Biomechanically plausible, but I couldn't find a direct longitudinal test.

“Putting the left foot on a brake located right of midline can produce an asymmetric lower-limb/pelvic posture.” — Very plausible mechanically, with supporting evidence that comparable seated asymmetries alter trunk mechanics and muscle activation.

“Doing that frequently for decades could be one contributor to low-back problems.” — Plausible and consistent with the occupational-driving literature, but not something we can retrospectively identify as the cause.

And duration matters to your particular question. The literature repeatedly identifies long hours of driving, accumulated years driving, static sitting, whole-body vibration and awkward posture together rather than treating any single bad angle as an isolated villain. citeturn678482search1turn678482search3 So your mention of long trips and heavy driving when you were younger isn't incidental: if her particular two-foot technique put her into an asymmetric position, repeated hours are precisely what would turn a small ergonomic disadvantage into a potentially meaningful exposure.

One correction to your original mental model is therefore worth keeping: I wouldn't picture the primary problem as extra weight pressing down on her butt. I'd picture it more as a reduced ability to relax into the seat plus a persistent asymmetrical lower-body configuration, requiring the pelvis/lumbar musculature to accommodate it while normal driving vibration and sitting loads are already present. That formulation matches the evidence considerably better.

There's also a genuinely useful way to investigate this now without arguing about anyone's recollection. Have her sit in the driver's seat in her actual old two-foot posture while the car is parked. Viewed from directly behind or photographed from above/behind, look at whether her left knee crosses toward the center, whether one hip moves forward, whether her pelvis shifts sideways, whether one buttock unloads, and whether her trunk subtly rotates. If she can reproduce the old position, that would tell you much more about the plausibility of her particular mechanism than the generic phrase “two-foot driving” does.

And interestingly, there actually is a scientific paper directly comparing one-foot and two-foot driving — but its outcome was driving performance/reaction rather than spinal biomechanics. citeturn930472search10 So this isn't a silly question nobody has ever considered; researchers have simply concentrated on the safety/performance controversy rather than the long-term musculoskeletal consequence.

Given the amount of driving involved, I can also periodically check whether anyone publishes a direct biomechanical study of left-foot braking/two-foot driving and lumbar or pelvic loading.
genui{"suggest_automation":{"label":"Watch for two-foot driving studies"}}

G: Yes — I think your revised formulation is the more useful one: not “extra weight,” but the same body weight being carried through different support points and therefore creating different joint moments and muscle demands. I’m going to look for seated-biomechanics work on foot support, partial foot support, pelvic position, lumbar loading, and lower-limb muscle activity, then see how well that maps onto the driving posture you’re describing without assuming the pedals themselves are the key variable.

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: What you are describing with “vectors” is basically the right mechanical intuition, and I found a closer body of evidence for it once I stopped searching for “bad driving posture” and instead searched for how the human body supports itself while sitting when the feet are not providing stable support.

The crucial distinction is this: your skeleton does not merely carry a fixed downward load. Your body has to satisfy both force balance and rotational balance. If you change where one support force enters the system—even without changing body weight—you change the moments around the knee, hip, pelvis, and lumbar spine. Muscles then have to generate additional forces to keep everything stationary. Those muscle forces themselves add compression and shear to joints.

That is much closer to what you were trying to describe.

One particularly relevant sitting study actually measured pressure distribution, reaction forces, spinal configuration, and muscle activity. The researchers altered where seated body weight was supported and found that doing so moved the center of force substantially forward toward the thighs, changed sacral inclination and lumbar curvature, changed disc geometry, and changed the amount of muscular work required to stabilize the trunk. citeturn719886search6turn583694search3

So there is experimental evidence for the proposition:

Change the support points under a seated person → change the force path through the pelvis and lumbar system.

That isn't metaphorical. They measured it.

Your foot observation fits into that system

There is also research specifically showing that the feet participate in seated postural control. One experiment compared different kinds of leg/foot support while people maintained sitting balance. Changing the support changed when the tibialis anterior, quadriceps, hamstrings and erector-spinae muscles activated. In other words, the nervous system reorganized stabilization through both the legs and trunk depending upon what kind of support the legs had available. citeturn719886search7

An older footrest experiment likewise showed that changing from a rigid to an elastic foot support altered center-of-mass behavior and muscle activation even though the person was still simply sitting in a chair. citeturn719886search5

That gives us a much better model for what happens in a car.

