Thursday, March 29, 2012

PDT for Cancer Depends on Improved Photosensitizers

Photodynamic therapy (PDT) is proving to be a more than viable option for cancer treatment. Compared with other treatments, such as chemotherapy and radiation therapy, PDT is more selective, causing far less damage to healthy cells near cancerous targets due to the precise way in which photosensitizers can locate and infiltrate tumor cells.

The task remains to find the best combinations of photosensitizers and conjugates to propel the technique past chemotherapy and other traditional methods.

Basically, a photoreactive chemical compound called a photosensitizer is introduced into a patient, where it aggregates near an active tumor site. A clinician then shines light from a diode laser or LED source onto the tumor region. The light, which has a specific wavelength, activates the photosensitizer without affecting surrounding healthy tissue. Once activated, the photosensitizer transfers some of its energy to nearby ground-state molecular oxygen, producing excited singlet oxygen. The result is oxidation of tumor cells in the site, destroying the cancer while harming as few of the adjacent healthy cells as possible.

Bringing light to the site is an ongoing issue. Early studies of PDT focused on skin cancers, such as various types of melanoma, because it was easier to shine near-infrared wavelengths a couple of millimeters through the skin’s surface to the tumor site. This drove design of the first photosensitizers to favor compounds that would preferentially react to light in that range. More recently, advances in endoscopic light-delivery systems have made deeper tumors easier to reach and have broadened the range of potential wavelengths and matching photosensitizers.

Different compounds are now used as photosensitizers, including phthalocyanine, chlorine, bacteriochlorin and porphyrin. None, however, is a perfect candidate.

Getting a photosensitizer to find and attach itself to a tumor cell is a major battle. The body’s immune system, for example, seeks out and annihilates some forms of photosensitizers, reducing the effectiveness of the overall treatment. Adding antibodies to photosensitizers can help their affinity for cancer cells, but some researchers feel that protecting them with shells composed of lipoproteins is a better way to go. Lipoproteins not only help their cargo locate and infiltrate tumors, but also help protect them from enzymes and macrophages that might alter or destroy them before they even arrive at the treatment site.

Gold nanoparticles and liposomes also have been considered as adjuncts that could help photosensitizers directly enter cancer cells.

Gold rush

Researchers at Rhodes University in Grahamstown and in the biophotonics department of the National Laser Center in Pretoria, both in South Africa, are among the groups looking at the possible improvements to photosensitizer action provided by gold nanoparticles.

Tebello Nyokong of Rhodes University and her colleagues had gold nanoparticles in mind during efficiency tests of a particular photosensitizer, as they reported in the Feb. 6 issue of the Journal of Photochemistry and Photobiology B: Biology.

Phthalocyanine compounds strongly absorb in the 600- to 800-nm range, yet tissues are transparent to a useful degree to these wavelengths. The result is an ability to reach deeply into tissue and provide sufficient energy to the photosensitizer to activate it.

Several attributes must be considered when designing a photosensitizer, said Nyokong, director of the Nanotechnology Innovation Center at Rhodes. One is that it should have a high specificity for cancer, which is achieved through inclusion and coordination of molecules such as folic acid and vitamin B12. Another highly valued attribute is good absorption in the red wavelengths, which is aided by sulfur linkages in the photosensitizer compound. The final product also should be water-soluble and initiate large production of singlet oxygen, which drives tumor cell death.

The group’s candidate was [2,9,17,23-tetrakis-(1,6-hexanedithiol)phthalocyaninato]zinc(II), a second-generation phthalocyanine-based compound. Its target: human malignant breast cancer cells (MCF-7).

The researchers chose zinc over more typical sulfur in their compound because it enhances the production of singlet oxygen while being somewhat easier to assemble. After forming the phthalocyanine complexes, they introduced some to gold nanoparticles, which self-assembled with the compound. Others were bound to liposomes as a delivery vehicle.

Using a Shimadzu spectrophotometer, a Varian Inc. spectrofluorimeter, and a single-photon counter and diode laser made by PicoQuant GmbH, the investigators measured the absorption spectra, fluorescence excitation and fluorescence lifetimes of their photosensitizer in action against MCF-7. 

