Carrots and pumpkin might reduce your risk of cancer, but beware taking them in pill form

A diet rich in fruit and vegetables is more than just a sum of its individual nutrients. From www.shutterstock.com

Simon Chapman, University of Sydney

In February this year, ABC’s Four Corners broadcast a critical and compelling program on complementary medicines, Swallowing it: How Australians are spending billions on unproven vitamins and supplements.

The program certainly tapped into a growing trend. The value of the global vitamins and dietary supplements market is predicted to reach US$59.6 billion by 2020; in Australia in 2014-15, 49% of women and 34% of men had bought vitamins in the past six months. Companies like Swisse and Blackmores have a lot riding on keeping up this demand.

Yet, the vast majority of this mass consumption, often helped along by celebrity endorsement, is just generating oceans of very expensive urine; relatively few people have medical conditions requiring specific nutrient supplements.

So why do so many people waste their money?

Seduced by reductionism

Scientific reductionism is the seductive “mental shortcut” or cognitive heuristic that assumes you can understand complex phenomena by analysing each of its elements: the whole is just the sum of its parts.

In reductionist reasoning, a piece of fruit is nothing more than the sum of all the compounds it contains. So if you don’t have enough time to buy, cook and eat a diet rich in the sources of vitamins and minerals we all need, you can buy a set of pills containing the vitamins and other nutrients that go to make up a carrot, a fish or a banana.

Right? No, actually.

A good example of the simplistic appeal of reductionism is the assumption that because tobacco smoke has over 70 known carcinogens, removing some of them will make smoking less dangerous. A no-brainer?

This is what three major US tobacco companies once tried to imply when they chemically engineered “reduced carcinogen” brands.

But a study of cigarette smoke emissions across different brands concluded that reducing some carcinogens in the smoke mix had two effects – “risk swapping”, when one specific carcinogen exposure was reduced at the cost of another’s exposure increasing, or “risk shifting”, when a specific exposure was reduced at the cost of that exposure increasing within another carcinogen group.

The impact on actual carcinogenic risk remains unknown when tobacco companies manipulate the presence of one or several carcinogens but sell products with all the 68 or so others intact.

Dietary reductionism

Reductionist thinking flourishes most in popular understanding of nutrition and is at the very epicentre of the appeal of complementary medicine. The vitamin and supplement shelves of pharmacies and complementary medicine shops are groaning with single and multi-vitamin and supplement bottles all promising swallowing their contents daily just must be good for you.

Perhaps the most famous of all salutary tales about the folly of reductionist thinking in medicine concerns beta-carotene. Beta-carotene is an organic red-orange pigment abundant in plants and fruits. It is a member of the carotenoid group, the main source of vitamin A in our diets (along with retinol in liver, butter, cheese and chicken skin). Beta-carotene levels in the diet are seen as a good indicator of overall fruit and vegetable consumption. Carrot, orange sweet potato and pumpkin are the richest sources of beta-carotene, with spinach and kale and any brightly coloured fruits and vegetables also good sources.

Studies of the diets of whole populations and their sub-groups (such as vegetarians) had long observed those who ate the most beta-carotene tended to have lower population-wide rates of several cancers.

Could beta-carotene pills prevent cancer?

By the early 1980s, leading epidemiologists like Oxford University’s Richard Doll and Richard Peto were speculating that diets high in beta-carotene protected people from developing cancer. This speculation stimulated several long-term trials of whether taking beta-carotene supplement pills might influence cancer rates.

The most famous was the Carotene and Retinol Efficacy Trial (CARET). In this study, people – including those at high risk of cancer like those exposed to asbestos at work, and smokers – were given daily 30mg of beta carotene plus 25,000IU of retinol and followed for an average four years between 1983 and 1997.

In May 1996, the bombshell results from the study were published in the New England Journal of Medicine. A total of 388 new cases of lung cancer were diagnosed. And the clanger? The study participants randomised to receive the beta-carotene and retinol supplements had a 28% higher incidence of lung cancer than those given placebos. As a result, the trial was stopped 21 months early.

The study provoked intense interest and commentary. In 2008, a meta-analysis of four studies of beta-carotene supplementation involving 109,394 people taking an average of 20-30mg of beta-carotene supplements a day confirmed the CARET results. It found that in smokers, those taking the supplements had a 24% increased risk of lung cancer. Beta-carotene was found in 70% of 47 common multivitamins used by people in the studies.

