What is Invokana?

What is Invokana?

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Invokana is a brand-name prescription drug. It’s FDA-approved for use in adults with type 2 diabetes to:

Improve blood sugar levels. For this use, Invokana is prescribed in addition to diet and exercise to lower blood sugar levels. Reduce the risk of certain cardiovascular problems. For this use, Invokana is given to adults with known cardiovascular disease. It’s used to lower the risk of heart attack and stroke that don’t lead to death. The drug is used to reduce the risk of death from a heart or blood vessel problem.
Reduce the risk of certain complications in people who have diabetic nephropathy with albuminuria. For this use, Invokana is given to certain adults who have diabetic nephropathy (kidney damage that’s caused by diabetes) with albuminuria* of greater than 300 milligrams per day. It’s used to lower the risk of:
End-stage kidney disease
death caused by a heart or blood vessel problem
doubled blood level of creatinine
the need to be hospitalized for heart failure
For more information about these uses of Invokana and certain limitations of its use, see the “Invokana uses” section below.

  • With albuminuria, you have high levels of a protein called albumin in your urine.

Drug details
Invokana contains the drug canagliflozin. It belongs to a class of drugs called sodium-glucose co-transporter 2 (SGLT-2) inhibitors. (A drug class describes a group of medications that work similarly.)

Invokana comes as a tablet that’s taken by mouth. It’s available in two strengths: 100 mg and 300 mg.

Effectiveness
For information on Invokana’s effectiveness for its approved uses, see the “Invokana uses” section below.

Invokana generic
Invokana contains one active drug ingredient: canagliflozin. It’s available only as a brand-name medication. It’s not currently available in generic form. (A generic drug is an exact copy of the active drug in a brand-name medication.)

Invokana side effects
Invokana can cause mild or serious side effects. The following list contains some key side effects that may occur while taking Invokana. This list doesn’t include all possible side effects.

To learn more about possible side effects of Invokana or how to manage them, talk with your doctor or pharmacist.

Note: The Food and Drug Administration (FDA) tracks side effects of drugs it has approved. If you would like to notify the FDA about a side effect you’ve had with Invokana, you can do so through MedWatch.

More common side effects
The more common side effects of Invokana can include*:

urinary tract infections / urinating more often than normal / thirstiness / constipation / nausea / yeast infections† in men and women / vaginal itching.

Most of these side effects may go away within a few days or a couple of weeks. If they’re more severe or don’t go away, talk with your doctor or pharmacist. You should also call your doctor if you think you have a urinary tract infection or yeast infection.

  • This is a partial list of more common side effects from Invokana. To learn about other mild side effects, talk with your doctor or pharmacist or visit Invokana’s medication guide.
    † For more information about this side effect, see the “Side effect details” section just below.

Serious side effects
Serious side effects from Invokana aren’t common, but they can occur. Call your doctor right away if you have serious side effects. Call 911 if your symptoms feel life-threatening or if you think you’re having a medical emergency.

Serious side effects and their symptoms can include the following:

Dehydration (low fluid level), which can cause low blood pressure. Symptoms can include:
dizziness/feeling faint/lightheadedness/weakness, especially when you stand up
Hypoglycemia (low blood sugar level). Symptoms can include:
drowsiness/headache/confusion/weakness/hunger/irritability/sweating/feeling jittery/fast heartbeat
Severe allergic reaction.*
Amputation of lower limbs.*
Diabetic ketoacidosis (increased levels of ketones in your blood or urine).*
Fournier’s gangrene (severe infection near the genitals).*
Kidney damage.* Bone fractures.*

Side effect details
You may wonder how often certain side effects occur with this drug. Here’s some detail on certain side effects this drug may or may not cause.

Allergic reaction
As with most drugs, some people can have an allergic reaction after taking Invokana. In clinical studies, up to 4.2% of people taking Invokana reported having mild allergic reactions.

Symptoms of a mild allergic reaction can include:

skin rash/itchiness/flushing (warmth, swelling, or redness in your skin)
A more severe allergic reaction is rare but possible. Only a few people in clinical studies reported severe allergic reactions while taking Invokana.

Symptoms of a severe allergic reaction can include:

swelling under your skin, typically in your eyelids, lips, hands, or feet
swelling of your tongue, mouth, or throat/trouble breathing
Call your doctor right away if you have a severe allergic reaction to Invokana. But call 911 if your symptoms feel life-threatening or if you think you’re having a medical emergency.

Amputation
Invokana may increase your risk of amputation of lower limbs. (With amputation, one of your limbs is removed.)

Two studies found an increased risk for lower limb amputation in people who took Invokana and had:

type 2 diabetes and heart disease, or
type 2 diabetes and were at risk for heart disease
In the studies, up to 3.5% of the people who took Invokana had an amputation. Compared with people who didn’t take the drug, Invokana doubled the risk of amputation. The toe and the midfoot (arch area) were the most common areas of amputation. Some leg amputations were also reported.

Before you start taking Invokana, talk with your doctor about your risk of amputation. This is especially important if you’ve had an amputation in the past. It’s also important if you have a blood circulation or nerve disorder, or diabetic foot ulcers.

Call your doctor right away and stop taking Invokana if you:

feel new foot pain or tenderness
have foot sores or ulcers
get a foot infection
Call 911 if your symptoms feel life-threatening or if you think you’re having a medical emergency. If you develop symptoms or conditions that increase your risk for lower limb amputation, your doctor may have you stop taking Invokana.

Yeast infection
Taking Invokana increases your risk of a yeast infection. This is true for both men and women, according to data from clinical trials. In the trials, up to 11.6% of the women and 4.2% of the men had a yeast infection.

You’re more likely to develop a yeast infection if you’ve had one in the past or if you’re an uncircumcised male.

If you get a yeast infection while taking Invokana, talk with your doctor. They can suggest ways to treat it.

Diabetic ketoacidosis
Although it’s rare, some people who take Invokana can develop a serious condition called diabetic ketoacidosis. This condition occurs when cells in your body don’t get the glucose (sugar) they need for energy. Without this sugar, your body uses fat for energy. And this can lead to high levels of acidic chemicals called ketones in your blood.

Symptoms of diabetic ketoacidosis can include:

excessive thirst/urinating more often than normal/nausea/vomiting/stomach pain/tiredness/weakness/shortness of breath/breath that smells fruity/confusion
In severe cases, diabetic ketoacidosis can cause coma or death. If you think you may have diabetic ketoacidosis, call your doctor right away. But if your symptoms are severe, call 911 or go to the nearest emergency room.

Before you start taking Invokana, your doctor will assess your risk for developing diabetic ketoacidosis. If you have an increased risk of this condition, your doctor may monitor you closely during treatment. And in some cases, such as if you’re having surgery, they may have you temporarily stop taking Invokana.

Fournier’s gangrene
Fournier’s gangrene is a rare infection in the area between your genitals and rectum. Symptoms can include:

pain, tenderness, swelling, or reddening in your genital or rectal area
fever malaise (overall feeling of discomfort)
People in clinical trials of Invokana didn’t get Fournier’s gangrene. However after the drug was approved for use, some people reported having Fournier’s gangrene while taking Invokana or other drugs in the same drug class. (A class of drugs describes a group of medications that work in the same way.)

More serious cases of Fournier’s gangrene have led to hospitalization, multiple surgeries, or even death.

If you think you may have developed Fournier’s gangrene, call your doctor right away. They may want you to stop taking Invokana. They will also recommend treatment for the infection.

Kidney damage
Taking Invokana can increase your risk of kidney damage. Symptoms of kidney damage can include:

urinating less often than normal
swelling in your legs, ankles, or feet
confusion
fatigue (lack of energy)
nausea
chest pain or pressure
irregular heartbeat
seizures
After the drug was approved for use, some people taking Invokana reported that their kidneys worked poorly. When these people stopped taking Invokana, their kidneys began to work normally again.

You’re more likely to have kidney problems if you:

are dehydrated (have a low fluid level)
have kidney or heart problems
take other medications that affect your kidneys
are older than age 65
Before you start taking Invokana, your doctor will test how well your kidneys are working. If you have kidney problems, you may not be able to take Invokana.

Your doctor may also test how your kidneys are working during your treatment with Invokana. If they detect any kidney problems, they may change your dose or stop your treatment with the drug.

Bone fractures
In a clinical study, some people who took Invokana experienced bone fractures (broken bones). The fractures weren’t usually severe.

Symptoms of bone fracture can include:

pain/swelling/tenderness/bruising/deformity
If you’re at high risk for a fracture or if you’re concerned about breaking a bone, talk with your doctor. They can suggest ways to help prevent this side effect.

Falls: In nine clinical trials, up to 2.1% of people who took Invokana had a fall. There was a higher risk of falls in the first few weeks of treatment.

If you have a fall while taking Invokana or if you’re concerned about falling, talk with your doctor. They can suggest ways to help prevent this side effect.

Pancreatitis (not a side effect)

Pancreatitis (inflammation in your pancreas) was extremely rare in clinical trials. Rates of pancreatitis were similar between people who took Invokana and those who took a placebo (treatment without active drug). Because of these similar results, it’s not likely that Invokana caused the pancreatitis.

If you have concerns about developing pancreatitis with Invokana, talk with your doctor.

