Francesca's post. Bone fractures and low weight

[Guest guest]

Hi All,

I caught the post from Francesca explaining that what she had said about

moderate CRON being the way to go was possibly unfortunately mistaken by

some of us. There has been much discussed of late on the other list since

than as well. To me it overall says that CRON needs to be extreme to be

become viable niche among the many other weight-loss and healthy eating

organizations. I agree with this.

I was alerted by:

/message/4475

From: " crdude35768 " <crdude35768@y...>

Date: Sat Sep 7, 2002 12:07 am

Subject: bone health.

To the, I think important, PDF-available paper below:

Int J Eat Disord 2002 Nov;32(3):301-8

Fractures in patients with anorexia nervosa, bulimia nervosa, and other

eating disorders-A nationwide register study.

Vestergaard P, Emborg C, Stoving RK, Hagen C, Mosekilde L, Brixen K.

“OBJECTIVE: To study fracture risk in patients with anorexia nervosa (AN),

bulimia nervosa (BN), or eating disorders not otherwise specified (EDNOS).

METHOD: Cohort study including all Danes diagnosed with AN (n = 2,149), BN

(n = 1,294), or EDNOS (n = 942) between 1977 and 1998. Each patient was

compared with three randomly drawn age- and gender-matched control subjects.

RESULTS: Fracture risk was increased in AN after diagnosis compared to

controls (incidence rate ratio: 1.98, 95% CI: 1.60-2.44), but not before

[1.22]. The increased fracture risk persisted more than 10 years after

diagnosis. A significant increase in fracture risk was found before

diagnosis in BN (1.31, 95% CI: 1.04-1.64), with a trend towards an increase

after diagnosis (1.44, 95% CI: 0.93-2.22). EDNOS patients had a significant

increase in fracture risk before (1.39, 95% CI: 1.06-1.81) and after

diagnosis (1.77, 95% CI: 1.25-2.51).

DISCUSSION: The increased fracture risk many years after diagnosis indicates

permanent skeletal damage.”

PMID: 12210644 [PubMed - in process]

Crdude said: “This study from Denmark suggests that eating disorders can

induce fairly permanent detrimental effects on skeletal structure. However,

the researchers were unable to rule out the possibility that abnormal

nutritional patterns that persisted due to incomplete treatment of the

eating disorders were generating the extra fractures”.

However, I think that “abnormal nutritional patterns” simply means continued

anorexia. Continued low weight is our patterns, I think.

The paper’s Table 2 is much more informative than the abstract would

suggest. Significant increased risk was seen before diagnosis in the femur

(incidence rate ratio 2.33) and femoral neck (3.49). After diagnosis, it

was significant in these (3.31, 7.17) as well as spine (3.49), upper arm

(2.86) and forearm (1.97).

Table 3 was important because if patients were </= 15 years old at

diagnosis, they had no significantly higher risk. If they were 16-25 years

old, risk was significant after diagnosis. If they were 26 years old, risks

were even higher (3.3 after diagnosis).

The PDF could not be copied and pasted from, unfortunately. It describes in

the discussion why younger patients may not be at so much risk – they

recover. In addition, older patients could have been low weight longer

before diagnosis. We are in CR for the long-term too, I think. Older first

recognized patients, maybe like older CRONies, cannot it is said do so. In

addition the normal aging-associated decline added to a low level bone

density ups the risk a lot.

Another to me very important point to note, was that they observed that the

bone density numbers determined by DEXA quite reliably predicted fractures.

Dean plays down the correlation among those who are light, I seem to recall.

They also said the loss of fat in the hips could predispose fractures. I

think the lack of muscle could be important too.

We are older, I think, also.

To me it spells out where low weight risks are distributed.

Looking back at my bone density scan data, my L2-L4 spine has increase from

the low in 1999 shortly before taking bisphosphonate in November to the one

last week, corrected for age and sex, by 19%. For the hip, it has increased

43%. It had gone down steadily before that. I feel that Saul

underestimates my response. My endocrinologist said at the time, as I said

earlier, that I made the greatest response to any of her other patients. My

latest 6% increase in the high-risk hip (femoral neck, as in the above

abstract) is above the level Saul says is typical of bisphosphonate-taking

patients.

When Warren ran into such problems, he boosted weight. Me, I remain like

many of the anorexia nervosa patients described above still at low weight.

is into CRON longer term also and has had no symptoms of bone loss

pathology to my recollection. His testosterone seems higher than mine and

Deans’s. Khurram’s testosterone at his young age is high too. is

older, though – almost my age of 55 versus his 54 years. Then there is

genetics, of course. My oldest aunt or uncle has my namesake and showed no

evidence of a problem in the bones at about 78 years as I recall it was from

eight years ago. There is nobody else in the family I am aware of with the

problem. They are or were mostly heavier than normal. But my frame was

always lower than most. I never had a problem putting my fingers around my

wrists. Now I easily do so for the narrow in my lower leg.

We are not CR rodents with their shorter life spans and walk erect. I am

unaware of monkey CR bone data.

Cheers, Al.

Alan Pater, Ph.D.; Faculty of Medicine; Memorial University; St. 's, NF

A1B 3V6 Canada; Tel. No.: (709) 777-6488; Fax No.: (709) 777-7010; email:

apater@...