Probiotics can protect the skeletons of older women

Probiotics can protect the skeletons of older women

Among older women who received probiotics, bone loss was halved compared to women who received only a placebo. The research opens the door to a new way to prevent fractures among the elderly.

Anna G. Nilsson, Daniel Sundh, Fredrik Bäckhed, Mattias Lorentzon. Lactobacillus reuteri reduces bone loss in older women with low bone mineral density – a randomized, placebo-controlled, double-blind, clinical trial. Journal of Internal Medicine, 2018; DOI: 10.1111/joim.12805

How Good Fats Build Bone

How Good Fats Build Bone

How Good Fats Build Bone
Researchers discover how DHA helps stem cells become bone forming cells

ω-3 polyunsaturated fatty acids direct differentiation of the membrane phenotype in mesenchymal stem cells to potentiate osteogenesis/ Science Advances  08 Nov 2017: Vol. 3, no. 11, eaao1193 DOI:10.1126/sciadv.aao1193

Common osteoporosis drug slows formation of new bone

Contact: Jenni Glenn Gingery 301-941-0240 The Endocrine Society

Study results suggest combination treatments may be needed to stop bone loss, fuel growth

Chevy Chase, MD––Although the drug zoledronic acid slows bone loss in osteoporosis patients, it also boosts levels of a biomarker that stops bone formation, according to a recent study accepted for publication in The Endocrine Society’s Journal of Clinical Endocrinology & Metabolism (JCEM).

Osteoporosis weakens bones and increases the risk patients will suffer fractures. The findings suggest combination therapy may be a more effective approach to battling this common condition.

“The key to effectively treating osteoporosis lies in increasing bone mass,” said the study’s lead author, Antonino Catalano, MD, PhD, of the University of Messina in Italy. “Zoledronic acid halts bone loss, but it also signals the body to stop forming new bone mass. The drug may need to be combined with other treatments to add bone mass.”

The prospective intervention study followed the treatment of 40 postmenopausal women at an ambulatory care center. Half of the women received zoledronic acid, and half received a placebo. Levels of sclerostin – a biomarker that inhibits bone formation – increased among the participants who were treated with zoledronic acid.

“The data points to an opportunity to increase bone mass by combining zoledronic acid with a drug that suppresses the resulting sclerostin’s effect,” Catalano said. “An innovative combination therapy using zoledronic acid and selective antibodies to block the sclerostin could simultaneously stop bone loss and encourage new bone formation. This is an important avenue for researchers to explore as they develop new osteoporosis treatments.”



Other researchers working on the study include: N. Morabito, G. Basile, S. Brancatelli, D. Cucinotta and A. Lasco of the University of Messina.

The article, “Zoledronic Acid Acutely Increases Sclerostin Serum Levels in Women with Postmenopausal Osteoporosis,” appears in the May 2013 issue of JCEM.

Founded in 1916, The Endocrine Society is the world’s oldest, largest and most active organization devoted to research on hormones and the clinical practice of endocrinology.  Today, The Endocrine Society’s membership consists of over 16,000 scientists, physicians, educators, nurses and students in more than 100 countries. Society members represent all basic, applied and clinical interests in endocrinology. The Endocrine Society is based in Chevy Chase, Maryland. To learn more about the Society and the field of endocrinology, visit our site at Follow us on Twitter at!/EndoMedia.

Building healthy bones takes guts : Lactobacillus reuteri, significant increase in bone density after four weeks

Building healthy bones takes guts

Contact(s): Andy McGlashen Media Communications office: (517) 355-5158 cell: (517) 420-1908, Laura McCabe Physiology and Radiology office: (517) 884-5152

In what could be an early step toward new treatments for people with osteoporosis, scientists at Michigan State University report that a natural probiotic supplement can help male mice produce healthier bones.

Interestingly, the same can’t be said for female mice, the researchers report in the Journal of Cellular Physiology.

