Bad News For Coffee Drinkers Who Get Headaches

People who consume high amounts of caffeine each day are more likely to suffer occasional headaches than those with low caffeine consumption, a team of researchers at the Norwegian University of Science and Technology (NTNU) reports in a study recently published in the Journal of Headache Pain.


 
But in findings that had “no obvious reason”, the researchers, led by Knut Hagen from NTNU’s Faculty of Medicine, also reported that low caffeine consumption was associated with a greater likelihood of chronic headaches, defined as headaches for 14 or more days each month.
 
The results are drawn from a large cross-sectional study of 50,483 people who answered a questionnaire about caffeine consumption and headache prevalence as a part of the Nord-Trøndelag Health Survey (HUNT 2), a county-wide health survey conducted in 1995-1997 on a wide range of health topics.

To drink or not to drink
Caffeine is the world’s most commonly consumed stimulant, and has long been known to have both positive and negative effects on headaches. For example, caffeine is a common ingredient in headache analgesics because it can help relieve headaches.

But research worldwide into the relationship between caffeine consumption and headache provides no relief to headache sufferers wondering whether they should drink more coffee or less. Some studies have shown that high caffeine consumption increases the prevalence of headaches and migraines, while other studies have shown no such relationship.

At the same time, headaches are costly to society, in work hours lost, and to individuals themselves. The World Health Organisation ranks migraine 19th in all causes of disability based on a measure called “years lived with disability”, as one example.

The issue is of particular interest in Scandinavia, because Scandinavians are heavy coffee drinkers, consuming on average about 400 mg of caffeine per day. That is roughly twice the average caffeine consumption in other European countries and in the US, and equates to roughly 4 cups of brewed coffee per day, although caffeine levels in coffee vary quite widely.

The power – and limitation -- of numbers

The HUNT study is powerful because it is large-scale, population-based and cross-sectional, but when it comes to headaches, these characteristics make it difficult to establish cause-and-effect. For example, the frequency of non-migraine headache was found by researchers to be 18 per cent more likely in individuals with high caffeine consumption (500 mg per day or more) than among those with the lowest consumption (with mean levels at 125 mg per day).

But does that mean that all that caffeine causes headaches – or that people who are more likely to suffer from headaches drink caffeinated beverages in search of relief? “Since the study is cross-sectional, it cannot be concluded that high caffeine consumption causes infrequent headache,” the researchers write.
Even more difficult is explaining why chronic headache was less likely among individuals with moderate or high caffeine consumption, the researchers said. One possibility is that caffeine consumption helps change chronic headache into infrequent headache.

Cutting back may help
But it is equally possible that chronic headache sufferers had reduced their intake of caffeine because they had experienced its headache precipitating properties – and that individuals with infrequent headaches were unaware that high caffeine might be the cause.

In an interview, Hagen said that people should consider cutting back on their coffee consumption if headaches were a problem. “People who suffer from headaches should be focused on their caffeine use, because it can be a cause of their headaches,” he said.

Soy Reduces Diabetes Risk

Nutrition scientists led by Young-Cheul Kim at the University of Massachusetts Amherst have identified the molecular pathway that allows foods rich in soy bioactive compounds called isoflavones to lower diabetes and heart disease risk. Eating soy foods has been shown to lower cholesterol, decrease blood glucose levels and improve glucose tolerance in people with diabetes.


According to Kim, the study shows that “what we eat can have tremendous impact on health outcomes by interacting with certain genes. Recent research also suggests that diet can even change the copy number of a certain gene, leading to biological changes.”

Soy is the most common source of isoflavones in food. In experiments with mouse cells, Kim, a molecular nutrition researcher who studies how fat cells develop in the body, and colleagues, focused on daidzein, one of the two main isoflavones found in soy. Many epidemiological observations and human clinical studies have shown that adding soy to one’s diet is associated with lower diabetes risk and improved insulin sensitivity, as well as lower cardiovascular disease risk, Kim notes. However, until now the direct target tissue and molecular pathways by which soy exerts its anti-diabetic effects was not clearly understood.

Kim and colleagues at Southern Illinois University, with others at the universities of Tennessee and Florida, had earlier found that dietary isoflavones reduced the severity of diabetes in an animal model of the disease by increasing the activity of certain transcription regulators in the fat tissue. For the current study, they hypothesized that daidzein and its metabolite, equol, are part of this activation process.

They found that daidzein and equol enhanced adipocyte differentiation, or the formation of fat cells, through activation of a key transcription regulator, the same receptor that mediates the insulin-sensitizing effects of anti-diabetes drugs. Thus, daidzein and equol daidzein and equol seem to work in a similar manner as anti-diabetic drugs currently in the market. Their findings are reported in a September online version of the Journal of Nutritional Biochemistry.

“Our results suggest that soy isoflavones exert anti-diabetic effects by targeting fat cell-specific transcription factors and the downstream signaling molecules that are important for glucose uptake and thus insulin sensitivity,” Kim notes. “The new findings help us to understand the cellular mechanisms.” That is, how these biologically active compounds in soy interact to regulate and initiate metabolic and biological functions.

Results demonstrate that daidzein and equol enhance adipocyte differentiation by activating a specific receptor. The downstream responses include increased expression of three proteins, resulting in enhanced glucose uptake and insulin sensitivity.

“Although some details remain to be worked out, our data provide an additional molecular basis for the mechanism of insulin-sensitizing action by soy isoflavones,” says Kim. “These new findings help fill a critical gap between epidemiological observations and clinical studies on the anti-diabetic benefits of dietary soy.”

Future studies will extend the work to primary cultures of human cells through collaboration with researchers at Pioneer Valley Life Science Institute and Baystate Medical Center in Springfield. If replicated, studies can move on to further work in whole body systems.

Knowing Me, Myself And I

How well do you know yourself? It's a question many of us struggle with, as we try to figure out how close we are to who we actually want to be. In a new report in Perspectives on Psychological Science, psychologist Timothy D. Wilson from the University of Virginia describes theories behind self-knowledge (that is, how people form beliefs about themselves), cites challenges psychologists encounter while studying it, and offers ways we can get to know ourselves a little better.

The study of self-knowledge has tended to focus on how accurate we are at determining our own internal states, such as our emotions, personality, and attitudes. However, Wilson notes that self-knowledge can be broadened to include memory, like recalling how we felt in the past, and prospection, predicting how we will feel in the future. Knowing who we were and who we will be are as important to self-knowledge as knowing who we are in the present. And while a number of researchers are conducting studies that are applicable to those various facets of self-knowledge, Wilson observes that there is not much communication between them, one reason this field is challenging to investigate.

