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Remember all the medical advice for years about not eating eggs frequently (high cholesterol! heart disease!) and to instead eat egg white omelettes if one absolutely wanted to eat eggs? Remember the obsession with dietary cholesterol? Well, this recent research followed 1032 men for 21 years and found that a relatively high intake of dietary cholesterol, or eating one egg every day, was not associated with an elevated risk of incident coronary heart disease - not in the entire study population nor in those with the APOE4 phenotype. Also, the study did not establish a link between dietary cholesterol or eating eggs with thickening of the common carotid artery walls. Time to enjoy eggs again! From Science Daily:

High-cholesterol diet, eating eggs do not increase risk of heart attack, not even in persons genetically predisposed, study finds

A new study from the University of Eastern Finland shows that a relatively high intake of dietary cholesterol, or eating one egg every day, are not associated with an elevated risk of incident coronary heart disease. Furthermore, no association was found among those with the APOE4 phenotype, which affects cholesterol metabolism and is common among the Finnish population.

In the majority of population, dietary cholesterol affects serum cholesterol levels only a little, and few studies have linked the intake of dietary cholesterol to an elevated risk of cardiovascular diseases. Globally, many nutrition recommendations no longer set limitations to the intake of dietary cholesterol. However, in carriers of the apolipoprotein E type 4 allele -- which significantly impacts cholesterol metabolism -- the effect of dietary cholesterol on serum cholesterol levels is greater. In Finland, the prevalence of the APOE4 allele, which is a hereditary variant, is exceptionally high and approximately one third of the population are carriers.

The dietary habits of 1,032 men aged between 42 and 60 years and with no baseline diagnosis of a cardiovascular disease were assessed at the onset the Kuopio Ischaemic Heart Disease Risk Factor Study, KIHD, in 1984-1989 at the University of Eastern Finland. During a follow-up of 21 years, 230 men had a myocardial infarction, and 32.5 per cent of the study participants were carriers of APOE4.

 Last fall a study came out that estimated that annually about 3.3 million deaths throughout the world were caused from air pollution. But a study was presented Friday at the American Association for the Advancement of Science (AAAS) that gave a much higher estimate of annual air pollution deaths: 5.5 million. A horrifying number. And yet... governments, companies, and people resist  measures to cut air pollution. Why? It costs money. And also many people are too poor (e.g., China and India) to use cleaner sources of heating and cooking fuel - so they are damaging their own health in their own homes. From Science Daily:

Poor air quality kills 5.5 million worldwide annually

New research shows that more than 5.5 million people die prematurely every year due to household and outdoor air pollution. More than half of deaths occur in two of the world's fastest growing economies, China and India.

Power plants, industrial manufacturing, vehicle exhaust and burning coal and wood all release small particles into the air that are dangerous to a person's health. New research, presented today at the 2016 annual meeting of the American Association for the Advancement of Science (AAAS), found that despite efforts to limit future emissions, the number of premature deaths linked to air pollution will climb over the next two decades unless more aggressive targets are set.

"Air pollution is the fourth highest risk factor for death globally and by far the leading environmental risk factor for disease," said Michael Brauer, a professor at the University of British Columbia's School of Population and Public Health in Vancouver, Canada. "Reducing air pollution is an incredibly efficient way to improve the health of a population."

For the AAAS meeting, researchers from Canada, the United States, China and India assembled estimates of air pollution levels in China and India and calculated the impact on health. Their analysis shows that the two countries account for 55 per cent of the deaths caused by air pollution worldwide. About 1.6 million people died of air pollution in China and 1.4 million died in India in 2013.

In China, burning coal is the biggest contributor to poor air quality. Qiao Ma, a PhD student at the School of Environment, Tsinghua University in Beijing, China, found that outdoor air pollution from coal alone caused an estimated 366,000 deaths in China in 2013....In India, a major contributor to poor air quality is the practice of burning wood, dung and similar sources of biomass for cooking and heating. Millions of families, among the poorest in India, are regularly exposed to high levels of particulate matter in their own homes.

