Restarting smoking after quitting is a problem that plagues those trying to kick the habit. Research into nicotine addiction and withdrawal in a mouse model is helping scientists understand the biological basis for the urge to restart. They have found that the signaling molecule dopamine, which is involved in feelings of reward, plays a key role in the body’s response to nicotine withdrawal.

Mark Twain said, “Giving up smoking is the easiest thing in the world. I know because I’ve done it thousands of times.” Many smokers would agree that it’s difficult to stay away from cigarettes. A new study in Biological Psychiatry this month now suggests that low dopamine levels that occur as a result of withdrawal from smoking actually promote the relapse to smoking.

Dopamine is a brain chemical messenger that is critically important in reward and motivation. Some research suggests that one of its central roles is to send a signal to the brain to ‘seek something enjoyable’. Indeed, dopamine is released during many rewarding experiences, including taking drugs, smoking, having sex, and eating food.

This signal seems to depend on the dopamine which is released in response to environmental cues, called phasic release, as opposed to the tonic seepage of small amounts of dopamine from nerve cells. The tonic release of dopamine is implicated in helping the dopamine system set the level of its reactivity to inputs.

Since dopamine is released by smoking, it makes sense that dopamine levels become abnormal when a smoker chooses to stop smoking. Researchers from Baylor College of Medicine in Texas undertook their study to characterize these changes.

They studied mice that were administered nicotine, the active constituent of cigarettes, for several weeks. The researchers then withheld the nicotine and measured the subsequent alterations in dopamine signaling during the withdrawal period.

They reported that withdrawal from nicotine produced a deficit in dopamine in which the basal dopamine concentration and tonic dopamine signals were disproportionately lower than the phasic dopamine signals. Re-exposure to nicotine reversed the hypodopaminergic state.

“This study is an elegant example of yet another way that addiction ‘hijacks’ the reward system. The phasic release of dopamine triggers us to seek things that, in theory, help us to adapt to our environment,” commented Dr. John Krystal, editor of Biological Psychiatry. “However, in addiction the phasic release of dopamine is heightened and it triggers the pursuit of abused substances. This disturbance of dopamine function would, conceivably, make it that much harder to avoid seeking drugs of abuse.”

According to the authors, these findings indicate that medications which could help elevate tonic dopamine levels during withdrawal may be successful treatment strategies for nicotine-dependent individuals attempting to quit smoking. Theoretically, such a treatment could help normalize any fluctuating dopamine levels from the sudden lack of nicotine, and also lessen the dopamine-influenced urges to seek out the nicotine, leading to relapse.

Reference: Elsevier

Children who are obese have a significantly increased risk of a certain class of bone fracture, according to new research. The study noted that the likelihood is much higher of fracturing the growth plate, the zone of new bone growth in kids, and most of the injuries are due to low-impact accidents.

Obese children are 74 percent more likely to sustain a fracture of the growth plate, the softer end of the bone where growth occurs. A new study presented today at the 2012 Annual Meeting of the American Academy of Orthopaedic Surgeons (AAOS), involved 224 children visiting a Maryland hospital with a fracture. Information was collected on each patient regarding their sex, age, height, weight, fracture location and pattern. Patients ages 2 to 16 were divided into two groups for comparison: a “normal weight” group and an “obese/overweight” group for children with a body mass index (BMI) greater than the 85 percentile.

The overweight/obese group represented 41.3 percent of the fracture population, and had a statistically significantly higher rate of growth plate injuries (40 percent versus 23 percent). The study, which is ongoing, also looked at the type of incidents causing the fractures, and found that the obese/overweight children had a greater number of injuries resulting from “low-energy” contact or impact, such as falling from a standing position. The findings could provide greater insight into the inherent risks for overweight and obese children pertaining to exercise and physical activity.

Reference: American Academy of Orthopaedic Surgeons

An anti-obesity drug currently in clinical trials may have worrying side effects, according to new research. The drug is actually a signaling molecule normally found in the body, called FGF21. However, high doses have harmful effects in mouse models, causing severe loss of bone mass.