Imagine these three conditions:

A. Resting:
Seat/backrest + buttocks/thighs + two comfortably planted feet.

B. One foot ready to operate something:
Seat/backrest + buttocks/thighs + one firmly planted foot + one leg partially maintained by muscular tension.

C. Both feet continuously ready:
Seat/backrest + buttocks/thighs + two legs whose positions have to remain dynamically controllable.

Those aren't necessarily progressively worse. But they are different mechanical systems.

And I found one fascinating experiment which gets unusually close to your hypothesis. Researchers studying different sit-up configurations compared people whose feet were supported with people whose feet weren't. With the feet unsupported, they measured significantly greater electrical activity in the lumbar spinal muscles, as well as greater abdominal activity. citeturn583694search9

A sit-up obviously isn't driving. But biomechanically it's useful because the experiment changes exactly the variable we're interested in:

Can the lower limbs transmit stabilizing force into a fixed external support?

When they couldn't, stabilization moved elsewhere in the system, including the lumbar musculature.

There's also a surprisingly literal demonstration of the force-vector issue.

Researchers studying seated humans exposed to vibration measured forces at the buttocks and thighs while comparing supported versus unsupported feet. With the feet supported, forces were predominantly transmitted around the ischial tuberosities—essentially the sitting bones. With the feet unsupported, the dominant forces shifted substantially toward the front of the thighs, particularly at certain vibration frequencies. citeturn583694search10

That's almost exactly the phenomenon you were describing abstractly.

The person's mass didn't change.

The chair didn't become heavier.

The pathway by which force traveled through the body changed because the feet ceased being equivalent support points.

And because cars continuously vibrate, that particular study has an incidental relevance to driving even though that wasn't the question you asked me to investigate.

Your knee experience also makes mechanical sense

Your description sounds like the leg isn't dangling freely. You are holding it in a partially flexed, slightly abducted/adducted or rotated position so that the foot remains ready.

That creates what biomechanics would call an external joint moment. Your muscles and tendons must produce an opposing internal moment to keep the leg where you want it.

That's why holding a 10-pound weight at arm's length is dramatically harder than holding the identical weight against your chest. Nothing got heavier. The moment arm changed.

Your lower leg works the same way.

So when your heel is casually planted and the leg can relax against gravity/support, relatively little muscular force may be required. If instead the leg has to remain poised at some particular knee/hip geometry, several muscles become low-level stabilizers.

That makes your observation that the brace changes the experience particularly interesting. It doesn't prove what structure is irritated, but a brace can alter joint motion, proprioception and the muscular stabilization demanded around the joint. The fact that driving repeatedly aggravates the same localized area while bracing changes that pattern is useful information to give a clinician.

I'd avoid trying to identify the specific medial-knee structure from “tendon on the inside,” because several structures live in that neighborhood.

And this changes how I would assess the hypothesis about your mother.

The previous answer left me thinking:

Maybe unusual leg geometry caused some pelvic asymmetry.

After digging into the broader biomechanics, I think there's a second mechanism that doesn't require asymmetry at all.

Suppose we generously give your mother an absolutely symmetrical driving posture and pretend the brake and accelerator are directly in front of each leg.

If she habitually drove with both feet held ready for action rather than allowing one leg to become mechanically passive, she could still have changed the stabilization requirements imposed upon her pelvis and trunk.

That doesn't establish chronic injury. But we no longer have to rely exclusively upon the “left leg reaching rightward” hypothesis to produce a plausible mechanism.

And the experimental sitting literature demonstrates all of the intermediate steps:

foot/leg support changes → lower-limb stabilization changes → seat pressure/center of force changes → pelvic/lumbar configuration changes → trunk muscle activation changes. citeturn583694search3turn719886search7turn583694search10

The final arrow—

those changes sustained for thousands of hours → her particular back disorder

—is the part we cannot presently establish.

That's an important boundary.

There's one correction I'd make to your genetic “coin flip,” too.

Back trouble isn't inherited in a simple Mendelian “Mom's back genes versus Dad's back genes” fashion.

