Young patients with heart disease are smoking more and twice as many suffer from diabetes compared to 12 years ago. Heart disease prevention in routine clinical practice is inadequate, with only a third of patients being referred to and joining prevention and rehabilitation programmes, whilst doctors are prescribing more and more drugs. Yet lifestyle programmes should be the backbone of preventive care. Saving people's lives from acute heart attacks is not sufficient, and an urgent investment in prevention is needed to address the lifestyle causes of heart disease. These are the conclusions of an Article published in this week's edition of The Lancet. The Article is one of four cardiology papers published in this edition, ahead of the American College of Cardiology meeting at the end of March.

Heart disease is preventable, yet it is the biggest killer in Europe causing 2 million deaths every year. The first (1995-96) and second (1999-2000) EUROASPIRE (European Action on Secondary and primary Prevention by Intervention to Reduce Events) surveys showed that in coronary patients cardiovascular risk factors such as smoking, high blood pressure, and high cholesterol were poorly managed in people with heart disease in Europe. Indeed, despite clear national and international guidelines on the best ways to prevent heart disease, they reported a widening gap between what is recommended and the results achieved in clinical practice.

In this study, Professor David Wood from Imperial College London, UK, and colleagues report the third (2006-7) EUROASPIRE survey outcomes*, examining more than a decade of heart disease prevention practices in 22 countries in Europe.

Findings showed a continuing and widening gap between the guidelines and patients' lifestyles in terms of stopping smoking, and reducing obesity and diabetes, and at the same time substantial increases in doctors prescribing of all of the major classes of cardioprotective drugs.

The authors report that over 12 years there has been no reduction in the proportion of patients with heart disease who smoke (20.3% in EUROASPIRE I, 21.2% in II, and 18.2% in III), but there has been a large increase in the proportion of younger female smokers. In addition, there has been a substantial increase in obesity and diabetes. In 1995-96, 25% of patients were obese and 17.4% had diabetes, this rose to 38% and 28% in 2006-7.

Further, despite large increases in the use of all classes of blood pressure lowering drugs, blood pressure management showed no improvement. Three out of five patients in all three surveys had raised blood pressure, and almost half of all patients remained above the recommended lipid targets. However, the number of patients with raised cholesterol has more than halved.

According to the authors, the results show how even when faced with a life-threatening disease it is difficult for people to change their behaviour. It is even harder when they don't have the professional support from a multidisciplinary team of nurses, dieticians, physiotherapists and doctors providing comprehensive prevention and rehabilitation programmes. They also point out that simply prescribing more cardioprotective drugs is clearly not enough and drug treatments need to be combined with professional lifestyle intervention.

They conclude by calling for comprehensive lifestyle programmes to be an integral part of health-care provision and health insurance plans for all patients with heart disease.

In an accompanying Comment, Mette Brekke and Bjørn Gjelsvik from The University of Oslo in Norway, say that the results give three messages: "First, to help patients with coronary heart disease achieve a healthy lifestyle should be mandatory and have high priority for doctors and health authorities. Second, therapeutic targets…[such as blood pressure and lipid targets] are too ambitious and might take focus away from important lifestyle issues. Finally…political action is needed to reverse the negative trends of obesity and sedentary habits, ranging from fighting against the fast food and sugar industries to safe bicycle paths and healthy school meals."

Pregnant women suffering from asthma run a greater risk of giving birth prematurely if they suspend their asthma treatments. According to a Université de Montréal study, published in Respiratory Medicine, the probability of suffering from hypertension during pregnancy also increases for women who interrupt their asthma treatment.

"Many pregnant women cease taking their asthma medication to protect the health of their child," says Faranak Firoozi, a researcher at the Université de Montréal's Department of Pharmacy. "However, they don't know that unchecked asthma can cause greater harm to the child than the medication."

According to Firoozi, there is no correlation between taking asthma medication, such as Pulmicort or Ventolin, and any congenital birth defect. In their study, Firoozi and colleagues debunk the myth that fetal gender has an affect on maternal asthma.

"Contrary to what some researchers have said, there is no difference between male and female hormones and how they impact bronchial sensitivity, which would in turn accentuate asthma symptoms when a woman carries a girl. This is good news," says Firoozi.

Firoozi used data collected by the Régie de l'assurance maladie, the Ministère de la santé et des services sociaux and the Institut de la statistique du Québec, on 13,000 pregnant women who consulted a physician for asthma between 1990 and 2002. The researcher analyzed the medication used by these women and their rate of hospitalization following their visit to the ER.

