75% Of Workers Are Tired During The Day: How To Boost Your Energy At Work

“All I’m doing is sitting at a computer for nine hours straight, but I’m incredibly exhausted throughout the day and by the time I get home. How is that possible?”

Most office workers have probably asked themselves this question. The nine-to-five routine can take a toll on our energy levels, despite the fact that we’re not being physically active at our jobs at all. Going to the gym in the morning might boost your energy for the first half of the day, but soon you’ll find that familiar exhaustion rolling back in by 3 p.m.

tired office worker

In a recently completed survey by Virgin Pulse and vielife —the former of which provides health incentives for AOL employees — researchers found that 76 percent of workers in the U.S. feel tired many days of the week. Nearly 15 percent of the people also said they fell asleep during the day while at work at least once a week; and about one-third of all the participants reported unhappiness with their sleep quality.

According to the National Sleep Foundation, more than 50 million Americans have poor sleep quality and sleep disturbances that negatively impact their work and personal lives. Virgin Pulse’s report notes that lack of sleep not only affects the physical, mental, and emotional health of company’s employees; but poor sleep quality can also affect the company’s overall performance. “Employee absence has been identified as an independent cost associated with poor sleep,” the authors write, “and tired employees, while present at work, may experience difficulties working to their capabilities.” Just think: when you’re tired, you’re more likely to spend an hour on a small task when you could have completed it much more quickly with your full energy and attention. Put quite simply, lost time is lost money.

“Maybe it might take me to do stuff like a little bit longer because either I just might forget an easier way to do it or just take the longer way to do something,” one participant was quoted as saying in the report.

So how can employers improve the sleep quality of their employees? First, let’s look into why people are losing sleep. The researchers found that 75.6 percent of the participants they surveyed watched television before going to bed, and studies have shown that being in front of a glowing TV or computer screen late at night can actually fool your body into thinking it’s still daytime, hindering your sleep cycle. Another 22 percent said they drank over three coffees or other caffeinated drinks every day. Other reasons why workers were tired had to do with work-related stress, long work hours, consuming alcoholic beverages frequently, or even sleeping in the wrong temperatures, all of which had an impact on sleep cycles. Having an overactive mental state, meaning you’re constantly worrying or thinking about stuff that occurs in your life, will also likely cause you to stay awake.

Here are some tips to improve your sleep cycle:

  • Get more exercise, but work out in the morning or during the day instead of late at night. You’ll experience a boost of energy if you exercise too close to bedtime.
  • Cut down on caffeine. Drink one or two cups of coffee if needed, but make sure it’s before 5 p.m.
  • Ease up on the Facebooking before you fall asleep: relaxing your mind is just as important as relaxing your body, so disconnect from checking e-mails or refreshing your news feed.
  • Set some time aside to wind down before you fall asleep. Reading can often make you tired, so choose a book instead of a computer screen.
  • Decrease sugar intake.
  • Walk more: some of the survey participants said that walking and physical activity helped them sleep better.

If you’re still tired at work, try these steps to boost your energy:

  • Take bathroom or walking breaks every hour. Walking improves concentration and gets your blood flowing.
  • Eat nutritious food — but not too much. Having a heavy lunch will make you want to hit the sack shortly after.
  • Reduce your stress levels. Anxiety can be exhausting, so pay more attention to taking care of yourself.
  • Drink more water, and stay away from the alcohol. We can all be reminded that battling a hangover at work is going to impair your work flow.

Green tea weight loss secrets proven by science – NaturalNews.com


From the desk of Zedie.

Blood Of Oldest Woman In The World Reveals Secrets Of Longevity, Suggests We Can Live Longer

It seems that 500 years after the death of Juan Ponce de Leon, science may have just discovered the mysterious fountain of youth. Only it’s not a fountain, and it’s definitely not in Florida. He actually had it all along — we all do. The secret to our longevity lies in our white blood cells. A study of blood and tissue samples from Hendrikje van Andel-Schipper, once the oldest woman in the world, revealed that death from old age is specifically caused by exhaustion of blood stem cells. Now that scientists have discovered what causes death, it automatically raises the question of what to do with this information. Some believe that manually replenishing these stem cells will result in the ability to fool Mother Nature and perhaps make death no longer inevitable.

