First comet landing site to be revealed

The European Space Agency (ESA) has planned to reveal the site selected for the first landing of a comet this week.

Philae, a landing module weighing about 100 kg that is part of Rosetta (robotic space probe), will probably touch down on Nov 11 on the surface of Comet Churyumov-Gerasimenko, which the unmanned spacecraft has been orbiting and observing from a distance of less than 100 km since Aug 6.

The ESA announced Aug 25 the five possible landing sites, photos of which scientists were examining in detail for three weeks to work out the operating and orbital strategies needed to get the probe to each one.

To do that, Rosetta approached to about 50 km from the comet, which allowed scientists to “gather more detailed information about each site”, in particular high-definition photos of the comet’s rocky, dusty and uneven surface, temperature readings and pressure measurements of the density of the gas surrounding the nucleus.

The ESA on Monday will announce the prime landing site and a backup site, and discuss what the specific challenges are with each one, and also other scientific results acquired so far.

Authorities have warned that the landing manoeuvre will be “complicated” and could last several hours because of the relatively small mass — and corresponding very light gravity — of the comet, which looks something like a potato the size of a mountain.

Once the probe has landed and attached itself to the surface, it is expected that Philae will be able to deliver valuable information to scientists for a period of about four months.

The orbiting module will continue observing the evolution of the comet’s activity through the end of 2015.

Rosetta was launched in 2004, and, over the past 10 years, has travelled almost 6.4 billion km on its odyssey to try and obtain data relating to the solar system’s origin.


Your lymphatic system – why and how to get it moving

When the lymphatic system is not working properly, our bodies cannot remove toxins; fight viral, fungal, and bacterial disease; or regulate the amount of fluid in our tissues. In order to achieve maximum health, we must keep this system functioning well and our lymph fluid flowing.

It is a complex system that includes organs, nodes, and vessels that perform three primary functions: fluid balance, fat absorption, and immunological defense.

When the blood reaches the capillaries, fluid is released from the thin-walled capillaries and flows into all of the tissues in the body. This fluid, called interstitial fluid, bathes the tissues with nutrients and gases as it washes over the cells.

The cells absorb nutrients and oxygen and release their waste products back into the interstitial fluid. Ninety percent of the interstitial fluid is reabsorbed by the venous capillaries, to recombine with the blood and flow back to the heart. The other 10% of the interstitial fluid, now called lymph, flows through the lymphatic system and is filtered through the lymph nodes before being returned, ultimately, to the bloodstream.

If the lymphatic system is not working properly, interstitial fluid builds up in the tissues, and the lymph fluid is not properly filtered and cleansed before being returned to the bloodstream.

Circulation of Lymph

The lymphatic system doesn’t have a big pump like a heart to force fluid through the vessels. Instead, our bodies rely on our muscles to move the fluid. Our diaphragms and rib cage as well as the blood pumping through our bodies, do assist in this movement. But body movement and exercise is the primary method of moving lymph. A sedentary lifestyle decreases lymph flow by 94%.

Why is it important to Move Our Lymph?

Lymph contains lymphocytes, (white blood cells: T-cells, B-cells, and natural killer cells) that seek out and kill pathogens. As the fluid is filtered through the lymph nodes, a concentration of lymphocytes clean up the fluid before it is returned to the blood.

If the fluid is backed up and not flowing properly, it becomes viscous. The flowing fluid can thicken until it becomes the consistency of cottage cheese. Fluids and waste are not properly drained from the cells, bacteria and other foreign invaders are not properly filtered and destroyed, and disease, including cancer, may result.

How to Move Lymph Through the Body and Assist the Lymphatic System

The major way to move lymph through the body is through movement of any kind. Walking, bending, stretching–any and all movement will assist with lymphatic movement. To really get it moving, bounce. Jump up and down, jump rope, or for the best result, bounce on a rebounder for 15-20 minutes a day. (See the link below.)

You will also benefit from massage, including self massage. (See the link below.) This will assist with flow and move any viscous fluid through the system. Find a massage therapist who is certified in lymphatic massage.

Be sure to hydrate well with clean (preferably spring) water.Beets, berries, and cherries all stimulate the lymphatic system. A healthy diet consisting of 80% raw vegetables and fruits supports healthy lymphatic function as well as general health.

One of Ayurveda medicine’s most popular blood purifiers, Manjistha, is known to be an excellent lymphatic tonic. Astragalus, echinacea, goldenseal, pokeroot, or wild indigo root tea are recommended. Detoxifying the blood, hot and cold hydrotherapy, candida cleansing, and rebounding are important components to detoxifying the lymph.

So get off the couch, jump up and down, and eat right to detox your lymphatic system. It’s the least you can do for a system that works so hard to protect you. Check out the first source for a more detailed look at the lymphatic system.


Sandy Ellis, Structure and Function of the Lymphatic System: an Overview, British Journal of Community Nursing, April 1, 2006

Alder, Richard, PhD, Lymphatic System, Salem Press Encyclopedia of Science, September, 2013

Learn more:

Researchers Trick E. Coli Into Making Propane .

Considering the costs of building new infrastructure and adapting to unfamiliar power sources, we aren’t likely to stop using fossil fuels anytime soon. What’s the next best solution? Make existing fuels greener and renewable.

That’s the idea behind new work from scientists at Imperial College London and the University of Turku in Finland, who aim to eventually coax photosynthetic bacteria to turn sunlight into propane gas. The technology has a long way to go before it’s commercially viable. But as a first step, the team has managed to trick E. coli, a bacteria found in our digestive system, into creating small amounts of engine-ready propane.

