Colonoscopy: Up Your Chances of Finding Flat Polyps.


Skilled doctor needed to spot all polyps in colonoscopy

It’s hard to say precisely how common flat polyps are because results are subject to variation between examiners and techniques. But doctors performing colonoscopies are finding them more easily and treating them more successfully as techniques improve.

Today, the incidence of flat polyps hovers around 10 percent. Still, they too often go undetected and unrecognized simply because they are, literally, flat, says colorectal surgeon Emre Gorgun, MD.

Intestinal polyps

“Endoscopists and surgeons may not consider flat polyps common at all, but in reality, if you recognize them early on, you will see how common they are,” Dr. Gorgun says.

“They tend to be under-recognized by inexperienced endoscopists or people untrained in removing that specific polyp. Usually endoscopists aren’t trained to notice them, and their eyes are more used to recognizing lesions emerging from the surface level.”

Well-trained doctor is key

There are some endoscopists, on the other hand, who recognize flat polyps but are not necessarily comfortable with treating them. For these cases, they will give patients a referral.

But the only step patients can take to ensure detection is to make sure they have a skilled endoscopist when they go in for a colonoscopy in the first place, Dr. Gorgun says. That’s especially important because flat polyps can grow and, eventually become cancerous, he says.

“Patients definitely should pick someone known for screening endoscopy as well as interventional endoscopy,” Dr. Gorgun says, adding that most Cleveland Clinic endoscopists are well trained in this area.

“Common endoscopists may not be skilled to recognize those flat polyps. It’s better to have a colonoscopy done at a good facility, which has physicians on board capable of recognizing and removing them.”

ESD and other removal techniques

A couple years ago, Dr. Gorgun helped pioneer an approach to remove flat polyps called endoscopic submucosal dissection (ESD). He’s still one of just a few physicians who perform this technique, which he learned in Tokyo where it’s more commonly performed.

Typical colonoscopy involves tying a snare around the polyp and cauterizing and cutting the tissue off, but the snaring technique doesn’t work with flat polyps, he says.

Instead, with ESD, endoscopists dissect the polyp, using a solution to lift, cut and burn the unwanted tissue, or sometimes they even create a tunnel underneath it to take it out in one piece.

“This allows you to remove these polyps oncologically, without destroying the tissue around them and without having to take out the whole colon,” Dr. Gorgun says.

Other techniques for removing polyps include:

  • Snare polypectomy, the classic polyp removal technique that most endoscopists use
  • Endoscopic mucosal resection (EMR), which combines the snaring technique with a solution, as in ESD
  • Endoscopic full-thickness resection (EFTR), which involves removing the colonic wall that contains the polyp and closing the opening internally, with clips, so there’s no need for a bowel resection

Natural News Blogs Read this Before Pigging Out on Dominos Pizza.


So how does one stoop lower in standards than McDonalds, Burger King and Wendys? Before you dial up Domino’s for your next pizza, you need to read this.  Regardless of whether you are a vegan, animal activist or absolutely can’t live without your big juicy steaks, I’m certain we all will agree that the behavior described below needs to be stopped.

Other fast food places have at least had the decency to stop the practice of using gestation crates for their pregnant pigs but Dominos still allows them.

image

Pregnant pigs are kept in gestation crates for about four months of pregnancy, their piglets are taken away after just a few weeks and then the pigs are impregnated again and forced into gestation crates for another cruel cycle. This madness goes on for years until the poor pigs are so worn down that her best use for the industry is slaughter. Companies like Domino’s should not tolerate this and consumers should not buy the product of such horrific suffering.

Whether you’re a vegan, vegetarian, the biggest carnivore on the planet or somewhere in between, please join us in asking Domino’s to do the right thing and stop using these cruel gestation crates.

McDonald’s even said it “believes gestation stalls are not a sustainable production system for the future,” and that there “are alternatives that are better for the welfare of sows.”

If all these huge companies can commit to getting rid of gestation crates, why is Domino’s unwilling to listen to the rest of the industry and consumer demand? Will ham, sausage, and pepperoni taste any different without this extreme cruelty? I doubt it!