An endocrine hormone used in clinical trials as an anti-obesity and anti-diabetes drug causes significant and rapid bone loss in mice, raising concerns about its safe use, UT Southwestern Medical Center researchers have shown.

The hormone, fibroblast growth factor 21 (FGF21), promotes bone loss by enhancing the activity of a protein that stimulates fat cells but inhibits bone cells, researchers report in a study available online in Proceedings of the National Academy of Sciences.

“This hormone is a very potent regulator of bone mass,” said Dr. Yihong Wan, assistant professor of pharmacology and senior author of the study. “When we oversupply FGF21 in mice, it results in substantial bone loss.”

UT Southwestern scientists had been investigating this hormone’s properties since its discovery in 2005 as a potential drug. Bone loss was a side effect of another class of compounds that had been commonly used in the treatment of diabetes – activating the same protein in a manner similar to FGF21 – and leading the research team to investigate the bone effect of FGF21 in three kinds of mice.

They found that rodents fed a drug form of the hormone over a two-week period lost 78 percent of their spongy bone. Mice engineered to produce excess FGF21 had similar effects. Conversely, researchers found mice completely lacking the hormone had comparable gains in bone mass.

While the insulin-sensitizing effects of FGF21 make it a potentially powerful anti-obesity drug, that could be canceled out by risk of osteoporosis and fractures associated with bone loss, the investigators report.

“The bone effect is clear,” said Dr. David Mangelsdorf, chairman of pharmacology, a Howard Hughes Medical Institute investigator at UT Southwestern and one of the study’s corresponding authors. “It’s a tradeoff of benefits and risks, and the key will be to design the drug in such a way to leverage the two against each other, dialing out the side effects and dialing in the positive.”

In a related study online in Cell, researchers at the medical center identified how FGF21 regulates the activity of a diabetes-fighting compound in fat tissue, altering metabolism in response to starvation and resumed eating for survival-driven energy conservation.

“FGF21 helps mobilize the fat in adipose tissue back to the liver and burn it. But when the animal is refed, it stops this process and immediately turns back to restoring fat. In one case, it turns this system on, and in the other, turns it off,” said Dr. Steven Kliewer, professor of molecular biology and pharmacology and senior author of the Cell paper.

UT Southwestern researchers involved in the PNAS study were Dr. Wei Wei, lead author and postdoctoral researcher in pharmacology; Dr. Paul Dutchak, postdoctoral researcher in neuroscience; Drs. Xunde Wang and Xushan Ding, postdoctoral researchers in pharmacology; Dr. Xueqian Wang, research associate in pharmacology; Angie Bookout, graduate student in internal medicine; Dr. Robert Gerard, associate professor of internal medicine; and Dr. Kliewer.

The scientists in the Cell study included Dr. Dutchak, lead author involved while a graduate student in pharmacology; Takeshi Katafuchi, instructor in pharmacology; Ms. Bookout; and Dr. Mangelsdorf.

Reference: UT Southwestern Medical Center

Parkinson’s disease is complex and difficult to study, given the complicated interactions between brain cells. A new model, however, is giving major new insights into what goes wrong in neurons in Parkinson’s patients. Scientists took skin cells from patients, and by changing their environmental signals in the laboratory, coaxed them into becoming neurons. Study of those neurons has revealed key properties, including abnormal levels of certain enzymes.

Parkinson’s disease researchers at the University at Buffalo have discovered how mutations in the parkin gene cause the disease, which afflicts at least 500,000 Americans and for which there is no cure.

The results are published in the current issue of Nature Communications.

The UB findings reveal potential new drug targets for the disease as well as a screening platform for discovering new treatments that might mimic the protective functions of parkin. UB has applied for patent protection on the screening platform.

“This is the first time that human dopamine neurons have ever been generated from Parkinson’s disease patients with parkin mutations,” says Jian Feng, PhD, professor of physiology and biophysics in the UB School of Medicine and Biomedical Sciences and the study’s lead author.

As the first study of human neurons affected by parkin, the UB research overcomes a major roadblock in research on Parkinson’s disease and on neurological diseases in general.

