Goodbye root canals? Researchers use lasers to regrow parts of teeth

Goodbye root canals? Researchers use lasers to regrow parts of teeth

Loren Grush

By Loren Grush
·Published May 28, 2014·

For the millions of Americans who suffer cavities each year, the ominous threat of a root canal may soon be a worry of the past.

Now, researchers from Harvard University claim they have discovered a novel way of regrowing parts of people’s teeth using an unlikely tool: Lasers.


In a new study published in the journal Science Translational Medicine, lead researcher Praveen Arany and colleagues detailed how they used focused laser light therapy on rats to stimulate the growth of lost dentin, the calcified tissue that comprises teeth. They noted that if the therapy proves effective in humans, it could potentially eliminate the need for crowns, fillings and other complex dental operations in the future.

The procedure’s success all revolves around a native protein called transforming growth factor beta, or TGF-beta. During preliminary tests of dentin tissues, the researchers discovered that this growth factor changed very drastically when introduced to a focused beam of light. Further analysis revealed that when hit with light, TGF-beta actually stimulated the stem cells already present in dentin.

“Once [TGF-beta] is activated by the laser, it can bind to stem cells resident in the tissue, and then it induces those stem cells to differentiate so they can proliferate and reform dentin,” David Mooney, the Pinkas Family Professor of Bioengineering at Harvard University, told

Numerous studies have focused on ways to manipulate stem cells in order to spur tissue regeneration, but most of these techniques have revolved around reintroducing altered stem cells into the patient or directing stem cell populations externally through added growth factors. With this form of laser therapy, the only external factor that is being introduced is light, which activates TGF-beta that’s already in the body.

According to Mooney, it’s not the laser’s heat that stimulates TGF-beta but the energy of its photons. When light is focused on dentin, the photons get absorbed into the tissue and activate molecules called reactive oxygen species (ROS), which naturally occur in the body. These ROS then stimulate TGF-beta, which spurs the chain reaction ultimately leading to dentin reformation.


However, Mooney noted that the power of the laser must be at a specific level of intensity and cannot produce any heat in order to be effective.

“It’s kind of like Goldilocks, too little won’t do enough and too much will become destructive,” Mooney said. “It has to be just right.”

To test their light therapy’s effectiveness, the researchers created a group of rats with tooth defects, by using a drill to remove pieces of their dentin. They then shined a laser on their exposed tooth structures and soft tissues underneath it. Sure enough, after 12 weeks, the team observed that new dentin had formed in the rats’ teeth.

Given their trial’s success, Arany and his team hope to test this type of dentin regeneration in human clinical trials, which could potentially alter modern dentistry. Currently, if a patient has a chipped or decayed tooth, dentists will use synthetic materials to fix the problem or perform a root canal if the tooth has become too infected. Yet, Arany noted that laser therapy could erase the need for these uncomfortable dental procedures, simply by regrowing the part of the tooth that is missing.

He also noted that focused laser therapy could be used to grow more protective dentin in teeth that have grown sensitive due to gum recession.

“As we grow older our gums recede, exposing our teeth root,” Arany, assistant clinical investigator for the National Institutes of Health, told “The root is covered by cementum, which is not as protective as enamel, so you get dentin sensitivity….What we hope is in tooth sensitivity, [laser therapy] is able to generate an intrinsic protective barrier on the inside of the tooth.”

Expanding beyond the world of dentistry, the researchers note that TGF-beta is found in other bodily tissues, such as skin and bone, and that laser therapy could potentially help regrow tissues in those systems, as well. Also, since TGF-beta is known to control tissue inflammation, the growth factor could perhaps be stimulated to control certain inflammatory diseases.

But for now, the team is focused on TGF-beta in relation to teeth, and they are hopeful that their laser therapy could be used in a clinical setting relatively soon.

“This laser is already a big part of the clinic, since so many of the clinicians use it for other purposes,” Arany said. “So the barrier to clinical trial translation is relatively low.”

Scientists discover new way of overcoming human stem cell rejection

Scientists discover new way of overcoming human stem cell rejection

By Loren Grush

Published January 02, 2014
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Human embryonic stem cells have the capacity to differentiate into a variety of cell types, making them a valuable source of transplantable tissue for the treatment of numerous diseases, such as Parkinson’s disease and diabetes.

But there’s one major issue: Embryonic stem cells are often rejected by the human immune system.

