You are what you drink

"There's an old expression you've probably heard a countless times… "you are what you eat." While this may be true, ultra athletes see the other side. 60% of a person's body weight is water therefore "You are what you drink". Water serves two critical functions:

1. Since water makes up most of our blood volume, it's an "energy supply line" that delivers oxygen to the muscles to allow them to do their essential work.
2. At the same time, water is the body's cooling system - sort of human radiator. When you exercise, you generate heat - literally 8 to 10 times what you do at rest. Blood conducts the heat to the skin which, in turn, makes you flush and dissipates the heat. When this process is not enough, you perspire and are cooled off by evaporating sweat.

Properly hydrated, you feel great, perform at your peak, and speed your recovery for you next activity. The problem comes when the body doesn't have enough water to perform all these functions. You can easily loose two quarts of water per hour in hot weather by exercising. When you do, the blood volume diminishes and the body struggles to supply oxygen to muscles. You feel weaker and start to experience headaches, cramps and nausea. In fact, dehydration is a key factor in "bonking" or "hitting the wall".
By the time you're thirsty it's too late. The body has to do something, and what it does is shut down the sweating mechanism. The body's temperature starts climbing rapidly, and you begin to experience heat exhaustion and heatstroke, the latter of which can be fatal. So what should you do? It's simple. Make sure you don't run out of water, and keep drinking. Drink before, after, and most of all drink during the run. Medical and training experts advise drinking at least 8 oz every 15-20 minutes during exercise. Don't wait till you're thirst-by then it's too late and you're becoming dehydrated."
http://www.ultrunr.com/hydrate.html

Water channels

"The hunt for the water channelsAs early as the middle of the nineteenth century it was understood that there must be openings in the cell membrane to permit a flow of water and salts. In the middle of the 1950s it was discovered that water can be rapidly transported into and out of cells through pores that admit water molecules only. During the next 30 years this was studied in detail and the conclusion was that there must be some type of selective filter that prevents ions from passing through the membrane while water molecules, which are uncharged, flow freely. Thousands of millions of water molecules per second pass through one single channel!
Although this was known, it was not until 1992 that anybody was able to identify what this molecular machinery really looked like; that is, to identify what protein or proteins formed the actual channel. In the mid-1980s Peter Agre studied various membrane proteins from the red blood cells. He also found one of these in the kidney. Having determined both its peptide sequence and the corresponding DNA sequence, he realised that this must be the protein that so many had sought before him: the cellular water channel.
Agre tested his hypothesis in a simple experiment (fig. 2) where he compared cells which contained the protein in question with cells which did not have it. When the cells were placed in a water solution, those that had the protein in their membranes absorbed water by osmosis and swelled up while those that lacked the protein were not affected at all. Agre also ran trials with artificial cells, termed liposomes, which are a type of soap bubble surrounded on the outside and the inside by water. He found that the liposomes became permeable to water if the protein was planted in their membranes.

What is osmosis?The liquid pressure in plant and animal cells is maintained through osmosis. In osmosis, small molecules (such as water) pass through a semi-permeable membrane. If the membrane does not admit macromolecules or salts that are in higher concentrations on one side of the membrane, the small molecules (water) will cross to this side, attempting to "dilute" the substance that cannot pass through the membrane. The osmotic pressure thus arising is the reason why cells are often swollen and stiff, in a flower stalk, for example.

Peter Agre also knew that mercury ions prevent cells from taking up and releasing water, and he showed that water transport through his new protein was prevented in the same way by mercury. This made him even more sure of that he had discovered what was actually the water channel . Agre named the protein aquaporin, "water pore".
How does the water channel work? A question of form and functionIn 2000, together with other research teams, Agre reported the first high-resolution images of the three-dimensional structure of the aquaporin. With these data, it was possible to map in detail how a water channel functions. How is it that it only admits water molecules and not other molecules or ions? The membrane is, for instance, not allowed to leak protons. This is crucial because the difference in proton concentration between the inside and the outside of the cell is the basis of the cellular energy-storage system.
Selectivity is a central property of the channel. Water molecules worm their way through the narrow channel by orienting themselves in the local electrical field formed by the atoms of the channel wall. Protons (or rather oxonium ions, H3O+) are stopped on the way and rejected because of their positive charges.