More Alpha-Synuclein in Spinal Fluid Linked to Faster Cognitive Decline


Alpha-synuclein — the protein that clumps in the cells of Parkinson’s patients — is currently the major focus of Parkinson’s biomarker studies. Researchers are analyzing biosamples (spinal fluid, blood, tissue) to make a connection between alpha-synuclein and risk, onset or progression of Parkinson’s disease (PD). The latest findings, published in The American Journal of Pathology, report that patients with higher levels in spinal fluid experienced faster cognitive decline.

In a project funded by The Michael J. Fox Foundation (MJFF), Jing Zhang, MD, PhD, and his team at the University of Washington in Seattle examined samples and data from PD patients obtained in the DATATOP study. Led by the Parkinson’s Study Group in the late 1980s, the deprenyl and tocopherol antioxidative therapy of parkinsonism (DATATOP) study collected samples and clinical data from PD subjects for up to eight years.

In this latest analysis, researchers compared alpha-synuclein levels to scores from tests of cognition, such as verbal learning and memory, visuospatial memory and processing speed, among 304 PD patients. They found that patients with higher levels of alpha-synuclein in spinal fluid had faster cognitive decline.

“This is a surprising conclusion,” says Mark Frasier, PhD, MJFF vice president of research programs. “One would think that people with more cognitive problems would have less alpha-synuclein in spinal fluid because more would be caught up in the brain causing those problems.”

Zhang’s group also reported that while alpha-synuclein levels decreased significantly over two years, that decline could not predict motor symptoms. These findings join a list of observations about how alpha-synuclein in spinal fluid relates to PD. Initial analysis from the MJFF-sponsored Parkinson’s Progression Markers Initiative (PPMI) reported last year that PD patients had lower alpha-synuclein levels in spinal fluid compared to controls. They also found that patients with posture/gait disturbance averaged lower alpha-synuclein than patients with tremor-dominant PD.

Further investigation into alpha-synuclein continues in PPMI and other studies. Zhang and his coauthors cited PPMI as a potential source for validation of their cognition findings. Since PPMI includes healthy controls, researchers could test whether those results are PD-specific or seen in healthy aging adults with cognitive decline, too.

To accelerate research around PD biomarkers, MJFF spearheaded an effort to make data and samples from varied Parkinson’s studies available to investigators. The Foundation also offers funding to use the data and samples, such as to Zhang for the DATATOP analysis.

Engineering team designs ‘living materials’


Justin Barone may just be a modern day alchemist.

But instead of turning ordinary metals into gold, he makes synthetic fibers that reproduce according to a genetic code embedded in their DNA.

“We live in a world today where we’re not stuck with what nature gave us,” said Barone, an associate professor in the Department of Biological Systems Engineering, which is in both the College of Agriculture and Life Sciences and the College of Engineering. “We decided we could start making our own proteins to create better fibers in the lab.”

Barone’s research seeks to make the fibers replicate and assemble of their own volition depending on the genetic code that is used to create them. His research could potentially be used to create muscle fibers and entire limbs in the future.

Knowing the genetic recipe of a fiber allows Barone to control the shape of the fiber and how much the proteins should interact with each other. By programming the proteins to interact with each other more, it’s possible to make a fiber tougher and stronger. If proteins are programmed to interact less, they are more pliable.

Barone’s lab is located in the new Human and Agricultural Biosciences Building 1, an airy building, with brand new laboratory facilities, natural lighting, and a large, open atrium entrance.

“You are inspired right as soon as you walk inside,” he said.

The larger lab space will help garner interest from industry for Barone’s other research endeavors that use keratin products like chicken feathers, animal hooves, and corn and soybeans to make biodegradable plastics.

“You have to show that you can do something in a lab on a large scale to get people interested,” said Barone. “It’s hard to show someone something in a beaker. We finally have the space we need to bring someone into a lab and show them we are processing large amounts of biomass — such, 10,000 pounds of corn an hour — and really show them how it works.”

Barone likes using chicken feathers and other keratin-based fibers because they are tough and versatile, and an agricultural waste product. His use of these products also directly benefits the agriculture industry in the state because the products either end up in landfills or in low cost animal feed, so his research could potentially create another revenue stream for farmers.