The beta-carotene supplementation story is a textbook illustration of the folly of reductionist thinking in preventive health. As one letter writer to the New England Journal of Medicine put it:

Beta-carotene was also acting as a marker of increased fruit and vegetable consumption and thus of many other components that have cancer-preventing potential (Vitamin C, folate, other carotenoids, polyphenols, and many plant compounds).

Others argued the dose of beta-carotene in the CARET study pill was too high. Others argued the specific form of beta carotene likely used in the CARET trial (all-trans-beta-carotene) was just one of 272 different isomers of beta-carotene and was probably chosen because it was the only one made commercially in large quantities (by BASF, Hoffmann-La Roche, and Sumitomo) and available for purchase. Perhaps the people who conducted the study, they argued, picked the wrong beta-carotene?

All these “what ifs?” may well have substance and we may one day find the holy grail of cancer preventing agents. But when the results are highly unlikely to be much different to the preventive effects of eating a mixed diet emphasising fruit and vegetables, I know which plan to continue to follow.

Simon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

New study: no increase in brain cancer across 29 years of mobile use in Australia

Simon Chapman, University of Sydney

Earlier this year, Australia saw a whirlwind tour from the electromagnetic radiation from mobile phones alarmist Devra Davis. Davis is an international champion of the belief that populations bathed in radiation emitted by mobile phones face epidemics of disease – particularly brain cancer.

Davis’ concerns were the focus of an ABC Catalyst program which attracted widespread criticism, including from me and Media Watch. The Catalyst presenter Maryanne Demasi was nominated for the Australian Skeptics bent spoon award.

At the time of the Catalyst program for which I declined to be interviewed, I had my hands tied behind my back because, with colleagues in cancer research, I had a paper in preparation examining the possible association between the incidence of brain cancer in Australia and the inexorable rise of mobile phone use here over the last three decades. Releasing our findings would have jeopardised publication, we could say nothing about what we had concluded.

Today the paper is published in early view in Cancer Epidemiology. Here’s what we set out to examine and what we found.

We examined the association between age and gender-specific incidence rates of 19,858 men and 14,222 women diagnosed with brain cancer in Australia between 1982-2012, and national mobile phone usage data from 1987-2012.

In summary, with extremely high proportions of the population having used mobile phones across some 20-plus years (from about 9% in 1993 to about 90% today), we found that age-adjusted brain cancer incidence rates (in those aged 20-84 years, per 100,000 people) had risen only slightly in males but were stable over 30 years in females.

There were significant increases in brain cancer incidence only in those aged 70 years or more. But the increase in incidence in this age group began from 1982, before the introduction of mobile phones in 1987 and so could not be explained by it. Here, the most likely explanation of the rise in this older age group was improved diagnosis.

Computed tomography (CT), magnetic resonance imaging (MRI) and related techniques, introduced in Australia in the late 1970s, are able to discern brain tumours which could have otherwise remained undiagnosed without this equipment. It has long been recognised that brain tumours mimic several seemingly unrelated symptoms in the elderly including stroke and dementia, and so it is likely that their diagnosis had been previously overlooked.

Next, we also compared the actual incidence of brain cancer over this time with the numbers of new cases of brain cancer that would be expected if the “mobile phones cause brain cancer” hypothesis was true. Here, our testing model assumed a ten-year lag period from mobile phone use commencement to evidence of a rise in brain cancer cases.

Our model assumed that mobile phones would cause a 50% increase in incidence over the background incidence of brain cancer. This was a conservative estimate that we took from a study by Lennart Hardell and colleagues (who reported even higher rates from two studies). The expected number of cases in 2012 (had the phone hypothesis been true) was 1,866 cases, while the number recorded was 1,435.

Using a recent paper that had Davis as an author we also modelled a 150% increase in brain cancer incidence among heavy users. We assumed that 19% of the Australian population fell into this category, based on data from the INTERPHONE study an international pooled analysis of studies on the association between mobile phone use and the brain. This would have predicted 2,038 expected cases in 2012, but only 1,435 were recorded.

