Judy Foreman

Nationally Sindicated Fitness, Health, and Medicine Columnist

“Cutting” – Understanding Self-Mutilation

by

Years ago, Boston University psychiatrist Dr. Bessel van der Kolk tried a simple experiment to understand one of the most disturbing, and bizarre, of all psychiatric disorders: self-mutilation, or more simply, cutting.

He asked his cutters, mostly young women, to come see him when they felt the urge to scratch, slash or burn themselves. When they came, he asked them to put their hands in ice water. They were able to keep their arms buried in ice much longer than normal people, he found, because they didn’t feel the pain.

Then, when he gave them an injection of a drug that blocks endorphins, the body’s natural painkillers, they felt pain again “and with that, a sense of feeling alive,” van der Kolk says.

To the uninitiated, cutting may seem like a suicide attempt or a cry for attention, and in rare cases that’s true. In reality, both cutters and psychiatrists say, the urge to self-mutilate is a coping behavior triggered by an inner sense of numbness or deadness. Far from a wish to die, cutting is a terrible urge to feel something , even physical pain, rather than nothing at all. And far from flaunting their cuts to get attention, cutters usually hide them.

The numbness that these teenagers – and some older cutters – feel is usually triggered by overwhelming trauma, family conflict, sexual or physical abuse, emotional neglect and, perhaps, genetics. This deadness “is so terrifying, that to feel one’s physicality brings relief — that one is still present and has definable boundaries,” says Dr. Michael Strober, a professor of psychiatry and director of the eating disorders program at the UCLA Neuropsychiatric Institute.

No one knows how prevalent cutting is, nor why it seems to be on the rise, though in some schools, contagion – kids copying each other’s strange behavior – may be involved. Nor do researchers know why roughly 75 percent of cutters are female, though one theory is that girls turn their feelings against themselves while boys attack others.

But researchers do know far more than they did a few years ago about what triggers cutting and, more important, and how to help kids stop.

Cutting often overlaps with anorexia or bulimia. In fact, roughly half of girls who cut themselves with pins, knives and razors start out with eating disorders, says New York psychotherapist Steven Levenkron, author of “Cutting: Understanding and Overcoming Self-mutilation.”

Curiously, black and Latina girls may be less prone to cutting than white girls, says psychologist Wendy Lader who, with Karen Conterio, started the SAFE program (Safe Alternative – Self Abuse Finally Ends) at Linden Oaks, a psychiatric facility at Edward Hospital in Naperville, Ill. 18 years ago. Perhaps darker-skinned girls, she says, may have more realistic ideas about what a healthy body looks like and may feel freer to express anger.

Levenkron agrees. Most of his cutters are white, perfectionistic and, contrary to outward appearances, filled with self-loathing. “I never met a cutter who liked herself.”
One way to help cutters is to teach them how to talk about their emotional pain so that they don’t express it nonverbally. “I teach cutters a full vocabulary for feelings and mental pain,” says Levenkron. By the time they learn to talk “in the language I taught them,” he adds, “they are not cutting anymore.”

All of this, of course, takes time, money and commitment. Levenkron sees patients twice a week for several years, and insurance rarely pays full freight. But like their desperate offspring, desperate parents often hang in, writing the checks and learning, slowly, how to deal with a more emotionally expressive, but less self-abusive, daughter.

He recalls one terrified teenager who came to him straight from a locked psychiatric ward and stayed in therapy for four years. “When I started seeing you,” Levenkron recalls her saying, “I thought I couldn’t breathe between appointments. I would kill to see you.” Three years later, she told him, “You’ve helped me a lot. Is it okay if I stop coming?”

That kind of intense support is also part of the SAFE approach, says psychologist Lader.
In the first phases of treatment, giving up the crutch of cutting – the one behavior that brings relief – can be terrifying, adds Lader.

“This is a nihilitive fear, the fear that they won’t exist, that they will explode… If we ask them to give up this coping strategy, we have to be there for them.”

But, despite some web sites that seem to glorify cutting, Lader says the emphasis should be teaching that cutting “is not a healthy coping strategy.” In fact, SAFE makes cutters sign a “no harm” contract. That’s partly common sense, but partly good biology as well.

That’s because cutting may produce transient good feelings by triggering trigger a flood of endorphins, the endogenous opiates. In fact, many doctors now do just what van der Kolk did in his early experiments – give opiate- blocking drugs such as Naloxone or Naltrexone.

By blocking the good feelings that cutting stimulates, cutters often stop injuring themselves because cutting no longer has the desired effect, says Dr. Alan Langlieb, a psychiatrist at The Johns Hopkins School of Medicine.
Other drugs help, too, because most girls who cut are “some combination of depressed and anxious,” says Dr. David Herzog, a psychiatrist at Massachusetts General Hospital who heads the Harvard Eating Disorders Center.

Some cutters, like Lydia Gibson, 38, a Baltimore woman who has been cutting herself off and on for 25 years, must take a number of drugs simultaneously. Gibson, who says she ” had to hurt myself because I had to get the anger out somehow,” now takes Buspar for anxiety, Paxil for depression, Naltrexone to blunt the positive effects of cutting, as well as Depakote, a mood stabilizer, and Seroquel, a tranquilizer.

In fact, not only do drugs and psychotherapy often work, cutting, perhaps surprisingly, is actually less dangerous than anorexia. Longterm outcome studies suggest that the mortality rate for anorexia is about 10 percent , says Herzog. Longterm mortality data from women without anorexia who cut themselves is scant, but doctors say that, except for accidentally deep cuts, the risk of death from any given cutting episode is minimal.

Herzog of MGH puts it this way. “It may sound nuts, but most of these girls are not nuts.” They’re stressed, depressed and scared. But what they really feel Herzog says is that they look good on the outside, but inside, they feel empty.

Meditation and the Brain ….?

by

For decades, open-minded Westerners – patients and doctors alike – have been touting the medical benefits of meditation, an ancient Eastern practice that comes in hundreds if not thousands of different flavors but consists basically of quieting the mind through moment-to-moment nonjudgmental awareness.

Considerable research suggests that regular meditation, or even just 10-20 minutes a day practising the “relaxation response” long promoted by Dr. Herbert Benson, president of the Mind/Body Medical Institute and associate professor of medicine at Harvard Medical School, can reverse many of the ill effects of stress.

Meditation, or the relaxation response, has been shown to lower blood pressure, heart rate and respiration; to reduce anxiety, anger, hostility and mild to moderate depression; to help alleviate insomnia, premenstrual syndrome, hot flashes and infertility; and to relieve some types of pain, most notably tension headaches.  

What nobody, until now, has even come close to explaining is how meditation may work. That is, what mechanisms within the brain might explain why changing one’s mental focus can have such large effects on mood and metabolism. Nor has there been until now, much collaboration between experts in meditation such as Buddhist monks and neuroscientists.

All that is changing – fast.

A new study, accepted for publication soon in Psychosomatic Medicine, is a significant first step in understanding what goes on in the brain during meditation. The study was led by Richard Davidson, director of the laboratory for affective neuroscience at the University of Wisconsin, and Jon Kabat-Zinn, founding director of the Stress Reduction Clinic and Center for Mindfulness at the University of Massachusetts Medical School.

The underlying theory is that in people who are stressed, anxious or depressed, the right frontal cortex of the brain is overactive and the left frontal cortex, underactive. Such people also show heightened activation of the amygdala, a key center for processing fear.