Now, researchers from the University of California San Diego may have found an effective way to prevent this rejection in humans.  Utilizing a novel humanized mouse model, the scientists have revealed a unique combination of immune suppressing molecules that stop the immune system from attacking the injected stem cells – without shutting the system down completely.

This discovery could ultimately help resolve some of the major problems currently limiting the use of embryonic stem cells for certain conditions, paving the way for the development of more effective human stem cell therapies.

“This is a generic way of immune suppression, so it could potentially be applied not just for stem cells therapies, but for organ transplants as well,” Yang Xu, a professor of biology at UC San Diego and lead author of the study, told  “It can be very broad.”

Embryonic stem cells are different from the other cells in a patient’s body, making them “allogenic.”  This means the immune system will recognize them as foreign agents and attack them.

One way of overcoming this rejection problem is to give patients immunosuppressant drugs, which suppress the entire immune system.  While short term use of immunosuppressants has been successful for many organ transplants, embryonic stem cell therapies for chronic diseases require long term use of these drugs – which can often be very toxic and increase the risk of cancer.

“In order for the patient to really use this therapy, they have to decide: Do they want a lifelong use of immunosuppressant drugs, or are they willing to live with the symptoms of their disease,” Xu said.

To figure out a way of bypassing this issue, researchers needed a relevant model that could closely mimic the human immune system’s response to embryonic stem cell transplantation.  To do this, they took immune deficient lab mice and grafted them with human fetal thymus tissues and hematopoietic stem cells derived from the fetal liver.

Essentially, this created a highly specialized mouse model with very robust T cells – capable of effectively rejecting foreign embryonic stem cells just like human T cells.

“The mouse immune system is very similar to humans but still very different,” Xu said.  “What we learn from mouse models does not really translate to the clinic.  So what we decided to do, rather than relying entirely on the mouse immune system, we tried to do a more human relevant system.  And it’s as close as can be at this moment.”

With these newly “humanized” mice, Xu and his team then tested various immune suppressing molecules after they had injected the mice with embryonic stem cells.  After some trial and error, they found that a combination of CTLA4-lg – an FDA-approved drug for treating rheumatoid arthritis – and a protein called PD-L1 – which induces immune tolerance in tumors – effectively protected the stem cells from rejection.

According to Xu, they don’t yet know why this specific combination protects embryonic stem cells, but they believe that both of the molecules may be suppressing the body’s T cells in two very different – and very important – ways.

“What was surprising was if you have these two together, you get nearly 100 percent local immune suppression and allow the graft to survive. But at the same time, there’s no effect on other parts of the body,” Xu said. “But if you only express one molecule, it has no impact.  That is the cool finding of this study.”

Since this drug combination was so successful in the humanized mice, the researchers hope to begin testing it on monkeys, before eventually moving on to human clinical trial.

“I think this is one of the few cases where we can have confidence that this combination would probably work in humans, because the system is so close,” Xu said.  “So the translation potential is very high.”

The research was published online in the journal Cell Stem Cell.

Bacteria-eating viruses found to effectively destroy C. difficile superbug

Bacteria-eating viruses found to effectively destroy C. difficile superbug

By Loren Grush

Published October 17, 2013
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    This image shows a burst open cell with phages escaping. (DR MARTHA CLOKIE/STEFAN HYMAN, SCHOOL OF BIOLOGICAL SCIENCES, UNIVERSITY OF LEICESTER)

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    This micrograph depicts Gram-positive C. difficile bacteria from a stool sample culture. (CDC.GOV)

Over the past decade, the superbug Clostrodium difficile (C. diff) has been on the rise in hospitals throughout the United States and England. The trend has many health experts concerned, as most strains of the bacteria are resistant to antibiotics, making them very difficult to treat and potentially deadly.

But now, researchers from the University of Leicester in England may have discovered a more potent, and seemingly unlikely, treatment for these highly infectious bacteria: viruses.

Through work funded by the British Medical Research Council (MRC), researchers have shown that a group of naturally occurring bacteria-eating viruses – known as phages – effectively target and destroy C. diff bacteria in cell cultures.

According to lead investigator Dr. Martha Clokie, while phages have often been used to target other forms of bacteria, they have yet to be used to target C. diff.