Secrets in Blood

Born in 1890, van Andel-Schipper was known for her remarkable health in old age. She had a clear mind and disease-free body until her death in 2005. As she wished, upon her death van Andel-Schipper’s body was donated to science, and her blood and tissue samples helped scientists understand how the body is affected by old age. What scientists found is that our lifespan is limited by the capacity for stem cells to replenish, New Scientist reported. When stem cells are eventually no longer able to self-replenish, they gradually die off. The individual will no longer be able to replace tissue, and cells will soon succumb to a natural death of old age.

At the end of her life, two thirds of van Andel-Schipper’s remaining white blood cells had originated from just two stem cells. This suggests that most or all of the blood stem cells she had started with in life had burned out and died. Also, the telomeres on van Andel-Schipper’s white blood cells were drastically worn down. Telomeres are the protective tips on chromosomes that burn down like a candle wick each time a cell divides. During life, the number of active stem cells shrinks, and their telomeres shorten to the point at which they die. This point is called stem-cell exhaustion.


‘Fountain of Youth’?

Does understanding the cause of death mean that we will be able to one day control death? Some scientists believe it may be possible to rejuvenate aging bodies with re-injections of stem cells saved from birth or early life. “If I took a sample now and gave it back to myself when I’m older, I would have long telomeres again—although it might only be possible with blood, not other tissue,” Henne Holstege, lead researcher of the study on van Andel-Schipper’s blood, told New Scientist. Rather than using this information to create a theoretical “fountain of youth,” scientists hope that the results can be used in correlation with studies on Alzheimer’s disease to reveal why some people are more susceptible to the disease at an early age.

Van Andel-Schipper’s blood also gave some important insight into our bodies’ natural defenses against cancer. Researchers found that although there were many mutations in van Andel-Schipper’s blood, they were all harmless. These mutations were the result of mistaken replication of DNA, but due to their absence of cancer, researchers concluded that van Andel-Schipper had an advanced system for repairing or aborting cells with dangerous mutations. “When there is a mutation, there’s an opportunity for selection and some somatic mutations lead to cancer. Now we see the range of somatic mutations in normal, non-cancerous tissues like blood, so we can start to think about health consequences,” said Chris Tyler-Smith of the Wellcome Trust Sanger Institute in Hixton, Texas.

What are stem cells?

Stem cells are essentially the body’s raw materials. Under the right conditions in the body, or in a laboratory, stem cells divide to form more cells. These new cells will either become new stem cells or specialized cells with a more specific function, such as blood cells or brain cells. Stem cells are the only cell in the body that has the natural ability to form new cells types.


Source: Holstege H, Pfeiffer W, Sie D, et al. Somatic mutations found in the healthy blood compartment of a 115-yr-old woman demonstrate oligoclonal hematopoiesis. Genome Research. 2014.

Worsening Heart Failure Tied to Higher Diabetes Risk

Heart failure severity correlated with a stepwise increase in diabetes risk, according to nationwide cohort study from Denmark.

Patients in the study taking the highest doses of loop diuretics, used as a proxy for heart failure severity, were three times as likely to develop diabetes as patients taking no diuretics over the study period (hazard ratio 3.02, 95% CI 2.66-3.43), reported Malene N. Demant of Copenhagen University Hospital Gentofte, and colleagues in Diabetologia.

However, concomitant use of renin-angiotensin system inhibitors (RASis) appeared to attenuate the risk (HR 1.76, 95% CI 1.61-1.92), they said.

“From an epidemiological perspective, the poor prognosis associated with diabetes in patients with heart failure has confused researchers for 35 years,” the authors wrote. “Our data add important insights to the understanding of the mechanisms underlying this poor prognosis, because it might be that the sickest patients are those who develop diabetes. Thus, diabetes may, in part, be a marker of heart failure severity in addition to being a causal risk factor for mortality in heart failure cohorts.”

More than 3 decades ago, findings from the Framingham Heart Study linked diabetes with a worse prognosis in patients with heart failure. Significant advances in diabetes treatments since then have not improved outcomes in patients with diabetes complicated by heart failure.

