Govt advisers urge people to limit red and processed meat intake

reposted from: http://info.cancerresearchuk.org/news/archive/cancernews/2011-02-25-Govt-advisers-urge-people-to-limit-red-and-processed-meat-intake-?rss=true

crabsallover highlights, key points, comments / links.

Friday 25 February 2011

A government-commissioned report has advised people who eat the highest levels of red and processed mean to limit their consumption of the foods in order to reduce the risk of bowel cancer.

Previous studies have indicated that substances in red meats such as beef, lamb and pork, and processed meats - including those that are smoked, cured, salted or chemically preserved - may increase people's risk of developing the disease.

For instance, a compound called haem - which gives red meat its colour - is broken down into harmful chemicals in the gut, and these chemicals can damage DNA in the cells lining the bowel.

In 1998, the Committee on Medical Aspects of Food and Nutrition Policy (COMA) suggested that people who eat large amounts of red and processed meat should cut back because of the possible risks.

However, red meat is an important source of iron, which is essential for health.

The Scientific Advisory Committee on Nutrition (SACN) has now reviewed the implications of reducing red and processed meat consumption and produced recommendations that aim to strike a balance between reducing the risk of bowel cancer and ensuring a sufficient intake of iron.

Its report concludes that red and processed meat is "probably" associated with an increased risk of bowel cancer.

Writing in a preface to the report, committee chair Professor Alan Jackson said: "Since the evidence does not allow quantification of the amount of red and processed meat that may be linked with increased colorectal cancer risk, SACN is advising high consumers of red and processed meat to consider reducing their intakes."

The research suggests that limiting consumption to about 70g (cooked weight) per day "would have little effect on the proportion of the population with iron intakes below the lower limit of recommended intake for iron".

This means about three rashers of bacon, three average slices of ham, or just under two large sausages per day.

At present, around 33 per cent of men and eight per cent of women are thought to consume more than 100g of red or processed meat each day.

Sara Hiom, Cancer Research UK's director of health information, said: "Eating lots of red and processed meat can increase your risk of bowel cancer and possibly stomach cancer. Red meat includes all forms of fresh, minced and frozen beef, lamb and pork. Processed meat includes sausages, bacon, ham and salami. White meat such as chicken is not likely to increase your risk of cancer. We advise people to eat smaller and fewer portions of red meat and to try using beans or pulses instead of meat in their recipes."

A large European study called EPIC, which was part-funded by Cancer Research UK, found that people who ate two 80g portions of red or processed meat each day were 30 per cent more likely to develop bowel cancer than those who ate just 20g per day.

She advised: "Keeping a healthy weight helps to reduce your risk of cancer so we recommend a balanced diet with plenty of fruit, vegetables and fibre and low in red and processed meat, salt and saturated fat."

Reference

• Scientific Advisory Committee on Nutrition - Iron and Health Report (2011)

New European guidelines on bowel cancer screening and diagnosis

reposted from: http://info.cancerresearchuk.org/news/archive/cancernews/2011-02-07-New-European-guidelines-on-bowel-cancer-screening-and-diagnosis-?rss=true

crabsallover highlights, key points, comments / links.

Tuesday 8 February 2011

The first-ever set of EU guidelines for bowel cancer screening and diagnosis has been published.

Coordinated by the International Agency for Research on Cancer (IARC) - the World Health Organisation's cancer research agency - the guidelines were drawn up by more than 90 experts from 32 countries.

Bowel cancer is the second most common cause of cancer deaths in Europe and the fourth worldwide, but screening can help to detect the disease at an early stage when it is easier to treat.

The new guidelines aim to improve the quality of screening across EU member states by providing benchmarks for all stages of the screening process, from the initial invitation and organisation through to diagnosis and the management of bowel abnormalities.

IARC director Dr Christopher Wild, said: "These guidelines are the result of a major international cooperation and the authors, editors and other contributors are to be congratulated.

"We must now turn to their widespread application to promote the vital international exchange of information and experience between programmes that is essential for continuous quality improvement across national borders."

Dr Wild also underlined the importance of primary prevention of bowel cancer alongside national screening programmes.

He revealed: "Reducing exposure to modifiable risk factors for colorectal cancer, such as physical inactivity, obesity, consumption of alcoholic beverages, red or processed meats and tobacco smoking, combined with screening will translate to a significantly reduced burden of this cancer."

