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Tuesday, 30 August 2011

Vaccines for Teens: Still Room for Improvement

Rates of HPV Shots Among Teens Lag Behind Other Recommended Vaccines

By Denise Mann
WebMD Health News

Aug. 25, 2011 -- More teens are getting their recommended vaccines, but there is still room for improvement. The numbers are especially low for human papillomavirus (HPV) or cervical cancer vaccines among U.S. girls, the CDC reports.

The recommended vaccines for all teens include:

Girls should also get three doses of an HPV vaccine to protect against genital warts, cervical cancer, and other cancers caused by HPV.

The flu vaccine is recommended annually for all people 6 months old and older.

Compared with 2009, vaccine rates among teens were up across the board in 2010.

Tdap rates increased from 55.6% to 68.7%
MenACWY rates increased from 53.6% to 62.7%.
Rates for one or more doses of HPV among females increased from 44.3% to 48.7%

The rate of increase in teen HPV vaccine rates was less than half of what was seen with the other vaccines.

Three doses of the HPV shot are needed to be fully effective. The shots should be given over a six-month period. Among females who had enough time to get all three, just 30.4% did. Teens who were black, Hispanic, and those who lived below the poverty line were among the least likely to get all three HPV shots.

About 20 million Americans are infected with HPV today. Each year, 12,000 women develop cervical cancer, the CDC states.

Bad News: Too Many Girls Not Getting HPV Shots

"U.S. girls are not getting the HPV vaccine that we know can prevent cervical cancer," the CDC's Melinda Wharton, MD, MPH, said during a teleconference. Wharton is deputy director for the National Center for Immunization and Respiratory Diseases.

This is "bad news" and "so very disappointing to us." But "the good news is that we can do better," Wharton says.

Cervical cancer is most often seen in women in their 30s and 40s. The HPV shot helps protect girls before they become infected with the types of genital warts linked to cervical cancer.

Why are rates of HPV trailing behind other teen vaccines?

Parents may not be aware of the HPV vaccine and what it does. They also may not be getting a strong enough recommendation from their daughter's pediatrician, Wharton says.

Also, HPV is given as three shots. "It is harder to get three doses in than one," Wharton says.

Some parents may have questions about their 11- or 12-year-old daughters getting a shot that prevents a sexually transmitted disease. But "this is a preventive vaccine, not a therapeutic one, and it won't work unless given prior to onset of sexual activity," Wharton says.

There was some pushback from parents in the early days of the vaccine because of potential side effects, but this vaccine is safe, Wharton says.

Jeff Levi, PhD, executive director of the Trust for America's Health, is also disheartened by the number of girls not getting HPV shots. "These rates are nothing short of tragic," he says in a written statement. "We could be sparing an entire generation from HPV, which can lead to a range of STDs, cervical cancer, and other cancers."

Boys may also get the HPV shot to prevent genital warts, but it's not part of the CDC's official vaccine recommendations. Just 1.4% of male teens got the HPV shot in 2010.

Teen Vaccine Rates Vary by State

Vaccine coverage rates also varied widely by states, the study showed.

Massachusetts, Rhode Island, and Virginia had the highest rates. More than 65% of teens got at least one dose of all three recommended teen vaccines in these states. These numbers still fall short of goals set by the government in its HealthyPeople 2020 campaign.

Overall, teen vaccine rates were lower for teens living in the Southeastern U.S. compared with other areas.

Teen vaccine rates based on the type of vaccine also varied by state -- sometimes by dozens of percentage points -- the study showed.

So why are some states doing so much better than others? School vaccination programs, reminders, and good communication between doctors and local public health officials may make a difference, the study suggests.

The CDC has tracked teen vaccine rates since 2006. The new findings appear in the CDC's Morbidity and Mortality Weekly Report.

SOURCES: CDC teleconference, Aug. 25, 2011.Morbidity and Mortality Weekly Report, Aug. 26, 2011; vol 60: pp 1018-1023.Jeff Levi, PhD, executive director, Trust for America's Health.Melinda Wharton, MD, MPH, deputy director, CDC's National Center for Immunization and Respiratory Diseases, Atlanta. �2011 WebMD, LLC. All Rights Reserved.