“This has led to the hypothesis that diabetes may in some cases be a marker of heart failure severity rather than a causal risk factor for adverse outcomes as such,” Demant and colleagues wrote. “In this context, chronic heart failure has been shown to be associated with hyperinsulinemia and increased insulin resistance in a severity-dependent manner.”

The impact of heart failure severity on the risk of developing diabetes has not been well studied, the researchers noted. In an 2010 investigation, which had a design similar to the current study, the researchers reported that heart failure increased diabetes risk in a severity-dependent manner in newly discharged myocardial infarction (MI) patients.

Study Details

Demant’s group followed patients discharged after hospitalization for heart failure from 1997 to 2010 and who had not previously been treated with hypoglycemic agents or loop diuretics. Data on these patients came from four nationwide administrative registries.

The patients were divided into five groups according to the dosage of prescribed loop diuretics based on arbitrary values:

  • Group 1: no loop diuretics (31% of patients)
  • Group 2: >0-40 mg/day (25%)
  • Group 3: >40-80 mg/day (17%)
  • group 4: >80-159 mg/day (12%)
  • Group 5: ≥160 mg/day (15%)

Mean patient age at hospitalization ranged from 72.1 in group one to 76.5 in group five. About half of the patients in all groups were women. Concomitant disease included ischemic heart disease, acute MI, and atrial flutter/fibrillation.

In all, 8% developed diabetes and the mean time to the first claimed prescription of a hypoglycemic agent was 1,080 days (interquartile range 475-2,037).

The higher the loop-diuretic dosage, the higher the proportion of patients who developed diabetes. Among those taking the highest dosage, the 10-year cumulative risk of developing diabetes exceeded 25%. Crude incidence rates for developing diabetes were 1.6 (95% CI 1.5- 1.7), 1.9 (95% CI 1.5- 2.0), 2.3 (95% CI 2.2-2.4), 2.6 (95% CI 2.5- 2.8) and 3.0 (95% CI 2.9-3.2) per 100 person-years in groups one-five.

In comparison with group one patients with and without ischemic heart disease, the hazard ratios associated with loop-diuretic dosage were found to be slightly lower for patients with ischemic heart disease than for those without in groups two-five (P<0.0001 for interactions):

  • HR 1.22 (95% CI 1.10-1.34) versus 1.29 (95% CI 1.19-1.41)
  • HR 1.38 (95% CI 1.24- 1.54) versus 1.50 (95% CI 1.38-1.64)
  • HR 1.55 (95% CI 1.38-1.75) versus 1.81 (95% CI 1.64-1.99)
  • HR 1.86 (95% CI 1.68-2.07) versus 2.00 (95% CI 1.83-2.20)

Just as with RASis, the use of beta blockers appeared to lower risk versus non-usage for groups two-five compared with group one (P<0.0001 for interactions):

  • HR 0.86 (95% CI 0.79-0.94) versus 1.60 (95% CI 1.46-1.75)
  • HR 0.97 (95% CI 0.88-1.07) versus 1.66 (95% CI 1.51-1.83)
  • HR 0.91 (95% CI 0.81-1.02) versus 2.03 (95% CI 1.82-2.26)
  • HR 1.03 (95% CI 0.93-1.14) and 2.17 (95% CI 1.96-2.40)

A total of 62,565 (63%) patients died during the study period, and the adjusted HR for death among those who developed diabetes was 1.16 (95% CI 1.12-1.19) compared with those who did not develop diabetes. Increasing loop-diuretic dosage was associated with increased risk for death: HRs 1.14 (95% CI 1.12-1.17), 1.17 (95% CI 1.14-1.20), 1.29 (95%CI 1.26-1.33) and 1.45 (95% CI 1.41-1.48) for groups two-five compared with group one.

The researchers noted that the results should be considered “hypothesis generating,” but the finding that RASis seemed to attenuate diabetes risk may be worthy of further study.

They noted that large-scale clinical studies have found that treatment with RASis or angiotensin II receptor antagonists reduced the relative risk of the development of diabetes by 14% to 34%, although newer studies have found less or no risk reduction. Other medications such as beta blockers have also been linked to increased risks of diabetes in some previous studies.

