Imagine a pacemaker or bionic ear that doesn’t require batteries but is powered by your very own cells.
That could be the future of biomedical implants once biofuel cells come to fruition, says an international team of scientists, who have taken the technology one step closer to reality.
The researchers have created a biofuel cell made from carbon nanotubes that generate energy from blood glucose.
The advance improves the power output and the lifetime of biofuel cells, they report in the journal Nature Communications.
Unlike batteries, which store chemical energy, conventional fuel cells convert a fuel such as hydrogen or methanol into electricity.
Biofuel cells, which have been in development since the 1960s, employ the same principle except they use biological enzymes to convert glucose into electricity inside the body.
However, there have been a number of serious technical hurdles that have impaired their performance, says study co-author Professor Gordon Wallace from the University of Wollongong.
One of the challenges is “immobilising” the enzyme that converts the fuel into electricity and making it stick to the electrodes of the fuel cell, rather than diffusing through the cell and into the fuel.
Another challenge is keeping the immobilised enzyme active for long periods of time.
“This is because the electrodes, like anything implanted in the body, tend to get fouled and performance drops off quite quickly with time,” says Wallace.
This has resulted in low power densities of only a few milliwatts per centimetre squared and a lifetime of only a few days, which is insufficient for practical use.
To tackle these problems Wallace and his colleagues turned to carbon nanotubes, which are microscopic cylinders made from long strings of interconnected carbon atoms.
They used a form of multi-walled carbon nanotube “yarn” to construct a microscopic structure for the biofuel cell.
“This provides an environment that gives stability to the enzymes and an environment that occludes the types of things that can poison the enzyme, therefore degrading its performance over time,” says Wallace.
The end result was a biofuel cell with an extended lifetime and a higher power density 2.2 milliwatts per square centimetre.
“In terms of the power density it’s a factor of two or three above what we were getting. That’s probably not staggering, but it is significant,” says Wallace.
“What is more significant is the length of time we can operate these biofuel cells for.”
Repair nerve damage
The researchers are aiming to develop the carbon nanotube yarn biofuel cells to power an implant that will help regenerate nerve damage.
“Our initial target is for peripheral nerve repair, whether that’s a finger or other limbs.”
The idea is to implant the conduit in the area where the nerves need to be regenerated, and the biofuel cells will produce a tiny electric current to stimulate nerve growth without requiring batteries or an external power source.
Wallace and his collaborators are also working on improving the power output and lifetime of biofuel cells even further.
“That then opens them up to powering all sorts of implants, not just this temporary power supply to repair a damaged area, but a power supply that will be able to service in an ongoing prosthetic, like the vagus nerve stimulators for epilepsy or for chronic pain management.”
The ultimate goal is to boost output and longevity to the point that biofuel cells can power a broad range of biomedical implants.
“If you can think of any type of device that is implantable that requires energy, this would be a great way to power it so you don’t have to go in and change the batteries all the time,” says Wallace.
Prof Rory Collins accuses GPs of unjustifiable suspicion of cholesterol-reducing drugs, but is himself accused of ‘fear-mongering’
Surgeons operate on a patient’s heart. Statins are taken in the UK by 7m people who have at least a 20% risk of heart attack or stroke in the next decade. Photograph: BSIP SA/Alamy
Doctors worrying about the safety of cholesterol-reducing statins are creating a misleading level of uncertainty that could lead to the loss of lives, according to one of the UK’s leading medical academics.
Professor Sir Rory Collins, from Oxford University, said he believes GPs and the public are being made unjustifiably suspicious of the drug, creating a situation that has echoes of the MMR vaccine controversy.
The academic, one of the country’s leading experts on the drug, is particularly unhappy with the British Medical Journal (BMJ), which has run well-publicised articles by two critics of statins that he argues are flawed and misleading.
“It is a serious disservice to British and international medicine,” he said, claiming that it was probably killing more people than had been harmed as a result of the paper on the MMR vaccine by Andrew Wakefield. “I would think the papers on statins are far worse in terms of the harm they have done.”
Statins are currently being taken in the UK by 7 million people who have at least a 20% risk of a heart attack or stroke in the next 10 years. Following a major study overseen by Collins’ team at Oxford in 2012, the National Institute for Health and Care Excellence (Nice) recommended in February that they should be given to people at only 10% risk – potentially dramatically increasing the number of people taking them.
