I discovered this article last night on a simple Google search - oops Podesta Group, (see more) you are not on the ball... According to the University of Chicago:
Evidence mounts for link between opioids and cancer growth
March 21, 2012
Opioid drugs used to relieve pain in postoperative and chronic cancer patients may stimulate the growth and spread of tumors, according to two studies and a commentary in the 2012 annual Journal Symposium issue of Anesthesiology, the academic journal of the American Society of Anesthesiologists.
"Epidemiologic findings suggest that the type of anesthesia we do for cancer surgery influences recurrence rate, and laboratory studies demonstrate that opioids influence tumor progression and metastasis," said Jonathan Moss, MD, PhD, professor of anesthesiology and critical care at the University of Chicago Medicine and co-author of the commentary, a summary of research on the topic. "These studies have caused anesthesiologists to re-evaluate how best to do anesthesia and pain control for cancer patients."
New studies provide new clues
Opioid-based painkillers, such as morphine, have been the gold standard for treatment of postoperative and chronic cancer pain for 200 years. Several studies published since 2002, however, suggest that opioids can stimulate the growth and spread of cancer cells. Laboratory research from the University of Chicago Medicine and a genetic study from the University of North Carolina Medical Center both argue that the mu opioid receptor plays an important role in tumor progression and support a therapeutic role for opioid antagonists.
One study presented in the journal -- from a group led by Patrick Singleton, PhD, assistant professor of medicine at the University of Chicago Medicine -- shows how opioids already present in the body can enhance the malignant tendencies of human lung cancer cells transplanted into mice, even without the addition of morphine.
Singleton's team found that cells from various types of human lung cancers have five to 10 times as many opioid receptors as non-cancerous lung cells. They mapped out two of the biochemical pathways -- Akt and mTOR, both targets for current chemotherapeutics -- triggered by contact between endogenous opioids and the receptors. They also show how this interaction can increase proliferation, migration and invasion of tumor cells, three hallmarks of cancer growth and spread.
In this study, human lung cancer cells with additional copies of the opioid receptor grew more than twice as fast as tumor cells that lacked extra receptors when transplanted into mice. More troubling, they were 20 times more likely to spread to distant sites. Medications that block the opioid receptors, such as naloxone or methylnaltrexone, reduced tumor growth and spread. "Our findings," they conclude, "suggest the mu opioid receptor may be a therapeutic target."
The other paper in the journal, a retrospective study by Andrey Bortsov, MD, PhD, assistant professor of anesthesiology and colleagues at the University of North Carolina, used human data to bolster the opioid-cancer link.
Bortsov's team looked at survival rates from an earlier study of more than 2,000 breast cancer patients. Women being treated for invasive breast cancer who had a tiny genetic mutation that made them less sensitive to opioids were much more likely to be alive 10 years after cancer treatment. Women with one copy of the protective mutation were nearly twice as likely to have survived; those with two copies were four times as likely.
"The results of this study," the authors wrote, "provide support for the hypothesis that endogenous and/or exogenous opioids, acting via the mu opioid receptor, may influence cancer outcomes."
Emergence of concern
The notion that opioids could encourage cancer growth started with a 2002 laboratory report from the University of Minnesota. Later, a randomized palliative-care trial from Virginia Commonwealth University found that patients who received spinal opiates (OK) rather than systemic pain relief survived longer. Then two retrospective studies showed that breast or prostate cancer patients who received local or regional anesthesia rather than systemic morphine had improved survival after surgery. More recent epidemiologic studies in colon cancer, however, failed to confirm the relationship.
Moss and University of Chicago colleagues approached the issue from a similar angle. They were involved in clinical trials of methylnaltrexone, a drug developed at the University of Chicago and approved by the Food and Drug Administration in 2008. This drug, marketed as Relistor™, was designed to block the peripheral side effects of opioids, such as nausea and constipation, without disrupting pain relief, which occurs in the brain. Following an early clinical study, Moss and colleagues noted that cancer patients receiving this peripheral opioid blocker in a compassionate-use protocol lived longer than expected.
"These were patients with advanced cancer and a life expectancy of one to two months," Moss recalled, "yet several lived for another five or six months. It made us wonder whether this was just a consequence of better GI function, or could there possibly be an effect on the tumors?"
They began a series of studies looking at the many peripheral effects of opioids and the potential benefits of blocking those effects. They found that those opioids enhanced tumor growth, angiogenesis, vascular permeability and metastasis. Drugs that blocked the opioid receptor reduced cancer growth and helped prevent invasion and metastasis. Tumors did not grow in mice that lacked the mu opioid receptor.
In a commentary in the journal, Moss, Singleton and Frances Lennon, PhD, summarize results from multiple studies to argue that opioids -- drugs like morphine or the body's own opioids, such as endorphins -- appear to have a significant and direct proliferative effect on cancer cells, aside from their effect suppressing immunity. They suggest a possible therapeutic role for mu opioid receptor antagonists on cancer growth and metastasis, but caution that "there are no clinical trials in humans demonstrating a direct effect."