“We know that inflammation in the gut can cause bone loss, though it’s unclear exactly why,” said lead author Laura McCabe, a professor in MSU’s departments of Physiology and Radiology. “The neat thing we found is that a probiotic can enhance bone density.”

Probiotics are microorganisms that can help balance the immune system. For the study, the researchers fed the mice Lactobacillus reuteri, a probiotic known to reduce inflammation, a sometimes harmful effect of the body’s immune response to infection.

“Through food fermentation, we’ve been eating bacteria that we classify as probiotics for thousands of years,” said co-author Robert Britton, associate professor in the Department of Microbiology and Molecular Genetics. “There’s evidence that this bacterium as a species has co-evolved with humans. It’s indigenous to our intestinal tracts and is something that, if missing, might cause problems.”

In the study, the male mice showed a significant increase in bone density after four weeks of treatment. There was no such effect when the researchers repeated the experiment with female mice, an anomaly they’re now investigating.

By 2020, half of all Americans over 50 are expected to have low bone density or osteoporosis, according to the National Osteoporosis Foundation. About one in two women and one in four men over 50 will break a bone due to osteoporosis.

Drugs to prevent bone loss in osteoporosis patients are already in wide use, but over the long term they can disrupt the natural remodeling of bone tissue and could potentially have negative side effects that include unusual bone fractures and joint and muscle pain.

McCabe and Britton are quick to point out that this line of research is in its early stages and that results in mice don’t always translate to humans. But they’re hopeful the new study could point the way toward osteoporosis drugs that aren’t saddled with such side effects, especially for people who lose bone density from an early age because of another chronic condition.

“People tend to think of osteoporosis as just affecting postmenopausal women, but what they don’t realize is that it can occur with other conditions such as inflammatory bowel disease and Type 1 diabetes,” she said. “You don’t want to put your child on medications that reduce bone remodeling for the rest of their life, so something natural could be useful for long-term treatment of bone loss that begins at childhood.”

The research was supported by grants from the National Institutes of Health and MSU. Research assistants Regina Irwin and Laura Schaefer co-authored the paper

Emerging cancer drugs may drive bone tumors

February 12, 2013
By Julia Evangelou Strait

Chang Yang, MD, PhD


Investigational cancer drugs, IAP antagonists, may increase the risk of tumors spreading to bone. Tumors often cause bone loss, but IAP antagonist treatment accelerates the problem.

Cancer drugs should kill tumors, not encourage their spread. But new evidence suggests that an otherwise promising class of drugs may actually increase the risk of tumors spreading to bone, according to researchers at Washington University School of Medicine in St. Louis.

The drugs, IAP antagonists, block survival signals that many cancer cells rely on to stay alive. Working in mice, the investigators found that targeting the same protein that makes tumors vulnerable to death also overactivates cells called osteoclasts, which are responsible for tearing down bone.

“These investigational drugs are getting broad attention right now because they seem to be very effective against primary tumors,” says senior author Deborah V. Novack, MD, PhD, associate professor of medicine. “There is also excitement because until now, these drugs have not appeared to have major side effects.”

The research appears in the February issue of Cancer Discovery.

In light of the study, Novack urges oncologists to think about protecting bone in patients taking IAP antagonists, including patients with cancers that don’t typically spread to bone. Numerous IAP antagonists are in early clinical trials against breast, lung, pancreatic, ovarian, prostate, liver, skin and blood cancers.

“For many of these cancers, doctors are not watching bone,” Novack says. “Osteoporosis is not the biggest concern when treating cancer, but if they’re not doing bone scans, they may miss a cancer spreading to bone.”

To maintain healthy bone, osteoclasts work in tandem with cells that build new bone. But IAP antagonists overactivate osteoclasts, destroying bone that is not replaced. In mice, the researchers showed that the drug led to osteoporosis, creating an environment that encouraged tumor growth in degrading bone, even while simultaneously killing breast cancer cells elsewhere.

