Good for you, Nicky!
My 1st wife had ridiculously "soft bones" and was in pain
for much of her last days.
The feeling of helplessness is overwhelming.

"Nicky" <ukc802466929@btconnect.com> a écrit ...

You may be too young for the effect to take hold. For those that have a
problem, the first article below shows a way out. The second citation
supports the notion that there is a problem with bone in diabetic women.

"OBJECTIVE—Alendronate sodium (ALN) increases bone mineral density (BMD)
in heterogeneous populations of postmenopausal women, but its effect is
unknown in women with type 2 diabetes. The objective of this project was
to compare changes in BMD during 3 years of ALN treatment versus placebo
in diabetic women.

RESEARCH DESIGN AND METHODS—We used data from the Fracture Intervention
Trial, a randomized blinded placebo-controlled trial conducted at 11
centers in which 6,458 women aged 54–81 years with a femoral neck BMD of
≤0.68 g/cm2 were randomly assigned to either placebo or 5 mg/day ALN for
2 years, followed by 10 mg/day for the remainder of the trial. BMD was
measured by dual-energy X-ray absorptiometry. Type 2 diabetes (n = 297)
was defined by self-report, use of insulin or other hypoglycemic agents,
or a random nonfasting glucose value ≥200 mg/dl.

RESULTS—In diabetic women, 3 years of ALN treatment was associated with
increased BMD at all sites studied, including 6.6% at the lumbar spine
and 2.4% at the hip, whereas women in the placebo group experienced a
decrease in BMD at all sites except the lumbar spine. The
safety/tolerability of ALN was similar to placebo, except for abdominal
pain, which was more likely in the ALN group.

CONCLUSIONS—ALN increased BMD relative to placebo in older women with
type 2 diabetes and was generally well tolerated as a treatment for
osteoporosis. Increases in BMD with ALN therapy compared with placebo
were similar between women with and without diabetes.

Abbreviations: ALN, alendronate sodium • BMD, bone mineral density •
BSAP, bone-specific alkaline phosphatase • CTx, COOH-terminal
telopeptide of type I collagen • FIT, Fracture Intervention Trial • NTx,
NH2-terminal propeptide of type I collagen" Source: Effect of
Alendronate on Bone Mineral Density and Biochemical Markers of Bone
Turnover in Type 2 Diabetic Women -
http://care.diabetesjournals.org/cgi/content/full/27/7/1547

"Objective: The objective of the study was to determine the risk of
fracture in postmenopausal women with type 2 diabetes and determine
whether risk varies by fracture site, ethnicity, and baseline bone density.

Design, Setting, and Participants: Women with clinically diagnosed type
2 diabetes at baseline in the Women’s Health Initiative Observational
Cohort, a prospective study of postmenopausal women (n = 93,676), were
compared with women without diagnosed diabetes and risk of fracture
overall and at specific sites determined.

Main Outcome Measures: All fractures and specific sites separately
(hip/pelvis/upper leg; lower leg/ankle/knee; foot; upper
arm/shoulder/elbow; lower arm/wrist/hand; spine/tailbone) were measured.
Bone mineral density (BMD) in a subset also was measured.

Results: The overall risk of fracture after 7 yr of follow-up was higher
in women with diabetes at baseline after controlling for multiple risk
factors including frequency of falls [adjusted relative risk (RR) 1.20,
95% confidence interval (CI) 1.11–1.30]. In a subsample of women with
baseline BMD scores, women with diabetes had greater hip and spine BMD.
The elevated fracture risk was found at multiple sites (hip/pelvis/upper
leg; foot; spine/tailbone) among black women (RR 1.33, 95% CI 1.00–1.75)
and women with increased baseline bone density (RR 1.26, 95% CI 0.96–1.66).

Conclusion: Women with type 2 diabetes are at increased risk for
fractures. This risk is also seen among black and non-Hispanic white
women after adjustment for multiple risk factors including frequent
falls and increased BMD (in a subset)."
Risk of Fracture in Women with Type 2 Diabetes: the Women’s Health
Initiative Observational Study -
http://jcem.endojournals.org/cgi/content/abstract/91/9/3404

Frank

My haemotologist found that my hip bone was unusually hard
and dense when drilling through it for my BMB. For osteo
that's good news; for painless BMB's it ain't:-)


Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraltraveloz.blogspot.com/
latest: Mossman Gorge in the Daintree Rainforest
http://loraldiabetes.blogspot.com/
latest: Self-Testing and Type 2 Management

OK, so I have great bones and therefore diabetes. : (

Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.6%  BMI 25

It's amazing how many people, including even doctors who ought to know
better, don't realise that bones grow in response to use, and atrophy
in response to disuse, just as muscles and brains do. So do
tendons. It's just that muscles can grow and atrophy faster than
tendons, and tendons faster than bones. That's why if you start heavy
muscle building exercises after many many years of idleness you can
grow your muscles fast enough to rip your tendons.

Of course heavy people have stronger bones! It's because they're
heavier! Start carrying a heavy backpack around *all* the time (the
equivalent of being a stone or two overweight) and you'll develop
stronger bones too!

I despair of the ridiculously defective biological education "they"
must have received!

You have to remember that we're dealing with dynamic processes
here. The only static bones are dead bones. A living bone is in a
process of continual destruction by osteoclasts and reconstruction by
osteoblasts, and the size and strength it is a dynamic balancing act
between those two processes. This process is complicated by the fact
that the body uses the skeleton as a calcium bank which it very
frequently raids for a short term calcium loan. The
thyroid/parathyroid balancing act is (among other things) concerned
with that business, and some bone problems are due to short term
calcium loan repayment problems arising from thyroid/parathyroid
problems.

It often happens with dynamic processes under feedback control that
supplemental interventions have the opposite effect to what you would
expect from a static model. In fact that's often a good sign that the
static model is wrong and a dynamic control system is involved.

For example, let's suppose someone has a metabolic defect which
inhibits the usual repayment of short-term calcium loans from the
skeleton. That would cause the bones to get lighter and weaker than
they should be, a process that would continue until bone stress became
large enough to stimulate bone growth, bone replacement then happening
for another reason in a longer feedback cycle. This person would then
end up with lighter weaker bones than they should have, plus a higher
level of osteocalcin because the rate of bone turnover in the
osteocalcin-controlled cycle was more rapid than it should be.

In other words, where dynamic processes are involved, it's quite
possible to have high osteocalcin levels associated with smaller
weaker bones -- it could be a pathology of increased bone turnover
rate due to a defect in one of the faster calcium control cycles.

Exactly. Mucking about with hormone control systems is hazardous and
often has not only unpredictable results, but results which are the
oppposite of what you expect.

In the absence of further research on the topic I'm currently disposed
to favour the idea of bone strengthening exercise as a way of
improving osteocalcin levels. Bone strengthening exercise is exercise
which strains the bone, of which there are two kinds -- weight-bearing
exercise, and sudden shock impact such as in hitting things.

By the way, did you know that one of the things which pulls calcium
from the bones in a supposedly short-term loan is stress? Just be
careful not to let that worry you :-)

Go for bone exercise! Break a leg! :-)