By contrast, people who are habitually calm and happy typically show greater activity in the left frontal cortex relative to the right. These lucky folks pump out less of the stress hormone cortisol, recover faster from negative events and have higher levels of natural killer cells, a measure of immune system function.

Each person has a natural “set point,” a baseline frontal cortex activity level that is characteristically tipped left or right and around which daily fluctuations of mood swirl. What meditation may do is nudge this balance in the favorable direction.

To find out, they recruited stressed-out volunteers from the Promega Corp, a high tech firm in Madison, Wisc. At the outset, all volunteers were tested with EEGs (electro-encephalographs), in which electrodes were placed on the scalp to collect brain wave information. The volunteers were then randomized into one of two groups – 25 in the meditation group and 16 into the control group.

The meditators took an 8-week course developed by Kabat-Zinn. At the end of 8 weeks, both meditators and controls were again given EEG tests and a flu shot. They also got blood tests to check for antibody response to the flu shots. Four months later, all got EEG tests again.

By the end of the study, the meditators’ brains showed a pronounced shift toward the left frontal lobe, while the nonmeditators’ brains did not, suggesting that meditation may have shifted the “set point” to the left. (The nonmeditators actually got slightly worse, perhaps because they were cranky from making several trips to the lab without the payoff of learning to meditate.) The meditators also had more robust responses to the flu shots. Indeed, the bigger the mood effect, the bigger the immune response.

The Wisconsin study fits with a smaller study published in May, 2000 by Sara Lazar, a neurobiologist at Massachusetts General Hospital, Benson and others that looked at 5 Sikh meditators using a brain scanning technique called functional MRI. It found a shift in blood flow in the brain during meditation.

The new meditation work also fits with data suggesting that certain drugs produce meditation-like effects on the brain, says Dr. Solomon Snyder, director of the department of neuroscience at  Johns Hopkins Medical School. Synder. “It’s reasonable to assume,”: he says, that meditation may increase serotonin, a calming neurotransmitter, in the brain.

No one has been more fascinated by this kind of  research than the Dalai Lama himself,  the leader (in exile) of Tibetan Buddhism.

The Dalai Lama spent 5 days in March, 2000 meeting with other Buddhis monks, philosophers and Western neuroscientists at a retreat in Daramsala, India that is chronicled in a new book called “Destructive Emotions” by Daniel Goleman, author of  “Emotional Intelligence.”

In addition to lots of esoteric debate, the conference had a practice outcome. One participant, Paul Ekman, professor of psychology at the University of California, San Francisco, School of Medicine, went on to study several monks in his California lab.

Ekman had previously developed a way to measure the facial expression of emotions and found that most people don’t do well when asked to decipher rapid changes in facial expression. But the monks were near-perfect decoders of facial expression. And one meditator, a 60-year old French intellectual who has been a monk for nearly 30 years

Appeared able to suppress the startle reflex while meditating – a stunning display of control over a basic, biological response.

None of this, of course, means that meditation is a cure-all.  As Barrie Cassileth, chief of the integrative medical service at Memorial Sloan-Kettering Cancer Center in New York, puts it, meditation is a wonderful tool “but it’s not going to let you fly to Europe on your own without a plane.”

But it is, as Ekman says cautiously, “an exercise for the brain that could be of some benefit.”

So, what does it all mean? Obviously, a few studies on several dozen amateur meditators and a handful of pros is not the final answer on how meditation acts on the brain to produce changes in mood and basic, biological functions.

Though it’s “a wonderful tool,” no one should expect meditation to work miracles, cautions psychologist-medical sociologist Barrie Cassileth, chief of the integrative medicine service at Memorial Sloan-Kettering Cancer Center in New York. It  “cannot bring about levitation. It cannot control cellular activity in the sense of getting rid of disease. …It’s not going to let you fly to Europe on your own without a plane.” 

But what these very preliminary studies do suggest is that, at long last, the subtleties of mind long known subjectively to proficient meditators may prove capable of being understood objectively as well.

New Approach Could Reduce the Need for Chemotherapy

by

There’s a revolution brewing in the diagnosis of cancer that could dramatically change how doctors figure out which tumors are truly life-threatening – and need chemotherapy — and which are not.

In the Netherlands, the new tool – called by various names, including gene expression profiling – is expected to be available for some women with breast cancer as soon as May. In the US, it could be several years before the technique is routinely available.But if gene profiling lives up to its promise, thousands of patients a year with tumors deemed unlikely to spread might safely skip chemotherapy. At the other extreme, people with cancers deemed lethal might skip chemotherapy if it’s unlikely to work, and go straight to experimental or alternative therapies.

With early stage breast cancer, for instance, doctors currently vastly over-treat because they can’t tell which patients need chemotherapy and which don’t.  Dr. Eric Winer, director of the breast oncology center at the Dana-Farber Cancer Institute in Boston estimates that in some situations, 100 women get chemotherapy for every 20 helped and in other cases, it’s 100 to 1.

With gene profiling – also known as genetic fingerprinting, molecular signatures and molecular profiling – the idea is to determine which genes are expressed, or turned on, in a given tumor.

Once genetically analyzed, tumors can then be categorized as having a good prognosis or not, and treatment can be chosen accordingly. Gene profiling will likely be used in addition to measures doctors already use, such as tumor size and whether the cancer has spread to lymph nodes. It will also be used to determine whether a tumor is likely to respond better to drug A or drug B.

Various teams of researchers have studied gene profiling in a number of different cancers and so far, perhaps surprisingly, there is very little overlap in the genetic patterns.

Several years ago, Charles Perou, now assistant professor of genetics at the University of North Carolina, with David Botstein and Pat Brown of Stanford University, identified a set of 450 genes that can predict outcome in breast cancer.

At Dana-Farber Cancer Institute in Boston, Dr. Sridhar Ramaswamy and his team have identified a set of 17 genes that seem to be harbingers of metastasis in various cancers. And in the Netherlands, Dr. Marc J. van de Vijver, Rene Bernards and others have identified a set of 70 genes that can predict which breast tumors will metastasize, or spread to other parts of the body, and which won’t.

Researchers have also used gene expression to predict outcome in cancers of the kidney, lung, and prostate. In B-cell lymphomas, they have identified one set of 16 genes and another of 13 genes that can do likewise. In one subtype of ALL (acute lymphocytic leukemia), researchers found a set of 20 genes that can predict which patients will develop a secondary cancer called AML (acute myelogenous leukemia).

This dazzling, even frightening, ability to predict the future is possible because of commercially available “gene chips” or DNA micro-arrays.

Imagine a thin, roughly one inch square plate of glass containing thousands of tiny spots of DNA, each spot representing a single human gene. Researchers then take genetic material called mRNA from a tumor and spread it on the DNA. If the mRNA finds its match on a spot of DNA, it sticks, and, because it’s been pre-treated, fluoresces under a special light. This technique – at roughly $1000 a test  – tells researchers which genes are active in that particular tumor.

The idea that a tumor’s potential to metastasize may be knowable while a tumor is still very small is both encouraging and distressing.

Historically, doctors believed tumors started off benign and mutated to acquire the ability to metastasize. ”Our study shows that this notion, at least for breast cancer, is wrong,” says Bernards, the senior author of the Dutch study on 70 predictive genes and head of the division of molecular carcinogenesis at the Netherlands Cancer Institute.

In other words, ”small does not mean benign,” he continues. ”We have seen small tumors that are poor in outcome and we have seen large tumors that have a good prognosis.”