After determining that a light dose of 4.5 J/cm2 provided adequate intensity without harming nearby healthy cells, the researchers compared how well the gold nanoparticles and the liposomes aided the overall phototoxic effect.

They found that, after photoactivation of the two complexes, 60.1 percent of the tumor cells treated with nanoparticle-enhanced phthalocyanine remained viable, whereas the liposome-enhanced complexes fared much better with 51.9 percent cell viability.

Nyokong’s work with PDT is focused on synthesizing bifunctional agents – compounds that serve two functions, generally enhancing location and attachment to tumor cells. In her lab, the desired result is agents that combine the action of PDT and other treatments, such as hyperthermia (destroying tumors with applied heat, which increases the uptake of oxygen, thus accelerating cell destruction). 

Nyokong’s lab also is looking at combinations of chemotherapy and PDT via introduction of platinum to common photosensitizers. Next up for her group is the ongoing search for water-soluble phthalocyanine compounds that include liposomes. Better water solubility, the researchers say, should improve the ability of phthalocyanine to generate singlet oxygen inside cells.



Before and after images show the effect of a porphyrin-based photosensitizer that was carried into HeLa cells by a ruthenium-based, cube-shaped cage. Courtesy of the Journal of the American Chemical Society.

Cage death matches

Phthalocyanine- and porphyrin-based photosensitizers struggle to reach the tumor site because they are fairly poorly water soluble. Placing either type of complex inside the hydrophobic cavity of an otherwise water-soluble vessel designed to wend its way breezily toward target cancer cells is thought by several research groups potentially to improve the situation.

The tricky part is getting the vessel to unload its cargo upon arrival.

Another way to bring the photosensitizer to the cell is to wrap it inside an organometallic cage. This helps address the water-solubility issue while offering control of photosensitizer release, according to Bruno Therrien, an associate professor at the University of Neuchâtel in Switzerland.


Side and top views show 3-D models of prism-shaped (left) and cubic (right) “metalla-cages” designed to transport photosensitizers to tumor cells. Courtesy of the Journal of the American Chemical Society.


Therrien and his colleagues at the university and at Centre Hospitalier Vaudois in Lausanne, Switzerland, devised and tested two types of carrier vessels to ferry porphyrin to its target. One, in the form of a prism, locks the porphyrin tightly; the other, a cubelike structure, is a more flexible jacket. Both vessels are made with ruthenium-based compounds.

“Within the ‘metalla-prism,’ it’s a ship-in-the-bottle system – only breakage of the cage can release the guest,” Therrien said. “However, from the ‘metalla-cube,’ the porphyrin is free to go through one of the apertures without [breaking] the cage.”

With either vessel, the porphyrin remains unreactive to light and only becomes photosensitive once released.

The group studied the uptake of both vessel types and their cargo into HeLa cells, and then used a 488-nm laser made by Spectra-Physics at various doses to release, then activate, the porphyrin once the metalla-cages were inside the cell membranes.


Fluorescence micrographs of HeLa cells show how the photosensitizer chlorin e6 (top row) and a complex of chlorin e6 and poly-L-lysine (bottom row) accumulate inside HeLa cells after 10 min (left), 1 h (center) and 2 h (right). Note how the photosensitizer alone remains in the cytoplasm near the cell membrane, while the conjugated pair works its way from the inner wall to the cell nucleus. Courtesy of Current Topics in Medicinal Chemistry.


Once released, porphyrin discharged from either cage performed well at generating singlet oxygen and thus destroying the HeLa cells. Interestingly, the porphyrin delivered via the cubelike metalla-cages packed more punch, requiring one-tenth the energy (0.2 J/cm2) to reach the threshold where half the cells are killed compared with the metalla-prism combo (2.1 J/cm2).

Both controlled release of the photosensitizer and its ultimate phototoxicity are important, according to Therrien. “Controlled release can eliminate side effects, such as skin photosensitivity after and during treatment, but the active treatment is phototoxicity, so you still need an efficient photosensitizer.”

The ultimate goal of Therrien and his colleagues is to be able to irradiate at a specific wavelength to break up the cage where and when it is desired and, after release, apply a second dose of light to activate the photosensitizer.