Dr Jodie Moffat, Cancer Research UK's health information manager, said: "We welcome these new bowel cancer guidelines. The cancer screening programmes that we have in this country together save several thousand lives every year, but making sure that every step in a programme works as it should is crucial to its effectiveness. It's important that the right balance between risk and benefit is kept."

Reference

• European guidelines for quality assurance in colorectal cancer screening and diagnosis First Edition

I am the very model of a singularitarian

reposted from:

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Sleep and heart risk link is uncertain

reposted from: http://www.nhs.uk/news/2011/02February/Pages/sleep-patterns-predict-heart-attack-risk.aspx

crabsallover highlights, key points, comments / links.

“Lack of sleep is a 'ticking time bomb',” The Independent reported. The newspaper said that people who regularly sleep less than six hours a night “have a 48 per cent greater chance of developing or dying from heart disease”.

The news is based on research that combined data on almost 475,000 adults, drawn from 15 studies on sleep duration and the risk of strokes and heart attacks. The review found that, compared with a normal 7-8 hours’ sleep a night, shorter or longer sleep was associated with increased risk of these heart problems.

The review has some important limitations. For example, many medical, psychological and lifestyle factors can affect both sleep and cardiovascular health but attempts to account for the influence of these factors varied widely between the studies. It is also unclear whether the participants did not have any cardiovascular disease at the start of the studies, so it should not be assumed that poor sleep was the cause of the cardiovascular problems eventually observed. As the researchers say, the reasons behind any associations between sleep and cardiovascular disease are not fully understood.

Where did the story come from?

The study was carried out by researchers from Warwick Medical School and the University of Naples in Italy. No sources of funding were reported. The study was published in the peer-reviewed European Heart Journal.

The newspapers generally reflected the findings of the research accurately, but did not address the wider issues and limitations of the study.

What kind of research was this?

This systematic review and meta-analysis combined observational studies that had assessed the relationship between duration of sleep and later development of coronary heart disease (CHD) or stroke, as well as the risk of death from these diseases.

A systematic review involves searching the global literature to identify all cohort studies relevant to the question of interest. It is the best way of combining all the evidence available to date on how an exposure (in this case sleep duration) relates to an outcome (in this case cardiovascular disease). The process involves the pooling of studies, which will inherently have different designs, methods and assessment outcomes. These differences can potentially lead to limitations in the results of systematic reviews.

It was important that this review studied people who were considered to have developed new cardiovascular disease during the follow-up period. To ensure that participants had truly developed the condition during the follow-up period and not before the study, the studies should have made sure that participants were truly free from disease at the start (baseline). This systematic review did not report whether the individual studies did this.

What did the research involve?

The researchers searched medical literature databases to identify prospective cohort studies published up to June 2009. These studies assessed the duration of sleep at baseline, then followed participants for at least three years to check for any recorded coronary heart disease (CHD), stroke or cardiovascular disease events, or death from these diseases.

Studies were required to have included only adults and to have recorded the number of cardiovascular outcomes that occurred in relation to different ranges of sleep duration. Most studies classed the duration of “normal sleep” as 7-8 hours a night, “short sleep” as less than or equal to 5-6 hours a night and “long sleep” as more than 8-9 hours. In this review, normal sleep was regarded as the reference category, which means that the effects of other sleeping durations were reported in relation to the effect of normal sleep.

After assessing the quality of the gathered studies, the researchers pooled risk figures for the associations between sleep duration and cardiovascular disease development, as well as death from cardiovascular disease.

The study did not give full details of the methods used, although the authors refer to a related 2010 publication that they wrote. This original publication (which searched for studies published up until March 2009) primarily identified studies that had recorded death due to any cause, which was the focus of the researchers’ first review and meta-analysis. It found that, compared with normal sleep, short and long sleep was associated with increased risk of death from any cause. A new search was conducted for this second publication, which specifically focused on deaths or disease attributed to cardiovascular causes.

The current review reported that all studies included had assessed death through death certificates and that non-fatal vascular events (such as strokes and heart attacks) were recorded through disease registers. As these were specific, recorded medical events, we can be sure that they occurred after the original assessment of sleep behaviour and, therefore, after certain sleep patterns. 

However, it would be more difficult to reliably examine any association between sleep duration and the development of new cardiovascular disease. The review does not tell us whether the individual studies gave the participants clinical checks to confirm they were free from the condition at the start of the study. This is problematic as, without knowing the details of the numerous individual studies, we cannot rule out that the condition preceded or even influenced the participants’ sleeping behaviours.