Our study follows those published about the United States, England, the Nordic countries and New Zealand where confirmation of the “mobile phones cause brain cancer” hypothesis was also not found.

In Australia, all cancer is notifiable. At diagnosis, all cases must by law be registered with state registries tasked with collecting this information. It has been this way for decades. So we have excellent information about the incidence of all cancers on a national basis.

The telecommunications industry of course also has information on the number of people with mobile phone accounts.

While touring Australia, Davis was confronted with the “flatline” incidence data on brain cancer. Her stock response was that it was far too early to see any rise in these cancers. She was here to warn us about the future.

However, prominent Sydney neurosurgeon Dr Charlie Teo would appear to disagree about it being too early. He told Andrew Denton on ABC-TV’s Enough Rope in 2008:

If you look at the science on mobile phones and the link with brain cancer, it is quite compelling … we know that radiation causes cancer, but it takes about ten years for it to develop, so we know that EMR electromagnetic radiation is going to take at least ten years to create brain tumours and possibly longer fifteen, twenty years.

In cancer epidemiology, the concept of the latency (or lag) period is well known. This refers to the time that it takes between initial exposure to a potentially carcinogenic agent (like cigarette smoke, asbestos, or nuclear radiation) and excess cases of cancers of interest to appear.

Davis would appear to be arguing that we would see a sudden rise many years later. That is not what we see with cancer; we see gradual rises moving toward peak incidence, which can be as late as 30-40 years (as with lung cancer and smoking).

For example, as I showed in a recent Conversation piece, this paper also reports on central nervous system cancers (including brain cancers) in those exposed to atomic bomb radiation in Japan in 1945. This graph shows 110 of 187 cases (58.8%) were diagnosed in the first 40 years (before 1985) (so before 40 years).

https://datawrapper.dwcdn.net/yJ7ej/3/

The incidence and type of cancers of those exposed to atomic bomb radiation varied over the years. And this quote from the methods section shows that there were another 27 who died before 1958 from central nervous system cancers, within 13 years of the bombs.

We excluded 73 tumours in individuals who were not in Hiroshima or Nagasaki at the time of the bombings, 35 individuals who did not have available organ dose estimates, and 27 individuals who died or were diagnosed before January 1, 1958.

Note here that A-bomb survivors were affected by ionising radiation (that is, radiation of sufficient energy to produce ionisation). This is where the energy is strong enough to remove electrons off their atoms or molecules, including causing DNA damage. Mobile phones produce non-ionising radiation which is low energy, sufficient only to ‘excite’ the electrons enough to make them just heat up.

We have had mobiles in Australia since 1987. Some 90% of the population use them today and many of these have used them for a lot longer than 20 years. But we are seeing no rise in the incidence of brain cancer against the background rate.

Simon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

 

Ten myths about smoking that will not die

Simon Chapman, University of Sydney

Across forty years I’ve come to recognise many factoid-driven myths about smoking that just won’t die. If I asked for a dollar each time I had to refute these statements, I’d have accumulated a small fortune.

Their persistence owes much to their being a vehicle for those who utter them to express unvoiced but clear sub-texts that reflect deeply held beliefs about women, the disadvantaged, mental illness, government health campaigns and the “natural”.

Let’s drive a stake through the heart of ten of the most common myths.

1. Women and girls smoke more than men and boys

Women have never smoked more than men. Occasionally, a survey will show one age band where it’s the other way around, but from the earliest mass uptake of smoking in the first decades of last century, men streaked out way ahead of women.

In 1945 in Australia, 72% of men and 26% of women smoked. By 1976, men had fallen to 43% and women had risen to 33%.

As a result, men’s tobacco-caused death rates have always been much higher than those of women. Women’s lung cancer rates, for example, seem unlikely to reach even half the peak rates that we saw among men in the 1970s.

Currently in Australia, 15% of men and 12% of women smoke daily.

But what about all the “young girls” you can see smoking, I’m always being told. In 2014, 13% of 17-year-old male high school students and 11% of females smoked. In two younger age bands, girls smoked more (by a single percentage point).

Those who keep on insisting girls smoke more are probably just letting their sexist outrage show about noticing girls’ smoking than their ignorance about the data.