After showing that the problem with IAP antagonists is specific to bone, Novack and her colleagues tested long-established drugs called bisphosphonates that inhibit osteoclasts and are used to treat osteoporosis.

“We found that bisphosphonate treatment protected bone from the negative effects of these drugs,” Novack says. “While bisphosphonates are common for breast cancer patients, they’re not, for example, commonly given to lung cancer patients. But since IAP antagonists are now in lung cancer trials, we’re saying doctors may want to consider bisphosphonate treatment for lung cancer or other cancer patients receiving these drugs. Or at least closely monitor the bone status.”

IAP antagonists are now only available to patients enrolled in phase 1 or 2 clinical trials. While these kinds of trials examine the short-term safety and effectiveness of new drugs, the researchers say they may not catch bone metastasis.

“These trials do not necessarily look for long-term effects of the drugs,” says Chang Yang, MD, PhD, staff scientist and the paper’s first author. “If the cancer is going to metastasize to bone, it may take six months to two years to see that outcome. This may not be seen during the clinical trial.”

Numerous drug companies are developing IAP antagonists intended for many kinds of cancer, but only Genentech agreed to provide Novack and her colleagues with its drug, called BV6, to evaluate in the study. Because the investigators could not obtain other proprietary IAP antagonists, they also made two other similar drug compounds and found them to have the same detrimental effects on the bone.

And to further ensure that over-stimulated osteoclasts are the only culprit in the bone metastasis associated with these new drugs, they performed studies in mice that lack the ability to dial up the production of osteoclasts. Even when given IAP antagonists, these mice were protected from osteoporosis and osteoclast activation.

Together, Novack says the studies have demonstrated that these results are unlikely to be a quirk of a particular compound.

“The osteoporosis and spread of tumors we see in bone are unintended side effects of IAP antagonists, but they’re not off-target effects,” she says. “They’re based on the mechanism of action for the entire class of drugs.”

Yang C, Davis JL, Zeng R, Vora P, Su X, Collins LI, Vangveravong S, Mach RH, Piwnica-Worms D, Weilbaecher KN, Faccio R, Novack DV. Anticancer IAP inhibition increases bone metastasis via unexpected osteoclast activation. Cancer Discovery. February 2013.

This study was supported by the National Institutes of Health (NIH), grant number AR052705, with additional support from AR52921 and AR53628, CA100730, and the Barnes-Jewish Foundation. Histological and microCT analysis was supported in part by the Washington University Center for Musculoskeletal Research NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), grant number AR057235. The Molecular Imaging Center was supported by NIH grant P50 CA94056. Genentech, Inc. provided BV6.

Washington University School of Medicine’s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked sixth in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.

New task force report on bisphosphonate use and atypical femur fractures in osteoporosis patients: 94 percent (291) of patients had taken the drugs, most for more than five years

2010 study posted for filing

Contact: Sara Knoll 301-652-1558 Burness Communications

Expert panel calls for additional product labeling, international patient registry

Washington, DC, SEPTEMBER 14, 2010– A widely prescribed class of drugs is highly effective in reducing common bone fractures in people with osteoporosis, but an expert panel announced today that these same drugs – when used long term – may be related to unusual but serious fractures of the thigh bone.   In the most comprehensive scientific report to date on the topic, the task force reviewed 310 cases of “atypical femur fractures,” and found that 94 percent (291) of patients had taken the drugs, most for more than five years.   The task force members emphasized that atypical femur fractures represent less than one percent of hip and thigh fractures overall and therefore are very uncommon.

The task force was convened by the American Society of Bone and Mineral Research – the leading scientific organization on bone science – in the wake of growing concern about the connection between these drugs, called bisphosphonates, and unusual femur fractures.  The Food and Drug Administration (FDA) said in March that it would await the report before making recommendations about bisphosphonates and has received a copy of the task force’s report.  The report was published in the Journal of Bone and Mineral Research.