That concerns Dr. Larry Norton, head of solid tumor oncology at Memorial Sloan-Kettering Cancer Institute in New York. ”It’s a big stretch to say if a cancer is bad, you might as well give up,” he says. ”It may be that those tumors are the most curable with therapy.”

Dr. Steven Goodman, a biostatistician and epidemiologist at the Kimmel Cancer Center at Johns Hopkins University is also cautious. So far, he says, ”there is absolutely zero evidence that by deferring chemotherapy based on these predictions you are better off.”

Despite concerns by some scientists that large prospective clinical trials should be conducted before gene expression profiling hits the clinic, the technique appears be on the fast track.

Bernards, who collaborated with scientists from Rosetta Inpharmatics (a wholly-owned subsidiary of Merck & Co.) on the study of 70 predictive genes, now has his own company, Agendia, Inc. in Amsterdam that, he says, ”allows us to offer this test.”

Celera Diagnostics is also doing a study correlating gene expression in breast tumors with progression of disease, with results expected later this year, says Tom White, chief scientific officer.

At Massachusetts General Hospital, a team led by Dr. Daniel Haber, director of the Center for Cancer Risk Analysis, with colleagues from Brigham and Women’s Hospital and Dana-Farber, has started testing 500 frozen breast cancer samples, in collaboration with the Dutch group. Funded by the Avon Foundation, the team hopes to test 5,000 samples in the next few years. ”Clearly, this is at the cutting edge of oncology,” says Haber, though he warns that it should be validated in a large prospective study before patients use it to make decisions about treatment.

One development that could speed things up is an idea being tested independently at Celera Diagnostics, Genomic Health, Inc. and researchers from Duke University and the University of North Carolina.

Instead of using frozen samples of tumor tissues, as the Dutch do and others do, these scientists are testing genetic profiling on tumor tissue that has been ”fixed” in formalin (formaldehyde) and embedded in paraffin wax for long term storage.

Until recently, scientists had thought formalin-fixed tissue “was unstudy-able,” says Dr. Matthew Ellis, clinical director of Duke’s breast cancer program, because the RNA in the tumors degraded. “That turns out not to be the case,” he says. ” We can do profiling on formalin-fixed tissue, and that is incredibly powerful.”

If this strategy works, “we can analyze 10 years’ worth of information in six months,” says Ellis.

Telomerase – a Promising Cancer Drug Stuck in Patent Hell?

by

Molecular biologists aren’t a particularly grumpy lot, but they are grumbling these days that corporate interests – particularly those of the California-based Geron Corp. – may be stifling development of a promising new class of anti-cancer drugs called telomerase inhibitors.

Telomerase is a weird enzyme – part protein (called hTERT), part RNA (hTR). Its job is to restore a tiny bit of DNA at the ends of chromosomes.As normal cells divide over the course of a lifetime, these tiny bits of DNA, called telomeres (prounounced TEE-low-mears), gradually get shorter and shorter until they virtually disappear. Without telomeres, the cell can no longer divide, and therefore dies.

Unlike normal cells, cancer cells have figured out a way to keep making telomerase so that telomeres are kept intact. The obvious implication is that blocking telomerase with drugs should destroy cancer cells – and indeed it does, at least in the lab.

The grumbling – by some of molecular biology’s biggest superstars – is unusually bitter because 90 percent of human cancers show over-activity of telomerase, suggesting that they would be vulnerable to anti-telomerase drugs.

At telomere meetings, it’s “common for people to sit around and tell Geron horror stories,” says  Elizabeth Blackburn, professor of biochemistry and biophysics at the University of California, San Francisco School of Medicine. The co-discoverer, in 1985, of telomerase, Blackburn consulted  briefly with Geron in the past but stopped that arrangement, citing potential conflict of interest. As a university employee, she is listed as a co-inventor of telomerase inhibition technology. She no longer has ties to Geron.

Carol Greider, the other co-discoverer of telomerase and a professor of molecular biology and genetics at the Johns Hopkins University School of Medicine, says that the legal agreements Geron writes to share materials with others “are often onerous,” she says, adding, “I have decided not to try to get material from them, knowing it would be difficult.”

Robert Weinberg, a professor of biology at the Massachusetts Institute of Technology and a member of the MIT-affiliated Whitehead Institute, is even more blunt. “No one in this country has had the temerity to move into this field – they didn’t want to risk the ligitation,” he says. “All this is a shame because telomerase is an extremely attractive target for anti-tumor therapy and Geron, by squatting on its patent estate, has really blocked other people from attempting to develop possible useful anti-tumor drugs.”

Not surprisingly, Geron strenuously disputes this.  “Those statements are simply not true,” says Geron’s chief scientific officer, Calvin Harley.  At a recent meeting in San Francisco and others over the last seven years, he says, “we have shown all our data. We’re highly collaborative. We have given our reagants [research materials] to hundreds of labs.”

And Nobel Laureate Tom Cech, president of the Howard Hughes Medical Institute and the co-discoverer, in 1997, of the protein portion of the telomerase enzyme, undertands that view. “I don’t see anything different in the way Geron is treating telomerase than the way any biotech company treats its intellectual property,”  he says, adding that he has “no connection” to Geron except that the company has licensed patents on discoveries made by Cech and his group at the University of Colorado.

Unlike most enzymes, which consist entirely of protein, telomerase is a combination of a protein called reverse transcriptase, which copies RNA into DNA, and a chunk of RNA, one form of genetic material that can also act as an enzyme.

Years ago, Blackburn noticed that the DNA on the ends of chromosomes “was growing and shrinking, which was not what DNA was supposed to do,” as she notes. She hypothesized that a special kind of enzyme called a polymerase must be at work. (Polymerases help create new chains of DNA.)

She and her then-graduate student Carol Greider found the enzyme and named it telomerase. It is highly active in early fetal development, when cells are rapidly dividing. But from birth through adulthood,  telomerase is made at low levels in normal cells and stored in a tiny structure called the nucleolus inside the nucleus. Just before a normal cell divides, telomerase moves to the nucleus where it restore telomeres to shrinking chromosomes.

In cancer cells, and normal cells that divide rapidly such as stem cells in the bone marrow and skin , telomerase goes back to its furious, fetal pace. As a drug target, this raises some concerns. Anti-telomerase drugs might harm some normal cells, though researchers say this is unlikely because tumor cells have shorter telomeres and therefore would be more susceptible than normal cells to anti-telomerase drugs. In addition, stem cells don’t divide often, and when they’re not dividing, they should not be impacted by the drugs.

Another concern is that, as cells “erode their telomeres, they may go into a state of genetic instability, which, ultimately, could fuel the emergence of resistance to telomerase and other anti-cancer therapies,” says Dr. Ron De Pinho, professor of medicine and genetics at the Dana-Farber Cancer Institute.

Despite such concerns and all the squabbling, telomerase research is chugging along. Studies on 20 different types of tumors in laboratory dishes and in at least 10 animal models show that blocking telomerase does indeed cause cells to die. (Internationally, Boehringer Ingelheim is also working on telomerase, though the company adds the “therapeutic benefit” from inhibitor drugs “remains an elusive target.”

Geron expects to start human trials later this year in patients with a kind of brain cancer called glioblastoma using a drug dubbed GRN163. This compound is a telomere-like bit of DNA that binds to the key region of the telomerase enzyme, blocking its action.