Source: http://www.medicinenet.com/guide.asp?s=rss&a=148684&k=Womens_Health_General

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You've Lost Weight, But Can You Keep It Off?

The Associated Press reports that a study published earlier this year in the New England Journal on a small European study can help you learn how to best keep off lost pounds.

If you've ever been on a weight loss diet, then you probably have experienced the difficulty of? keeping off lost pounds. Maintaining weight loss is often an incredible roller coaster ride with your scale going up and down.

So what does it take to keep off lost pounds?

The researchers, in this study,? looked at 773 overweight and obese adults who had families. The participants were from eight countries in Europe. Each of the 773 adults lost an average of 24 pounds after spending two months on a low fat diet prior to participating in the study. The families of the participants were included because researchers believed it would help the overweight and obese family members stick to their assigned weight loss maintenance diets.

One of five different weight loss maintenance diets was assigned to each study participant. Each of four different diets were a combination of high or low amounts of protein and carbs. A fifth diet was used as a control diet. This diet was a combination of moderate protein with no restriction on carbs.

Study participants received counseling, recipes, and cooking tips. There were no restrictions on the amount of food eaten on any of the five diets. Participants were instructed to keep food diaries, and gave periodic blood and urine samples for laboratory evaluation.

After six months on the weight loss maintenance diets, only one group was able to not only keep the lost weight off, but lose additional pounds. This group was the one that was assigned a high protein, low carb diet.

The weight loss maintenance group assigned a low protein, high carb diet regained a significant amount of weight at almost 4 pounds.

The high protein, low carb group also had far fewer dropouts than all of the other diet groups who had significant numbers of dropouts. The researchers believe the difficulty with dropouts was caused by problems keeping families motivated.

While this study is promising and offers more hope to yo-yo dieters who find it not so hard to lose the weight, but often impossible to maintain weight loss. However, more studies with larger groups is necessary before any firm conclusions can be reached.

Have you been able to maintain weight loss long term? How have you done it?

10 Steps For Healthy And Permanent Weight Loss

Source: http://womenshealth.about.com/b/2011/08/26/keeping-off-lost-pounds.htm

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Choosing The Most Promising Oocytes For In-vitro Fertilization

Main Category: Fertility
Also Included In: Women's Health / Gynecology
Article Date: 30 Aug 2011 - 0:00 PDT

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Most cells rely on structural tethers to position chromosomes in preparation for cell division. Not so oocytes. Instead, a powerful intracellular stream pushes chromosomes far-off the center in preparation for the highly asymmetric cell division that completes oocyte maturation upon fertilization of the egg, report researchers at the Stowers Institute for Medical Research.

Their findings illustrate how oocytes repurposed a dynamic cellular mechanism capable of generating considerable intracellular forces and widely used by migrating cells to propel them forward, to set the stage for asymmetric cell division - the kind of cell divisions that generate two different daughter cells. It might also lead to improvements in the selection criteria used to choose the most promising oocytes for in-vitro fertilization.

As a mammalian egg develops, it undergoes two highly asymmetric cell divisions, known as meiosis I and II. During each of these divisions, the cytoplasm divides unequally, giving rise to a large egg and two polar bodies that are much smaller than the developing oocyte. To achieve this uneven distribution of the cytoplasm, the meiotic spindle - the structure that separates the chromosomes into daughter cells - has to be positioned close to the so-called cortical cap, the region where the polar body will form.

"Conventional thinking predicted some sort of physical tether that moors the meiotic spindle at the cortical cap," says Rong Li, Ph.D., Stowers investigator and senior author of the study published in the August 28, 2011, advance online edition of Nature Cell Biology. "It came quite as a surprise that, instead, a continuous intracellular flow pushes the spindle into the correct position and keeps it there."