Although it can be fairly simple to assess how people's attitudes change over time--that is, have them predict how they will feel at certain time and then actually measure their feelings at that time-- it is more difficult to measure people's current self-knowledge accurately. Some methods of acquiring accurate information on a person's feelings or their personality are to compare reports from their peers and study their nonverbal behavior. However, Wilson has "great faith in the methodological creativity" of his "fellow social psychologists" and is confident that questions raised by these types of experiments will be answered in the next few years.
Although Wilson acknowledges all the interesting findings that have come out of new technologies, such as fMRI, he cautions that those type of studies may not be very relevant to studying issues associated with self-knowledge.
There are a number of theories that aim to describe self-knowledge by a dual-process model, pitting the unconscious against the conscious. Wilson notes that these theories are pessimistic in that they view the unconscious as something that cannot be breached. However, he remarks that "self-knowledge is less a matter of careful introspection than of becoming an excellent observer of oneself."
Wilson suggests some ways that can help us learn more about ourselves, such as really attempting to be objective when considering our behaviors and trying to see ourselves through the eyes of other people. Another way of knowing ourselves better is to become more aware of findings from psychological science. Wilson concludes, "Most of us pay attention to medical findings that inform us about our bodies (e.g., that smoking tobacco is harmful), and can learn about our psychological selves in the same way."

Males Have More Personality

Males have more pronounced personalities than females across a range of species -- from humans to house sparrows -- according to new research. Consistent personality traits, such as aggression and daring, are also more important to females when looking for a mate than they are to males. Research from the University of Exeter draws together a range of studies to reveal the role that sexual selection plays in this disparity between males and females.



The study shows that in most species males show more consistent, predictable behaviours, particularly in relation to parental care, aggression and risk-taking. Females, on the other hand, are more likely to vary their behaviour. They are also more likely to respond to these traits and therefore seem to be 'choosier' about the personality of a potential mate.
The research, which is published in the journal Biological Reviews (18 November 2009) draws on several studies, dating back to 1972. It is the latest study in a growing body of research from a University of Exeter team that links gender personality differences to sexual selection.
The authors believe sexual selection may hold the key to this variation. A concept originally developed by Charles Darwin, sexual selection is the theory that evolutionary traits can be explained by competition between one sex -- usually males -- for mates and by (female) mate choice. While the physical attributes resulting from sexual selection -- from dazzling peacocks tails to over-sized antler horns -- are well known, there has been much less of a focus on the impact on personality.
Lead author Dr Wiebke Schuett of the University of Exeter says: "Our study is the first to bring together research about the impact of sexual selection on personality in humans and other animals. Our study suggests that, while males tend to exhibit more pronounced personalities, including more predictable behaviour, in a range of different contexts, females are more receptive to these traits in males. We found a surprising level of similarity across a range of species."
This paper supports research carried out by the same team, published in the journal Animal Behaviour (February 2009). The team studied the social and feeding behaviours of a population of zebra finches. They found that although the male zebra finches did not explore their environment more than the females, they were more consistent in their exploratory behaviour. The team concluded that males are more likely to be selected as mates if they are consistent in any behaviour that would be beneficial to a partnership and its offspring. This would include finding food or seeing off predators.

Dr Sasha Dall of the University of Exeter, the team leader, says: "This body of research suggests that male personality could have evolved in much the same way as signs of physical attractiveness -- to help attract a mate. Scientists have not given the role of sexual selection in shaping animal personality much consideration in the past. We hope that our work will pave the way for further research in this rather overlooked subject."

Heart Disease Found in Egyptian Mummies

Hardening of the arteries has been detected in Egyptian mummies, some as old as 3,500 years, suggesting that the factors causing heart attack and stroke are not only modern ones; they afflicted ancient people, too.

Study results are appearing in the Nov. 18 issue of the Journal of the American Medical Association (JAMA) and are being presented Nov. 17 at the Scientific Session of the American Heart Association at Orlando, Fla.
"Atherosclerosis is ubiquitous among modern day humans and, despite differences in ancient and modern lifestyles, we found that it was rather common in ancient Egyptians of high socioeconomic status living as much as three millennia ago," says UC Irvine clinical professor of cardiology Dr. Gregory Thomas, a co-principal investigator on the study. "The findings suggest that we may have to look beyond modern risk factors to fully understand the disease."

The nameplate of the Pharaoh Merenptah (c. 1213-1203 BC) in the Museum of Egyptian Antiquities reads that, when he died at approximately age 60, he was afflicted with atherosclerosis, arthritis, and dental decay. Intrigued that atherosclerosis may have been widespread among ancient Egyptians, Thomas and a team of U.S. and Egyptian cardiologists, joined by experts in Egyptology and preservation, selected 20 mummies on display and in the basement of the Museum of Egyptian Antiquities for scanning on a Siemens 6 slice CT scanner during the week of Feb. 8, 2009.

The mummies underwent whole body scanning with special attention to the cardiovascular system. The researchers found that 9 of the 16 mummies who had identifiable arteries or hearts left in their bodies after the mummification process had calcification either clearly seen in the wall of the artery or in the path were the artery should have been. Some mummies had calcification in up to 6 different arteries.

Using skeletal analysis, the Egyptology and preservationist team was able to estimate the age at death for all the mummies and the names and occupations in the majority. Of the mummies who had died when they were older than 45, 7 of 8 had calcification and thus atherosclerosis while only 2 of 8 of those dying at an earlier age had calcification. Atherosclerosis did not spare women; vascular calcifications were observed in both male and female mummies.

The most ancient Egyptian afflicted with atherosclerosis was Lady Rai, who lived to an estimated age of 30 to 40 years around 1530 BC and had been the nursemaid to Queen Ahmose Nefertiri. To put this in context, Lady Rai lived about 300 years prior to the time of Moses and 200 prior to King Tutankhamun (Tut).

In those mummies whose identities could be determined, all were of high socioeconomic status, generally serving in the court of the Pharaoh or as priests or priestess. While the diet of any one mummy could not be determined, eating meat in the form of cattle, ducks and geese was not uncommon during these times.

"While we do not know whether atherosclerosis caused the demise of any of the mummies in the study, we can confirm that the disease was present in many," Thomas says.

In addition to Thomas, Dr. Adel Allam of the Al Azhar Medical School in Cairo, Egypt, is the study's co-principal investigator. Dr. Randall Thompson of the Mid America Heart Institute in Kansas City, Mo.; Dr. L. Samuel Wann of the Wisconsin Heart Hospital in Milwaukee; and Dr. Michael Miyamoto of UC San Diego also contributed to the JAMA report.

The Egyptology and preservationist team consisted of Abd el-Halim Nur el-Din and Gomma Ab el-Maksoud of Cairo University; Ibrahem Badr of the Institute of Restoration in Alexandria, Egypt; Hany Abd el-Amer of the National Research Center in Dokki, Giza, Egypt.
The authors express their appreciation to Zahi Hawass, secretary general of the Supreme Council of Antiquities, for allowing them to scan these mummies and perform this investigation.

Yoga Boosts Heart Health

Heart rate variability, a sign of a healthy heart, has been shown to be higher in yoga practitioners than in non-practitioners, according to research to be published in a forthcoming issue of the International Journal of Medical Engineering and Informatics.