The problem has been that human neurons live in a complex network in the brain and thus are off-limits to invasive studies, Feng explains.

“Before this, we didn’t even think about being able to study the disease in human neurons,” he says. “The brain is so fully integrated. It’s impossible to obtain live human neurons to study.”

But studying human neurons is critical in Parkinson’s disease, Feng explains, because animal models that lack the parkin gene do not develop the disease; thus, human neurons are thought to have “unique vulnerabilities.”

“Our large brains may use more dopamine to support the neural computation needed for bipedal movement, compared to quadrupedal movement of almost all other animals,” he says.

Since in 2007, when Japanese researchers announced they had converted human cells to induced pluripotent stem cells (iPSCs) that could then be converted to nearly any cells in the body, mimicking embryonic stem cells, Feng and his UB colleagues saw their enormous potential. They have been working on it ever since.

“This new technology was a game-changer for Parkinson’s disease and for other neurological diseases,” says Feng. “It finally allowed us to obtain the material we needed to study this disease.”

The current paper is the fruition of the UB team’s ability to “reverse engineer” human neurons from human skin cells taken from four subjects: two with a rare type of Parkinson’s disease in which the parkin mutation is the cause of their disease and two healthy subjects who served as controls.

“Once parkin is mutated, it can no longer precisely control the action of dopamine, which supports the neural computation required for our movement,” says Feng.

The UB team also found that parkin mutations prevent it from tightly controlling the production of monoamine oxidase (MAO), which catalyzes dopamine oxidation.

“Normally, parkin makes sure that MAO, which can be toxic, is expressed at a very low level so that dopamine oxidation is under control,” Feng explains. “But we found that when parkin is mutated, that regulation is gone, so MAO is expressed at a much higher level. The nerve cells from our Parkinson’s patients had much higher levels of MAO expression than those from our controls. We suggest in our study that it might be possible to design a new class of drugs that would dial down the expression level of MAO.”

He notes that one of the drugs currently used to treat Parkinson’s disease inhibits the enzymatic activity of MAO and has been shown in clinical trials to slow down the progression of the disease.

Parkinson’s disease is caused by the death of dopamine neurons. In the vast majority of cases, the reason for this is unknown, Feng explains. But in 10 percent of Parkinson’s cases, the disease is caused by mutations of genes, such as parkin: the subjects with Parkinson’s in the UB study had this rare form of the disease.

“We found that a key reason for the death of dopamine neurons is oxidative stress due to the overproduction of MAO,” explains Feng. “But before the death of the neurons, the precise action of dopamine in supporting neural computation is disrupted by parkin mutations. This paper provides the first clues about what the parkin gene is doing in healthy controls and what it fails to achieve in Parkinson’s patients.”

He noted in this study that these defects are reversed by delivering the normal parkin gene into the patients’ neurons, thus offering hope that these neurons may be used as a screening platform for discovering new drug candidates that could mimic the protective functions of parkin and potentially even lead to a cure for Parkinson’s.

While the parkin mutations are only responsible for a small percentage of Parkinson’s cases, Feng notes that understanding how parkin works is relevant to all Parkinson’s patients. His ongoing research on sporadic Parkinson’s disease, in which the cause is unknown, also points to the same direction.

Reference: University at Buffalo

New models of Alzheimer’s disease are helping scientists better understand how the condition progresses in the brain. Researchers have discovered part of the process through which a key protein is transferred between brain cells. Further insights into the movement of the protein could suggests ways to stop disease progression.

Two different research groups have independently made the same important discoveries on how Alzheimer’s disease spreads in the brain, according to a February 2 New York Times story. The groups’ findings have the potential to give us a much more sophisticated understanding of what goes wrong in Alzheimer’s disease and, more importantly, what can be done to prevent or repair damage in the brain.

The Times reported on the research teams of Bradley T. Hyman, MD, Ph.D., at Massachusetts General Hospital in Boston, and Karen E. Duff, Ph.D., of Columbia University Medical Center in New York.