Earlier studies had ruled out microtubules, which help position the spindle during mitotic cell divisions, as potential tethers while older studies had hinted at actin as a possible candidate. Actin, one of the most abundant protein in animal cells, forms dynamic filament networks that play a crucial role in many cellular processes, including cell migration, intracellular transport.

To find out whether and how actin might play a role in the position of the meiotic spindle, postdoctoral researcher and first author Kexi Yi, Ph.D., incubated mouse oocytes with several known inhibitors of the actin cytoskeleton. "Within minutes of applying CK-666, a brand new and very specific inhibitor, the spindle drifted away from the cortical cap towards the center of the oocyte."

CK-666 inhibits the Arp2/3 complex, a major regulator of the actin cytoskeleton that is known to play a role in cell locomotion and membrane trafficking. It binds to existing actin filaments and initiates the growth of new "branch" filaments. Further experiments revealed that myosin-II contractility, better known for producing muscle contractions, pushes the spindle away from the cortical cap when the Arp2/3 complex is inhibited.

Previous work by Li and her team had shown that meiotic chromosomes, when positioned close to the cortex of an oocyte in meiosis II, induces the formation of a cortical actin cap by propagating the regulatory signal from the Ran protein. When Yi tested the effect of intercepting the Ran signal, they found that Ran also regulates Arp2/3 localization and by extension, spindle position.

Yi then turned to high-resolution time-lapse confocal microscopy and spatiotemporal correlation spectroscopy (STICS), in collaboration with Stowers imaging experts, Jay Unruh, Ph.D., and Brian Slaughter, Ph.D., both co-authors on the paper, to track the dynamics of the cytoplasmic actin network in oocytes labeled with a live F-actin probe.

"STICS analysis showed that the actin flow originates at the cortical cap and continues down along both sides of the lateral cortex before it converges near the center of the oocyte and reverses direction toward the spindle," says Yi. When he treated the oocytes with jasplakinolide, an actin filament-stabilizing drug, actin flow in the cells' interior almost immediately ceased.

"The actin flow drives cytoplasmic streaming away from the cortical cap region along the cell periphery. When it arrives at the opposite pole of the oocyte, it circulates back in a pattern similar to that of the actin flow toward the spindle," says Li. A theoretical analysis by physicist and co-author Boris Rubinstein, Ph.D., a research advisor at the Stowers Institute, found that the observed cytoplasmic streaming generates pressure on the spindle and pushes it towards the cortex.

In many vertebrate species including mammals, oocytes may arrest in meiosis II for hours or even days awaiting fertilization. "During this time the asymmetric spindle position must be stably maintained," explains Li. "Maintaining spindle position under an active force could prevent slow and random drift of spindle position or orientation if the meiotic arrest is prolonged."

Loss of asymmetric positioning of the meiosis II spindle is a known cause of impaired reproductive potential in aging females and spindle position is used as a clinical index to evaluate the quality of oocytes arrested in meiosis II for in-vitro fertilization.

Manqi Deng, Ph.D., in the Department of Obstetrics and Gynecology and Reproductive Biology in the Brigham and Women's Hospital at Harvard Medical School, Boston, MA, also contributed to the study,

The study was funded in part by the National Institutes of Health and the Stowers Institute for Medical Research.

What Is Iron Deficiency Anemia?

While there are several types of anemia, iron deficiency anemia is by far the most common anemia that women experience. Menstruating girls and women are most likely to experience iron deficiency anemia. Pregnant women have a 50 percent chance of experiencing iron deficiency anemia.

Brittle nails, fatigue, pale skin and nail beds are just a few of the symptoms of iron deficiency anemia.

Iron deficiency anemia can cause other problems such as restless legs syndrome (RLS). RLS often strikes at night making sleep difficult, if not impossible.

Fortunately, treating iron deficiency anemia is often as simple as making some changes to your diet.

If you think you may have iron deficiency anemia, contact your healthcare provider for testing and treatment recommendations. The consequences of untreated low iron is the possibility of heart damage due to the fact that your heart is working harder to pump blood because of the low oxygen levels that occur in iron deficiency anemia.