“For the vast majority of patients with osteoporosis, these drugs are an important weapon against fractures and their benefits far outweigh the risks of using them,” said task force co-chair and lead author Elizabeth Shane, M.D., of Columbia University.  “Most of the patients who experienced these atypical femur fractures had been taking bisphosphonates for more than five years.  However, we are concerned that there may be a relationship between these fractures and long-term bisphosphonate use and, although the risk is low, we want to make sure that people know about the warning signs,” she said.

The task force is calling for additional product labeling, better identification and tracking of patients experiencing these breaks, and more research to determine whether and how these drugs cause the serious but uncommon fractures.

The international, multi-disciplinary task force conducted an extensive review of both published and unpublished data and interviewed scientists at pharmaceutical companies that sell the drug and at the FDA, which maintains the MedWatch database that tracks reported side effects of approved medications.

The task force expressed concern about the lack of awareness of atypical femur fractures, their warning signs and their association with long-term use of bisphosphonates.   More than half of patients with atypical femur fractures reported groin or thigh pain for a period of weeks or months before fractures occurred, according to the report.  More than a quarter of patients who experienced atypical femur fractures in one leg experienced a fracture in the other leg as well.

Millions of people, primarily women, have been treated with bisphosphonates since they were approved in 1995.  Bisphosphonates include the drugs Aclasta, Actonel, Aredia, Bondronat, Boniva, Didronel, Fosamax, Fosavance, Reclast, Skelid, and Zometa.   Bone diseases, such as osteoporosis, drastically affect the way people function.  Individuals who suffer broken bones as a result of osteoporosis can suffer severe pain, loss of height and stooped posture that can affect breathing and digestion.  One in five patients who walked before their hip fracture needs long-term care afterward. And although the rate of hip fractures is two to three times higher in women, after one year, the death rate in men is nearly twice as high.

Among the task force recommendations:

  • Product labeling should be changed to alert health professionals and patients to the possibility of atypical femur fractures for patients on bisphosphonate therapy and the associated warning signs; cases should be reported to the FDA MedWatch program.
  • New diagnostic and procedural codes should be developed for atypical femur fractures to improve the quality of case reporting and enable better review of medical records.
  • An international registry of patients experiencing atypical femur fractures should be established to track cases and facilitate future research.

“We know that bisphosphonates prevent many, many common fractures.  For this reason, we want to emphasize that patients should not stop taking these drugs because they are afraid of the much more uncommon femur fractures.  They should talk to their health professionals about their concerns and should let them know if they experience any new groin or thigh pain.  Patients can also report any side effects of these medications to the FDA by phone or online,” Shane said.

“Health professionals should reserve bisphosphonates for patients with certain cancers, Paget’s disease of bone, and patients with osteoporosis who are at high risk of having a fracture. Drug labels should include information about this side effect.  Although the risks are very low, health professionals should know the warning signs of atypical femur fractures and regularly ask patients on these drugs about groin or thigh pain.  They also should assess annually whether this therapy is appropriate for each patient,” she added.


The task force report will be the topic of a session at the ASBMR 2010 Annual Meeting in Toronto on Saturday, October 16 and is available at

About the Task Force

A full list of task force members and their affiliations is listed below.  All task force members were required to disclose any potential conflicts of interest and their disclosures are published as part of the task force report. To ensure the objectivity of its findings, the task force included a physician and bioethicist with expertise in conflict issues affecting biomedical researchers and a scientist who does not work directly on osteoporosis or bisphosphonates or with pharmaceutical companies that make or market bisphosphonates.  Additionally, the report underwent a rigorous peer review process prior to its acceptance for publication by the Journal of Bone and Mineral Research.

About ASBMR and the Journal of Bone and Mineral Research

The ASBMR is a professional, scientific and medical society that brings together clinical and experimental scientists involved in the study of bone and mineral metabolism.  The Society has a hard-earned reputation for scientific integrity.  The majority of the Society’s revenue comes from membership dues, fees paid to attend the Society’s annual meeting and subscriptions to ASBMR publications.  Like many scientific, professional, and medical organizations, ASBMR also accepts grants from pharmaceutical companies, the federal government and other entities to support its mission.  To ensure that the Society adheres to the highest ethical practices ASBMR has an ethics committee, consults with experts in health care ethics and reviews its practices with regard to managing potential conflicts of interest.