Who knows? If Barone’s research with chicken feathers becomes widely used, he actually may be somewhat of an alchemist for Virginia farmers by spinning feathers into cash.

Nationally ranked among the top research institutions of its kind, Virginia Tech’s College of Agriculture and Life Sciences focuses on the science and business of living systems through learning, discovery, and engagement. The college’s comprehensive curriculum gives more than 3,100 students in a dozen academic departments a balanced education that ranges from food and fiber production to economics to human health. Students learn from the world’s leading agricultural scientists, who bring the latest science and technology into the classroom.

Death Spreads From Cell To Cell In A Wave: How New Findings Show Old-Age Deaths Happen From Multiple Processes Breaking Down.


In contrast to cell death, the processes leading to an organism’s systemic collapse are less understood. This has prompted researchers to examine the nature of death in one organism’s cells as the necrosis propagates throughout its entire body, the findings for which could shed considerable light on how human death takes place, especially in old age.

nematode

The new study, which comes from theInstitute of Health Aging at University College London, paints death as a wave of cell necrosis that spreads across the body like a cascade. Using nematodes as the basis for their study, researchers examined the way a unique molecule emitted a fluorescent blue light as the worms’ cells died. This molecule is similar to a product of oxidative damage in mammals that have died of old age.

“In the nematode Caenorhabditis elegans, intestinal lysosome-related organelles (or “gut granules”) contain a bright blue fluorescent substance of unknown identity,” wrote theresearchers. “This has similar spectral properties to lipofuscin, a product of oxidative damage known to accumulate with age in postmitotic mammalian cells.”

The researchers’ theory assumes that people in old-age could have multiple processes whose cell pathways are dying and that age-related deaths are effectively the result of parallel waves of cell deaths. Despite not knowing which processes are taking place simultaneously, the findings bode well for understanding the nature of death as a gradual wave because of multiple processes, not a consequence of accumulated molecular damage.

“We’ve identified a chemical pathway of self-destruction that propagates cell death in worms, which we see as this glowing blue fluorescence traveling through the body,” David Gems, the study’s lead author, told Discovery News. “It’s like a blue grim reaper, tracking death as it spreads throughout the organism until all life is extinguished.”

The implications for such a finding suggest the ability to delay death, or even stop it, in cases where infections cause mass necrosis. Old-age death works in ways that are less well-known, so the technique cannot apply.

“We found that when we blocked this pathway, we could delay death induced by a stress such as infection, but we couldn’t slow death from old-age,” Gems said, referring to the stress cells undergo when they’re required to perform at higher intensities than a body is equipped for — extreme temperatures being one example. “This suggests that aging causes death by a number of processes acting in parallel.”

Gems expressed great optimism for the future of studying cell death as it applies to old-age necrosis, as the parallel processes not yet understood could provide groundbreaking opportunities for fighting infections and preserving life into old-age.

“Inhibition of necrosis pathway components can delay stress-induced death, supporting its role as a driver of organismal death,” the researchers concluded. “This necrotic cascade provides a model system to study neurodegeneration and organismal death.”

Source: Coburn C, Allman E, Mahanti P. Anthranilate Fluorescence Marks a Calcium-Propagated Necrotic Wave That Promotes Organismal Death in C. elegans. PLoS Biology. 2013.

His Fertility Advance Draws Ire.


To most people, the word “mitochondria” is only dimly familiar, the answer to a test question in some bygone high-school biology class. But to Shoukhrat Mitalipov, the mysterious power producers inside every human cell are a lifelong obsession.

“My colleagues, they say I’m a ‘mitochondriac,’ that I only see this one thing,” he said recently in his modest, clutter-free office at Oregon Health and Science University. He smiled. “Maybe they are right.”

With a name that most Americans can’t pronounce (it is Shoe-KHRAHT Mee-tuhl-EE-pov) and an accent that sounds like the villain’s in a James Bond film, Dr. Mitalipov, 52, has shaken the field of genetics by perfecting a version of the world’s tiniest surgery: removing the nucleus from a human egg and placing it into another. In doing so, this Soviet-born scientist has drawn the ire of bioethicists and the scrutiny of federal regulators.