Location, location, location

One of the most troubling disadvantages of first- and second-generation photosensitizers, according to researchers at the Tokyo Institute of Technology, is that they do not locate cancer cells as well as they might. The more specifically diseased cells are targeted, the more healthier viable cells can remain. 

“(A) photosensitizer which shows high tumor localization shows low phototoxicity for normal tissue,” said Shun-Ichiro Ogura of the institute’s department of biomolecular engineering. “It is quite important for tumor therapy.”

But as importantly, the short lifetime of singlet oxygen (measured in no more than microseconds) means that the closer they are to the right target, the more damage they can do. Therefore, improving localization can improve PDT efficacy.

Some photosensitizers, such as porphyrin-based constructions, accumulate in a target cell’s plasma membrane. However, the nucleus is the place to be if you want maximum destructive impact. Ogura and his colleagues found that one possible way to get to the cell nucleus effectively is to combine the popular photosensitizer chlorin e6 with poly-L-lysine. By itself, chlorin e6 stays in the cytoplasm of the cell, but the conjugated pair ultimately travels to the nucleus. After subsequent light exposure, the complex offered high phototoxicity. The group presents its findings on the localization capabilities of several photosensitizer types in the February issue of Current Topics in Medicinal Chemistry.

Wednesday, March 28, 2012

Theralase Reports Cancer Therapy Breakthrough

Toronto, ON – March 28, 2012 - Theralase Technologies Inc. (TSXV: TLT) announced today that its anti-cancer Photo Dynamic Compound (PDC) technology was found to completely destroy  subcutaneous (under the skin) colon cancer tumours in a mouse model. Four weeks post treatment; the mice continue to be cancer free.

Dr. Arkady Mandel, Chief Scientific Officer of Theralase said, “In cancer treatment, destroying the tumour is half the battle, while the other half is preventing the cancer from recurring. These findings are important because they demonstrate that our leading drug candidate in combination with a specific dose of light can prevent the cancer from returning. Preventing cancer from recurring in animal models is an important benchmark in developing new cancer therapeutics aimed at prolonging life."

Roger Dumoulin-White, President and CEO of Theralase Inc. stated, "The achievement of this important milestone signifies that Theralase’s leading drug PDC candidate is effective in the destruction of cancer in a live animal model and can prevent the cancer from recurring. Theralase's PDC technology was able to completely destroy subcutaneous cancer in mice and allow them to live cancer free for up to 4 weeks. Mice not treated with our PDC technology did not survive even 2 weeks. Based on recent successes in our research, we are confident that Theralase is well positioned to expedite the required steps to initiate human trials in the near future.”

Theralase’s work in this area will be presented at an International Symposium on “Photodynamic Therapy and Photodiagnosis in Clinical Practice” conference in Brixton, Italy in October 2012.

The following summarizes the research conducted by Theralase scientists:
  • In early February, mice were injected under the skin with 350,000 colon cancer cells.
  • All tumours were allowed to grow until they reached 5 mm in size.
  • On February 21, 2012, half the mice were used as a control group where no therapy was administered, while the remaining animals became the treatment group and were administered an intratumour injection of Theralase’s lead PDC.
  • The PDC was allowed to distribute within the cancerous tumour for 4 hours.
  • The PDC was then activated by Theralase’s proprietary laser light protocol for 32 minutes.
  • After 24 hours, the tumours were no longer visible on the treated mice.
  • All mice were monitored and examined daily thereafter.
  • Tumours in the control mice grew to the maximum allowable size of 12 mm, as determined by the study protocol, and did not survive for longer than 2 weeks.
  • The mice treated with Theralase’s PDC technology continue to be cancer free four weeks post treatment.

Theralase has a growing portfolio of intellectual property patents protecting the Theralase PDC technology for many years. Theralase’s anti-cancer technology pipeline includes drug candidates, in various advanced stages of preclinical development thus preparing Theralase’s anti-cancer PDC technology the ability to enter human clinical trials as early as 2013.

About Theralase Technologies Inc.:
Theralase Technologies Inc. founded in 1995, designs, develops, manufactures and markets patented, superpulsed laser technology utilized in biostimulation and biodestruction applications. The technology is safe and effective in the treatment of chronic pain, neural muscular-skeletal conditions and wound healing. When combined with its patented, light-sensitive Photo Dynamic Compounds (PDCs), Theralase laser technology is able to specifically target and destroy cancers, bacteria and viruses, as well as microbial pathogens associated with food contamination. For further information please visit www.theralase.com, regulatory filings may be viewed by visiting www.sedar.com.  