The GRN163 drug is not perfect, in part because it’s 10 times bigger than most drugs. (In general, the smaller the drug molecule, the more easily it gets into cells.) But so far, says Harley of Geron, GRN163 has shown “no significant toxicity.”

Geron is also conducting a clinical trial of a telomerase vaccine in 20 men with prostate cancer with researchers from Duke University.

Unlike conventional vaccines, this one is designed to treat, not prevent, disease. The Geron vaccine is made individually for each patient, using the patient’s own immune cells, which are removed from the bloodstream and coaxed to display tiny pieces of the telomerase molecule, like little flags, on their surfaces. These cells are then re-injected in hopes of triggering a widespread immune response to cells carrying telomerase “flags.”

Other ideas are in the pipeline, including using detection tests for telomerase to diagnose cancer from blood samples, making “toxic telomeres” to destroy cancer cells, using viruses controlled by telomerase regulators to kill tumor cells, and seeing whether newly-discovered proteins that regulate the binding of telomeres to the ends of chromosomes might also be drug targets.

All this will, of course, take time. But it may also take tinkering with the delicate balance of corporate interests and public health. 

As Tyler Jacks, director of the Center for Cancer Research at the MIT puts it, “There is a desperate need for more specific and more effective drugs for treating cancer. It would be extremely unfortunate if, due to intellectual property considerations, a very promising cancer target were not pursued as vigorously and as broadly as possible.”

Blood Pressure Drugs – Confusing but Crucial

by

In December, a study of more than 42,000 white and black Americans found that old-fashioned, cheap diuretics – “water pills” – work at least as well and sometimes better than more expensive drugs to treat high blood pressure and certain heart problems.  The study, dubbed ALLHAT, was published in JAMA, the Journal of the American Medical Association.

In February, a study of more than 6,000 mostly white Australians came to a different conclusion – that drugs called ACE inhibitors were better than diuretics, although only for men (for unclear reasons). This study was published in the New England Journal of Medicine.

Between now and May, it falls to Dr. Aram Chobanian, dean of the Boston University School of Medicine, and his committee of experts picked by the National Heart Lung and Blood Institute to reconcile the studies and tell America’s 50 million hypertensives what to do.

Their conclusions are crucial. Hypertension doubles the risk of heart attack and is the leading risk factor for stroke and heart failure. One in four adult Americans has hypertension – defined as a reading of 140/90 millimeters of mercury or higher.

(The top number is the systolic pressure, taken as the heart muscle contracts. The lower number is the diastolic, as the heart relaxes. Normal blood pressure is 120/80, but even readings of 130/ 85 should be considered a red flag.) 

High blood pressure is so common, especially among older people,  that many patients don’t’ take it as seriously as they should. “High blood pressure doesn’t make you feel bad,” says Dr. Michele Hamilton, co-director of the heart failure program at the University of California, Los Angeles. This makes it harder for people to change their diets (and reduce salt), lose weight, reduce stress and take medications.

High blood pressure is also tricky for doctors because they usually don’t know what causes it. In 5 percent of cases, it’s caused by kidney and adrenal problems, or legal and illegal substances such as prednisone, cocaine, ephedrine, even licorice. But 95 percent of hypertension is deemed “essential” or “primary” because the cause is unknown.

Basically, blood pressure is a matter of hydraulics. If the pressure inside artery walls is too low, a person can go into shock and die. If the pressure is too high, because vessels are too narrow or rigid or the heart beats too hard, a person can develop heart and kidney failure and stroke. 

With age, the risks get worse because blood vessels become more rigid. Indeed, data from the Framingham Heart Study show that a person who has a normal blood pressure at 55 has a 90 percent chance of developing high blood pressure eventually.

Regulation of blood pressure is complex. Short term fluctuations are controlled by the nervous system, specifically hormones such as adrenalin and noradrenalin. Longer term, a key player is angiotensin II, a kidney hormone that makes vessels constrict.

If you have hypertension, the first remedy to try is behavioral: exercise and nutrition. This means losing weight if you’re heavy, adopting the DASH diet and restricting salt. Even losing just 10 pounds can lower blood pressure significantly.

It’s not fully clear whether consuming too much salt actually causes hypertension. But age-related increases in blood pressure can be minimized by reducing salt (sodium) intake to about  2.4 grams of sodium a day. (This equals 6 grams, about 1 teaspoon, of salt.)  In practice, this means not adding salt when cooking or eating and avoiding many canned and fried foods, including foods containing soy sauce.

The DASH diet, plus salt restriction, clearly lowers blood pressure. The DASH diet is rich in fruits, vegetables, lowfat diary foods, potassium, calcium, magnesium, fiber and protein. It’s low in total and saturated fat, red meat, sweet foods and sugary drinks.

Stress reduction helps, too. Dr. Thomas Graboys,  chairman of the Lown Cardiovascular Foundation, asks patients two questions: Do you look forward to going to work? And, do you look forward to going home at night? “If someone says no to either,” he says, stress may be contributing to that person’s problems.

To combat stress, Dr. Herbert Benson, president of the Mind/Body Medical Institute and associate professor of medicine at Harvard Medical School, recommends the “relaxation response.” That means taking 10 to 20 minutes a day to meditate, pray or quiet the mind and body through focused concentration. Stress reduction, he says, can minimize the “vicious cycle” in which people panic about their hypertension, making it worse.

If you’ve done all this and still have high blood pressure, you probably need medication. And that’s where doctors disagree – not on whether medication is needed, but on which drugs to try first. If hypertension is stubborn, you’ll probably need several drugs, and there are many to choose from.

Diuretics such as hydrochlorothiazide (Hydrodiuril) or chlorthalidone (Hygroton) flush excess water and salt from the body, allowing the heart to work less hard. One reason diuretics fared well in the ALLHAT study is that 32 percent of participants were black. Blacks, perhaps for genetic reasons, tend to be sensitive to salt and hence, highly responsive to diuretics.

Beta-blockers such as propanolol (Inderal) are another staple. They reduce nerve impulses to the heart and blood vessels, making the heart beat more slowly and with less force.

A similar class of drugs is the alpha blockers such as doxazosin (Cardura), which also reduce nerve impulses to blood vessels. But the Doxazosin arm of the ALLHAT study was stopped early because those patients had higher rates of cardiac problems.

ACE-inhibitors such as lisinopril (Zestril) relax blood vessels by blocking the formation of angiotensin II. (A newer class of drugs called angiotensin antagonists such as losartan (Lotrel Cozaar) act differently, by blocking receptors for angiotensin II in vessels.)

And then there are the calcium channel blockers (CCBs), drugs such as amlodipine  a combination of amlodipine and benazepril (Lotrel). They lower pressure by blocking calcium, which causes vessels to constrict.

Granted, it’s a bit confusing. But it’s “very reassuring” that the ALLHAT study found diuretics to be so effective, says Dr. Sid Smith, past president of the American Heart Association and professor of medicine at the University of North Carolina at Chapel Hill.

And because diuretics are cheap – about 13 cents a pill versus 10 times that for other medications – “there is no cost-quality tradeoff,” as Dr. Lawrence J. Appel, a hypertension specialist at Johns Hopkins Medical Institutions noted in a JAMA editorial.

As to which drug to start with, stay tuned for the findings from Chobanian’s committee. In the meantime, work with your doctor until you find a drug, or combination of drugs, that get your blood pressure out of the danger zone.

The Glycemic Index – Should You Worry?

by

If you haven’t heard of it yet, get ready to grapple with the “glycemic index,” the latest wrinkle in America’s endless diet debate.

