Good health and disease prevention are usually toward the bottom of the list when we consider where and how we live. In America, a healthy lifestyle and disease prevention have not been priorities for community planners. With suburban sprawl, wider streets make less room for sidewalks. Malls and superstores have replaced local shops. Driving is no longer a convenience; for most people it is a necessity.
To help people take personal responsibility for staying healthy, we need to make it easier to live healthier. This requires studying different designs for our homes, offices and communities. It also means changing our priorities, putting health and disease prevention ahead of convenience, at least some of the time.
We are already getting a glimpse of the future based on some key developments in prevention, earlier diagnosis and treatment of Alzheimer’s disease. In a study published in the September issue of Lancet Neurology, researchers identified the seven factors most closely associated with Alzheimer’s disease and then devised a risk profile based on these factors. Although not validated yet, four of the seven are similar to risk factors for heart attack and stroke–hypertension, an abnormal cholesterol profile, obesity and physical inactivity. Since changes in the brains of people with Alzheimer’s start years before symptoms occur, modifying these risk factors in midlife and perhaps sooner may be the best way to prevent or at least delay onset of the disease.
Spinal-fluid sampling and analysis for a protein called beta amyloid has shown promise as a diagnostic test prior to symptom onset. People with Alzheimer’s accumulate beta amyloid in the brain. People who have a genetic predisposition for Alzheimer’s tend to have lower levels in their fluid, indicating higher deposition of brain beta amyloid. But many people with abnormal spinal fluid do not develop Alzheimer’s.
Genetic testing can identify some individuals who are at higher risk. However, like spinal-fluid analysis, it is far from perfect. Diagnostic evaluation with genetic testing and spinal-fluid analysis will become more valuable over time. Test accuracy will improve and scientists will discover methods of prevention beyond a healthy lifestyle.
On the treatment front, there were high hopes for a nasal Alzheimer’s vaccine designed to attack brain beta amyloid. While the vaccine did seem to slow down mental decline in some patients, the results were not conclusive. More important, the clinical trial was stopped because of significant side effects.
There is a host of new medications in various stages of development. Some are enhancements of types of drugs already on the market. Others have completely new actions, such as facilitating the transmission of nerve signals between brain cells. Other drugs are designed to block the formation and deposit of amyloid in the brain.
We know a lot about how to prevent coronary-artery disease. Four changes in our lifestyle can substantially decrease our risk–taking in fewer calories to keep body weight in check, getting more physical activity combined with at least 30 minutes of dedicated exercise time daily, avoiding tobacco use and making healthy food choices.
Knowing what we should do has not translated into action. What we need are the right incentives to get more people engaged in lifestyle change and to stick to it. We are starting to see this happen. Some companies are offering financial incentives for people to join programs to stop smoking, exercise more and lose weight. This is a good first step. For financial incentives to result in major lifestyle improvements, signing up for a program won’t be enough. The incentives must be linked to results. The dilemma is determining fair and equitable ways to define personal goals and distribute the rewards.
Meanwhile, statins are here to stay. These drugs do much more than lower cholesterol levels. They lower the risk of heart attack and stroke, and slow down the buildup of fatty deposits called plaque in arteries throughout the body. Heart attacks occur most often when a plaque in a coronary artery breaks, releasing chemicals that cause a clot to form on top of the plaque. Statins help keep the surface of plaques from breaking. They also dampen the inflammation associated with plaque instability.
Neuroscientists have made great progress in understanding the likely mechanisms involved in migraine. Based on these findings, researchers have discovered therapies that modify these responses. To date, the scientists have been more successful in their work on acute attacks than on prevention. Prior to sumatriptan, the first of the many triptans to be approved, migraine sufferers found variable success at stopping a migraine attack with aspirin, another NSAID such as ibuprofen or naproxen, or an ergot derivative. For the nausea, patients would also take an anti-emetic such as prochlorperazine (Compazine). The triptans have multiple actions related to activation of serotonin receptors inside and outside the brain. They seem to work by keeping blood vessels from dilating and blocking painful nerve impulses. Potential targets for new abortive therapies include nitric oxide and glutamine inhibitors.