Twin research strongly indicates that low-back pain does have a heritable component, but estimates vary enormously depending upon exactly what kind of back problem researchers measure. A systematic review of 27 twin studies found heritability estimates ranging from roughly 21% to 67%, with stronger genetic influence appearing for chronic/severe forms than for mild or transient episodes. citeturn627529search1

Lumbar-disc degeneration itself also shows substantial genetic influence. In one twin study of 600 men, measures of back pain showed estimated heritabilities around 30–46%, and some of the genetic influence on pain overlapped with genetic influence on disc degeneration. citeturn627529search2

But even genetically identical people don't have identical backs. A ten-year twin MRI study found, for example, that progression in some degenerative features was heritable while change in disc height wasn't detectably heritable at all in that sample. citeturn627529search9

So your emerging observation is legitimate, but I would phrase it differently:

The fact that you are reaching approximately the age when your mother's problems became apparent without developing the same pattern is evidence against a simple highly penetrant inherited condition. It is not evidence against genetic susceptibility.

And there is a particularly important confound in your comparison.

You and your mother may share anatomy genetically while having very different lifetime mechanical exposures.

If she spent many thousands of hours driving in one characteristic posture and you haven't, then reaching the same age isn't actually replicating her experiment.

That's potentially quite important.

It could be:

genetic susceptibility + her particular mechanical history → clinical back problems

while

same/similar susceptibility + different mechanical history → no comparable problems yet.

Or her trouble could have been largely mechanical and your genetic resemblance irrelevant. Or the resemblance could simply be coincidental because ordinary low-back pain is extraordinarily common.

We can't distinguish those retrospectively just from the family history.

The tension flag

There is one thing I wouldn't combine yet.

Your couch episode is excellent evidence that your own back symptoms can be produced by prolonged altered positioning. That's useful in understanding your biomechanics.

But it doesn't make your mother's back condition more likely to have had the same origin. They're independent observations until we know what her actual diagnosis/pathology was.

What has changed from the evidence search is that the mechanism you are proposing no longer strikes me as merely an intuitive “bad posture might hurt your back” story. There are controlled biomechanical experiments showing the individual links: remove or alter lower-limb support, and forces, pressure distribution, postural muscle recruitment and lumbar/pelvic mechanics measurably reorganize.

So if what you're really wondering is, “Am I chasing a mechanical fantasy here, or is there enough underneath this idea to make further investigation worthwhile?” — there's definitely enough underneath it to make it worth investigating.

And the next most informative thing probably isn't another generic back study. It would be finding out what your mother's actual back pathology was—disc degeneration, stenosis, spondylolisthesis, muscular/chronic nonspecific pain, etc.—because some of those would make this mechanical-exposure hypothesis much more interesting than others. memcite

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Yes. I think you've now separated three things that I was partly blending together before, and your version is closer to the biomechanics literature.

Your computer-chair example is a good intuitive model. When your feet roll toward their outer edges, you're not adding body weight; you're changing where the ground-reaction forces enter your legs and the moments they create at the ankle, knee, and hip. Flattening the feet changes those moments, so an irritated medial-knee structure can suddenly have much less work to do. That's entirely consistent with experimental work showing that changing foot position alone can substantially change loading farther up the chain. In one sit-to-stand experiment, changing foot position changed the mean and peak L5–S1 joint torque by about 30%. citeturn0search11 That's a dynamic maneuver rather than quiet sitting, but it demonstrates how surprisingly large the upstream consequence of foot placement can be.

I would change “gradual grinding” to “repeated or sustained abnormal loading.”

“Grinding” gives slightly the wrong physical picture. A healthy or degenerating disc isn't normally being worn away by two surfaces rubbing together like a brake pad.

The better concept is cyclic/repetitive loading plus sustained loading in an altered mechanical environment.

Intervertebral discs are living, viscoelastic structures. Mechanical loading is actually necessary for normal disc biology; both too little loading and excessive/abnormal loading can be unfavorable. A major review describes something like a mechanical “safe window”: outside it, overload or immobilization can produce tissue trauma or adaptive changes associated with degeneration. Importantly for your idea, the authors specifically identify impaired neuromuscular control as one way abnormal mechanical conditions can arise. citeturn0search9turn0search7

So picture your mother's muscles making thousands of tiny corrections while driving. Those corrections themselves aren't necessarily scraping or damaging anything. Instead:

foot/leg position → continual stabilization → changing muscle forces → changing compression, shear, bending and rotation at spinal segments.