“We found the opposite in the present study, i.e. a lowered risk of diabetes associated with [beta blockers], which, as for RASis, may have been due to blockage of a high sympathetic tone and/or improved cardiac function,” they said, adding that a selection bias for prescribing beta blockers to generally healthier patients couldn’t be ruled out.

Diabetes Awareness in HF Management

Study limitations included the lack of data on possibly relevant variables such as body mass index, smoking status, blood glucose values, New York Heart Association class, hypertension, and left ventricular ejection fraction. In addition, both heart failure severity and diabetes were defined from prescription claims, which were characterized by the authors as “rough phenotypic markers” of true severity.

The authors also did not explore the mechanisms for these effects in this study, but they did suggest several possibilities, such as patients with heart failure having decreased cardiac output and diminished oxygen; glucose and insulin distribution to peripheral muscular tissue which may lead to increased insulin resistance and decreased insulin release; lack of physical activity in those with the most severe heart failure; and potential side effects of loop-diuretic drugs.

Nevertheless, the findings emphasize the need to closely monitor and treat patients with heart failure if necessary with the goal of preventing diabetes, the researchers concluded.

“Future strategies for heart failure management should include increased awareness of risk of diabetes in patients with severe heart failure,” they wrote.

The study was funded by the Copenhagen University Hospital Gentofte.

Demant reported no relevant relationships with industry.

Two co-authors reported support from the Danish Agency for Science, Technology and Innovation and Novo Nordisk Foundation.

One co-author reported equity ownership in Novo Nordisk A/S and receiving honoraria from the company.

One co-author reported holding stock in Novo Nordisk A/S.

DNA nanotechnology places enzyme catalysis within an arm’s length.

Using molecules of DNA like an architectural scaffold, Arizona State University scientists, in collaboration with colleagues at the University of Michigan, have developed a 3-D artificial enzyme cascade that mimics an important biochemical pathway that could prove important for future biomedical and energy applications.

The findings were published in the journal Nature Nanotechnology. Led by ASU Professor Hao Yan, the research team included ASU Biodesign Institute researchers Jinglin Fu, Yuhe Yang, Minghui Liu, Professor Yan Liu and Professor Neal Woodbury along with colleagues Professor Nils Walter and postdoctoral fellow Alexander Johnson-Buck at the University of Michigan.

Researchers in the field of DNA nanotechnology, taking advantage of the binding properties of the chemical building blocks of DNA, twist and self-assemble DNA into ever-more imaginative 2- and 3-dimensional structures for medical, electronic and energy applications.

In the latest breakthrough, the research team took up the challenge of mimicking enzymes outside the friendly confines of the cell. These enzymes speed up chemical reactions, used in our bodies for the digestion of food into sugars and energy during human metabolism, for example.

“We look to Nature for inspiration to build man-made molecular systems that mimic the sophisticated nanoscale machineries developed in living biological systems, and we rationally design molecular nanoscaffolds to achieve biomimicry at the molecular level,” Yan said, who holds the Milton Glick Chair in the ASU Department of Chemistry and Biochemistry and directs the Center for Molecular Design and Biomimicry at the Biodesign Institute.

With enzymes, all moving parts must be tightly controlled and coordinated, otherwise the reaction will not work. The moving parts, which include molecules such as substrates and cofactors, all fit into a complex pocket just like a baseball into a glove. Once all the chemical parts have found their place in the pocket, the energetics that control the reaction become favorable, and swiftly make chemistry happen. Each enzyme releases its product, like a baton handed off in a relay race, to another enzyme to carry out the next step in a in the human body.

For the new study, the researchers chose a pair of universal enzymes, glucose-6 phosphate dehydrogenase (G6pDH) and malate dehydrogenase (MDH), that are important for biosynthesis—making the amino acids, fats and nucleic acids essential for all life. For example, defects found in the pathway cause anemia in humans. “Dehydrogenase enzymes are particularly important since they supply most of the energy of a cell”, said Walter. “Work with these enzymes could lead to future applications in green energy production such as fuel cells using biomaterials for fuel.”


In the pathway, G6pDH uses the glucose sugar substrate and a cofactor called NAD to strip hydrogen atoms from glucose and transfer to the next enzyme, MDH, to go on and make malic acid and generate NADH in the process, which is used for as a key cofactor for biosynthesis.