In the last 50 years, North America, Western Europe and Japan have made massive strides to combat pollution by using cleaner fuels, more efficient vehicles, limiting coal burning and putting restrictions on electric power plants and factories. 

Additional facts about air pollution: - World Health Organization (WHO) air quality guidelines set daily particulate matter at 25 micrograms per cubic metre. - At this time of year, Beijing and New Delhi will see daily levels at or above 300 micrograms per cubic meter metre; 1,200 per cent higher than WHO guidelines..... According to the Global Burden of Disease study, air pollution causes more deaths than other risk factors like malnutrition, obesity, alcohol and drug abuse, and unsafe sex.... - Cardiovascular disease accounts for the majority of deaths from air pollution with additional impacts from lung cancer, chronic obstructive pulmonary disease (COPD) and respiratory infections. Video: https://youtu.be/Kwoqa84npsU 

Another famous long-running study (Framingham Heart Study) finds more bad news for middle-aged coach-potatoes (that is, those who don't exercise or have poor physical fitness). It's an observational study (thus they found an association), but the finding is pretty damn convincing: that poor physical fitness (basically a sedentary life-style) may be linked to a smaller brain size (brain volume) 20 years later. The reason this is significant is because shrinking brain volume means that accelerated brain aging is occurring.

Researcher Nicole Spartano said: "Brain volume is one marker of brain aging. Our brains shrink as we age, and this atrophy is related to cognitive decline and increased risk for dementia. So, this study suggests that people with poor fitness have accelerated brain aging." Bottom line: if you don't get much exercise or lead a sedentary life-style, then increase your activity levels for hopefully better brain health decades later. Just getting out daily (or several times a week) and walking briskly would improve fitness. From Medical Xpress:

Couch potatoes may have smaller brains later in life

Poor physical fitness in middle age may be linked to a smaller brain size 20 years later, according to a study published in the February 10, 2016, online issue of Neurology, the medical journal of the American Academy of Neurology."We found a direct correlation in our study between poor fitness and brain volume decades later, which indicates accelerated brain aging," said study author Nicole Spartano, PhD, with Boston University School of Medicine in Boston.

For the study, 1,583 people enrolled in the Framingham Heart Study, with an average age of 40 and without dementia or heart disease, took a treadmill test. They took another one two decades later, along with MRI brain scans. The researchers also analyzed the results when they excluded participants who developed heart disease or started taking beta blockers to control blood pressure or heart problems; this group had 1,094 people. 

The participants had an average estimated exercise capacity of 39 mL/kg/min, which is also known as peak VO2, or the maximum amount of oxygen the body is capable of using in one minute. Exercise capacity was estimated using the length of time participants were able to exercise on the treadmill before their heart rate reached a certain level. For every eight units lower a person performed on the treadmill test, their brain volume two decades later was smaller, equivalent to two years of accelerated brain aging. When the people with heart disease or those taking beta blockers were excluded, every eight units of lower physical performance was associated with reductions of brain volume equal to one year of accelerated brain aging.

The study also showed that people whose blood pressure and heart rate went up at a higher rate during exercise also were more likely to have smaller brain volumes two decades later. Spartano said that people with poor physical fitness often have higher blood pressure and heart rate responses to low levels of exercise compared to people with better fitness. Spartano noted that the study is observational. It does not prove that poor physical fitness causes a loss of brain volume; it shows the association. (Link to study in journal Neurology.)

Now and then I hear people wondering whether the many hours we spend staring at computer, cell phone, and tablet screens is damaging our eyes. And what about fluorescent lighting (which seems to bother many people) and LED lights? After all, the blue light of all our device screens seems intense, and researchers have long known that blue light is toxic to the retina.

Recently researchers measured the blue light on various device screens and lamps (including over extended time periods) and compared it to looking at a clear blue sky in June (but not looking at the sun). They found that most devices put out less blue light than the blue sky on a clear day and all were less than international standards for blue light exposure limits. Whew...we're all OK. But don't use them for a long time at night because their bright emissionInternational Commission on Non-Ionizing Radiation Protectisuppresses melatonin (needed for sleep). From Medscape:

Blue Light From Screens, Bulbs Won't Damage Retina

Despite concerns that staring at devices putting out high amounts of the blue light wavelength could damage human retinas, a recent study finds that most devices put out less of that light than the blue sky on a clear day. "Even under extreme long-term viewing conditions, none of the low energy light bulbs, computers, tablets and mobile phones we assessed suggested cause for concern for public health," said lead author John O'Hagan, head of the Laser and Optical Radiation Dosimetry Group of Public Health England in Chilton, U.K., in an email.