"Yes, asthma can have an important impact on pregnancy," says Firoozi. "Asthmatic women must be closely followed during pregnancy given the risks they pose to their own health and the health of their child. But the sex of the fetus has nothing to do with the asthmatic condition of pregnant women.

Human problems rarely occur in a vacuum, but persist as part of ongoing social interaction in which causes and effects are interwoven. One person's behavior can set the stage for what another does. A new study in the journal Family Process reveals that smoking can promote emotional connection for couples when both partners smoke. Health-compromising behaviors, such as smoking or weight gain, may sometimes persist because they preserve stability in a vital close relationship.

Researchers led by Michael J. Rohrbaugh and Varda Shoham of the University of Arizona had 25 couples discuss a health-related disagreement before and during a period of actual smoking, then use joysticks to rate how they had felt from moment to moment (from very positive to very negative) while watching themselves on video. One partner in each couple smoked despite having a heart or lung problem, and in some couples the other partner was a smoker as well.

The joy-stick ratings of partners in dual-smoker couples became more positive and more synchronous contingent upon lighting up - as if they were dancing to the same emotional tune. In single-smoker couples, however, both partners (smokers and non-smokers alike) report decreased positive emotions and less affective synchrony.

While most people think of health-compromising habits like smoking as a purely individual matter of motivation or addiction, this study shows that social factors beyond the smoker are important as well.

Having a partner who also smokes makes a huge difference in how smoking fits the couple's relationship (e.g. as an irritant or an ally), which in turn has implications for helping one or both partners quit.

"Looking beyond the patient can help to predict health outcomes, and relational processes are an important focus for intervention," the authors conclude. "Although prevailing conceptualizations cast nicotine addiction almost exclusively as an 'individual problem,' (findings such as ours) add credence to alternative, more contextual avenues of intervention."

A new 18-year nationwide study of US cities found that long term exposure to high levels of ground ozone, a main component of smog, was linked to significantly higher risk of dying from respiratory diseases.

The study was the work of Dr George Thurston, a professor in the Department of Environmental Medicine at New York University School of Medicine (NYU) School of Medicine, a part of NYU Langone Medical Center, and colleagues, and is published online on 12 March in the New England Journal of Medicine, NEJM.

Many studies have linked atmospheric ozone to poor health, and others have shown that a high-ozone day, for example as a result of city smog, is linked to an increased risk of acute health problems the next day, such as more asthma and heart attacks. However, until this study, the effect of long term exposure to ozone in air pollution (the summertime haze) on health and deaths in particular was somewhat uncertain.

Thurston, who directed the air pollution exposure assessment part of the study, said in a separate press statement that:

"What this study says is that to protect the public's health, we can't just reduce the peaks, we must also reduce long-term, cumulative exposure."

For this study, Thurston and colleagues looked at the potential contribution of exposure to ozone to the risk of death from cardiopulmonary or heart and lung related causes and specifically to death from respiratory causes. It is the first study to separate the effect of ozone from that of fine particulate matter, the tiny particles of pollutant material that cars, factories and power plants release into the atmosphere.

They used data from the American Cancer Society Cancer Prevention Study II and correlated it with air pollution figures for 96 metropolitan areas of the US. They analyzed study records from 448,850 people, including 118,777 deaths over an 18 year period from 1982 to 2000.

The study records included cause of death (where relevant), and things like age, smoking status, body mass index, and diet, plus where the subjects lived, so these potential confounding factors could be taken into account in the statistical analysis.

They were able to find data on daily maximum ozone levels from April 1 to September 30 from 1977 to 2000, and data on fine particles in the air (2.5 microns or smaller in diameter, called PM2.5) for 1999 and 2000.

The researchers found that:

* When they used a single pollutant model, increased levels of either PM2.5 or ozone were significantly linked to increased risk of death from cardiopulmonary causes.

* When they used a two pollutant model, increased PM2.5 was linked to increased risk of death from cardiovascular disease, while ozone was linked to increased risk of death from respiratory causes.

* The risk of dying from respiratory disease was more than 30 per cent higher in metropolitan areas with the highest ozone levels than those with the lowest.

* The estimated risk of dying from respiratory disease went up by 4 per cent for each increase in 10 parts per billion (ppb) of ozone.

* The city with the highest mean daily maximum ozone concentration over the 18 years of the study was Riverside, California (104 ppb).

* This corresponded to about 50 per cent higher risk of dying from lung disease compared to no exposure to ozone.

* Los Angeles came a close second, with an estimated 43 per cent increased risk of dying from lung disease.

* Northeast cities were generally lower in ozone than California.