On the surface, the glycemic index is a simple concept – a way to measure how much blood sugar goes up in the two hours after eating carbohydrates. Carbohydrates with a high glycemic rating, like cake with icing, trigger huge, rapid spikes in blood sugar, followed by steep spikes in insulin, the hormone that escorts sugar into cells. Carbohydrates with low glycemic ratings, like whole grains and fresh fruits and vegetables, trigger more modest, slower rises.

The basic idea is that high glycemic carbohydrates are bad because they leave the stomach fast and trigger a rapid rise in blood sugar and insulin, which is soon followed by a crash in blood sugar that prompts renewed hunger. The result can be more calories consumed and more weight gained.

Using the index in real life is dicey. For instance, carrots have a high glycemic rating, but they’re good for you. French fried potatoes could be interpreted as having a better (lower) rating than a naked baked potato, because they contain fat, which causes slower emptying of the stomach and hence, a more modest rise in blood sugar and insulin, notes Karen Chalmers, a registered dietician and director of nutrition services at the Joslin Diabetes Center in Boston.

But what is important about the glycemic index is its symbolic value as a reminder to ever fatter, ever more confused Americans that carbohydrates, the big no-no of current fad diets, are not a monolithic entity. There are “good” carbs – found in whole grains, fruits and veggies – and “bad” ones, found in highly refined baked goods, candy and many processed foods, a message that some nutritionists, most notably Dr. Walter Willett, chairman of the department of nutrition at the Harvard School of Public Health and author of “Eat, Drink and Be Healthy, have long been trying to get across.

The glycemic index has actually been around for 20 years, but a series of recent studies, and popular books like “The Glucose Revolution” by Jennie Brand-Miller et al, have propelled it to center stage.

In the last several years, for instance, Dr. David Ludwig, director of the obesity program at Children’s Hospital in Boston, and others have published studies suggesting that obese people put on low-glycemic diets lose more weight than those on reduced-fat diets.

 In one such study, Ludwig gave some obese youngsters high glycemic index meals and others, low-glycemic ones. The number of calories given to both groups was the same. But the kids on the high glycemic diet ate almost twice as much when allowed free access to food as the others. Obviously, more snacks mean more calories and more weight gain.

That said, there are limits to the logic behind the glycemic index. It is incorrect to infer, as some do, that sugar is “addictive.”  Nor is it correct, as some diet gurus say, that carbohydrates turn into body fat more easily than fat. It’s fat that’s most efficiently converted into body fat, that is, it takes the fewest calories for the conversion. Carbohydrate is the next most efficient, then protein.

More important, a calorie is still a calorie is still a calorie. No matter what combination of protein, fat and carbohydrate you eat, if you take in more calories than you burn, you’ll get fat.

And getting fat triggers a dangerous cascade of biochemical events. Excess body weight causes the pancreas to work overtime to produce enough insulin, a phenomenon called insulin resistance, notes Dr. Edward Horton, director of clinical research at the Joslin Diabetes Center in Boston.

Insulin resistance, in turn, is associated with a whole cluster of metabolic problems, even if it never leads to outright diabetes. Syndrome X, also called Insulin Resistance Syndrome or Metabolic Syndrome, is characterized by elevated triglycerides (fats), low HDL (“good” cholesterol), high blood pressure, changes in blood clotting patterns and a build-up of plaque in artery walls. High insulin prevents fat cells from dumping fatty acids into the blood stream (thereby making the body store more fat) and makes the liver convert more fatty acids to triglycerides, which raises the risk of heart disease.

High insulin can also raise the level of PAI-1, or plasminogen activator inhibitor, which prevents the breakdown of potentially dangerous clots. With high PAI-1 levels, clots are not broken down and the risk of heart attack and stroke goes up. Insulin resistance is also associated with high levels of C-reactive protein, a marker for heart disease.

Eating too many calories – from any source, protein, fat or carbohydrate – can lead to obesity. But part of the problem today – two-thirds of Americans are overweight and one third, obese – is that for years, we were all told to cut down on fats. There’s still some truth in this message-saturated fats and trans-fats (like those in some margerines) are dangerous because they boost cholesterol and the risk of heart disease. Some fats, though,  are good, notably the monounsaturated and polyunsaturated fats found in olive, canola or peanut oils, nuts, other plant products and fish. These fats can lower the bad kind of cholesterol (LDL) without lowering the good (HDL).

The lesson that most of us have absorbed over the years, however, was not this mixed message but a starker one: all fat is bad. That, not surprisingly, prompted consumer demand for “low fat” foods, the food industry responded, with a vengeance.  

 In recent years, “the food industry has screwed around with fat-free foods to keep the taste up,” says Dr. David Heber, director of the University of California, Los Angeles Center for Human Nutrition and author of “What Color is Your Diet?”

“They lowered the fat content but raised the sugar,” he says, noting that many processed foods are now loaded with high fructose corn syrup, in part because “corn is subsidized by the federal government.” Indeed, one reason for the current obesity epidemic is all the high fructose corn syrup added to processed foods.

So whee does this leave us, besides fat and frustrated? It’s pretty straightforward, actually. Don’t take the glycemic index itself too literally. It’s too complicated and you could spend hours trying to calculate the glycemic rating for each food on your plate.  

But do use the concept as a valid, potent way of remembering that not all carbohydrates are created equal. After all, as Ludwig points out, lumping all carbohydrates together as a diet rationale has clearly not worked to help people lose weight.

Bottom line? Stick to whole grains and fresh fruits and veggies, avoid refined carbohydrates as much as you can. Chances are, you’ll be less hungry and much healthier.

Sleep and Memory – Are they Intertwined?

by

In July, researchers led by Robert Stickgold, an assistant professor of psychiatry at Harvard Medical School, reported that a full eight hours’ sleep after learning a motor task boosts performance by 20 percent the next day.

Even a one-hour nap can improve scores on a simple visual task, others reported in May.

Perhaps even more compelling, Belgian researchers, using a brain imaging technique called PET scanning, reported two years ago that when people perform reaction time tests, certain areas of the brain become activated. These same areas “light up” again when the people experience REM (rapid eye movement, or dreaming) sleep, as if their brains were actively rehearsing what had been learned.

Over the years, researchers have found tantalizing evidence that sleep may enhance learning and memory. Some have showed that infants who learn a head-turning response have more REM sleep than those who failed to learn the response. Others, that people given 90 minutes of training in Morse code showed an increase in REM sleep. Still others, that people who did well learning French increased their REM sleep, while poorer learners did not – and that the sooner the good learners started dreaming in French, the higher their scores on French tests. (The poor learners never did dream in French.)

Case clinched, right? Sleep, particularly REM sleep, seems to boost memory, just as many scientists – and mothers – have been saying for years.

Would that it were that simple.

“Everybody knows sleep has something to do with memory – except people who study sleep and memory,” says Stickgold.

Brain researchers would like nothing better than to come up with a neat paradigm of how sleep affects memory.

It would go something like this: Learning creates chemical changes in specific cells in specific parts of the brain. When a person sleeps shortly after learning, and perhaps especially when she dreams that night, the brain takes these fragile, new memories, shuffles them around into a more permanent home, or at least a more permanent set of neural circuits. And  – Presto! – the memories would be firmly “consolidated” by morning.

There are two main reasons why confidence in such a nice, simple scenario is impossible, as least for now: At the electrical and biochemical level, sleep itself is devilishly complicated. Memory, arguably, is even more so.