If you have two or more migraine attacks per month, consider preventive therapy, especially if the attacks are severe and not responsive to treatments. Finding the right drug or combination of drugs is less of a science and more trial and error. There are many to choose from. I try to prescribe an agent that not only prevents migraine, but also has some other additional health benefit. For example, a person with high blood pressure and migraine might start with a beta blocker or an angiotensin inhibitor.
There are three parts to migraine management–identifying what triggers your attacks, stopping an attack before severe symptoms set in and preventing attacks from starting. Newly diagnosed migraine sufferers should keep a diary of foods and beverages they ingest prior to each migraine and the events leading up to the attack. Avoiding triggers may be low tech, but it can be very effective.
True, psychiatric diagnoses cannot be confirmed by blood tests, brain imaging or biopsy. As neuroscientists figure out more of the details of how the brain works, we will begin to see helpful diagnostic tests.
Psychiatry is already a science. Psychiatrists use scientific principles to make diagnoses. They do this mostly by defining syndromes (groups of symptoms that tend to occur together). Indeed, because of the brain’s complexity, discovering the biological mechanisms for anxiety disorders, depression and psychoses is a daunting challenge. But there is already hope that genetic testing will tell us, for example, how well a person may respond to a given antidepressant. This kind of test could guide more accurate medication choices.
You are correct–prescribing a therapy for someone with a mental-health disorder is a far cry from prescribing penicillin for a strep throat. But a strep infection is a very straightforward illness, with a well-understood cause and a treatment that makes a direct hit on the target. In contrast, psychiatric illnesses have multiple causes, which also make the science harder.
In my view, the science of psychiatry is very hard to understand. The best scientists in the field recognize what they don’t know, which spurs them to learn more. Despite the limits of our knowledge, we are fortunate to have many excellent treatments for psychiatric problems.
title: “Let S Live Healthier” ShowToc: true date: “2022-12-19” author: “Ray Gonzales”
Good health and disease prevention are usually toward the bottom of the list when we consider where and how we live. In America, a healthy lifestyle and disease prevention have not been priorities for community planners. With suburban sprawl, wider streets make less room for sidewalks. Malls and superstores have replaced local shops. Driving is no longer a convenience; for most people it is a necessity.
To help people take personal responsibility for staying healthy, we need to make it easier to live healthier. This requires studying different designs for our homes, offices and communities. It also means changing our priorities, putting health and disease prevention ahead of convenience, at least some of the time.
We are already getting a glimpse of the future based on some key developments in prevention, earlier diagnosis and treatment of Alzheimer’s disease. In a study published in the September issue of Lancet Neurology, researchers identified the seven factors most closely associated with Alzheimer’s disease and then devised a risk profile based on these factors. Although not validated yet, four of the seven are similar to risk factors for heart attack and stroke–hypertension, an abnormal cholesterol profile, obesity and physical inactivity. Since changes in the brains of people with Alzheimer’s start years before symptoms occur, modifying these risk factors in midlife and perhaps sooner may be the best way to prevent or at least delay onset of the disease.
Spinal-fluid sampling and analysis for a protein called beta amyloid has shown promise as a diagnostic test prior to symptom onset. People with Alzheimer’s accumulate beta amyloid in the brain. People who have a genetic predisposition for Alzheimer’s tend to have lower levels in their fluid, indicating higher deposition of brain beta amyloid. But many people with abnormal spinal fluid do not develop Alzheimer’s.
Genetic testing can identify some individuals who are at higher risk. However, like spinal-fluid analysis, it is far from perfect. Diagnostic evaluation with genetic testing and spinal-fluid analysis will become more valuable over time. Test accuracy will improve and scientists will discover methods of prevention beyond a healthy lifestyle.
On the treatment front, there were high hopes for a nasal Alzheimer’s vaccine designed to attack brain beta amyloid. While the vaccine did seem to slow down mental decline in some patients, the results were not conclusive. More important, the clinical trial was stopped because of significant side effects.