Traditionally, propane is created as a by-product of natural gas and petroleum processing. It’s removed from natural gas to make transport along pressurized pipelines safer, and oil refineries produce it when they break down petroleum into either gasoline or heating oil.

In a three-step process, the scientists used enzymes to first free up fatty acids in E. coli that are normally used in the creation of cell membranes. One of these, butyric acid, was then converted with another enzyme into butyraldehyde—a derivative of butane. Finally, the team transformed the butyraldehyde into propane. Stimulating the converting enzyme with electrons enhances the process, the team found.

Recently described in the journal Nature Communications, the project is in its early stages. But Patrik R. Jones, one of the paper’s authors, says the method is simpler than similar attempts at creating fuel with living organisms. Yeast or bacteria play a role in producing ethanol from sugar or corn, and engineered photosynthetic bacteria create diesel from crops as well. Ethanol is now commonly added to gasoline in the United States, thanks mostly to government subsidies and incentives. But bacteria-derived biodiesel hasn’t yet seen widespread use, due largely to continued issues with costs and efficiency.

“In the case of [photosynthetic] biodiesel, there are many steps in the process, and each of these steps has a penalty in terms of efficiency,” says Jones. “If we could cut down the number of steps, at least theoretically, we could then have a more efficient process.”

The focus on propane as opposed to other fuels also simplifies the process, because propane separates from the organisms’ cells easily due to its compact chemical structure. Ethanol, which can be created from corn, sugar and other crops, needs to be physically separated from water in a process that is energy intensive. Current methods for harvesting diesel fuel from algae involve breaking open their cells and, in doing so, killing the organisms that are making the fuel. With propane, the fuel can be separated without destroying E. coli.

Propane is simple to collect as a gas, and yet easier to safely store than hydrogen, which is very dangerous as a gas, especially when mixed with air. It was also chosen, Jones says, because it’s easy to liquefy for transportation, and it’s compatible with the existing infrastructure. Propane is mostly associated with outdoor grills in the United States, but it’s also used to power forklifts and boat motors. Cars can even be converted to run on propane; the process is fairly common in the United Kingdom, where gas prices are much higher than in the United States.

The team is using E. coli at this stage because it’s simple to work with, Jones says. But eventually, the researchers hope to transplant the process from E. coli into photosynthetic bacteria so that sunlight provides the energy to power the cells, rather than the diet of nutrients that E. coli requiresThis will again cut down the number of steps in the process, but there’s a lot of work left to be done before the scientists get to that point.

“Only theoretically perfect or near-theoretically perfect systems will ever have a chance of being commercialized,” says Jones. “That’s why it’s important to try and reach [a process] that works as well as possible.” At the moment, Jones estimates they’ll have to produce 1,000 to 5,000 times more fuel from their process before industry will show an interest. And from that point, more engineering and refinement would have to take place before it could be commercially viable as an alternative to existing fossil fuels.

“Some issues lie in the enzymes we use,” says Jones. “So there will need to be some search for alternative enzymes, or improvement of the enzymes we have, and these will be big projects on their own.”

It’s clear that we won’t be driving cars or grilling burgers using propane produced by bacteria and the sun anytime soon. But in an Imperial College London article, Jones said that he hopes the process will become commercially viable in the next 5 to 10 years.

Even if that estimate is generous, solar-powered propane production may be ready in time to help speed up the switch from dirty fuels to more environmentally friendly alternatives.


Total Revascularization Gets CvLPRIT Push

If a patient is undergoingpercutaneous coronary stenting for treatment of an acute myocardial infarction, researchers here suggested that all dangerous lesions in the coronary arteries should be addressed — not just the culprit lesion.

At 12 months, 21.1% of patients who had only the culprit lesion treated experienced a major adverse cardiovascular event compared with 10% of the patient who underwent more extensive treatment of all dangerous lesions observed with angiography (P=0.009), said Anthony Gershlick, MD, honorary professor of interventional cardiology at the University of Leicester and Glenfield Heart Centre in England.

In the breakdown of the components of the primary endpoint, Gershlick reported at the annual meeting of the European Society of Cardiology:

  • Six people in the group that only had the culprit lesion treated died compared with two of the patients who underwent complete revascularization (P=0.14).
  • Four people in the group that only had the culprit lesion treated experienced a recurrent myocardial infarction compared with two patients who had complete revascularization (P=0.39).
  • Nine people in the culprit lesion group experienced heart failure compared with four patients who underwent complete revascularization (P=0.14).
  • Twelve people in the culprit lesion group required revascularization compared with seven patients who underwent complete revascularization (P=0.20).

“While none of these differences were significantly significant on their own, it does show that the overall outcome was driven by hard events and not by the need for revascularization,” Gershlick explained at a press conference.

Gershlick and colleagues attempted to answer the controversial question of how to manage patients being treated for an acute ST-segment elevated myocardial infarction (STEMI) who present with a culprit lesion causing the heart attack and also one or more other lesions that would be considered worrying.

Retrospective registry data and meta-analyses suggested that outcomes improved by treating non-infarct-related lesions but, he said, questions persisted about how to judge the significance of the non-infarct lesions and when to treat these lesions.

He told MedPage Today that lesions that occluded a coronary artery by 70% or more were addressed in doing a complete revascularization. Lesions of 50% or greater occlusion were addressed if they occurred in more than one plane, he said.

“We had a median stent placement of about two in the patients where we did complete revascularization,” Gershlick said.

The CvLPRIT (Complete versus Lesion-only Primary PCI Trial) was initiated in 2008, and enrolled 298 patients — 150 underwent complete revascularization and 146 had the culprit lesion treated and then had other lesions considered at a later date.