Source: http://womenshealth.about.com/b/2011/08/02/what-is-iron-deficiency-anemia.htm

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Years spent obese increase health risks

The BBC News today reported that the ?health hazards of obesity may have been grossly underestimated because we are not measuring the condition adequately?. Its website says that we should not focus on weight gain alone, but also look at how long it persists.

This news story was based on an analysis of data from the Framingham Heart Study, a long-running research project started in 1948 that went on to study participants for up to 48 years. As part of the study, researchers measured whether participants were obese every two years, as well as recording various aspects of their health. This new analysis found that the longer people stayed obese the greater their risk of dying from any cause (all-cause mortality), as well as cardiovascular diseases specifically.

This study further highlights the health risks of obesity. The researchers say that the duration of obesity is particularly important in today?s society where people are becoming obese at an earlier age. A healthy body mass index (BMI) is considered to be between 18.5 and 24.9, whereas obesity is classified as having a BMI above 30. People who are concerned about their weight can obtain help and advice from their GP.

�

Where did the story come from?

The study was carried out by researchers from Monash University, Australia. It was funded by an AusAID scholarship, a fellowship from VicHealth and the Australian National Health and Medical Research Council. The study was published in the�peer-reviewed International Journal of Epidemiology.

The BBC News gave a top line review of this research and reported the research well.

�

What kind of research was this?

This was an analysis of a�prospective�cohort study that had followed people for up to 48 years. The researchers were interested in seeing whether there was a specific association between mortality and the length of time a person was obese, rather than just the fact that they were obese.

It has been well established that being obese increases the risk of death and numerous health conditions, for example heart disease, diabetes and cancer. The researchers say that when quantifying the risks of numerous diseases the measures used have generally been body weight and BMI, which are related to the severity of obesity. However, the researchers wanted to know the role that duration of obesity plays, e.g. whether the risks would be the same for a person who had been obese for one year compared to a person who had been obese for 20 years. They refer to this factor as either one ?obese year? or 20 ?obese years?.

To understand the association the researchers assessed how the number of years lived with obesity related to the risk of all?cause mortality, death due to cardiovascular disease, cancer and other conditions.

�

What did the research involve?

The researchers used data from a long-running cohort study called the Framingham Heart Study. In 1948 this extensive cohort study enrolled 5,209 participants aged between 28 to 62 years, following them up for around 48 years. The participants had been examined at two-yearly intervals. The current study included those participants who were free from pre-existing diseases of diabetes, cardiovascular disease or cancer at the start of the study - 5,036 people in total.

The study recorded demographic and health behaviour variables such as age, educational level, country of birth, marital status, smoking status, number of cigarettes smoked per day, alcohol consumption and physical activity. A participant was considered obese if their BMI was more than 30 kg/m2. Among the chronic diseases that were regularly measured and included in the analysis were diabetes, cancer and cardiovascular disease (CVD) outcomes such as heart disease and stroke.

The researchers calculated the cumulative duration of obesity for each participant at each examination. As people who were borderline obese or overweight could have fluctuated over the course of the follow-up period, the researchers defined obese individuals as people who were obese at two consecutive examinations, i.e. continuously obese for at least two years. People could have multiple periods of obesity during follow-up (with weight loss in between). For these people, the researchers added all of their obese periods together to generate a cumulative score.

The researchers calculated a ?time to event? score for each individual, which represented either their survival time in days from study start to their death, their loss to follow-up or the end of the study (examination number 24, given in year 48 of the study).

For parts of the analysis the researchers grouped the duration of obesity into the following periods:

Short: 1 to 4.9 obese years
Medium: 5 to 14.9 obese years
Long: 15 to 24.9 obese years
Over 25 obese years

What were the basic results?

The researchers found that 75% of the eligible study participants were not obese in any of the 24 examinations. Among participants who had two consecutive obese examinations, the average age of onset of obesity was around 50 years. The average number of years that this group lived with obesity was 13 years (time spent as obese ranged from 2 to 46 years).