A night’s sleep typically goes from light (Stages 1 and 2 sleep to deeper stages 3 and 4, known as slow wave sleep). All of these are called non-REM sleep. Non-REM sleep alternates with REM, or dreaming sleep, with REM periods getting longer and non-REM periods getting shorter as the night progresses.

One reason for thinking that REM sleep may be involved in memory consolidation is that the brain behaves differently during slow wave and REM sleep. During deep sleep, the brain is relatively inactive, and electrical patterns are slow and synchronized; during REM, it is extremely active, and desynchronized..

Brain chemistry changes, too. During REM, some neurotransmitters, or chemical  messengers, especially norepinephrine and serotonin  are virtually shut off while others, notably acetylcholine, believed to be a memory booster, go up.

Memory is even trickier. Scientists divide memory into two basic categories, declarative and procedural. That’s the difference between “knowing that” and “knowing how,” notes psychologist Carlyle Smith of Trent University in Peterborough, Ontario.

Declarative memory involves learning facts – knowing that the French Revolution began in 1789. Knowing how is knowing, often without knowing that you know, how to turn the key in the ignition to start the car. Declarative memory is “explicit,” and usually consciously acquired; procedural memory is “implicit,” often unconsciously acquired.

The trouble is, although declarative memory is what most of us mean when we talk about memory, most of what researchers study is procedural memory – the less juicy stuff like learning finger-tapping exercises.

For declarative memory, there is little evidence that sleep, even REM sleep, has any effect, says Smith of Trent University.

“No matter what I have done – I have deprived people of sleep, I have deprived people of REM sleep, I have deprived them of non-REM sleep –  and I have never seen any difference [in declarative memory] between people who got a good night’s sleep and those who didn’t,” says Smith of Trent University.

Dr. Jerome Siegel, professor of psychiatry at the David Geffen School of Medicine at UCLA and chief of neurobiology research at the VA Greater Los Angeles Healthcare System Sepulveda, agrees, noting in a paper in Science in 2001 that the evidence for such a link is “weak and contradictory.”

And a link between sleep and procedural memory? That’s stronger.

In 1991, researchers studied people learning trampolining, which required  new, complex motor skills. The best learners showed increases in REM sleep (and no differences in non-REM sleep); those in control groups who expended the same number of calories but didn’t learn new motor skills showed no difference in either REM or non-REM sleep.

REM and some non-REM sleep may help with a different type of procedural task – visual learning. In a paper published in 2000, Stickgold and his team found that improvement on a visual task increased with stage 3 and 4 slow wave sleep in the first part of the night, and with REM later in the night. The real payoff, he finds, is with REM sleep in the final two hours of an 8-hour sleep.

In a sequel to Stickgold’s studies, doctoral student Sara Mednick wanted “to see if napping had the same effect as a night’s sleep.” To find out, she used the same visual memory task and tested volunteers on it at four points in the same day. They all got worse as the day went on.

So she let some volunteers take a half-hour nap between the second and third session and others, an hour nap. The half-hour nappers were able to stop the decline in performance. The hour-nappers not only stopped the decline but performed as well as they had first thing in the morning. The long nappers, by the way, exhibited both slow wave sleep and some REM sleep as well.

The bottom line in all this? There is still much that remains a mystery. Someday, maybe they’ll figure it all out. For now, “the simple answer is that we don’t know,” says Stickgold of  Harvard. “You  push this system just a bit and you stumble onto complete ignorance.

New Trial to Detect Early Lung Cancer

by

Sadly enough, it often seems to take a celebrity patient to get the rest of us to sit up and take notice of certain diseases, especially diseases  in which the patient’s own behavior contributes to the risk.

This time, the celebrity is an active, young mother, Kara Kennedy , 42, the daughter of Sen. Edward M. Kennedy (D-Mass.). And the disease is lung cancer – the biggest cancer killer in the country, whose primary cause is smoking – an addiction, to be sure, but a potentially modifiable behavior as well.Kara Kennedy, a smoker, had a cancerous portion of her right lung removed 12 days ago at Brigham and Women’s Hospital in Boston and was recuperating last week before starting chemotherapy.

Though she may receive lots of emotional support, the societal prejudice against many lung cancer patients runs deep.

But this longstanding attitude is beginning to lift, thanks in part to a massive new study launched last fall by the National Cancer Institute. The $200 million, 8-year study is called the National Lung Screening Trial (NLST). It will involve 50,000 healthy smokers and former smokers at 30 medical centers across the country. So far, almost 10,000 have signed up. (For more information, visit http://cancer.gov/nlst or call, 1 800 422 6237 begin_of_the_skype_highlighting              1 800 422 6237      end_of_the_skype_highlighting.)

The trial is designed to determine which screening test, chest X-rays or a relatively new technology called spiral CT scanning, is more effective at reducing deaths by catching cancers at an earlier stage. (Currently, neither test is recommended for routine screening.) Researchers will also collect and store blood, urine and sputum samples to see which participants might be at higher genetic risk of lung cancer.

This year, 171,900 Americans will be told they have lung cancer and most will have spreading disease at the time of diagnosis. (Breast cancer, by contrast, will strike more people (212,600), but most cases will be caught before the cancer has spread.)

In a sense, there might appear to be no need for the big lung cancer trial. Everybody already knows that smoking causes lung cancer, or to be more precise, that it causes 80 to 85 percent of cases. (It’s not clear why nonsmokers also get lung cancer, why lung cancer is rising among nonsmokers, or why female nonsmokers are more likely than male nonsmokers to get the disease.)

So, if all smokers just quit, much of the lung cancer problem could disappear, which would free researchers (and funds) for cancers with less obvious causes.

But in reality, there’s an enormous need for this trial, says Dr. Denise Aberle, chief of radiology at the David Geffen School of Medicine at UCLA and one of the two co-principal investigators in the study.

Historically, lung cancer has gotten less funding than other cancers, even though it is responsible for more cancer deaths per year than cancer of the colon, breast, prostate and pancreas combined.

In 2001, the latest year for which figures are available, the National Cancer Institute spent a relatively paltry $206.5 million on lung cancer, compared to $475.2 million on breast cancer. Yet lung cancer is projected to kill 157,200 people this year, according to the American Cancer Society – nearly four times the deaths expected from breast cancer.

And the “reservoir” of people at risk is huge – 45 million current smokers and 45 million former smokers. Moreover, if the $200 million trial, as hoped, shows that early detection translates into lives saved, it could make a sizeable dent in the nearly $5 billion the country now spends annually to treat lung cancer patients, Aberle notes.

“This is an incredibly important trial,” agrees Dr. Phillip Boiselle, director of thoracic imaging at Beth Israel Deaconess Medical Center in Boston, one of the Massachusetts sites for the study. (The other is at Brigham and Women’s Hospital). “Even if widespread efforts at smoking cessation are successful, lung cancer will continue to be a major problem because the risk among former smokers, though less than for smokers, is still high.”

Not only does the trial address “the most lethal cancer that we face,” adds Dr. Andrew C. von Eschenbach, director of the National Cancer Institute, it should point the way to better detection at a stage of disease when therapy can do the most good. “We need a proven effective way to detect lung cancer when it is still curable.”

In recent years, studies of smokers and former smokers (including one in Japan in 1996 and one in New York in 1999) have convinced researchers of the need for a truly definitive trial.