Each research group found that the Alzheimer’s disease protein called tau can apparently spread from one part of the brain to other connected areas by effectively “jumping” from one nerve cell (neuron) to another. This is good news for scientists exploring pathways for treating Alzheimer’s disease, which is now a growing epidemic with the aging of the Baby Boomer generation and the sixth leading cause of death in the U.S. If scientists can determine how tau jumps from neuron to neuron, Alzheimer’s disease can potentially be stopped from spreading.

Results of Dr. Hyman’s AHAF-funded research will be published later this month in the journal Neuro. Dr. Duff’s research was published this week in PLoS ONE.

The two research groups also made similar advances in how to study the development of the disease in mice, by making new “mouse models” that better represent the human form of Alzheimer’s at later stages of the disease. This will allow scientists to develop a much more detailed understanding of what goes awry with the spread of Alzheimer’s disease over time, and what can be done to stop it.

It is important to note that these scientists’ findings build on an idea studied by a number of others over the years—the idea that cells can infect neighboring cells. This concept—now significantly advanced by the work of Hyman and Duff—was previously pursued by several scientists including AHAF grantees Joanna Jankowsky, Ph.D., of Baylor College of Medicine in Houston, and Marc Diamond, M.D., of Washington University School of Medicine in St. Louis.

The announcement this week reminds us why early-stage basic research is so crucial to fighting costly and devastating diseases. Only with solid investment in this type of research will solutions ultimately be developed that improve the lives of people affected by this disease.

On that front, important bipartisan legislation was unveiled this week by Senators Barbara Mikulski (D-MD) and Susan Collins (R-ME) and Representatives Chris Smith (R-NJ) and Ed Markey (D-MA). The Spending Reductions through Innovations in Therapies (SPRINT) Agenda Act of 2012 would ultimately reduce America’s healthcare costs, by spurring public and private research funding and streamlining the regulatory review of treatments needed for Alzheimer’s and other costly diseases. Read more information from Sen. Mikulski, and Sen. Collins.

Reference: AHAF-American Health Assistance Foundation

The flow of zinc in and out of cells could have an impact on the way breast cancer cells grow, according to a new study. The research determined that changing levels and activity of zinc transporter proteins are linked to cancer development. Using drugs to modify the flow of zinc could be an effective way to control tumor growth, and clinical trials are underway.

The body’s control mechanisms for delivering zinc to cells could be key to improving treatment for some types of aggressive breast cancer.

New research by Cardiff University and King’s College London has identified the switch which releases zinc into cells, with important implications for a number of diseases.

Zinc has long been known to play a vital part in human health. Too much zinc, or too little, can cause cell death. A growing body of evidence links zinc to disease states including neurodegeneration, inflammation, diabetes and cancer.

Zinc levels in cells are controlled by protein molecules called zinc transporters. These move zinc in and out of the cell to ensure correct levels are maintained. Until now, scientists have not understood how the transporters release the zinc. The Cardiff and King’s research team have identified a switch, known as CK2, a protein which opens one transporter, called ZIP7, and allows the zinc to flow.

Earlier research by the team has already linked zinc delivery to types of breast cancer. Higher levels of intracellular zinc and the ZIP7 transporter were found in tamoxifen-resistant breast cancers. CK2 was also known to be more common in cancers which encourage cell growth. The discovery that CK2 opens ZIP7 suggests that drugs which block this release of zinc could also block cancer development. Early results from clinical trials of CK2 inhibitors suggest they are performing well.

Dr Kathryn Taylor, of Cardiff University’s School of Pharmacy and Pharmaceutical Sciences, said: “We know that zinc, in the right quantities, is vital for development, our immune systems and many other aspects of human health. But when something goes wrong with the body’s zinc delivery system, it looks as though disease can result. In particular, our research has shown a link to highly aggressive forms of breast cancer. Our better understanding of how exactly zinc is delivered suggests if we can block malfunctioning transporter channels, we can potentially halt the growth of these forms of cancer. We believe this makes zinc, and zinc delivery, a high priority for future cancer research.”