Joint pain (not a side effect): Joint pain wasn’t a side effect of Invokana in any clinical trials.

However, some other diabetes drugs may cause joint pain. In fact, the Food and Drug Administration (FDA) released a safety announcementTrusted Source for a class of diabetes drug called dipeptidyl peptidase-4 (DPP-4) inhibitors. (A drug class describes a group of medications that work in the same way.) The announcement said that DPP-4 inhibitors may cause severe joint pain.

But Invokana doesn’t belong to that drug class. Instead, it belongs to a class of drugs called sodium-glucose co-transporter-2 (SGLT2) inhibitors.

If you have concerns about joint pain with Invokana use, talk with your doctor.

Hair loss (not a side effect)/Hair loss wasn’t a side effect of Invokana in any clinical trials.

If you’re concerned about hair loss, talk with your doctor. They can help you determine what’s causing it and ways to treat it.

Invokana dosage
The Invokana dosage your doctor prescribes will depend on several factors. These include:

the type and severity of the condition you’re using Invokana to treat
your age
other medical conditions you may have
how well your kidneys are working
certain other medications you may be taking with Invokana
Typically, your doctor will start you on a low dosage. Then they’ll adjust it over time to reach the amount that’s right for you. Your doctor will ultimately prescribe the smallest dosage that provides the desired effect.

The following information describes dosages that are commonly used or recommended. However, be sure to take the dosage your doctor prescribes for you. Your doctor will determine the best dosage to suit your needs.

Drug forms and strengths
Invokana comes as a tablet. It’s available in two strengths:

100 milligrams (mg), which comes as a yellow tablet
300 mg, which comes as a white tablet
Dosage for lowering blood sugar levels
Recommended dosages of Invokana to lower blood sugar levels are based on a measurement called estimated glomerular filtration rate (eGFR). This measurement is done using a blood test. And it shows how well your kidneys are working.

In people with an:

eGFR of at least 60, they have no loss of kidney function to mild loss of kidney function. Their recommended dosage of Invokana is 100 mg once daily. Their doctor may increase their dosage to 300 mg once daily if needed to help manage their blood sugar level.
eGFR of 30 to less than 60, they have mild-to-moderate loss of kidney function. Their recommended dosage of Invokana is 100 mg once daily.
eGFR of less than 30, they have severe loss of kidney function. It’s not recommended that they begin using Invokana. But if they’ve already been using the drug and are passing a certain level of albumin (a protein) in their urine, they may be able to continue taking Invokana.*
Note: Invokana shouldn’t be used by people who are using dialysis therapy. (Dialysis is a procedure that’s used to clear waste products from your blood when your kidneys aren’t healthy enough to do so.)

  • For this use, people would be taking Invokana at a dosage of 100 mg to lower the risk of certain complications of diabetic nephropathy. See the “Invokana uses” section for more information.

Dosage for reducing cardiovascular risks
Recommended dosages of Invokana to reduce cardiovascular risks are the same as they are to lower blood sugar levels. See the section above for details.

Dosage for reducing the risk of complications from diabetic nephropathy
Recommended dosages of Invokana to lower the risks of complications from diabetic nephropathy are the same as they are to lower blood sugar levels. See the section above for details.

What if I miss a dose?
If you miss a dose of Invokana, take it as soon as you remember. If it’s almost time for your next dose, skip the missed dose and take the next dose at the normal time. Don’t try to catch up by taking two doses at once. This can cause dangerous side effects.

Using a reminder tool can help you remember to take Invokana every day.

Be sure to take Invokana only as your doctor prescribes.

Will I need to use this drug long-term?
If you and your doctor agree that Invokana is working well for you, you’ll likely use it long-term.

New test may predict which IBD patients have higher colorectal cancer risk

New test may predict which IBD patients have higher colorectal cancer risk

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Individuals who suffer from inflammatory bowel disease (IBD) are more likely to develop colorectal cancer. Every one to three years, people with IBD frequently undergo colonoscopies to screen for colorectal cancer. Previous studies have demonstrated that identifying precancerous cells in individuals with IBD can be difficult. A new test created by researchers at London’s Institute of Cancer Research claims to be able to predict bowel cancer risk in individuals with IBD with 90% accuracy. According to earlier studies, individuals with inflammatory bowel disease (IBD), which includes Crohn’s disease and ulcerative colitis, are more likely to develop colorectal cancer than those without IBD.

Due to the chronic inflammation associated with IBD, which can lead to the growth of abnormal cells called dysplasia and the development of precancerous polyps in the intestinal tract, people with IBD are more likely to develop colorectal cancer, also known as bowel cancer. Currently, a colonoscopy is performed every one to three years to screen for colorectal cancer in individuals with IBD. Nevertheless, prior research indicates that it can be challenging to identify precancerous cells in IBD patients. Researchers at London’s Institute of Cancer Research have now created a new test that they claim can more than 90% accurately predict bowel cancer risk in individuals with IBD.

The study’s senior author, Trevor Graham, PhD, a professor of genomics and evolution and director of the Centre for Evolution and Cancer at The Institute of Cancer Research in London, stated that while individuals with IBD are more likely to develop bowel cancer, there is currently no reliable method to predict that risk. Graham told Medical News Today that the only effective treatment for people who are believed to be in imminent danger of developing cancer is surgery to remove part or all of the large bowel. This procedure may save a life. However, people are undergoing needless surgery that can change their lives because we are currently unable to determine whether a patient actually needs the procedure. However, he added, those whose risk of bowel cancer is deemed low and for whom we do not perform surgery still experience anxiety due to the uncertainty surrounding their cancer risk.

Increased risk of cancer with cellular DNA changes
Researchers discovered that individuals with IBD who had precancerous cells that either gained or lost multiple copies of DNA were more likely to develop bowel cancer. The researchers then used the precise pattern of the altered DNA in the precancerous cells to create an algorithm that would predict the risk of colorectal cancer in the future. According to Graham, individuals with IBD in the UK undergo routine colonoscopies, which involve a camera being inserted up their butt to check for early indications of cancer. A biopsy is a tiny sample of tissue taken if something odd is observed. The test we run on the biopsy is a genetic test. According to him, we have developed a test to predict an individual’s risk based on the genetic signals in their biopsy after comparing the genetic signals of those who did and did not develop cancer.

Test predicts colorectal cancer risk with over 90% accuracy
Graham and his colleagues discovered that their novel test could more than 90% accurately predict which IBD study participants who developed precancerous cells would later develop colorectal cancer within five years. Graham stated, “We hope that by accurately identifying those at risk of cancer, we will be able to provide appropriate treatment.”. Surgery can be used to remove the colon and reduce the risk of cancer in people who are at a high risk of getting the disease. We can spare people who are not at high-risk needless anxiety and care. In clinical trials that we intend to conduct in the future, we must demonstrate that our predictions are accurate for patients to benefit from this, he said.

Although bowel cancer is more likely to strike people with inflammatory bowel disease, most IBD patients do not go on to get the disease. By predicting who is actually at risk, our new test enables all patients to receive the best possible care. To demonstrate that our predictions are accurate in practical situations, we will next conduct clinical trials. In the upcoming years, we hope to be able to administer the test within the NHS.

A less invasive predictive test
Regarding this study, a board-certified gastroenterologist at Providence Saint John’s Health Center in Santa Monica, California, commended it as fantastic, outstanding, and wonderful. The truth is that we frequently perform colonoscopies and biopsies on our IBD patients to check for dysplasia or cells or tissue that may develop into cancer. After that, we must have these conversations with them. Bedford clarified, “What do we do if they do have these low-grade dysplastic cells? Do we remove your colon or do we do more frequent surveillance?

It sounds like the speaker is expressing enthusiasm about a new test for predicting cancer risk in patients with inflammatory bowel disease (IBD). A test with 90% accuracy could significantly improve clinical decision-making by identifying those at risk for cancer and allowing doctors to target therapy more effectively. This could reduce the need for invasive procedures, which is always a win for patient comfort and safety. Additionally, if the test could be adapted into a blood or stool test, it would make it even more convenient for patients, potentially improving adherence to monitoring and early intervention.
It’s exciting when advancements like this can make a real difference in patient care! Would you like more information on current developments in diagnostic tests for IBD or related cancer risks?

Determining who is at higher risk
It seems like Dr. Nilesh Vora is also highlighting the potential of this study, emphasizing how valuable it would be for gastroenterologists to have a more accurate way of identifying which patients with inflammatory bowel disease (IBD) are at higher risk for colon cancer. This would help doctors make more informed decisions on how to manage these patients and which individuals might benefit from closer monitoring or more aggressive treatments.

Dr. Vora’s perspective points to the benefit of targeted care by identifying at-risk patients, healthcare providers can potentially avoid unnecessary procedures for those not at risk, while ensuring higher-risk patients are managed more carefully. This kind of approach could streamline care and improve outcomes for patients with IBD, who already face challenges related to their condition.

It’s fascinating to see how medical fields are working together to improve outcomes for patients, and studies like this really highlight how advances in one area of medicine (in this case, diagnostic tools for cancer risk) can have a ripple effect on multiple specialties, improving patient care overall. Does this kind of collaboration between specialists and new diagnostic tests interest you?