The Journal of Bone and Mineral Research is the leading source worldwide for cutting-edge basic and clinical research in the hormones that regulate bone and mineral metabolism and the treatment of bone and mineral disorders.


Elizabeth Shane, Task Force Co-Chair, Columbia University

David Burr, Task Force Co-Chair, Indiana University School of Medicine

Bo Abrahamsen, Copenhagen University Hospital Gentofte

Robert A. Adler, McGuire Veteran’s Administration Medical Center

Thomas D. Brown (Reviewer Scientist), University of Iowa

Angela M. Cheung, University Health Network – University of Toronto

Felicia Cosman, Helen Hayes Hospital

Jeffrey R. Curtis, University of Alabama at Birmingham

Richard Dell, Kaiser Permanente Bellflower

David Dempster, Columbia University

Peter R. Ebeling, University of Melbourne

Thomas A. Einhorn, Boston Medical Center

Harry Genant, University of California at San Francisco

Piet Geusens, Maastricht University Medical Center, The Netherlands & University Hasselt, Belgium

Klaus Klaushofer, Hanusch Hospital – Ludwig Boltzmann Institute of Osteology

Kenneth Koval, Dartmouth-Hitchcock Medical Center

Joseph M. Lane, Hospital for Special Surgery

Fergus McKiernan, Marshfield Clinic

Ross McKinney (Ethicist), Duke

University School of Medicine

Alvin Ng, Singapore General Hospital

Jeri Nieves, Helen Hayes Hospital

Regis O’Keefe, University of Rochester Socrates Papapoulos, Leiden University Medical Center

Howe Tet Sen, Singapore General Hospital

Marjolein C.H. van der Meulen, Cornell University

Robert S. Weinstein, University of Arkansas for Medical Sciences

Michael Whyte, Shriners Hospital for Children

42nd Health Research Report 28 OCT 2008 – Reconstruction

Editors top five:

1. Biotech experts urge industry to work with researchers or risk federal action

2. Splenda may damage gut bacteria, boost weight gain: study

3. What the election means to the nutrition industry?


5. How drug companies covertly promote off-label drug use



In this issue:

1. Biotech experts urge industry to work with researchers or risk federal action

2. Fructose Sets Table For Weight Gain Without Warning

3. LEDs may help reduce skin wrinkles, researchers report.

4. 10 Things the Food Industry Doesn’t Want You to Know

5. Do cell phones increase brain cancer risk?

6. US suicide rate increasing

7. Splenda may damage gut bacteria, boost weight gain: study

8. How eating fruit and vegetables can improve cancer patients’ response to chemotherapy

9. Green tea may delay onset of type 1 diabetes

10. Rheumatoid arthritis rising among women


12. How drug companies covertly promote off-label drug use

13. How toxic environmental chemical DBT affects the immune system



16. Methylmercury warning

17. Grapes and grape extracts may lower cardiovascular disease risk, says review in Nutrition Research

18. What the election means to the nutrition industry?


Health Technology Research Synopsis

42nd Issue Date 28 OCT 2008

Compiled By Ralph Turchiano

Osteoporosis Drugs, Reduce Fracture Risk by ONLY 0.9% according to studies

Contact: Emma Dickinson 44-020-738-36529 BMJ-British Medical Journal

Value of drugs for pre-osteoporosis exaggerated

Drugs for pre-osteoporosis: Prevention or disease-mongering?

Public release date: 17-Jan-2008

A series of recent scientific publications have exaggerated the benefits and underplayed the harms of drugs to treat pre-osteoporosis or “osteopenia” potentially encouraging treatment in millions of low risk women, warn experts in this week’s BMJ.