The autonomic nervous system regulates the heart rate through two routes -- the sympathetic and parasympathetic nervous systems. The former causes the heart rate to rise, while, the parasympathetic slows it. When working well together, the two ensure that the heart rate is steady but ready to respond to changes caused by eating, the fight or flight response, or arousal.
The ongoing variation of heart rate is known as heart rate variability (HRV), which refers to the beat-to-beat changes in heart rate. In healthy individuals HRV is high whereas cardiac abnormalities lead to a low HRV.
Now, Ramesh Kumar Sunkaria, Vinod Kumar, and Suresh Chandra Saxena of the Electrical Engineering Department, at the Indian Institute of Technology in Roorkee, in Uttrakhand, India, have evaluated two small groups of men in order to see whether yoga practitioners can improve heart health. Anecdotal evidence would suggest that yoga practice may improve health through breathing exercises, stretching, postures, relaxation, and meditation.

The team analyzed the HRV "spectra" of the electrocardiograms (ECG) of forty two healthy male volunteers who are non-yogic practitioners, and forty two who are experienced practitioners, all volunteers were aged between 18 and 48 years.
The spectral analysis of HRV is, the team says, an important tool in exploring heart health and the mechanisms of heart rate regulation. The power represented by various spectral bands in short-term HRV are indicative of how well the heart responds to changes in the body controlled by the sympathetic and the parasympathetic nervous systems.

The team explains that very low frequency (VLF) variations in the spectra are linked to the body's internal temperature control. Low frequency peaks are associated with the sympathetic control and high frequency with parasympathetic control.

The team concludes that in their preliminary study of 84 volunteers, there is strengthening of parasympathetic (vagal) control in subjects who regularly practice yoga, which is indicative of better autonomic control over heart rate and so a healthier heart.

Moderate-to-Heavy Exercise May Reduce Risk of Stroke for Men

Men who regularly take part in moderate-to-heavy intensity exercise such as jogging, tennis or swimming may be less likely to have a stroke than people who get no exercise or only light exercise, such as walking, golfing, or bowling, according to a study published in the November 24, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology.

However, exercise did not have a protective effect against stroke for women. Women who took part in moderate-to-heavy intensity exercise did not have a reduced risk of stroke.

The study involved 3,298 people living in northern Manhattan, NY, with an average age of 69 who were followed for about nine years. During that time, there were 238 strokes. A total of 41 percent of the participants reported that they participated in no physical activity. Twenty percent regularly participated in moderate-to-heavy intensity activities.

Men who participated in moderate-to-heavy intensity activities were 63 percent less likely to have a stroke than people with no physical activity. The baseline risk of ischemic stroke over five years in the entire group was 4.3 percent; among those with moderate-to-heavy intensity activities the risk was 2.7 percent, and among those with no activity it was 4.6 percent.

"Taking part in moderate-to-heavy intensity physical activity may be an important factor in preventing stroke," said study author Joshua Z. Willey, MD, of Columbia University Medical Center and New York Presbyterian Hospital at Columbia. Willey is also a member of the American Academy of Neurology. "A large percentage of the participants were not taking part in any physical activities. This may be true of many elderly people who live in cities. Identifying ways to improve physical activity among these people may be a key goal for public health."

These results are contrary to some other studies that found that even light intensity physical activity reduced the risk of stroke. Willey said the number of participants may not have been large enough to detect subtle differences in the group that took part in only light physical activity.

Stroke is the leading cause of disability and the third-leading cause of death in the United States.
The study was supported by the National Institutes of Health

S k i n a n d s u n

How does the sun affect the skin?

Sunlight is an essential source of energy and is vitally important to life. However, absorption of
incident solar energy by components of the skin causes premature skin aging, known as photoaging
(Berneburg, 2000; Hadshiew, 2000). Photoaged skin displays textural and pigmentary changes as
well as prominent alterations in the organization of connective tissue (breakdown of collagen and
elastin fibers) and cell death. The skin becomes wrinkled, less elastic, dry and rough, and uneven in
pigmentation.

What are the differences between UVA and UVB rays?

Most of the photobiological effects of the sun, including sunburn, sun tanning, and immunosuppression,
are attributed to UVB rays (290-320 nm). However, UVA rays (320-400 nm) can cause
more significant damage to the skin. Because they permeate more deeply into the dermal matrix
than UVB rays, UVA rays can induce long-lasting skin lesions and contribute to the formation of free
radicals (these are involved in the alteration of all skin compounds and in skin aging). UVA rays can
thus cause irreversible skin alterations and induce skin cancer (Mariéthoz, 1998).

What can you do to protect your skin?

The best protection against photoaging is avoidance of sunlight, particularly when it is at its strongest
(during the summer and in between 11 am and 3 pm). Remember to always wear sun protection, even
on winter days. Your sunscreen should block out both UVA and UVB rays and be SPF (Sun Protection
Factor) 30 or above. Clothes are also an effective means of protection against the sun

Heavy, Daily Drinking Increases Risk Of High-Grade Prostate Cancer; Makes Preventive Drug Ineffective

Current research is inconclusive regarding the relationship between alcohol consumption and prostate cancer risk. Researchers led by Zhihong Gong Ph.D. of the University of California San Francisco, examined the associations of total alcohol, type of alcoholic beverage, and drinking pattern with risks of total, low- and high-grade prostate cancer.


They used data from more than 10,000 men participating in the Prostate Cancer Prevention Trial (PCPT). They found participants who reported heavy alcohol consumption (≥50 g alcohol/day) and regular heavy drinking (≥4 drinks/day on ≥5 days per week) were twice as likely or more to be diagnosed with high-grade prostate cancer (RR: 2.01, and 2.17, respectively). Less heavy drinking was not associated with risk.

They also compared drinking patterns with treatment outcome among men enrolled on this placebo-controlled trial of the drug finasteride. They found finasteride's ability to lower prostate cancer risk was blocked in men drinking <50g alcohol per day.

They conclude heavy, daily drinking increases the risk of high-grade prostate cancer and that heavy drinking made finasteride ineffective for reducing prostate cancer risk.

Men with lower cholesterol are less likely than those with higher levels to develop high-grade prostate cancer -- an aggressive form of the disease with a poorer prognosis

In a prospective study of more than 5,000 U.S. men, epidemiologists say they now have evidence that having lower levels of heart-clogging fat may cut a man's risk of this form of cancer by nearly 60 percent.

"For many reasons, we know that it's good to have a cholesterol level within the normal range," says Elizabeth Platz, Sc.D., M.P.H., associate professor at the Johns Hopkins Bloomberg School of Public Health and co-director of the cancer prevention and control program at the Johns Hopkins Kimmel Cancer Center. "Now, we have more evidence that among the benefits of low cholesterol may be a lower risk for potentially deadly prostate cancers."
Normal range is defined as less than 200 mg/dL (milligrams per deciliter of blood) of total cholesterol.
Platz and her colleagues found similar results in a study first published in 2008, and in 2006, she linked use of cholesterol-lowering statin drugs to lower risk of advanced prostate cancer.
For the current study, Platz, members of the Southwest Oncology Group, and other collaborators analyzed data from 5,586 men aged 55 and older enrolled in the Prostate Cancer Prevention Trial from 1993 to 1996. Some 1,251 men were diagnosed with prostate cancer during the study period.