There is a host of new medications in various stages of development. Some are enhancements of types of drugs already on the market. Others have completely new actions, such as facilitating the transmission of nerve signals between brain cells. Other drugs are designed to block the formation and deposit of amyloid in the brain.
We know a lot about how to prevent coronary-artery disease. Four changes in our lifestyle can substantially decrease our risk–taking in fewer calories to keep body weight in check, getting more physical activity combined with at least 30 minutes of dedicated exercise time daily, avoiding tobacco use and making healthy food choices.
Knowing what we should do has not translated into action. What we need are the right incentives to get more people engaged in lifestyle change and to stick to it. We are starting to see this happen. Some companies are offering financial incentives for people to join programs to stop smoking, exercise more and lose weight. This is a good first step. For financial incentives to result in major lifestyle improvements, signing up for a program won’t be enough. The incentives must be linked to results. The dilemma is determining fair and equitable ways to define personal goals and distribute the rewards.
Meanwhile, statins are here to stay. These drugs do much more than lower cholesterol levels. They lower the risk of heart attack and stroke, and slow down the buildup of fatty deposits called plaque in arteries throughout the body. Heart attacks occur most often when a plaque in a coronary artery breaks, releasing chemicals that cause a clot to form on top of the plaque. Statins help keep the surface of plaques from breaking. They also dampen the inflammation associated with plaque instability.
Neuroscientists have made great progress in understanding the likely mechanisms involved in migraine. Based on these findings, researchers have discovered therapies that modify these responses. To date, the scientists have been more successful in their work on acute attacks than on prevention. Prior to sumatriptan, the first of the many triptans to be approved, migraine sufferers found variable success at stopping a migraine attack with aspirin, another NSAID such as ibuprofen or naproxen, or an ergot derivative. For the nausea, patients would also take an anti-emetic such as prochlorperazine (Compazine). The triptans have multiple actions related to activation of serotonin receptors inside and outside the brain. They seem to work by keeping blood vessels from dilating and blocking painful nerve impulses. Potential targets for new abortive therapies include nitric oxide and glutamine inhibitors.
If you have two or more migraine attacks per month, consider preventive therapy, especially if the attacks are severe and not responsive to treatments. Finding the right drug or combination of drugs is less of a science and more trial and error. There are many to choose from. I try to prescribe an agent that not only prevents migraine, but also has some other additional health benefit. For example, a person with high blood pressure and migraine might start with a beta blocker or an angiotensin inhibitor.
There are three parts to migraine management–identifying what triggers your attacks, stopping an attack before severe symptoms set in and preventing attacks from starting. Newly diagnosed migraine sufferers should keep a diary of foods and beverages they ingest prior to each migraine and the events leading up to the attack. Avoiding triggers may be low tech, but it can be very effective.
True, psychiatric diagnoses cannot be confirmed by blood tests, brain imaging or biopsy. As neuroscientists figure out more of the details of how the brain works, we will begin to see helpful diagnostic tests.
Psychiatry is already a science. Psychiatrists use scientific principles to make diagnoses. They do this mostly by defining syndromes (groups of symptoms that tend to occur together). Indeed, because of the brain’s complexity, discovering the biological mechanisms for anxiety disorders, depression and psychoses is a daunting challenge. But there is already hope that genetic testing will tell us, for example, how well a person may respond to a given antidepressant. This kind of test could guide more accurate medication choices.
You are correct–prescribing a therapy for someone with a mental-health disorder is a far cry from prescribing penicillin for a strep throat. But a strep infection is a very straightforward illness, with a well-understood cause and a treatment that makes a direct hit on the target. In contrast, psychiatric illnesses have multiple causes, which also make the science harder.
In my view, the science of psychiatry is very hard to understand. The best scientists in the field recognize what they don’t know, which spurs them to learn more. Despite the limits of our knowledge, we are fortunate to have many excellent treatments for psychiatric problems.