A number of doctors are among those who have questioned the wisdom of dosing essentially healthy people to prevent – rather than treat – illness. Some of them doubt the data from the drug company trials, which has been made available to Collins and his team but to nobody else.Collins criticised two papers published by the BMJ – one by John Abramson, a clinician working at Harvard medical school, and the other by Aseem Malhotra, a cardiologist in the UK. Both doctors said statins did not reduce mortality and that side effects meant they did more harm than good.
The Oxford academic said the side-effect claims were misleading and particularly damaging because they eroded public confidence. “We have really good data from over 100,000 people that show that the statins are very well tolerated. There are only one or two well-documented [problematic] side effects.” Myopathy, or muscle weakness, occurred in one in 10,000 people, he said, and there was a small increase in diabetes.
But the two researchers criticised by Collins said the side effects were real, with one accusing the professor of “fear-mongering”.
Abramson said the analysis by him and his team, published in the BMJ, showed statins did not significantly reduce mortality in the 20% or 10% risk groups. “This raises two issues,” Abramson said. “First, Dr Collins is fear-mongering when he says that ‘lives will be lost’ as a result of our calculations. Second, if Dr Collins believes our analysis is not correct, then he should release the patient-level data … so this discussion can be based on direct analysis of the data rather than relying upon their representation of the manufacturers’ data. At this point, I believe there is no excuse for not making this data public and the ongoing secrecy only raises the public’s level of suspicion.”
Although Malhotra accepted the benefits of statins for people who already had heart disease and prescibed them for such patients, he said “prescribing them to a low-risk group, potentially putting millions more of the UK population [on statins] would in my view be a public health disaster, contributing to chronic suffering to patients and placing a great strain on the NHS”.
The data did not show that statins prevented death or serious illness in people at low risk, he said. “Real world data also reveal that up to 20% of people suffer disabling side effects that result in discontinuation of the drug. The side effects include fatigue, muscle pain, stomach complaints, short-term memory loss, and erectile dysfunction.”
Dr Fiona Godlee, editor of the BMJ, said major issues were raised in the papers that deserved public debate – particularly the potential medicalisation of a large proportion of the population and the lack of access to data held by drug companies. Although Collins had seen the full data, Ebrahim and the Cochrane collaboration had not. “To rely on one meta-analysis by one group is no longer acceptable,” she said.
She dismissed Collins’ suggestion that there was a similarity between the BMJ’s publication of the statin papers and the Lancet’s 1997 decision to publish the controversial paper by Andrew Wakefield that wrongly suggested a link between MMR and autism.
“This is a debate that has been ongoing – the BMJ did not start it. Extending the statins to healthy people at low risk is an enormously important decision which should be subject to debate and question.”
The BMJ had already invited Collins to write a critique of the papers for publication, she added.
A study two weeks ago in the European Journal of Preventive Cardiology, which looked at drug company trial data, found that as many people experienced side effects on placebo dummy pills as on the statins. Dr Ben Goldacre, one of the authors of the study, said participants may have experienced the “nocebo” effect – where people believe they are experiencing the side effects they have heard the drugs may induce. But the flaw in the study, he said, was that the authors did not have access to the full data from the pharmaceutical companies behind the drugs.
‘I suffered terrible aching limbs’
Claire Rumble suffered aching limbs when she began taking statins to control her cholesterol level. Photograph: Dimitris Legakis/Athena Pictures
Claire Rumble has experienced both sides of the coin when it comes to the side effects of statins.
The 47-year-old, from Llanelli, Wales, was put on a cholesterol-lowering drug after having three heart attacks within 36 hours in 2009. The diagnosis was a blocked artery and despite her cholesterol not being particularly high, the consultant said that she should start taking statins. Rumble was prescribed Simvastatin but, as with others who have reported side effects from using statins, she developed muscle pains.
“I suffered terrible aching limbs,” she recalled. “I got it for six to eight months. I thought my body was adapting to the tablets. My arms and legs just felt very heavy, it could make you feel quite fluey.”
After the aches failed to disappear, Rumble, a fundraiser for Hafan Dda NHS trust and supporter of the British Heart Foundation, went back to the doctor, who put her on a different statin, Rosuvastatin.
“Within days of changing, I felt much much better and haven’t had a day’s problem since. I would recommend that if you are suffering aching muscles, go and see your GP and change [your medicine],” she said.
Despite her problems with Simvastatin, Rumble is philosophical. “Maybe Simvastatin wasn’t suitable for myself but I’m sure many people could take it without experiencing side effects.”