Remaking this enzyme pair in the test tube and having it work outside the cell is a big challenge for DNA nanotechnology.

Credit: ASU Biodesign Institute / Nature Nanotechnology.

To meet the challenge, they first made a DNA scaffold that looks like several paper towel rolls glued together. Using a computer program, they were able to customize the chemical building blocks of the DNA sequence so that the scaffold would self-assemble. Next, the two enzymes were attached to the ends of the DNA tubes.

In the middle of the DNA scaffold, they affixed a single strand of DNA, with the NAD+ tethered to the end like a ball and string. Yan refers to this as a swinging arm, which is long, flexible and dexterous enough to rock back and forth between the enzymes.

Once the system was made in a test tube by heating up and cooling the DNA, which leads to self-assembly, the enzyme parts were added in. They confirmed the structure using a high-powered microscope, called an AFM, which can see down to the nanoscale, 1,000 times smaller than the width of a human hair.

Like architects, the scientists first built a full-scale model so they could test and measure the spatial geometry and structures, including in their setup a tiny fluorescent dye attached to the swinging arm. If the reaction takes place, they can measure a red beacon signal that the dye gives off—-but in this case, unlike a traffic signal, a red light means the reaction works.

Next, they tried the enzyme system and found that it worked just the same as a cellular enzyme cascade. They also measured the effect when varying the distance between the swinging arm and the enzymes. They found there was a sweet spot, at 7nm, where the arm angle was parallel to the enzyme pair.

With a single swinging arm in the system working just like the cellular enzymes, they decided to add arms, testing the limits of the system with up to 4 added arms. They were able to show that as each arm was added, the G6pDH could keep up to make even more product, while the MDH had maxed out after only two swinging arms. “Lining enzymes up along a designed assembly line like Henry Ford did for auto parts is particularly satisfying for someone living near the motor city Detroit,” said Walter.

The work also opens a bright future where biochemical pathways can be replicated outside the cell to develop biomedical applications such as detection methods for diagnostic platforms.

“An even loftier and more valuable goal is to engineer highly programmed cascading enzyme pathways on DNA nanostructure platforms with control of input and output sequences. Achieving this goal would not only allow researchers to mimic the elegant enzyme cascades found in nature and attempt to understand their underlying mechanisms of action, but would facilitate the construction of artificial cascades that do not exist in nature,” said Yan.

Old Gout Drug Could Help Your Heart, Hurt Your Wallet.

A decades-old medication used to treat gout has taken on a new life in preventing multiple episodes (greater than 2) of recurrent pericarditis. But with its new name comes a hefty price increase.

Attendees at the American College of Cardiology’s 63rd Annual Scientific Session and Expo heard a report on the CORP-2 trials. The trials looked at how well and how safely colchicine helps prevent recurrent bouts of pericarditis. This study builds on the previous CORP trial to help prevent recurrent pericarditis.

Recurrent pericarditis is a well-known complication of acute pericarditis (inflammation of the sac that lines the heart). It troubles over 30 percent of pericarditis patients.

Even though research results on treating with colchicine look promising, patients will face sticker shock at the pharmacy. The patent medication is very expensive. However, there are programs that may offer to help patients pay for the drug.

Natural cure now under patent protection

Originally used to treat gout, colchicine derives from a centuries-old, plant-based cure that used autumn crocus, or Colchicum autumnale, in its preparation.

Currently, the patent version of the drug, Colcrys, has FDA approval as a treatment for gout. The trials aim to gain its official approval as first-line treatment for acute and recurrent pericarditis.

The problem is that the formerly inexpensive generic colchicine is no longer available. The cost of the patented version for the drug ballooned from nine cents to five dollars per pill – a price hike that might make even healthy patients swoon.

Research trials presented at ACC conference

The Colchicine for Recurrent Pericarditis 2 Study (also known as ASLT02 and conducted under the support of the Italian National Health Service) looked at data from a total of 240 patients over a period of six months.

The patients had recurrent pericarditis, 82 percent of which was of idiopathic (unknown) origin. Half the patients received colchicine (0.5 mg by mouth twice a day) treatment in addition to traditional treatment including standard NSAID’s. The other half did not.