“(Researchers) haven’t really found C. diff phages before, partly because they looked in the wrong places,” Clokie, from the University of Leicester’s department of infection, immunity and inflammation, told “We know C. diff to be a gut pathogen, causing huge problems in hospital settings, but it also has a strong presence in environmental settings… And wherever you find bacteria in a natural environment, you will almost always find viruses (that target them).”

With this theory in mind, Clokie and her team searched environmental areas where C. diff is known to exist, such as in soil, rivers and estuaries.  Together, they managed to isolate around 40 different viruses associated with the bacteria – the largest known set of C. diffphages ever collected.

The researchers then tested the phages on clinically relevant strains of C. diff bacteria in cell cultures.  Ultimately, they were able to identify a mixture of seven viruses that effectively destroyed the most problematic strains of the bacteria.

“When we add the viruses to the bacteria, the bacteria die in petri dishes,” Clokie said.  “We can also grow gut cells on plates, infect our gut cells with C. diff, and show that adding these viruses gets rid of theC. diff.”

Given the success of their research, Clokie and her team have partnered with the AmpliPhi Biosciences Corporation, a U.S.-based biopharmaceutical company that specializes in the development of phage-based treatments for bacterial infections.  Through their partnership, they have patented Clokie’s virus mixture, hoping to develop it further into a viable treatment option.

“It’d be like an oral pill – a little capsule of viruses,” Clokie explained.  “It’d allow viruses to pass through the stomach, degrade at that point and access C. diff where it needs to.  We’re at an exciting stage for this; we’re not quite there yet, but we’re in an exciting place.”

A phage-therapy such as this one is desperately needed in both the United States and England. While hospital acquired infections (HAIs) have declined in the United States in recent years, C. diff still remains at historically high levels.  According to the Centers for Disease Control and Prevention, the superbug is linked with 14,000 American deaths each year.  C. diff is also extremely difficult to treat as many of the clinically significant strains of the bacteria are naturally resistant to antibiotics.

Additionally, the people most at risk for C. diff infection – which often involves severe dehydration and diarrhea – are sick or elderly patients who have recently been treated with antibiotics in a hospital or other medical setting.

Although antibiotics are valuable for their ability to destroy harmful bacteria in the body, they also effectively kill the body’s “good” bacteria, which help protect against unwanted infection. As a result, this makes patients more susceptible to contracting C. diff from contaminated surfaces or the unwashed hands of health care workers.

Clokie said one of the great things about her team’s phage mixture is that it bypasses this very significant problem.

“The viruses are so specific (to C. diff) that they won’t even kill other bacterial species,” Clokie said.  “Antibiotics kill other bacteria you actually need, but these viruses are so specific that they just take outC. diff. They can’t even recognize human cells and use them as hosts.”

With further funding from AmpliPhi, Clokie is working on having a fully developed phage mixture ready to go into phase 1 and phase 2 clinical trials relatively soon.  She believes that a shift towards phage-based therapies could help eliminate the negative impact antibiotics have had on increasing HAIs and spurring antibiotic resistance.

“It would really allow doctors to have another way of treating patients,” Clokie said.  “As soon as people get a little sick with C. diff, you could give them this virus mixture.  We hope to lower patient death rate and reduce their stays in hospital, so we would be reducing the health care burden in general.”

New blood test can detect lung and prostate cancers

New blood test can detect lung and prostate cancers

By Loren Grush

Published October 16, 2013
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A new blood test can help detect the presence of early-stage lung and prostate cancers – as well as any recurrences of these diseases.

In a new study presented at the Anesthesiology 2013 annual meeting, researchers have found that an increased level of serum-free fatty acids and their metabolites in the blood stream can help indicate the presence of lung cancer in the body.

According to the study’s authors, such a test could be extremely beneficial for the detection and management of the disease.

“Lung cancer is the leading cause of cancer death in the U.S., and unlike some other cancers, there is no easy way to diagnose it,” senior author Dr. David Sessler, professor and chair of the department of outcomes research at the Cleveland Clinic, told  “The current standard is a spiral CT, which works well, but they are expensive, and they expose patients to radiation.  So having a blood test for lung cancer would be very helpful.”

Sessler said that he and his research team stumbled upon these biomarkers for lung cancer while conducting an entirely different experiment.

“It was complete serendipity,” Sessler said.  “We were looking for inflammatory markers associated with a particular type of anesthesia – general anesthesia versus epidural anesthesia.  There was no difference in inflammation, but we noticed that patients with lung cancer had higher incidences of these fatty acids and their metabolites.”