What were the basic results?

The review included 15 studies, reporting on 24 cohorts (including some studies also featured in the researchers' 2010 review). These covered 474,684 adults from eight different countries. Four of the studies investigated women only, and the other 11 covered a mixed population. Duration of follow-up varied from 6.9 to 25 years. All studies assessed sleep duration using questionnaires and deaths by looking at death certificates. Non-fatal, new cases of cardiovascular events were recorded through disease registers. The total number of cardiovascular events reported (assumed to include both fatal and non-fatal events) was 16,067 (4,169 cases of CHD, 3,478 strokes, and a further 8,420 cases recorded as any cardiovascular event).

When the researchers analysed their pooled results, they found that short sleep, compared to normal sleep, was reported to be associated with increased risk of developing or dying from CHD (relative risk [RR] 1.48, 95% confidence interval [CI] 1.22 to 1.80), as was long sleep (RR 1.38, 95% CI 1.15 to 1.66). Pooled analysis similarly found that long sleep was associated with increased risk of developing or dying from stroke (RR 1.65, 95% CI 1.45 to 1.87). The increase in stroke risk with short sleep was only just statistically significant (RR 1.15, 95% 1.00 to 1.31). For studies examining total cardiovascular disease, the researchers found that, compared with normal sleep, long sleep was associated with increased risk of developing or dying from any cardiovascular disease (RR 1.41, 95% CI 1.19 to 1.68). There was no association between short sleep and any cardiovascular disease (RR 1.03, 95% CI 0.93 to 1.15).

How did the researchers interpret the results?

The researchers concluded that their review found that shorter-than-normal or longer-than-normal sleep was associated with increased risk of “developing or dying of coronary heart disease and stroke”.

Conclusion

This study found that, compared with 7-8 hours of sleep a night, shorter and longer sleep was associated with increased risk of fatal or non-fatal coronary heart disease or stroke.

There are some important points to consider when interpreting this research:

• The review does not specify whether the identified cohort studies excluded existing cardiovascular disease at baseline or looked for new disease development during follow-up. Therefore, it is not clear how reliably it can tell us whether sleep duration is associated with the development of cardiovascular disease.
• The participants reported their own sleep duration, which was only measured at one point at the beginning of the study. It cannot easily be assumed that this represents a life-long sleeping pattern for the subject. Also, it is not clear whether all respondents reported sleep in a similar way, for example whether they only considered time in bed or time asleep, including naps as well.
• The studies included in the meta-analyses had some variation in their methods. They varied in the time period they assessed (studies commenced between 1970 and 1999), age range of their included population (varying between studies from people aged 31 and over to people aged 69 and over), duration of follow-up (from 6.9 to 25 years) and methods of outcome assessment.
• Many factors may affect sleep duration and quality of sleep, including illness, mental health and a person’s life circumstances. The individual studies variably accounted for the participants’ lifestyle, medical and psychological health at the time of assessing sleep, including smoking status, raised blood pressure, diabetes and stress. Such variable lifestyle, medical and psychological health factors could affect the relationship between sleep duration and cardiovascular disease (for example, stress could be the cause of both poor sleep and poor cardiovascular health).

Confirmation that extremes of sleep, both long and short, are associated with poor cardiovascular outcomes is of interest. However, as the researchers say, the “mechanisms that underlie these associations are not fully understood”. As such, the reasons for poor sleep patterns also need consideration, as sleeping for longer or shorter periods may only be a by-product of factors that also affect cardiovascular disease and death.

Links to the headlines

Lack of sleep is a 'ticking time bomb'. The Independent, Februaury 9 2011

Why late to bed, early to rise is a recipe for a heart attack. Daily Mail, Februaury 9 2011

Warwick scientists say lack of sleep 'bad for health'. BBC News, Februaury 9 2011

Links to the science

Cappuccio FP, Cooper D, D'Elia L et al. Sleep duration predicts cardiovascular outcomes: a systematic review and meta-analysis of prospective studies. European Heart Journal, February 7 2011 (first published online)

Prostate cancer mutations identified

reposted from: http://www.nhs.uk/news/2011/02February/Pages/mutations-behind-prostate-cancer.aspx

crabsallover highlights, key points, comments / links.