2. Quit campaigns don’t work on low socioeconomic smokers

In Australia, 11% of those in the highest quintile of economic advantage smoke, compared with 27.6% in the lowest quintile. More than double.

So does this mean that our quit campaigns “don’t work” on the least well-off?

Smoking prevalence data reflect two things: the proportion of people who ever smoked, and the proportion who quit.

If we look at the most disadvantaged groups, we find that a far higher proportion take up smoking than in their more well-to-do counterparts have never smoked (39.5% vs 50.4%) – see table 9.2.6).

When it comes to quitting, 46% of the most disadvantaged have quit compared to 66% of the least disadvantaged (see table 9.2.9).

There is a higher percentage of the disadvantaged who smoke mainly because more take it up, not because disadvantaged smokers can’t or won’t quit. With 27.6% of the most disadvantage smoking today, the good news is that nearly three-quarters don’t. Smoking and disadvantage are hardly inseparable.

3. Scare campaigns ‘don’t work’

Countless studies have asked ex-smokers why they stopped and current smokers about why they are trying to stop. I have never seen such a study when there was not daylight between the first reason cited (worry about health consequences) and the second most nominated reason (usually cost).

For example, this national US study covering 13 years showed “concern for your own current or future health” was nominated by 91.6% of ex-smokers as the main reason they quit, compared with 58.7% naming expense and 55.7% being concerned about the impact of their smoking on others.

If information and warnings about the dire consequences of smoking “don’t work”, then from where do all these ex-smokers ever get these top-of-mind concerns? They don’t pop into their heads by magic. They encounter them via anti-smoking campaigns, pack warnings, news stories about research and personal experiences with dying family and friends. The scare campaigns work.

4. Roll-your-own tobacco is more ‘natural’ than factory made

People who smoke rollies often look you in the eye and tell you that factory made cigarettes are full of chemical additives, while roll-your-own tobacco is “natural” – it’s just tobacco. The reasoning here that we are supposed to understand is that it’s these chemicals that are the problem, while the tobacco, being “natural”, is somehow OK.

This myth was first turned very unceremoniously on its head when New Zealand authorities ordered the tobacco companies to provide them with data on the total weight of additives in factory made cigarettes, roll-your-own and pipe tobacco.

For example, data from 1991 supplied by WD & HO Wills showed that in 879,219kg of cigarettes, there was 1,803kg of additives (0.2%). While in 366,036kg of roll-your-own tobacco, there was 82,456kg of additives (22.5%)!

Roll-your-own tobacco is pickled in flavouring and humectant chemicals, the latter being used to keep the tobacco from drying out when smokers expose the tobacco to the air 20 or more times a day when they remove tobacco to roll up a cigarette.

5. Nearly all people with schizophrenia smoke

It’s true that people with mental health problems are much more likely to smoke than those without diagnosed mental health conditions. A meta-analysis of 42 studies on tobacco smoking by those with schizophrenia found an average 62% smoking prevalence (range 14%-88%). But guess which study in these 42 gets cited and quoted far more than any of the others?

If you said the one reporting 88% smoking prevalence you’d be correct. This small 1986 US study of just 277 outpatients with schizophrenia has today been cited a remarkable 1,135 times. With colleagues, I investigated this flagrant example of citation bias (where startling but atypical results stand out in literature searches and get high citations – “wow! This one’s got a high number, let’s quote that one!”).

By googling “How many schizophrenics smoke”, we showed how this percolates into the community via media reports where figures are rounded up in statements such as, “As many as 90% of schizophrenic patients smoke.”

Endlessly repeating that “90%” of those with schizophrenia smoke does these people a real disservice. We would not tolerate such inaccuracy about any other group.

6. Everyone knows the risks of smoking

Knowledge about the risks of smoking can exist at four levels:

• Level 1: having heard that smoking increases health risks.
• Level 2: being aware that specific diseases are caused by smoking.
• Level 3: accurately appreciating the meaning, severity, and probabilities of developing tobacco related diseases.

Level 4: personally accepting that the risks inherent in levels 1–3 apply to one’s own risk of contracting such diseases.

Level 1 knowledge is very high, but as you move up the levels, knowledge and understanding greatly diminish. Very few people, for example, are likely to know that two in three long term smokers will die of a smoking caused disease, nor the average number of years that smokers lose off normal life expectancy.