The procedure is intended to help women conceive children without passing on genetic defects in their cellular mitochondria. Such mutations are rare, but they can cause severe problems, including neurological damage, heart failure and blindness. About one in 4,000 babies in the United States is born with an inherited mitochondrial disease; there is no treatment, and few live into adulthood.

A healthy rhesus monkey, born at Dr. Mitalipov’s lab after the nucleus of the mother’s egg cell was removed and placed in the egg cell of another female that is healthy.

LEAH NASH FOR THE NEW YORK TIMES

Mitochondria have their own sets of genes, inherited solely from mothers, and women who carry mitochondrial mutations are understandably eager to not pass them to their children. Dr. Mitalipov’s procedure would allow these women to bear children by placing the nucleus from the mother’s egg into a donor egg whose nucleus has been removed. The defective mitochondria, which float outside the nucleus in the egg’s cytoplasm, are left behind.

“It was a major breakthrough,” said Douglas C. Wallace, a professor of pathology and laboratory medicine at the University of Pennsylvania. “He’s an exceptionally talented person.”

But the resulting baby would carry genetic material from three parents — the mother, the host egg’s donor and the father — an outcome that ethicists have deplored.

That specter drew critics from all over the country to a hotel in suburban Maryland late last month, where Dr. Mitalipov tried to persuade a panel of experts convened by the Food and Drug Administration that the procedure, which he has pioneered in monkeys, was ready to test in people.

Stored materials at Oregon Health and Science University’s National Primate Research Center.

LEAH NASH FOR THE NEW YORK TIMES

Some told the officials that the technique could introduce new genetic mutations into the human gene pool. Others warned that it could be used later for something ethically murkier — perhaps, said Marcy Darnovsky, executive director of theCenter for Genetics and Society, “to engineer children with specific character traits.”

Back in his office, Dr. Mitalipov waved off those warnings. Mitochondrial DNA comprises just 37 genes, which direct the production of enzymes and molecules that the cell needs for energy, he noted. They have nothing to do with traits like eye and hair color, which are encoded in the nucleus.

“There are always people trying to stir things up,” said Dr. Mitalipov, an American citizen who grew up in what is now Kazakhstan. “Many of them made their careers by criticizing me.”

The United States is not the only country weighing mitochondrial replacement. In Britain, the government has issued draft regulations that would govern clinical trials in people. If accepted into law by Parliament, such trials, which are how banned, would be allowed to go forward, although regulators would have to license any clinical application.

Dr. Mitalipov’s fixation on mitochondria began in graduate school in Russia in the 1990s. After graduating from an agricultural institute — and a brief, unhappy stint as a manager on a collective farm — he began work on his doctoral thesis at theResearch Center of Medical Genetics, a prestigious state-funded institution in Moscow. He focused on embryonic stem cells, which can be grown in the laboratory and turned into any type of cell in the body.

He noticed a strange thing. When stem cells were extracted from a mouse embryo and put in a petri dish, they stopped aging but remained healthy and growing, as if frozen in time. Somewhere in the cell, it seemed, was a clock that determined its life span.

The search for the clock took him to Utah State University for postdoctoral research in the mid-1990s. He developed an interest in cloning, a process in which the cellular clock is not only stopped but reset. Why, he wondered, do cloned animals have normal life spans?

The answer to the riddle of cellular aging was not to be found in the cell’s nucleus, Dr. Mitalipov concluded, but in the surrounding cytoplasm. In the mitochondria.

“Everything was falling into place in my head,” he said.

As researchers began to suspect defective mitochondria as a cause in more diseases, Dr. Mitalipov wondered whether replacing them might be possible.

Scientists already had experimented with combining genetic material from three people to make a baby. About 15 years ago, researchers in New Jersey injected a bit of cell fluid from donor eggs into the eggs of women who were having fertility problems. Those experiments, which came shortly after the cloning of Dolly the sheep, set off such a uproar that the F.D.A. eventually told researchers that they could not perform them without special permission.