This press release contains forward-looking statements which reflect the Company's current expectations regarding future events. The forward-looking statements involve risks and uncertainties. Actual results could differ materially from those projected herein. The Company disclaims any obligation to update these forward-looking statements.

Neither TSX Venture Exchange nor its Regulation Services Provider (as that term is defined in the policies of the TSX Venture Exchanges) accepts responsibility for the adequacy or accuracy of this release.


For More Information

Roger Dumoulin-White                                                                      
President & Chief Executive Officer                          
416-447-8455 ext. 225                                   
rwhite@theralase.com

Monday, March 26, 2012

Comparison of Class 3 vs Class 4 Lasers

Comparison of Class 3 vs Class 4 Lasers



Dear Costumers,

Please join us at our Comparison of Class 3 vs Class 4 Lasers webinar.

Best Regards,
Theralase Team 






Comparison of Class 3 vs Class 4 Lasers

Beloware a few items that will be covered in the Webinar:

Is more power better?
What is the correct therapeutic dose?
Optimal laser wavelength will be examined
Clinical and scientific research will be discussed 

Date & Time

Date: Tuesday, March 27, 2012
Time: 1:00 PM - 2:PM EDT


Spaceis limited.
Reserve your Webinar seat now at:

https://www2.gotomeeting.com/register/369312378




Thursday, March 15, 2012

Young Arms and Curveballs: A Scientific Twist

For decades, it has been an article of faith for parents of young pitchers: Do not let them throw curveballs. The reason was simple. Contorting elbows — all in the service of ever more competitive baseball at ever younger ages — puts more strain on the joint than arms can handle. 


 Gene J. Puskar/Associated Press


Studies show curveballs aren't more harmful to youngsters. 


 But as the research into the biomechanics of pitching has evolved, the debate has grown more robust, and more perplexing. A recent major study shows curveballs pose no greater risk than that of other pitches. And many studies lately have shown that the greatest threat to young arms is not throwing curves but making too many pitches of any kind. 


 “Science is banging heads with intuition and gut instinct,” said Glenn Fleisig, the research director of the American Sports Medicine Institute, who has conducted studies on breaking balls and young arms since 1996. “For years, we told people that curveballs were bad. Then we set out to prove it. We did not prove curveballs are safe, but we could not prove they were dangerous.” 


 Like a pitcher and a catcher disagreeing on pitch selection, the opposing sides in the debate could not be more closely allied. Dr. James Andrews, the orthopedic surgeon to many athletes, is a founder of the American Sports Medicine Institute and has written with Fleisig some of the studies that have failed to prove that curveballs are hazardous to young arms. It has not stopped Andrews from challenging the results. 


 “What we found out in the lab is true,” Andrews said. “For pitchers with proper mechanics, the force of throwing a curveball is no greater than for a fastball. But that’s not what happens in reality on the baseball field. Many kids don’t have proper mechanics or enough neuromuscular control, or they are fatigued when throwing curveballs. Things break down. 


 “Those are the kids I’m seeing every day in my operating room.” 


 Little League Baseball imposed strict per-game pitch limits five years ago, but Andrews said he performed about seven times the number of arm operations on young pitchers that he did 15 years ago. 


 Last year, the findings of a study conducted on more than 1,300 pitchers from 8-year-olds to college students, were released by Little League Baseball, which had commissioned it with USA Baseball. Three University of North Carolina researchers surveyed the pitchers over five years, annually assessing multiple factors: number of innings pitched, kinds of pitches thrown, number of teams played for and any arm pain or injuries experienced. The answers were analyzed to judge which factors influenced injury risk. The test group included 410 Little League pitchers. 


 “There was no association between throwing curveballs and injuries or even arm pain,” said Johna Mihalik, who wrote the study. “It was surprising in a sense because of the conventional thinking about curveballs, but we were well aware that the studies by Dr. Andrews and Glenn Fleisig had come to similar conclusions. That’s what fueled our study.” 


