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Research Articles and Papers on:

Bones, Skeletal, Osteoporosis

 

Long-term Risk of Incident Vertebral Fractures

Jane A. Cauley, DrPH; Marc C. Hochberg, MD, MPH; Li-Yung Lui, MA, MS; Lisa Palermo, MS; Kristine E. Ensrud, MD, MPH; Teresa A. Hillier, MD, MS; Michael C. Nevitt, PhD, MPH; Steven R. Cummings, MD

JAMA. 2007;298(23):2761-2767.

Taking a single bone mineral density (BMD) test could help women predict their risk of developing osteoporosis up to 15 years later.

“Vertebral fractures are the most common osteoporotic fracture. Women with low bone mineral density (BMD) and prevalent vertebral fractures have a greater risk of incident vertebral fractures over the short-term, but their absolute risk of vertebral fracture over the long-term is uncertain.”

As we know, we are constantly told that if we take too much thyroxine, we will get osteoporosis.  One of the most common things I tell people is to ask their doctor for a bone density test if they say this to them when the patient asks for an increase in their thyroxine.  Unfortunately, it is very rare for a doctor to do this and in one case, the patient got crossed off the list for asking!

The researchers of this study examined the absolute risk of incident vertebral fracture by BMD and prevalent vertebral fracture status over 15 years.
A total of 9704 white women were recruited at 4 US clinical centres and enrolled in the Study of Osteoporotic Fractures, a longitudinal cohort study. Of these, 2680 attended a clinic visit an average of 14.9 years after the start; average age of 68.8 years at entry and 83.8 years at follow-up.

Researchers took lateral radiographs of the thoracic and lumbar spines of the women and measured their BMD and body weight.
At the end of the study, they found that 18 per cent of women had experienced spinal fractures.

The researchers concluded that “Low BMD and prevalent vertebral fractures are independently related to new vertebral fractures over 15 years of follow-up. Women with a prevalent vertebral fracture have a substantially increased absolute risk of an incident fracture, especially if they have osteoporosis diagnosed by BMD.”


 

Endocrine Regulation of Energy Metabolism by the Skeleton

Na Kyung Lee, Hideaki Sowa, Eiichi Hinoi, Mathieu Ferron, Jong Deok Ahn, Cyrille Confavreux, Romain Dacquin, Patrick J. Mee, Marc D. McKee, Dae Young Jung, Zhiyou Zhang, Jason K. Kim, Franck Mauvais-Jarvis, Patricia Ducy, and Gerard Karsenty

An international team of scientists has discovered that bone plays an important role in controlling sugar metabolism, energy balance and weight, suggesting the skeleton is actually a member of the endocrine system. The finding may lead to new ways to prevent and treat type 2 diabetes.

The study which is published in the August 10th issue of the journal Cell, was carried out on laboratory mice by researchers in New York, Chicago and Hershey, Pennsylvania in the US, Seoul  in  Korea,  Lyon  in  France,  Cambridge  in the UK, and Montreal in Canada.
 
Most people imagine the skeleton to be an inert calcified structure that just stops us collapsing inside our skin.

Senior author of the paper, Dr Gerard Karsenty, chair of the department of Genetics and Development at Columbia University Medical Center, and Paul Marks Professor in the Basic Sciences, explained: "The discovery that our bones are responsible for regulating blood sugar in ways that were not       known before completely changes our understanding of the function   of   the  skeleton  and  uncovers  a  crucial  aspect  of energy metabolism." 
"These results uncover an important aspect of endocrinology that was unappreciated until now," he added.

Karsenty and colleagues had a hunch that bone might be involved in metabolism because leptin, a hormone released by fat cells, is also involved in the control of bone formation. So they decided to look for other molecules that might be communicating between bone forming cells and the endocrine system.

Using laboratory mice they discovered previously unknown metabolic processes where a hormone called osteocalcin that   is known to regulate mineralization and is released in bone forming cells known as osteoblasts, also regulates glucose (blood sugar) and the deposition of fat.