As people are using computers and phones more often and low-energy lighting like fluorescent and LED bulbs is becoming more common, the types of light human eyes are encountering is changing, the researchers pointed out January 15 online in the journal Eye. Compared to traditional incandescent bulbs, electronic screens and low-energy light bulbs tend to emit more blue light, which has long been known to be toxic to the retina, they write.

Based on that toxicity research, the International Commission on Non-Ionizing Radiation Protection (ICNIRP) has proposed a safe exposure limit, below which blue light is unlikely to harm a viewer's eye. O'Hagan and his team measured the blue light emitted by several sources, including mobile phones, tablet computers, laptops and lamps, over time periods similar to the way people use the devices. Then they compared the emissions to the ICNIRP's exposure limits.

After comparing multiple colors on device screens, the researchers found that a white screen had the highest blue light emissions, so they used a white screen set at maximum brightness for their measurements.They also compared the blue light emissions from various devices to the levels people would encounter when looking at a clear blue sky in summertime in Chilton, in southern England, and also to an overcast winter sky in the same location.

The blue light exposure on a clear day in June was around 10 percent of the ICNIRP safe limit. A cloudy day in December produced around 3 percent of the limitComparing these natural exposures with light from lamps, computer screens and mobile devices like smartphones, the study team found that the artificial light produced even lower exposures than people normally encounter outdoors. That is, provided they're staring just at the sky, not directly at the sun.

 

Even considering that people may stare at computer screens for hours in the course of work or play, the study team concludes that there's no danger to the retina.They caution, however, that the amount of light that gets transmitted from the surface of the eye to the retina is age-related, so children may be more sensitive to blue light. Light sources that are comfortable for adults could be distressing for children, the authors warn.

Once again, research shows that "BPA-free" plastic does not mean it is safer than BPA plastic. Both BPA and BPS (the usual replacement for BPA) leach estrogenic chemicals into the foods and beverages, which means negative health effects when ingested. Both BPA and BPS mimic the effects of estrogen, as well as the actions of thyroid hormone. Yes, this study was done on zebrafish, but think of them as "the canaries in the mine" - if it affects them, it could affect humans also, especially developing fetuses and young children.

BPA  and BPS can leach into food, particularly under heat, from the lining of cans and from consumer products such as water bottles, baby bottles, food-storage containers, sippy cups, and plastic tableware. BPA can also be found in contact lenses, eyeglass lenses, compact discs, water-supply pipes, some cash register and ATM receipts, as well as in some dental sealants. A good way to minimize exposure to BPA , BPS, and other estrogenic chemicals is to try to avoid food and beverages in plastic containers and cans, but instead try to buy and store food in glass containers, jars, and bottles. From Science Daily:

'BPA-free' plastic accelerates embryonic development, disrupts reproductive system

Companies advertise "BPA-free" as a safer version of plastic products ranging from water bottles to sippy cups to toys. Many manufacturers stopped used Bisphenol A to strengthen plastic after animal studies linked it to early puberty and a rise in breast and prostate cancers.Yet new UCLA research demonstrates that BPS (Bisphenol S), a common replacement for BPA, speeds up embryonic development and disrupts the reproductive system.

Using a zebrafish model, Wayne and her colleagues found that exposure to low levels of BPA and BPS -- equivalent to the traces found in polluted river waters -- altered the animals' physiology at the embryonic stage in as quickly as 25 hours. "Egg hatching time accelerated, leading to the fish equivalent of premature birth," said Wayne, who is also UCLA's associate vice chancellor for research. "The embryos developed much faster than normal in the presence of BPA or BPS."