That’s a crucial next step! Getting FDA approval for this test would be a significant milestone. If it’s approved, it could become a standard tool in clinical practice, helping doctors more accurately determine which IBD patients need frequent colonoscopies and which could safely extend the interval between screenings. Reducing the number of unnecessary colonoscopies would not only ease the burden on patients but also reduce healthcare costs and free up resources for those who truly need more frequent monitoring.

The potential for a more personalized approach to care where screenings are tailored to an individual’s actual risk—could be a game changer in managing IBD patients. The idea of offering more tailored and less invasive options for ongoing care could improve patient experience, both physically and psychologically.

If the test proves to be both accurate and accessible, it could help revolutionize the way doctors approach cancer prevention and monitoring for IBD patients. What do you think are some of the biggest hurdles in getting something like this approved by the FDA?

Common sleep medication may prevent the brain from clearing ‘waste’

Common sleep medication may prevent the brain from clearing ‘waste’

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Up to 70 million people suffer from persistent sleep problems. A person’s risk of developing dementia and cognitive decline is increased when they don’t get enough sleep each night. Using a mouse model, a new study explains for the first time how the brain’s glymphatic system is powered by synchronized oscillations during sleep to help eliminate “waste” linked to neurodegenerative diseases. Additionally, researchers discovered that a frequently prescribed sleep aid may suppress those oscillations, interfering with the brain’s ability to eliminate waste while you sleep. It’s critical to consider every factor that could increase the risk of cognitive decline, especially in light of recent studies showing that the risk of dementia in Americans has more than doubled after the age of 55.

According to the most recent data, many adults over the age of 18 may experience persistent sleep problems like insomnia and sleep apnea, despite doctors’ recommendations that they get at least 7 hours of good sleep every night. It is estimated that 39 percent of adults over 45 in the United States alone were not getting enough sleep in 2022. According to previous research, a person’s risk of developing some illnesses, including brain-related disorders like dementia and cognitive decline, can be raised by not getting enough sleep each night. Natalie Hauglund, PhD, a postdoctoral fellow at the Universities of Copenhagen in Denmark and Oxford in the United Kingdom, told Medical News Today that sleep enables the brain to go offline, stop processing information from the outside world, and concentrate on maintenance functions like waste removal and immune surveillance. Disease development and cognitive decline are linked to sleep deprivation.

But could some sleep aids also lead to worse brain health as we age? Researching all the potential causes of cognitive decline is more crucial than ever, especially in light of a recent study in Nature Medicine that found that Americans’ risk of developing dementia after the age of 55 has more than doubled compared to previous estimates. For the first time, Hauglund is the first author of a study that uses a mouse model to describe the synchronized oscillations that occur during sleep and power the brain’s glymphatic system, which helps remove waste linked to neurodegenerative diseases. The study was published in the journal Cell. According to the survey, zolpidem, a popular prescription sleep aid sold under Ambien, may suppress these oscillations and interfere with the brain’s ability to eliminate waste while you sleep.

What powers the brain’s ‘waste-removal’ system?
For this study, scientists recorded the brain activity of mice both awake and asleep using a variety of technologies. Researchers found that the brain’s waste-removing glymphatic system is essentially powered by slow, synchronized oscillations of the neurotransmitter norepinephrine, cerebral blood, and cerebrospinal fluid (CSF) during non-REM sleep. The brain uses cerebrospinal fluid, a fluid produced inside the brain, to flush the brain tissue and wash away unwanted molecules. This makes our brain unique because it lacks lymphatic vessels, which remove waste products like dead cells and bacteria from the rest of our body, she explained.

The glymphatic system is the brain’s cleaning mechanism. Crucially, the glymphatic system only activates during non-REM sleep, which is the deepest phase of sleep. This is due to a neuromodulator called norepinephrine, which is released in slow cycles approximately every 50 seconds during non-REM sleep. Nedergaard informed us that norepinephrine causes the arteries to constrict by binding to their muscle cells. Consequently, a gradual fluctuation in the brain’s blood volume and artery diameter is caused by the slow oscillation in norepinephrine concentration. Cerebrospinal fluid is transported through the brain’s tissue and along the arteries by this dynamic change in blood volume, which functions as a pump. She explained that norepinephrine thus controls the glymphatic system by coordinating the synchronized dilatation and constriction of the blood vessels.

Sleep aids may disrupt the brain’s glymphatic system
The possibility that sleep aids could mimic the natural oscillations required for the glymphatic function was also investigated. They concentrated their investigation on zolpidem, a sedative. They found that zolpidem seemed to stop norepinephrine oscillations, which disrupted the brain’s glymphatic system’s ability to remove waste while you slept. Although our research indicates that sleep medication may not have the same positive effects as natural, restorative sleep, sleep aids may offer a shortcut to sleep, according to Hauglund. Our results highlight the importance of using sleep aids sparingly and only as a last resort. Sleep is essential because it allows the brain to complete homeostatic housekeeping functions like eliminating waste. Conversely, sleep aids hinder the brain’s ability to properly prepare for each new day by blocking the neuromodulators that control the waste removal system.

Should sleep-aid users be concerned?
As per Segal’s perspective, not being part of the recent study, the advantages derived from enhanced sleep due to the use of sleep aids like zolpidem seemingly fail to surpass any alleged negative impact this medication may have on decreasing REM sleep, consequently lowering brain neurotransmitter levels, subsequently affecting brain protein levels. The numerous ‘in turn’ assertions do not instill any worry in me that this research holds any substantial clinical relevance, he mentioned. Clinical neurologists, including myself, are not apprehensive about the possibility of zolpidem misuse leading to dementia in the elderly population struggling with insomnia.

It is difficult for clinical neurologists like me to agree that sleeping pills will cause dementia. I would tell my patients that the advantages of getting a good night’s sleep outweigh any potential risks that may arise, such as dementia or memory loss as they age. The relationship between brain health, sleep quality, and general healthPolos, who was not involved in the study, said he found the results intriguing. “There is no question that the glymphatic system can work in synchrony with different transmitters and waste products in the brain,” he said.

According to this study, changes to this delicate balance may have cellular and possibly therapeutic repercussions. Though intriguing, we must keep in mind that this is an animal study and that extrapolating results from it to humans should be done carefully, as is frequently the case. It does, however, provide physicians with a phenomenon that merits some discussion. “We definitely would like to see if studies could assess the impact of sleep aids on human glymphatic flow if more work were to be done in this area,” Polos added. Naturally, noninvasive methods and possibly some sophisticated imaging would be needed for this. Even in small quantities, such data would be useful.

He went on to say that it is impossible to overstate the connection between the brain, restful sleep, and general health. As sleep physicians, we fully support ongoing research into the relationship between the brain, sleep, and general health because the rhythmic nature of sleep and the regular cycling of sleep stages have been thoroughly studied. We have learned a lot about the effects of changes in the brain and how they affect sleep, but we still have a lot to learn.

Alzheimer’s: Are newly approved drugs making a real-life difference?

Alzheimer’s: Are newly approved drugs making a real-life difference?

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In 2021, the Food and Drug Administration (FDA) finally approved some new medications to treat Alzheimer’s disease after a nearly two-decade hiatus. The majority of these medications are antibody treatments that target harmful protein clusters in the brain. Their endorsement has generated equal parts excitement and controversy. In this Special Feature, we look into the fundamental question of whether these medications are actually having an impact. The neurodegenerative condition known as Alzheimer’s disease causes a slow and irreversible loss of thinking, memory, and ultimately the capacity to carry out daily tasks. Alzheimer’s disease is primarily caused by aging, and as the population ages quickly, it has become a public health emergency.

Alzheimer’s disease affected 57 million people worldwide in 2019; by 2050, that figure is predicted to rise to 153 million. This emphasizes the necessity of disease-modifying therapies that alter the course of the illness permanently and slow its progression. The development of disease-modifying treatments for Alzheimer’s disease, however, has not been successful until recently. The beta-amyloid protein, whose aberrant accumulation is generally thought to be the cause of Alzheimer’s disease, has been the focus of the majority of clinical research aimed at creating disease-modifying treatments for the condition. Regarded as the first disease-modifying treatment for Alzheimer’s disease, aucanumab, an antibody that targets amyloid-beta protein deposits, was approved by the Food and Drug Administration (FDA) in 2021.

Nevertheless, aducanumab’s manufacturer, Biogen, announced that it will eventually halt sales after clinical trials failed to yield consistent improvements in cognitive function. Since then, phase 3 clinical trials have shown that two additional anti-amyloid antibodies, lecanemab from Biogen and donanemab from Eli Lily, can slow cognitive decline in people with early-stage Alzheimer’s disease. These antibodies have been approved by the FDA. Clinicians and researchers have welcomed the approval of lecanemab and donanemab as a breakthrough after decades of clinical research that failed to yield effective disease-modifying therapies. The modest clinical benefits of these anti-amyloid treatments have, however, drawn criticism from some researchers who point to safety concerns and a lack of cost-effectiveness.