“CvLPRIT demonstrated a 55% reduction in major adverse cardiovascular events in those patients presenting for primary percutaneous coronary interventions when the non-infarct-related artery is treated on the index admission,” Gershlick said. “We saw no adverse safety signal.”

The trial appears to confirm outcomes seen in the PRAMI (Preventive Angioplasty in Myocardial Infarction) in which a 65% reduction in adverse events was observed if complete revascularization was performed at the time of initial percutaneous intervention.

Dipti Itchhaporia, MD, past chair of the American College of Cardiology and Georgia and Robert Roth’s Chair for Cardiac Excellence at Hoag Memorial Hospital Presbyterian, Newport Beach, Calif., told MedPage Today, “CvLPRIT is an anticipated trial coming on the heels of PRAMI. I think the interest was to see if this does make a difference. Here they looked at the two groups and found, indeed, if you do a complete revascularization at the time of the initial treatment, there is a 55% decrease in the rate of major adverse cardiovascular events.

“I think that most of us who were cautious after the PRAMI data are a little bit more excited now,” she said. “Will it completely make us change? No, because the guidelines still tell us to do infarct-related angioplasty, but all of a sudden there is going to be much more interest among people in doing the other vessels that are involved at the same time.”

“We think this strategy may need to be considered by future STEMI guideline committees,”Gershlick said.

“I think this is potentially a practice-changing study,” Deepak Bhatt, MD, MPH, professor of medicine, Harvard Medical School/Brigham & Women’s Hospital, Boston, told MedPage Today. ” Most interventionalists have intuitively believed that STEMI patients should undergo nonculprit percutaneous coronary intervention prior to discharge and this study supports that belief — whether that should be during the initial procedure or the next couple of days likely depends on lesion complexity and patient comorbidities.”

Cardiac Amyloidosis: The Great Imitator

Total Revascularization in Primary PCI: Will CvLPRIT Change US Guidelines?

Nonculprit PCI Now or Never?

Gilles Montalescot, MD, PhD: Hello. I am Gilles Montalescot, a cardiologist from Paris, and I’m here in Barcelona at the European Society of Cardiology Congress with Tony Gershlick. Welcome, Tony.

Anthony H. Gershlick, MBBS: Thank you.

Dr. Montalescot: You are presenting a very important study[1]here in the Hot Line Session. It’s the same question that we have been asking for years. What should we do with the coronary arteries other than the culprit when we are in the middle of a percutaneous coronary intervention (PCI) in a patient with ST-elevation myocardial infarction (STEMI) in the cath lab? Of course we treat the culprit artery, but what should we do with the others? You did a fantastic randomized study. Can you tell us about it?

Dr. Gershlick: You and many other clinicians who are watching this know that when you do a primary PCI in a left anterior descending artery, and there is a very tight stenosis in the right coronary artery, we have never known what to do. Some people leave it. Some people treat it. Some people defer treatment. Some people wait for a myocardial perfusion scan (MPS) or a nuclear scan. Some people don’t do anything. The original question (and there are many different questions, including how to judge severity) was: What should we do? Should we treat it during the admission, or should we not treat and wait and see what happens? That was the basic question that struck me as a clinician.

We had STEMI patients who had lesions in their non-infarct-related artery. The previous guidelines and the current American guidelines[2] suggested that these non-infarct-related lesions shouldn’t be treated. We can — and should — discuss why what we did was different from those guidelines. Patients were randomly assigned after the PCI had been started on their infarct-related artery. If there was a lesion in the non-infarct-related artery that was more than 70% in a single plane or more than 50% in orthogonal planes, patients were randomly assigned to either treating the infarct-related artery alone and leaving any other significant stenosis or to treating both, preferably at the same session so the patient didn’t have to come back and have a second puncture. The interventionist could defer it if clinically he or she felt it was right to do so. I deferred one case when it was 2:00 AM and the team was tired. It was a right coronary artery occlusion, a significant stenosis in the circumflex artery.

Dr. Montalescot: So, the other lesion would be treated but not in the same sitting?

Dr. Gershlick: It had to be done during the same hospital admission, and in 59% of patients, it was done at the same sitting. We preferred to do it in the same sitting because we might have lost patients who did not want to come back and also because we wanted to shorten the length of stay.

We didn’t want patients to have more than one puncture. There were all sorts of reasons why we wanted to do it during the same admission.

These were significant stenoses. The randomization was different from some of the other trials in that it was done while the infarct-related artery was being treated. In PRAMI,[3] the infarct-related artery treatment was finished, and then randomization was done, so there could have been a degree of selection.

Total Revascularization Cuts MACEs in Half

Dr. Montalescot: How many patients were there? What did you find?

Dr. Gershlick: We planned for 144 patients per group, based on the Politi data.[4] There were some crossovers. It was an intent-to-treat protocol, and I have some per-protocol/per-treatment analyses as well. We found a 55% reduction in composite major adverse cardiac events (MACEs) at 12 months in patients who had complete revascularization at the time of their index admission. This was across the board. There was as much difference in hard endpoints — death and myocardial infarction — as there was in revascularization. It’s always different with open trials involving revascularization when the patient [and physician] knows they still have a lesion. We did a subanalysis looking at only the hard endpoints, and they were still significantly different, regardless of concerns about revascularization and objectivity.

The hazard ratio was 0.45 with a P value of .009 across all endpoints.

Dr. Montalescot: That is good.

Dr. Gershlick: It is interesting. It’s difficult because it prevents us from understanding the mechanism when you see differences across all composite endpoints. But we do have some cardiac magnetic resonance substudy data. We have a nuclear substudy that we put in at six weeks for safety, so that patients with a high ischemic burden weren’t left, but we nested it. We didn’t look at it unless we were notified by the core lab that there was more than 20% ischemic burden.