Professor Christer Hogstrand from the Diabetes and Nutritional Sciences Division at King’s College London, said: “Our discovery provides a mechanistic explanation for how the cell uses zinc to regulate different functions. The evidence that zinc is released on command in the cell and then regulates cellular processes seems to set it apart from other transition metals, such as copper and iron, in the way that it is used by the body. These findings should open the door for new research into the roles of zinc in health and disease.”

The research, funded by a Wellcome Trust University Research Award to Dr Taylor, is published tomorrow (February 7) in the leading journal Science Signaling.

Reference: Cardiff University

Our tastes and food preferences are influenced by our genetic background, according to a new research study. Scientists have found that certain variations in a certain gene, involved in signalling, correlate with a preference for high-fat foods. The work may explain why some people have more trouble than others in sticking to a healthy diet, and could help researchers understand the genetics of those more prone to obesity.

A preference for fatty foods has a genetic basis, according to researchers, who discovered that people with certain forms of the CD36 gene may like high-fat foods more than those who have other forms of this gene.

The results help explain why some people struggle when placed on a low-fat diet and may one day assist people in selecting diets that are easier for them to follow. The results also may help food developers create new low-fat foods that taste better.

“Fat is universally palatable to humans,” said Kathleen Keller, assistant professor of nutritional sciences, Penn State. “Yet we have demonstrated for the first time that people who have particular forms of the CD36 gene tend to like higher fat foods more and may be at greater risk for obesity compared to those who do not have this form of the gene. In animals, CD36 is a necessary gene for the ability to both detect and develop preferences for fat. Our study is one of the first to show this relationship in humans.”

Keller and a tem of scientists from Penn State, Columbia University, Cornell University and Rutgers University examined 317 African-American males and females because individuals in this ethnic group are highly vulnerable to obesity and thus are at greatest risk for obesity-related diseases.

The team gave the participants Italian salad dressings prepared with varying amounts of canola oil, which is rich in long-chain fatty acids. The participants were then asked to rate their perceptions of the dressings’ oiliness, fat content and creaminess on a scale anchored on the ends with “extremely low” and “extremely high.”

The team also gave participants questionnaires aimed at understanding their food preferences. Participants rated how much they liked each food on a scale anchored with “dislike extremely” and “like extremely.” Foods included on the questionnaire were associated with poor dietary intake and health outcomes, such as half-and-half, sour cream, mayonnaise, bacon, fried chicken, hot dogs, French fries, cheese, chips, cake, cookies and doughnuts. The researchers collected saliva samples from the participants to determine which forms of CD36 they had. From the saliva samples, they extracted DNA fragments and examined differences in the CD36 gene contained within the fragments.

They found that participants who had the “AA” form of the gene — present in 21 percent of the population — rated the salad dressings as creamier than individuals who had other forms of the gene. These individuals reported that the salad dressings were creamier regardless of how much fat was actually in them. The researchers also found that “AA” individuals liked salad dressings, half-and-half, olive oil and other cooking oils more than those who had other forms of the gene. The results are published in a recent issue of the journal Obesity.

“It is possible that the CD36 gene is associated with fat intake and therefore obesity through a mechanism of oral fat perception and preference,” said Keller. “In other words, our results suggest that people with certain forms of the CD36 gene may find fat creamier and more enjoyable than others. This may increase their risk for obesity and other health problems.”

According to Keller, having certain forms of a gene that help in the perception and enjoyment of fats in foods might once have been an advantage.

“Fats are essential in our diets,” she said. “In our evolutionary history, people who were better able to recognize fats in foods were more likely to survive. Such forms of the gene, however, are less useful to us today as most of us no longer have to worry about getting enough fats in our diets.”

In fact, she added, having such forms of a gene can be detrimental in today’s world of fat-laden convenience foods.

“Our results may help explain why some people have more difficulty adhering to a low-fat diet than other people and why these same people often do better when they adopt high-fat, low-carbohydrate diets such as the Atkins diet,” said Keller. “We hope these results will one day help people select diets that are easier for them to follow. We also think the results could help food developers create better tasting low-fat foods that appeal to a broader range of the population.”