After making this discovery, the researchers decided to further analyze these potential biomarkers. They examined blood samples from 55 patients with lung cancer and 40 patients with prostate cancer, comparing them to samples from people without cancer. The blood samples from the cancer patients had one- to six-times greater amounts of the serum-free fatty acids and their metabolites than the samples from cancer-free patients.

In a second phase of the study, the researchers examined blood samples from 24 patients with lung cancer before they underwent curative surgery.  They then analyzed the patients’ blood at six and 24 hours after surgery.  The level of serum-free fatty acids and their metabolites decreased three to 10 times within 24 hours after the cancerous tumors were removed.

The researchers didn’t assess why the level of these compounds increased, but they said their findings are consistent with previous research on the relationship of serum-free fatty acids and cancer.

“The three fatty acids are necessary for cancer cell growth, and some cancers stimulate the release of these fatty acids,” Sessler said.

Though the blood test was shown to be effective in detecting the disease, the researchers argue that it should not be used as the go-to test for lung cancer screenings.  However, it could be helpful for a certain population of patients.

“It’s by no means a perfect test; blood tests rarely are,” Sessler said. “It is about 75 percent for sensitivity and specificity.  It is probably not a good enough test to use for routine screening, but it well could be helpful for high risk patients or patients who have found a nodule but don’t know if it’s cancerous enough.”

Sessler also said the blood test could be helpful for those who have already undergone lung cancer surgery to better understand if they will suffer recurrence.

“If someone who has lung cancer and has surgery, you might use this as a follow up,” Sessler said. “Presumably the fatty acids go down after surgery, and an increase in concentration might tell you if patient is having a relapse.”

While other blood tests do exist for some cancers – most notably the prostate-specific antigen (PSA) test for prostate cancer – Sessler said this is still an exciting discovery for the future of lung cancer treatment.

“Yes, there are some biomarkers for some cancers, but there’s no general cancer biomarker, nor has there ever been an established biomarker for lung cancer,” Sessler said.

Newly discovered biomarker can better guide treatment for melanoma patients

Newly discovered biomarker can better guide treatment for melanoma patients

By Loren Grush

Published October 22, 2013
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    This image depicts the gross appearance of a cutaneous pigmented lesion, which had been diagnosed as superficial spreading malignant melanoma (SSMM). (CDC.GOV)

Researchers have discovered a new biomarker that can predict whether melanoma patients with mutations in the BRAF gene will respond to certain kinds of cancer medications.

The discovery could help better guide treatment for patients with the disease, as they are often subjected to ineffective therapies to which their bodies are resistant.

The BRAF gene has been found to be an effective drug target for treating melanoma cancers, and the Food and Drug Administration (FDA) has approved two drugs inhibiting this gene.  However, patients with melanomas harboring mutations in the BRAF gene are sometimes resistant to these medications, and most people who initially respond to BRAF-targeting therapies eventually relapse, as their tumors become resistant to the drugs.

While BRAF mutations are present in only 7 percent of all human cancers, they are seen in approximately 50 percent of melanomas.  And there’s no concrete way of knowing which patients with BRAF mutations will respond to BRAF-targeting treatments and which ones will not.

“For virtually untreatable cancers, we’re seeing response rates of 60 to 80 percent with BRAF-targeting drugs.” Dr. Ryan Corcoran, a clinical investigator and assistant professor at the Massachusetts General Hospital Cancer Center and Harvard Medical School in Boston, Mass., told   “…But 60 to 80 percent response rate means there are still 20 to 40 percent of patients who don’t respond.  Determining which patients are most likely to respond (to these drugs) and perhaps should be diverted to an alternative therapy could be really beneficial.”

Corcoran said that previous research has identified numerous mechanisms behind the resistance to BRAF inhibitors, but it can be a daunting task screening patients for these mechanisms. So he and his team decided to analyze them further.

“We thought, ‘Perhaps all these resistance mechanisms converge into a key downstream pathway,’” Corcoran said.  “Then maybe we could get a more universal yes-or-no predictor to see if patients respond to the drugs.”

After analyzing genetic models in the lab, Corcoran and his team found that the signaling pathway TORC1 was a key converging point for these mechanisms and that the presence of a protein called S6 could serve as a good predictor of sensitivity to BRAF-inhibiting medication.

