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LIFTING THE BLACK CLOUD

Existing antidepressants leave a lot to be desired. They can take weeks to start working, and they fail many people. Researchers are scouting for better options

By Robin Marantz Henig

Click here to view the entire article

Structural changes in the hippocampus have long been implicated in depression. Brain autopsies of clinically depressed people often show atrophy in that region and a significant reduction in volume. The SSRIs and SNRIs already in use ease depression not only by manipulating serotonin levels but also by increasing new hippocampal cell growth. That growth happens slowly, though, which is probably part of why the pills’ benefits take so long to kick in. Scientists at the small pharmaceutical company Neuralstem in Rockville, Md., are hoping they have found a different way to spark neurogenesis—and to maintain it even after the drug has been stopped.

To find their spark, Neuralstem researchers relied on cultures of neural stem cells derived from human hippocampal cells—the only such cultures in the world, according to the company. First, they screened some 10,000 compounds for their effect on the hippocampal
cells in culture. The goal, chief scientific officer Karl Johe says, was to see which compounds increased the rate of cell proliferation after seven days. Fewer than 200 made the cut, he says, and from those the Neuralstem team devised a dozen candidate compounds that seemed most likely to stimulate hippocampal neurogenesis. In 2004 the workers began animal testing, injecting the preparations into healthy normal mice. The compounds best at provoking growth of new hippocampal cells were given to mice with depressive behavior, and from this protocol the single most promising one emerged.

Now Neuralstem is conducting early safety tests (phase I trials) of a pill form of the substance, called NSI-189, in humans. If all goes as planned, Neuralstem officials expect to begin tests of efficacy later this year. These studies will use magnetic resonance imaging to determine whether the drug increases neurogenesis and will use other measures to determine whether it relieves symptoms of depression. Even if NSI-189 works, though, it will not have rapid effects. “It’s not like somebody having epilepsy, where you give a drug to stop the epilepsy instantaneously,” Johe says. “This treatment requires changes in the cell at the genetic level.” Hippocampal atrophy takes years to occur, he adds, and “to reverse the process will also require a long period of time.” He hopes, however, that the effect will be long-lasting, so that NSI-189 may be needed only intermittently. That notion still has to be demonstrated, but it is “an exciting possibility,” Johe says.

A young woman who calls herself blueberryoctopus had been taking antidepressants for three years, mostly for anxiety and panic attacks, when she recounted her struggles with them on the Web site Experience Project. She said she had spent a year on Paxil, one of the popular SSRIs (selective serotonin reuptake inhibitors), but finally stopped because it destroyed her sex drive. She switched to Xanax, an antianxiety drug, which brought back her libido but at the cost of renewed symptoms. Then Paxil again, then Lexapro (another SSRI), then Pristiq, a member of a related class of antidepressants, the SNRIs (serotonin and norepinephrine reuptake inhibitors). At the time of the post, she was on yet another SSRI, Zoloft, plus Wellbutrin (a cousin of SNRIs that affects the activity of dopamine as well as norepinephrine), which was intended to counteract the sexual side effects of Zoloft. “I don’t notice much of a difference with the Wellbutrin, but I’m on the lowest dose now,” she wrote. “I’m going back to my psychiatrist next week, so maybe he’ll up it. Who knows.”

This is the typical trial-and-error approach to prescribing antidepressants, not only for depression per se but also for related disorders such as blueberryoctopus’s. The tactic, Andrew Solomon wrote in The Noonday Demon, his landmark book about depression,
“makes you feel like a dartboard.”

Troubling side effects are not the only reason for the dartboard approach. The SSRIs and SNRIs that have dominated the antidepressant market since their introduction in the 1980s and 1990s do not help everyone and eventually fail in more than a third of users. A pill that seems to be working today might well stop helping tomorrow. And the drugs can take several weeks to start having a marked effect, a waiting period that can be especially perilous. According to a 2006 report in the American Journal of Psychiatry, among depressed older adults (age 66 and older) taking SSRIs, the risk of suicide was fivefold higher during the first month of treatment than in subsequent months.