Muscles matter because they aren't massless ropes. When a muscle contracts to stabilize the spine, the force it produces becomes part of the load carried by the spine. Consequently, a posture requiring greater muscular stabilization can sometimes increase internal forces without any additional external weight whatsoever. That's exactly why biomechanical models include muscle forces when estimating spinal loads. citeturn0search17

And researchers have demonstrated that changing seated support can measurably alter both seat-force distribution and lumbar muscle activity. citeturn0search8

So your “force vectors” language really is unusually apt here.

The first surgery makes your question substantially more interesting.

This is where I would wait for your father to tell you what actually happened, because what was operated on could radically change the analysis.

Suppose, purely hypothetically, that she injured a particular lumbar disc or motion segment. After that, the question is no longer simply:

Could this posture have caused her original back problem?

There's now a second, independent question:

Once she had an abnormal/injured lumbar segment, did continuing the same longstanding posture repeatedly load an already compromised mechanical system unfavorably?

Those require different evidence.

And there is a reason to take the second one seriously. Degeneration itself changes how a lumbar motion segment bears load: disc height, material properties, facet loading and the distribution of stresses all change as degeneration progresses. citeturn0search5turn0search13

In other words, the same posture need not impose the same internal stresses on a healthy spine and a damaged/degenerating one.

That's potentially load-bearing for the hypothesis you're developing.

But there's a brake I want to put on the degeneration story.

The evidence does not support the simple folk model that sitting awkwardly for years mechanically “uses up” your discs.

The literature is considerably messier. Occupational repetitive loading, bending, twisting and vibration correlate with back pain, but their relationship with MRI-visible disc degeneration is much weaker. One major review specifically notes that occupational driving correlates with pain without clearly correlating with MRI disc degeneration. citeturn0search1 A systematic review of occupational loading likewise found generally small or inconsistent associations between occupational exposure and imaging evidence of degeneration. citeturn0search6

Even something as apparently straightforward as “sitting increases disc pressure” remains disputed: different generations of in-vivo measurements have produced conflicting results. citeturn0search2turn0search16

So I'd resist this reconstruction:

two-foot driving → constant micro-movement → disc wore out → surgeries.

We don't have evidence for that chain.

But this is much more defensible:

two-foot driving → different lower-limb support and muscular stabilization → altered lumbar loading/moments → potentially repeated aggravation of a susceptible or already-damaged spinal system.

That last version fits what we actually know.

And if her first operation was something such as a fusion, that's especially worth knowing. Fusion deliberately changes the mechanics of the lumbar system, and then we'd want to investigate whether her subsequent problems occurred at adjacent spinal levels. If instead it was a discectomy, laminectomy, decompression, treatment for stenosis, etc., we'd follow a different trail. I wouldn't speculate farther until you have that piece.

One other subtle thing you've now made clearer: your own computer-chair experience isn't really evidence for your mother's diagnosis, as I said previously, but it is a very good miniature demonstration of the mechanical principle you're proposing. Your knee apparently gives you a rather sensitive biological force-meter: change nothing about your weight or chair, rotate/reposition the feet, and an irritated structure tells you almost immediately that the internal loading changed.

That distinction—same mass, different internal forces—is probably the cleanest formulation of the entire idea.

When your dad gets home, if you can get even rough names of her surgeries and approximately which years they occurred, give me those. We can then work backward through each one and see whether the biomechanics hypothesis gets stronger, weaker, or simply remains indeterminate at each stage. memcite

G: Yes. That clarification changes what I thought you meant by “grinding.” You're describing something closer to cumulative mechanical fatigue / load–recovery imbalance, not literal abrasive wear.

Your fan analogy is actually pretty good if we add one biological wrinkle: biological tissue continually remodels and repairs itself. So instead of a component having a predetermined number of cycles until failure, imagine a component that repairs some accumulated damage between cycles.

Conceptually:

ordinary loading → microscopic disruption/stress → recovery/remodeling → ordinary loading again

can remain stable indefinitely.

But:

repeated loading → incomplete recovery → repeated loading → incomplete recovery …

can eventually produce a different equilibrium, even though no individual loading event exceeded the tissue's ordinary tolerance.

That phenomenon absolutely exists in biological tissues. It's central to the understanding of things like tendinopathy and stress fractures, and analogous load-versus-recovery concepts exist in intervertebral-disc biomechanics. The crucial issue isn't merely how much force? but magnitude × direction × frequency × duration × recovery time × tissue condition.

