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Of all the health issues that loom large with age, memory loss is among those that provoke the most worry. A big reason is the uncertainty: people often wonder if their occasional memory slips are just a normal part of growing old or early signs of Alzheimer’s disease, the most common form of dementia. A study, published in today’s issue of the journal Neurology, sheds some light—and perhaps offers a bit of reassurance—about the connection between self-reported memory loss and a diagnosis of dementia.
The study included 531 people with an average age of 73 and no signs of Alzheimer’s or signs of dementia. They took memory and thinking tests every year for an average of 10 years. Researchers also asked participants if they noticed any changes in their memory over the past year. Slightly more than half reported memory changes, at an average age of 82.
About 1 in 6 developed dementia during the study, and 80% of those had previously reported memory changes. But it took about nine years from the first self-report of a memory change, a possible early sign of dementia, to a diagnosis of mild cognitive impairment, an intermediate stage between normal memory loss and dementia. The transition to dementia usually took about 12 years.
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That relatively long time period means that if you notice troubling memory changes, there’s no cause for immediate alarm, as the study authors note (see “Memory loss warning signs: When should you worry?”). That period could offer a window for intervention during those first early signs of dementia, but we don’t yet have any proven therapies to prevent or stop Alzheimer’s disease or other memory-related illnesses.
Still, this study is a valuable addition to our understanding of Alzheimer’s progression, says neuropsychologist Rebecca Amariglio, PhD, an instructor in neurology at Harvard Medical School. “We’re never going to cure or delay Alzheimer’s if we don’t start to identify what goes on early in the disease. Early intervention is where things are headed,” says Amariglio, who studies early indicators of Alzheimer’s disease.
If you’re concerned about your memory, see a doctor and get a baseline assessment. It can be used as a comparison in the future. If you’re between 65 and 85 years of age and have normal memory and thinking skills, you might be eligible to enroll in large, nationwide study to test a new investigational treatment to slow memory loss cause by Alzheimer’s disease. You can learn more about the “A4” (Anti-Amyloid Treatment in Asymptomatic Alzheimer’s) study, led by Harvard Medical School professor of neurology Dr. Reisa Sperling, at http://a4study.org.
The FDA’s approval in 2010 of the blood-thinner dabigatran (Pradaxa) got many doctors excited. This drug got the green light after a head-to-head trial with warfarin (generic, Coumadin) in people with an irregular heart beat from atrial fibrillation.
Pradaxa was at least as effective as warfarin for preventing stroke-causing blood clots, and possibly caused fewer bleeding side effects. In addition, it is easier to use. Pradaxa doesn’t require frequent blood tests, and isn’t affected by food, like warfarin is.
“Clinicians in the United States are excited to have the first new oral anticoagulant in over half a century,” said Dr. Richard Becker, Director of the Cardiovascular Thrombosis Center at Duke School of Medicine in North Carolina, in an interview with the medical journal Nature Reviews Drug Discovery. “This approval gives clinicians an opportunity to select therapies based on patient need.”
Since then, studies of Pradaxa have slightly dampened the enthusiasm for the new drug. Take, for example, the results of a University of Pittsburgh survey of 9,400 men and women covered by Medicare. All had atrial fibrillation, an irregular heart rhythm that lets blood clots form in the heart. None had damaged heart valves. When these clots get into the bloodstream, they can cause strokes. In this group, 1,300 had been prescribed Pradaxa and 8,100 took warfarin. The researchers followed these men and women until they either stopped using the drug, switched to a different blood thinner, died, or until December 2011.
Among those taking Pradaxa, 9% experienced a major bleed, compared with 6% among those taking warfarin. The bleeding sites tended to differ. Bleeding in the stomach and intestines was slightly higher among Pradaxa users. Bleeding in the head was slightly higher among warfarin users. Black patients and those with chronic kidney disease were more likely to bleed from Pradaxa. The results were reported online in the journal JAMA Internal Medicine.
