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Harrison 07-31-2009 08:56 PM

Gut Drives Bone Makeovers
I meant to post this a long time ago! For me, it begs the question: how critical is good intestinal health to proper bone growth? I think these researchers are on to something. It is said that much of the body’s immune function – and strength – comes from the GI tract. And now, this...

Gut Drives Bone Makeovers

Posted by Jennifer Evans

The signals that tell your skeleton to lay down new bone come from an unlikely source -- your gut, according to a study published today (Nov. 26) in Cell.

"This study revolutionizes how we think about the skeleton,"
Cliff Rosen, a bone biologist from Maine Medical Center Research Institute who was not involved in the research, told The Scientist.

"We, as bone [researchers], thought of the skeleton as functioning independent of everything else," Rosen said. This group "asked the question, 'could there be other regulators outside the skeleton that are regulating bone?' and found the answer to be 'yes.'"

The skeleton undergoes constant
remodeling and through the steady process of absorbing and laying down new bone, renews itself roughly every 10 years, Rosen said. That remodeling process is thrown off balance in certain bone diseases or simply with age, resulting in low bone mass, or osteoporosis.

Earlier studies in patients with two types of rare bone diseases that cause high and low bone density, respectively, identified a hormone called LDL-receptor related protein 5 (Lrp5) as a key player in bone remodeling. This finding sparked enthusiasm among bone researchers hungry to identify a drug that could repair bone damage, Columbia University molecular geneticist Patricia Ducy, coauthor on the Cell study, told The Scientist. The majority of drugs on the market arrest bone loss, but fail to promote bone repair, she said.

Gerard Karsenty, a geneticist also at Columbia and senior author on the Cell paper, was studying Lrp5 knockouts, which develop osteoporosis. Microarray studies of gene expression in bone cells identified a surprisingly high expression of tryptophan hydroxylase 1 (Tph1), an enzyme that regulates serotonin production in the gut, in knockouts compared to normal mice.

Researchers have long known the duodenum, a region of the small intestine, produces the majority of serotonin found in the body, but unlike serotonin's well-understood role in the brain, its role in the body was less clear. However, there have been
reports that some patients taking selective serotonin reuptake inhibitors (SSRI), which increase serotonin levels throughout the body, experience decreases in bone mass.

The microarray findings led researchers to take a closer look at the duodenum cells of their Lrp5-deficient mice, Ducy said, where they discovered Tph1 was expressed 15,000-times higher than levels seen in normal mice, suggesting the gut was somehow involved in controlling bone remodeling.

To confirm the link between the gut and bone formation, the researchers created transgenics with cell-specific Lrp5-deficiency in the duodenum and bone cells. When Lrp5 was absent in gut cells, circulating serotonin levels were 5- to 8-fold higher than in normal mice and bone mass decreased whereas mice with Lrp5 deficiency in bone cells remained normal.

Conversely, blocking Tph1 in the gut cells, but not bone cells, of Lrp5-deficient mice led to increased bone mass. Normal mice experience osteoporosis following menopause, but the Tph1 deficiency was enough to protect the knockouts from osteoporosis. In further gene deletion experiments, they identified the receptor on bone cells through which serotonin signals.

"Lrp5 and Tph1 are two partners in crime," Ducy said, with Lrp5 inhibiting expression of Tph1 and serotonin. "In the absence of Lrp5, you have more Tph1 and serotonin" expressed in the gut.

The group also obtained serum from patients with the high and low bone density diseases linked to Lrp5, Karsenty said. Patients with the low bone density disease had raised serotonin levels, and those with high bone mass disease had suppressed serotonin levels, suggesting "this is more than just a mouse study," he said.

Serotonin is "a schizophrenic molecule, working differently in the body depending on whether it's upstairs or downstairs," Ducy said. "What's important is serotonin does not cross blood-brain barrier," she added, making it an attractive drug target for treating osteoporosis -- inhibiting Tph1 in the body wouldn't affect serotonin levels in the brain.


Harrison 10-12-2009 08:04 PM

Coeliac bone loss link uncovered
Another data point that may explain why GI health is so important to "good bones." Personally, I don't believe our immune systems attack "our own bone tissue" specifically; that's a story for another day.