The genetic map of prostate cancer has been “cracked”, The Daily Telegraph reported. The newspaper said that new research into prostate cancer has provided a “breakthrough that could transform our understanding of the disease”.

The research scanned the entire genetic sequences of prostate tumours and compared them to the genetics of healthy cells from the same patient. The research identified a range of mutations and genetic patterns that showed the way that the DNA is sometimes rearranged in these tumours. The researchers suggest that these patterns may be unique to prostate cancer and may have a role in initiating it.

Such research helps to further our understanding of the complex genetic reasons why some men may develop prostate cancer while others do not. However, it will be some time before this knowledge can be used in diagnosis or treatment as several thousand mutations were identified in each tumour and it is unclear what effect each mutation has. The study also looked at only seven tumours, so further research must verify the presence of these mutations in more samples.

Where did the story come from?

Numerous researchers from several research institutions across the US contributed to this research. The study was funded by several US organisations, including the Prostate Cancer Foundation Movember campaign, the Howard Hughes Medical Institute, the National Human Genome Research Institute, the Kohlberg Foundation, the National Cancer Institute and the National Institutes of Health. It was published in the peer-reviewed scientific journal Nature.

The newspapers generally reported the study clearly, although the Daily Mail did not highlight that this study has limitations due to the small number of samples tested. Given that the research only studied samples from seven men, it needs to be repeated on a larger scale.

What kind of research was this?

This genetic study set out to sequence the entire DNA code of prostate cancer cells. Prostate cancer is a major disease and the second most common cause of cancer deaths in men in the UK. Previous research, through genome-wide association studies, has identified that certain single-letter variants within the DNA code are associated with an increased risk of cancer. In fact, nine such variants were identified by four studies covered by Behind the Headlines in September 2009, where it was concluded that many regions in the DNA appear to contribute to the risk of prostate cancer and that further variants are likely to be discovered.

The methods of this research differed from those employed in genome-wide association studies, which look at associations that may exist between specific DNA variations traits and the risk of developing a particular disease. In this current study, researchers “read” (sequenced) the entire genetic code of a person’s prostate cancer cells and compared it with the genetic sequence of that person’s healthy prostate cells. Using this method, the researchers could see what genetic changes and mutations occurred in these cells as they became cancerous.

What did the research involve?

The researchers used DNA extracted from prostate tumour samples from seven men given a radical prostatectomy (removal of the prostate and related tissue). They also had blood samples from these men. DNA extracted from the blood was used as a control in the experiments, to show what the men’s DNA was like in non-cancerous cells.

The researchers sequenced the entire genome of the prostate cancer cells, looking for mutations and variations that did not exist in normal cells from the same patient. They looked for small differences in the sequence of the DNA, larger-scale changes in the chromosome arrangements and instances where part of one chromosome had broken off and attached to another chromosome to form a hybrid. The DNA was sequenced using established methods in this field and the information was processed by complex software that could identify the presence of mutations in the DNA.

A portion of the mutations detected were checked using different methods to validate the original process. The researchers reported how many mutations they detected in the tumour cells and their observations on the common types of genetic rearrangements. They then discussed how certain variations may increase the risk of prostate cancer developing.

What were the basic results?

The researchers found about 3,866 single-letter mutations of the genetic code in each tumour, a rate of mutation that they say is similar to that seen with acute myeloid leukemic and breast cancer but lower than that seen in small cell lung cancer and skin cancer.

Two of the seven tumours tested had mutations within two genes called SPTA1 and SPOP. In three of seven tumours, there were mutations in three genes called CHD1, CHD5 and HDAC9, which are responsible for producing chromatin modifier proteins. These proteins are known to play a role in suppressing tumours, regulating how genes are switched on and off, and stem cells’ capacity to develop into different body cells. Three of seven tumours also had mutations in HSPA2, HSPA5 and HSP90AB1, a set of genes linked to cells’ response to environmental stress and damage. Other genes were mutated in only one of the seven tumours.

The researchers identified 90 chromosome rearrangements in each tumour and noted that this number was similar to that seen in breast cancer cells. The rearrangements showed a distinctive pattern that had reportedly not been seen in other solid tumours before.

Some of the rearrangements involved genes that were affected by single-letter mutations in other tumours, including the chromatin modifier gene CHD1. A number of rearrangements also occurred  near multiple known cancer genes.