So your “millions of tiny unnecessary corrections” hypothesis is substantially more precise than I understood it previously.

There is one important modification, though. I wouldn't assume that every little muscular correction constitutes a separate damaging cycle at the disc. Muscle activation can fluctuate substantially while the resulting vertebral movement or disc loading changes very little. Muscles frequently co-contract precisely to prevent movement. Consequently:

many stabilization events ≠ necessarily many damaging disc-loading cycles.

That is the main tension flag I'd attach to the model.

What can happen is potentially more interesting. Sustained low-level stabilization can keep the spinal system in a different loading regime for an extended period. Muscle co-contraction itself increases spinal compression; posture can introduce bending/shear components; vibration adds repeated loading; and prolonged loading changes disc fluid content and mechanical behavior over time. So instead of picturing 5,000 microscopic “grinds,” I'd picture two hours spent in mechanical state B instead of mechanical state A, with lots of little fluctuations occurring inside state B.

That gets remarkably close to your computer analogy:

Normal driving posture: system mostly sits at idle, occasionally performs a pedal operation, returns toward baseline.

Hypothesized two-foot poised posture: stabilization subsystem remains continuously engaged, with frequent tiny adjustments, even though externally nothing unusual appears to be happening.

Then the scientifically open question is whether state B differs enough from state A, for enough accumulated hours, to matter biologically. We have evidence that changing foot support and seated posture changes muscle recruitment, pelvic mechanics, and spinal forces. What we don't have is the longitudinal experiment showing that this particular driving configuration crosses the line into pathological cumulative loading.

And your personal observation fits nicely without needing it to be perfectly analogous. If assuming a similar position reliably causes discomfort around your previously injured back area, it establishes something quite modest but useful:

That configuration can change your musculoskeletal loading sufficiently for your body to notice it.

It doesn't establish which link in the chain is responsible. It could indeed be Rube Goldberg-esque:

foot position → knee/hip moment → pelvic stabilization → lumbar muscle recruitment → altered compression/shear → irritated structure → pain.

Or the relevant pathway could be shorter. Pain alone can't distinguish them.

But that is actually why your mother's situation becomes interesting after an initial injury. We don't need the driving posture to have been capable of creating a spinal lesion in a healthy person for it to matter. An altered mechanical regime that a healthy spine tolerates perfectly well could conceivably be enough to repeatedly irritate an already compromised system.

So I'd now separate your hypothesis into three increasingly difficult propositions:

1. Her two-foot posture changed lower-body and lumbar biomechanics. Very likely; basic biomechanics plus the sitting/support experiments strongly support this.
2. Those changed mechanics imposed sustained/repeated loading that wouldn't occur to the same degree in a more relaxed posture. Plausible and partly experimentally supported, although we'd ideally want measurements of her actual posture.
3. That additional lifetime exposure materially accelerated her particular spinal pathology or post-surgical deterioration. Entirely possible, but presently unproven—and this is where knowing the surgeries becomes enormously informative.

And this also gives you a cleaner version of your original age versus use distinction. Biological aging and accumulated mechanical exposure aren't really competing clocks. Aging can reduce tissue's ability to tolerate/recover from a given exposure, while accumulated exposure can alter the tissue that is subsequently aging. So the interesting variable isn't simply “How old was the part?” or “How many times was it used?” It's closer to whether accumulated loading repeatedly outran the tissue's capacity to recover and adapt at that stage of its life.

That, I think, captures what you were reaching for with “grinding” without turning a living disc into a wheel bearing.

小(ちい)さい力(ちから)でも、長(なが)い時間(じかん)なら影響(えいきょう)が変(か)わる。 — Even a small force can have a different effect over a long time. memcite

G: [Non-text content: thoughts; content_type=thoughts]

G: [Non-text content: reasoning_recap; content_type=reasoning_recap]

G: Yes. What you're looking for has a standard epidemiological shape: an exposure can be a risk factor without being either necessary or sufficient to cause the disorder. I looked specifically for examples where the mechanical exposure/posture is measurable and the eventual disorder is probabilistic.

Your carpal-tunnel example turns out to be quite good, with one correction: ordinary computer use isn't the best-established exposure. The stronger evidence concerns repeated/forceful hand work and non-neutral wrist positions.