Reducing stroke risk from atrial fibrillation
For decades, the best way to prevent stroke from atrial fibrillation was by taking warfarin (Coumadin). But warfarin is a kind of “Goldilocks” drugs. You need regular blood tests to make sure the amount in your blood isn’t too high (which puts you at risk of bleeding) or too low (which puts you at risk of having a stroke). You also need to pay attention to what you eat, because a sudden meal with a lot of vitamin K can counteract warfarin.
Then came Pradaxa. After doctors had been prescribing it for a while, they noticed that it was causing more episodes of major bleeding than had been expected. The FDA ordered that additional studies be performed on the safety of Pradaxa in the real world.
Some studies, like the one from, the University of Pittsburgh, showed a higher bleeding risk with Pradaxa than with warfarin. Other studies show the opposite.
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FDA approves other blood thinners
Since 2010, two other blood thinners have been approved to prevent strokes in people with atrial fibrillation and no heart valve problems: apixaban (Eliquis) and rivaroxaban (Xarelto). Post-approval studies on the safety of these drugs are still ongoing.
One downside of the three new drugs: they are much more expensive than warfarin. One upside: none require regular blood tests to adjust the dose. One big unknown: the long-term side effects.
Choosing the right blood thinner
How do you and your doctor decide which drug is right for you if you have atrial fibrillation? There is no right answer. Here are the questions I ask my patients:
Is cost an issue? If yes, warfarin will be the likely choice.
Are you sure you will take the medicine as prescribed? This is important for all drugs. But warfarin stays in the body longer, so you have a longer protection time if you miss a dose. That isn’t the case with the other three.
Is it relatively easy for you to get a blood test? If the answer is no, then one of the newer drugs might be better.
I usually start my patients with atrial fibrillation on warfarin. I do this mainly because I take a conservative approach to new drugs. Also I have many years of experience with warfarin. If the patient has trouble keeping his or her warfarin levels in the proper range, I then consider switching to one of the newer drugs.
I might start with a newer blood thinner in a person a higher-than-average risk of bleeding into or around the brain. Examples include a person with:
Jogging is one of those activities that seem to perfectly embody the concept of healthy physical activity. I know people who run for an hour or more a day. I admire their commitment to physical activity and sometimes envy their seeming good health. But a new study from Denmark has me rethinking the benefits of strenuous jogging.
Researchers with the ongoing Copenhagen City Heart Study have been following the health of more than 1,000 joggers and 400 healthy but inactive non-joggers. Between 2001 and 2014, 156 of these study participants died. Using the death rate of the sedentary non-joggers as a point of comparison, the researchers found that the death rate of light joggers was 90% lower than that of the non-joggers, while that of moderate joggers was about 60% lower. Here’s the big surprise: the death rate for strenuous joggers was no different than that of sedentary non-joggers. This kind of relationship is known as a U-shaped curve (see figure).
In this study, jogging for just an hour a week was associated with a significantly lower death rate. The most beneficial combination was jogging at a slow or moderate pace two to three times a week, for a total of 60 to 145 minutes across the week. These results were published in the February 5, 2015 Journal of the American College of Cardiology.
This is just one study among hundreds that have looked at the link between exercise and mortality. It certainly isn’t a stop-the-presses kind of study, nor should this study alone change the current recommendations for physical activity — 150 minutes of moderate physical activity a week. But it does make me think about how much exercise, and what kind, is best.
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The Copenhagen City Heart Study results certainly help debunk the “no pain, no gain” myth associated with exercise. Slow- to moderate-pace jogging for 20 minutes three times a week should be a no-pain activity for many, and comes with a clear gain.
The current U.S. exercise guidelines have some strong science behind them. But they are daunting to many people, leading some to forgo exercise entirely. The message from this study and others is that lower amounts of activity that are manageable as part of a normal lifestyle can still have significant health benefits.