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The medical significance of the water channels

"During the past ten years, water channels have developed into a highly topical research field. The aquaporins have proved to be a large protein family. They exist in bacteria, plants and animals. In the human body alone, at least eleven different variants have been found.

The function of these proteins has now been mapped in bacteria and in plants and animals, with focus on their physiological role. In humans, the water channels play an important role in, among other organs, the kidneys.

The kidney is an ingenious apparatus for removing substances the body wishes to dispose of. In its windings (termed glomeruli), which function as a sieve, water, ions and other small molecules leave the blood as 'primary' urine. Over 24 hours, about 170 litres of primary urine is produced. Most of this is reabsorbed with a series of cunning mechanisms so that finally about one litre of urine a day leaves the body.

From the glomeruli, primary urine is passed on through a winding tube where about 70% of the water is reabsorbed to the blood by the aquaporin AQP1. At the end of the tube, another 10% of water is reabsorbed with a similar aquaporin, AQP2. Apart from this, sodium, potassium and chloride ions are also reabsorbed into the blood. Antidiuretic hormone (vasopressin) stimulates the transport of AQP2 to cell membranes in the tube walls and hence increases the water resorption from the urine. People with a deficiency of this hormone might be affected by the disease diabetes insipidus with a daily urine output of 10-15 litres."
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Dense Breasts Raise Cancer Risk

(HealthDay News) -- Two new studies suggest breast density is nearly as important as age in predicting who is going to develop breast cancer.
The information may help better identify women at high risk for the disease, the researchers noted.
"After age, it's probably the most important factor," said William E. Barlow, lead author of one of the studies and a senior investigator at Group Health Cooperative in Seattle. "If we wanted to identify women who were really at high risk for chemoprevention efforts or more intense screening surveillance, then any model that incorporates breast density is going to be better at picking out those women."
Both studies are in the Sept. 6 issue of the Journal of the National Cancer Institute.
Since the late 1980s, medical professionals have relied on the Gail model to assess breast cancer risk in women undergoing annual mammography. That model uses risk factors known at the time, such as current age, age at first menstrual period, age at birth of first child, number of first-degree relatives with a family history of breast cancer and number of previous breast biopsies. More recently, race and atypical hyperplasia were added to the model.
Experts had speculated that adding newly identified risk factors for breast cancer such as breast density and use of hormone therapy might improve the test's predictive powers.
Barlow and his colleagues looked at 11,638 women who had developed breast cancer, out of a larger group of about 1 million.
Among premenopausal women, age, breast density, family history of breast cancer and a previous breast procedure were significant risk factors for developing breast cancer. Having any type of prior breast procedure was associated with about a 50 percent increased risk. Women with extremely dense breasts had about a fourfold greater risk than women whose breasts were not dense.
For postmenopausal women, factors included age, breast density, race, ethnicity, family history of breast cancer, a prior breast procedure, body-mass index, natural menopause, hormone therapy and a prior false-positive mammogram.
The model may perform better than the Gail model, although the accuracy was far from perfect. This suggests that the major determinants of breast cancer are still unknown.
A second study, conducted at the National Cancer Institute, used an updated version of the Gail model to assess the absolute risk of developing breast cancer. This model also included breast density, along with weight, age at first live birth, number of previous benign biopsies and number of first-degree relatives with breast cancer.
Again, this model predicted that women with high breast density had an increased risk of breast cancer.
It's unclear if breast density can be considered a modifiable risk factor.
"It may be modifiable, but we don't know that for sure," Barlow said. "It is related to hormone use in women. Their breasts can be denser during the time they're on hormone replacement therapy."
It's also not clear exactly how this new information will be incorporated into practice. Breast density generally needs to be measured by a radiologist. "It's not something that a woman can judge for herself," Barlow explained. "There really isn't a feedback mechanism from the radiologist back to the woman to say what the breast density is."
In the future, however, Barlow envisions mammography facilities becoming more like risk-counseling facilities that incorporate breast density along with other risk factors and past mammogram results. "But that would require an evolution of mammography centers," he noted.
Even in the more immediate present, the findings reinforce the notion of taking steps to prevent breast cancer in high-risk and other women.
"We as a medical community still have not accepted the paradigm that we can identify women who are at a high risk for developing breast cancer," said Dr. Jay Brooks, chairman of hematology/oncology at Ochsner Health System in Baton Rouge, La. "We could intervene with a treatment to reduce their risk."
"We don't use the tools we already have to identify women at a high risk for breast cancer and offer them potential treatment to reduce their risk like we do for cholesterol and heart disease," he continued. "Now, we're further defining the model that will predict even better who could potentially benefit from these tools."