As if to prove her point, Susan Saul, an insulin-dependent diabetic from Stanmore, north-west London, had a completely different experience with the same two drugs.
With a history of high cholesterol and heart problems in her family, Saul was prescribed Simvastatin more than 10 years ago as a precaution. But after about a year she was moved on to Rosuvastatin, in the belief that it might be more effective. “Within a few days I noticed I was getting very severe leg cramps,” said Saul, a supporter of Heart UK. “It was awful, mostly at night.”
She read the accompanying leaflet which identified her symptoms as a possible, if rare, side effect. “I persevered for about two weeks but if anything they were getting more frequent and intense. I got changed back to the original [Simvastatin] and they went away almost immediately.” Saul said she has experienced no problems since.
The research from Imperial College London’s National Heart and Lung Institute that prompted the side-effects row suggested that some of the ailments suffered by statins users were not as a consequence of the drugs, but Saul believes her cramps were.
“My feeling on statins is that, as with any drug, different drugs suit different people,” she said. “You have side effects with any medication. Each time I go to my diabetes clinic and get my cholesterol checked, if it’s gone down further, I think the statins are doing the job, they are working. I think the benefits outweigh the risks.”
Though we can’t say that exercise will prevent dementia, evidence does suggest it can help reduce the risk of the condition as part of a healthy lifestyle”
Whether these benefits improve quality of life is still unclear, but the study authors say the findings are reason for optimism.
Dementia affects some 800,000 people in the UK. And the number of people with the condition is steadily increasing because people are living longer.
It is estimated that by 2021, the number of people with dementia in the UK will have increased to around one million.
With no cure, ways to improve the lives of those living with the condition are vital.
Researcher Dorothy Forbes, of the University of Alberta, and colleagues who carried out the Cochrane review, said: “Clearly, further research is needed to be able to develop best practice guidelines to enable healthcare providers to advise people with dementia living at home or in institutions.
“We also need to understand what level and intensity of exercise is beneficial for someone with dementia.”
Dr Laura Phipps of Alzheimer’s Research UK said: “We do know that exercise is an important part of keeping healthy, and though we can’t say that exercise will prevent dementia, evidence does suggest it can help reduce the risk of the condition as part of a healthy lifestyle.”
The device will work in a similar way to the cochlear implant, with electrodes implanted into the frontal area of the brain, which will provide electrical stimulation and growth factors to improve brain function in schizophrenia and allied disorders.
“Brain abnormalities in neuronal growth, microstructure and inter-neuronal communication underlie the prefrontal cortical pathology of many psychiatric diseases, including schizophrenia,” Professor Huang said.
Professor Huang recently told the Herald Sun that there had been virtually no technological breakthroughs for the treatment of schizophrenia (which ranks among the top 10 causes of disability in developed countries worldwide) in 50 years.
“Largely we rely on antipsychotics that not only have side-effects but also they can’t address the disease effects on cognitive function and communication,” he said.
“Through a number of years of study we’ve proven these materials have many benefits transmitting electrical signals to both nerve and muscle cells, and therefore influencing the developing and behaviour of those cells,” Professor Wallace said.
The team will initially evaluate and optimise the technology in vitro before creating a 3D nano-structured drug-loaded electrical stimulation device that will be tested in animal trials, with the potential to translate to clinical trials.
Professor Huang, who is also the Director of the Centre for Translational Neuroscience at UOW (which has been supported by the Schizophrenia Research Institute since 1999), is working on an additional five National Health and Medical Research Council projects (totalling $3 million) into mental illness.
The guidelines were first penned nearly a half century ago, in 1964, at a meeting of the World Medical Association in Helsinki, Finland, and have since been updated 7 times. Before this most recent update, the last time the document saw revisions was 2008.
The newest update,published onlineOctober 19 inJAMA, covers a wide range of topics organized under several headings, including:
Research Registration and Publication and Dissemination Results
Unproven Interventions in Clinical Practice
TwoViewpoints, both published in the same issue of the journal, help put the revisions in context. In some cases, the editorialists point out perceived shortcomings.
he revised document includes several subsections that give added emphasis to specific issues as well as improve readability, notes Paul Ndebele, PhD, from the Medical Research Council of Zimbabwe, Causeway, Harare, in oneperspective. “By so doing, the Declaration of Helsinki is a better and more important authority at what it is aimed at achieving — providing guidance on conducting medical research involving humans.”