Dr. Montalescot: The curves diverged quite rapidly, didn’t they? The advance in this control arm occurred when — within the first two weeks, three weeks, four weeks?

Dr. Gershlick: We did the analysis with the Kaplan-Meier curves up to one month. Although the P value wasn’t significant at .055, it told me that if you look at the curves, there is early divergence across all the endpoints. No one thing in particular caused this early divergence. But it tells you, although this is all speculative because it’s a small study, that if you decide to bring the patient back in two months’ time to treat the non-infarct-related artery stenosis, you may have missed your chance because the divergence with these curves was very early.

No Safety Issues

Dr. Montalescot: Many times, we would take the patient back to the cath lab two or days later. This is different from what you did in the control arm, right?

Dr. Gershlick: You could do that. Is there another study where you randomize to treating at the time or doing it within two or three days? I don’t think so. Clinicians know when not to do something at the time of the primary PCI. If you had a patient, you would know immediately. The blood pressure is a little low. The patient is a bit peaky. It’s complex. You have spent time on the primary, but there is a tight stenosis somewhere else. You wouldn’t do it at the time. We don’t need to do that trial. There are other trials that need to be done, such as fractional flow reserve for determining stenosis, doing nothing vs doing it at admission vs stage. Other trials have asked slightly different questions, such as doing nothing vs a staged procedure, but they may have missed the in-hospital patient.

Dr. Montalescot: Did patients in your control group receive medications including antiangina agents?

Dr. Gershlick: Yes. We had a very high incidence of secondary prevention medications — 98% were on antiplatelet therapy or beta blockers, and 100% were on statins. It was very good. One of the pleasing things about the study is the optimal medication arm — we can’t be criticized there. Then we waited. Obviously we had a data and safety monitoring board (DSMB). Unlike PRAMI, the trial was not interrupted. The DSMB let us continue to the end of the study. That was very useful — we were not exaggerating the effect by stopping the trial early.

Dr. Montalescot: Did the physicians feel confident in leaving 98% stenosis in the contralateral artery?

Dr. Gershlick: We reassured them by having the MPS. We don’t know the results of the MPS yet because it’s still being analyzed. We know that no patients had more than 20% ischemic burden because no one was informed by our independent callout that such a situation needed to be addressed. These are hard studies. I take my hat off to all of the physicians who were prepared to leave the 98% right coronary artery stenosis because no trial existed previously to tell us that we shouldn’t do that. PRAMI had been completed. There were no safety issues in doing both lesions at the same time, even though it was a longer procedure and it was more dire, but it was not associated with any excess bleeding or contrast-induced nephropathy — no safety issues at all.

A Change in Thinking

Dr. Gershlick: This was in contrast with data from many of the previous registries[5,6] that said that this approach was associated with harm. I suspect that the reason for those findings (which led to the American guidelines giving this a class III indication) was selection. We are taught that patients with cardiogenic shock(although we had very few cases because they shouldn’t be included) need total revascularization. If a sick patient comes in, we do everything. If you look at the registry data, many of the patients who had complete revascularization were sicker. Only approximately 20% of patients in the registries had complete revascularization initially. That suggests that they may not have died because they had complete revascularization but because they were sicker, which led them to do the revascularization.

It has changed my thinking. People who are better at this than me will decide about guidelines, but for now, we have two trials with very strong signals.

Dr. Montalescot: Two trials from your country, PRAMI and CvLPRIT, say that we should look very carefully at these other coronary arteries and probably treat them rapidly.

Dr. Gershlick: One would believe that you would now question leaving a tight stenosis in a non-infarct-related artery. They are not the same as stable patients.

Dr. Montalescot: While awaiting the change in the guidelines, what are you going to do tomorrow? Are you going to treat all of the arteries in the same sitting? Or are you going to take the patient back to the cath lab the next day?

Dr. Gershlick: It depends. We can only be guided by the evidence base. If people believe that this is part of the evidence base, then we have to be guided by it. It’s not the whole evidence base — it’s a small part of it. We should dampen down any extreme views about this.

What would I do tomorrow? If my patient had a blocked left anterior descending artery, with a very tight right coronary artery, I would treat it at the time unless the patient wasn’t doing well. It’s always easier to do things in trials than it is in real life. We have to believe the evidence. This was a very robust trial, independently funded by the British Heart Foundation and the National Institute for Health Research. We had an independent clinical trials unit and an independent Chair of the Steering Committee, with lay membership. I was very “hands-off” during this trial.

Dr. Montalescot: It is beautiful work. Congratulations to you and the others. I’m sure that it is going to have an impact on the guidelines. Thank you very much.

Dr. Gershlick: Thank you.

Four-Month Moxifloxacin Regimens Less Effective for TB Treatment .

In a randomized, controlled trial, two 4-month moxifloxacin regimens were both inferior to the standard 6-month regimen.

The need to treat tuberculosis (TB) patients with 6-month drug regimens creates problems with adherence, adverse effects, and cost of care. The finding that moxifloxacin has antimycobacterial activity has raised the possibility that use of this agent might shorten treatment duration.

In a recent multinational, randomized, placebo-controlled, noninferiority trial involving 1931 adults with newly diagnosed, previously untreated, drug-sensitive TB, researchers compared the standard 6-month regimen (8 weeks of ethambutol/isoniazid/rifampin/pyrazinamide, followed by 18 weeks of isoniazid/rifampin) with two 4-month moxifloxacin-based regimens — one isoniazid-based (8 weeks of moxifloxacin/isoniazid/rifampin/pyrazinamide followed by 9 weeks of moxifloxacin/isoniazid/rifampin and 9 weeks of placebo) and the other ethambutol-based (8 weeks of moxifloxacin/ethambutol/rifampin/pyrazinamide followed by 9 weeks of moxifloxacin/rifampin and 9 weeks of placebo). The predefined definition of noninferiority was a <6% between-group difference in favorable treatment outcomes within 18 months after the end of treatment.