Clearly, patients critically need antidepressants that work faster and better, yet the pipeline for novel drugs is drying up. In fact, in the past couple of years such pharmaceutical giants as Glaxo-SmithKline have announced their intention to abandon psychiatric drug development, finding it too expensive, too hard and too much of a long shot.
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Some scientists in government and academic laboratories and at small pharmaceutical companies are trying to pick up the slack. Whether their efforts will succeed remains an open question.  But new drugs cannot come too fast for the nation’s approximately 15 million depressed patients. Many remain unhelped by talk therapy and medicines and are desperate to try anything to relieve the psychic pain, including such experimental treatments as putting electrodes in their head or burning holes in their brain.

IN SEARCH OF SPEED

investigators aiming to find faster-acting antidepressants have been studying compounds known to be lightning-quick mood lifters, hoping to figure out why they work so much more rapidly than the SSRIs, which enhance levels of serotonin, a signaling molecule, in the brain. One such compound is ketamine.

Ketamine is an anesthetic, an analgesic and a recreational drug known on the street as Special K. It can, among other things, affect consciousness and cause hallucinations, and experiments in rodents show it can be toxic to nerve cells—all of which make it a less than ideal candidate for an antidepressant. But it has proved to be a fascinating compound to study for ideas about how to make antidepressants reduce symptoms faster. As Ronald Duman and George Aghajanian of Yale University and their colleagues have demonstrated, within only two hours after an injection of ketamine lab rats start increasing production of proteins needed to build new synapses—the contact points through which signals flow between nerve cells—in the prefrontal cortex. This region of the brain, located right behind the eyes, is known to behave abnormally in depressed individuals. By 24 hours after the ketamine shot, the rats also start sprouting new synaptic spines, like cloves in a Christmas orange, along dendrites, which are the nerve cell projections that receive signals from other neurons. The more spines, the quicker the transmission. And in Duman and Aghajanian’s experiments, the more synaptic spines, the less the animals display depressionlike behavior (such as abandoning activities they would normally engage in).

“A lot of work over the past 10 years or so has shown that in depression, there is atrophy, not growth, in the prefrontal cortex and also the hippocampus,” says Duman, who directs Yale’s Laboratory of Molecular Psychiatry. “Ketamine can rapidly reverse that atrophy” and restore normalcy. Just how rapidly is the subject of current research, as the Yale scientists examine rat brains only a few hours after the ketamine injection to see if the increase in synaptic spines occurs even sooner than 24 hours.

Additional research in a different group of depressed rats has revealed how ketamine makes these synaptic spines grow: by activating an enzyme in neurons known as mTOR. Duman and his colleagues discovered this connection by giving rats a drug that blocks the enzyme’s action. Then they gave ketamine to the mTOR-blocked rats. Nothing happened, which meant that when mTOR was inhibited, ketamine had no effect on synaptic spine proliferation or reversal of depressionlike behavior. In other words, mTOR needs to be functioning for the ketamine to do its spine-sprouting work.

Given that ketamine is too risky to use routinely as a medicine, the researchers began searching for other mTOR activators. They knew that ketamine stimulates the enzyme by preventing glutamate (the main excitatory neurotransmitter in the brain) from acting on a particular docking molecule—termed an NMDA receptor—on the surface of neurons. They therefore tested another NMDA blocker and found that it, too, led to mTOR activity and quickly promoted spine formation and produced antidepressant effects in rats. Now, Duman says, he and his co-workers are examining other compounds that block NMDA receptors to see if any have promise as safe, fast-acting antidepressants.

Another compound that elevates mood swiftly is, like keta-mine, already on the market for another purpose: scopolamine, sold as a skin patch for treating motion sickness.  Scopolamine influences a different brain circuitry than ketamine does: it impedes binding of the neurotransmitter acetylcholine—involved in attention and memory—to molecules known as muscarinic receptors.

Click here to view the entire article

 

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* Running Against the Odds

http://bayweekly.com/articles/people/article/running-against-odds

One in a thousand on the B&A Trail Marathon

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Sunday, March 4, a thousand men and women lined up to run the Annapolis Striders’ B&A Trail Marathon. Among them, 71-year-old Minnesotan Don Wright stood poised to begin his 63rd marathon in 44 states.