The UCLA team, which included first author Wenhui Qiu, a visiting graduate student from Shanghai University, chose to conduct the study in zebrafish because their transparent embryos make it possible to "watch" cell growth as it occurs.... In a second finding, the team discovered that the number of endocrine neurons increased up to 40 percent, suggesting that BPA overstimulates the reproductive system.... "We saw many of these same effects with BPS found in BPA-free products. BPS is not harmless."

After uncovering her first finding about BPA in 2008, Wayne immediately discarded all of the plastic food containers in her home and replaced them with glass. She and her family purchase food and drinks packaged in glass whenever possible. "Our findings are frightening and important," emphasized Wayne. "Consider it the aquatic version of the canary in the coal mine."

Finally, the researchers were surprised to find that both BPA and BPS acted partly through an estrogen system and partly through a thyroid hormone system to exert their effects"Most people think of BPA as mimicking the effects of estrogen. But our work shows that it also mimics the actions of thyroid hormone," said Wayne. "Because of thyroid hormone's important influence on brain development during gestation, our work holds important implications for general embryonic and fetal development, including in humans."

Researchers have proposed that endocrine-disrupting chemicals may be contributing to the U.S.' rise in premature human births and early onset of puberty over the past couple of decades. "Our data support that hypothesis," said Wayne. "If BPA is impacting a wide variety of animal species, then it's likely to be affecting human health. Our study is the latest to help show this with BPA and now with BPS."

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Once again, two opposing views about beards have been in the news - that they harbor all sorts of nasty disease-causing bacteria vs they are hygienic. An earlier May 5, 2015 post was about the question of whether bearded men have more bacteria on their faces than clean shaven ones. I cited a 2014 study found that they don't, and that we are all covered with bacteria, all sorts of bacteria, and this is normal.

Now another study has looked at the issue of hospital workers with and without beards and whether they carry infectious bacteria. Researchers swabbed the faces (center of the cheek and the skin of the upper lip under the nostrils) of both clean shaven individuals and individuals with facial hair (beards) that worked in two hospitals (they all had direct contact with patients) and looked at the bacteria present. They especially looked for the presence of the bacteria Staphylococcus aureus, which surprisingly was found more in the clean-shaven men.

Also to their surprise, it was more of the clean shaven men who carried the pathogenic bacteria Methicillin-resistant Staphylococcus aureus (also known as MRSA). For those bacterial groups most closely associated with hospital acquired infections, such as Klebsiella species, Pseudomonas species, Enterobacter species., and Acinetobacter species, prevalence was low in both groups, and less than 2% for each group.

For other, less harmful bacteria, researchers found that bearded employees harbored no more bacteria than their clean-shaven colleagues. In summary: The researchers say that "results suggest that male hospital workers with facial hair do not harbour more potentially concerning bacteria than clean-shaven workers, and that in some instances, clean-shaven individuals are significantly more likely to be colonized with potential nosocomial pathogens". (NOTE: nosocomial means a disease originating or acquired in a hospital.)

And why is that? According to the study, one explanation is "microtrauma to the skin," which occurs during shaving and results in abrasions, which could support bacterial colonisation and growth of bacteria on the clean-shaven men. However, some other researchers have a different hypothesis — that beards themselves actually fight infection.

This stems from an experiment carried out by Dr. Michael Mosley who recently swabbed the beards of a variety of men and sent the samples to Dr. Adam Roberts, a microbiologist at University College London. Roberts grew more than 100 different bacteria from the beard samples, but found that in a few of the petri dishes a microbe was killing the other bacteria -  a bacteria called Staphylococcus epidermidis, and which they believe has antibiotic properties.

From the Journal of Hospital Infection: Bacterial ecology of hospital workers’ facial hair: a cross-sectional study

Summary: It is unknown whether healthcare workers' facial hair harbours nosocomial pathogens. We compared facial bacterial colonization rates among 408 male healthcare workers with and without facial hair. Workers with facial hair were less likely to be colonized with Staphylococcus aureus (41.2% vs 52.6%, P = 0.02) and meticillin-resistant coagulase-negative staphylococci (2.0% vs 7.0%, P = 0.01). Colonization rates with Gram-negative organisms were low for all healthcare workers, and Gram-negative colonization rates did not differ by facial hair type. Overall, colonization is similar in male healthcare workers with and without facial hair; however, certain bacterial species were more prevalent in workers without facial hair.