Conversion to culture-negative status occurred more quickly with the moxifloxacin regimens than with the standard one. However, per-protocol analysis showed that both moxifloxacin regimens were inferior to the standard regimen: Favorable outcome rates were 85% with isoniazid-based moxifloxacin, 80% with ethambutol-based moxifloxacin, and 92% with the standard regimen. The most common reason for an unfavorable outcome was relapse after conversion to culture-negative status. Comparable results were found in a modified intention-to-treat analysis.


Although one could imagine other 4-month moxifloxacin regimens that might be investigated, the present results discourage studying them at this time. A key finding of this trial is that the shorter time to culture conversion seen with the moxifloxacin regimens did not accurately predict long-term outcomes. A better understanding of why this occurred is needed.

– See more at:

7 Ways You’re Sabotaging Your Workout

Exercise can reduce your risk of heart disease, cancer, and depression, and it can increase your energy levels, help you think clearer, and even slow down the aging process. However, there are pitfalls that can hamper your workout progress.

I was guilty of mistake #3 and #4 below. For thirty years, my only form of exercise was long distance running with little to no strength or interval training.

As noted in the featured CNN article,1 your setbacks may be due to certain bad habits, and by nipping them in the bud you can start reaping results again. Here, I’ve chosen seven common mistakes that may be thwarting your fitness efforts.

Mistake #1: Skipping the Warm-Up

While you can get away with skipping the warm-up when you’re doing a low to moderate impact workout, not warming up can easily lead to injury when you’re doing high-intensity interval training (HIIT) exercises, especially sprinting.

As noted by John Paul Catanzaro, a Certified Kinesiologist and exercise physiologist, it takes 10-15 seconds of muscular contractions to raise your body temperature by 1°C, and a proper warm-up should raise your body temperature by 1-2°C (1.4-2.8°F).

This is enough to cause sweating, and is really all that’s required in terms of warm-up. So, all you really need are a few repetitions of motions that increase the blood flow to the appropriate muscles. Aerobic activity isn’t necessary, and will actually take longer as its target is non-specific.

A more comprehensive list is included in Catanzaro’s original article, but here are a few examples of simple movements that will get your blood flowing. Start slow and shallow and gradually increase speed and range with each repetition; 5-10 reps per movement are all you really need:

  1. Squat
  2. Side bends
  3. Trunk twists
  4. Arm circles
  5. Shoulder shrugs

Whether or not you really need to stretch before your workout is another source of confusion for many. The answer really depends on the type of exercise you’re about to do—in some cases it’s very important, and in other cases it may even be contraindicated.

For example, a study published in The Journal of Strength and Conditioning Research2 concluded that stretching should be avoided prior to strength training, noting that the passive stretches may impair strength by causing joint instability.

In other instances, such as when you’re doing high intensity sprinting exercises, prior stretching is imperative, and should NOT be skipped. Failing to stretch in this case can easily lead to injury. For a demonstration of proper stretching technique, please see the following video.

Mistake #2: Not Feeding Your Muscles After a Strenuous Workout

One way to boost your fitness results is to work out while fasting. When you exercise in a fasted state, it essentially forces your body to shed fat, as your body’s fat burning processes are controlled by your sympathetic nervous system (SNS), and your SNS is activated by exercise and lack of food.

Intermittent fasting calls for you to exercise in late morning or early afternoon, and fasting (or eating only light raw foods, vegetable juice, and/or whey protein, or eggs) until 30 minutes after your workout. If you have trouble exercising on an empty stomach, you can include 20 grams of a fast-assimilating protein like a high-quality whey protein concentrate 30 minutes before your workout.

Of course, a number of individual factors play a role in whether it’s appropriate to exercise while fasting, such as your age, when you last ate, whether or not you’re pregnant, taking medications, your medical history, level of fitness, and the type of workout you engage in.

That said, it’s important to remember that whether you’re fasting or not, you do need to eat something after exercising. This is particularly important if you’re doing strength training, in which case you need to eat  a fast assimilating protein within 30 minutes after your workout. Whey protein is a useful option here.

After a cardiovascular workout, wait 30-45 minutes, and then consume a high-quality source of protein (whole food) and vegetable-type carbohydrate. An example would be a spinach salad and some chicken.

After a resistance/strength training workout you need a different approach. The meal after a resistance workout needs to be absorbed rapidly to help repair your damaged muscles. As a general rule, you have a one hour window of opportunity to shuttle in the required nutrients. Ideally, you’ll want to eat your post workout meal around 15-30 minutes after an intense weight training session.

If you miss this one hour window after your intense workout, your muscles’ ability to repair themselves and grow bigger and stronger significantly diminishes. What makes whey protein such an ideal choice here is that it does not require your stomach and digestive tract to work very hard to assimilate it.

Your digestive tract is very vascular and uses significant amounts of blood to do its job. But after a strenuous workout, much of your blood is in your muscles. As a result, your digestive system doesn’t have an adequate amount of blood to digest a whole lot of food. The whey protein, however, is already pre-digested so it’s rapidly absorbed.

Mistake #3: Concentrating on a Single Body Area, and Working in a Limited Range of Motion

It’s wise to think of your body as a composition of symmetry, and focusing on certain movements and muscle groups while excluding others can cause imbalances. This in turn can lead to reduced balance and weaknesses in certain areas, such as your back, for example. You could say your body is only as strong as its weakest link.