These studies showed that spiral CT scans (an improved version of the standard computed tomography X-rays) are good at catching cancers while they are small) and in fact, are better than chest X-rays. But because these studies were small and did not randomize participants to get CT scans or chest X-rays, they could not show whether earlier detection saves lives, says Robert Smith, director of cancer screening at the American Cancer Society.

Another study, by the Mayo Clinic in 2002, also showed that spiral CT scans are better than chest X-rays at finding small tumors, but it highlighted a problem that the earlier studies also suggested: spiral CT scans are so sensitive that they often pick up tiny abnormalities that turn out not to be cancer.

Indeed, most of the abnormal nodules detected in the Mayo study turned out to be false alarms, often just tiny patches of scar tissue from bronchitis or pneumonia. But finding any suspicious nodule often sets a patient on a path of follow-up and further testing, sometimes including surgery.

The high rate of false positives “is a big drawback” to CT scans, says Aberle of UCLA. “You convert healthy participants into patients and expose them to additional tests or additional anxiety.”

Despite the risk of false positives, some worried smokers and former smokers already get spiral CT scans on their own. (The test costs $300 to $400 and is often not covered by insurance unless a doctor suspects lung cancer and orders it.)

Though it might seem obvious that CT scans constitute a better detection method, there are actually significant pros and cons to both the scans and chest X-rays.

The advantage of a spiral CT scan is that it can pick up abnormalities smaller than a dime, while chest X-rays find nodules only if they are the size of a quarter.

CT scans also give doctors a 3-D image, while chest X-rays provide only a 2-D image. On the other hand, while chest X-rays can miss up to 30 percent of suspicious nodules, they also are far less likely to yield false positives. Then again, chest X-rays expose a person to low dose radiation, while the exposure from spiral CT scans is roughly 15 times higher. (Even so, the CT scan is a lower dose of radiation than a person gets from environment radiation every year.)

The bottom line, of course, is that no knows yet which method is better. But the strong hope is that whichever one is, that earlier detection will indeed save lives.

Our Columnist Goes Under the Knife

by

I was very scared, shivering as much from fear as from the chilly room temperature. I was waiting on a gurney at Brigham and Women’s Hospital to be wheeled in for a catheter ablation, an invasive cardiac “procedure.” (Ah, the euphemisms.)

In a totally bizarre twist of fate, I had several weeks earlier interviewed Dr. Laurence Epstein, chief of the cardiac arrhythmia service, in preparation for a column I was working on about new treatments for arrhythmias.

He had shown me his very cool, animated PowerPoint presentations and explained the details of the procedure. As a medical writer, I was fascinated. The process involves inserting catheters through veins in the patient’s groin, snaking them up into the heart, then using the wires to record the heart’s electrical activity – from the inside. Once this activity is “mapped,” the catheters deliver radio frequency waves to ablate (i.e., kill) the clusters of cardiac cells that trigger the abnormal rhythms.

As Epstein showed me his pictures and scholarly articles, I casually mentioned that, once a year or so, I got tachycardia – very rapid heart beat. He instantly drew me pictures of what he guessed was wrong – SVT, or supra-ventricular tachycardia, which affects an estimated 500,000 to 1 million people with varying severity.

Like many of these people, I had probably been born with two electrical pathways through a key switching station in the heart, the atrial-ventricular (AV) node, instead of the normal one. In people like me, electrical signals from the right atrium (one of the upper chambers of the heart) that tell the heart when to beat sometimes go down the wrong pathway and then back up the normal pathway, creating an electrical circuit that causes the heart to beat very rapidly.

“We can cure that with catheter ablation, you know,” he said. “Great,” I said nervously. “If it ever gets worse, I’ll be back.”

Several weeks later, totally out of the blue, it did get worse, much worse. I’m pretty fit – I either swim a mile or do 10 miles on my exercise bike nearly every day. But suddenly, I couldn’t walk a block without sending my heart rate up to 190 beats a minute. Even just washing my hair in the shower triggered it. I was fast becoming a cardiac cripple, afraid of climbing even one set of stairs lest I become short of breath or pass out.

The whole thing was frightening, even though, rationally at least, I knew that SVT was not life-threatening.

But fear and discomfort weren’t the only things I had to cope with. Suddenly, I had a brand new, tricky role: Patient. On the plus side, telling people about my unexpected medical problem meant that I got a huge amount of support from friends.

But becoming a Patient also meant that I instantly became the target of masses of unsolicited advice from people. I was a Rorschach ink blot upon people could now feel free to foist their pet theories.

Interestingly, the doctors I talked to – both friends who are doctors and doctors I consulted for this- were uniformly terrific listeners, contrary to the bad rap they often get. They listened calmly, respectfully, and took me seriously.  When I asked, they offered advice, including one doctor-friend’s very useful mantra, “Stay cool.”

My close friends did all the right things, too. They called during the interminable weekend while I waited to have the procedure. They emailed. They hugged.  They brought flowers, and excellent squash soup. But most important, they neither pooh-poohed my problem nor rushed in to solve it. They had a natural way of simply listening, with attention and kindness, taking in to their own hearts what I was going through, without trying to take over or tell me what to do.

On the other hand, I rapidly came to the conclusion that my friends are pretty special because a number of other people were truly awful at listening and giving support. Their insensitivity ended up putting the burden of patience and diplomacy on me, as a tried to fend off unsolicited advice diplomatically – at a time when I had little patience to spare.

For instance, some people couldn’t stand to let me finish before interrupting with their own horror stories.

Others insisted, quite adamantly, that my problem must be “stress.” This was especially annoying, first, because it seemed to imply that my arrhythmia was my own fault and, second, because it seemed to invalidate the reality of my symptoms, which had been confirmed by cardiac testing. As one friend put it, “Telling someone they sound stressed blames them. Saying, ‘What a stressful situation you’re in’ doesn’t.”

Sure, stress can sometimes boost the chances of getting some diseases, mostly notably, the common cold. But it shouldn’t be the explanation of first resort, partly because it blames people and partly because lots of people get very stressed and never get sick.

Indeed, military studies show that soldiers discharged during World War II for neuroses had no high cancer rates 24 years later than their mentally healthier comrades. And a report in the November 15 issue of Cancer shows that even extreme stress (such as losing a child) is not a risk factor for cancer.

If some people were too eager to blame the victim, others were almost too kind – so eager to DO SOMETHING that they trampled a bit on my autonomy, not giving me the open space to decide what concrete help, if any, I really wanted.

Some people, I discovered, also seem programmed to pounce on someone else’s illness as an opportunity to promulgate their religious views. Several years ago, when a dear friend of mine got a bad diagnosis, one woman actually said to me, “It’s up to God, not the doctors.” Whether this is true or not, it was her worldview, not mine. Which meant I had the burden of fending it off, as tactfully as I could.

Why are some people such naturally good listeners and others find listening so hard?  I wondered aloud about this with my across-the-street neighbor, a psychiatrist, in the count-down days before my procedure. His conclusion makes sense: “When you tell people how helpless you feel,” he said, “they feel helpless. They can’t stand feeling helpless, so they jump in with advice.”

Mercifully, the big day came and, scared though I was, the procedure was substantially less awful than I expected. The nice guys with the great drugs konked me out briefly while they inserted the catheters and when I woke up (the type of anesthesia I had is called “conscious sedation”)  the procedure was already underway. I could feel the arrhythmias as Epstein and his team intentionally triggered them. But none of these was anywhere near as disconcerting as the ones I’d been having spontaneously. I also knew that they could stop any arrhythmia at any time, a huge comfort.