More information
For more on breast cancer, visit the American Cancer Society.

Gene Test May Improve Breast Cancer Treatment

(HealthDay News) -- A test that checks the expression of 70 genes associated with breast cancer can help doctors determine a patient's risk of cancer recurrence or death, an international study finds.
The study included 307 breast cancer patients assigned to high- and low-risk groups based on their scores from the 70-gene signature test and standard risk-assessment using a software program. The patients were followed for 13.6 years.
The gene-signature test was a more accurate predictor of cancer recurrence and death than the software, the researchers found. The study also concluded that the gene test included most of the prognostic information provided by traditional risk classifiers.
"These results indicate that the gene signature adds independent prognostic information," reported scientists at the Netherlands Cancer Institute in Amsterdam.
The findings were published in the Sept. 6 issue of the Journal of the National Cancer Institute.
The 70-gene signature test will be evaluated in a larger study of 6,000 women with node-negative early-stage breast cancer. The trial will assess whether the test can improve identification of women who can safely be spared adjuvant chemotherapy.

More information
The U.S. National Library of Medicine has more about genetics and breast cancer.

Scientists Map Genetic Codes for Breast, Colon Cancers

(HealthDay News) -- In what experts are calling a milestone achievement, U.S. researchers have sequenced the genetic "blueprints" of two major cancer killers -- breast and colon cancer.
Identifying nearly 200 genes thought responsible for these diseases, the work gives researchers new insight into these malignancies and lays the foundation for the gene-targeted therapies that may one day cure them.
"Only by understanding this blueprint of cancer will we be fully able to understand the mechanism of what makes a cancer a cancer and to think about strategies for diagnosis, prevention and therapy," explained Dr. Victor Velculescu, senior researcher on the project and an assistant professor of oncology at Johns Hopkins University's Kimmel Cancer Center.
Experts elsewhere were similarly optimistic. In a statement, Dr. Elias A. Zerhouni, director of the U.S. National Institutes of Health, which funded the project, described the new genetic maps as "groundbreaking work."
"This research approach holds great promise for providing an understanding of the genomic contributions to cancer," he said.
Velculescu's team outlined the findings in the Sept. 8 issue of the journal Science.
Just as the human body has its genetic code, so, too, do cancer cells.
"Work from the past two decades has shown us that cancer is a genetic disease," said Velculescu. He explained that a malignancy occurs when specific genes in healthy cells undergo unhealthy mutations.
"A mutation is really like a typo in a blueprint that's 3 billion letters long," he said, so spotting any one mutation has been like finding the proverbial needle in a haystack.
A new $100 million federal initiative, The Cancer Genome Atlas project, seeks to change all that by mapping the myriad genetic "typos" that cause specific tumor types to form. The project described in Science is the first major step in that effort.
In their research, Velculescu and his colleagues from across the United States focused on cracking the gene codes for breast and colon cancers, which together make up one-fifth of all cancer diagnoses worldwide. Other initiatives, focused on other tumor types, are currently under way.
The team analyzed more than 13,000 genes from tumor tissues taken from 11 patients with breast cancer and 11 patients with colorectal cancer.
What they found surprised them.
"Many of us might have expected that only a few of the 'building blocks' in a cell to be mutated, but we actually found quite a number of them," Velculescu said. "It looks like each cancer has about 100 different genes that are mutated, at least 20 of which are thought to be important for the tumor's progression."
The research also confirmed that there's no one disease called cancer.
"It looks like there are quite a bit of differences between the blueprint of different cancer types," the Johns Hopkins expert noted. "Colon and breast cancers are different, and, in addition, each individual's cancer is different. This, in part, may explain the differences that clinicians for a long time have seen among their cancer patients."
But the team also found "commonalities" between colon and breast cancers as well -- mutations that affected similar cellular pathways. "As we learn more and more about how these genes interact, about pathways and how these genes control processes that occur inside cancer cells, we may be able to find simpler [treatment] targets," Velculescu said.
Another expert agreed. "This achievement is important because, to the degree that those genes are proven now to be related to the cancer process, they provide targets that can be potentially used either for diagnostic or treatment purposes," said Dr. Len Lichtenfeld, deputy chief medical officer at the American Cancer Society.
For example, doctors may someday use sensitive nanotechnology early detection tests to spot tiny amounts of cancer-linked proteins produced by these aberrant genes. "That would be a test that would enable you to diagnose a cancer long before you are actually able to see it," Lichtenfeld said.
In terms of treatments, drug developers can target specific genes and their proteins to create treatments that stop a cancer cold without harming the patient. Gleevec -- the "wonder" drug now used to halt chronic myelogenous leukemia -- is one such targeted therapy, Lichtenfeld said.
"So, this new achievement is a really important step and an important link between where we are today and where we have been talking that we will be in five, 10, 15 years," he said.
Velculescu said he shares that vision.
"We are predicting that cancer is an individualized disease, and there will come a day when people will go into the clinic and their tumor will be analyzed for specific mutations," he said. "Based on the combination of genes that are mutated, they will receive a particular combination of therapies that will treat the disease."
"We're not there yet, and there's still a long way to go," Velculescu said. "But without knowing what's broken inside a cancer cell, we have no hope of fixing it."