ARCHIVED CONTENT: As a service to our readers, Harvard Health Publishing provides access to our library of archived content. Please note the date each article was posted or last reviewed. No content on this site, regardless of date, should ever be used as a substitute for direct medical advice from your doctor or other qualified clinician.
Every so often a medical advance comes along that rewrites the script for treating a disease or condition. After today’s announcements of impressive results of a new type of cholesterol-lowering drug, that scenario just might happen in the next few years.
The new drugs, called PCSK9 inhibitors, are monoclonal antibodies. They target and inactivate a specific protein in the liver. Knocking out this protein, called proprotein convertase subtilisin kexin 9, dramatically reduces the amount of harmful LDL cholesterol circulating in the bloodstream. Lower LDL translates into healthier arteries and fewer heart attacks, strokes, and other problems related to cholesterol-clogged arteries.
If you have high cholesterol, it’s best to try to lower it with a healthy diet like the Mediterranean diet and exercise. The combination of diet and exercise does the trick for some people. Others need help from medicine.
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Statins have been the first-line drugs for lowering cholesterol since the late 1980s. They’ve been shown to prevent repeat heart attacks in people who have already had one and first heart attacks in a wide range of at-risk individuals. In about one in five people, though, a statin doesn’t lower cholesterol enough. Adding a second drug that lowers cholesterol by a different mechanism doesn’t always help. And some people can’t take a statin because of side effects like muscle pain, liver damage, or the development of diabetes.
The results of three clinical trials presented today at the annual meeting of the American College of Cardiology, and simultaneously published in the New England Journal of Medicine, suggest that an even better cholesterol-lowering medication may be on the horizon.
The trials show that PCSK9 inhibitors are extremely powerful cholesterol-lowering agents. In all three trials, all of the participants took a statin. Half got a PCSK9 inhibitor (either evolocumab or alirocumab) every two to four weeks; the other half got a placebo. After a year, LDL levels were 60% lower in the PCSK9 groups.
“Among people treated with evolocumab, the average LDL after one year of treatment was 48 milligrams per deciliter of blood, the lowest LDL ever seen in the experimental arm of a lipid-lowering trial,” Dr. Marc Sabatine, professor medicine at Harvard-affiliated Brigham and Women’s Hospital, told me. Dr. Sabatine was the principal investigator for two of the trials presented at the cardiology meeting. For comparison, a “healthy” LDL is 100 mg/dL.
In some of the trial participants, treatment with evolocumab lowered LDL below 25 mg/dL, and the individuals appeared to do fine, said Dr. Sabatine.
There is no such thing as a small stroke…
Strokes are the fifth leading cause of death in the United States and a significant cause of disability. Learn from Harvard Medical School experts how to understand your odds for having a stroke, evidence-based steps that can lower your risk, how to recognize the early signs of a stroke, and what to do to get rapid, brain-saving treatment.
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Cholesterol lowering is good only if it translates into better health. That was the case in the three trials. Participants taking the PCSK9 inhibitors were 50% less likely to have had a heart attack or stroke or develop heart failure over the course of the one-year trials.
As with all drugs, there are downsides. At least for now, PCSK9 inhibitors must be given by injection every 2 to 4 weeks. Neurocognitive problems, such as mental confusion or trouble paying attention, were seen in some of the study participants. And if the cost of other monoclonal antibody drugs is any indication, PCSK9 inhibitors won’t be cheap. CVS officials have estimated that a year’s worth of treatment could cost between $7,000 and $12.000.
PCSK9 inhibitors are still experimental drugs. The three trials presented at the American College of Cardiology meeting were designed to look at how well the drugs lowered LDL, not how well they prevent heart attack, stroke, and other cardiovascular problems. Other trials now underway aim to do just that. The FDA can’t begin to evaluate whether PCSK9 inhibitors should become part of the cholesterol-lowering armamentarium until after the results of these trials have been presented and published, and better information is available about the drugs’ side effects.