The researchers then combined all the years of follow-up for the whole cohort. This resulted in 166,130 person years of follow-up. Over this time 3,397 (75%) of the participants died. Of the deaths, 39% were caused by CVD, 25% by cancer and 36% by other non-CVD and non-cancer causes.

The researchers adjusted their results within several models. The one used for the main results adjusted for the influence of sex, age at baseline, marital status, education level, country of birth, time-varying smoking, alcohol consumption and BMI.

Relative to people who had never been obese, the researchers calculated the increased risks of death due to any cause (all-cause mortality) during the study period:

Short duration of obesity increased the risk by 51% (Hazard ratio(HR) 1.51, 95%�confidence interval [CI] 1.27 to 1.79).
Medium duration of obesity increased the risk by 94% (HR 1.94, 95% CI 1. 71 to 2.20).
Long duration of obesity more than doubled the risk (HR 2.25, 95% CI 1.89 to 2.67).
Obesity for over 25 years more than doubled the risk (HR 2.56, 95% CI 1.89 to 2.67).

For CVD-related deaths relative to people who had never been obese, the pattern was similar:

Short duration of obesity increased the risk by 68% (HR 1.68 95% CI 1.29 to 2.18).
Medium duration of obesity more than doubled the risk (HR 2.18, 95% CI 1.78 to 2.68).
Long duration of obesity more than doubled the risk (HR 2.53,95% CI 1.99 to 3.23).
Obesity for over 25 years almost tripled the risk (HR 2.76, 95% CI 2.08 to 3.68).

For cancer-related deaths the risk increase associated with obesity was smaller:

Short duration of obesity ? no increased risk relative to non-obese people.
Medium duration of obesity increased the risk by 41% (95% CI 1.06 to 1.88).
Long duration of obesity increased the risk by 69% (95% CI 1.20 to 2.39).
Obesity for over 25 years increased the risk by 50% (95% CI 1.00 to 2.24).

They found that every two years living with obesity, relative to people who were never obese, resulted in a 6% increased risk of death due to any cause, a 7% increase in the risk of death following cardiovascular disease and a 3% increase in cancer-related mortality.

�

How did the researchers interpret the results?

The researchers said that ?the number of years lived with obesity is directly associated with the risk of mortality; this needs to be taken into account when estimating its burden on mortality".

The researchers said that their study ?confirmed that prior analyses examining the association between obesity and the risk of mortality? but ?by only considering the severity of obesity and ignoring the duration of obesity may have underestimated the adverse effects of current obesity?.

�

Conclusion

This analysis of data from a prospective cohort study shows that duration of obesity is associated with mortality risk, particularly CVD-related mortality. The researchers said the key strength of this study was its long follow-up (up to 48 years), but they highlight that this is also a limitation due to the demographic and medical changes that have occurred since the study began. For example, they say that rates of obesity and type 2 diabetes were relatively low in 1948 when the study commenced, but that the contemporary obesity epidemic is characterised by a much earlier onset of obesity, which would mean that people today may have an even longer duration of obesity than the study population. Likewise, advances in medical treatments since 1996 (the last follow-up date in this study) may have affected the prevalence of CVD or cancer-related deaths.

The researchers also pointed out that for the people who were obese at baseline, there is no indication of when they became obese. Therefore the estimation of duration of obesity in these people may be imprecise.

Taking these limitations into consideration, the researchers said that in current and future studies the duration of subjects? obesity needs to be taken into account in estimating the future life expectancy and burden of disease for the general population.

This research again highlights the health dangers of being obese. People who are obese and are looking for ways to lose weight can consult their GP for help and advice. Further research is needed to see whether weight loss following being obese lowers these risks over time.