 Stephen D. Keener, the president and chief executive of Little League International, said that deliberations among youth baseball leaders about banning, by rule, all breaking pitches had led to the commissioning of the study. When the findings did not link curveballs to injury, he said, Little League felt compelled to maintain the status quo. 


 “It doesn’t mean we’re advocating throwing breaking balls,” Keener said. “We don’t promote it. We just think it’s very difficult to regulate it out of the game, and there is no data to show that throwing breaking balls is at the root of arm injuries.” 


 Dr. Timothy Kremchek, an Ohio orthopedic surgeon who is the Cincinnati Reds’ physician and whose practice frequently treats youth pitchers, called Little League’s stance irresponsible. 


 “They have an obligation to protect these 12-year-old kids and instead, they’re saying, ‘There’s no scientific evidence curveballs cause damage, so go ahead, kids, just keep throwing them,’ ” Kremchek said. “It makes me sick to my stomach to watch the Little League World Series and see 12-year-olds throwing curve after curve. Those of us who have to treat those kids a few years later, we’re pretty sure there is a cause and effect.” 


 Kremchek said he performed 150 elbow ligament reconstructions a year, a complex operation named after the former major league pitcher Tommy John, who had the surgery when it was developed in the 1970s.



“Seventy percent of those surgeries are pitchers who haven’t hit college yet,” Kremchek said. “I ask each one the same question: when did you start throwing curveballs? And they say: ‘I was 10. I was 11.’ Sometimes, it’s 9.” 

Karena Cawthon for The New York Times


Dr. James Andrews says he performs more arm surgeries now than he did 15 years ago. 


 Kremchek coaxed about eight Ohio youth leagues to prohibit breaking pitches. The umpire issues a warning the first time he suspects a pitcher has thrown a curveball, slider or other breaking pitch. A second offense means the player must stop pitching. 


 “The mothers in those leagues are the biggest fans of those rules,” Kremchek said. “It’s not a hard call for the umpires. A 12-year-old trying to throw a breaking ball is pretty demonstrative as he does it. You can tell.” 


 But Keener said that rule, if enacted by Little League, would be hard to enforce across its more than 7,000 leagues. 


 “I applaud people for trying to do it,” Keener said. “But we often have volunteer umpires in a Little League trying to make balls-and-strikes calls and basepath calls, and it would be a very hard thing to ask them to also decide if a pitcher intentionally tried to throw a breaking pitch. What if that pitcher just has natural movement on his fastball?” 


 One aspect of the curveball debate, and the studies it has spawned, that everyone agrees on is that throwing too many pitches of any type is the biggest danger. 


 As surprised as Mihalik might have been about her study’s findings on curveballs, what alarmed her most was the number of pitches thrown. 


 “So many were playing for three teams at once,” she said. “And the data was extremely clear that overuse led to injury more than any other factor.” 


 That, too, is consistent with the findings of more than 15 years of research at the American Sports Medicine Institute, and similar studies around the country. 


 “Maybe asking whether the curveball is safe is the wrong question,” Fleisig said. “Maybe the question should shift to this: Are you overdoing it? Because there is no question, scientifically or anecdotally, that too much throwing leads to injury, and often it’s serious injury.” 


 Little League instituted pitch limits based on research conducted by Andrews and Fleisig. This season, the limits are 85 pitches a day for 11- to 12-year-olds and 75 pitches for 9- to 10-year-olds. Rules also mandate days off between pitching appearances. Other recommendations by Andrews, who is on Little League’s board, and Fleisig, who acts as a Little League adviser, include a break of months from overhand throwing and competitive pitching, a 100-inning annual limit, avoiding radar guns and barring pitchers from playing catcher. 


 In 2007, the first year of the Little League pitch restrictions, Tyler Richards and Kyle Cotcamp logged many innings as their Hamilton, Ohio, team reached the World Series. They also pitched for a travel team. 


 Two years later, Richards had Tommy John surgery. Kremchek performed the operation, as he did for Cotcamp last year. 


 “I just pitched way too much,” said Richards, now a high school junior who has resumed pitching. 


 He added: “I should have just said no. I should have rested my arm.”