While there are challenges at the clinical, societal, and healthcare levels, we should not forget the opportunities and the breakthrough that after decades of very costly negative trials, we finally have unequivocal evidence that it is possible to reduce the progression of the disease, said Dag Aarsland, MD, professor of old age psychiatry at King’s College London in the United Kingdom, in an interview with Medical News Today. Paresh Malhotra, PhD, who teaches clinical neurology at Imperial College London in the United Kingdom, is comparable. K. pointed out that even though these anti-amyloid treatments are only moderately effective, it’s crucial to understand that they are the first to show clinical effects that seem to be connected to a major mechanism of disease progression. Their introduction could speed up the development of new treatments and revolutionize clinical services for Alzheimer’s disease, the most prevalent cause of dementia in the world.

The amyloid cascade theory is the foundation for the creation of anti-amyloid antibody therapies like lecanemab and donanemab. This theory states that Alzheimer’s disease develops as a result of additional alterations in the brain brought on by the buildup of beta-amyloid protein. In particular, it is thought that the development of beta-amyloid aggregates causes oxidative stress, inflammation, neuronal damage, the loss of synapses the connections between neurons that enable communication and, eventually, cognitive decline. This is supported by the fact that beta-amyloid protein buildup occurs several years before cognitive function, such as memory and decision-making, deteriorates.

Secretase enzymes cleave a larger amyloid precursor protein to produce the beta-amyloid protein. Each beta-amyloid protein unit is known as a monomer, and these monomers can combine to form oligomers, which are soluble short chains made up of two to more than fifty monomers. Larger, soluble protofibrils and insoluble fibrils can also be formed by the aggregation of beta-amyloid monomers. In the extracellular space between neurons, the insoluble fibrils subsequently come together to form plaques.

Amyloid plaques were once believed to be poisonous and to be the cause of Alzheimer’s disease. However, over the last 20 years, research has indicated that beta-amyloid oligomers are more harmful than amyloid plaques and may be more involved in the onset of Alzheimer’s disease. It is believed that poor production or clearance of beta-amyloid protein is the cause of the buildup of beta-amyloid aggregates. Over the last 20 years, some medications have been created that either target the enzymes that produce beta-amyloid or make it easier to remove beta-amyloid aggregates. However, because of their serious side effects or inability to produce the intended clinical effects, these medications have failed to obtain FDA approval.

The only FDA-approved treatments that target beta-amyloid aggregates are the anti-amyloid antibodies lecanemab, aducanumab, and donanemab. The affinity of these antibodies for the different kinds of beta-amyloid protein aggregates varies. While aducanumab and lecanemab bind to beta-amyloid oligomers, protofibrils, and plaques, donanemab binds to a particular type of beta-amyloid that is exclusively present in plaques. While aducanumab has a greater affinity for insoluble fibrils, lecanemab exhibits the highest affinity for beta-amyloid protofibrils.

Activating an immune response against beta-amyloid aggregates and causing their removal is one of the hypothesized mechanisms by which anti-amyloid antibodies generate their therapeutic effects. Additionally, anti-amyloid antibodies may neutralize the plaques by binding to oligomers or destabilizing them. In 2021, the FDA gave aducanumab accelerated approval for the treatment of Alzheimer’s disease because of its capacity to remove amyloid plaques. Although aducanumab was effective in removing amyloid plaques from the brain, different clinical trials showed different effects on cognitive function.

The FDA’s approval process caused controversy, and doctors were reluctant to prescribe aducanumab because of the lack of evidence supporting its therapeutic effects. Additionally, as was already mentioned, Biogen has halted aducanumab’s development and sales as of 2024. On the other hand, lecanemab and donanemab have both demonstrated the capacity to remove amyloid plaques while delaying the course of the illness. People with early-stage Alzheimer’s disease and lower baseline beta-amyloid levels respond better to these treatments. The FDA has approved the intravenous infusion of lecanemab and donanemab for use in patients with early-stage Alzheimer’s disease, including those with mild cognitive impairment or mild Alzheimer’s disease.

Donanemab must be administered every four weeks, while lecanemab should be given every two weeks. Donanemab’s ability to allow patients to stop treatment once they have achieved total plaque clearance is one of its special qualities. Amyloid plaques develop over some years, and it is thought that people may only need minor additional care. Lecanemab and donanemab phase 3 trial participants demonstrated slower declines in cognitive function by 27% and 36%, respectively, when compared to placebo.

These results, according to some researchers, are mild and on par with symptomatic treatments like acetylcholinesterase inhibitors, which reduce symptoms without altering the course of the illness. Additionally, the Clinical Dementia Rating Sum of Boxes (CDR-SB) was used to measure the cognitive changes mentioned above. Additionally, when comparing the anti-amyloid antibody treatment groups to the placebo group, researchers found that the absolute difference in decline in cognitive function, as measured by the difference in scores on the CDR-SB scale, did not indicate a clinically significant effect of these anti-amyloid therapies.

Donanemab treatment only resulted in a 14–8% slower decline in cognitive function, according to more objective measures of cognition like the Mini-Mental State Examination [MMSE]. Stated differently, it has been suggested that the evidence currently available indicates that the clinical benefit of these anti-amyloid medications may be minimal. These medications’ effectiveness only results in a statistically significant but clinically meaningless slower decline rather than improvements. The clinical advantages of anti-amyloid antibodies, according to some researchers, support the amyloid cascade theory. Others, however, contend that there are still a lot of unanswered questions, making this conclusion premature.

The amyloid-beta hypothesis states that Alzheimer’s disease should have progressed more slowly as a result of aducanumab’s capacity to remove plaque. Nevertheless, detractors contend that aducanumab trials demonstrated efficient amyloid plaque removal without consistently yielding therapeutic benefits. Similarly, donanemab only caused a 14–8% slower decline in cognitive function as determined by MMSE scores, despite removing roughly 85% of plaques from patients in the phase III trial. Crucially, the amyloid cascade theory served as the foundation for the FDA’s decision to approve aducanumab. The buildup of tau protein within neurons is another aspect of Alzheimer’s disease, and the degree of tau accumulation—rather than beta-amyloid—is linked to the severity of cognitive decline.

The notion that beta-amyloid plays a key role in the development and progression of Alzheimer’s disease is being leveraged by pharmaceutical interventions that aim to reduce beta-amyloid or its production. Many people have contested this theory. Additionally, the outcomes of clinical trials for these drugs show a high associated risk and little efficacy. Therefore, some researchers contend that the modest effectiveness of anti-amyloid antibodies suggests that the beta-amyloid pathway contributes to the development of Alzheimer’s disease along with other pathways, rather than suggesting that the beta-amyloid pathway plays a focal role in the disease’s development.

This theory holds that Alzheimer’s disease develops as a result of a complex network of factors, including those linked to the environment, oxidative stress, inflammation, metabolic factors, and genes unrelated to the amyloid pathway. This perspective also suggests that anti-amyloid treatments, when used in conjunction with other therapies, may play a part in the treatment of Alzheimer’s disease. On the other hand, beta-amyloid aggregation might be a sign of other compromised biological pathways or a downstream phenomenon. According to Perlmutter, it is now evident that the activation of the brain’s microglial cells is largely dependent on metabolic dysfunction upstream of amyloid plaque formation. This phenotypic shift both promotes the formation of beta-amyloid and decreases its degradation.

Furthermore, microglial activation causes synaptic degradation and jeopardizes neuron viability, two key characteristics of Alzheimer’s disease. As has now been shown in early research employing GLP-1 agonists, treatments that target brain metabolism will therefore probably offer significant benefits for Alzheimer’s disease, Perlmutter continued. It is necessary to balance the risks, expenses, and accessibility of anti-amyloid antibody therapies against the limited clinical benefits they offer. A considerable percentage of participants in the phase 3 clinical trials for lecanemab (45%) and donanemab (89%) experienced adverse effects.

For example, amyloid-related imaging abnormalities (ARIA) are alterations in the brain that frequently occur in patients receiving anti-amyloid antibody treatments. These changes, which include either small areas of bleeding from blood vessel rupture (microhemorrhage) or brain swelling (edema), are seen during routine follow-up magnetic resonance imaging (MRI) scans. In the phase 3 trials, for example, ARIA was observed in 21 percent and 36 percent of patients treated with lecanemab and donanemab, respectively. The majority of ARIA cases are asymptomatic and go away in ten weeks.

Even though ARIA symptoms are usually mild to moderate, there have been reports of serious side effects like seizures and even death. In the phase III donanemab clinical trial, for example, approximately 1 in 6 participants experienced severe adverse effects related to ARIA, while the donanemab group experienced a death rate of 0 in 35. The long-term consequences of amyloid-related imaging abnormalities, even those that are mild to moderate in severity, are unknown, in addition to worries about these grave side effects. Adverse effects like nausea, fever, rash, and dizziness are also linked to the infusion of these anti-amyloid antibodies.

Of patients treated with lecanemab and donanemab, respectively, 24 and 8 percent experienced such infusion-related reactions. Regular MRI scans and clinical follow-ups are required due to these amyloid-related imaging abnormalities and other side effects. In the phase III trials for lecanemab and donanemab, people who had at least one copy of the APOE4 gene a gene associated with an increased risk of Alzheimer’s disease—were more likely to experience brain swelling.