7. You can reduce the health risks of smoking by just cutting down

It’s true that if you smoke five cigarettes a day rather than 20, your lifetime risk of early death is less (although check the risks for one to four cigarettes a day here).

But trying to “reverse engineer” the risk by just cutting down rather than quitting has been shown in at least four large cohort studies such as this one to confer no harm reduction.

If you want to reduce risk, quitting altogether should be your goal.

8. Air pollution is the real cause of lung cancer

Air pollution is unequivocally a major health risk. By “pollution”, those who make this argument don’t mean natural particulate matter such as pollen and soil dusts, they mean nasty industrial and vehicle pollution.

The most polluted areas of Australia are cities where pollution from industry and motor vehicle emissions are most concentrated. Remote regions of the country are the least polluted, so if we wanted to consider the relative contributions of air pollution and smoking to smoking-caused diseases, an obvious question to ask would be “does the incidence of lung cancer differ between heavily polluted cities and very unpolluted remote areas?”

Yes it does. Lung cancer incidence is highest in Australia in (wait for this …) in the least polluted very remote regions of the country, where smoking prevalence happens also to be highest.

9. Smokers should not try to quit without professional help or drugs

If you ask 100 ex-smokers how they quit, between two-thirds and three-quarters will tell you they quit unaided: on their final successful quit attempt, they did not use nicotine replacement therapy, prescribed drugs, or go to some dedicated smoking cessation clinic or experience the laying on of hands from some alternative medicine therapist. They quit unaided.

So if you ask the question: “What method is used by most successful quitters when they quit?” The answer is cold turkey.

Fine print on this English National Health Service poster states a bald-faced lie by saying that “There are some people who can go cold turkey and stop. But there aren’t many of them.” In the years before nicotine-replacement threapy and other drugs were available, many millions – including heavy smokers – quit smoking without any assistance. That’s a message that the pharmaceutical industry was rather not megaphoned.

Not true. NHS poster.

10. Many smokers live into very old age: so it can’t be that harmful

In just the way that five out of six participants in a round of deadly Russian roulette might proclaim that putting a loaded gun to their head and pulling the trigger caused no harm, those who use this argument are just ignorant of risks and probability.

Many probably buy lottery tickets with the same deep knowing that they have a good chance of winning.

Simon Chapman, Emeritus Professor in Public Health, University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

 

Cancer drug promises to break down barrier to HIV cure

Nicola McCaskill, The Conversation and Sasha Petrova, The Conversation

Researchers have found a promising way of kicking the AIDS virus out of its hiding place in infected cells, potentially removing the main obstacle to curing HIV.

While antiretroviral treatment successfully suppresses HIV replication in an infected person, it can’t completely remove the virus. This is due to the virus’ ability to integrate itself into the DNA of cells, where it can lie dormant and invisible to the body’s immune system for years.

These so-called “reservoirs” of what is known as “latent virus” are the primary barrier to an HIV cure. Recent research has focused on a “shock and kill” method, to shock the dormant virus out of its comfortable place in the reservoir. When the virus is active, it becomes a visible target to kill.

Previous attempts with agents called histone deacetylase (HDAC) inhibitors have shown inconsistent results. HDACs, that enable a virus to coil tightly around a cell’s DNA, are the primary reason for its successful ability to hide undetected.

If an HDAC inhibitor is potent enough, it could stimulate the unravelling and activation of the virus. Research published today in PLOS Pathogens shows the HDAC inhibitor, romidepsin – a drug currently being used to treat cancer – to be the most potent, and thus successful, inhibitor trialled so far.

Six patients, who had been on antiretroviral treatment for around 10 years, each received three transfusions of romidepsin. The dormant HIV was activated in five of the participants, making it a detectable target for elimination.

University of Melbourne Professor and Director of the Doherty Institute, Sharon Lewin, said the results were promising.

“It is an interesting study because it shows the effects of a more potent drug, which can activate or kick the virus out of hiding,” she said.

Researchers also found romidepsin coaxed the virus out of its reservoir without suppressing the body’s broader immune response.

“There’s been some concern that these drugs will suppress an immune response to the virus, and they looked pretty comprehensively to show that there was no suppression of immune function, so that was encouraging as well,” said Professor Lewin, who was not involved in the study.