“There’s a protein substraight called S6, which is involved in protein translation in the cell,” Corcoran said. “It’s basically used as an indicator of TORC1 activity.  When the pathway is active, the presence of S6 is elevated, and vice versa.”

In their models, the researchers found that melanoma cancers that were sensitive to BRAF inhibitors saw a suppression of S6 after treatment.  In contrast, almost all melanoma cancers that were resistant to the drugs maintained higher levels of S6 post treatment.

To further verify this finding, the researchers collected tumor biopsies from nine melanoma patients, which had been taken before and after treatment with BRAF-targeting drugs.  The found that one subset of patients had an effective shutdown of S6 after treatment, compared to the other patients who had maintained levels of S6 after treatment.  Ultimately, the group of patients with effective suppression of S6 had a more than fivefold increase in repression-free survival compared to the those who had maintained S6.

“That suggests that if we can identify early on these patients who down regulate or fail to down regulate S6, we can predict who is most likely to respond,” Corcoran.

Applying this new knowledge, Corcoran and his team developed a new technique that can rapidly monitor, in real time, the levels of S6 in tumor cells.  Using fine-needle aspiration biopsies from melanoma patients before and during the first couple weeks of their treatment with BRAF-targeting drugs, they could assess the activity of the S6 signaling pathway and quickly determine a patient’s resistance.

“It’s still in concept phase, but …if you have a way of determining (resistance), you can spare (a patient) unnecessary treatment,” Corcoran said. “By identifying this subgroup, you can do that at a much earlier point, rather than waiting two months, as is done, for a repeat CT scan.  So this is really a way to guide treatment more rapidly and divert more patients to more effective therapy.”

The research was presented at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics.

New protein found to control deadly cancer metastasis

Stopping cancer’s spread: New protein found to control deadly cancer metastasis

By Loren Grush

Published June 15, 2013
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    This image shows metastasized human breast cancer cells (magnified 400 times, stained brown) in lymph nodes. (National Cancer Institute)

Researchers have found a critical element that may explain why some cancers spread farther and faster than others, a discovery that could lead to one of the Holy Grails of cancer treatment: containing the disease.

Scientists from the University of California, San Diego School of Medicine have identified a protein that seems to serve as a switch, regulating the spread of cancer from the primary tumor to distant spots in the body – a process known as metastasis.  The protein is used by embryo cells during early development, but then disappears from the body after an individual comes out of the womb.

According to the researchers, the protein was only found in people with metastatic cancer, leading them to belive that the regulation of this protein could potentially stop the dangerous progression of this killer disease.

“The protein seems to get turned off (after embryonic development), and we’ve only identified a small sub-population of cells that can turn it on,” lead investigator, Dr. Thomas Kipps, Evelyn and Edwin Tasch Chair in Cancer Research at UC San Diego, told  “By and large, we looked at the brain, lungs, heart, kidney and other organs, and it wasn’t there. Then we looked at a variety of cancers – breast, ovarian, prostate – and it seems to be a common theme to express this embryonic protein.”

Kipps said they stumbled upon this protein while conducting immunotherapy research on leukemia patients, in which they reengineered the patients’ leukemia cells and injected them into their bodies.  This technique is meant to enhance the body’s natural immune response to cancer.

“We did have patients respond to their leukemia cells, but part of the immune response was a cell that targeted (this protein),” Kipps said. “Anecdotally, these patients did well. So we wanted to know (what) it is doing.”

The protein, called Receptor-tyrosine-kinase-like Orphan Receptor 1, or ROR1, is involved in a process known as epithelial mesenchymal transition (EMT), which occurs during early embryonic development.  Throughout the EMT process, embryonic cells migrate and eventually grow into new organs.

Kipps explained that ROR1’s role during embryonic development may explain how it helps cancers to grow and spread.

“It’s a protein that sits on the surface of the cancer, so it has the ability to bind to other proteins outside of the cell and may have the ability to bind to other proteins on the cancer cell membrane,” Kipps said.  “Half of it sits outside the cell and half inside the cell.  It’s like having an antenna sticking out, and then you have a transmitter below the surface.  That transmitter conveys important signals to the cell, and it seems to allow itself to assume a better state of migration.”