More information
For more on gene therapy and cancer, head to the American Cancer Society.

Teenage Alcoholism Can Have Lifelong Effects

(HealthDay News) -- Becoming alcoholic as a teenager doesn't just spell a booze-soaked adolescence.
It can also portend trouble for decades, apparently contributing to more severe levels of alcoholism and a reluctance to seek help, a new federal study found.
The study revealed that 58 percent of those interviewed who became alcoholics before age 18 became drunk at least once a week during adult episodes of dependence, compared to 19 percent of those who became alcoholics at age 30 or older.
"This tells us that it's very important to try to delay the onset of drinking," said study author Ralph W. Hingson, director of the National Institute on Alcohol Abuse and Alcoholism's division of epidemiology and prevention research. "That's not to say there aren't some who become dependent at an early age and overcome the problem. It's just more difficult."
An estimated 12.5 percent of Americans are alcoholics or have been so during their lives, according to federal statistics. And previous studies have linked teenage drinking to a variety of ills, from smoking and drug use to fights, car accidents and unprotected sex.
In the new study, the researchers examined the results of a 2001-2002 survey by the National Institute on Alcohol Abuse and Alcoholism that included 43,093 people over the age of 18. The researchers zeroed in on face-to-face interviews with 4,778 people who appeared to have been alcoholics at some time in their lives.
Of all the people who were ever alcoholics, 15 percent appeared to have become dependent before the age of 18, while 47 percent were dependent before age 21.
"The thing that is probably most surprising to the general population is that these problems begin so early," Hingson said. "The conventional image is that people who have alcoholism or alcohol dependence are middle-aged. That's not the case. The problem begins much earlier in life."
The study findings are published in the September issue of Pediatrics.
The researchers found that those drinkers who became alcoholics before 18 were more likely to show more symptoms of alcoholism later in life: 44 percent displayed six to seven symptoms, compared to 33 percent of those who became dependent on alcohol after age 30.
The researchers adjusted the figures to account for other possible influences such as race, gender and family history of alcoholism.
Compared to those drinkers who became addicted after age 30, the early alcoholics were also more likely to want to continue drinking (26 percent vs. 16 percent among the older group); thought they didn't need help (44 percent vs. 30 percent); and didn't know where to turn for help (14 percent vs. 3 percent).
It's not clear why people who drink heavily earlier are at higher risk later in life, but it may have something to do with biologic changes in the brain due to alcohol consumption, Hingson said.
The study does have weaknesses. It doesn't definitively suggest a cause-and-effect relationship between teenage alcoholism and alcohol dependence later in life. And it relies on people's recollections about a sensitive subject -- alcoholism.
Still, the study included a large number of people, and the question format that was used for the survey doesn't mean the results are invalid, said Dr. J.C. Garbutt, a professor of psychiatry at the University of North Carolina at Chapel Hill.
What should you do if a teen you know is having problems with alcohol? "Talk with them about it, and if it is serious, get help for them," Garbutt said. "Stick with it even if the adolescent doesn't want treatment -- and few do. The alternative could be serious alcoholism with risk of legal, health, relationship problems and even death."