If approved, these drugs would probably be used first in people who don’t respond to statins or who develop side effects from them. But because it appears that PCSK9 inhibitors reduce the risk of heart attack and other cardiovascular problems in those taking a statin, combining a statin and a PCSK9 inhibitor may be a good option for people at especially high risk for cardiovascular disease.
We’ve never before had medications that can reduce LDL cholesterol levels this much. Time will tell if PCSK9 inhibitors safely prevent heart attack and stroke. As a cardiologist who has seen many people have their lives cut short by cardiovascular disease or who survived but with a poorer quality of life, I have my fingers crossed that a new class of cholesterol-lowering drugs may someday reduce the burden of heart and blood vessel disease.
About the Author
Gregory Curfman, MD, Assistant Professor of Medicine, Former Editor-in-Chief, Harvard Health Publishing
Dr. Gregory Curfman is Assistant Professor of Medicine at Harvard Medical School and former editor-in-chief of Harvard Health Publishing. He is also on the affiliated faculty of Harvard Law School. Before joining Harvard Health Publishing, Dr. … See Full Bio
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Is brain damage an inevitable consequence of American football, an avoidable risk of it, or neither? An editorial published yesterday in the medical journal BMJ poses those provocative questions.
Chad Asplund, director of sports medicine at Georgia Regents University, and Thomas Best, professor and chair of sports medicine at Ohio State University, offer an overview of the unresolved connection between playing football and chronic traumatic encephalopathy, a type of gradually worsening brain damage caused by repeated mild brain injuries or concussions.
This condition was first described in a football player in 2005, after University of Pittsburgh experts performed an autopsy on Pittsburgh Steelers center Mike Webster, whose life had taken a downward turn after his retirement from professional football. Since then, researchers have linked chronic traumatic encephalopathy to the wasting away of brain tissue, the buildup of brain proteins linked to dementia and Alzheimer’s disease, memory loss, depression, anger, and other behavioral and emotional problems.
So far, all cases of autopsy-proven chronic traumatic encephalopathy have been in players who sustained repeated blows to the head. That’s a fact of life for almost all professional football players. But some of those with the condition had never been diagnosed with a concussion. According to Asplund and Best, this suggests that a series of head injuries that don’t cause concussions may lead to chronic traumatic encephalopathy or be an important risk factor for it.
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So here’s the big question: does playing football cause chronic traumatic encephalopathy, or are some people who play football already at higher risk for developing it? Repeated head injuries may, indeed, directly cause chronic traumatic encephalopathy. At the same time, it’s possible that the players who sustain brain injuries are genetically prone to them or to other factors that increase the likelihood of developing dementia, emotional or behavioral issues, or premature death.
It’s essential to answer the cause and effect question, in part because not knowing the answer has generated fear among players. San Francisco 49ers linebacker Chris Borland, one of the National Football League’s top rookies in 2014, recently announced his retirement from professional football because of his worries about the long-term effects of repetitive head injuries. In addition, some parents of even younger players, fearing the potential hazard from head injuries, are keeping their kids from playing football, soccer, and other sports.
The Football Players Health Study at Harvard University aims to provide some solid answers. Its organizers hope it will do for football what the Framingham Heart Study has done for heart health and the Nurses’ Health Study has done for nutrition.
The 10-year study, launched in 2013, aims to explore more than just head injuries. It includes a variety of medical conditions that affect football players’ quality of life and length of life. The study is funded by the National Football League Players Association. It has begun by recruiting former NFL players. Let’s hope that this study and other research on sport-related head injury and later brain damage can provide the guidance that players and parents need.
The placebo effect is a mysterious thing. I’ve long been fascinated by the idea that something as inert and harmless as a sugar pill could relieve a person’s pain or hasten their recovery just by the expectation that it would.
Studies use placebos — an inactive treatment, such as a sugar pill — in an attempt to understand the true impact of the active drug. Comparing what happens to a group of patients taking the active drug with the results of those taking a placebo can help researchers understand just how good the active drug is.