Wednesday, March 14, 2012

Theralase Identifies Leading Anti-Cancer Drug Candidate

Pivotal Milestone Achieved – Theralase Advances Towards FDA Clinical Approval

Toronto, ON – March 14, 2012 - Theralase Technologies Inc. (TSXV: TLT) announced today that it is pursuing FDA Phase 1 approval for its patented Photo Dynamic Compounds (PDCs).

Theralase has successfully identified the leading drug candidate, which will be used for safety and efficacy clinical testing in human cancer patients. In multiple preclinical studies, the leading drug candidate has been selected from Theralase’s library of PDCs and has repeatedly demonstrated:
  • extremely high efficacy, virtually 100% kill rate, in various cancer cell lines including brain and colorectal cancers
  • robust destruction of sub cutaneous (under the skin) cancerous tumours in animals
  • extremely low toxicity
  • high stability, allowing for a long shelf life

The preclinical results have been reviewed by SPIE (The International Society for Optics and Photonics) and were accepted by the Conference Chairs for presentation at the SPIE Photonics Europe conference slated for April, 2012 in Brussels, Belgium.

Theralase will validate its extensive data with additional cancer animal models and toxicology analyses. This will provide the results required by the FDA to design a FDA Phase 1 clinical human study to commence in 2013 with scheduled completion in 2014.

Roger Dumoulin-White, President and CEO of Theralase Inc. stated, "Achievement of this critical milestone represents irrefutable proof that the Theralase leading drug PDC candidate is effective in the destruction of cancer in live animal models. The treatment was well tolerated by the animals, eliminating their cancer without any adverse effects. The Theralase leading drug candidate has been proven to be superior to any currently approved FDA PDC drug on the market, tested in our lab.


About Theralase Technologies Inc.
Theralase Technologies Inc. founded in 1995, designs, develops, manufactures and markets patented, superpulsed laser technology utilized in biostimulation and biodestruction applications. The technology is safe and effective in the treatment of chronic pain, neural muscular-skeletal conditions and wound healing. When combined with its patented, light-sensitive Photo Dynamic Compounds (PDCs), Theralase laser technology is able to specifically target and destroy cancers, bacteria and viruses, as well as microbial pathogens associated with food contamination. For further information please visit www.theralase.com, regulatory filings may be viewed by visiting www.sedar.com.  

This press release contains forward-looking statements which reflect the Company's current expectations regarding future events. The forward-looking statements involve risks and uncertainties. Actual results could differ materially from those projected herein. The Company disclaims any obligation to update these forward-looking statements.

Neither TSX Venture Exchange nor its Regulation Services Provider (as that term is defined in the policies of the TSX Venture Exchanges) accepts responsibility for the adequacy or accuracy of this release.


For More Information

Roger Dumoulin-White                                                                      
President & Chief Executive Officer                         
416-447-8455 ext. 225                                   
rwhite@theralase.com                                   

Kristina Hachey
Chief Financial Officer
416-447-8455 ext. 224

Dr. Arkady Mandel
Chief Scientific Officer
416-447-8455 ext. 242
amandel@theralase.com                  

