 |
submitted by /u/Andonly [link] [comments] |
Recent studies from G.I specialists and doctors from around the world uncover why certain spicy foods make us poop more.
Recent studies from G.I specialists and doctors from around the world uncover why certain spicy foods make us poop more.
Recent studies from G.I specialists and doctors from around the world uncover why certain spicy foods make us poop more.
https://ift.tt/35dEO03 December 12, 2019 at 08:39AM https://ift.tt/1R552o9
|
submitted by /u/Andonly [link] [comments] |
Exercise advice on food labels could help reduce obesity, researchers say
Exercise advice on food labels could help reduce obesity, researchers say
https://ift.tt/36vjsvl December 12, 2019 at 06:33AM https://ift.tt/1R552o9
 |
submitted by /u/2293201518O [link] [comments] |
Low-Dose Aspirin May Not Reduce Heart Risks for Black Americans, Study Finds
It’s fairly established medical science that people who have had heart attacks can take regular low doses of aspirin to significantly lower their risk of having another heart attack, or other heart problems including stroke. But it is still an open question whether or not people who haven’t had a heart event, but are at higher risk of one (because, for example) they have diabetes, high blood pressure, or elevated cholesterol levels), can also benefit from the over-the-counter painkiller and anti-inflammatory drug.
A new study, published in the Journal of the American Heart Association, adds to that debate by addressing a gap in the research on the subject: whether race or ethnicity makes a difference in how aspirin affects their risk of heart disease.
The U.S. Preventive Services Task Force (USPSTF), an independent body of experts convened by the U.S. government to explore such health questions, determined in 2016 that people could prevent a first heart attack by taking low-dose aspirin if they are between 50 to 59 years old and have a greater than 10% risk of a heart event in the next 10 years. (That overall risk is calculated by taking into account a variety of risk factors such as weight, blood pressure, cholesterol and diabetes.)
But for those between 60 and 69 years old, the USPSTF recommends discussing the benefits and risks with a doctor; while aspirin can lower the inflammation that pushes plaques in the blood vessels to rupture and then form clots that can cause heart attacks, it can also lead to bleeding in the gastrointestinal tract. Because of this risk, some experts have been backing away from advising older people who have not yet had any heart events from taking daily aspirin.
In the recent study, Dr. Rodrigo Fernandez-Jiminez, a researcher at the Spanish National Center for Cardiovascular Research, and his team analyzed data from the Southern Community Cohort Study, which included more than 62,000 people from 12 states in the southeastern U.S. The participants answered questions about their lifestyle behaviors, including exercise and diet, and the researchers collected information on the subjects’ medical profile, including their medication use and heart disease risk factors. What set the cohort apart was the fact that most of the participants came from lower socioeconomic backgrounds, making it a relatively homogeneous population when it came to access to health care and insurance. About two-thirds of the volunteers identified as African-American or non-Hispanic black.
That allowed Fernandez-Jiminez and his team to explore race’s potential role in aspirin’s ability to prevent first heart events, something previous research hasn’t adequately addressed. “Most trials that have happened so far do not include different racial and ethnic groups,” he says. “And African-Americans are totally under-represented in these studies, so the guidelines have no conclusions about the potential differential effect aspirin could have on different racial groups. We didn’t have any hypotheses going into the study because this was almost the first data analyzing this issue.”
Despite identifying with a range of ethnic backgrounds, the study participants were similar socioeconomically, which means that factor wasn’t likely to explain differences the researchers found: After a median follow up of 11 years, the scientists learned that for people reporting taking low-dose aspirin, the risk of dying from a heart event increased by 18% among those identifying as black, while in participants identifying as non-Hispanic white, that risk declined by 14%.
However, it’s important to note that this doesn’t mean categorically that aspirin isn’t effective in this population. Income-related factors, such as access to health care and medications, aren’t likely to play a role, since this study controlled for those, but there may be other social factors at play. There could, for example, be differences in how faithfully people in a given population take a daily pill like aspirin, as well as what other medications they might be taking that could interfere with aspirin’s beneficial effects on the heart. In the study’s highest-risk group, for example, 18% of black participants reported being on a low-dose aspirin regime, compared to 27% of white participants. Genetic factors may also contribute to how people from different racial and ethnic backgrounds biologically respond to drugs like aspirin.
Fernandez-Jiminez says the current study was not designed to tease out what might be causing the difference in aspirin’s effect on heart deaths among those identifying as black vs. those identifying as white. But documenting the disparity is the first step toward understanding it better. “Our work is not enough to make specific recommendations or change guidelines,” he says. “But it points to the need for more information in general about the differential effect drugs can have on different racial or ethnic groups.”
Gene Testing for Antidepressants & Psychotropics: Not There Yet
An increasingly common question I get asked is, “Will gene testing help my doctor know which antidepressant to prescribe?” Popular tests such as GeneSight suggests that they can “shorten your road to recovery” and how you, as an individual, will respond to specific antidepressant medications.