Men with cholesterol levels lower than 200 mg/dL had a 59 percent lower risk of developing high-grade prostate cancers, which tend to grow and spread rapidly. High-grade cancers are identified by a pathological ranking called the Gleason score. Scores at the highest end of the scale, between eight and 10, indicate cancers considered the most worrisome to pathologists who examine samples of the diseased prostate under the microscope.
In Platz's study, cholesterol levels had no significant effect on the entire spectrum of prostate cancer incidence, only those that were high-grade, she says.
Platz cautions that, while the group took into account factors that could bias the results, such as smoking history, weight, family history of prostate cancer, and dietary cholesterol, other things could have affected their results. One example is whether men in the study were taking cholesterol-lowering drugs at the time of the blood collections, a data point the researchers expect to analyze soon.
Results of the current study are expected to be published online Nov. 3 in the journal Cancer Epidemiology, Biomarkers & Prevention. Also in the journal is an accompanying paper from the National Cancer Institute showing that lower cholesterol in men conferred a 15 percent decrease in overall cancer cases.
"Cholesterol may affect cancer cells at a level where it influences key signaling pathways controlling cell survival," says Platz. "Cancer cells use these survival pathways to evade the normal cycle of cell life and death."
She says that targeting cholesterol metabolism may be one route to treating and preventing the disease, but this remains to be tested.
Funding for the study was provided by the National Cancer Institute.

Authors of the study include Cathee Till, Phyllis J. Goodman, Marian L. Neuhouser and Alan R. Kristal from the Fred Hutchinson Cancer Research Center; Howard L. Parnes, William D. Figg, and Demetrius Albanes from the National Cancer Institute; Eric A. Klein from the Cleveland Clinic; and Ian M. Thompson Jr., from the University of Texas Health Sciences Center.

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Lost on the Way- Short Story

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Economic Stress—How Bad Is It Really?

Before the financial collapse, Dr. Jonathan Whiteson says his patients made predictable small talk. "It used to be, 'How are the children? Where did you go on vacation?'" he recalls.
"Now," he says, "they come in with a [newspaper] tucked under their arm and say, 'Did you see this?'" Usually they're pointing to a story about the market's dismal fortunes or the fallout of yet another Ponzi scheme.

Whiteson, director of cardiac and pulmonary wellness and rehabilitation at New York University's Langone Medical Center, says the change in tone has been accompanied by complaints about ailments small and large, including chest pain, gastrointestinal distress and muscle aches.

That's unsurprising given that scientific research has long demonstrated a link between poor health outcomes and declining employment and gross domestic product. Since the recession began in December 2007, the economy has shed 5.1 million jobs and the unemployment rate has reached 8.5 percent. Meanwhile, U.S. GDP decreased at an annual rate of 6.3 percent in the fourth quarter of 2008.

And since the economy began quickly unraveling last fall, there have been numerous reports about how this dynamic is playing out in the current recession: Americans are sleeping less, seeing doctors less frequently and slowing prescription drug refills.
But some reports may be exaggerating how bad the recession has been for Americans' health.

By the numbers
To be fair, various polls and surveys have accurately tracked some of the effects. In March, the National Sleep Foundation reported that more than a quarter of 1,000 survey participants were sleeping less because of the economy.

The recession has also forced Americans to skimp on health care. In a February telephone poll of 1,200 adults conducted by the nonprofit Kaiser Family Foundation, 53 percent of respondents said they cut back on health care costs by avoiding doctor's visits, skipping dental check-ups and not filling prescriptions, among other strategies.

The American Hospital Association, a national trade organization, recently reported that total visits to 650 hospitals across the country were down in the fourth quarter of 2008 compared to the previous year, with nearly 3 percent fewer visits to the emergency room and 2 percent fewer patient surgeries. The sample is not nationally representative, but is still considered a leading indicator of hospital performance.

Despite such research, it remains challenging to gauge what is happening across the nation. That's because the government rarely collects data about health outcomes in real-time. The Centers for Disease Control and Prevention, for example, surveys the public about contraceptive use once over a several-year period and those figures aren't released until a year or two later. As such, it often requires rigorous statistical and epidemiological analysis to link a single negative health outcome to the economy.

Even some major insurers are reluctant to discuss the situation. UnitedHealth Group and Aetna declined to comment on how the recession might be reducing the frequency of treatments and procedures, citing insufficient data on usage trends in the past six months.

Perception vs. reality
The dearth of statistics may explain why some are turning to individual providers for answers about what's happening to patients nationwide.

At his clinic, Dr. Whiteson has noticed that patients more frequently complain of shortness of breath, fatigue, dizziness and palpitations. They seem to be experiencing sexual dysfunction more often and report drinking more frequently.

But extrapolating such observations beyond one practice can be deceiving. Craig Wolf, president and CEO of the Wine and Spirits Wholesalers of America, Inc., says that per capita alcohol consumption has remained flat for the past 30 years—even in the past six months.

Even during deep recessions of the '70s and '80s, Americans annually drank about 2.7 gallons of alcohol per capita, a figure that has never decreased more than a half-gallon in the decades since.
Other potentially misleading anecdotes have popped up recently. A report by the Associated Press found that some regional and state health clinics and hospitals had seen a significant increase in the number of local abortions and vasectomies since last year. Last month the Washington Times reported that dentists nationwide had noticed an uptick in the number of teeth grinding cases since 2007.

But as it turns out, neither trend could be confirmed by outside sources. Planned Parenthood and the American Dental Association both lacked national data to verify the anecdotal reports.
"It's reasonable and it's plausible," says Dr. Matthew Messina, a consumer adviser for the ADA, "but it still is an urban myth."
Ted Joyce, a professor of economics at Baruch College at the City University of New York, says that there's little evidence that abortions follow business cycles. Verifying this would require comparing monthly unemployment data to monthly abortion rates, which is not collected by nonprofit organizations or the government. Looking at the raw data—abortions stayed level at 1.6 million annually throughout the '80s—doesn't help establish a pattern, either.

Skeptics might want to consult research pioneered by Dr. Harvey Brenner, a professor of public health at the University of North Texas Health Science Center and at John Hopkins University's Bloomberg School of Public Health, which has shown a correlation between economic downturns and a rise in suicides and cardiovascular mortality.

This has been proven in "sharp and complete statistical studies," says Brenner, which "all lead to a fairly strong case that major disturbances to peoples' economic lives make a real difference in life expectancy."

That's partly because high-stress events elicit an immunological response from the body, leaving it vulnerable to everything from the common cold to a heart attack. Couple the stress response with the cutback in preventive care prompted by the floundering economy, and personal health suffers.

But even Dr. Whiteson, who is certain the economy is negatively affecting his patients' health, is struggling to separate persistent symptoms from ones temporarily brought on by stress.

"It's becoming an increasing challenge to work out what's real and what's not real," he says

What gives you that feel-good feeling

Are we hard-wired to be good people? Is helping our fellow man a natural instinct of our kind?
It's inviting to believe we share species-wide morality when we see U.N. rations drop into a destitute village or watch a rescue worker pull a toddler from a well. Altruism needn't come on such a grandiose scale, either; we feel the same swell of pride and humility from everyday overtures like shoveling the neighbor's walk or offering directions to a lost stranger.
Granted, we don't live it 24/7. Anyone who's spent more than five minutes on the phone with the cable company's customer service line has danced with his darker demons. But we know when we're morally and ethically on track.