Additionally, these medications were less effective in people who had one or more copies of APOE4. Therefore, before beginning anti-amyloid therapy, people must undergo genetic screening. Anti-amyloid immunotherapies are also linked to an increase in the volume of the brain’s fluid-filled ventricles and a decrease in the volume of the entire brain. Reduced cognition is linked to both a decrease in the volume of the entire brain and an increase in the volume of the ventricles. It’s unclear, though, if these alterations in brain volume and cognitive function are causally related. Therefore, it is necessary to investigate the effects of these alterations in brain volume following anti-amyloid therapies. It’s interesting to note that donanemab treatment led to a lesser decrease in the volume of the hippocampus, a part of the brain essential for memory and learning.

It is unlikely that many people with Alzheimer’s disease will fit the requirements to be enrolled in lecanemab or donanemab clinical trials. These studies’ participants were younger and had fewer co-occurring illnesses. Therefore, treating a real-world population of people with Alzheimer’s and co-occurring conditions is likely to result in more side effects or decreased effectiveness. The healthcare system faces additional challenges in diagnosing and screening patients who qualify for anti-amyloid therapies, in addition to managing side effects.

The majority of people with Alzheimer’s disease are not identified until the disease is advanced, and early detection would necessitate screening a large number of people with imaging tests or measuring biomarkers in cerebrospinal fluid. Therefore, widespread availability would require a significant financial outlay for APOE4 genetic testing, early Alzheimer’s disease screening, and diagnosis, and the monitoring and treatment of ARIAs and infusion-related reactions, regardless of their severity. A third of dementia patients in the UK do not receive a diagnosis at all, and certain diagnostic tests are necessary to confirm eligibility for new treatment. To make sure that those who qualify for new treatments can get them when they work best, which seems to be in the early stages of Alzheimer’s disease, we need to invest in diagnostic infrastructure and personnel.

Common Medications for Other Conditions in People with Lupus

Common Medications for Other Conditions in People with Lupus

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Lupus is an autoimmune disease that causes the body’s immune system to attack healthy tissue. This inflammation can affect many parts of the body, including the skin, joints, heart, lungs, and kidneys. Lupus can be a life-threatening disease, but with the right care and treatments, individuals can live long, happy, and healthy lives. Most often, serious issues come from heart disease, kidney failure, or infections.

Doctors often use The following medications to treat other conditions that commonly occur in people with lupus. Although these drugs do not specifically address the underlying cause of lupus, they are used to treat other conditions that may be compounded or indirectly caused by lupus. Since lupus affects people differently, treatment courses are highly individualized. Please remember to take your medications exactly as directed by your physician and notify him/her of any concerns upon your next visit. Never take any medications until they are approved by your doctor – in other words, do not self-medicate!

Aspirin Low doses of aspirin are often recommended for lupus patients who have antiphospholipid antibodies and may reduce the risk of heart attack and stroke.

Antidepressants Anti-depressant medications are used to treat depression and anxiety, present in almost half of all people who have lupus. You must speak with your doctor if you feel you are experiencing clinical depression because many people who are physically ill respond well to anti-depressant medications. In addition, your doctor may treat your depression in different ways depending on the cause.

Antiplatelet Medications (Platelet Antagonists) Some lupus patients are at an increased risk for blood clots due to the prevalence of a condition known as antiphospholipid antibody syndrome (APS). Platelet antagonists help prevent these clots and in doing so, also help to prevent heart attack, stroke, and other complications.

Osteoporosis Medications (Bisphosphonates) Bisphosphonates are medications used to treat and prevent osteoporosis. People with lupus are at an increased risk for this condition due to the inflammation they experience with the disease. Certain medications taken by lupus patients also increase the risk of osteoporosis, especially corticosteroids such as prednisone.

Blood Pressure Medications (Anti-hypertensives) 25-30% of people with lupus experience hypertension (high blood pressure). The most common causes of high blood pressure in people with lupus are kidney disease and long-term steroid use. Other medications, such as cyclosporine (Neoral, Sandimmune, Gengraf) can also cause elevations in blood pressure. It is important to remember that while diet and exercise are essential for optimal cardiovascular health, these elements alone may be insufficient in controlling your blood pressure; in this case, your doctor will prescribe a medication.

Anticoagulants Anticoagulants (“blood thinners”) are medications that decrease the ability of the blood to clot and are used in lupus patients with antiphospholipid antibodies to reduce the risk of deep venous thrombosis (DVT), stroke, and heart attack.

Gastrointestinal Medications Many people with lupus suffer from gastrointestinal problems, especially heartburn caused by gastroesophageal reflux disease (GERD). Peptic ulcers can also occur, often due to certain medications used in lupus treatment, including NSAIDs and steroids. Certain medications may be prescribed or recommended by your doctor to control these conditions.

Cholesterol Medications (Statins) Statins are medications that lower the level of cholesterol in your blood by reducing the production of cholesterol in the liver. People with high levels of cholesterol in their blood face an increased risk of cardiovascular disease, which can lead to chest pain, heart attack, stroke, and peripheral vascular disease. Studies have shown that people with lupus are more likely to have clogged arteries that can lead to heart attack and stroke at a younger age. This increased risk is caused by elevated cholesterol levels, high blood pressure, diabetes, and inflammation, conditions that occur often in people with lupus. Certain medications, such as corticosteroids (e.g., prednisone) can provoke or compound these symptoms. For this reason, the cholesterol-lowering properties of statins are commonly called upon for lupus patients.

Thyroid Medications Autoimmune thyroid disease is common in lupus. It is believed that about 6% of people with lupus have hypothyroidism (underactive thyroid) and about 2% have hyperthyroidism (overactive thyroid). A thyroid gland that is functioning improperly can affect the function of organs such as the brain, heart, kidneys, liver, and skin. Hypothyroidism can cause weight gain, fatigue, depression, moodiness, and dry hair and skin. Hyperthyroidism can cause weight loss, heart palpitations, tremors, and heat intolerance, and eventually lead to osteoporosis. Treatment for both underactive and overactive thyroid involves getting your body’s metabolism back to normal.

Fibromyalgia Medications Fibromyalgia is a chronic disorder characterized by widespread pain and tenderness, general fatigue, and non-restful sleep. Many people with lupus have fibromyalgia; in fact, much of the pain that people with lupus feel is due to this condition. Three medications are used to reduce some of the physical and emotional symptoms of fibromyalgia.

Restasis (Dry Eye Medication) Restasis is an immunosuppressive medication used to treat eye symptoms related to Sjogren’s syndrome, a chronic autoimmune disorder in which the glands that produce tears and saliva do not function correctly.

Can antibiotics, vaccines, and antivirals help lower dementia risk?

Can antibiotics, vaccines, and antivirals help lower dementia risk?

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A recent systematic review found that anti-inflammatory medications such as ibuprofen, as well as antibiotics, antiviral drugs, and vaccines, were linked to a lower risk of dementia. Up to 70% of those with dementia have Alzheimer’s disease, and the condition affects over 55 million people globally at an estimated cost of over $1 trillion. Before drawing any conclusions about repurposing current medications for the treatment of dementia, experts point out that more research is necessary due to the complexity of dementia in various individuals. In a recent systematic review, researchers from the Universities of Cambridge and Exeter in the United Kingdom found that anti-inflammatory drugs like ibuprofen, antibiotics, antiviral drugs, and vaccines, were linked to a lower risk of dementia.

Published in Alzheimer’s and Dementia: Translational Research and Clinical Interventions, the review examined data from 14 studies that included 1 million dementia cases and over 130 million people. Antimicrobials, vaccinations, and anti-inflammatory drugs (NSAIDs) were linked to a lower risk of dementia. In contrast, vitamins, supplements, antipsychotics, and diabetes medications were somewhat linked to a higher risk, according to the researchers’ analysis of medical and administrative records as well as large clinical datasets. Evidence regarding antidepressants and certain blood pressure medications was inconclusive. The authors observed that overall, there was a lack of consistency across studies in identifying specific medications that alter the risk of Alzheimer’s disease or all-cause dementia and that some limitations and false positives may have impacted findings.

It’s crucial to keep in mind that dementia, which merely characterizes a collection of progressive symptoms, can result from a variety of pathological conditions. Furthermore, according to Dr. Dot MacSweeney, Alzheimer’s disease, the most prevalent cause of dementia as we age, is not a single illness. It is complicated and has a lot of aberrant biomarkers. However, it is widely acknowledged that the majority of conditions that eventually lead to dementia do, in large part, have a neuroinflammatory origin, just like many other diseases. Large-scale, longitudinal, randomized controlled trials (RCTs) are required to prove a causal relationship between dementia risk and particular medications, according to MacSweeney.

Confounding variables such as age, gender, and comorbidities should be controlled for, and lifestyle and genetic data should be included to find effects specific to subgroups, and biomarkers (e.g. G. levels of tau or amyloid) to gauge how drugs affect the body. She also suggested that they concentrate on long-term results to verify a lower incidence of dementia. Given how common these drugs are already worldwide, Clifford Segil, DO, a neurologist at Providence Saint John’s Health Center in Santa Monica, CA, who was not involved in the review, expressed some skepticism to MNT regarding its findings: Studies frequently surface expressing concern for prescription and over-the-counter medications causing dementia that are not clinically observed. For instance, studies have shown that taking allergy drugs like Benadryl/diphenhydramine increases the risk of dementia; however, in my clinical neurology practice, I have never observed this to be the case.