In the future, the team plans to expand the population they examine to include children.

“By the time we are adults it is very hard for us to change our eating behaviors,” said Keller. “So if we can determine which children have forms of the CD36 gene, as well as other genes that are associated with greater liking of fats, we can help them develop healthier eating behaviors at a young age.”

Keller also plans to incorporate novel techniques, such as functional magnetic resonance imaging (fMRI), to better understand why certain forms of the CD36 gene are linked to higher fat preferences.

“We plan to scan children while they are tasting high-fat foods and beverages so that we can see how their brains react to fats,” she said. “By doing this, we may be able to develop foods that are perceived by the brain as palatable high-fat treats, even though in reality, they are low-fat and healthy.”

Reference: Penn State

While eating whole soy has been touted as one way to reduce your risk of developing breast cancer, taking supplements with compounds isolated from soy do not have the same effect. The new study assigned women to take soy isoflavone supplements or a placebo pill, and found no difference in breast cancer cell growth. In pre-menopausal women, however, women taking the supplement showed higher breast cancer cell growth.

Soy isoflavone supplements did not decrease breast cancer cell proliferation in a randomized clinical trial, according to a study published in Cancer Prevention Research, a journal of the American Association for Cancer Research.

Lead researcher Seema A. Khan, M.D., professor of surgery at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University, said the results of this study are consistent with the findings of previous studies that were designed to test cancer prevention benefits of dietary supplements.

“Simply put, supplements are not food. Although soy-based foods appear to have a protective effect, we are not seeing the same effect with supplementation using isolated components of soy, so the continued testing of soy supplements is likely not worthwhile,” said Khan.

Khan said that beta-carotene and selenium supplementation have also been shown to lack benefit in lung cancer prevention studies.

“Foods are very complex and there are likely traveling companions that we haven’t identified that are protecting against cancer,” said Khan.

For the current study, Khan and colleagues randomly assigned 98 women to receive a mixed soy isoflavones supplement or placebo. Isoflavones are components of soy foods that were expected to have anti-estrogen activity.

These women had more than 4,000 breast cancer epithelial cells identified by fine needle aspiration biopsy. At six months, researchers evaluated the levels of Ki-67, an established protein marker of cancer cell growth. In the overall population, no difference was seen after six months in either group. However, among pre-menopausal women, the level of Ki-67 increased from 1.71 to 2.18, suggesting a negative effect of the supplementation.

“This was a small finding, but one that should suggest caution,” said Khan.

Reference: American Association for Cancer Research

A new study confirms a healthy benefit of drinking coffee: researchers have found that patients with nonalcoholic fatty liver disease drinking coffee have a reduced risk of liver fibrosis. Previous work suggests the key ingredient is caffeine.

Caffeine consumption has long been associated with decreased risk of liver disease and reduced fibrosis in patients with chronic liver disease. Now, newly published research confirms that coffee caffeine consumption reduces the risk of advanced fibrosis in those with nonalcoholic fatty liver disease (NAFLD). Findings published in the February issue of Hepatology, a journal of the American Association for the Study of Liver Diseases, show that increased coffee intake, specifically among patients with nonalcoholic steatohepatitis (NASH), decreases risk of hepatic fibrosis.

The steady increase in rates of diabetes, obesity, and metabolic syndrome over the past 20 years has given rise to greater prevalence of NAFLD. In fact, experts now believe NAFLD is the leading cause of chronic liver disease in the U.S., surpassing both hepatitis B and C. The majority of patients will have isolated fatty liver which has a very low likelihood of developing progressive liver disease. However, a subset of patients will have NASH, which is characterized by inflammation of the liver, destruction of liver cells, and possibly scarring of the liver. Progression to cirrhosis (advanced scarring of the liver) may occur in about 10-11% of NASH patients over a 15 year period, although this is highly variable.