Ethical behavior's effect on the brain

We know because the brain tells us so in its strange chemical language. Research in the young field of social neuroscience has revealed that the brain is activated in response to compassion and ethical behavior.

Several studies have focused on the brain's reward circuit to try to connect the dots between neurological function, emotion and ethics. The reward circuit is an interacting group of brain areas including the ventral striatum and ventromedial prefrontal cortex (a small region behind the forehead), and it's understood to be a hub of the brain's emotional network.
It's here that we manage reason and emotions like compassion and shame, and where we process pleasure in response to stimuli like an attractive face or a big bite of chocolate. Over the past two years, studies have linked the reward circuit to altruism, the perception of justice, and a sense of fairness.

Another study by world-class neuroscientists suggests the same area of the brain is engaged in deeper moral judgments. Working with 30 subjects, researchers posed classic morality scenarios such as: If one person in a life raft had to be thrown over so that several others could live, could you toss her over?
Each of the six subjects who had suffered injuries to the prefrontal cortex—and only those six—responded without reservation that they were willing to harm one individual to save themselves and the others.

"In those circumstances most people without this specific brain damage will be torn," said one author of the study. "But these particular subjects seem to lack that conflict." The research has been noted for linking the block of emotions with a failure of moral judgment.
Studies on oxytocin (more widely recognized for its role in childbirth and parent/child bonding) also have linked brain activity with higher moral functions. Acts of selflessness, the touch of another's hand, the glance of a mother into her newborn baby's eyes—all are known to trigger release of the hormone, which in turn promotes the release of dopamine. The flooding of dopamine into the brain's reward center elicits that warm surge of satisfaction we get from doing good things or being in the company of people we love and trust. It's the pleasure response.

Soul stirring
While these findings represent some terrific leaps in neuroscience, they also stir up some troubling questions. People get uneasy when science rubs up against philosophy or, heaven forbid, theology.

We've taken it on good scientific authority that all stimuli and responses course through the brain. Yet we still credit our loftier inclinations to the mind, the soul, or even to the heart. We say music is "good for the soul" or that a child's smile "fills the heart" with joy. No one ascribes a vision of peace and brotherhood to their ventromedial prefrontal cortex. No romantic wants to equate a flow of emotion with a flow of oxytocin.

While this all may sound like groundwork for an argument that we are a robotic and soulless race, science is not laying claim to the impulses at the origin of ethical thought. Neither has it been able to find a clear evolutionary advantage for all of these brain reactions, suggesting humans are wired for more than survival of the species.
This line of study does approach an understanding of how humans process moral and ethical choices. Structures and chemicals in the brain help set the magnet of our moral compass. But so too do we feel within ourselves something greater than ourselves.

Brain loves the good kind and the bad

A friend offers you a smoke while you're tailgating at the game. You have one every now and then, and you're not hooked, so sure, thanks. Besides, it does look good with your drink. This, my friend, is your brain battling a bad habit—and losing. As we continually perform a behavior—smoking socially, say, or texting while driving—neural pathways in our brains form new patterns, according to a recent MIT review. Once the prompt arrives, your brain shifts into autopilot. "Situational cues bring out habits that are deeply embedded," says Ellen Peters, Ph.D., who studies risk perceptions at Decision Research, a psychological research firm in Eugene, Ore. "When that habit surfaces, it's hard not to let it overcome you." The problem, of course, is that these proclivities can endanger your health. So follow our guide to rid yourself, once and for all, of a few distinctly unhealthy habits.

A quick drag every now and again ...
While regular smokers have a chemical component fueling their addiction, people who smoke only occasionally succumb mainly to social and environmental triggers. "The most powerful prompt is often being around other people who are smoking or drinking," says Michael Fiore, M.D., director of the University of Wisconsin Center for Tobacco Research and Intervention. In stressful situations, a cigarette can put you at ease: 10 minutes after you take a puff, your brain releases a surge of dopamine, a neurotransmitter that can make you feel relaxed and happy. (Want to boost your mood without cigarettes or drugs?

Why it's bad: Lighting up even a few times a week is still poisoning yourself. "There's no lower limit of exposure to tobacco smoke that is safe. Period," says Richard D. Hurt, M.D., director of the Mayo Clinic Nicotine Dependence Center. In fact, a single cigarette can almost instantly injure the inner walls of your blood vessels. That damage can lead to heart disease and blood clots. Looming in the background, of course, is also the risk of developing a full-blown addiction. Some research suggests that about a quarter of "occasional" smokers go full-time.

Break the habit: When you can't steer clear of the smokestacks, benign substitutes can work wonders, Dr. Hurt says. For instance, grab a drink stirrer and hold it between your fingers like a cigarette. Set it between your lips while you take out your wallet or phone. This keeps your mouth and hands busy. And carry nicotine gum or lozenges—these can mimic the effects of nicotine from cigarettes, Dr. Fiore says.

Evenings in front of the tube ...
Grabbing some snacks and firing up the plasma after work is okay once or twice a week. But every night? Yes, bad habit. "People who are under high levels of stress and who may not have a large network of friends are prone to isolating themselves after work," says Leonard Jason, Ph.D., a DePaul University psychologist who studies the challenges of breaking bad habits. "Eventually, it becomes their default."
Why it's bad: Slumming it on the couch plays havoc with your body and your brain. For one thing, people can consume up to 71 percent more food while they're glued to the tube, so it's no surprise that watching more than 19 hours a week increases your odds of being overweight by 97 percent, according to a 2007 Belgian study. And researchers at Case Western Reserve University found that for every hour of TV beyond 80 minutes that you watch daily, your risk of developing Alzheimer's increases by a whopping 30 percent.

Break the habit: If you have a digital video recorder, use it to record shows, and simply start your descent to bedtime later in the evening, Jason suggests. Zipping through the commercials can cut about half an hour off every 2 hours of couch time. Then, at least three times a week, make afterwork plans that specifically involve people—meet friends for dinner, or join a recreational sports team. "Finding alternatives that you can do with others helps reduce passive TV viewing," Jason says. How about taking her out? But not just for dinner and a movie—plan one of these unforgettable adventures for a date like she's never gone on before.

Your caffeine drip ...
The human body embraces some vices with gusto, effectively launching lifelong habits by punishing you for skipping even a single hit. That's caffeine's MO. When a caffeine fanatic doesn't get that fix, bloodflow in the brain spikes, according to a 2009 study in Psychopharmacology. This expansion of blood vessels results in a headache, while you suffer from symptoms such as fatigue and grumpiness. To avoid this, you visit the vending machines or the office java pot. (Makes us wonder: Why can't fruits and vegetables hook us like this?)
Why it's bad: A constant infusion of caffeine can set your nerves on edge. "High daily caffeine intake may decrease hand steadiness and increase anxiety," says Russell Keast, Ph.D., a caffeine-consumption researcher at the School of Exercise and Nutrition Sciences at Deakin University, in Australia. Then there's a 2007 study from Dartmouth medical school, which found that people who consumed 400 milligrams of caffeine a day (about four 8-ounce cups of coffee) for a week experienced a 35 percent decrease in insulin sensitivity, which may increase the risk of diabetes. And if you commonly drink any of the worst frozen coffee drinks in America, you could be slurping down a day's worth of calories in minutes.