More information
To learn more about underage drinking, visit the U.S. Substance Abuse and Mental Health Services Administration.

Early Treatment Helps People With Prehypertension

(HealthDay News) -- People with the early signs of hypertension appear to benefit from early treatment with blood pressure medication, new research shows.
During the four years of the Trial of Preventing Hypertension (TROPHY) study, researchers found that people with prehypertension who received candesartan -- an antihypertensive drug -- had a significantly reduced risk of developing high blood pressure compared with those who received a placebo.
The findings suggest that people with prehypertension should receive treatment to prevent high blood pressure from developing. This concept has caused some controversy, since it would mean treating perhaps millions of people.
In a discussion Friday at the American Society of Hypertension in New York City, the findings and implications of TROPHY were discussed. The research appeared in the New England Journal of Medicine last month.
People with prehypertension can progress rapidly to full blown hypertension and its consequences, said lead researcher Dr. Stevo Julius, an emeritus professor of internal medicine at the University of Michigan. "This study gives us some hope that if you start treating these people early, you may be able to prevent hypertension."
In the study, Julius and his colleagues randomly selected 772 people with prehypertension to receive the antihypertension drug candesartan or a placebo. Over two years, those taking candesartan experienced significant reductions in blood pressure compared with those receiving placebo.
After two years, candesartan therapy was stopped, and all the patients continued on placebo for another two years. During that time, blood pressures in both groups continued to rise, the researchers found.
During the first two years of the study, 13.6 percent of the patients taking candesartan became hypertensive compared with 40.4 percent of those receiving placebo. Over the next two years, 53.2 percent of those who had been taking candesartan became hypertensive, compared with 63 percent of those who had been taking the placebo throughout.
"We have shown the possibility of treating people with prehypertension," Julius said. "We are by no means recommending this. This is the first step; further studies using other drugs are needed," he added.
One of the objections raised to treating prehypertension is the expense of such a program and the fact that insurance might not cover the expense of the medications. "People are spending a lot of money on vitamins or herbs or massages or a number of unproven things, and they are very glad to do so," Julius responded.
Because of the importance of controlling blood pressure, Julius believes that insurance would cover the costs, but, in any case, such a program could be worthwhile.
Another problem is identifying those who would benefit most from a program directed at prehypertensives. The key to identifying those most at risk is simple, Julius said. "Not surprisingly, the biggest identifier is blood pressure," he said. "People who have the highest blood pressure are those most likely to develop hypertension."
One expert thinks that treating prehypertension is important.
"My personal opinion, one that isn't supported by any guidelines, is that, yes, patients with prehypertension should be treated," said Dr. Thomas Giles, a professor of medicine at Tulane University and president of the American Society of Hypertension.
"Most hypertension experts, I believe, think that lowering blood pressure in patients who are at risk is a good thing to do," Giles said. However, Giles doesn't believe that just putting people on drugs is the answer. He thinks that each patient needs to have a personalized treatment program, including lifestyle changes. "There needs to be a precise regimen designed for you," he said.
In an unrelated report at the same meeting, Dr. Michael Doumas, from the Department of Internal Medicine at the University of Athens, in Greece, presented results of a study of 417 women that showed that sexual dysfunction is linked to high blood pressure.
Among 216 women with high blood pressure, 42 percent suffered from sexual dysfunction, compared with 19 percent of the 201 women with normal blood pressure, Doumas said. In addition, 51 percent of the women who had uncontrolled high blood pressure also had sexual dysfunction, compared with 27 percent of the women whose high blood pressure was controlled.
Why this link exists is unclear, Doumas said. "We really don't know very much about sexual dysfunction in women," he added.