Only six states stand between Wright and his goal to complete a marathon in all 50 states.

Wright is training, traveling around the country and completing several marathons every year, as he has been for the last eight years — while fighting multiple myeloma, an incurable blood cancer.

“When I got the disease, it wasn’t hurting me yet, so I was in denial,” Wright says. “I am still in denial, and I plan on staying in denial.”

Multiple myeloma is a cancer of plasma cells that attacks and destroys bone. There are about 100,000 patients with 20,000 new cases diagnosed each year in the U.S. Causes are unknown; however, certain professions involving exposure to nuclear radiation, pesticides and petrochemicals have a higher risk factor.

One State at a Time

Wright started running a decade ago to lose weight. He ran his first marathon about two years later, days before his diagnosis. He kept running, determined to qualify for the coveted Boston Marathon, a goal he achieved in the first race after his diagnosis, Minnesota’s Twin Cities Marathon. Next, Wright headed to Arizona for a downhill marathon in Tucson.

His marathon quest evolved one state at a time.

“We started to pick off other states, never expecting that we’d be able to do 50 states,” Wright says. “It takes time if you want to do a few marathons a year, and I didn’t know how much time I had.”

Eight years ago, Wright’s survival time was estimated at about five years.    He attributes his energy and his cancer’s stability to a pill he has taken every night for the last four years. It’s an investigational drug still in the trial stages.

“I’ve met people who are no longer with us because of this disease,” Wright says. “It’s a serious thing, but because of this drug, we’re going all over the country celebrating life and really having a wonderful time.”

We is Wright plus his wife and daughter, who travel with him to each race and run either alongside him or in an accompanying half-marathon.

Cancer isn’t slowing Wright down, but he has suffered from a sports hernia — an abdominal wall strain — since August. His usual schedule of running 30-plus miles each week has been reduced to long walks, often through his local mall in Lake Elmo, just east of Minneapolis-St. Paul, to stay out of the cold winter mornings.

To help heal, Wright has adopted a routine of 30 seconds of running followed by 90 seconds of walking throughout a race. At that pace, he can finish within the race cutoff time (six hours for the B&A Trail Marathon) while avoiding further injury.

On Sunday, Wright finished in 5:32:47. Time, however, matters less to him than the running itself.

“I like to imagine that I’m just floating, that there’s no effort to it at all,” Wright says. “I’m just kind of drifting across the landscape, watching the houses and the trees and the other people go by. That’s one of my favorite things.”

Wright attributes his active lifestyle in helping hold off the cancer. His next marathon is in June in Alaska, followed by races in Vermont, New Hampshire, West Virginia, New Mexico and, in December, Hawaii. That’s 50.

“I think about the people I know who can’t do this,” Wright says, “and how lucky I am to be able to do it.”

Wright’s running raises money for two charities, Team Continuum (www.teamcontinuum.com) and Tackle Cancer (http://tacklecancerfoundation.org). Both help cancer patients and their families pay for living expenses.

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* New antidepressant studied here



http://abclocal.go.com/wpvi/story?section=news/health&id=8545273

ROOMALL, PA.; February 15, 2012 (WPVI) — There is new hope for people who suffer from depression. Final trials are underway on a new antidepressant.

Dr. Ronald Fuchs of Sproul Medical Center in Broomall, says it’s a common story. A patient on antidepressants needing higher and higher doses to get any relief, only to develop side effects that drive the sufferer to stop taking the medication altogether.

He’s taking part in the TRIADE trial, phase 3 tests of a new type of antidepressant.

Amitifadine is intended for people who failed with other medications.

It elevates levels of 3 chemicals in the brain – serotonin, dopamine, and norepinephrine. Other antidepressants only act on one or two of those.
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Dr. Ronald Fuchs, of Sproul Medical Center in Broomall, says, “By working on 3 different pathways, at different percentages of these mechanisms, the potential for remission of symptoms – or control of symptoms – is higher because you’re not just coming at it from one direction.”