The word “placebo” comes from Latin and means “I shall please.” And “please” it does. In study after study, many people who take a placebo show improvement in their symptoms or condition.
The placebo effect is for real
Recent research on the placebo effect only confirms how powerful it can be — and that the benefits of a placebo treatment aren’t just “all in your head.” Measureable physiological changes can be observed in those taking a placebo, similar to those observed among people taking effective medications. In particular, blood pressure, heart rate, and various blood test results have been shown to change among subsets of research subjects who responded to a placebo.
Of course, not everyone has a therapeutic response to a placebo. If that were the case, we wouldn’t need medications at all. Instead, we could simply wield the power of suggestion. Understanding why certain people improve with placebo treatment and others do not is the “holy grail” of placebo research.
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Nocebo: Placebo’s evil twin
The power of suggestion is a double-edged sword. If you expect a treatment to help you, it may be more likely to do so. And if you expect a treatment will be harmful, you are more likely to experience negative effects. That phenomenon is called the “nocebo effect” (from the Latin “I shall harm”). For example, if you tell a person that a headache is a common side effect of a particular medication, that person is more likely to report headaches even if they are actually taking a placebo. The power of expectation is formidable and probably plays a significant role in the benefits and the side effects of commonly prescribed medications.
Is the power of the placebo effect rising?
A fascinating study examined the impact of the placebo effect in 84 trials of nerve pain treatments that took place over the prior 23 years. The researchers found that the placebo effect has become remarkably stronger, but this observation was only noted in U.S. studies. Why? One theory is that the flood of direct-to-consumer drug advertising in the U.S. (which is not allowed in most other countries) increases patients’ expectations that a medication will help them. Stronger and higher expectations of a drug’s effectiveness may translate into a bigger placebo effect.
Another theory links the rising effectiveness of placebos to the research trials themselves: the larger, more expensive, and more elaborate the trial, the higher the expectations of the study participants. Trials of this type tend to be more common in the U.S. than elsewhere.
Whatever the reason, there is a downside to this trend. A powerful placebo effect makes it harder for researchers to prove that a new medication is effective. The stronger the placebo effect, the more difficult it becomes to demonstrate a significant difference between a placebo and an active drug — even if the active drug is pretty good. As a result, some effective drugs might “fail” in clinical trials. And that could drive researchers to move their studies outside the U.S.
Chances are you’ve seen one of these ads in your local newspaper or on television: “Do you suffer from (insert common medical condition here)? Would you like to participate in a research study to evaluate a new treatment?” Many people are curious about such studies but hesitate to take the next step.
Nothing obligates you to join a study, but it’s an option worth examining. “If you participate in a study, you’ll be advancing scientific knowledge to help the next patient like you. In fact, you’ve already benefited from all the people who took part in earlier clinical research,” says Harvard professor Dr. Christopher Cannon, executive director of Cardiometabolic Trials at the Harvard Clinical Research Institute.
Types of studies
One of the most famous studies is the long-running Framingham Heart Study, which has yielded a wealth of information about the causes of heart disease and stroke. It’s an example of a cohort study, which follows a large group of people over a long period of time. Through questionnaires or interviews, researchers gather information on a wide range of things—diet, exercise, and medical and family history, for example. They may also measure different variables (such as blood pressure or cholesterol level) or do other testing to assess a person’s health status.
A clinical trial is type of study in which volunteers receive a new treatment, which may be a medication, a procedure, or a device. Most often, volunteers are randomly assigned to receive either the investigational treatment or the comparison, which may be a placebo (an inactive therapy) or a treatment that’s already available.
All clinical trials have very specific guidelines about who can participate. Some seek healthy participants, while others require people with a specific condition or illness. Researchers also use a variety of criteria—including age, blood test results, and other medical conditions—to include or exclude people from a trial. This helps protect the participants’ safety and ensures the investigators get the information they need.
