Think about that fleeting moment when you get up after sitting or lying down—your head spins, your heart pounds, maybe you feel lightheaded or nauseated. If this scene has become all too familiar, you might be dealing with postural orthostatic tachycardia syndrome—POTS. It’s rare, but for the 1–3 million people in the U.S. who have it, it’s daily life. Now, a heart failure drug is showing real promise in taming the symptoms.

Ivabradine isn’t new—it’s been used for years to manage chronic heart failure, slowing the heart without dropping blood pressure. But a new pilot study, published in the Journal of Cardiovascular Pharmacology, suggests this drug might be a breakthrough for POTS patients. Researchers from UVA Health and Virginia Commonwealth University treated 10 young adults (average age 28, most of them women) with the drug. Normally, when these patients stood, their heart rates surged by around 40 beats per minute. After ivabradine? The spike shrank to only 15 bpm. And symptoms like faintness dropped by nearly 70%, chest pain by 66%—the difference wasn’t just physiological, it was life-changing.

Dr. Antonio Abbate from UVA Health called the findings compelling: cutting heart rate alone—without affecting blood pressure—appeared to break the chain of symptoms. “The inappropriate increase in heart rate is exactly why patients feel sick,” he said.

UVA Health Newsroom

What Is POTS?

Postural orthostatic tachycardia syndrome may sound technical, but its components describe the experience: "postural" (related to posture), "orthostatic" (standing upright), "tachycardia" (a fast heart rate), and "syndrome" (a bundle of symptoms). When someone with POTS stands, their autonomic system fails to constrict blood vessels effectively. The result? Blood tanks into the legs, the heart overcompensates, and you get hit by symptoms: dizziness, pounding heart, fatigue, brain fog, chest discomfort, sweating, nausea—anything but ordinary.

This isn’t a heart-muscle issue or a brain problem: it’s more like a software glitch in how your body regulates itself. It often affects young women between 15 and 50 and can stem from triggers like infections, trauma, pregnancy, or autoimmune diseases.

The recent UVA pilot study isn’t standalone. Earlier research supports the same direction. A 2017 retrospective study of 49 patients—almost all women—found 88% saw palpitations improve and 76% felt less lightheaded, with heart rates dipping and no significant change in blood pressure.

Then a 2021 randomized, placebo-controlled crossover trial—including 22 adults with hyperadrenergic POTS—took it further. The results showed substantial heart rate drops, improved physical and social quality of life, and even reduced norepinephrine levels (the stress hormone that tends to over-react upon standing). None of the participants developed dangerously low blood pressure.

And even earlier studies, including student-case reports and case series, all support the conclusion: ivabradine reduces heart rate without bringing blood pressure down—and that matters because traditional beta blockers can drop both, making some patients feel worse.

How Ivabradine Interrupts the Vicious Vagus Loop?

Here’s what researchers suspect is happening behind the scenes: when someone with POTS stands, the body overreacts with a surge of norepinephrine—our classic fight-or-flight hormone. The heart races, the brain kicks into panic mode, symptoms amplify, and the loop perpetuates itself. Ivabradine, by slowing the heart without altering blood pressure, effectively breaks that cycle at the source. Patients stop spinning, both literally and metaphorically.

What You Should Know POTS?

It's worth noting that these are still early results. The studies are relatively small, but statistically compelling. There's enough here, though, to encourage more formal trials—and for doctors and patients to take notice.

If POTS symptoms sound familiar—if you get faint when you stand, your heart races, and doctors struggle to pinpoint the cause—ivabradine may be a conversation worth having. It’s not a universal cure, but it’s different from other treatments. Rather than forcing blood vessels to tighten or increasing blood volume, it focuses squarely on the heart rate itself.

POTS has always been a misunderstood syndrome—a tricky physiological dance that leaves patients frustrated and clinicians unsure. But treating the pulse directly, instead of chasing blood pressure or fluid levels, looks like a game changer. Ivabradine isn’t a cure-all, but it's poised to offer relief where little existed before.

For anyone sick of dizzy spells, pounding hearts, or unexplained fatigue whenever they stand, it’s time to explore if this one medication could be the difference between feeling trapped and regaining control.

Multiple sclerosis (MS) tends to be viewed as an abrupt disease—vision loss, numbness, tiredness, and other neurological interruptions. But based on a revolutionary new study at the University of British Columbia (UBC), the body could begin to send warning signals as much as 15 years before a diagnosis is officially made.

This study, which appeared in JAMA Network Open, contradicts decades of premises on when MS really gets started. It proposes that the disease can enter an extended and insidious prodromal phase, with such nonspecific symptoms as fatigue, dizziness, headache, depression, and anxiety—often ignored or misdiagnosed. These could all be early whispers of MS in the making.