Since the first declaration in 1964, research oversight has improved. However, Dr. Ndebele says, improved oversight has sometimes led to an underrepresentation of certain groups in research protocols. The new version of the declaration recommends that heretofore underrepresented groups need to be more involved in clinical trials so they have a chance, along with other groups, of benefiting from successful research. “Instead of excluding groups that have been ordinarily excluded from research, such as minority groups, women, and children, researchers need to clearly justify why these groups have been excluded from research,” he writes.
In addition, he notes that the newer version is more relevant for countries with limited resources as it includes clear language that specifically addresses issues of importance in poor countries. Dr. Ndebele points to one example: “The 2013 version of the Declaration of Helsinki recommends use of unproven interventions in cases for which proven interventions do not exist, after the physician has sought expert advice as well as the patient’s informed consent.”
The 2013 version also discusses issues related to dissemination of health research information. That includes making sure that trials are registered in publicly accessible databases and that those databases include not only trials with positive results but also those with findings that are negative or inconclusive.
Dr. Ndebele emphasizes that informed consent must be a cornerstone of ethical research. The new declaration acknowledges that in some closely knit societies, gaining consent needs to involve other people than the patient, such as community leaders and significant others. “By addressing this reality, the new version is emphasizing respect for culture and community norms as part of the research process,” he writes.
The new guidelines also encourage researchers to make use of videos, vignettes, and other innovative means to explain the rationale for their studies.
Once trials are complete, it is important to give participants feedback on the results, he adds. He believes that doing so demonstrates respect for research participants and also helps demystify research.
Dr. Ndebele concedes that in recent years there has been considerable debate regarding the ethics of conducting medical research in developing countries. However, he says the 2013 update of the guidelines makes progress in addressing the issues surrounding that debate.
In thesecondViewpoint, Joseph Millum, PhD, from the Department of Bioethics, Clinical Center, and the Fogarty International Center, National Institutes of Health, Bethesda, Maryland, acknowledge that the 2013 update represents progress. However, they also see a number of challenges that still need to be addressed.
For one, they say, “While the document purports to be a statement of enduring ethical principles, the nearly continuous process of revision undermines its authority.”
In addition, the 2013 document, similar to previous versions, is aimed primarily toward physicians. That is a mistake, they say, as the document offers recommendations for other health professionals, research ethics committees, sponsors, and governments, as well as editors and publishers. “It is time for the [World Medical Association] to recognize that the Declaration of Helsinki should address physicians as well as other health professionals and personnel involved in research,” they write.
Dr. Millum and colleagues add that the 2013 version’s treatment of informed consent remains inadequate. “It fails to recognize the possibility of waiving consent for some research involving competent adults, even though such research is common and widely endorsed.”
Neither does the declaration provide guidance on when it is appropriate to ask participants in studies to give broad consent for donating biological samples that could be used for wide-ranging studies in the future.
Dr. Millum and colleagues also take issue with the way the declaration treats “nonbeneficial studies,” or studies that pose risks to patients without offering compensating benefits.
Research combined with medical care is an increasingly popular way of conducting studies, note Dr. Millum and colleagues, but the declaration only allows such studies if, in the words of the declaration, “this is justified by its potential prevention, diagnostic or therapeutic value.”
In the view of Dr. Millum and colleagues, “The declaration’s lack of clear and consistent guidance regarding when net risks are acceptable creates unnecessary confusion and fuels the unfounded concern that all medical research is inherently exploitative.”
The authors further take issue with the new declaration’s protection of research participants who are vulnerable to harm in 1 or more ways, saying that the document “is confused about what constitutes appropriate protections and the appropriate means to achieve those protections.”
They concede that creating an international document to guide global research is an enormously difficult and complicated task. Hence, they say, it is not surprising that the newest version contains flaws. In spite of those flaws, however, they see the update as a step forward.
Over the past decade, doctors have become increasingly aggressive at initiating treatment for borderline hypothyroidism, possibly raising the risk for thyroid suppression as an unintended consequence, a new study suggests.
The American Thyroid Association recommends considering levothyroxine therapy at thyroid-stimulating hormone (TSH; thyrotropin) levels of 10 mIU/L or lower if symptoms of hypothyroidism, positive thyroid autoantibodies, or evidence of atherosclerotic cardiovascular disease or heart failure are present. But starting levothyroxine at or below 10 mIU/L in those without symptoms may do more harm than good, it cautions.
Yet in this new 9-year survey of more than 52,000 individuals in the United Kingdom, the number of individuals who received levothyroxine for a thyrotropin level of less than 10 mIU/L increased by 30% over the course of the study.