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Safeguards in place
Anyone who volunteers for a research study must undergo a process known as informed consent, which is designed to help them clearly understand what to expect as well as the risks and benefits of participating. An independent committee known as an Institutional Review Board ensures the study is performed in a way that protects the rights and welfare of the participants.
In addition, the FDA reviews proposed studies of new drugs or devices and approves only those for which they deem the potential benefit is greater than the possible risk, Dr. Cannon explains. Still, there can be unforeseen side effects from any experimental treatment, and they can be unpleasant, serious, or even life-threatening. Another possible downside is the inconvenience, as the study may require extra clinic visits and complex treatment regimens.
On the other hand, the extra medical attention—which is in addition to your usual care—may be helpful, because any changes in your health are more likely to be noticed. Another potential advantage is access to new therapies before they are widely available or affordable, although in any clinical trial, you won’t know if you get the new treatment or not, notes Dr. Cannon.
For more information
If you’re considering joining a clinical trial, your doctor may be able to steer you to a study appropriate for your condition. The National Library of Medicine maintains a current list of public and privately supported clinical trials at www.clinicaltrials.gov where you can search by condition, location, and other criteria.
Before signing up for a study, carefully read the informed consent form and be sure to get answers to these questions:
Are there alternative treatments other than the one being tested in the trial?
How will you monitor my safety during the trial?
After the trial ends, can I opt to stay on (or switch to) the treatment being tested if it proves successful?
What happens if I am harmed by the trial?
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If you are like me, when you get the flu you head straight to the pharmacy and grab the most powerful over-the-counter medicine you can find. But is that really the best approach? After all, your condition, symptoms, and reaction to the virus may be quite different from someone else’s, so why use the same medicine? Instead, you may benefit more from a treatment specifically designed just for you and your ailment.
That’s the philosophy behind precision medicine (sometimes referred to as personalized medicine), an approach to cancer prevention and treatment that takes into account a person’s genes, environment, and lifestyle and eliminates the one-size-fits-all concept.
“As you get older, you are more likely to battle diseases and ailments, like cancer, and you do not want to waste your time with trial-and-error treatments that may not work and could expose you to various side effects,” says Dr. Paul Avillach, assistant professor of biomedical informatics at Harvard Medical School. “Precision medicine can help take out the guesswork.”
It works like this: doctors rely on family history, lifestyle habits (like diet, exercise, and smoking), and environmental factors (such as where you grew up and where you now live) to determine if you’re more likely to get certain forms of cancer. This can help create preventive strategies like adopting a healthier diet and increasing screenings.
If you have a family history of cancer, a genetic test can help clarify whether you inherited a specific genetic mutation. This involves taking a sample of either blood or saliva to look for mutations in several genes related to certain cancers.
If you are diagnosed with cancer, doctors can use genetic testing on tumors in order to find the best possible drug treatment. Tumors have genetic changes that cause cancer to grow and spread, and researchers have learned that the changes that occur in one person’s cancer may not happen in other people with the same type of cancer.
For genetic testing of tumors, doctors remove a sample of the tumor tissue and a machine called a DNA sequencer looks for genetic changes that may cause the cancer to grow. With this information in hand, doctors then try to match the cancer with existing drugs.
“With a tumor’s genetic profile, we can screen 1,000 different drugs to see which ones might work best,” says Dr. Avillach.
This way, a person is less likely to receive a drug that may not work or causes severe side effects, like blood clotting. That, in turn, cuts down on the odds of having to start treatment over again with a new drug.
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Practical applications of precision medicine still evolving
Despite its name, precision medicine is not yet as precise as it should be. A study published Oct. 19, 2017, in BMC Medical Genomics suggested that genetic targeting for cancer therapy is more accurate for people of European decent and less so for those whose ancestry is Latin American, African, or Asian. Another downside: genetic testing for cancer treatment is practiced mostly at larger research hospitals and cancer centers and thus is not available everywhere.
Still, for some, it can offer a better way to prevent and treat possible cancer.