Dr Kersten Koelsch, who was involved in the study, explained there had been concerns the HDAC inhibitors might negatively affect T cell responses, which play an important part in fighting infection.

“We know that the HIV reservoir needs to be controlled to some extent by T cell responses,” said Dr Koelsch, who is a senior lecturer at UNSW Australia’s Kirby Institute. “So if you had a weak T cell response after an intervention, that would be counterproductive. But it appears that this is not the case with these HDAC inhibitors.”

But Dr Koelsch also stressed that although the results were positive, researchers were by no means close to a HIV cure.

“Unless a miracle happens, there’s not going to be a cure for HIV for at least 10 or even 20 years,” he said.

“Small studies like this can be very informative for the next study which can then build upon it, and the next study will then be another piece in the puzzle that will be important to design the study afterwards.”

He said romidepsin was a “promising agent to check in future studies in combination with immunotherapies or vaccines.”

This will indeed be the next phase of the two-part trial, which will use a combined therapy of romidepsin with a HIV vaccine to kill the infected cells.

“Combination studies are of highest interest now. We need to know whether the combination of activation of the virus with boosting the immune system will actually clear the infected cell. That’s really what we’re after now,“ said Professor Lewin.

Senior Research Officer at the Burnet Institute, Lachlan Gray said the latest research was extremely promising. But he added there were limitations to current HIV research as it focused only on eliminatig the viral reservoir in the blood.

“Tackling the blood reservoir has been the major focus of cure research to this point, predominantly because it is the major HIV reservoir. Importantly, this research sets the scene for efforts focused on non-blood reservoirs such as the gut, and brain” said Dr Gray, who researches HIV replication in brain cells.

“To completely eradicate HIV from the infected individual, that is, where there’s a complete elimination of every HIV infected cell in the body, we need to target all reservoirs, not just the predominant blood reservoir.”

“I think we’re making inroads, and the more research, the more information gathered from important studies such as this, the closer we get to the end goal, which is curing HIV,” he said.

Nicola McCaskill, Editor, The Conversation and Sasha Petrova, Editor, The Conversation

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.
 

Cluster bomb of new research explodes tobacco industry lies about plain packs

Simon Chapman, University of Sydney

There is near-universal agreement that Australia’s implementation of tobacco plain packaging in December 2012 has seen the most virulent opposition ever experienced from the global tobacco industry.

While the industry bravely insisted early in its campaigning that plain packs “would not work” their legal actions, campaign expenditure, lobbying and general apoplexy rather suggests they feared it would be a devastating policy, with long term global ramifications.

Indeed, eleven other nations (Ireland, England, New Zealand, France, Norway, Finland, Chile, Brazil, India, South Africa, Turkey) have either legislated plain packaging or are now warming up to do so.

University of Sydney researcher Becky Freeman and I catalogued the full range of industry lies in our recently released (free) book Removing the Emperor’s Clothes. The Cancer Council Victoria has also published extremely detailed rebuttals to the major industry scuttlebutt.

Now today, the British Medical Journal’s specialist journal Tobacco Control has published a special collection of new research which puts further 10,000 watt arc lights on specious industry claims.

Key industry claims have included that plain packs would:

• Drive prices down, as smokers turn away from buying expensive premium brands because they look exactly the same as cheap brands (other than brand names). More affordable cigarettes, they argued, would cause more smoking, including among children
• Flood Australia with illegal tobacco
• Cause smokers to stop buying cigarettes at small convenience stores
• Prompt smokers to use special covers to conceal the large-scale graphic warnings on packs.

Price falls?

One of the new Tobacco Control papers monitors changes in recommended retail prices RRPs from one year before plain packs were introduced until one year after. Prices were adjusted to 2013 prices, and for inflation and average cigarette price stick and grams of roll-your-own tobacco.

The RRPs of tobacco products were higher in real terms one year after the legislation was implemented. Importantly, these increases exceeded increases resulting from consumer price indexation of duty and occurred across all three major manufacturers for both factory made and roll-your-own brands, all three cigarette market segments and all major pack sizes.