In a series of lab experiments, Kipps and his team found that high-level expression of ROR1 in breast cancer cells were associated with higher rates of relapse and metastasis.  However, when they used therapies to silence the expression of ROR1, the researchers were successfully able to inhibit metastatic spread of the cancer cells in animal models.

“It’s like taking the antenna away; you can’t hear the radio or TV station anymore,” Kipps said. “The cancer cells become more fragile and don’t grow as well.”

After cardiovascular disease, cancer is the second leading cause of death in the United States, with 575,000 Americans dying from the disease each year. One of the scariest aspects of receiving a cancer diagnosis is learning how far the disease has spread throughout the body.  An individual’s prognosis can vary greatly depending on the extent of the cancer’s progression; if it has spread too much, modern treatments can do little to stop it. This explains why the vast majority of cancer-related deaths – approximately 90 percent – are due to metastasis of the original tumor cells.

Since ROR1 is only expressed in cancer cells, Kipps said it provides a singular target for future therapies aimed at containing and reversing metastasis.  Then, once the cancer becomes more localized, traditional therapies such as radiation and surgery can help remove the original tumor from the body.

“I think it’s an exciting time for cancer treatment,” Kipps said.  “I do think it’s a great time for discoveries, and hopefully we’ll be able to cure many forms of cancer – turning it into a bad experience rather than a life threatening event.”

The research was published in the June 15 issue of the journal Cancer Research.

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The 7 Minute Back Pain Solution

Words of Wellness: ‘The 7 Minute Back Pain Solution’


Published May 02, 2012

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Having a bad back can be as simple as a daily nuisance or as severe as a debilitating condition.  While it’s important to have a strong back, not everyone suffering from back pain needs to take drastic measures to fix the problem.

In his book The 7 Minute Back Pain Solution, Dr. Gerard Girasole, a board-certified orthopaedic spin surgeon in New York City, explains the common causes of back pain and details different exercises a person can do to strengthen the muscles in their core.

What made you want to write this book?

I’m a spinal surgeon, but there’s never been a concise go-to article about how to strengthen your back.  In therapy places they had different exercises, but nothing was very to the point.

Cara, my co-author, was a patient of mine, and I thought she needed surgery.  But one day I saw her in the gym, and she looked great.  She told me she had designed these exercises to help her back, so we decided to both write a book about it together.

How prevalent is back pain in America?

In the work place, 93 million work days are lost every year due to back pain, resulting in $5 billion in health care costs.  Plus eight out of 10 people will have back pain at some point in their lives.  Not all will end up having surgery, but back pain is one of the leading causes of people losing time at work.

Back pain is the also one of the leading causes of relationship problems, medication abuse and more.  If people don’t treat it, it can become a chronic problem that can significantly affect the quality of their life.

What are some suggestions in your book?

Since I’m an orthopedic spine surgeon, I’m the one that gives you concise instructions on stretching the key muscles that attribute to low back pain.  The book encompasses every walk of life: How to run with back pain, play golf, have sex – everything.  My job as a surgeon was to explain why you have back pain and the myths surrounding it, like that you’re doomed and need surgery.  Fifty percent of the battle of back pain is understanding it.

The rest of the book contains easy routines to follow written by Cara.  These are exercises you can do in your home, workspace, in the car and anywhere else.  It’s designed for anybody: if you have chronic back pain, post-op back pain or people who just want to strengthen their backs in general.

What are the key muscles people should focus on?

The key to understanding your lower back is to focus on the core muscles.  The core muscles encompass the abdominal muscles, pelvic muscles, hip muscles and lower back muscles.  All of these muscles work together to provide all of your daily motion.  So proper body movement require a strong core.  The biggest misnomer is that when you work your abdomen, you work your core, but you’re really just working a third of your core.  When the core is weak, meaning one of the other muscles is not working properly, it can result in pain or injury.

We coined a phrase in the book called ‘back mindfulness’ and how crucial your back is for every move you take.  People have to understand that from the moment you wake up in the morning to when you go to bed at night, you’re using your back.

Any other tips?

In the seven minute stretches we outline, you’re stretching each one of these muscles for a minute per stretch.  Everybody has the time to do this.  We make them very simple and easy to do anywhere.

The cost of lower back pain is expensive and can greatly impact your life.  You don’t need any kind of gimmicks or additive equipment, you can just use this book as a guide.  It’s a great guide for your specific problems – shoveling snow, travel, how you pack your bag, etc.  It’s simple to read and simple to understand.

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