Coeliac bone loss link uncovered

People with coeliac disease may be more susceptible to osteoporosis because their own immune system attacks their bone tissue, a study suggests.

Osteoporosis is a known risk of coeliac disease and has been explained by a failure to absorb calcium or vitamin D.

But a study in the New England Journal of Medicine suggests coeliac patients produce antibodies which attack a key protein that maintains bone health.

They could easily be treated with drugs to prevent bone loss, researchers say.

It also explains why osteoporosis in those with the digestive disorder may not respond to calcium and vitamin D.

Coeliac disease is caused by a reaction to gluten, a protein found in wheat, barley, rye and oats which damage the small finger-like villi that line the small intestine and play a key role in digestion.

When damaged and inflamed, the villi are unable to absorb food properly, causing diarrhoea and malnutrition.

It affects one in 100 people, and of these a significant proportion may go on to develop osteoporosis - a disease of bone that leads to an increased risk of painful and disabling fractures.

Protein clue

Scientists at the University of Edinburgh say it may be a protein called osteoprotegerin which holds the key to the link between coeliac disease and osteoporosis.

Our traditional understanding of its cause has left some people with the condition with little hope that
their symptoms and quality of life will improve ” -- Sarah Sleet, Coeliac UK

In 20% of the coeliac patients tested, antibodies were produced which stopped this protein - crucial for maintaining bone strength - from working effectively.

Lead researcher Professor Stuart Ralston from the Institute of Genetics and Molecular Medicine, said: "This is a very exciting step forward. Not only have we discovered a new reason to explain why osteoporosis occurs in coeliac disease, but we have also found that it responds very well to drugs that prevent bone tissue removal.

"Testing for these antibodies could make a real and important difference to the lives of people with coeliac disease by alerting us to the risk of osteoporosis and helping us find the correct treatment for them."

Sarah Sleet, head of Coeliac UK said: "Osteoporosis is a damaging complication of coeliac disease and our traditional understanding of its cause has left some people with the condition with little hope that their symptoms and quality of life will improve.

"This new breakthrough in understanding and treatment will give renewed hope to our members struggling with their condition."

Dr Claire Bowring, medical policy officer with the National Osteoporosis Society said: "We already know that coeliac disease is a risk factor for osteoporosis and that early diagnosis and treatment of coeliac disease gives the best chance of improving bone density.

"A better understanding of the relationship between coeliac disease and osteoporosis will enable clinicians to manage both conditions more effectively.
"Although this research is at an early stage it is certainly interesting and we look forward to more extensive work to identify how prevalent this antibody is in people with coeliac disease."

Story from BBC NEWS:

Harrison 09-18-2015 09:16 PM

The Gut and Bone Growth
I am just refreshing this topic tonight. I am reviewing this subject doing prep for my next documentary.

A reminder that there is more and more evidence that pesticides and GMO foods are causing these problems! Eat organic and support your local farmer.

Harrison 01-21-2016 12:35 PM

Scurvy of the Bone
Osteoporosis Is Scurvy of the Bone, Not Calcium Deficiency

“…in my opinion, a more constructive supplementation regimen could include Vitamin C, Vitamin K2, vitamin D3( in winter months, sun in summer) and boron, silica and magnesium. These are all far more important to preventing fracture and keeping bone healthy than calcium…”

Fathub 01-21-2016 05:58 PM

I guess since I gotta go for a bone density scan (was -2.8) in Bogen.....I should be on Vitamin C, Vitamin K2, vitamin D3( in winter months, sun in summer) and boron, silica and magnesium......
Richard does anyone (reputable) supply a supplement with those components?

Harrison 01-31-2016 09:29 PM


I am sure it should be easy to find. I am slowly changing my mind about supplementation, even though I still supplement several times weekly with enzymes and fatty acids.

I recommend you juice 2 or 3 times weekly, instead of supplementing. Now I know I am mixing apples with oranges (punny), but food-based, whole plant nutrition is way better to help your body repair itself. And go organic!

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