Dr. Fuchs, who is one of the local doctors involved in the study, says the three-pronged approach may also reduce the side effects of other antidepressants

Those side effects, such as weight gain or sexual dysfunction, drive some patients to give up their medications.

To find out more about the study, call 610-356-0662, or see TRIADE trial.

(Copyright ©2012 WPVI-TV/DT. All Rights Reserved.)

 

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Scientists Transform Deadly Plant Into Cancer Killing Smart Bomb

Scientists Transform Deadly Plant Into Cancer Killing Smart Bomb

By Kristen Philipkoski
Feb 2, 2012 4:40 PM

The ancient Greeks called the thapsia garganica plant “deadly carrot,” because their camels would eat it and quickly die. The Roman emperor Nero mixed it with frankincense to treat bruises. Until the early 20th century it was used in a plaster to treat rheumatism—the side effects, however, were barely worth the cure.

But what happens when you deploy thaspia on a molecular level? You get a teeny tiny, very precise, cancer-killing grenade. It’s an entirely new approach that has its creators throwing around the word “cure.”

Thapsigargin, the active ingredient in the thapsia plant, does a fantastic job of killing tumor cells by destroying their calcium balance. But it will do that to any cell that crosses its path. So Genspera, a biotech company in San Antonio, Texas, found a way to strictly guide and control the drug through the bloodstream until it finds its target.

“That’s why we came up with the concept of producing a molecular grenade, so it activates only in the tumor,” said Craig Dionne, GenSpera’s president, CEO and director.

That’s no easy task. One of the reasons many cancer drugs cause such terrible side effects is because they leak into the bloodstream on their way to the tumor. The bone marrow is ravaged, hair falls out, and the liver and cardiovascular system can be damaged.

“We have none of that nonsense,” Dionne says.

The key to the cancer grenade’s precise explosive effect is its “pin,” a 5-amino-acid-long peptide that can be pulled only by an enzyme, called PSMA, found on the surface of blood vessels that feed cancer cells. Only when the peptide comes into contact with PMSA will it release the thapsigargin.
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Other chemotherapy drugs slow the growth of cancer, and doctors consider them a success if they prolong a patient’s life for just a few months.

“We’re not trying to slow the growth,” Dionne told me. “We’re dropping a neutron bomb in the neighborhood. Everything in the neighborhood dies and goes away.”

Traditional chemotherapy is also designed to kill fast-growing cells, i.e. cells that are dividing out of control like cancer tumor cells do. The problem is that cancer stem cells, which continuously give rise to new tumors, actually divide very slowly, which can lead to a relapse. In animal studies, Genspera’s drug killed all the cancer cells plus the stem cells, leaving nothing behind that could seed more cancer growth—hence the talk of a cure.

“It looks like what we’ve seen in animals will be replicated in humans—that’s what we expect to see,” Dionne said.

Not to get too overly optimistic: the drug is in the earliest phase of FDA clinical trials. So far, researchers are excited and hopeful because they’ve cranked up the dosage more than they ever thought possible, and still have not seen side-effects in patients. Twenty-six patients with various types of late-stage “solid tumor” cancer have participated in the trial and researchers will soon add 18 more. After that they hope to move on to the second phase of trials (FDA clinical trials usually include three phases: the first for safety, the second for safety and efficacy, and the final one to confirm safety and efficacy.)

Prostate cancer cells also grow slowly, so they can escape cancer treatments focused on killing fast-growing cells. Genspera’s next drug, which will be based on the same grenade technology, will target that disease. Also in the queue are brain and stomach cancer. Here’s hoping they bomb the crap out of all of them.

Image: Luigi Rignanese

http://gizmodo.com/5881640/scientists-transform-deadly-plant-into-cancer-killing-smart-bomb

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Scientists Use Spectroscopy to Study Black Holes, Stars, and Now Cervixes

Scientists Use Spectroscopy to Study Black Holes, Stars, and Now Cervixes

Scientists use spectroscopy to examine the make-up of celestial objects. Now, they’re taking the technology in a decidedly different direction and using it to detect cervical cancer.