Break the habit: Start by keeping a food diary for a few days to identify all the sources of caffeine in your diet—soda, coffee, tea, energy drinks—and tally the total milligrams you're consuming, says Chad Reissig, Ph.D., a researcher at Johns Hopkins University who studies the behavioral effects of caffeine. (Consult beverage manufacturer Web sites for the actual amounts.) Then reduce your caffeine intake by about 10 percent. This could be as simple as drinking a 12-ounce can of cola instead of the 20-ounce bottle. "You can also mix decaf with your cup of full-strength coffee, and slowly increase the ratio," says Reissig. Keep dialing back by 10 percent every few days until your craving subsides. The gradual reduction should minimize fatigue and headaches, but plan for them anyway: Go to bed earlier to keep drowsiness at bay, Reissig says, and carry Advil or Tylenol to treat brain pain.
Cranking the tunes ...
This habit sneaks up on you: You listen to your music through your headphones at a higher volume than you should a few times, and your ears become accustomed to it. Then you play it at that level all the time. Eventually, you max out the volume controls on the iPod. "It's possible to quickly adapt and become accustomed to louder and louder sounds without realizing it," says Robert Fifer, Au.D., the director of audiology and speech language pathology at the University of Miami's Mailman Center for Child Development.

Why it's bad: Blasting Nickelback at full volume through earbuds for long intervals can cause permanent hearing damage, because your body lacks a self-defense mechanism for loud noise. While you won't feel pain in your ears until the volume exceeds 120 decibels, the damage can begin earlier than that. The cells in your inner ear that process sound begin working overtime to keep up with the onslaught, and eventually die off under stress, says Dr. Fifer. The fewer of these cells you have, the more difficult it becomes to hear soft sounds. You may also experience a constant ringing in your ears, called tinnitus.
Break the habit: You have to retrain your brain to perceive lower volume levels as normal and to automatically tune out background noise. Start by turning down the volume on your iPod or car stereo until you can hear other people talking to you—they shouldn't have to shout. "If you force yourself to listen to music at a lower level, your brain will begin to perceive it as normal after about a week," says Catherine Palmer, Ph.D., the director of audiology at the University of Pittsburgh Medical Center Eye & Ear Institute. Also, think about using Loud Enough earphones ($40, loudenough.com), which reduce your music player's maximum volume by up to 20 decibels. And for ways to improve your eyesight, posture, and more with these 17 problems you can fix right now.
Talking and texting while driving ...
We keep doing this because while we intuitively know that the combination is unsafe, we assume nothing would ever happen to us. "If you do it once and nothing happens, your experience tells you that it's OK," says Peters. "Those repeated safe experiences build up a sense of invulnerability."
Why it's bad: The hard reality is that our habit of talking and texting while driving, which springs from our still-bubbling enthusiasm for our mobile devices, conflicts directly with proof that we suck at it. Look no further than the September 2008 train crash in Los Angeles that killed 25 people; a commuter train's engineer had just sent a text message before the collision with a freight train. Even having a hands-free cellphone conversation while driving slows your reaction time by more than 20 percent, a French study found.
Break the habit: Switching your cellphone ringer to silent when you step in the car is an easy, effective fix. But many people forget to do that, or they forget to turn the ringer up again, so a better strategy is to train yourself to not want to pick up the phone. "You can teach yourself to have a negative emotional association with cellphone use while driving," Peters says. When your phone rings or beeps with a new text message, visualize what could happen if your attention is distracted—picture yourself plowing into the car ahead of you. Be graphic about it. Then imagine the effect that an accident would have on your family and on the family of the person you hit. Over time, you'll start associating the ringing cellphone with a crash, and you'll have less desire to answer it.

Regulating Emotion After Experiencing A Sexual Assault

After exposure to extreme life stresses, what distinguishes the individuals who do and do not develop posttraumatic stress disorder (PTSD)? A new study, published in the October 1st issue

suggests that it has something to do with the way that we control the activity of the prefrontal cortex, a brain region thought to orchestrate our thoughts and actions.
Researchers at the Mount Sinai School of Medicine examined women who had been the victims of violent sexual assault, some of whom developed PTSD and others who did not develop any serious emotional symptoms afterwards. Using a brain imaging technique, they evaluated the ability of these women to voluntarily modify their own responses to unpleasant emotional stimuli and found that it was the trauma history itself, not how well they endured this sort of trauma, that influenced their ability to dampen subsequent emotional responses.
Surprisingly, however, the ability of the subjects to amplify their emotional responses to unpleasant stimuli was related to psychological outcome after the sexual assault. The resilient individuals, that is, those who endured sexual assault without developing emotional symptoms, were able to enhance the activation of emotional brain circuitry in response to unpleasant stimuli more than either those with PTSD or healthy controls who had never experienced a serious sexual assault.
Corresponding author Dr. Antonia New explained the findings: "This raises the possibility that the ability to focus on negative emotions permits the engagement of cognitive strategies for extinguishing negative emotional responses, and that this ability might be related to resilience. This is important, since it has implications for how we might enhance resilience."
These findings suggest that exposure to extremely stressful situations may leave an "emotional scar" that may influence the capacity to be resilient to the impact of subsequent stressors, even when one does not develop PTSD. "These data seem to support an idea that has emerged from clinical descriptions of resilient people, i.e., that people who are resilient are able to be flexible in the way that they respond to changing emotional contexts. It would be helpful to know how we can enhance the flexible activation of these prefrontal cortex networks in people with compromised resilience," commented Dr. John Krystal, Editor of Biological Psychiatry.
Dr. New agrees, adding that "perhaps the enrichment of the broad capacity to tolerate negative emotional experiences might be helpful in promoting resilience. Further work needs to be done on whether the feature of this capacity that relates to resilience is about the ability to tolerate one's one responses, or whether it is the ability to respond distress in others."
Journal reference:
New et al. A Functional Magnetic Resonance Imaging Study of Deliberate Emotion Regulation in Resilience and Posttraumatic Stress Disorder. Biological Psychiatry, 2009; 66 (7): 656 DOI: 10.1016/j.biopsych.2009.05.020

Men With Erectile Dysfunction Have Increased Risk For Cardiovascular Events

Men with erectile dysfunction have a higher risk of subsequent cardiovascular events such as heart attack, stroke, and angina, according to a study in the December 21 issue of JAMA.
See also:

More than 10 million men in the United States are affected by erectile dysfunction (ED), with an estimated 100 million men affected worldwide, according to background information in the article. The risk of erectile dysfunction is related to many factors, including age, smoking, diabetes, heart disease, depression, and hypertension. Because cardiovascular disease and erectile dysfunction share etiologies as well as pathophysiology (endothelial dysfunction) and because of evidence that degree of erectile dysfunction correlates with severity of cardiovascular disease, it has been postulated that erectile dysfunction is a sentinel symptom in patients with cardiovascular disease.
Ian M. Thompson, M.D., of the University of Texas Health Science Center at San Antonio, and colleagues studied a group of men who were assessed for ED and subsequent cardiovascular disease over the course of 7 years. The study included men aged 55 years or older who were randomized to the placebo group (n = 9,457) in the Prostate Cancer Prevention Trial at 221 U.S. centers. Participants were evaluated every 3 months for cardiovascular disease and erectile dysfunction between 1994 and 2003. In analysis, factors at study entry taken into account included age, body mass index, blood pressure, serum lipids, diabetes, family history of heart attack, race, smoking history, current use of antihypertensive medication, physical activity, and quality of life.
Of the 9,457 men randomized to placebo, 8,063 (85 percent) had no cardiovascular disease at study entry; of these men, 3,816 (47 percent) had erectile dysfunction at study entry. Among the 4,247 men without erectile dysfunction at study entry, 2,420 men (57 percent) reported incident erectile dysfunction after 5 years. After adjustment, incident erectile dysfunction was associated with a 25 percent increased risk for subsequent cardiovascular events during study follow-up. For men with either incident or prevalent erectile dysfunction, the increased risk was 45 percent.
"Our analysis of men in the placebo group of this study demonstrates the substantial association between incident as well as prevalent erectile dysfunction and subsequent cardiovascular disease, including angina, myocardial infarction, stroke, and transient ischemic attack," the authors write.
"The implications of this study are substantial. With the availability of effective pharmacotherapy, an increasing number of men are seeking care for erectile dysfunction. It is estimated that more than 600,000 men aged 40 to 69 years in the United States develop erectile dysfunction annually. Our data suggest that the older men in this group have about a 2-fold greater risk of cardiovascular disease than [younger] men without erectile dysfunction. With 70 percent to 89 percent of sudden cardiac deaths occurring in men and with many men not having regular physical examinations, this analysis suggests that the initial presentation of a man with erectile dysfunction should prompt the evaluating physician to screen for standard cardiovascular risk factors and, as appropriate, initiate cardioprotective interventions," they write.
"Our data provide the first evidence, to our knowledge, of a strong association between erectile dysfunction and subsequent development of clinical cardiovascular events. Acknowledging this association over a 5-year period and the high prevalence of vasculogenic/atherogenic etiologies in men of this age, the presenting symptom of erectile dysfunction should prompt an assessment of cardiovascular risk factors and vigorous interventions as appropriate. While a full cardiovascular evaluation is not necessary in response to findings of erectile dysfunction in asymptomatic patients, such findings should prompt diligent observation of at-risk men and reinforces the need for intervention for cardiovascular risk factors," the researchers conclude.

Younger Men With Erectile Dysfunction

Men who experience erectile dysfunction between the ages of 40 and 49 are twice as likely to develop heart disease than men without dysfunction, according to a new Mayo Clinic study. Researchers also found that men with erectile dysfunction have an 80 percent higher risk of heart disease.

"The highest risk for coronary heart disease was in younger men," says researcher Jennifer St. Sauver, Ph.D. The study was published in the February 2009 issue of Mayo Clinic Proceedings. The results suggest that younger men and their doctors may need to consider erectile dysfunction a harbinger of future risk of coronary heart disease -- and take appropriate steps to prevent it, says Dr. St. Sauver.
"The importance of the study cannot be overstated," writes Martin Miner, M.D., in an editorial in the same issue of Mayo Clinic Proceedings. The results "raise the possibility of a 'window of curability,' in which progression of cardiac disease might be slowed or halted by medical intervention," writes Dr. Miner, who practices at the Men's Health Center, Miriam Hospital, Providence, R.I.
Erectile dysfunction is common, and prevalence increases with age. It affects 5 to 10 percent of men at age 40. By age 70, from 40 to 60 percent of men have the condition.
Dr. St. Sauver says researchers wanted to learn more about the connections between age, cardiovascular disease and erectile dysfunction. Two previous studies, both published in 2005, laid groundwork for the Mayo Clinic study. One found that erectile dysfunction predicted an increased risk of heart disease, but the erectile dysfunction of the study participants was not assessed with an externally validated questionnaire and cardiac events were not subjected to standardized review for diagnostic accuracy [Thompson et al, JAMA, 2005]. The second predicted that future cardiovascular disease would be higher in younger men with erectile dysfunction, but wasn't able to follow the men to determine if heart disease developed [Ponholzer et al, Eur Urol, 2005].
For the Mayo Clinic study, the investigators identified 1,402 men who lived in Olmsted County, Minn., in 1996 and did not have heart disease. Every two years for 10 years, these men were assessed for urological and sexual health.
Answers to questions from the Brief Male Sexual Function Inventory, a statistically validated questionnaire, were used to determine erectile dysfunction. The baseline prevalence of erectile dysfunction in study participants was: 2.4 percent in men aged 40-49; 5.6 percent in men aged 50-59; 17 percent in men aged 60-69 and 38.8 percent in men 70 years and older. Those initial data and the increasing incidence of erectile dysfunction over time were linked to data from a long-term study of heart disease in Olmsted County residents, led by Veronique Roger, M.D., Mayo Clinic cardiologist.
Over 10 years of follow-up, researchers found that men with erectile dysfunction were 80 percent more likely to develop coronary heart disease compared to men without erectile dysfunction. The highest risk of new heart disease was seen in the youngest study participants who had erectile dysfunction. In men 40 to 49 years old when the study began, the number of new cases in men with erectile dysfunction was more than 50-fold higher than in men without erectile dysfunction. Statistically, that's a cumulative incidence of 48.52 per 1,000 person years in those with erectile dysfunction compared to 0.94 per 1,000 person years in those without erectile dysfunction).
In men in their 50s, 60s and 70s, the total incidence of new cases of heart disease also was higher in those with erectile dysfunction. However, the differences were not as striking as those seen among the 40- to 49-year- olds.
"In older men, erectile dysfunction may be of less prognostic importance for development of future heart disease," says Dr. St. Sauver.
This study did not determine reasons for the increased risk of heart disease among men with erectile dysfunction. Some have theorized that erectile dysfunction and coronary artery disease may be different manifestations of the same underlying disease process. A buildup of plaque that can block arteries around the heart may plug the smaller penile arteries first, causing erectile dysfunction. Alternatively, arteries may lose elasticity over time, contributing to heart disease. This arterial stiffening may affect the smaller penile arteries first.
Other Mayo Clinic researchers were: Brant Inman, M.D.; Debra Jacobson; Michaela Mc Gree; Ajay Nehra, M.D.; Michael Lieber, M.D.; Dr. Roger; and Steven Jacobsen, M.D., Ph.D.

Erectile dysfunction

Erectile dysfunction, also known as impotence, is a sexual dysfunction characterized by the inability to develop or maintain an erection of the penis for satisfactory sexual intercourse regardless of the capability of ejaculation.