[Excerpts from Discussion]:Several studies to date have demonstrated that physician white coats and neck ties can act as significant sources of nosocomial bacteria. Our study suggests that facial hair does not increase the overall risk of bacterial colonization compared to clean-shaven control subjects. Indeed, clean-shaven control subjects exhibited higher rates of colonization with certain bacterial species. This finding may be explained by microtrauma to the skin during shaving resulting in abrasions, which may support bacterial colonization and proliferation. This may be akin to the enhanced risk of surgical site infections in patients shaved with razors prior to surgery. Further, our results are consistent with prior evidence pertaining to bacterial colonization on the hands and nares of HCWs (Health care workers).

A recent study using mice, and following them for 4 generations, has implications for Americans who typically eat a low-fiber diet (average of 15 grams daily). Note that current dietary guidelines recommend that women should eat around 25 grams and men 38 grams daily of fiber. The researchers found that low-fiber diets not only deplete the complex microbial ecosystems residing in the gut, but can cause an irreversible loss of diversity within those ecosystems in as few as three or four generations.

This is because fiber feeds the millions of microbes in the gut - and so a fiber-rich diet can nourish a wide variety of gut microbes, but a low-fiber diet can only sustain a narrower community. As the generations went by, the rodents’ guts became progressively less diverse, as more and more species were extinguished. If the fourth-generation mice switched to high-fiber meals, some of the missing microbes rebounded, but most did not. It took a fecal transplant (mice style) to get back the missing microbes. From Science Daily:

Low-fiber diet may cause irreversible depletion of gut bacteria over generations

A study by Stanford University School of Medicine investigators raises concerns that the lower-fiber diets typical in industrialized societies may produce internal deficiencies that get passed along to future generations. The study, conducted in mice, indicates that low-fiber diets not only deplete the complex microbial ecosystems residing in every mammalian gut, but can cause an irreversible loss of diversity within those ecosystems in as few as three or four generations.

Once an entire population has experienced the extinction of key bacterial species, simply "eating right" may no longer be enough to restore these lost species to the guts of individuals in that population, the study suggests. Those of us who live in advanced industrial societies may already be heading down that path.

This study showed an association of eating lots of flavonoid rich foods (strawberries, blueberries, cherries, blackberries, red wine, apples, pears, and citrus products) and lower rates of erectile dysfunction. A higher intake of several flavonoids also reduces diabetes and cardiovascular disease risk. Keep in mind that erectile dysfunction is thought to be of vascular etiology (the cause) and so shares risk factors (such as hypertension, obesity, and smoking) with cardiovascular disease. Studies have shown that lifestyle factors such as plenty of exercise, being of normal weight, and a Mediterranean style diet rich in whole grains, fruit, vegetables, nuts, legumes, and olive oil was associated with both lower rates of erectile dysfunction and an improvement in erectile function in men. So don't focus just on the flavonoids, but on the whole lifestyle package. From Science Daily:

Blueberries, citrus fruits, red wine associated with reduced erectile dysfunction

Flavonoid-rich foods are associated with a reduced risk of erectile dysfunction -- according to a new collaborative study from the University of East Anglia (UEA) and Harvard University. Research published in The American Journal of Clinical Nutrition reveals that eating foods rich in certain flavonoids is associated with a reduced risk of erectile dysfunction in men, with the greatest benefit in those under 70. Of all the different flavonoids, Anthocyanins (found in blueberries, cherries, blackberries, radishes and blackcurrant), flavanones and flavones (found in citrus fruits) were found to offer the greatest benefits in preventing the condition.

It is already known that increased exercise can improve erectile function, but this research shows that eating a flavonoid-rich diet is as good for erectile function as briskly walking for up to five hours a week. The study also showed that a higher total fruit intake was associated with a 14 per cent reduction in the risk of erectile dysfunction. And that a combination of consuming flavonoid-rich foods with exercise can reduce the risk by 21 per cent.