Over the past decade, Guided Therapeutics has identified cellular markers specific to cervical cancer cells, which their new device identifies by shining a spectrum of light on the tissue. Like spectroscopy for planets and stars, the company’s LuViva Advanced Cervical Scan shines light on the object of interest, then analyzes how that light is reflected. The technique is non-invasive and doesn’t require tissue samples or lab tests, which is reason to celebrate for anyone who’s had a Pap-smear or cervical biopsy.

“Every molecule has a spectral fingerprint. If you hit it with a specific wavelength of light any tissue will reveal its nature and tell you something about itself,” Mark Faupel, CEO of Guided Therapeutics, told me during a phone interview. “We’ve adapted this technology used by NASA to identify whether there’s life on other planets to detect cancer cells in tissue in vivo (i.e. in a live person).”

In studies looking at 1,600 cervixes, the company’s scientists found that the device detected 90 percent of cervical cancers an average of two years earlier than Pap smears, the technique currently used by doctors for early diagnosis. Pap smears are a good way to detect cervical cancer early but they also lead to a lot of false positives—only 20 percent of patients who have abnormal Paps actually require treatment. That’s an 80 percent false positive rate. The test also completely misses two-thirds of pre-cancerous cells.

False positive or not, an abnormal Pap smear typically leads to a colposcopy, which is basically a quick but sometimes painful scrape of the cervix’s surface cells to obtain a biopsy.

Cervical cancer, which is usually caused by human papilloma virus, is a major killer of women, especially in developing countries where women have less access to Pap smears. In the United States where Pap smears are routine, most women catch pre-cancerous cells early enough that it’s 100 percent treatable by removing the abnormal cells with cryosurgery or laser therapy. But in places where Pap tests are not routine and cervical cancer often goes undetected until it has spread, LuViva could save lives. The device will be relatively inexpensive at about $20,000, so Faupel hopes smaller clinics will be able to afford one.

“We wanted to make it accessible to use on a reservation for Native Americans or rural clinics in developing countries,” he says. “This can be used for the underserved population, not just afforded by large industrial hospital complexes.”

The National Cancer Institute has granted Guided Therapeutics $6 million to develop the technology, and the company hopes to receive final FDA approval to market the device sometime this month.

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Scientists Use Spectroscopy to Study Black Holes, Stars, and Now Cervixes

Scientists use spectroscopy to examine the make-up of celestial objects. Now, they’re taking the technology in a decidedly different direction and using it to detect cervical cancer.

Over the past decade, Guided Therapeutics has identified cellular markers specific to cervical cancer cells, which their new device identifies by shining a spectrum of light on the tissue. Like spectroscopy for planets and stars, the company’s LuViva Advanced Cervical Scan shines light on the object of interest, then analyzes how that light is reflected. The technique is non-invasive and doesn’t require tissue samples or lab tests, which is reason to celebrate for anyone who’s had a Pap-smear or cervical biopsy.

“Every molecule has a spectral fingerprint. If you hit it with a specific wavelength of light any tissue will reveal its nature and tell you something about itself,” Mark Faupel, CEO of Guided Therapeutics, told me during a phone interview. “We’ve adapted this technology used by NASA to identify whether there’s life on other planets to detect cancer cells in tissue in vivo (i.e. in a live person).”

In studies looking at 1,600 cervixes, the company’s scientists found that the device detected 90 percent of cervical cancers an average of two years earlier than Pap smears, the technique currently used by doctors for early diagnosis. Pap smears are a good way to detect cervical cancer early but they also lead to a lot of false positives—only 20 percent of patients who have abnormal Paps actually require treatment. That’s an 80 percent false positive rate. The test also completely misses two-thirds of pre-cancerous cells.

False positive or not, an abnormal Pap smear typically leads to a colposcopy, which is basically a quick but sometimes painful scrape of the cervix’s surface cells to obtain a biopsy.

Cervical cancer, which is usually caused by human papilloma virus, is a major killer of women, especially in developing countries where women have less access to Pap smears. In the United States where Pap smears are routine, most women catch pre-cancerous cells early enough that it’s 100 percent treatable by removing the abnormal cells with cryosurgery or laser therapy. But in places where Pap tests are not routine and cervical cancer often goes undetected until it has spread, LuViva could save lives. The device will be relatively inexpensive at about $20,000, so Faupel hopes smaller clinics will be able to afford one.