Funding for the studies was provided by the National Cancer Institute, the University of North Carolina and the University of Chicago. Moss, one of the developers of methylnaltrexone, receives royalties from its sale and is a paid consultant for its distributor, Salix Pharmaceuticals Inc.
While researching common opiods that people may not recognize to be opioids, such as Tramadol, I found out that Egypt bans Tramadol and has even possibly given the death penalty out to people who traffick it into their country:
What is tramadol, how dangerous is it – and where is it illegal?
November 7, 2017
An Englishwoman named Laura Plummer is in jail in Egypt on suspicion of drug trafficking 290 tramadol tablets. The tablets (available on prescription in the UK) were found in her suitcase when it was examined at Hurghada international airport on Egypt’s Red Sea coast on October 9. She’s reported to have been given them by a colleague to treat her Egyptian husband’s sore back and has said that she had “no idea” they were illegal in the country. So what is tramadol and why are the Egyptian authorities so concerned?
Tramadol, which does not occur in nature, was first synthesised in 1962 by chemists at the German pharmaceutical company Grünenthal as a painkiller. The company became notorious 50 years ago as the firm that marketed thalidomide, which when taken by pregnant women as a sedative and treatment for “morning sickness” led to the birth of thousands of children with malformed or missing limbs. Tramadol is an entirely different drug but there is a real possibility of taking a lethal overdose.
Patents were taken out on tramadol in 1972 and it was brought to market in 1977. The drug is recognised as a painkiller with a potency around 10% that of morphine and it is used to treat moderate to severe acute and chronic pain. Like morphine, it works by binding to the mu-opioid receptor found in the brain and in other regions of the body, stopping pain messages from getting through. It inhibits re-uptake of the neurotransmitter messenger molecules norepinephrine (noradrenalin) and serotonin and also has antidepressant and anti-anxiety properties.
In the body, tramadol is metabolised into a number of different molecules, the most important of which is O-desmethyltramadol; this binds much more strongly to the mu-opioid receptor than tramadol does, making it more potent than the parent compound. So tramadol is really a pro-drug, a molecule that is converted by the body’s metabolism into the pharmacologically active drug.
Widespread use
Perhaps not surprisingly, tramadol has reared its head in sport. After he retired in 2012, the professional cyclist Michael Barry wrote in his autobiography, Shadows on the Road, that he’d used tramadol while cycling in the Sky team. He took tramadol (which after all is a legal painkiller in most countries) when he broke his ribs in a crash. He said that it alleviated the pain, made him feel “slightly euphoric” and reckoned that he could push harder than usual when on it.
Because of concerns about the use and abuse of painkillers in sport there have been calls for WADA, the World Anti-Doping Agency, to prohibit the use of tramadol (like many steroids, EPO, amphetamines and other stimulants) and put it on its prohibited list, but currently it remains on their list of medications whose use is monitored, such as caffeine, nicotine, codeine and certain others. A research programme is being run to see if tramadol confers advantages upon sportsmen.
Painkiller abuse and addiction is a major problem in the US, where events have moved on from the days when heroin was the drug of choice that killed rock stars such as Jim Morrison and Janis Joplin. Now, it is prescription painkillers, such as oxycodone (in its formulation as OxyContin, “hillbilly heroin”) and fentanyl (which killed Prince) which are proving lethal in the wrong hands.
Tramadol’s first 20 years on sale were unspectacular and it was not until around the time that it was introduced onto the US market in the 1990s that addiction started to be a problem. This has now spread to the Far East, including China, as well as much of Africa.
It is widely abused in Cameroon, for example, where it is even fed to cattle to enable them to plough in the hottest weather.
Because of this consumption by humans and animals, excreted tramadol (and its metabolites) can be present in soil in some parts of the Cameroon so that it is taken up by plants. At one stage, this led scientists to believe that it occurred naturally in the pincushion tree – although it has subsequently been shown that plants are incapable of producing it.
The Egyptian problem
Egypt has a particular problem with tramadol. It is a prescription drug in the UK and a Schedule IV controlled substance in the US, but in Egypt, any opioid, including tramadol and codeine, is a controlled substance. Consequently, bringing it into the country without prior permission, especially in large quantities (Laura Plummer had 290 tablets), will land you in trouble. The Egyptian authorities have come down hard on people in possession of significant amounts of tramadol, and the courts dish out stiff punishments – possibly even the death penalty.
Nevertheless, tramadol is popular in Egypt and is misused widely. Indeed, besides it being a recreational drug, many people – especially from the poor working class – take tramadol to give them more energy, to work for longer or to hold down two jobs.
It has been a particularly serious problem in places such as Gaza, where addiction has led to an illegal trade in tramadol, often smuggled in through underground tunnels. This has led the government to take a particularly hard line on it.
So if you are going to take drugs abroad, even your own medications, you should check carefully how they are viewed at your destination. A legal drug in one country could lead to a very long prison sentence – or even worse – in another.