The scientists showed that an increase in osteocalcin effectively prevents the development of type 2 diabetes and obesity in the laboratory mice.  This is an exciting finding because it suggests increasing levels of osteocalcin in patients with type 2 diabetes could be a promising treatment route, especially since such patients tend to have low levels of the hormone.

Osteocalcin was thought only to be involved in bone development, but it seems it has a second crucial role in the endocrine system: it increases the secretion of insulin and it increases sensitivity to insulin. It also boosts production of pancreatic beta cells that make insulin (a much sought but currently unattainable path in new treatment research for type 2 diabetes) and reduces fat deposits by interacting with fat cells.

When Karsenty and colleagues analyzed mice that did not have osteocalcin, they found they had type 2 diabetes, increased fat deposits, a decrease in insulin, a decrease in adiponectin expression (a protein that regulates fat deposits), and a much lower count of beta cells in the pancreas.
 
It came as a complete surprise to the research team, to discover that endocrine processes in the pancreas and fat cells were also being controlled by signals from the skeleton.
 
Karsenty and colleagues concluded that:   "By revealing that the skeleton exerts an endocrine regulation of sugar homeostasis this study expands the biological importance of this organ and our understanding of energy metabolism."
Their next step is to look at the link between osteocalcin, blood sugar, type 2 diabetes and obesity in humans.

Reprinted with permission of www.medicalnewstoday.com


 

The Lancet. Vol. 340: 9-13, July 4, 1992.
Long-term Thyroxine Treatment and Bone Mineral Density - J.A. Franklin, J. Betteridge, J. Daykin, R. Holder, G.D. Oates, J.V. Parle, J. Lilley, D.A. Heath, M.C. Sheppard

In most cases, if you go to your GP and ask for your thyroxine replacement to be raised, you will be told, “No, No, you’ll get osteoporosis!”   In actual fact, I could not find any research that shows a risk of osteoporosis in thyroxine treatment, only in Graves Disease.

I was extremely pleased, therefore to find a study published in the Lancet on this very subject.  The researchers studied 49 patients who had all received a constant dose of thyroxine since thyroidectomy with most doses being sufficient to suppress TSH levels to below normal.  The result was that there was no significant difference in bone mineral density between patients and control.  The researchers suggested that, “thyroxine alone does not have a significant effect on bone mineral density and hence on risk of osteoporotic features…  Most other studies have included patients with preceding thyrotoxicosis or land-standing goitre.”  They felt that, “indeed, it is possible that preceding thyrotoxicosis or goitre are more important risk factors for osteoporosis than thyroxine treatment itself.”



American Journal of Clinical Nutrition, Vol. 74, No. 3, 343-347, September 2001

Carbonated beverages and urinary calcium excretion1,2,3 - Robert P Heaney and Karen Rafferty  - Creighton University Osteoporosis Research Center, Omaha.

Perhaps the docs that keep reducing our thyroxine dosages should worry more about our drinking habits if they want to prevent us getting osteoporosis.  It’s been known for some time that the drinking of fizzy drinks has been associated with increased fracture risk in observational studies. It was thought that one or more of the ingredients contained in the drinks increases urinary calcium.

Researchers, R P Heaney and K Rafferty assessed the short-term effects on urinary calcium excretion of fizzy drinks of various compositions.  20–40 year old women who drank fizzy drinks daily were studied.  2 carbonated drinks with caffeine and 2 without were tested.  Two contained phosphoric acid as the acidulant and 2 contained citric acid. The study included one neutral control (water) and one positive control (skim or chocolate milk).  The drinks were taken with a light breakfast after an overnight fast and no other foods were eaten until urine collection was complete.

Urinary calcium rose significantly with the milks and the 2 caffeine-containing beverages. It was concluded that the excess calcium associated with consumption of carbonated beverages is confined to caffeinated beverages. We should all, therefore, be aware that drinking both fizzy drinks and caffeinated drinks can cause calcium loss.