Led by Dr. Marta Ruiz-Algueró, a postdoctoral fellow at UBC, the study analyzed the medical histories of 2,038 Canadians with MS and compared them to more than 10,000 people without the condition. Using detailed administrative and clinical records that spanned 25 years, researchers tracked how often patients visited healthcare providers before their first classical MS symptoms.

15 years before diagnosis, people who later developed MS were already visiting general practitioners more frequently. Their complaints often centered on fatigue, pain, dizziness, headaches, and mental health concerns like anxiety and depression.

12 years before: Psychiatrist visits began to rise.

8 to 9 years before: Visits to neurologists and ophthalmologists increased, often due to vision issues or unexplained nerve-related symptoms.

3 to 5 years before: More visits to emergency medicine and radiology departments.

1 year before diagnosis: Healthcare use spiked across multiple specialties, especially neurology and emergency medicine.

“These patterns suggest that MS has a long and complex prodromal phase where something is happening beneath the surface but hasn’t yet declared itself as MS,” said Dr. Ruiz-Algueró.

Is Mental Health One of the First Clues?

One of the most striking revelations was the presence of mental health conditions, particularly anxiety and depression, in the earliest stages of the disease's progression. These symptoms were found to be significantly more common in people who eventually developed MS—often more than a decade before diagnosis.

“We’re only now starting to understand what these early warning signs are, with mental health-related issues appearing to be among the earliest indicators,” added Ruiz-Algueró.

However, the researchers are clear: not everyone with depression or fatigue has MS, and most people with such symptoms will never develop the condition. But in combination with other red flags and patterns, these findings could help doctors detect MS earlier.

Why These Findings Could Change How MS is Diagnosed?

Traditionally, MS diagnosis hinges on a demyelinating event, such as vision loss or difficulty walking. But this study shifts the focus further upstream, suggesting that the disease process starts silently, even while symptoms seem unrelated or mild.

Dr. Helen Tremlett, senior author of the study, emphasized that early detection is key:

“By identifying these earlier red flags, we may eventually be able to intervene sooner—whether that’s through monitoring, support, or preventive strategies.”

The implication is profound: if clinicians know what to look for, they could start identifying people at risk much earlier and possibly even slow the progression before major damage occurs.

How MS Works?

Multiple sclerosis is an autoimmune condition where the immune system mistakenly attacks the protective covering of nerves—the myelin sheath. Over time, this leads to inflammation, scarring, and disruption in the brain’s ability to communicate with the rest of the body. Common symptoms include:

• Chronic fatigue
• Numbness or tingling
• Loss of coordination or balance
• Vision problems
• Muscle weakness
• Memory and cognitive changes

Despite decades of research, the exact cause of MS remains unknown. Genetics, viral infections, environmental factors, and immune system dysfunction are all believed to play roles. Previous studies have also identified MS-specific antibodies in blood up to five years before symptoms, suggesting the immune system may go rogue much earlier than expected.

This extended prodromal phase isn't unique to MS. Parkinson’s disease, for instance, has long been known to begin with subtle mood changes, constipation, and sleep disturbances years before motor symptoms appear.

Tremlett and her team say MS is now showing similar patterns, and it’s time to recognize that the disease doesn’t start with the first lesion—it starts long before that.

“This is the most comprehensive picture to date of how patients engage with a range of healthcare providers in the years leading up to a diagnosis,” said Tremlett. “Our findings dramatically shift the timeline for when these early warning signs are thought to begin.”

While there's still no cure for MS, early detection could pave the way for better disease management, fewer relapses, and slower progression.

If you're experiencing chronic fatigue, unexplained pain, dizziness, or persistent mental health concerns—and you’re not getting answers—it’s worth advocating for yourself. While these symptoms are common and non-specific, studies like this show they may sometimes be the earliest signs of something more serious, like MS.

Dementia doesn’t happen overnight. It’s the result of a long chain of biological and lifestyle factors that quietly stack up over decades. A major new study from Oxford University now sheds light on just how early some of these risks can start—and it’s sooner than you might think.

According to the research published in Brain Communications, developing certain health conditions in your 40s and 50s—decades before memory loss begins—can sharply raise your chances of developing dementia later in life. Specifically, heart disease, atrial fibrillation, diabetes, anxiety, depression, and stroke were all linked to a significantly increased risk. And it’s not just having one condition that matters—multiple illnesses over time (a phenomenon called multimorbidity) appears to compound the risk dramatically.

Researchers at the University of Oxford analyzed data from more than 280,000 participants in the UK Biobank, focusing on the timing and combination of 46 chronic illnesses. They found that up to 80% of dementia patients had two or more health conditions leading up to their diagnosis. But more critically, the age at which these conditions first appeared had a major influence on dementia risk.

Before age 55: Heart disease, atrial fibrillation, and diabetes had the strongest connection to later dementia.

Between ages 55 and 70: Stroke, anxiety, and depression doubled the risk.

These findings don’t just point to correlation—they suggest there are “critical time windows” when certain illnesses may do the most damage to long-term cognitive health.