Although sleep aids are frequently linked to deteriorating memory loss in the elderly, I think the advantages of getting a good night’s sleep exceed any possible hazards. According to him, there are too many cooks in the kitchen these days, and if dementia is a concern, you should speak with a specialist like me who makes it their career to diagnose and treat dementia patients. The best strategy to lower one’s risk of dementia, according to Segil, is to alter one’s lifestyle, since middle-aged habits shape one’s later years. He informed us that some tests related to the genetics of dementia do not ensure the onset of dementia and that false-positive test results are common. I would suggest leading a healthy lifestyle to prevent the need for a doctor’s prescription medication. If medication is required, I would suggest consulting a board-certified neurologist for guidance on which medications to take as you age.

Over 55 million people worldwide suffer from dementia, which is estimated to cost more than $1 trillion. Up to 70% of those affected have Alzheimer’s disease, which is typified by the accumulation of two proteins, tau and amyloid. Adults with early symptomatic Alzheimer’s disease, including those with mild cognitive impairment (MCI) and mild dementia with confirmed amyloid plaques, can now receive treatment with the monoclonal antibody donanemab, which was approved by the Food and Drug Administration (FDA) in July 2024. In 2024, the FDA granted accelerated approval to two additional monoclonal antibodies, lecanemab and aducanumab, after encouraging trial outcomes.

Alzheimer’s disease can be managed with the help of current treatments, but the disease’s progression is unaffected. In a global phase 3 clinical study, donanemab reduced cognitive decline in individuals with low/medium tau levels by 35% when compared to a placebo. There is broad agreement that multiple approaches are likely required to provide maximally effective treatment and the authors of the new review point out that these treatments target a single pathway in a complex condition and carry a significant risk of severe side effects. Although they emphasize that repurposing current medications for potential dementia treatment is a global priority, experts argue that, given the complexity of dementia and Alzheimer’s disease, more research is necessary to determine the specific effects of such medications.

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Common thyroid drug levothyroxine linked to bone mass loss

Common thyroid drug levothyroxine linked to bone mass loss

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In the United States, levothyroxine is a commonly prescribed medication, especially for elderly patients, because aging can be linked to decreased thyroid function. However, because of the potential for side effects, there are still concerns about how it should be prescribed. The use of levothyroxine in individuals with normal hormone ranges may eventually result in decreased bone mass and density in older adults, according to a recent abstract presented at the annual meeting of the Radiological Society of North America.

A small cohort study found that older adults with normal thyroid levels who take levothyroxine, a medication used to treat hypothyroidism, may have decreased bone mass and density. Over a 6-year follow-up period, researchers from Johns Hopkins University School of Medicine in Baltimore, Maryland, demonstrated that adults over 65 who received levothyroxine experienced a decrease in both total body bone mass and density. On November 25, 2024, they presented the findings at the Radiological Society of North America’s Annual Meeting. A peer-reviewed publication has not yet published these findings.

The findings came from a small study with 81 participants taking levothyroxine and having normal thyrotropin levels, which are used to show thyroid function. Levothyroxine is one of the most often prescribed medications in the US, especially for older adults, according to the study’s authors. Not involved in this study was Sean Ormond, MD, of Atlas Pain Specialists, who holds dual board certifications in anesthesiology and interventional pain management.

Since thyroid issues are more likely to occur as we age, levothyroxine is a very common medication. Older adults are more likely to have hypothyroidism, a condition in which the thyroid slows down and produces insufficient hormones to maintain bodily functions. When thyroid function is compromised, people frequently experience fatigue, weight gain, cold sensitivity, or even depression. Because these symptoms can make life difficult, doctors frequently recommend levothyroxine to help people feel better by restoring hormone levels. In situations where untreated thyroid problems could endanger the heart or other organs, it’s particularly crucial, he added.

Why is the thyroid gland important?
The thyroid, which is located in the neck, is in charge of making hormones that affect metabolism, children’s growth and development, temperature regulation, and the operation of the heart and digestive system. The pituitary gland, another hormone-producing organ in the head, produces thyroid stimulating hormone (TSH). T3 and T4 are then produced by the thyroid as a result, and they are involved in the previously mentioned processes. Fatigue, weight gain, cold intolerance, dry, flaky skin, hair loss, and difficulty concentrating are all signs of low thyroid hormone levels. On the other hand, weight loss, muscle weakness, elevated blood pressure and heart rate, and a tense, irritable mood are all linked to hyperthyroidism, a condition in which thyroid levels are excessively high.

Levothyroxine: Can it raise osteoporosis risk?
The recent study’s team had previously demonstrated that levothyroxine use can result in a number of undesirable side effects, especially in those who use it excessively. In a previous study, the authors demonstrated that levothyroxine use in individuals with elevated thyroid hormone levels negatively impacted older adults’ leg mass; the findings were published in Frontiers in Aging. Both their most recent research and that study included an analysis of the Baltimore Longitudinal Study of Aging.

In their most recent study, the authors examined 32 males and 49 females who were 65 years of age or older at the beginning of the study, with a mean age of 73, in order to examine the effects of levothyroxine use on a comparable cohort of adults. To establish a quasi-control group, they matched these participants to five other cohort members based on biological sex, body mass index (BMI), age, race, history of alcohol use, history of smoking, other treatments they were undergoing, and TSH levels.

This cohort was analyzed after two visits during which Dual-Energy X-ray Absorptiometry was used to measure their bone mass and density. Over the course of the study, researchers found that people taking levothyroxine and having normal thyroid hormone levels had less bone mass and density. The findings imply that even when levothyroxine is taken at the recommended dosage, bone loss may occur in older adults, raising the possibility of osteoporosis.

Is levothyroxine overprescribed?
There have long been concerns about the overprescription of levothyroxine for elderly patients; a 2023 letter in Clinical Chemistry suggested that many people had been overdiagnosed with hypothyroidism. It referenced studies demonstrating that TSH levels fluctuate greatly throughout the year, reaching their highest in the winter and falling in the summer. By comparing the ratio of free thyroxine (T4) levels to those of people with elevated TSH levels, hypothyroidism can be diagnosed.

Hypothyroidism is the diagnosis given to people with low T4 and high TSH. Subclinical hypothyroidism is diagnosed in people with slightly elevated TSH and slightly low T4, and levothyroxine may be used as a treatment. The letter made the argument that many people were being prescribed medications that might not be helpful to them and might even cause bad, preventable side effects because normal seasonal variation in TSH levels was not taken into consideration. For patients who have unpleasant side effects, deprescribing is an option, according to Sue Clenton, MD, a consultant clinical oncologist at Sheffield, UK’s Weston Park Cancer Centre.

Levothyroxine is prescribed for symptoms such as fatigue, weight gain, cognitive slowing, and elevated TSH levels, which indicate an underactive thyroid. Deprescribing, however, might be taken into consideration if a patient’s thyroid function tests return to normal or if they experience adverse effects like anxiety, rapid heartbeat, or bone loss. The significance of careful monitoring and customized treatment plans, especially in older adults, she said, was underscored by the study.

References:
https://www.medicalnewstoday.com/articles/common-thyroid-drug-levothyroxine-linked-to-bone-mass-loss
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Lenacapavir injection lowers HIV risk by 96%

Lenacapavir injection lowers HIV risk by 96%

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Infection with the human immunodeficiency virus (HIV) is still a major public health concern. The best pre-exposure prophylactic options and other HIV prevention strategies are of interest to experts. According to one study, giving at-risk people an injection of lenacapavir every six months could significantly lower their risk of contracting HIV. The immune system is impacted by the human immunodeficiency virus, or HIV. To stop HIV from developing into acquired immunodeficiency syndrome (AIDS), people with the virus can take medication.

But there is currently no treatment for HIV. Prevention measures are therefore crucial to HIV-related research. To prevent HIV, pre-exposure prophylaxis, or PrEP, entails taking medication. Lenacapavir, an antiretroviral medication commonly used to treat HIV infections, was assessed as a PrEP strategy in a recent study that was published in the New England Journal of Medicine. Lenacapavir injections were more than 96% successful in preventing HIV infection. Additionally, researchers discovered that this option was more effective than the daily dose of emtricitabinetenofovir disoproxil fumarate (Truvada), which is the PrEP option. Lenacapavir use has the potential to significantly increase PrEP options for at-risk groups.

Lenacapavir for HIV prevention: Does it work?
This study was a multicenter, active-controlled, phase 3 double-blind randomized trial. The effectiveness of lenacapavir subcutaneous injections in preventing HIV infection was being investigated by the researchers. The study’s sample was broad and included a variety of groups that are frequently affected by HIV infection. Participants who have not frequently participated in HIV clinical trials were specifically targeted by the researchers. Participants were people who had receptive anal intercourse without condoms with partners who were assigned male at birth. Participants who identified as transgender and gender nonbinary were included in the study, along with cisgender men.

All possible participants were tested for HIV even though their status was initially unknown. HIV-negative individuals were included in PrEP treatment. Researchers randomly divided the 3,265 trial participants into two groups. One group was given emtricitabine-tenofovir disoproxil fumarate (F/TDF), marketed under the brand name Truvada, orally every day, along with a placebo injection every six months.