“Precision medicine is only one added element in an ongoing equation,” adds Dr. Avillach. “It’s not the solution to everything, and it won’t replace the testing and treatments currently in place, but it can help to get a more targeted answer for some.”
It’s a bit like clockwork: Soon after an important scientific finding about health, a slew of self-help products arrive to support it. Added sugars are unhealthy? Try this diet. A sedentary lifestyle leads to disease? Do this workout.
So it’s not surprising that increasing knowledge about DNA markers for longevity called telomeres has spawned yet another round of self-help tools. The latest encourages you to measure the stuff via doctor’s office or a home kit. But should you?
Telomeres and aging
Telomeres are strings of DNA that protect the ends of chromosomes. Telomeres tend to shorten over time as they do their job, so they’re considered biological markers of aging. Unhealthy lifestyle habits — such as smoking, eating junk food, obesity, inactivity, and chronic stress — are also associated with shorter telomeres. Shorter telomeres, in turn, are associated with a lower life expectancy and higher rates of developing chronic diseases, such as cardiovascular disease.
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Telomere testing to show biological aging?
According to telomere testing companies, learning your telomere length might provide insight into your “biological” age.
You’ll find the tests in several places. One is the Internet. For as little as $100, some companies will sell you a home kit that allows you to send your DNA (in a drop of blood or a cheek swab) to a lab. After a few weeks, the company mails you the test results, which tell you what your telomere length is and how that length compares to your peers.
For more money, you can talk to a company “coach,” who explains the results to you and helps you come up with a plan for healthier living.
Other (more expensive) ways to get the test include:
going to a walk-in clinic with a doctor who’ll order the test for you and then talk you through the results
buying and ordering a test from a company that directs you to a lab or a doctor who works in your area
asking your own physician to order the test for you.
What the tests don’t tell you
There’s no way to know how accurate various telomere tests are. “There are a few published methods for telomere measurements. Some are better than others in terms of quality control and robustness. The most common method is called the real-time PCR method. “We run it in my lab at the Harvard Cancer Center. But it requires expertise to run the test, and there are a lot of variables,” explains Dr. Immaculata De Vivo, a Harvard Medical School professor and genetics researcher at the Dana-Farber/Harvard Cancer Center.
Having just one telomere test — even in a research lab — can’t tell you how fast your telomeres are shortening. This is because we’re not all born with the same quantity of telomeres, and because you’d need a baseline test followed over time to find out how much telomere length you’re losing.
Plus, even if your telomeres are shortening, it doesn’t mean something bad will happen. “And if your telomeres are long, it doesn’t guarantee that something bad won’t happen,” says Dr. William Hahn, a Harvard Medical School professor and chief research strategy officer at Harvard-affiliated Dana-Farber Cancer Institute.
Should you try telomere testing?
The commercial labs and clinics plugging telomere tests suggest that the results will help you make better lifestyle decisions to slow telomere shortening and increase telomere length.
Is it really possible? “There’s nothing that has been proven to prevent the shortening of your telomeres,” says Dr. Hahn.
However, since stress and unhealthy lifestyle habits have been linked to shorter telomeres, it is reasonable to suppose that stress reduction and healthy lifestyle might be beneficial. “There is mounting evidence that a healthy lifestyle buffers your telomeres,” Dr. De Vivo says.
Learning your telomeres’ status could then be a wake-up call to change behaviors associated with telomere shortening, such as eating a healthier diet, losing weight, stopping smoking, or reducing stress.
But do you really need to pay for a test to tell you that? It may be easier to adopt healthy habits associated with a longer life.
I am now 11 years into recovery from my battle with opiate addiction, and I have always been fascinated with two related questions: is there truly such a thing as an “addictive personality,” and do people substitute addictions?
The myth of the addictive personality
The recently deceased writer and television personality Anthony Bourdain was criticized by some for recreationally using alcohol and cannabis, in what was seemingly a very controlled and responsible manner, decades after he quit heroin and cocaine. Was this a valid criticism? Can a person who was addicted to drugs or alcohol in their teens safely have a glass of wine with dinner in their middle age?