“This practice may be harmful, given the high risk of developing a suppressed thyrotropin level after treatment,” say the researchers, led by Peter N. Taylor, MRCP, from the Thyroid Research Group at the Institute of Molecular and Experimental Medicine, Cardiff University School of Medicine, United Kingdom, and colleagues, whose findings arepublished onlineOctober 7 inJAMAInternal Medicine.
Asked to comment on the findings forMedscape Medical News, Leonard Wartofsky, MD, chair of the department of medicine, Washington Hospital Medical Center, Washington, DC, said the authors are “raising the red flag that there is potentially overdiagnosis and overtreatment that has some risks.”
Most healthy people have thyrotropin levels less than 2.5 mIU/L, he explained. “If you simply go by the numbers, it’s hard to reconcile a TSH level of 7.9 as being normal when the rest of the population has numbers of 2.5 or less.” However, he added, thyrotropin levels do rise with age, so higher levels are normal for people 70 years of age or more and do not necessarily indicate treatment is necessary.
“Part of the problem is that this is a mild abnormality, and in most published studies it’s been difficult to show a clear benefit of intervention, because the number of subjects participating has been small, the abnormalities are minor, and you can’t show a major clinical effect of intervention,” Dr. Wartofsky observed. “This is a controversial issue, and it’s still unsettled.”
Threshold Lowered After 2004
Using the General Practice Research Database (GPRD; now called the Clinical Practice Research Datalink), which contains the records of more than 5 million patients in 508 primary-care practices across the United Kingdom, Dr. Taylor and coauthors conducted a retrospective cohort study of 52,298 adults who initiated levothyroxine therapy between January 1, 2001, and October 30, 2009, at a median age of 59 years.
Excluded from the study were people with a history of hyperthyroidism, pituitary disease, or thyroid surgery; those who were taking medication that affected thyroid function or whose thyroid problems were related to pregnancy; and/or those whose thyrotropin had been measured more than 3 months prior to beginning treatment.
To gauge the effect of therapy on thyroid function, they also studied thyrotropin levels at 30 to 36 months and 54 to 60 months after treatment began. Female patients outnumbered males by almost 4 to 1.
Following multivariate adjustment, the odds ratio of a patient receiving a levothyroxine prescription for a presenting thyrotropin level of less than 10.0 mIU/L in 2009 compared with 2001 was 1.30 (P< .001), and the number of new levothyroxine prescriptions increased by 74% over the study period.
The median thyrotropin level for initiating treatment fell from 8.7 mIU/L in 2001 to 7.9 mIU/L in 2009.
Individuals prescribed levothyroxine with a thyrotropin level between 4.0 and 10.0 mIU/L instead of exceeding 10.0 mIU/L were more likely to be female, have cardiovascular risk factors, and be older than 70 years when prescribed levothyroxine after 2004, with trends also observed for tiredness and depression, the authors write.
They conclude that “large-scale, prospective studies are required to assess the risk/benefit ratio of current practice.”
Overtreatment Can Lead to Problems, but So Can Undertreatment
Dr. Wartofsky said the study was designed to address whether starting levothyroxine therapy too early may result in overtreatment
Follow-up data showed that the percentage of patients with thyrotropin levels less than 0.1 mIU/L increased from 2.7% to 5.8% and the percentage of those with levels between 0.1 and 0.5 mIU/L increased from 6.3% to 10.2%, suggesting the presence of thyroid suppression. This “could lead to cardiac problems, arrhythmias, and atrial fibrillation and over the long term could lead to loss of bone mineral, osteopenia, and osteoporosis,” he explained.
But, he added, “I’m not particularly overwhelmed by the fact that only 5.8% of the patients were so oversuppressed. I think that is not unusual, even in the hands of expert endocrinologists — sometimes you oversuppress inadvertently.”
And the study does not show what the benefits of earlier treatment might be, probably because it takes longer for them to become apparent, he said. “In my view, there are compelling data that treating these populations does have a salutary effect”: lower serum cholesterol, a lower risk of coronary artery disease, and general symptom relief, among other things.
Over the past decade, doctors have become increasingly aggressive at initiating treatment for borderline hypothyroidism, possibly raising the risk for thyroid suppression as an unintended consequence, a new study suggests.