Links To The Headlines

Call to measure duration of obesity. BBC News, August 23 2011

Links To Science

Abdullah A, Wolfe R, Stoelwinder JU et al. The number of years lived with obesity and the risk of all-cause and cause-specific mortality. International Journal of Epidemiology. (2011) 40 (4): 985-996

Source: http://www.nhs.uk/news/2011/08August/Pages/time-spent-overweight-important-health-marker.aspx

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Monday, 29 August 2011

Latest generation of children will live 20 years longer than their grandparents

Lifespan tables show a 65-year-old man can expect to live another 17 years, and a woman of the same age another 20. A man now in his late 70s can also expect to continue to live for a further nine years and a woman for more than 11. Elderly people can expect more of their longer years of life will be spent in good health, the report in the ONS journal Social Trends also said.

Explaining the 20-year increase, the report said: ?One of the main reasons is the considerable decrease in infant mortality rates which were at their lowest recorded level in 2010.?

It added: ?As well as living longer, men and women are staying healthy and disability free for more of their lives.?

The life expectancy tables - calculated on evidence from 2009 - follow recent evidence that the middle classes have benefited far more from better health and living standards than those on lower incomes.

The character of neighbourhoods also has an effect and people in rural areas live longer, it added.

In 1930 the infant mortality rate stood at 6.3 per cent, with more than one in 20 children dying before their first birthday. Last year that rate was down more than tenfold to less than half of one per cent - 0.45 per cent.

Today, deaths overall are at a record low. Last year was the second in a row in which fewer than 500,000 people died in England and Wales. There were 493,242 deaths, nearly 45,000 fewer than in 2000.

Source: http://telegraph.feedsportal.com/c/32726/f/569020/s/16aee165/l/0L0Stelegraph0O0Chealth0Chealthnews0C86395690CLatest0Egeneration0Eof0Echildren0Ewill0Elive0E20A0Eyears0Elonger0Ethan0Etheir0Egrandparents0Bhtml/story01.htm

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Does stress cause grey hairs?

?When the going gets tough, the tufts get greying,? according to The Sun,�which�was among many�newspapers which today reported that stress causes hair to go grey by damaging people?s DNA. The Daily Mail also reports that this DNA damage might cause stress to bring on cancer.

The news is based on laboratory research, which infused mice with an adrenaline-like chemical for four weeks and found that this led to DNA damage and lower levels of a protein called p53. The protein is thought to protect our DNA from damage and prevent tumours forming. This complex research managed to tease out the series of reactions in a cell that led to the DNA damage in response to adrenaline. The study did not look at whether stress caused grey hair, a link which appears to be based on speculation.

As this research was conducted in mice and cells, it is not clear how its results would relate to people with chronic stress. It is particularly unclear whether the constant infusion of adrenaline into the mice represents the way that the body releases adrenaline in people with chronic stress, a condition that also involves other processes such as release of the stress hormone cortisol.

Additionally, this study did not look at the health consequences of this treatment on the mice, e.g. whether they had a greater chance of developing a tumour or heart problems. However, the results of this study warrant further investigation to assess the role of stress in the likelihood of developing disease in humans.

�

Where did the story come from?

The study was carried out by researchers from Duke University Medical Center, and it was funded by the Howard Hughes Medical Institute. The study was published in the�peer-reviewed scientific journal Nature.

The headlines in the newspapers suggested that this study had looked at the effects that stress has on hair greying. In fact, this study had looked at the effect of adrenaline on DNA damage. It was only speculation that this research had potential implications linking greying to stress.

�

What kind of research was this?

This was a laboratory study which used human cells and mice to investigate the role that stress chemicals play in DNA damage. They were particularly interested in the hormone adrenaline, which is sometimes known as the ?flight or fight? chemical due to the responses it can cause in emergency situations.

The researcher discovered a series of reactions in the cell, which lead to changes in the levels of a protein called p53. This protein is important in regulating how a cell divides, and it is thought to have a role in preventing mutations in DNA and tumours occurring. Because of this role the protein is of interest in current cancer research.

This study was looking at cell biology pathways in mice and human cells. As such, it cannot say what physical symptoms too much stress would typically cause in humans, i.e. grey hair, or indeed what constitutes too much stress.