Greg Bewsh
Director of Investor Relations,
416-447-8455 ext. 262

Monday, March 12, 2012

The OxyContin Switch - The Lost Battle on the War on Pain


OxyContin, a powerful painkiller, disappeared from Canada on March 1. It was replaced by OxyNEO, a chemically identical, but tamper-resistant version. The anger, confusion and physical pain that has resulted from this seemingly benign upgrade speaks volumes about what’s wrong with our approach to drugs in this country
We pay far too little attention to the effectiveness of medications used for legitimate purposes like pain control. At the same time, we fret incessantly about drug abuse while doing virtually nothing to prevent or treat addiction. Worse yet, we behave as if these challenges are somehow unrelated when, in fact, they are intricately linked.
The OxyContin story is a prime example of this public-policy hash and underscores the crying need for a plan, a strategy. We need a War on Pain a lot more than we need a War on Drugs.
Getting rid of OxyContin – a drug that can be crushed by addicts who want to snort or inject it rather than use it for its intended purpose, to relieve severe pain – is a good thing, at least superficially.
Concomitant with the disappearance of OxyContin, however, a number of provincial and federal drug plans have “de-listed” OxyNEO – meaning it is no longer paid for by public drug plans. While most patients already prescribed OxyContin will be able to get OxyNEO and have it paid for by the drug plan for a transitional period of up to a year, it will be very difficult for new patients to get the drug, other than those being treated for cancer or requiring it for palliative care.
This too is a good thing, at least theoretically.
Annual prescriptions for oxycodone (the generic name for OxyContin/OxyNEO) have soared nearly 80-fold since the drug was introduced in 2000. Far too many people are taking this highly addictive drug for far too long, especially since there is no research showing that long-term use is safe or effective.
Governments hope the new rules will slow the soaring number of oxycodone prescriptions – 1.6 million last year alone – and reduce drug plan costs, which exceed $150-million annually.
So why so much angst over a seemingly sensible change in public policy?
Two reasons: 1) Because the OxyContin decision will have a ripple effect, one that could have many unintended negative consequences; and 2) The decision, while well-intentioned, seems to ignore the harsh reality that chronic pain and addiction are sprawling societal problems that extend far beyond access – legitimate or otherwise – to a single drug.
Let’s start with the immediate consequences. There are an estimated 200,000 prescription drug addicts in Canada. (More than there are addicts hooked on illicit drugs, by the way. And the distinction is also an artificial one: Oxycodone is only a couple of molecules removed from heroin.) For many, OxyContin – known as hillbilly heroin – is the fix of choice.
With the new rules, one of two things will happen to Oxy addicts: Without access to OxyContin, they will suffer severe withdrawal, or they will switch to another form of opioids like hydromorphone (brand name Dilaudid) or heroin.
There are fewer than 100 “detoxification” beds (for those suffering withdrawal) in Canada; the waits for treatment stretch to six months and beyond. There are treatment programs that offer methadone and suboxone, but those too are in short supply.
There have been dire warnings of mass withdrawal in some first nations where OxyContin addiction is at epidemic levels, but this is unlikely. Far more likely is that new drugs will fill the void, and they will be even more costly. (The pharmacy price for OxyContin was between $1.25 and $6 a pill, depending on dosage; on the street, prices ranged from $5 to $80 a pill.) Bottom line: Those who want help kicking their opioids addiction will have little chance of getting it, and those who remain addicted will have an even more costly, desperate addiction.
But street users of OxyContin are just one part of the issue.
An estimated six million to seven million Canadians suffer from serious chronic pain. In the past decade, they have been treated increasingly with opioids, OxyContin in particular. That’s because it’s a slow-release drug that the maker, Purdue Pharma Canada, cleverly marketed as being less addictive. (Purdue’s parent company was fined more than $600-million for these misleading claims. The drug brings in $3.1-billion a year worldwide, so the fines weren’t too burdensome.) One of the principal reasons painkillers are overprescribed is that physicians get little formal training in dealing with pain; they tend to get their information from drug reps. Moreover, alternatives to drugs like physiotherapy and psychological counselling are not funded.
And while governments are cracking down on prescribing of OxyContin’s substitute, OxyNEO, they are not extending those measures to other opioids.
Without better physician education and improved prescribing guidelines, it is unlikely opioid use will be reduced.
Rather, patients will be switched to other drugs, like Dilaudid, which are just as addictive and far more powerful. These “conversions” are difficult for physicians and patients alike; the Ontario Pharmacists’ Association has warned its members that “unintentional dose escalation” is a serious concern. For many patients, the risk of overdose is very real – and one death has already been linked to conversion. (Opioids depress the central nervous system, meaning people can stop breathing if the dose is too high. OxyContin alone kills an estimated 1,000 people a year in Canada.)
This double whammy – the fear of being cut off painkillers and the risk of alternatives being even more dangerous than OxyContin – is concerning. It is certainly not what policymakers had in mind.
“We cannot let people with serious pain become collateral damage of the war on prescription drug abuse,” the Canadian Pain Society said in a statement.
But the reality is that people with chronic pain are already collateral damage. Frequently their physical pain is treated – often ineffectually – and the price is steep: addiction. In addition to their injuries and illnesses, those with chronic pain have been victims of aggressive marketing by Big Pharma, lack of investment in rehabilitation, inadequate research in pain control and short-sighted public policy.
It’s time for some relief from the suffering, and that will require concerted action.