After six months, patients treated with colchicine had a disease recurrence rate of just over 20 percent. The group that did not receive colchicine had a 42 percent recurrence rate. The medication also helped similarly reduce short-term persistence of symptoms (measured at 72 hours).


Allan L. Klein, MD, Director of Cleveland Clinic’s Center for the Diagnosis and Treatment of Pericardial Diseases, did not participate in the study. After reviewing the results, he says it does “perhaps confirm its utility as first-line therapy for multiple episodes of recurrent pericarditis in the absence of contraindications (reasons to withhold a certain medical treatment).” However, he tempers the optimistic findings with caution. He notes that colchicine is not without side effects. It can cause diarrhea and the dose will need adjusted in patients who have reduced kidney function. Of note in the U.S., the drug is off-label with a dose of 0.6mg by mouth twice a day and is currently used in patients with acute and recurrent pericarditis.

Thermal Touch can turn any surface into a tablet.

One of the biggest problems for range finding cameras like Kinect is physical touch; it’s often important to be able to tell whether someone’s finger is hovering a millimetre over the surface of a table, or actually touching it. The resolution necessary to do that accurately, quickly enough to follow professional typist for instance, is very hard to come by. But a new innovation from a German company called Metaio takes a simple insight and applies it to great effect: with a simple thermal camera, they use the heat signatures left by our fingertips to turn virtually any surface into a touch interface. It’s called Thermal Touch.

thermal touch head

Notice that it’s a tablet-like touch interface, rather than a touch screen. While sometimes the technology might be applied to objects that already have a visual structure on them (say, a chess board), most others will be flat and featureless (the surface of a table on which you want to play chess). In those cases, the technology utilizes existing augmented reality tech to live-edit some interface element into a video feed, and uses Thermal Touch tracking to coordinate your input with the functional elements. Keeping with the example of chess, your augmented reality glasses might layer the board over your view of the table, and then track which squares you touch for control.

The applications are nearly endless. Security passwords could be input on a custom keypad, unique to every user or even to every trip through security. With a sophisticated enough augmented reality system hooked to a Google Googles-like service, this technology could allow you to “click” on every image in a catalogue, or every ad in a magazine. A restaurant could hand out interactive menus with touch-to-order functionality… and they could be made of paper. You’d have to have an AR setup for that to work, however, and the restaurant would have to provide a (preferably passive and unprotected) wireless connection with it.

Consumer electronics could get quite a bit out of this as well, for instance projecting the controls for your MP3 player onto the arm of whichever shirt or jacket you happen to be wearing. Skin itself will likely be difficult, since by its nature skin won’t show a lasting heat signature of skin. Thermal cameras don’t have to be any more expensive than regular ones, and most of us already have two of those in a single handset.

This is the current test setup, bulky but effective.

This is the current test setup, bulky but effective.

Right now the technology is working with a webcam mounted to a tablet PC, but the team is working based on the assumption that some sort of video-computing hybrid will be strapped to a large number of people’s faces soon enough. Whether that might come in the form form of some future Google Glass is up in the air, but this technology does require actual augmented-reality capabilities — that is, you need a screen between your eye and the interface, a feature that doesn’t mesh with the off-in-a-corner display on Glass.

The team basically stumbled onto this innovation because some thermal cameras happened to be lying around the lab. That’s how easily this technology can be adapted to work; just by fiddling with the technology, you can immediately see the heat signatures we leave on virtually every object. A combination of remote thermal sensing like this, capitative touch sensing like we have in our touch screens, and broad motion-tracking like Kinect could allow truly incredible levels of control.

If nothing else, innovations like this one will be necessary if we’re to see the expansion of advertising continue. We can’t make everything into a touchscreen, but the onset of wearable computing and user-friendly augmented reality hardware mean that, very likely, we won’t have to.

Rare Disease Genetics: A New Frontier


From the desk of Zedie.

Deficiency of the sunshine vitamin

Deficiency of the sunshine vitamin: http://www.thehindu.com/news/national/kerala/deficiency-of-the-sunshine-vitamin/article6043850.ece

From the desk of Zedie.

Why your children don’t listen to you

Why your children don’t listen to you http://www.bbc.co.uk/news/health-27538195

From the desk of Zedie.