There are various underlying causes, such as diabetes, many of which are medically reversible. The causes of erectile dysfunction may be physiological or psychological.
Psychological impotence can often be helped by almost anything that the patient believes in; there is a very strong placebo effect.
Erectile dysfunction is characterized by the inability to maintain an erection.
Normal erections during sleep and in the early morning suggest a psychogenic cause, while loss of these erections may signify underlying disease, often cardiovascular in origin.
Other factors leading to erectile dysfunction are diabetes mellitus (causing neuropathy) or hypogonadism (decreased testosterone levels due to disease affecting the testicles or the pituitary gland)..

Disrupting Male Fertility

ScienceDaily (Nov. 2, 2009) — The sexual function of male rodents can be impaired by in utero and/or neonatal exposure to external molecules that disrupt normal hormone functioning, giving rise to concerns that low-level exposure to such molecules might cause similar effects in humans. Examples of such molecules include the synthetic nonsteroidal estrogen DES, which was used as a treatment for various diseases until the mid 1990s, and BPA, which is found, among other places, in some plastic containers.
See also:

New research, by David H. Volle and colleagues, at INSERM U895, France, has identified the molecular mechanism underlying many of the harmful effects of DES on the mouse testis.
The research is reported in the Journal of Clinical Investigation.
The pivotal experiments demonstrated that neonatal exposure to DES led to a much more dramatic reduction in fertility in male mice with the protein NR0B2 than it did in male mice lacking the protein because NR0B2 deficiency protected male mice against the negative effects of DES on testis development and function. NR0B2 deficiency also protected male mice from the detrimental effects of postnatal and adult exposure to DES.
Future work will determine whether similar pathways link human exposure to molecules such as DES that disrupt normal hormone functioning to the increased incidence of male reproductive disorders.

Blood Vessels Might Predict Prostate Cancer Behavior

The answer may lie in the size and shape of the blood vessels that are visible within the cancer, according to research led by investigators at The Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute in collaboration with the Harvard School of Public Health.
The study of 572 men with localized prostate cancer indicates that aggressive or lethal prostate cancers tend to have blood vessels that are small, irregular and primitive in cross-section, while slow-growing or indolent tumors have blood vessels that look more normal.
The findings were published Oct. 26 in the Journal of Clinical Oncology.
"It's as if aggressive prostate cancers are growing faster and their blood vessels never fully mature," says study leader Dr. Steven Clinton, professor of medicine and a medical oncologist and prostate cancer specialist at Ohio State's Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute.
"Prostate cancer is very heterogeneous, and we need better tools to predict whether a patient has a prostate cancer that is aggressive, fairly average or indolent in its behavior so that we can better define a course of treatment -- surgery, chemotherapy, radiotherapy, hormonal therapy, or potentially new drugs that target blood vessels -- that is specific for each person's type of cancer," Clinton says.
"Similarly, if we can better determine at the time of biopsy or prostatectomy who is going to relapse, we can start treatment earlier, when the chance for a cure may be better."
Prostate cancer is the most common cancer in men and the second leading cause of cancer death in American men.
This study analyzed tumor samples and clinical outcome data from men participating in the Health Professionals Follow-Up Study, which involves 51,529 male North American dentists, optometrists, podiatrists, pharmacists and veterinarians.
After an average follow-up of 10 years, 44 of the 572 men had developed metastatic cancer or died of their cancer.
Men whose tumors had smaller vessel diameters were six times more likely to have aggressive tumors and die of their disease, and those with the most irregularly shaped vessels were 17 times more likely to develop lethal prostate cancer.
The findings were independent of Gleason score, a widely used predictor of prognosis based on a prostate tumor's microscopic appearance, and of prostate specific antigen (PSA) level, a blood test used to identify the presence of prostate cancer.
These findings currently apply to men with local disease, whose PSA is only modestly elevated, and who are younger and more likely to choose surgery.
"If our findings are validated by larger studies, particularly in biopsy specimens, the measurement of tumor blood vessel architecture might help determine the choice of therapy, with the goal of improving long-term survival."
Funding from the National Cancer Institute and the Prostate Cancer Foundation supported this research.

Men with lower cholesterol are less likely than those with higher levels to develop high-grade prostate cancer

In a prospective study of more than 5,000 U.S. men, epidemiologists say they now have evidence that having lower levels of heart-clogging fat may cut a man's risk of this form of cancer by nearly 60 percent.
"For many reasons, we know that it's good to have a cholesterol level within the normal range," says Elizabeth Platz, Sc.D., M.P.H., associate professor at the Johns Hopkins Bloomberg School of Public Health and co-director of the cancer prevention and control program at the Johns Hopkins Kimmel Cancer Center. "Now, we have more evidence that among the benefits of low cholesterol may be a lower risk for potentially deadly prostate cancers."
Normal range is defined as less than 200 mg/dL (milligrams per deciliter of blood) of total cholesterol.
Platz and her colleagues found similar results in a study first published in 2008, and in 2006, she linked use of cholesterol-lowering statin drugs to lower risk of advanced prostate cancer.
For the current study, Platz, members of the Southwest Oncology Group, and other collaborators analyzed data from 5,586 men aged 55 and older enrolled in the Prostate Cancer Prevention Trial from 1993 to 1996. Some 1,251 men were diagnosed with prostate cancer during the study period.
Men with cholesterol levels lower than 200 mg/dL had a 59 percent lower risk of developing high-grade prostate cancers, which tend to grow and spread rapidly. High-grade cancers are identified by a pathological ranking called the Gleason score. Scores at the highest end of the scale, between eight and 10, indicate cancers considered the most worrisome to pathologists who examine samples of the diseased prostate under the microscope.
In Platz's study, cholesterol levels had no significant effect on the entire spectrum of prostate cancer incidence, only those that were high-grade, she says.
Platz cautions that, while the group took into account factors that could bias the results, such as smoking history, weight, family history of prostate cancer, and dietary cholesterol, other things could have affected their results. One example is whether men in the study were taking cholesterol-lowering drugs at the time of the blood collections, a data point the researchers expect to analyze soon.
Results of the current study are expected to be published online Nov. 3 in the journal Cancer Epidemiology, Biomarkers & Prevention. Also in the journal is an accompanying paper from the National Cancer Institute showing that lower cholesterol in men conferred a 15 percent decrease in overall cancer cases.
"Cholesterol may affect cancer cells at a level where it influences key signaling pathways controlling cell survival," says Platz. "Cancer cells use these survival pathways to evade the normal cycle of cell life and death."
She says that targeting cholesterol metabolism may be one route to treating and preventing the disease, but this remains to be tested.
Funding for the study was provided by the National Cancer Institute.Authors of the study include Cathee Till, Phyllis J. Goodman, Marian L. Neuhouser and Alan R. Kristal from the Fred Hutchinson Cancer Research Center; Howard L. Parnes, William D. Figg, and Demetrius Albanes from the National Cancer Institute; Eric A. Klein from the Cleveland Clinic; and Ian M. Thompson Jr., from the University of Texas Health Sciences Center.