As noted in the featured article: “Muscle imbalances can lead to overuse injuries, such as PCL tears from quad dominance, which will keep you out of the gym for a minimum of nine months.”

High intensity exercises can make a dramatic difference here, because these exercises automatically help create muscle definition all over your body, while simultaneously improving your aerobic fitness.

While I don’t recommend doing just one form of exercise, IF that’s all you have time for, then doing short but high intensityPeak Fitnessexercises will give you the greatest all-around benefits, and this form of exercise differs from others in that it benefits your entire body.

High intensity exercises sequentially recruit all types of muscle fibers, starting with the smaller motor units made up of slow-twitch fibers—which are primarily aerobic in metabolism, have a lot of endurance, and recover quickly—to the intermediate fibers; followed by the fast-twitch fibers. The key to activating your fast-twitch muscle fibers is intensity, or speed.

When these muscles are recruited, it creates the stimulus needed to grow muscle. At the same time, it enlarges the glucose storage reservoir in the muscle, which in turn enhances your insulin sensitivity. I’ve often stated that normalizing your insulin is one of the primary health benefits of exercise, and this is particularly true in the case of high-intensity exercise. Conventional aerobics does not do this as efficiently. Activating your fast-twitch fibers also prompts your body to create human growth hormone (HGH), also known as “the fitness hormone,” which plays an important role in slowing down the aging process.

Another common mistake relates to range of motion, which is also important for overall functioning, balance and movement in everyday life. When performing strength exercises using weights, it’s important to employ a full range of motion. One example offered in the featured article is when someone tears a knee ligament simply by stepping off a curb. This could be the result of not doing full-depth squats. Basically, your body is unaccustomed to stabilizing your knee during motion outside the limited range of a partial-depth squat. The other side of the coin here is avoiding using heavy weights beyond your normal range of motion. Doing so will place you at risk of injury as well. So, when you start out, use a weight that allows you to perform the exercise through a full range of motion, without overstraining.

Mistake #4: Training Too Long and Too Frequently

Exercising too much, either by working out too long or too frequently, can backfire in a number of ways. Many fail to appreciate the importance of recovery between sessions, and research has shown that endurance training can do more harm than good in the long run. As noted in the featured article: “A common physiological response to training is the release of certain hormones into the bloodstream, such as testosterone and dopamine. Going past 45 to 55 minutes per workout can put the body into a negative hormonal state.” Adrenal fatigue and reduced performance can result when you exercise excessively.

To maximize your workout efforts, it is important to strive for that “Goldilocks’ Zone” where you’re pushing hard enough to challenge your body at your current level of fitness, while allowing your body to recuperate in between. Recovery is particularly important when you’re doing high intensity exercises. When you work your fast-twitch fibers, it takes about 48 hours for that fiber to heal and fully recover. This is twice the recovery time needed for long and slow exercise. An equation to keep in mind is that as intensity increases, frequency can be diminished. In fact, you need to allow your body to fully recuperate in between sessions, so it’s NOT recommended to do high intensity exercises more than three times a week.

Both Phil Campbell and Dr. Doug McGuff have addressed this in previous interviews. If you don’t allow your body to fully recuperate and rebuild, your efforts will not pay off beneficial dividends. Remember, while your body needs regular amounts of stress like exercise to stay healthy, if you give it more than you can handle your health can actually deteriorate. So it’s crucial to listen to your body and integrate the feedback into your exercise intensity and frequency. The following seven symptoms may signal that you need to cut back a bit and allow your body to recover between sessions:

  1. Exercise leaves you exhausted instead of energized
  2. You get sick easily (or it takes forever to get over a cold)
  3. You have the blues
  4. You’re unable to sleep or you can’t seem to get enough sleep
  5. You have ”heavy” legs
  6. You have a short fuse
  7. You’re regularly sore for days at a time

So, how do you know if you’re sufficiently recovered from your exercise? One tip gleaned from Dr. Doug McGuff is that you know you’re recovered when you have that restless energy and feel like you have to engage in some type of physical activity. You will just want to work out.

Mistake #5: Inadequate Sleep

I believe it is very important to strive for eight hours of sleep. That does not mean time in bed. Many fitness trackers like UP24 can help you determine how long you are really sleeping, but it is likely more than 30 minutes less than you think you are. While I do recommend exercising first thing in the morning, I don’t advise sacrificing sleep to do so. A high intensity interval session only requires about 20 minutes or less, two or three times a week, opposed to an hour or more on the treadmill, several times a week. Most people can carve out 20 minutes without losing sleep over it. Getting enough sleep is an important aspect of health, and lack of sleep can hamper weight loss efforts and contribute to a wide range of health problems.

Disrupted sleep cycles have the potential to stimulate cancer growth by altering hormone levels, such as melatonin, for instance, showing just how important it is to regulate your circadian rhythm. It’s commonly suggested that it’s best to avoid exercising late in the evening, as the increases in your adrenaline levels, heart rate, and body temperature may keep you from falling asleep. Without a doubt, many are sensitive to late-night exercise, such that a vigorous session will keep them awake. For others, it can have the opposite effect, so you’ll have to experiment to find what works best for you.