�

What did the research involve?

The researchers infused mice either with artificial adrenaline (isoproterenol) or a salt solution for four weeks and looked at whether it caused DNA damage by looking at chemical changes to histones, the proteins which package the DNA. Alteration of the histones is thought to be one of the earliest indicators of DNA damage. They then looked at p53 levels in the thymus (a specialised organ of the immune system) of the mice.

The researchers then conducted a series of investigations in cells, examining:

the effect of isoproterenol on human bone cancer cells, skin cells and a type of kidney cell line
the location of p53 in the cells in response to the isoproterenol
what types of adrenaline receptors were behind the changes in p53 levels by using inhibitors that stopped specific subtypes of adrenaline receptor from working
the numerous proteins in the cell which are involved in regulating where in the cell p53 is found, its clearance (breakdown) and its activity, to see how these proteins responded to the isoproterenol

Finally, the researchers produced a genetically modified mouse which did not produce beta-arrestin 1, one of the proteins that they had found to be involved in the adrenaline (isoproterenol) response.

�

What were the basic results?

The researchers found in the animal experiments that four weeks of isoproterenol infusion was enough to cause DNA damage and a lowering of p53 levels in the thymus organs of the mice. This finding was replicated in the cell studies.

They found that isoproterenol caused a reduction of p53 levels by causing p53 to be broken down by proteins in the cell. They also found that the treatment caused the p53 to be transported out of the nucleus of the cell, where the DNA is found.

The researchers found three proteins that were involved in the suppression of p53 levels. Beta arrestin 1, AKT and MDM2. They deduced that when adrenaline attached to a particular type of receptor this led to the activation of beta-arrestin 1 protein. This then allowed AKT to activate the MDM2 protein, causing it to bind to p53 and break it down. They further found that mice that did not produce the beta-arrestin 1 protein (the first step of this reaction pathway) had less DNA damage when exposed to isoproterenol.

�

How did the researchers interpret the results?

The researchers highlighted that beta-arrestin 1 may have some emerging roles in protein clearance pathways. They said that their research reveals how DNA damage may accumulate in response to chronic stress.

�

Conclusion

This laboratory research teased out a complex series of protein reactions in cellular tests. These reactions were then analysed in an experimental mouse model to underpin the finding that adrenaline exposure leads to DNA damage.

Like all animal research, the implications for humans are currently limited and remain to be determined. This research will undoubtedly lead to further study of these proteins, although it is not clear whether the amount of adrenaline the mice were exposed to is similar to the adrenaline levels that could be found in humans during chronic stress.

For example, the primary role of adrenaline is to allow the body to immediately deal with sudden, emergency situations such as physical threats or impending danger, but it is not fully known how the adrenaline system functions in chronic stress. As such, further research would be needed to determine�whether the mechanism is of relevance when considering the effects of typical day-to-day stresses or long-term stretches of feeling stressed.

The newspapers have reported that this research could explain why people?s hair greyed or were at higher risk of developing cancer if suffering from chronic stress. This study did not assess the physical symptoms of the adrenaline treatment in the mice (e.g. whether they went on to develop tumours at a higher frequency than non-treated mice).

This early stage research was well-conducted. Following these findings, further research is warranted to assess whether stress reduction techniques can lower rates of disease.

Links To The Headlines

Stress really does turn your hair grey. The Daily Telegraph, August 23 2011

Too much stress 'turns you grey': Adrenaline from being put under pressure could cause hair to change colour. Daily Mail, August 23 2011

When the going gets tough, the tufts get greying...�Sun, August 23 2011

Stress does make your hair go grey. Metro, August 23 2011

Links To Science

Hara MR, Kovacs JJ, Whalen EJ et al. A stress response pathway regulates DNA damage through b2-adrenoreceptors and b-arrestin-1. Nature, August 2011 [Awaiting online publication]

Source: http://www.nhs.uk/news/2011/08August/Pages/stress-grey-hair-dna-damage.aspx

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