Dr. Mitalipov persevered. At Oregon Health and Science University’s National Primate Research Center, one of eight in the country, he spent years perfecting a way to create monkey eggs with donated mitochondria. He persuaded software developers to adapt a program that would allow real-time viewing of the necessary microsurgery. A special microscope was developed so that human hands, too blunt an instrument on their own, could conduct the operation with joysticks that look like upside-down flashlights.

“He’s just a really practical guy,” said Daniel M. Dorsa, senior vice president for research at the university. “He just nose-to-the-grindstone plowed through and figured out what it took.”

Success came in 2008 in a darkened, hot laboratory room. On April 24, 2009, twin male rhesus monkeys, Mito and Tracker, were born with replaced mitochondria. Later, with some adjustments Dr. Mitalipov replicated the procedure in human eggs. Because of federal rules against genetic manipulation, the eggs were not allowed to mature.

His research has brought persistent criticism. “If these procedures are carried out, it crosses a very bright line,” said Ms. Darnovsky of the genetics center.

She said that the current goal, mitochondrial replacement, may be narrow, but that Dr. Mitalipov’s genetic techniques could lead to broader applications and eventually to a situation in which scientists or governments “compete to enhance future generations,” such as producing soldiers who never need sleep.

Sheldon Krimsky, a bioethicist who attended the F.D.A. meeting on behalf of theCouncil for Responsible Genetics, argues that mitochondrial replacement is simply unnecessary. There are other options for women with mitochondrial defects to have healthy children, such as getting an egg from a donor, or having prenatal genetic diagnosis to find eggs with fewer mutations, he said.

“There’s that genetic chauvinism that says unless my DNA is in the child, it will not be truly my child,” he said.

Would-be parents, on the other hand, have been following Dr. Mitalipov’s work with the intensity of the hungry waiting for food. When he came back from the meeting in Maryland, his inbox contained an avalanche of emails from women with mitochondrial mutations and other fertility problems.

Dr. Dorsa said the university still has not decided whether to formally ask the F.D.A. for permission to move forward with clinical trials.

Dr. Mitalipov, for his part, is determined.

“We are ready now to move on to the next stage,” he said. “Not in 10 years, but in the next few years.”

Ebola outbreak confirmed in Guinea, death toll reaches 59 — RT News


The deadly epidemic, which has killed at least 59 people, in Guinea, West Africa, and could have spread to neighboring Sierra Leone, has been confirmed to be Ebola, according to government officials.

Health workers, dressed in head-to-toe "Ebola suits", leaving in a pick-up truck in Uige, about 300km north of the Angolan capital, Luanda, to collect a man dying from haemorrhagic fever. (AFP Photo / Florence Panoussian)

Following failed attempts by medical experts in Guinea to identify the disease, which started claiming lives six weeks ago, samples of the virus were sent to scientists in the French city of Lyon, who confirmed the virus was Ebola.

The Ebola fever epidemic raging in southern Guinea, including the prefectures of Gueckedou and Macenta, since February 9 has left at least 59 dead out of 80 cases identified by our services on the ground,” the Guinean health ministry’s chief disease prevention officer, Sakoba Keita, announced on Saturday, according to AFP.

The disease, which has diarrhoea, vomiting and bleeding among its symptoms and kills between 25 and 90 percent of those who fall sick, depending on the virus’s strain, has never before been registered in Guinea. It has now been found in three southeastern towns and in the capital, Conakry.

The disease could have also spread to neighboring Sierra Leone, according to World Health Organization (WHO) officials, who reported cases showing similar symptoms there.

A 14-year-old boy died in Sierra Leone’s eastern Kailahun District, reportedly after he attended a funeral in Guinea of one Ebola victim, chief medical officer, Dr. Brima Kargbo said, as cited by Reuters.

The official said a medical team was investigating the death and looking for people the boy might have been in contact with before he died.

The international humanitarian organization, Medecins Sans Frontieres (MSF), announced on Saturday it already had 24 doctors, nurses, logisticians and experts in hygiene and sanitation in Guinea and was further reinforcing its team there.

MSF also said it was flying in 33 metric tons of medicines and equipment and was setting up isolation units in the affected towns in Guinea.