More than 50,000 middle aged men were included in this large population based study. They were asked about their ability to have and maintain an erection sufficient for intercourse -- dating back to 1986. Data on dietary intake was also collected every four years.....More than one third of the men surveyed reported suffering new onset erectile dysfunction. But those who consumed a diet rich in anthocyanins, flavones and flavanones were less likely to suffer the condition.

Prof Cassidy said: "The top sources of anthocyanins, flavones and flavanones consumed in the US are strawberries, blueberries, red wine, apples, pears, and citrus products.""We also found that the benefits were strongest among younger men," she added. The team also looked at other lifestyle factors and found that men who consumed a high intake of anthocyanins and flavanones and who were also physically active had the lowest risk of erectile dysfunction.

Could the bacteria described in this research be another probiotic or beneficial bacteria (besides Lactobacillus sakei) that helps protect against sinusitis? New research found that the harmless bacteria Corynebacterium accolens is "overrepresented" in children free of Streptococcus pneumoniae (pneumococcus) -  which commonly colonizes in children's noses (and that can live harmlessly as part of a healthy microbiome), but it is also an important infectious agent. Streptococcus pneumoniae is a major cause of pneumonia, septicemia, meningitis, otitis media (ear infections), and sinusitis in children and adults worldwide.

The researchers did an analysis on the microbes in the nasal passages of children and found that the nasopharyngeal (nostrils) microbiome was different in children with and without pneumococcal nasopharyngeal colonization. This revealed that Corynebacterium species and Dolosigranulum were "overrepresented" in children negative for pneumococcal colonization, whereas Streptococcus was "overrepresented" in children positive for Streptococcus  pneumoniae colonization.

The researchers found that higher numbers of  Corynebacterium accolens cells deter and limit S. pneumoniae nostril colonization, which might partly explain why children without S. pneumoniae colonization have higher levels of nasal Corynebacterium species. The researchers write that "there is direct antagonism" between Corynebacterium spp. and S. pneumoniae in the human nose. How do children get this beneficial bacteria? Interestingly, at 6 weeks of age, Corynebacterium species. and Dolosigranulum species are also "overrepresented" in the nasopharyngeal microbiota of breastfed infants compared to formula-fed infants. From Science Daily:

Good bacteria might help prevent middle ear infections, pneumonia

A new study is helping to shed more light on the important connections among the diverse bacteria in our microbiome. According to research published in mBio, scientists at Forsyth, led by Dr. Katherine P. Lemon, along with their collaborator at Vanderbilt University, have demonstrated that a harmless bacterium found in the nose and on skin may negatively impact the growth of a pathogen that commonly causes middle ear infections in children and pneumonia in children and older adults.

This study provides the first evidence that Corynebacterium accolens, a harmless bacterial species that commonly colonizes the nose, can help inhibit Streptococcus pneumoniae (S. pneumoniae) -- a major cause of pneumonia, meningitis, middle ear infection and sinusitis. According to the World Health Organization, S. pneumoniae leads to more than 1 million deaths each year, primarily in young children in developing countries. Although most people that host S. pneumoniae do not develop these infections, colonization greatly increases the risk of, and is a perquisite for, infection and transmission.

The study, titled, "Corynebacterium accolens (C. accolens) Releases Antipneumococcal Free Fatty Acids from Human Nostril and Skin Surface Triacylglycerols," is published on January 5, 2016 in mBio. In this study, first-author Dr. Lindsey Bomar and her colleagues show that C. accolens are overrepresented in the noses of children that are not colonized by S. pneumoniae, which is commonly found in children's noses and can cause infection. In laboratory research, the team further found that C. accolens modifies its local habitat in a manner that inhibits the growth of S. pneumoniae by releasing antibacterial free fatty acids from representative host skin surface triacylglycerols. The team went on to identify the C. accolens enzyme needed for this. These results pave the way for potential future research to determine whether C. accolens might have role as a beneficial bacterium that could be used to control pathogen colonization.