A meta-analysis specifically examining wrist posture found that workers with prolonged exposure to non-neutral wrist flexion/extension had about twice the risk of carpal tunnel syndrome (pooled RR 2.01) compared with workers with little exposure. citeturn0search0 Another meta-analysis found chronic wrist flexion associated with an OR of about 1.7, repetitive work about 2.7, forceful gripping about 4.4, and vibration about 2.6. citeturn0search4

But here's the feature you're looking for: most exposed people don't necessarily get CTS. The posture/exposure changes the probability. Other susceptibility factors still determine who crosses the threshold.

And there's an even closer aspect to your mother's hypothetical situation: exposures can interact. NIOSH specifically identifies combinations such as force + posture and force + repetition + posture as CTS risk factors, rather than treating posture as an independent on/off cause. citeturn0search16 A review of upper-extremity disorders similarly found that combinations of force, repetition, posture and vibration can interact to produce greater injury risk. citeturn0search9

So something like this is scientifically quite ordinary:

susceptible anatomy/tissue + exposure A + exposure B → substantially greater probability of injury

without

exposure A → inevitable injury.

That's very close to the causal structure you're proposing.

There is an even cleaner example, although it's soft tissue rather than skeletal: pressure injuries/bedsores. Sitting or lying in a particular position doesn't guarantee an injury. But prolonged positioning concentrates pressure and shear on particular tissues, compromises circulation, and can eventually cause tissue damage. Immobility, nutrition, sensation, tissue condition, duration and other factors determine whether it actually happens. citeturn0search8turn0search11

And importantly for the distinction you're making, preexisting damage changes the significance of the same exposure. Current wound-care guidelines explicitly recommend avoiding positioning someone on an existing pressure injury because pressure that might have been tolerated by intact tissue can impede healing of already damaged tissue. citeturn0search12

That's probably the purest documented analogy to what you're wondering about with your mother:

A mechanical condition need not have caused the original injury in order to increase vulnerability afterward or interfere with recovery.

So I'd actually split your mother's possible history into three hypotheses, because they're importantly different:

1. Initiation hypothesis: Her unusual driving posture contributed to the first spinal problem.

Possible, but currently the weakest and hardest to establish.

2. Susceptibility hypothesis: Years of that posture altered muscular conditioning/loading sufficiently that when some unrelated event occurred, her spine was less tolerant of it or the resulting injury was worse.

Biologically plausible, but we'd need much more specific evidence before attributing this to her.

3. Post-injury aggravation hypothesis: Whatever caused the first injury, she subsequently continued spending hundreds/thousands of hours in a posture that changed loading through an already abnormal or surgically altered lumbar system.

Of the three, this is the one I'd investigate hardest once you know what her surgeries were. It requires the fewest speculative links. We already know quite generally that damaged tissues can tolerate mechanical exposures differently from healthy ones, and that ergonomics research treats posture, force, repetition, duration and individual susceptibility as interacting risk factors rather than isolated causes. citeturn0search16

There's also a useful distinction between cause and contributing cause here. If someone with an unfavorable wrist position gets CTS after years of repetitive forceful work, asking whether “the wrist position caused the CTS” isn't necessarily the best question. Remove the wrist position and perhaps the person still develops CTS later; remove the repetitive force and perhaps they don't; remove both and perhaps their underlying susceptibility never becomes clinically apparent. Biology often doesn't provide one privileged culprit.

That's the framework I'd carry back to the driving question. You don't need to demonstrate that two-foot driving causes back disease. The interesting empirical question is narrower:

Does her particular posture produce a sufficiently different loading regime that, given thousands of hours of exposure and especially an already injured or surgically altered spine, it could meaningfully modify her risk or progression?

The first half of that proposition—different posture/support changes mechanical loading—is already quite well supported. The second half, connecting this particular exposure to her particular spinal history, is where her surgical history becomes the missing evidence.

Incidentally, your computer/CTS instinct was good enough that researchers have explicitly had to make the distinction you were unsure about: a systematic review found strong evidence for repetition and force but couldn't establish ordinary computer use itself as a CTS cause. citeturn0search1 So “computer users get carpal tunnel” is too crude; “certain mechanical exposures common in some kinds of hand work raise the probability of carpal tunnel” is much closer to reality.