“We wanted to make it accessible to use on a reservation for Native Americans or rural clinics in developing countries,” he says. “This can be used for the underserved population, not just afforded by large industrial hospital complexes.”

The National Cancer Institute has granted Guided Therapeutics $6 million to develop the technology, and the company hopes to receive final FDA approval to market the device sometime this month.

Posted on

The Pill That Could Cure Depression by Growing Your Brain

http://gizmodo.com/5874433/the-pill-that-could-cure-depression-by-growing-your-brain

Kristen Philipkoski:  January 9, 2012

If you are depressed, or schizophrenic or have Alzheimer’s, scientists say you probably have a shrunken hippocampus. The good news: a drug that just entered human trials promises to re-grow that part of the brain.

It’s an entirely new approach to treating clinical depression, which is the first of several diseases scientists at biotech company Neuralstem are hoping to address with their experimental oral drug. Most antidepressants work on brain chemistry, tweaking levels of neurotransmitters including serotonin, norepinephrine, and dopamine. This is the first drug that aims to re-grow patients’ atrophied brains.

Dr. Karl Johe, Neuralstem’s CEO, believes that depression is a three-headed beast that affects neurotransmitter levels, neurons, and hippocampus size. And he says their new drug could address all three. He also hopes the drug will reverse the disease to the point that patients could permanently go off the drug.

“If we can show by MRI that we’ve increased hippocampus volume and at the same time reversed depression symptoms for six months after patients have stopped taking the drug, then we’ll have a cure.”
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That a too-small hippocampus causes depression and other diseases is still technically a theory in humans (though it’s been demonstrated in rats and chimps). So if the drug grows hippocampus volume and thereby treats depression, we’ll not only have a new treatment, but the study results would be proof that a shriveled hippocampus is at least in part the culprit.

The scientists showed first that the drug worked in the lab: They started with dishes of neural stem cells and added several compounds they thought might instigate growth. Seven showed promise, but they could only afford to develop one, so they chose NSI-189. They then tested it in mice; after taking the drug, the rodents had larger hippocampi.

Thirty-five healthy humans have now taken the drug with no ill effects, so the FDA gave the company the OK to start testing in depressed patients. They’ll give the pill to 18 volunteers (six will get a placebo) in three groups, each receiving a progressively larger dose, each over 28 days. They expect this phase, which is mainly to make sure the drugs is safe, to take about six months. If all goes well they hope to proceed to phase two clinical trials later this year, which will test to determine whether the drug is both safe and effective. (After that, a final phase three trial to confirm safety and efficacy will remain before the company can market the drug.)

I couldn’t help thinking about those healthy test subjects who took the drug. Will they get super brain powers? The healthy mice that received the drug did grow extra large hippocampi, the seahorse-shaped part of the brain involved with both short and longterm memory and spatial navigation. Johe isn’t ruling out the possibility of souped-up brains:

“It’s an exciting possibility and we’ll definitely be looking out for it.”

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Stem Cells: Plural Paths to Harnessing Pluripotency

Stem Cells: Plural Paths to Harnessing Pluripotency

By Anette Breindl
Science Editor

Monday, January 9, 2012

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The most obvious way to use stem cells is to differentiate them in a petri dish and transplant the resulting cells into tissues or organs that are damaged or diseased.

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* Solace in numbers

http://www.thestarnews.com/chula-vista/solace-in-numbers/

The Star-News

Solace in numbers

Sat, Jan 07 2012 12:00 PM Posted By: Allison K. Sampité

In October 2006, Guadalupe Moreno was taken to the emergency room for severe bone and kidney pain and a fever.  During the second day of her one-week stay at Scripps Hospital in Chula Vista, doctors told Moreno something that would change the rest of her life.

Moreno, now 64, was diagnosed with multiple myeloma, an incurable blood cancer where abnormal cells collect in the bone marrow and form tumors.

It’s the second most common blood cancer after lymphoma, affecting an estimated 750,000 people worldwide.

In July 2007, Moreno went to the University of California, San Diego, where she received a stem cell transplant.