A provocative and thought-provoking article in which the title says it all: Cancer screening has not been shown to 'save lives'. The following is from the Medscape analysis/reporting of the original British Medical Journal article and accompanying editorial ( BMJ. January 2016, Article, Editorial), and both the original and Medscape analysis are well worth reading. From Medscape:

Cancer Screening Has Not Been Shown to 'Save Lives'

Debates about cancer screening programs tend to focus on when to start, who to screen, and the frequency of screening. But some investigators are asking a far more provocative question: Do screening programs actually save lives?

We do not know the answer to that question, and would need to conduct massive clinical trials to find out, said Vinay K. Prasad, MD, MPH, assistant professor of medicine at the Oregon Health Sciences University in Portland."Proponents of cancer screening say that screening tests have been shown to save lives. What we're trying to show is that, strictly speaking, that's sort of an overstatement," he told Medscape Medical News.

In an analysis published online January 6 in the BMJ, Dr Prasad and his colleagues argue that although cancer screening might reduce cancer-specific mortality, it has not conclusively been shown to have an effect on overall mortality. The researchers go on to suggest that the harms of screening might actually contribute to overall mortality rates. These potential harms include false-positive results that lead to unnecessary biopsies or therapeutic interventions and overdiagnosis, in which treatment is delivered for a condition that is unlikely to affect patients during their natural lifespans.

"There are two chief reasons why cancer screening might reduce disease-specific mortality without significantly reducing overall mortality," the researchers write. "Firstly, studies may be underpowered to detect a small overall mortality benefit. Secondly, disease-specific mortality reductions may be offset by deaths due to the downstream effects of screening." "The bar to say that screening saves lives should be overall mortality, and we haven't met that bar," Dr Prasad told Medscape Medical News.

The rationale for cancer screening is based on the assumptions that screening will reduce deaths from cancer and that lowering cancer-specific deaths will decrease overall mortality. These assumptions remain unsupported by facts, Dr Prasad's team contends.

They illustrate this point with data from the National Lung Cancer Screening Trial (NLST). Although there was a 20% relative reduction in lung cancer deaths with low-dose CT screening, compared with chest x-ray, and a 6.7% relative reduction in overall mortality, the absolute reduction in risk for overall mortality was just 0.46%....The team also notes that "the benefit in lung cancer mortality of CT screening (estimated to avert over 12,000 lung cancer deaths in the United States annually) must be set against the 27,034 major complications (such as lung collapse, heart attack, stroke, and death) that follow a positive screening test."

The decision to undergo screening should be part of an informed discussion between the patient and clinician that takes into account personal preferences and the risks and benefits of screening. Dr Prasad explained. "Declining screening may be a reasonable and prudent choice for many people," the researchers write. "Doctors should be comfortable with whatever choice people make when they hear about all the potential benefits and the known harms," Dr Prasad added.

However, in an accompanying editorial, Gerd Gigerenzer, PhD, from the Max Planck Institute for Human Development in Berlin, argues that "rather than pouring resources into 'megatrials' with a small chance of detecting a minimal overall mortality reduction, at the additional cost of harming large numbers of patients, we should invest in transparent information in the first place." He explains that information about screening should be presented in a "fact box" that lays out the benefits and risks of mammography with numbers for how many women would be affected."It is time to change communication about cancer screening from dodgy persuasion into something straightforward," he concludes.

Richard L. Schilsky, MD, chief medical officer for the American Society of Clinical Oncology (ASCO), said that although, in general, ASCO supports cancer screening, "it's a very imperfect process....The often high variability in the natural history of many cancers has been the source of particular confusion and uncertainty surrounding screening, he noted. For example, there is little value in screening for aggressive cancers for which interventions are unlikely to make a difference in outcomes, no matter how early the disease can be detected. Conversely, "if the cancer is never going to kill you, no matter what the doctors do, then screening won't help either," he said. Additionally, there are some cancers for which treatments are sufficiently effective that they can be successfully managed whether they are diagnosed at an early or later stage. "When you consider all these factors, the number of individuals who will actually benefit from detecting a screen-detected cancer is very small," Dr Schilsky said.