It depends on which model of addiction and recovery you subscribe to. If you are a traditionalist who believes that addictions last a lifetime, that people readily substitute addictions, and that people have ingrained “addictive personalities,” the answer is: absolutely not. This would be playing with fire.
During my 90 days in rehab, it was forcefully impressed upon me that addictions are routinely substituted, and that if one is ever addicted to any substance, then lifelong abstinence from all potentially addictive substances is one’s only hope of salvation. This seemed to make sense, as a person would have the same lifelong predispositions to an addiction: genetic makeup, childhood traumas, diagnoses of anxiety or depression — all of which could plausibly set them up to become addicted to, say, alcohol, once they have put in the hard work to get their heroin addiction under control. In medical terms, the concern is that different addictions can have a common final pathway in the mesolimbic dopamine system (the reward system of our brain), so it is logical that the body might try to find a second pathway to satisfy these hungry neurotransmitters if the first one is blocked, a “cross-addiction.”
I learned early in my own recovery how critical it is to apply logic and evidence to the field of addiction, and that just because things make sense, and because we have thought about them in a certain way for an extended period of time, that doesn’t mean that they are necessarily true. While in rehab, I was actually told a lot of other things that turned out to have no basis in scientific evidence. For example, I was told on a daily basis that “a drug is a drug is a drug.” This mentality doesn’t allow for there being a difference between, for example, the powerful opiate fentanyl, which kills thousands of people every year, and buprenorphene (Suboxone) which is a widely-accepted treatment for opioid use disorder.
I have come to believe that an uncompromising “abstinence-only” model is a holdover from the very beginnings of the recovery movement, almost 100 years ago, and our understanding has greatly evolved since then. The concepts of addiction and recovery that made sense in 1935, when Alcoholics Anonymous was founded, and which have been carried on by tradition, might not still hold true in the modern age of neurochemistry and functional MRIs. That said, mutual help groups today do have a place in some people’s recovery and they can encourage the work of changing and maintaining change.
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Recovery may improve resiliency to new addictions
It seems as if no one definitively knows the answer about whether people substitute addictions. According to the National Institute on Drug Abuse in response to a request for comment from the website Tonic: “A previous substance use disorder is a risk factor for future development of substance use disorder (SUD),” but “It is also possible that someone who once had an SUD but doesn’t currently have one has a balance of risk and protective genetic and environmental factors that could allow for alcohol consumption without developing an AUD [alcohol use disorder].”
One study published in JAMA in 2014 showed that, “As compared with those who do not recover from an SUD, people who recover have less than half the risk of developing a new SUD. Contrary to clinical lore, achieving remission does not typically lead to drug substitution, but rather is associated with a lower risk of new SUD onset.”
The authors of this study suggest that factors such as “coping strategies, skills, and motivation of individuals who recover from an SUD may protect them from the onset of a new SUD.” In other words, by making the life-affirming transition from addicted to recovered, we gain a recovery “toolbox” that helps us navigate life’s challenges and stresses in a much healthier way. We learn to connect with people, push our egos aside, and to ask for help if we need it. Thus, when faced with stressful situations that formerly would trigger us to drink or drug, we might respond by exercising or calling a friend, rather than using a substance. As such, we substitute addictions with healthier activities that perform the function that the drink or drug used to, albeit in a much more fulfilling way.
This issue is also, partly, a question of semantics, and of how narrowly or widely we define addictions. Many hold that an addiction can be to either a substance or a process: gambling, eating, video game playing, Internet use, sex, work, religion, exercise, or compulsive spending. Lots of people gain weight when they quit smoking. Is that a case of substituting an addiction? I like to joke that, in my observations, the only reliable outcome from a stay at rehab was a nicotine addiction, because many people, in an attempt to cope with the trauma and dislocation of being sent away to rehab, pick up cigarettes.
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