More information
The American Heart Association can tell you more about high blood pressure.

Painkillers Don't Boost Blood Pressure in Healthy Men

(HealthDay News) -- Contradicting some previous research, a new study finds that frequent use of painkillers including nonsteroidal anti-inflammatory drugs (NSAIDs) does not substantially increase a healthy man's risk of developing hypertension.
The findings, which appear in the Sept. 12 issue of Archives of Internal Medicine, may muddy the picture more than clarify it.
"It's inconclusive," said Dr. Joel S. Bennett, a spokesman for the American Heart Association who is with the division of hematology/oncology at the University of Pennsylvania School of Medicine. "Most epidemiological studies have to be done multiple times before you can be sure."
Past research involving women had suggested there might be a link between pain relievers and hypertension, also known as high blood pressure.
"We don't know what all the answers are," conceded senior author Dr. J. Michael Gaziano, a cardiologist and epidemiologist at Brigham and Women's Hospital in Boston. "We need to better understand what's going on in larger observational studies and randomized trials. We need careful additional study of the question."
Hypertension is a major risk factor for cardiovascular disease, including stroke, heart attack and heart failure, as well as for kidney disease.
While the authors of this study stated that obesity is probably the major contributing factor to an increased risk for heart disease, they pointed to suspicions that other factors, such as NSAID use, may also play a role. NSAIDs inhibit production of prostaglandin, which helps regulate blood pressure.
The study researchers looked at 8,229 healthy male physicians aged 53 to 97 enrolled in the Physicians' Health Study. None of the participants had hypertension at the beginning of the trial. All completed detailed questionnaires about use of analgesics (pain relievers) and blood pressure over a six-year period.
After about six years of follow-up, there appeared to be no association between use of painkillers and hypertension. Specifically, the study looked at three types of pain relievers: NSAIDs, aspirin and the non-NSAID acetaminophen (Tylenol).
When a more detailed analysis was performed, the data indicated there might be a small-to-moderate increase of hypertension risk tied to acetaminophen use, the study found.
The study was funded by the National Institutes of Health and by an unrestricted research grant from McNeil Consumer & Specialty Pharmaceuticals, the maker of Tylenol. It was concerned only with the disease of hypertension and not with transient changes in blood pressure that these drugs can cause.
Despite the contradictory findings involving women, the study authors don't believe that gender affects reaction to the drugs.
"We don't think that women and men are different," said Gaziano, who serves as a consultant for McNeil Consumer & Specialty Pharmaceuticals. "This is observational epidemiology. A lot of people might conclude incorrectly that men must be different than women, and rather than that conclusion, we don't fully know the whole story of analgesics and their ability to cause hypertension in men or women."
It's possible, however, that pain relievers might heighten the risk of hypertension in certain groups of people. "These were healthy men and some of those blood pressure changes seen in other trials may be more pronounced in susceptible populations," Gaziano said.
Gaziano believes that short-term use of over-the-counter pain killers is probably safe, as long as the drugs are taken as indicated.
"Even if there are going to be any effects on blood pressure, they're going to be transient and are not going to translate into any meaningful risk," he said.
But, he added, "we really need better trial data on the long-term consequences."
Bennett said, "This suggests that over the long term, these analgesics are not going to cause hypertension."

More information
The American Heart Association has more on hypertension.