These structures are essential to prevent the spread of the disease, which is highly contagious,” Dr. Esther Sterk, MSF’s tropical medicine adviser, said in a statement. “Specialized staff are providing care to patients showing signs of infection.

Ebola haemorrhagic fever is one of the deadliest viral diseases known to humankind, according to the WHO. There’s no vaccine against the virus and the disease is treated by general supportive therapy.

It was first identified in 1976 in Sudan and Congo. It is believed to have been passed onto humans from sick animals – chimpanzees, gorillas, monkeys, forest antelope, and fruit bats.

The highly contagious virus is transmitted by direct contact with the blood, body fluids and tissues of those infected.

Scientist makes fibers in a bottle | Virginia Tech News | Virginia Tech


http://www.vtnews.vt.edu/articles/2014/03/031914-cals-habbibarone.html#

From the desk of Zedie.

Why dark chocolate really IS good for you: Stomach microbes turn cocoa into a natural drug that reduces blood pressure.


  • Previous studies found dark chocolate reduces blood pressure
  • Now scientists have discovered this is due to how our guts ferment cocoa
  • By breaking down chocolate compounds, microbes produce molecules that act like a natural anti-inflammatory
  • This ‘drug’ enters the bloodstream and helps protect arteries from damage
  • Dark chocolate contains a higher cocoa content than milk chocolate
Dark chocolate, pictured, can reduce blood pressure because gut microbes ferment fibres in cocoa and produce a natural anti-inflammatory

Dark chocolate, pictured, can reduce blood pressure because gut microbes ferment fibres in cocoa and produce a natural anti-inflammatory

Love dark chocolate?

Now you can eat it with much less guilt because scientists have discovered why it is so good for us.

Previous studies have found daily consumption of dark chocolate reduces blood pressure and is good for the heart.

Now scientists have discovered why this happens – and its down to how our guts ferment the fibre in cocoa beans.

Researcher Maria Moore, from Louisiana State University said: ‘We found that there are two kinds of microbes in the gut: the ‘good’ ones and the ‘bad’ ones.

‘The good microbes, such as Bifidobacterium and lactic acid bacteria, feast on chocolate.

‘When you eat dark chocolate, they grow and ferment it, producing compounds that are anti-inflammatory.’

This naturally forming anti-inflammatory enters the bloodstream and helps protest the heart and arteries from damage.

Bad gut bacteria, such as Clostridia and some strains of Escherichia coli (E.coli) trigger inflammation, leading to bloating, diarrhoea and constipation.

The team tested three types of cocoa powder, the raw ingredient used to make chocolate, in an artificial digestive tract consisting of a series of modified test tubes.

Cocoa contains so-called antioxidant polyphenol compounds, such as catechin and epicatechin, and a small amount of dietary fibre.

Both components are poorly digested and absorbed, but are readily processed by the friendly bacteria in the colon.

Cocoa, stock image pictured, contains so-called antioxidant polyphenol compounds, such as catechin and epicatechin, and dietary fibre. These components are poorly digested, but are readily processed by friendly bacteria in the colon. This turns large polymers into smaller molecules with an anti-inflammatory effect

Cocoa, stock image pictured, contains so-called antioxidant polyphenol compounds, such as catechin and epicatechin, and dietary fibre. These components are poorly digested, but are readily processed by friendly bacteria in the colon. This turns large polymers into smaller molecules with an anti-inflammatory effect

HOW COCOA IS DIGESTED

Cocoa contains so-called antioxidant polyphenol compounds, such as catechin and epicatechin, and a small amount of dietary fibre.

Both components are poorly digested and absorbed into the body, but are readily processed by the friendly bacteria in the colon.

‘In our study we found that the fibre is fermented and the large polyphenolic polymers are metabolised to smaller molecules, which are more easily absorbed,’ said Dr John Finley, who led the Louisiana research team.

‘These smaller polymers exhibit anti-inflammatory activity. When these compounds are absorbed by the body, they lessen the inflammation of cardiovascular tissue, reducing the long-term risk of stroke.’

Dark chocolate contains a higher cocoa content, increasing this process.