“The transplant worked for 20 months — my cancer was in remission then it began slowly coming back and I started chemo again,” she said.

Moreno, like many people who are diagnosed with multiple myeloma, have never heard of the disease and think of it as melanoma, the leading cause of death from skin disease.

Years ago, multiple myeloma mostly affected men in their 60s and older, but today, diagnosis includes women and those younger than 30.

There are approximately 19,900 new cases of myeloma in the United States each year, according to the International Myeloma Foundation, which works to improve treatment options to improve the quality of life for patients.

Although multiple myeloma is treatable with medication, radiation and chemotherapy, the condition can cause bone pain, frequent infections, dizziness and fatigue.

Moreno takes steroids and two chemotherapy treatments in cycles, which helps minimize her pain, but causes side effects such as nausea.

While symptoms of multiple myeloma can be strong, they are not easy to detect at an early stage.

For some people like Elliot Recht, who was diagnosed during an annual physical 14 years ago, there are no symptoms at all.

Recht is one of two leaders for the San Diego Multiple Myeloma Support Group, but started off as a member when he was first diagnosed, taking over after group founder Fred Gloor passed away.

“I am very fortunate,” Recht said. “I’ve been pretty asymptomatic the whole time.”
Still, patients must manage their symptoms.

Because multiple myeloma affects plasma cells responsible for producing antibodies, it often affects the immune system, making patients more susceptible to infections, colds and viruses. It can also cause build-up of the M protein, which thickens the blood.
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Moreno explained the importance of washing her hands and dishes well and often to rid them of bacteria and how she can’t eat fruit or vegetables that grow underground because of pesticides.

When Recht was diagnosed, the life expectancy of patients was only three years, so he decided to stop working full time as a photographer.

“Why work so hard when you have such a short time to live?” he said.

Dr. Brian Durie, chairman of the foundation’s board, said that in the last decade, six new agents have been created to fight myeloma.

“Novel therapies are much better tolerated and work for a whole lot longer than chemotherapy does,” Durie said. “On average, life expectancy has doubled in the last decade from three to six years … allowing patients to return to a longer, fuller life.”

Chula Vista resident Lanorris Sewell was diagnosed at Scripps Hospital in Chula Vista in April after his back went out. Blood tests, a bone marrow biopsy and MRI confirmed he had multiple myeloma.

Sewell, 49, retired from the Navy in 2003 after 20 years working with chemicals to strip rust off airplanes. Prior to being diagnosed Sewell hadn’t heard of multiple myeloma.

“One thing I have learned about the cancer thing is that you have to stay positive if you want to beat it, otherwise you’re defeated,” he said.

Although the reason why people develop multiple myeloma is unknown, there are man-made risk contributors that include environmental pollution, stress and pesticides.

In Recht’s case, he grew up in Pittsburgh where he said he believes that air pollution, caused by the burning of coal and production of steel and iron, might have contributed to his condition, in addition to medal casting, oil paints, turpentine and clay.

“It’s a fine line between awareness and susceptibility,” Durie said. “Only a small percentage of those exposed have a genetic predisposition to it. People who do get myeloma aren’t able to break down these chemicals because they are slow metabolizers.”

Sewell and Moreno live on disability, unable to work, but attend support group meetings, which offer information on finances, give emotional support, and provide a better understanding of myeloma.

“It helps them realize that they are not alone in this battle and struggle,” Recht said.

“This is a type of cancer where education is the best possible thing.”

Moreno also attends meetings at Sharp Medical Center’s Leukemia and Lymphoma Society in Chula Vista.

“It’s good to learn and talk with other people that are like you and exchange your experiences,” she said. “I think when you have cancer, you have to fight to get well—you have to think positive.”

For information on support groups visit www.multiplemyelomasandiego.org.

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Washington area business diary for week of Jan. 2

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Short takes on the week’s announcements and deals.

Pharmaceuticals

Rockville-based Neuralstem has received approval from the Food and Drug Administration to advance to Phase Ib in its ongoing clinical trial to test its neuroregenerative compound NSI-189 for the treatment of major depressive disorder.