Blood Pressure Drugs Keep Hypertension in Check

(HealthDay News) -- Using drugs to treat prehypertension reduced the risk of developing full-blown hypertension, a new study finds.
Although using pharmaceuticals may one day offer increased hope for millions of people with high blood pressure, the authors of this study stress that this treatment is not yet ready for prime time.
"It only shows the feasibility of this approach," said study author Dr. Stevo Julius, active emeritus professor of medicine and physiology at the University of Michigan, in Ann Arbor. "It is safe and it can be done, but it is a relatively small study and the time frame on the drug was only two years and generally, in our field, we want to see longer-term studies, so we're not ready to recommend this as a massive way of treating patients."
The study is nevertheless a breakthrough in the field. "We are the first, and we truly had to work for that," Julius said. "It's quite unusual. People are not given to adventures in our field. We've done it and we are very pleased."
The study was presented Tuesday at the American College of Cardiology annual meeting in Atlanta, and will also appear in the April 20 issue of the New England Journal of Medicine.
People who have blood pressure higher than normal but less than what is considered hypertension have prehypertension. Like people with hypertension, people with prehypertension are at an elevated risk for heart disease. They will also typically go on to develop hypertension.
Prehypertension is defined as systolic blood pressure in the range of 120 to 139 mm/Hg and diastolic blood pressure of 80 to 89 mm/Hg. Some 70 million Americans have the condition.
But the division is an artificial one. "High blood pressure is a continuum," said Dr. Gary Orin, a board-certified internist and nephrologist at Lenox Hill Hospital in New York City. "You can't really draw a line. There's no magic number."
Over the years, hypertension has been defined at lower and lower numbers, he noted.
Whatever the number, current guidelines recommend lifestyle modifications, rather than pharmaceuticals, for the management of prehypertension. But given the increasing prevalence of prehypertension, this approach does not seem to be working.
For this study, about 800 participants were randomized to receive Atacand (candesartan cilexetil) or a placebo for two years. Atacand is an angiotensin receptor blocker (ARB), which relaxes the blood vessels and widens them. This lowers blood pressure.
The study was sponsored by AstraZeneca, which makes Atacand.
All participants had prehypertension, defined here either as systolic pressure of 130 to 139 mm Hg and diastolic pressure of 89 mm/Hg and lower, or a systolic pressure of 139mm/Hg or lower and diastolic pressure of 85 to 89 mm/Hg. The mean age of the participants was 48.5 years; 59.6 percent were men.
After two years, 154 participants taking a placebo and 53 taking Atacand developed hypertension. This means that those in the intervention group had a 66.3 percent lower risk of developing hypertension. The authors calculated that four participants with prehypertension needed to be treated for two years to prevent one case of hypertension.
After four years (or two years after participants stopped taking the drug), hypertension had developed in 240 people in the placebo group and 208 in the Atacand group. In other words, people taking Atacand had a 15.6 percent lower risk of developing hypertension.
The drug also appeared safe, with serious adverse events reported in 3.5 percent of those taking Atacand and 5.9 percent of those receiving a placebo.
"We are trying to find out whether this is safe in the long term," Julius said. "It looks good. In two years of treatment, there was no difference in side effects between the placebo and the other group, and there was considerable postponement of hypertension."
Another heartening aspect of the trial, an accompanying editorial pointed out, is that Atacand seemed to affect the actual progression of the disease, rather than just mask symptoms.
Before this becomes practice, however, more studies need to be done.
"We are trying to find patients at the highest risk and treat them for a longer period of time," Julius said.

More information
For more on hypertension, visit the American Heart Association.

Hypertension in Teens Predicts Adult Heart Woes

(HealthDay News) -- Adolescents who have pre-hypertension or hypertension and don't exercise, eat better or receive drugs to treat the conditions are more likely to have hypertension when they're young adults, a U.S. study finds.
"Knowing which youngsters are most likely to progress to hypertension would provide the ability to target preventive measures," Dr. Bonita Falkner, professor of medicine and pediatrics at Thomas Jefferson Medical College in Philadelphia, said in a prepared statement.
Her team compared single blood pressure readings taken two years apart among 4,147 boys and 4,386 girls, ages 13 to 15, who were in the National Childhood Blood Pressure Database.
The study found that there was a linear increase -- from normal blood pressure, to pre-hypertension, to hypertension -- among teens who had hypertension at the second blood pressure reading. The progression of pre-hypertension to hypertension is about seven percent per year, the researchers said.
Among boys in the study, weight was an important predictor of higher blood pressure, while age was a significant factor among girls -- those aged 15 showed higher blood pressure than those aged 13.
The study was expected to be presented Friday at the American Society for Hypertension's annual scientific meeting, in New York City.
More information
The Nemours Foundation has more about teens and hypertension.