‘In our study we found that the fibre is fermented and the large polyphenolic polymers are metabolised to smaller molecules, which are more easily absorbed,’ said Dr John Finley, who led the Louisiana team.

‘These smaller polymers exhibit anti-inflammatory activity. When these compounds are absorbed by the body, they lessen the inflammation of cardiovascular tissue, reducing the long-term risk of stroke.’

The findings were presented at the American Chemical Society’s annual meeting in Texas.

Combining cocoa with prebiotics – indigestible food ingredients that stimulate bacterial growth – is likely to enhance the process with beneficial results, said Dr Finley.

‘When you ingest prebiotics, the beneficial gut microbial population increases and out-competes any undesirable microbes in the gut, like those that cause stomach problems,’ he added.

Prebiotics are found in foods such as raw garlic, raw wheat bran, and cooked whole wheat flour, and are especially abundant in raw chicory root. They can also be obtained from widely available supplements.

Combining dark chocolate with fruits such as pomegranates or acai may also boost its benefits, said Dr Finley.

What Everyone Should Know About Blood Clots.


To prevent deep vein thrombosis, get up and move often

Just like a traffic jam on the highway, blood clots impede normal circulation in your body and can be dangerous. Here are some blood clot basics and information on steps you can take to help avoid the problem.

Signs of a serious blood clot

Thrombosis is a medical term for blood clot. Deep vein thrombosis (DVT) occurs in one of the large veins, usually in your legs. DVT can cause pain and swelling in the area where blood clots form. The area might also be reddened and feel warm to the touch.

The most common complication from DVT is pulmonary embolism (blockage), which occurs when a clot or part of a clot breaks off and lodges in the lungs. Symptoms of pulmonary embolism include shortness of breath and sudden pain in the chest that gets worse when you breathe deeply.

Risk factors and ways to avoid DVT

Anybody can get DVT, but surgery or injury increases your risk, as does increasing age and weight gain. Some people have clotting disorders that increase their risk for DVT.

Ways to avoid DVT include:

  • Quitting smoking, maintaining a healthy weight and exercising regularly.
  • If you are hospitalized, ask your healthcare providers about available DVT prevention, such as mechanical devices to aid circulation.
  • If you are on a long flight, or if you sit for hours, wear compression stockings and get up and move around or perform stretching exercises.

“As many as 60 percent of all people who suffer an episode of deep vein thrombosis will also develop post-thrombotic syndrome,” says vascular medicine specialist Natalie Evans, MD.

This syndrome can cause long-term pain, swelling and even ulcers.

Blood thinners and what not to eat

Physicians prescribe blood thinners to some DVT patients to prevent future clotting. Warfarin or Coumadin is a type of blood thinner that has been used for decades, but frequent blood tests are needed to monitor dosage.

Dr. Evans adds, “Patients should talk with their doctor or pharmacist…to learn about potential interactions with foods and drugs.”

The Vitamin K found in greens and other foods can interfere with Coumadin’s effects. There’s a long list of foods that you should eat only in moderation while you are on the drug.

Cranberries and cranberry products like cranberry juice can intensify Coumadin’s effect, so it’s best to avoid them while you are on the drug.

Pros and cons of new medications

Newer blood-thinner medications, including rivaroxaban (Xarelto), apixaban (Eliquis) and dabigatran (Pradaxa), can be used for DVT prevention and do not require frequent blood tests, making them more convenient.

These new-generation blood thinners also may have fewer negative interactions with foods and other drugs. However, they are also more expensive than warfarin, and a specific antidote, in cases of bleeding, is not available. Patients should talk to their physician about the risks and benefits of taking these medications.

Beware of high impact sports

If you’re taking blood thinners, participating in high-impact sports can lead to potentially dangerous bleeding. Dr. Evans says that during exercise, “people who’ve had DVT and PE in the past need to be aware of the symptoms of recurrent clots, that is, leg pain and swelling, shortness of breath, chest pain that’s worse with deep breathing.”

While you are on blood thinners, there’s always a danger from cuts or bruising, even in going about your everyday activities like shaving or gardening.

Keep a medical card in your wallet that says you are on blood thinners, and never take any prescription or non-prescription medications without talking with your doctor first.