To enhance understanding of the correlation between coffee consumption and the prevalence and severity of NAFLD, a team led by Dr. Stephen Harrison, Lieutenant Colonel, U.S. Army at Brooke Army Medical Center in Fort Sam Houston, Texas surveyed participants from a previous NAFLD study as well as NASH patients treated at the center’s hepatology clinic. The 306 participants were asked about caffeine coffee consumption and categorized into four groups: patients with no sign of fibrosis on ultrasound (control), steatosis, NASH stage 0-1, and NASH stage 2-4.

Researchers found that the average milligrams in total caffeine consumption per day in the control, steatosis, Nash 0-1, and Nash 2-4 groups was 307, 229, 351 and 252; average milligrams of coffee intake per day was 228, 160, 255, and 152, respectively. There was a significant difference in caffeine consumption between patients in the steatosis group compared to those with NASH stage 0-1. Coffee consumption was significantly greater for patients with NASH stage 0-1, with 58% of caffeine intake from regular coffee, than with NASH stage 2-4 patients at only 36% of caffeine consumption from regular coffee.

Multiple analyses showed a negative correlation between coffee consumption and risk of hepatic fibrosis. “Our study is the first to demonstrate a histopatholgic relationship between fatty liver disease and estimated coffee intake,” concludes Dr. Harrison. “Patients with NASH may benefit from moderate coffee consumption that decreases risk of advanced fibrosis. Further prospective research should examine the amount of coffee intake on clinical outcomes.”

Reference: Wiley-Blackwell

Although previous studies have found that binge drinking is linked to an increased risk of cardiovascular disease, a recent study has called this conclusion into question. A large scale study of over 25,000 individuals failed to find a difference between those binge drinking and drinking moderately, in terms of the incidence of ischemic heart disease.

Most studies have found that binge drinking is associated with a loss of alcohol’s protective effect against ischemic heart disease (IHD) and most studies have found an increase of coronary risk among binge drinkers.

This study followed 26,786 men and women who participated in the Danish National Cohort Study in 1994, 2000, and 2005 and sought to see if binge drinking increased the risk of IHD or all-cause mortality among “light-to-moderate” drinkers: (up to 21 drinks/week for men and up to 14 drinks/week for women). A “drink” was 12g.

“Binge drinking” (more that 5 drinks on an occasion) did not show differences in risk of ischemic heart disease (coronary disease) or total mortality than among always moderate drinkers. These results are somewhat different from results of many other epidemiologic studies that have shown increased risk of health problems (even higher risk of coronary disease) to be associated with what was referred to as “binge drinking.”

Why there were no adverse effects of binge drinking in this study has provoked considerable discussion among members of the Forum. The assessments of alcohol were based on consumption in the week prior to the examination, so data was not available to judge whether or not binge-drinking episodes occurred rarely or regularly. Data was available for smoking, education, physical activity, BMI, and self-reported hypertension and diabetes. There was a strong increase in IHD risk and mortality from binge drinking among heavy drinkers, but the authors were comparing outcomes in binge vs. non-binge drinkers among subjects in the “light-to-moderate” categories, and so in all comparisons, the relative risk of IHD and all-cause mortality was higher for non-drinkers than for all other categories of drinkers.

The general consensus of opinion among Forum members is the definition of “binge drinking.” The rapid consumption of more than 5 drinks on an empty stomach surely has different effects than the consumption of alcohol over several hours with food, such as during a prolonged dinner. The rate of consumption strongly affects the consequences of alcohol; the speed of drinking and context should constitute part of the definition of ‘bingeing’ and not just the total number of drinks.

The Forum concludes that “binge drinking,” however defined, is not a healthy pattern of alcohol consumption. But the circumstances of consumption (rate of consumption, with or without food, etc.) may also be important in its definition and in judging its effects on health.

The Forum does not take the results of this single study to support binge drinking. What the Danish results suggest is that the occasional “excess” embedded in a moderate consumption pattern is not shown to be harmful in this study. As recognized in responsible drinking guidelines from Australia, Canada and the US, occasional episodes of consumption greater than the recommended daily levels do not necessarily change the classification of a normally moderate drinker into that of an abuser.

Reference: Boston University Medical Center