Does drug-gene testing, also referred to as pharmacogenomics or pharmacogenetics, work? And if so, does it only work for certain types of medications? Let’s find out.
The Promise of Gene Testing
The idea of gene-drug testing is pretty simple. By testing your DNA, companies hope to be able to predict your response (or likely non-response) to specific types of antidepressants. It’s also being marketed for a number of other diseases and medications.
Just a year ago, GeneSight had some pretty strong marketing language on its site. The company was strongly suggesting its test could help your doctor choose the best antidepressant for you:
Fortunately, the GeneSight genetic test can provide doctors answers that quickly lead to relief. Pharmacogenomic testing helps empower your doctor with the exact information needed to prescribe you the best medication for you. By examining how your DNA responds to specific medications such as antidepressants, this simple, painless test lets doctors know which medications may not work for you, so you can get back to feeling like yourself again. […] Through pharmacogenomic testing, your doctor can identify the correct medication and create a personalized treatment for you.
In the 2018 announcement of its own antidepressant test, another gene-drug testing company called Color says it “now analyzes a number of these genes, starting with two that can impact your response to certain mental health medications like Zoloft, Paxil, and Lexapro.” The blog entry cites seven research studies, but none of them have anything to do with antidepressants.
The Problems of Gene-Drug Testing
Few genetic researchers feel as positive about the current usefulness of gene-drug testing than companies marketing these tests. The American Psychiatric Association’s research council reviewed the evidence last year and found that such genetic testing is not really ready for mass consumption.
Greden et al. (2019) looked at using pharmacogenomics directly to help in depression treatment. Because the researchers didn’t find a significant difference (either statistically or clinically) in their primary outcome measure, they instead emphasized the statistical significance they found in two of the 25 secondary outcome measures they examined.
In treatment research, scientists increasingly use a statistic called Number Needed to Treat (NNT) that allows for cross-comparisons of the real-world efficacy of different kinds of treatment. The National Institute for Clinical Excellence (NICE) in the UK recommends that for a treatment to be clinically significant, the NNT should be in the single digits.
According to a critique of the researchers (Goldberg et al., 2019), the Greden study had an NNT of 17 for a response to an antidepressant and an NNT of 19 for remission of a depressive episode. Not exactly powerful numbers. In fact, combined with the non-significance of the primary outcome studied, Greden ironically demonstrated that pharmacogenomics doesn’t appear to very good at its primary goal of helping to guide antidepressant treatment.
In short, the science today doesn’t support the mainstream use of these tests for antidepressants.
Selling You on Personalized Results
Personalized medicine is the new New Thing marketed by anyone who has access to a DNA lab. The problem is that the marketing of gene-drug testing far overshadows the science. In early 2019, the U.S. Food and Drug Administration updated its guidance on gene-drug testing:
[The] FDA is aware of genetic tests that claim results can be used to help physicians identify which antidepressant medication would have increased effectiveness or side effects compared to other antidepressant medications. However, the relationship between DNA variations and the effectiveness of antidepressant medication has never been established. […]
Do not change or stop taking any medicine based on a report from a genetic test you took on your own. […]
[And to doctors:] If you are using, or considering using, a genetic test to predict a patient’s response to specific medications, be aware that for most medications, the relationship between DNA variations and the medication’s effects has not been established.
Goldberg et al. (2019) said it best:
[Researchers] have noted that commercial […] test manufacturers promote their products with a zeal that is disproportionate to the existing evidence base — particularly when marketing to the lay public and clinicians who are likely unfamiliar with the limited statistical power of candidate gene association studies.
You’d be wasting your money by purchasing one of these tests in hopes of getting better results from your antidepressant treatment. The science simply doesn’t support use of these tests at this time.
Online health information isn’t always accurate on this issue — even from trusted sources. For instance, the Mayo Clinic suggest these tests can help, but it’s unclear whether the anonymous, unlisted author of that article has examined the primary research (as there are no research references listed in the article). Harvard Health Publishing, on the other hand, got it right by noting that the research of gene-drug testing “showed no evidence of effectiveness.
Someday, the hope is that pharmacogenetics may meaningfully inform treatment decisions, as it does in oncology. But we’re not yet there.
References
Goldberg, J.F., Rosenblat, J.D., McIntyre, R.S., Preskorn, S.H., de Leon, J. (2019). Letter to the Editor: Clinical versus statistical significance of pharmacogenomic-guided antidepressant therapy: What’s really being measured and marketed? Journal of Psychiatric Research, 114, 208-209.
Greden, J.F., Parikh, S.V., Rothschild, A.J., et al. (2019). Impact of pharmacogenomics on clinical outcomes in major depressive disorder in the GUIDED trial: a large, patient-and rater-blinded, randomized, controlled study. J. Psychiatr. Res. 111, 59–67. https://doi.org/10.1016/j.jpsychires.2019.01.003
Subscribe to:
Comments (Atom)
Popular Posts
|