Tobacco prices rose most for leading and premium brands 10.0% and 10.1%, respectively) and among packs of 30s (18.3%) and 50s (12.5%). So far from seeing cigarette prices fall across the board, the industry raised prices.

Floods of illicit tobacco?

The tobacco industry’s most common claim was that plain packs would see smokers turn away from buying the purposefully confronting and unattractive plain packs and seek out illegal products not in plain packs.

Tobacco spokespeople made the outrageous claim that about one in seven of all cigarettes being smoked were such illegally obtained cigarettes. Apparently, while ordinary smokers across the country knew where to buy these easily, the full might and resources of the Australian Federal Police could not work out where these were being sold.

Tobacco companies have been proven wrong. Source: Curran Kelleher/Flickr, CC BY

Another study in the collection questioned 8,679 smokers across the country in telephone surveys conducted continuously, from six months before plain packs until 15 months afterwards.

The study found no significant increases in reported purchasing of “cheap whites” (illegally imported Asian sourced brands), of international brands selling for 20% or more less than the normal retail price, or of unbranded loose tobacco (so-called “chop chop”).

Rates of purchase of cheap whites and heavily discounted products were at around half of one per cent of smokers, nothing remotely like one in seven.

Small shops losing customers?

One of the most bizarre claims the industry made was that plain packs would see smokers deserting corner stores for larger retail outlets like supermarkets. This was an appeal designed to tap into wider public sentiment about local corner store owners being crushed under the dead weight of government regulation.

Those making the claim never explained why smokers would abandon small retailers for large ones because of plain packs when the very same packs would be sold in both. Consumer preference for larger retailers is entirely driven by price discounting, something never mentioned in the industry propaganda.

A third paper in the collection examined where smokers purchased their cigarettes. Unsurprisingly, it found no changes from prior to and after the introduction plain packs in where smokers bought their supplies.

Covering up the packs?

In the month that plain packs were introduced, a Queensland small businessman got his 15 minutes of fame from publicity about special pack covers that could block out the unforgettable graphic warnings. Like children covering their eyes from scary scenes in movies, the idea was that many smokers would rush to do the same, outsmarting the hapless bureaucrats who planned the legislation.

A fourth paper which reports on unobtrusive observations of smokers handling their packs in outdoor cafés found that prior to plain packs, just 1.2% of outdoor café smokers used pack covers. This rose to 3.5% in the early months of plain packs and then fell back to 1.9% one year later.

In any event, evidence shows that smokers who actively try to avoid exposure to pack warnings by covering them up, have higher subsequent rates of quit attempts than those who don’t.

Importantly too, these observations recorded that of all café outdoor patrons, one in 8.7 displayed a pack prior to the introduction of plain packs with this reducing to one in 10.3 afterwards. Such a fall is consistent with both a reduction in smoking prevalence and with growing self-consciousness among smokers about showing that they smoke in public.

Impact on adolescents?

There were several principal objectives of the plain packs legislation. But outstanding among these was the goal of making smoking less desirable among young people. This would continue the trend away from smoking, as each successive cohort of children chose not to take up the habit.

A fifth paper used school-based surveys prior to and after plain packs to examine students’ ratings of the “character” of four popular cigarette brands, and variables including perceived harmfulness, look of pack and positive and negative perceptions of pack image.

Positive character ratings for each brand reduced significantly between 2011 and 2013. Significantly fewer students in 2013 than 2011 agreed that “some brands have better looking packs than others” and packs were rated more negatively, with positive ratings decreasing most in smokers.

The tobacco industry and its acolytes can be expected to try to torture these reports to spin yet more denials of the impact it fears will quickly inspire even more countries to follow Australia’s lead.

Australia is fortunate in having some of the very best researchers in the world whose work has contributed to the development of plain packs and now to the evaluation of its impact.

Editor’s note: please ensure your comments are courteous and on-topic.

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

Why the causes of cancer are more than just random bad luck

By Darren Saunders, Garvan Institute

What causes cancer? This deceptively simple question has a devilishly complex answer. So when US researchers proposed a relatively simple mathematical formula to explain a long-standing conundrum in cancer earlier this year, it was bound to get a lot of attention.

The study published in the journal Science suggested a correlation between the variation in cancer occurrence between different tissues and the number of stem cell divisions in each tissue. In other words, it said the tissues most vulnerable to cancer are those with the greatest number of stem cell divisions.