Overall, sixteen genes affected by a rearrangement mutation were found in at least two tumours.

How did the researchers interpret the results?

The discovery of many mutations in the genetic code of prostate cancers, some of which are associated with known genes, led the researchers to conclude that these mutations may contribute to the development of tumours in the prostate.

They also say that the high number of “recurrent gene fusions” suggests that rearrangements in the DNA may be critical events in initiating prostate cancer. These are complex rearrangements and the researchers note that a “whole-genome approach”, looking at the whole of a tumour cell’s genetic code, is necessary to profile them.

Conclusion

This important study looked at the entire genetic sequence in a sample of prostate tumour cells and compared this with that of normal tissue. It has revealed that there are many mutations and rearrangements of DNA, which the researchers suggest could increase the risk of this cancer type. Importantly, only seven tumour samples were used in this analysis, and the mutations identified were not present in all tumour samples. This confirms what is already suspected about the disease, that factors affecting prostate cancer are complex, particularly the genetic elements.

The methods of this study will need to be replicated in a larger sample of individuals, a process which is likely to be extensive and time consuming. Such research will also need to confirm the extent to which each mutation or DNA rearrangement increases the risk of the disease and the normal function of the genes around the mutation sites. Such information could be critical in the development of screening or treatment approaches in the future.

While this study has importantly applied a whole genome approach to understanding the genetics of prostate cancer, this now needs to be applied to more samples. Only then can the full implications of the genetic changes found through this research be appreciated.

Links to the headlines

Genetic map of prostate cancer cracked. The Daily Telegraph, February 10 2011

Prostate cancer's genetic code cracked by U.S. scientists in breakthrough set to transform treatment of the disease. Daily Mail, February 10 2011

Links to the science

Berger MF, Lawrence MS, Demichelis F et al. The genomic complexity of primary human prostate cancer. Nature: 470, 214–220 February 10 2011

Ray Kurzweil: Explains The Singularity, Longevity, exponential growth of IT

reposted from: http://singularityhub.com/2010/12/01/time-presents-10-questions-for-ray-kurzweil-hello-mainstream-video/

crabsallover highlights, key points, comments / links.

Law of Accelerating Returns - Exponential increase (doubling per year) eg Genetic Sequencing, computer power, reprogram biology - turn off fat insulin receptor gene. Humans transcend our limitations.

Bridge to a bridge to a bridge. Bridge 1: eating right and exercising >> 10-20 years - Bridge 2 - change our genes >> Bridge 3 - nanorobots will keep us healthy. Parkinsons Disease. The sky is the limit! Exponential growth of IT - protect us from those who will abuse it.

Government campaign highlights signs of bowel cancer

reposted from: http://info.cancerresearchuk.org/news/archive/cancernews/2011-02-02-Government-campaign-highlights-signs-of-bowel-cancer-?rss=true

crabsallover highlights, key points, comments / links.

Wednesday 2 February 2011

The Department of Health has launched a new cancer awareness campaign focusing on the early signs and symptoms of bowel cancer.

Pilot campaigns costing £1.75 million will run for seven weeks in the east and south-west of England, before being rolled out nationwide if successful.

The 'Be Clear on Cancer' adverts will appear on regional TV and radio and in newspapers, and feature GPs encouraging patients to tell them about any changes in their bowel movements or abnormal bleeding, as these may be early signs of bowel cancer.

If bowel cancer is diagnosed at the earliest stage, the chances of successful treatment are higher with more than nine out of ten people surviving for at least five years. But the disease is harder to treat when it is diagnosed at an advanced stage.

The coalition government has made earlier diagnosis of cancer one of its priorities and the new campaign is part of a broader programme of work to improve cancer services and outcomes.

Launching the campaign, health minister Paul Burstow said that it uses "simple messages to make people aware of the early signs of bowel cancer and to give them the confidence to talk to their GP about them".

He explained: "To make sure we get it right, we're testing this campaign in two regions and, if it works, we'll roll it out nationally."

Sarah Lyness, Cancer Research UK's executive director of communications and information, said: "We welcome this campaign because spotting cancer early saves lives. Most changes in bowel habits probably won't be cancer, but if they are it is much better to be diagnosed and treated as quickly as possible.

"So if people notice a change that lasts three weeks or more - whether it's looser poo, bleeding or anything else that is unusual for them - they should report the symptoms to their doctor without further delay."