The authors believe that this represents a classic case of disease-mongering: a risk factor being transformed into a medical disease in order to sell tests and drugs to relatively healthy people.

Osteopenia or “pre-osteoporosis” is said to affect around half of all older women and, in at least one country, drug companies have already begun to market their drugs to women with osteopenia, based on re-analyses of four osteoporosis drug trials.

But the authors of this week’s BMJ paper argue that this move raises serious questions about the benefit-risk ratio for low risk individuals, and about the costs of medicalising and potentially treating an enormous group of healthy people.

These reanalyses tend to exaggerate the benefits of drug therapy, they say. For example, the authors of one reanalysis cite a 75% relative risk reduction, though this translates into only a 0.9% reduction in absolute risk.

In other words, up to 270 women with pre-osteoporosis might need to be treated with drugs for three years so that one of them could avoid a single vertebral fracture.

Most of the reanalyses also play down the harms of drug therapy, they add. For example, the reanalysis of data for the drug raloxifene focuses solely on the potential benefits, with no mention of an increased risk of blood clots.

Finally, like much of the published literature on osteoporosis, these analyses have potential conflicts of interest, they write. For instance, all of the original drug trials being re-analysed were funded by industry and, in three out of four cases, drug company employees were part of the team conducting the reanalyses.

The World Health Organisation is currently developing guidance on how to deal with women categorised as having osteopenia. Whether this will stop industry efforts to encourage treatment in low risk women is, however, questionable, they say.

“We need to ask whether the coming wave of marketing targeting those women with pre-osteoporosis will result in the sound effective prevention of fractures or the unnecessary and wasteful treatment of millions more healthy women,” they conclude.

Repsoted study from 2008…Requested repost

23rd Health Research Report 23 JAN 2008 – Reconstructed

Health Technology Research Synopsis

23rd Issue Date 22 JAN 2008

Compiled By Ralph Turchiano

Editors Top Five:

1.      Lipoic acid could reduce atherosclerosis, weight gain
2.      Probiotics affect metabolism, says new study
3.      Value of drugs for pre-osteoporosis exaggerated
4.      Selective reporting of antidepressant trials exaggerates drug effectiveness
5.      4 health behaviors can add 14 extra years of life

In this issue:

1.      More sun exposure may be good for some people
2.      Muscles are affected by cigarette smoking
3.      4 health behaviors can add 14 extra years of life
4.      New statistical technique shows more informative picture of survival
5.      Evidence for Dopamine Toxicity in Neurodegeneration
6.      UCLA study finds brain response differences in the way women with IBS anticipate and react to pain
7.      High degree of resistance to antibiotics in Arctic birds
8.      Stem cells make bone marrow cancer resistant to treatment
9.      Editorialist: Scientific Journals Must Provide a Forum for New Discoveries Based on Clinical Observation
10.  Vitamin D2 supplements may help prevent falls among high-risk older women
11.  Diets high in lutein, zeaxanthin and vitamin E associated with decreased risk of cataracts
12.  Selective restraints and reduced medication could reduce nursing home falls says 4-year study
13.  Aggression as rewarding as sex, food and drugs
14.  Lipoic acid could reduce atherosclerosis, weight gain
15.  Celecoxib can adversely affect heart rhythm
16.  Combined HRT increases risk of lobular breast cancer fourfold after just 3 years of use
17.  Probiotics affect metabolism, says new study
18.  Popular osteoporosis drugs triple risk of bone necrosis
19.  Cholesterol-lowering drugs may not prevent Alzheimer’s disease
20.  Selective reporting of antidepressant trials exaggerates drug effectiveness
21.  Indian medicinal plant Acanthus ilicifolius may combat liver cancer
22.  How does Fu-Zheng-Jie-Du-Decoction act on PTEN expression in hepatocellular carcinoma?
23.  Weight gain induced by antipsychotic drugs can be avoided
24.  Toxoplasma Infection Increases Risk of Schizophrenia, Study Suggests
25.  Newly discovered virus linked to deadly skin cancer
26.  Value of drugs for pre-osteoporosis exaggerated
27.  Saline nasal wash helps improve children’s cold symptoms

Deer antlers inspire a new theory on osteoporosis

The loss of manganese could mean that calcium does not stick to bones and could cause osteoporosis. This is the new theory put forward by researchers at the University of Castilla-La Mancha (UCLM) in Spain after studying deer antlers. The hypothesis published this month in the Frontiers of Bioscience journal still needs to be confirmed by the scientific community.