Most of the reporting about the research ran with the line that “cancer is all down to bad luck”, implying that developing the disease is out of our hands and that preventative efforts might be useless. But is that really the case?

Much of the misunderstanding seems to have arisen from the authors’ statement that a third of the variation in cancer risk among tissues is attributable to environmental or inherited factors, with the majority due to random mutations during DNA replication in normal cells. This statement about relative risk was overblown into blanket conclusions about the underlying causes of cancer.

The wonder of replication

Cancer emerges when one of the cells that make up your tissues (and organs) grows and divides without control, losing its specialised function and invading other tissue. This happens when normal control of cell growth and division is compromised through changes, or mutations, in your genome (the chemical instruction book for life).

Mutations lie at the heart of cancer biology.

The genome is made from a chemical alphabet of just four letters (A,T,G, and C) “written” into DNA. It works like a kind of computer software for our cells, with strict instructions for growth and function.

Each of the 100 trillion cells in your body contains roughly six billion letters (called nucleotides) of this code, condensed into a thin strand of DNA about two metres long. To put this into perspective, if you stretched out all the DNA in a human body it would reach around the moon and back several times.

Every time a cell divides, the genome must be copied accurately and quickly. This synthesis of new DNA is called replication, and the numbers behind it are staggering. UK researcher John Diffley has calculated that you will have synthesised the equivalent of a light-year of DNA (10 trillion kilometres) by the time you’re 50.

Words simply cannot do this amazing process justice, but this short video by award-winning animator Drew Berry will blow your mind:

http://bcove.me/byqhourx

DNA replication has evolved to be incredibly efficient and reliable, but random mistakes (mutations) occasionally happen. Still, they occur at a rate of less than once per genome per cell division, thanks to some impressive molecular proofreading machines, which constantly survey the newly copied DNA and correct errors.

But with so many cells dividing so often, DNA replication still represents a major source of mutations. And every cell division increases the chance of accumulating mutations in important genes, increasing the likelihood of cancer.

Other sources of mutation

Mutations can take many forms and can emerge in a number of ways – not just through replication errors. We inherit between 50 and 100 mutations from our parents at birth, for instance, and any new or de novo mutations act on this inherited genetic background.

Even normal cellular metabolism damages DNA through the production of reactive oxygen. And, in a sinister twist, many of the inherited mutations that predispose people to cancer hit genes that control the DNA proofreading and repair systems (such as the breast cancer genes BRCA1 and BRCA2). This has the effect of amplifying the rate of new mutations.

The other major causes of DNA mutation are lifestyle or environmental factors. We are exposed to a range of these in our everyday lives, such as UV radiation from sunshine, and chemicals including asbestos or from smoking cigarettes.

Lifestyle factors including diet and alcohol consumption may also contribute. Some viruses and bacteria are known to cause DNA damage leading to cancer. They include the human papillomavirus (HPV) for cervical cancer and H. pylori for gastric cancer.

Not off the hook: alcohol and diet can contribute to DNA mutations. Source: Erik/Flickr, CC BY-NC

Although these different agents leave unique chemical signatures in the DNA, they are still essentially random events. Random mutations are, in fact, the raw material driving evolution. And the processes of mutation and evolution are accelerated in cancer. Indeed, we are only now starting to understand the importance of evolution in driving cancer emergence and spread, as well as its resistance to therapy.

Minimising risk

Where does this leave the idea that cancer is all down to bad luck? Is modifying your lifestyle to minimise exposure to risk factors futile?

As usual, reality lies somewhere in the middle of competing narratives. Life is a kind of genetic gamble. We have to play the cards dealt us, but we can stack the odds in either direction by altering our exposure to environmental and lifestyle factors. Suggesting cancer is all down to bad luck dilutes the important message that risk can be modified by behaviour.

The cancer lexicon is littered with notions of guilt and blame. Death is often framed as “losing the battle with cancer”, for instance. And patients and their families are bombarded by gurus profiteering from various diet and lifestyle interventions. Their implicit messages can often leave people feeling that their cancer is all their own fault and wondering if there was something they could have done differently.

The fact remains that, in many cases, there isn’t.

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

<

Ricky Gervaise on religion