The American Thyroid Association recommends considering levothyroxine therapy at thyroid-stimulating hormone (TSH; thyrotropin) levels of 10 mIU/L or lower if symptoms of hypothyroidism, positive thyroid autoantibodies, or evidence of atherosclerotic cardiovascular disease or heart failure are present. But starting levothyroxine at or below 10 mIU/L in those without symptoms may do more harm than good, it cautions.
Yet in this new 9-year survey of more than 52,000 individuals in the United Kingdom, the number of individuals who received levothyroxine for a thyrotropin level of less than 10 mIU/L increased by 30% over the course of the study.
“This practice may be harmful, given the high risk of developing a suppressed thyrotropin level after treatment,” say the researchers, led by Peter N. Taylor, MRCP, from the Thyroid Research Group at the Institute of Molecular and Experimental Medicine, Cardiff University School of Medicine, United Kingdom, and colleagues, whose findings arepublished onlineOctober 7 inJAMAInternal Medicine.
Asked to comment on the findings forMedscape Medical News, Leonard Wartofsky, MD, chair of the department of medicine, Washington Hospital Medical Center, Washington, DC, said the authors are “raising the red flag that there is potentially overdiagnosis and overtreatment that has some risks.”
Most healthy people have thyrotropin levels less than 2.5 mIU/L, he explained. “If you simply go by the numbers, it’s hard to reconcile a TSH level of 7.9 as being normal when the rest of the population has numbers of 2.5 or less.” However, he added, thyrotropin levels do rise with age, so higher levels are normal for people 70 years of age or more and do not necessarily indicate treatment is necessary.
“Part of the problem is that this is a mild abnormality, and in most published studies it’s been difficult to show a clear benefit of intervention, because the number of subjects participating has been small, the abnormalities are minor, and you can’t show a major clinical effect of intervention,” Dr. Wartofsky observed. “This is a controversial issue, and it’s still unsettled.”
Threshold Lowered After 2004
Using the General Practice Research Database (GPRD; now called the Clinical Practice Research Datalink), which contains the records of more than 5 million patients in 508 primary-care practices across the United Kingdom, Dr. Taylor and coauthors conducted a retrospective cohort study of 52,298 adults who initiated levothyroxine therapy between January 1, 2001, and October 30, 2009, at a median age of 59 years.
Excluded from the study were people with a history of hyperthyroidism, pituitary disease, or thyroid surgery; those who were taking medication that affected thyroid function or whose thyroid problems were related to pregnancy; and/or those whose thyrotropin had been measured more than 3 months prior to beginning treatment.
To gauge the effect of therapy on thyroid function, they also studied thyrotropin levels at 30 to 36 months and 54 to 60 months after treatment began. Female patients outnumbered males by almost 4 to 1.
Following multivariate adjustment, the odds ratio of a patient receiving a levothyroxine prescription for a presenting thyrotropin level of less than 10.0 mIU/L in 2009 compared with 2001 was 1.30 (P< .001), and the number of new levothyroxine prescriptions increased by 74% over the study period.
The median thyrotropin level for initiating treatment fell from 8.7 mIU/L in 2001 to 7.9 mIU/L in 2009.
Individuals prescribed levothyroxine with a thyrotropin level between 4.0 and 10.0 mIU/L instead of exceeding 10.0 mIU/L were more likely to be female, have cardiovascular risk factors, and be older than 70 years when prescribed levothyroxine after 2004, with trends also observed for tiredness and depression, the authors write.
They conclude that “large-scale, prospective studies are required to assess the risk/benefit ratio of current practice.”
Overtreatment Can Lead to Problems, but So Can Undertreatment
Dr. Wartofsky said the study was designed to address whether starting levothyroxine therapy too early may result in overtreatment
Follow-up data showed that the percentage of patients with thyrotropin levels less than 0.1 mIU/L increased from 2.7% to 5.8% and the percentage of those with levels between 0.1 and 0.5 mIU/L increased from 6.3% to 10.2%, suggesting the presence of thyroid suppression. This “could lead to cardiac problems, arrhythmias, and atrial fibrillation and over the long term could lead to loss of bone mineral, osteopenia, and osteoporosis,” he explained.
But, he added, “I’m not particularly overwhelmed by the fact that only 5.8% of the patients were so oversuppressed. I think that is not unusual, even in the hands of expert endocrinologists — sometimes you oversuppress inadvertently.”
And the study does not show what the benefits of earlier treatment might be, probably because it takes longer for them to become apparent, he said. “In my view, there are compelling data that treating these populations does have a salutary effect”: lower serum cholesterol, a lower risk of coronary artery disease, and general symptom relief, among other things.
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