Through the study of deer antlers, researchers of the Research Institute of Hunting Resources (IREC, joint centre UCLM-CSIC-JCCM) suggest that the origin of osteoporosis could not be directly linked to the lack of calcium but rather to the lack of a mineral essential to calcium absorption. In particular they believe that this could be manganese, according to a new theory published in the latest issue of the Frontiers of Bioscience journal.

According to Tomás Landete, sub-director of the IREC and one of team’s researchers, “previous antler studies show that manganese is necessary for calcium absorption. Our hypothesis is that when the human body absorbs less manganese or when it is sent from the skeleton to other organs that require it, such as the brain, the calcium that is extracted at the same time is then not properly absorbed and is excreted in the urine. It is in this way that osteoporosis can slowly strike.”

The theory must now be validated with more studies and medical trials but its creators believe that it is a “step in a totally new direction in osteoporosis research as it considers calcium loss to be a consequence of the disease and not the origin.”

The idea for the new proposal came from a dramatic increase in antler breakages seen in Spain in 2005. When scientists analysed these antlers in detail, they realised that weakening was due to manganese depletion caused by the deer’s diet. That year saw an intensely cold winter which in turn caused plants to reduce their manganese concentrations in response to such stress.

“Antlers grow by transferring 20% of the skeleton’s calcium towards their structure. We therefore saw that it was not calcium deficiency that caused the weakening but rather the deficiency of manganese,” clarifies Landete. “The lack of manganese was almost as if the ‘glue’ that sticks calcium to antlers bones was missing.”

Links to Alzheimer’s and Parkinson’s Disease

In the case of humans, the researchers suggest that manganese is extracted from the bones when it is required by the “most important” organs, such as the brain. The researcher adds that “maintaining the bones is important, but even more so is sustaining the working of the brain, which uses 25% of our energy intake when at rest.”

The team also points out that when this vital mineral runs out after the onset of osteoporosis, conditions like Alzheimer’s disease, Parkinson’s disease, and senile dementia could strike. To put this theory to the test, they analysed data from 113 patients who were operated on for osteoporosis and osteoarthritis (wear and tear of joint cartilage) at Hellín Hospital in Albacete, Spain between 2008 and 2009. Some 40% of those operated on for osteoporosis showed some form of cerebral dysfunction whereas this was not the case in any of the 68 patients operated on for osteoarthritis.

Furthermore, the percentage increased with age and only amongst those patients with osteoporosis. The exhaustion of manganese reserves could be behind the bone disease and the cerebral degeneration. “We are collecting human bones to confirm this. However, studies on rats in which Alzheimer’s disease has been induced by aluminium intoxication show that as the severity of this disease increases, manganese levels in the bones decrease,” says Landete.

The researcher also recalls studies that link manganese to Parkinson’s disease and show that astrocytes, which provide support to neurons, have specific enzymes that require manganese. In any case, researchers outline that their theory “is not a final solution to such diseases but constitutes the first step in a new direction” – a new direction that requires validation and confirmation from the scientific community.



Tomas Landete-Castillejos, Inmaculada Molina-Quilez, Jose Antonio Estevez, Francisco Ceacero, Andrés José García, Laureano Gallego. “Alternative hypothesis for the origin of osteoporosis: The role of Mn”. Frontiers in Bioscience (Elite Edition) 4: 1385-1390, January 2012. Doi: 10.2741/468