The other group was given a daily oral placebo and an injection of lenacapavir every six months. Two initial oral loading doses of lenacapavir were also given to the lenacapavir group. Regular HIV infection testing was performed on the participants. In addition to this comparison of medications, researchers examined the background incidence of HIV infection by examining broader data from the population that was first screened.

According to the study, lenacapavir injections were the best way to prevent HIV. Compared to nine participants in the F/TDF group, only two participants in the group of more than 2,100 receiving lenacapavir developed HIV. Lenacapavir’s results were also significantly better than the background incidence estimate. In general, lenacapavir adherence was significantly higher than F/TDF adherence. Researchers point out that there was proof that individuals in the F/TDF group who contracted HIV either stopped taking F/TDF more than a week and a half prior to being diagnosed with HIV, or had poor or no adherence.

Among the 2,179 trial participants who received twice-yearly injections of lenacapavir, there were only two incident cases of HIV infection. This translates to a 96 percent risk reduction in comparison to the estimated background HIV incidence rate among the study population, meaning that 99.9 percent of trial participants receiving lenacapavir for pre-exposure prophylaxis (PrEP) did not contract HIV. Furthermore, lenacapavir taken twice a year was 89% more effective than Truvada taken once daily.

Are there any concerns about the study findings?
There are certain limiting factors to take into account in this research. The Food and Drug Administration (FDA) halted lenacapavir injections for approximately five months during the trial. As a result, during this period, some participants were unable to receive their initially prescribed regimen. Initially, participants who were scheduled for injections during this period were given either emtricitabinetenofovir alafenamide fumarate (F/TAF) or F/TDF instead.

The FDA lifted the injection hold after a little over a month, allowing participants in the lenacapavir group to receive weekly oral lenacapavir. The results of the study might have been impacted by this. Second, the sample was impacted by the inclusion criteria that the researchers used. The results might have been impacted by the small number of ineligible participants who continued to go through randomization screening and randomization.

Furthermore, not all participants who qualified for randomization were randomized. It should also be noted that adherence to injections was higher than adherence to daily oral medication. Researchers only used a cross-sectional incidence cohort to estimate the background incidence of HIV infection. Regarding this data point, researchers did not conduct long-term follow-up. They also admit that their methodology might have resulted in an underestimation of the prevalence of HIV infection.

Overall, the study found no safety issues with the use of lenacapavir. Researchers do admit, though, that the two lenacapavir-using group members who got HIV most likely developed some sort of resistance as a result of using lenacapavir alone. Future studies may need to address this.

Two-yearly lenacapavir for PrEP is being studied in other populations and regions in non-pivotal PURPOSE trials. These investigations are in progress. Furthermore, open-label lenacapavir is being or has been offered to participants in the PURPOSE 1 and PURPOSE 2 trials, which are investigating twice-yearly lenacapavir for PrEP in cisgender women. We will also keep an eye on those who receive lenacapavir injections. Gilead Sciences, the company that makes lenacapavir, provided funding for the current study.

Twice-yearly lenacapavir could act like an HIV vaccine
This study offers a practical way to shield at-risk people from HIV infection. Because lenacapavir is currently only approved for use by specific individuals with multidrug-resistant HIV, researchers point out that more approval will be needed before it can be used more widely.

Its use might also be hampered by other factors. The main concern with long-acting injectable PrEP is access and affordability, according to Charles Flexner, MD, a professor of clinical pharmacology and infectious disease at John Hopkins School of Medicine and principal investigator of the Long-Acting and Extended-Release Antiretroviral Research Resource Program (LEAP). Although he was not involved in the current study, Gilead has funded his research.

According to recent estimates, it may take years for generic or affordable versions of these medications to become available in low- and middle-income countries, where the majority of new HIV infections worldwide are occurring, even though they are probably available in high-income countries, he said. But according to Flexner, lenacapavir, which is administered twice a year, is becoming as effective as a vaccine at preventing an infection for which there may never be a suitable vaccine.

Lenacapavir administered twice a year is a revolutionary option for HIV prevention among cisgender men and transgender communities, according to the findings of the PURPOSE 2 study. With a 96% decrease in HIV incidence when compared to the background rate, lenacapavir is not only efficient but also novel and covert, assisting in removing major obstacles for marginalized groups that frequently experience stigma and difficulties following daily oral regimens. This emphasizes how crucial it is to include lenacapavir in our HIV prevention plans, especially as the U.S. K. and the global community strives to meet the 2030 UNAIDS targets.

References:
https://www.medicalnewstoday.com/articles/lenacapavir-injection-lowers-hiv-risk-by-96#Twice-yearly-lenacapavir-could-act-like-an-HIV-vaccine
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People with kidney disease, diabetes may develop heart disease 28 years earlier

People with kidney disease, diabetes may develop heart disease 28 years earlier

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According to a recent study, individuals who have type 2 diabetes, chronic kidney disease, or both may be at higher risk for cardiovascular disease (CVD) 8–28 years earlier than those who do not have these conditions. Type 2 diabetes and chronic kidney disease are parts of the cardiovascular-kidney-metabolic (CKM) syndrome, which has a major effect on the risk of CVD.

These findings could aid in the early diagnosis of CVD in patients and aid in disease prevention. Chronic kidney disease, type 2 diabetes, or both may increase the risk of cardiovascular disease (CVD) 8 to 28 years earlier than people without these conditions, according to a recent study presented at the American Heart Association’s Scientific Sessions 2024.

To ascertain the relationship between age and risk factors linked to CKM syndrome, researchers employed simulated patient profiles. These findings could guide early detection and intervention strategies in CVD prevention, even though they haven’t been published in a peer-reviewed journal yet. Type 2 diabetes and chronic kidney disease are two of the four components of cardiovascular-kidney-metabolic (CKM) syndrome, which increase this risk.

According to current CVD prevention guidelines, if a person has a 7 5% chance of having a heart attack or stroke within the next ten years, their risk is elevated. CKM syndrome is defined by the American Heart Association as the relationship among metabolic diseases such as type 2 diabetes and obesity, kidney disease, and cardiovascular disease.

Developing cardiovascular risk profiles
To represent men and women aged 30 to 79 with and without type 2 diabetes and/or chronic kidney disease, researchers created risk profiles. They estimated the age at which each profile would probably reach elevated CVD risk using the Predicting Risk of Cardiovascular Disease EVENTs (PREVENT) calculator from the American Heart Association. Data from the 2011–2020 National Health and Nutrition Examination Survey was used to create the risk profiles.

An estimated glomerular filtration rate (eGFR) of 44.5, which denotes stage 3 kidney disease, was used to categorize chronic kidney disease. A “yes” answer to the PREVENT calculator question, Any history of diabetes, indicated type 2 diabetes. According to the American Heart Association, almost half of all U.S One in three adults has at least three risk factors linked to CKM syndrome, and all adults suffer from cardiovascular disease (CVD) in some capacity. Early identification of high-risk individuals can enhance primary prevention initiatives and reduce the likelihood of early death from CVD.

According to our research, a person’s age and other medical conditions have a substantial impact on their risk of cardiovascular disease. In particular, people with diabetes or kidney disease have a significantly increased risk of heart disease, even in their 30s, which can now be determined using the PREVENT equations. According to Krishnan, the Pooled Cohort Equations, which began at age 40 and excluded kidney function, could not previously be used to evaluate this.

A better understanding of cardiovascular disease risk, which includes heart attacks, heart failures, and strokes, should be made possible by the study, she continued. Even in the absence of a formal diagnosis, people with borderline high blood pressure, glucose, or kidney function may be at risk for unidentified health issues.

For people with CKM (Cardiovascular-Kidney-Metabolic) disorders like diabetes or kidney disease, these risks manifest earlier. For instance, elevated cardiovascular risk can manifest decades earlier in individuals with CKM, particularly when combined with other conditions, whereas it begins around age 68 for women and 63 for men without CKM.

References:
https://www.medicalnewstoday.com/articles/chronic-kidney-disease-type-2-diabetes-may-develop-heart-disease-28-years-earlier#Developing-cardiovascular-risk-profiles


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In Conversation: Investigating the power of music for dementia

In Conversation: Investigating the power of music for dementia

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There is mounting evidence that music can improve mood, calm people down, and help them regain some aspects of their memory. But why does music have such a powerful effect on our brains, and does this effect last? You may have seen a video of an elderly person suffering from dementia swaying to a piece of music, recalling a plethora of memories, or even playing the notes to a song they used to know on the violin or piano, even though they cannot recall their family members.

Many people are perplexed by this phenomenon regarding dementia, a neurological disorder. One of the many questions we sought to address in our April podcast, In Conversation: Investigating the Power of Music for Dementia, was how someone could forget the names of their own children while remembering something as intricate as a classical piece of music. Beatie Wolfe, a singer, songwriter, and representative of the nonprofit organization Music for Dementia, and Dr. Kelly Jakubowski, an assistant professor of music psychology at Durham University, joined the discussion this month. This month’s episode is available to listen to below or on your favorite streaming service.

Whether instrumental or lyrical, music is a creative fusion of harmony, rhythm, and emotional expression. Its numerous health benefits have also been confirmed by numerous studies. For instance, a 2013 study discovered that music can help the nervous system recover more quickly and have a calming effect before stressful situations. According to a different study conducted that same year, music therapy helped hospitalized kids feel less anxious and in pain. In addition to its physiological advantages, studies have shown that music has a positive effect on cognitive function.