* For example, Washington DC and New York City, showed a 27 and 25 increased risk of death from respiratory causes linked to ozone exposures.

* The lowest ozone levels were in San Francisco with a 33 ppb long term average daily maximum that was linked to a 14 per cent estimated increase of death from respiratory causes.

* The link between ozone and risk of death from respiratory causes did not change when confounders were taken into account, and neither did it change when they used different statistical models.

The researchers concluded that:

"In this large study, we were not able to detect an effect of ozone on the risk of death from cardiovascular causes when the concentration of PM2.5 was taken into account. We did, however, demonstrate a significant increase in the risk of death from respiratory causes in association with an increase in ozone concentration."

When it is high in the atmosphere, ozone protects us against the harmful UV (ultraviolet) rays of the sun. But at ground level, inhaled ozone causes inflammation of respiratory tissue, according to the Canadian Center for Occupational Health and Safety (CCOHS). Here it is primarily a byproduct of pollution, a secondary pollutant created when nitrogen dioxide from cars, power plants and factories meets with oxygen in the presence of sunshine.

This type of ozone takes time to form and is more likely to found downwind of cities in suburbs and rural areas, unlike fine particulate matter, a primary pollutant which hangs around where it is produced, in the inner cities, near roads and industrial sites.

Lead author Dr Michael Jerrett, associate professor, Division of Environmental Health Sciences, at the University of California, Berkeley, said that in line with rising death rates from respiratory disease, "background levels of ozone have at least doubled since pre-industrial-revolution times".

Thurston said that even though New Yorkers were breathing air with ozone levels very nearly in compliance with the Environmental Protection Agency short term ozone limit of 75 ppb, their estimates showed they were at a significant 25 per cent higher risk of dying from respiratory causes compared to non exposure.

The researchers said that San Francisco has low levels of ozone pollution because the city is often covered with a blanket of fog that stops the sun coming through to catalyze the photochemical reaction between nitrogen dioxide and oxygen. And Los Angeles, which has high levels, sits in a basin which stops the air pollution from dispersing as rapidly as it does in other cities like San Francisco.

Thurston said the current EPA air quality standards only address the health effects of short-term daily peaks in ozone exposure and do not protect against the long-term cumulative effects. The current EPA level for short term (8-hour) ozone exposure is 75 ppb, which is higher than the 60 ppb recommended by the agency's own scientific advisors, the American Lung Assocation and several other public health bodies. The EPA is going to review the standard in the next 12 months.

Revered in India as "holy powder," the marigold-colored spice known as turmeric has been used for centuries to treat wounds, infections and other health problems. In recent years, research into the healing powers of turmeric's main ingredient, curcumin, has burgeoned, as its astonishing array of antioxidant, anti-cancer, antibiotic, antiviral and other properties has been revealed.

Yet little has been known about exactly how curcumin works inside the body.

Now, University of Michigan researchers led by Ayyalusamy Ramamoorthy have discovered that curcumin acts as a disciplinarian, inserting itself into cell membranes and making them more orderly, a move that improves cells' resistance to infection and malignancy.

"The membrane goes from being crazy and floppy to being more disciplined and ordered, so that information flow through it can be controlled," said Ramamoorthy, a professor of chemistry and biophysics. The findings were published online March 3 in the Journal of the American Chemical Society.

The research project melds Ramamoorthy's past with his current scientific interests. As a child in India, he was given turmeric-laced milk to drink when he had a cold, and he breathed steam infused with turmeric to relieve congestion. Now as researcher he is fascinated with proteins that are associated with biological membranes, and he uses a technique called solid-state NMR spectroscopy to reveal atom-level details of these important molecules and the membranous milieu in which they operate.

"Probing high-resolution intermolecular interactions in the messy membrane environment has been a major challenge to commonly-used biophysical techniques," Ramamoorthy said. His research group recently developed the two-dimensional solid-state NMR technique that they used to probe curcumin-membrane communication in this study.

Scientists have speculated that curcumin does its health-promoting work by interacting directly with membrane proteins, but the U-M findings challenge that notion. Instead, the researchers found that curcumin regulates the action of membrane proteins indirectly, by changing the physical properties of the membrane.

Ramamoorthy's group now is collaborating with chemistry professor Masato Koreeda and U-M Life Sciences Institute researcher Jason Gestwicki to study a variety of curcumin derivatives, some of which have enhanced potency. "We want to see how these various derivatives interact with the membrane, to see if the interactions are the same as what we have observed in the current study," Ramamoorthy said. "Such a comparative study could lead to the development of potent compounds to treat infection and other diseases."