Mistake #6: Talking Too Much

While having workout buddies are a great way to keep motivated and help each other stay accountable, constant chatter can reduce your fitness payout in the gym. As noted in the featured article, “talking during a workout can decrease the metabolic, or fat burning, effect of your workout… The reason? When rest intervals increase, ‘the body will cool down, leading to a slowed metabolism,’ [New York-based trainer Nick] Ebner says. Also, talking during a set of squats and shifting your focus from the exercise form to the conversation “can lead to form breakdown, and in turn, serious risk of injury…”

In short, talking while exercising can lead to, or worsen, mouth breathing, and this has consequences for your health and fitness. In fact, the amount of benefit you derive from your exercise efforts is largely controlled by your breathing habits, which affect your performance, endurance, post-exercise energy levels, and even your ability to metabolize fat. The Buteyko Breathing Method—named after the Russian physician who developed the technique—is a powerful methodology for reversing problems associated with improper breathing, the most common of which are overbreathing and mouthbreathing.

The Buteyko Method teaches you how to bring your breathing volume back toward normal, reversing chronic hyperventilation or chronic overbreathing. When your breathing is normal, you have better oxygenation of tissues and organs, including your brain. This is particularly important during exercise. If you tend to hyperventilate through your mouth during exercise, you’re actually decreasing oxygen delivery.

The key here is to breathe through your nose, not your mouth. Nitric oxide is found in your nose, so when you breathe through your nose, you carry a small portion of the gas into your lungs. Nitric oxide plays a significant role in homeostasis, or the maintaining of balance within your body. It’s also a significant bronchodilator and vasodilator. The elasticity of your lungs also depends on nasal resistance, which you only get from nasalbreathing due to the smaller diameter of your nasal passages. Poor breathing is even associated with poor posture. So, breathing through your nose helps maintain your health in a number of important ways.

Mistake #7: Using Incorrect Form

Proper form is essential for most exercises. Done incorrectly, virtually any exercise can lead to injury. At best, you’ll end up with inferior results. So, make sure you get some guidance on how to perform each exercise correctly. The better your form is, the more effective your workout will be, and the faster you’ll see results. One of the key ingredients of proper form is to engage every single muscle to its full potential. This requires some mental focus, and not just half-heartedly going through the motions.

As just one example, when doing a controlled deep squat, you’ll engage not just your thighs and knees, but your entire core, back and muscle fibers throughout your legs and buttocks all the way down to your ankles and feet. Squats have long been criticized for being destructive to your knees, but when done properly, squats actually improve knee stability and strengthen connective tissue. As you can see, there are many ways to negate your efforts in the gym. But the solutions are there, and they are usually quite simple. Being mindful of these mistakes, and correcting them, can help you maximize your results.

Why male birth control is a million disasters waiting to happen.

It was 100 degrees out but I couldn’t stop shivering. I wore two shirts, jeans, and a heavy hoody but was still colder than I had ever been in my life.

Several months prior to the chills I started to have trouble sleeping. The urge to urinate woke me up about every two hours. I woke up about four times a night to take a piss. Each time hardly anything would actually come out.

At first I wrote it off.

Maybe I’m drinking too much water before bed, I thought. After all, I did drink tons of water throughout the day.

Then I started having problems urinating during the day. I’d whip it out to piss and then…nothing. Sometimes it’d be a full minute until I could actually get a stream going.

The pain started a few weeks later. It felt like a burning-hot screwdriver was being shoved up my phallus every time I tried to pee. There was pain even when I didn’t go to the bathroom. The sensation was as if everything beneath my stomach was crammed into a blender, torn apart, and then lit on fire. There was also pain in my sides. I don’t have quite as dramatic an explanation for that pain. If you’ve ever been punched before, imagine that but coming from the inside.

Regular visits to the gynecologist are essentially a must for a woman. While this has to suck, the upshot is that it forces them to understand their sexual health and reproductive health better than any man understands their own. It also, presumably, makes them less afraid of invasive tests since they have to endure them on a semi-regular basis. That’s why I put off going to the urologist for so long, because I was afraid of getting a tube put in my dick. Eventually, I couldn’t stand the pain and constant chills anymore, and I saw the doctor.

The doctor said I had a severe bacterial kidney infection that spread to the bladder and prostate—so basically a kidney infection, a urinary tract infection, and prostatitis.

I took the most powerful antibiotics they’re allowed to prescribe and after a while the pain went away…but the nocturia (getting up to pee a lot during the night) and the long delay before urinating. I went back to the doctor and he said the bladder muscle had become spastic and overactive as a result of the prolonged infection.

He prescribed a medicine to help me with my symptoms. I can’t remember the name, but I know it belonged to a class of medicines calledAlpha Blockers.

“One thing about this medicine,” the doctor said as he typed the prescription into the computer. “There’s a chance it can cause retrograde ejaculation.”

“Um…what?” I asked. I obviously knew what ejaculation meant but “retrograde” could’ve meant anything.

“Dry orgasms. No seminal fluid,” he said. In more specific terms, retrograde ejaculation is when semen gets sent into the bladder rather than out into a sock, condom, or, if you’re lucky, a crevasse belonging to your significant other.

I was weirded out but he said there was only a chance, right? So that meant there was a chance it didn’t cause retrograde ejaculation.

This pathetic bit of self delusion lasted until my first jerk-off session on the medicine. I felt the familiar build-up of pleasure and tension (I call it plension) and then… nothing. Not only was there no semen, there was no electric rush, no hip-bucking, and no release.

After about a month of this, I asked to switch to a different medicine. As far as I knew, that’d be the last time I’d ever have to think or hear about dry orgasms and retrograde ejaculation.

I was wrong.

Male birth control is swift becoming a highly discussed issue among social justice circles and the Internet in general.

One proposed method of male birth control is the use of alpha blockers to intentionally cause dry orgasms. Another, more recently publicizedstrategy is using gel to block the vas deferens—the tube sperm travels through—thereby preventing sperm from ever coming out of the penis (forgive the pun). The latter product could be available in three years.