According to a recent study, individuals between the ages of 62 and 78 may experience a slower decline in cognitive function if they actively practice and listen to music. According to the researchers, playing music enhances the gray matter in certain parts of the brain, increasing neuroplasticity the brain’s capacity to rewire itself which is essential for memory formation and learning. Regarding actively practicing music, a 2023 study also revealed that sustained music training might help maintain the brain’s youth and offer possible functional advantages. According to these findings, music has the potential to be a very effective treatment for dementia, a condition marked by a variety of symptoms such as memory loss and issues with thinking, speaking, and solving problems.

Another way that music can support cognitive health is by serving as a communication tool. Loneliness and social isolation have been linked to accelerated dementia progression in numerous studies. Beatie stated, I think music is the most potent instant connector, almost of any experience and of the arts.. According to the singer/songwriter, the arts in general not just music can be medicinally potent, transcending its use as a kind of amusement. The ubiquitous nature of music does not necessitate one to get up and dance or draw. A person can simply take in the words, the frequencies, and the entire soundscape. Without a doubt, music has always been a strong tool that I use to feel good. You have a great deal of respect and admiration for music after seeing the reactions I’ve witnessed to it, she said.

But just as much, if not more, of an influence on our health, comes from the absence of silence than from sound and music. Silence can be therapeutic and calming, lowering blood pressure and brain wave frequency, according to a 2020 study. Indeed, studies have demonstrated the detrimental effects of excessive noise and loud noises on cognitive function. Chronic exposure to loud noises, like heavy traffic, maybe a particular risk factor for dementia, according to a 2022 study. Beatie, our guest, talked about how she was affected by total silence by sharing her experience recording her Raw Space album in the Bell Labs anechoic chamber, which is the quietest room in the world.

I think it was one of the most profound experiences I’ve ever had, and I keep thinking about it. Even now, it seems to have practically gained more relevance. As the world has become more noisy, both sonically and informationally, we are being inundated with notifications and social media, among other things that are bombarding us and causing us to feel frazzled, she said. You experience silence; it’s almost as if your nervous system relaxes and you hear sound in its most unadulterated form, devoid of echo, reverb, or enhancements. Do you also realize that we use technology far too much these days to fix all of these issues that are fundamentally what makes us human?

Beatie ended up spending quite a few hours in that exact chamber, seemingly enjoying the experience far more than most people do. Because you could hear the blood pounding through your veins and the engineers usually had to take breaks due to the intensity, I was told that I would probably be able to stay in there for fifteen minutes. She claimed that I ultimately spent at least 100 hours.

I spent several hours in there for the first time and found it to be very soothing; perhaps I’m an exception. However, I reacted differently to people’s freakouts, which I believe are also related to being truly alone. You are there very much with yourself, there are no distractions, and there is nothing to pull you out of that internal space, she added, adding, I do think there is an element of it in the chamber. Regarding the issue of dementia patients remembering song lyrics but not their own children’s names, Dr. Dot Guite highlighted the power of repetition and the way that music can simultaneously activate multiple brain networks and regions.

We’ve discussed the universality of music in the brain, but even though a child’s name is repeated throughout their life, the song may only be played once a month or once a year. She inquired, How can we explain that?. Dr. According to Jakubowski, procedural memory is linked to the capacity to fill in the lyrics of songs. When people may no longer have this type of semantic memory for names and places, they still have this type of memory for the motor sequence of singing along lyrics, likely because they have sung along to that song many times before, or at least have sung along to that piece of music in their minds many times before, she explained. Procedural memories are similar to remembering motor sequences, such as being able to ride a bike.

She added that some people with dementia may be able to play an old song on an instrument or remember lyrics because the brain may spare specific areas of this kind of memory. According to her, if a person has played the piano before, they can frequently continue to play those well-known pieces even after they have developed a serious illness. Beatie started a study in 2014 called The Power of Music in a collection of assisted living facilities in the United States. The UK. The Priory Group is in charge.

The video and pictures of that experience make it clear how the dementia patients in those assisted living facilities begin to clap their hands, tap their feet, and sing along to some of them with their eyes shining. She explained to us how it all began when she performed original English-language songs in a Portuguese nursing home. I had intended to perform for my father-in-law alone, but instead, I performed for the entire ward, which consisted of about 100 Portuguese individuals suffering from dementia and Alzheimer’s. Except for this relative, none of them could speak English. Additionally, I was playing brand-new English-language songs that they had never heard before. She added I was witnessing people clapping, waking up, and singing along as much as they could.

Beatie was inspired by this to test the theory that music, whether or not you were already familiar with it, had a powerful effect. In his book Musicophilia, neurologist Oliver Sacks made the prediction that prior knowledge of music was not necessary for its influence, which served as her inspiration. She performed original songs for residents of care facilities in the United States. K. The impact of one song in particular on the audience was noteworthy. Dr. Jakubowski shared her thoughts on why she believes the song Wish was especially popular with the people Beatie visited at the assisted living facility. Beatie, in particular, tends to use brief sentences. The fact that you can practically guess the next word or rhyme is a great way to get people to try singing along. A lot of things are repeated. As a result, you begin to anticipate, and it offers this lovely framework for others to follow along, she said.

Dr. Jakubowski stated that the very obvious beat is an additional contributing element in addition to rhyme and alliteration. The music’s tempo is actually quite similar to what is known as the human-preferred tempo. According to her, if I asked someone to tap a beat without listening to anything, they would typically do so at a pace of about 120 beats per minute, which is comparable to the tempo of that song. This is known as spontaneous motor tempo. We feel at ease clapping at that pace, so it’s a very simple piece to follow along with. I believe that encourages participation as well, she continued. Dr. Jakubowski added that the music’s structure makes it simple to follow. If you don’t have complex lyrics and you have this ‘oh, oh,’ every now and then, that’s pretty easy to understand, she said.

In addition to studying MEAMS (music-evoked autobiographical memories) in general, Dr. Dot Jakubowski thinks there are many implications for its relationship to dementia. She began by discussing the cascade effect of music on memory recall. A memory can be triggered by music or any other cue, which can then trigger related memories. According to her, the theory is that if music can arouse a memory associated with it, it may also aid in reviving other memories from that era or memories that are connected.

Dr. Jakubowski contrasted music with other forms of cues for autobiographical memories in one of her pieces. Across several studies, we consistently discovered that music generally evokes more positive memories from our lives than other cues. Therefore, I believe that music appears to be a particularly powerful cue for recalling happy memories from our past, which is one obvious potential therapeutic benefit. According to her, this actually appears to be further enhanced in older adults. Dr. To determine whether these findings apply to individuals with dementia, particularly those who are in the later stages of the illness, Jakubowski hopes that this will stimulate further research in this field. Dr. Jakubowski also discussed how music can help restore a sense of identity that frequently wanes with memory loss in individuals with dementia.

Beyond that, I believe the significance of autobiographical memories lies in the fact that recalling a small portion of our lives really strengthens our sense of personhood and identity, reminding us of our origins and identity. According to her, that’s crucial for those who experience some form of memory loss because it keeps them from connecting with their former selves and makes them feel trapped in the present, which can harm their mental health.

Family members and carers are also impacted by this sense of past, personhood, and reconnecting. Therefore, it’s crucial to catch a glimpse of the person you once knew. This supports family members and caregivers in realizing that this person is still a person with a rich past. Dr. While the immediate health benefits of music are obvious, Jakubowski pointed out that regular exposure is necessary to discuss long-term benefits. You can’t expect to benefit from listening to music for years on end just because you heard one song three years ago. According to her, listening to music for a longer period has more advantages than just hearing it once and then never hearing it again. People can interact with music in a variety of ways, she added.

For those with dementia, even regular, recorded music listening has long-lasting benefits, such as lowering agitation, lowering apathy, elevating mood, occasionally strengthening a sense of identity, and more. According to her, there are various ways to interact with music. Dr. Jakubowski emphasized that there might be drawbacks to using music therapy to treat dementia. Regardless of whether a person has dementia or not, there are possible drawbacks to music because, on occasion, it may be connected to a traumatic memory from their past, she said.

It might remind someone of a funeral or the death of a family member, even if it isn’t a traumatic memory. Therefore, she added, we must exercise caution when choosing music and consider these factors. She also discussed personal taste and the wide variety of musical styles available. Unwanted consequences could result from this, particularly for those suffering from dementia. According to her, choosing the music for sessions requires careful consideration on the part of music therapists.

Music is less likely to be useful for controlling agitation and mood if someone despises it. This relates to our discussion at the outset, which was that noises in our surroundings can occasionally be harmful and bothersome. According to her, we don’t want to force people to listen to music they don’t particularly enjoy or that they don’t relate to because that could cause them to react negatively.

Regardless of preferences, these experiences demonstrate the positive effects of music on health and well-being. Further research is necessary to determine whether it can truly slow the progression of dementia, but before I go, I would like to ask our readers this: What is the one song that always makes you feel something, whether it’s a reminder of a heartbreaking heartbreak or the happiest day of your life?

References:
https://www.medicalnewstoday.com/articles/in-conversation-investigating-the-power-of-music-for-dementia#Can-music-be-detrimental-to-people