The actual ablation felt a bit hot from my left hip bone to my left collar bone, but not uncomfortable. In fact, I found I was able to chat with the nurse through much of the procedure. I was also lucky. Sometimes, catheter ablations take three to four hours or longer, but mine was quick – an hour and a half.

Then it was OVER! I was ecstatic. I had to lie still for four hours so the puncture wounds in my leg veins could begin to heal, but that was easy.

I went home that same night, feeling terrific. No more tachycardia. No more worries about walking, or climbing stairs. Not even a hangover from the drugs.

I had trusted Epstein and his team and they were magnificent. Thanks to them, I could trust my own heart again.

As for the creepiness of researching a medical problem, then actually getting it. That’s solved, too. I’m writing about hangnails and pimples from now on.

New Fixes for Electrical Problems in the Heart

by

Until last winter, Joseph Moniz, 50, a Fall River man with congestive heart failure was waiting, like 4,000 other Americans, for a heart transplant to save his life.

He never got it. But he got something better: a small device called an implantable cardioverter defibrillator (ICD) like the one Dick Cheney got, a familiar gadget but with a new twist.

Like older defibrillators, Moniz’ device can shock his heart back to normal if the lower chambers, or ventricles, start beating in a rapid, life-threatening rhythm. This kind of arrhythmia, called ventricular fibrillation, causes 350,000 sudden deaths every year.

But the new device in Moniz’ chest can also do something else – re-synchronize the beating of the ventricles so that they work efficiently. This is a potentially a huge boon for many of the 5 million Americans with congestive heart failure, a condition in which the heart beats inefficiently and fluid accumulates in tissues.

Other heart patients, at a handful of medical centers around the country, are getting a variety of other novel treatments for the electrical problems in their hearts, including a promising technique called catheter ablation for atrial fibrillation and other arrhythmias.

For decades, cardiology was ruled by medical plumbers, doctors whose main concern was fixing crucial coronary arteries that become clogged with cholesterol. But now, a number of (literally) electrifying advances has put a new batch of cardiac gurus in the limelight as well: the cardiac electricians, or more precisely, the electrophysiologists.

In the heart, the electrical signals that control rhythms originate in a built-in pacemaker, the SA, or sinoatrial node, a small bit of tissue at the top of the right atrium. Normally, the SA node produces about 60 heartbeats a minute. The electrical signal spreads through the right and left atrium, then activates the AV, or atrioventricular node, a relay point between the upper and lower chambers.

From there, the electrical signal spreads through the ventricles. After the ventricles contract, the signal dies out and the heart waits for a new signal from the SA node.

When these electrical signals become deranged, cardiac hell can break loose, including atrial and ventricular fibrillations, in both of which the heart beats wildly and very rapidly. Such arrhythmias “are becoming an epidemic” because the risk goes up with age and the population is aging, notes Dr. Valentin Fuster, director of the Cardiovascular Institute and Health Center at Mt. Sinai Medical Center in New York.

But treatments often help. Last March, the New England Journal of Medicine published a major study called MADIT II that was stopped early because the results were so clear. It involved more than 1,200 patients and showed that those randomly assigned to get standard ICDs to shock their hearts back into normal rhythm when ventricular arrhythmias occurred had a 31 percent decreased risk of death compared to those receiving standard drug (non-ICD) therapy. Roughly one million Americans have heart attacks every year, and more than a third wind up with poor ventricular function as a result.)

The new generation of ICDs not only can shock the heart back to normal rhythm but can synchronize the coordination of the ventricles by way of an extra wire, or lead, that runs from a pacemaker in the chest to the left ventricle, the main pumping chamber of the heart.

Several new ICDs – Contak CD by Guidant and InSync ICD by Medtronic – were approved for marketing this summer. (A third such device, Epic HF made by St. Jude Medical, is in US testing now and is on the market in a limited way in Europe.)

Some congestive heart failure patients now getting resynchrozining ICDs are “turning their beepers in and feeling so well with ventricular resynchronization that they no longer need a heart transplant,” says Dr. Lynne Warner Stevenson, co-director of the cardiomyopathy and heart failure program at Brigham and Women’s Hospital.

Just as ever-improving ICDs are transforming care for patients with ventricular arrhythmias, so, too, is catheter ablation improving care for people with atrial fibrillation, a problem that strikes more than 2 million Americans.

In “A Fib,” electrical signals in the heart’s upper chambers, or atria cause the heart muscle to flutter wildly, which in turn reduces the efficiency of the ventricles. This allows blood to pool and form clots that can lead to strokes.

Some people with A Fib don’t mind the symptoms and mainly need to worry about the risk of stroke from blood clots. Others find the erratic heartbeats drive them crazy.

In a recent study published in the New England Journal of Medicine, researchers found that for older patients who were at risk of stroke from atrial fibrillation, treatments to control heart rhythm were no better at preventing death than treatments to control heart rate.

But other data suggest that for people whose main concern is disruption of quality of life because of A Fib, catheter ablation may provide substantial relief.

In this treatment, electrophysiologists place catheters, or tubes, into the heart and use them to send use radio waves to burn away specific, tiny areas, particularly those on veins going from the lungs to the heart, that trigger arrhythmias.

“Until a year or two ago, no one ever thought you could use catheters to approach this problem,” says Dr. Kalyanam Shivkumar, director of interventional cardiac electrophysiology at the David Geffen School of Medicine at UCLA.

Now, says Dr. Davendra Mehta, director of the cardiac electrophysiological lab at Mt. Sinai Medical Center in New York, the technique could become for some patients “the treatment of choice.”

Indeed, catheter ablation is a potential “cure” for atrial fibrillation, says Dr. Laurence M. Epstein, chief of the arrhythmia service at Brigham and Women’s Hospital in Boston, although Dr. Jeremy Ruskin, director of Cardiac Arrhythmia Service at Massachusetts General Hospital, is more cautious. The technique is “results in dramatic outcomes in some patients,” Ruskin agrees,  but “the long-term cure rate is only about 50 percent in the best hands.”

Initially, electrophysiologists thought they had to carefully map out the regions of the heart that were triggering the arrhythmias, says Epstein of Brigham and Women’s Hospital.

To do this, doctors threaded a tube (the catheter) through a blood vessel in the groin up to the heart. Under X-ray guidance, doctors then watched on TV screens as they passed the catheter over different regions of heart muscle, recording electrical activity. Areas of the heart that produced bursts of rapid beats were deemed to be arrhythmia trigger centers. To stop the arrhythmias, doctors then delivered radio waves to the troublesome regions.

But recently, electrophysiologists have found that the mapping step is not always necessary because in many cases of atrial fibrillation, the trigger is the region where the pulmonary veins attach to the heart.  Destroying this region can get rid of arrhythmias.

Researchers are also experimenting with destroying electrically-dangerous tissue with ultrasound, microwaves and cryogenic techniques that burn by freezing tissue.

There is still, as Ruskin of MGH and others warn, a long way to go before all arrhythmias can be controlled. But it’s “a very exciting area – there’s a tremendous amount happening.”

Nobody needs to tell that to Joseph Moniz, whose electrophysiologist, Epstein of Brigham and Women’s Hospital, says, “He’s like a new man.” Now off the heart transplant list, Moniz is climbing stairs, playing drums and doing other things he thought he’d never do again.

“I washed my truck for the first time in a couple of years,” Moniz says jubilantly. He still can’t work, but says, “I feel excellent.”