The Daily Beast’s Samantha Allen, who is also a frequent contributor at the Daily Dot, noted that male birth control could have a multitude of wondrous impacts on society, and would greatly aid women since they would no longer be subject to the deleterious affects of The Pill.

Allen’s interpretation of the facts is accurate, but it paints too rosy a picture. The coming wave of male birth control will make conversations about reproductive health more vitriolic and hateful, not less.

First, insertion of gel into the vas deferens is an invasive procedure—far more invasive than popping a pill every day. A significant percentage of America’s 150 million-plus men will not go for it no matter how economical it is or how beneficial to society it is. American culture is too patriarchal and while #NotAllMen are this selfish, most are.

The bigger concern, however, isn’t the procedure but the dry orgasm.

“Dry orgasm” is a misnomer. Yeah it’s dry, but calling it an orgasm is just wrong. My dry “orgasms” felt like being 12 again—old enough to get a boner looking at porn illegally downloaded from Napster but not actually old enough for your member to spew forth any precious fluids.

I’m not alone in realizing that dry orgasms remove pleasure from sex. Astudy performed in 2009 found that “a strong decline in ejaculatory volume is associated with reduced sexual pleasure” when they gave men alpha blockers. The study noted the men were “greatly dissatisfied with the ejaculatory dysfunction” from the alpha blockers.

I lost all sex drive almost immediately once I started having dry orgasms. I didn’t even respond to a “booty call” I got while I was on the alpha blockers because I just didn’t care. What was the point of having sex if I knew I was incapable of enjoying it?

Cynics and jokesters would say “Well, if male birth control reduces libido then mission accomplished: No kids!”

Birth control isn’t just a preventative measure; it enables people to fully enjoy sex while avoiding the grave biological and financial consequences of sex. Male birth control, however, prevents pleasure as well as pregnancy.

Look, I’m not a men’s rights activist. I’m not trying to say women should be subjugated and forced to take the pill for as long as they live. I’m just saying that male birth control is highly imperfect. If you’re expecting it to take the world by storm in 2017, don’t. Once the first crop of men feel what a dry orgasm is like, it’ll start a new culture war. Imagine the GIF vs. JIF debate, but 10,000 times worse because it’ll be filled with more hate and it’ll be an issue that actually matters.

I guarantee you there will be a contingent of men comparing male birth control to female circumcision in that it robs both groups of pleasure. The web will be inundated with articles just like this one explaining just how awful male birth control is for men’s sexual health. And maybe we don’t deserve sexual health for all the atrocities we’ve committed against females, but good luck convincing America of that.

This birth control innovation isn’t a solution, it’s 150 million problems waiting to happen.

Will the ‘God particle’ destroy the world?

World-famous physicist Stephen Hawking recently said the world as we know it could be obliterated instantaneously.

Basically, we would be here one minute and gone the next.

A proton-proton collision produced in the Large Hadron Collider shows characteristics in line with the decay of a Higgs boson particle.

Don’t you love physics? When we speculate about catastrophes, we don’t mess around.

The physics underlying this speculation is related to the Higgs particle, whose discovery was announced July 4, 2012, at the Large Hadron Collider, the world’s largest particle accelerator, in Geneva, Switzerland.

A leading physicist dubbed it the “God particle” — a name I wish would disappear, as the particle and the laws of physics tell us nothing whatsoever about God, and God, if she exists, has not opined about the Higgs particle.

So, the simplified argument goes like something like this — the Higgs particle pervades space roughly uniformly, with a relatively high mass — about 126 times that of the proton (a basic building block of atoms). Theoretical physicists noted even before the Higgs discovery that its relatively high mass would mean lower energy states exist. Just as gravity makes a ball roll downhill, to the lowest point, so the universe (or any system) tends toward its lowest energy state. If the present universe could one day transition to that lower energy state, then it is unstable now and the transition to a new state would destroy all the particles that exist today.

This would happen spontaneously at one point in space and time and then expand throughout the universe at the speed of light. There would be no warning, because the fastest a warning signal could travel is also at the speed of light, so the disaster and the warning would arrive at the same time.

We know spontaneous events do happen. The universe began in a rapid expansion called inflation that lasted only a tiny fraction of a second. We owe our existence to that sudden event.

Spontaneous change is something you might have seen in chemistry class. Super-cooled water will rapidly crystallize to ice if you drop a snowflake into it, just as a salt crystal will grow when added to a supersaturated salt solution.

Back to the universe. Whether the existence of Higgs boson means we’re doomed depends on the mass of another fundamental particle, the top quark. It’s the combination of the Higgs and top quark masses that determine whether our universe is stable.

Experiments like those at the Large Hadron Collider allow us to measure these masses. But you don’t need to hold your breath waiting for the answer. The good news is that such an event is very unlikely and should not occur until the universe is many times its present age.

Probability is the key. Many bad things are possible A large asteroid destroying the Earth. Getting hit by a bus. Having space time gobbled up by instability in the Higgs field. (For an engaging discussion of the many ways humans can be done in by the cosmos, see the marvelous “Death from the Skies!” by Bad Astronomer Phil Plait.)

Are they likely? Humans have to prioritize by considering both outcome (death or destruction) and probability.

Rare events like the collision of a massive asteroid with the Earth could destroy life as we know it and perhaps the planet itself. However, the chances of a sufficiently massive asteroid intersecting the Earth in the vast emptiness of space is pretty low. Collisions with much less massive asteroids are much more likely but much less destructive.

So don’t lose any sleep over possible danger from the Higgs boson, even if the most famous physicist in the world likes to speculate about it. You’re far more likely to be hit by lightning than taken out by the Higgs boson.