Dr. Sana Suri, associate professor and senior fellow at Oxford Brain Sciences, emphasized the importance of identifying not just which conditions matter, but when they matter most: “This study has identified how specific illnesses tend to co-exist with each other, and also the critical time windows in which they could pose the greatest risk.”

Conditions That Could Set the Stage for Dementia

1. Heart Disease

Cardiovascular issues—especially those that start before age 55—appear to set the stage for dementia decades later. Poor heart health means reduced blood flow to the brain, which can lead to structural changes, shrinkage, and even microinfarcts (tiny strokes). Over time, this damages the brain's ability to process and retain information.

Studies have long linked hypertension and atherosclerosis to cognitive decline. But this study reinforces the idea that early-onset heart disease isn't just a heart issue—it's a brain issue too.

2. Atrial Fibrillation (AFib)

AFib, a common heart rhythm disorder, was strongly associated with increased dementia risk—particularly when diagnosed early in life. It may contribute to the formation of blood clots, which can travel to the brain and cause strokes, even small ones that go undetected.

AFib also leads to inefficient blood circulation, which deprives brain cells of oxygen over time, potentially accelerating cognitive decline.

3. Diabetes

Type 2 diabetes damages blood vessels throughout the body—including the brain. It also increases inflammation and oxidative stress, both of which are implicated in dementia. Chronically high blood sugar levels can impair memory, learning, and executive function over the years.

The Oxford study suggests that diabetes diagnosed before midlife (age 55) is especially dangerous for long-term brain health. Managing blood sugar early could be a powerful intervention strategy.

4. Anxiety

Anxiety isn’t just an emotional state—it also has biological consequences. Chronic anxiety floods the body with stress hormones like cortisol, which, over time, can damage the hippocampus (the area of the brain responsible for memory formation).

The study showed that anxiety diagnosed between ages 55 and 70 had a strong link to future dementia, potentially due to cumulative stress or co-existing health problems like insomnia or cardiovascular disease.

5. Depression

Like anxiety, depression can cause neurobiological changes in the brain, including reduced brain volume in key areas like the prefrontal cortex and hippocampus. It also disrupts sleep, appetite, and motivation—factors that are all linked to cognitive decline when persistent.

Importantly, depression may not just be an early symptom of dementia, as once believed—it may actually play a causal role in increasing risk, particularly if it arises in midlife.

6. Stroke

Stroke was one of the most powerful predictors of dementia risk identified in the study. Whether large or small, strokes damage brain tissue, disrupt communication between brain regions, and increase the likelihood of future vascular events.

When strokes occur between ages 55 and 70, the risk of dementia appears to double. Preventing stroke through better blood pressure control, physical activity, and managing cholesterol could play a major role in reducing dementia burden globally.

How Lifestyle Habits Increase Risk Of Dementia?

While these conditions pose serious risks, they’re often tied to modifiable behaviors. That’s why lifestyle matters just as much as biology when it comes to preventing dementia.

• Poor sleep, especially in midlife, is now linked to structural brain changes.
• Chronic stress and high cortisol levels are known to impair memory and shrink the brain.
• Excess alcohol, particularly over many years, can lead to alcohol-related brain damage (ARBD).
• Ultra-processed foods, low in fiber and high in sugar, are associated with increased inflammation and dementia risk.
• Lack of physical activity contributes to vascular damage, insulin resistance, and reduced brain resilience.
• Social isolation has been shown to speed cognitive decline—engagement and social interaction are critical to brain longevity.

Is Dementia Prevention Possible?

This study changes the way we think about dementia prevention. It’s not something to start worrying about at 70. It’s something to pay attention to in your 40s, 50s, and 60s—especially if you’re already living with chronic health issues.

Dr. Suri stresses that prevention needs to be dynamic and age-sensitive: “Future studies could examine whether efforts to manage or prevent cardiovascular problems in early-to-midlife, followed by mental health and neurological disorders when people are in their 50s and 60s, might reduce the risk of dementia.”

In other words- the earlier, the better. But it’s never too late to change course. Dementia isn’t inevitable. While you can’t change your genes or erase your age, you can manage the conditions that may tip the scales toward cognitive decline. This study is a wake-up call to healthcare providers and patients alike—start the conversation early, monitor chronic illnesses proactively, and don’t underestimate the power of midlife choices.

If heart disease, diabetes, stroke, anxiety, or depression are part of your story, now’s the time to treat not just the symptoms—but the long-term risk that may be quietly building.

A hair transplant is a surgical procedure, and like any medical intervention, it comes with a recovery period. While the healing of the scalp typically takes one to two weeks, visible results in terms of hair growth take much longer. It can take up to 12 months for the full results to show, depending on individual healing patterns, the technique used, and how well post-procedure care is followed.

Hair does not magically grow overnight. Recovery is a journey that requires a bit of patience and some TLC.

Here is what really happens post-transplant, week by week.

First 24-72 Hours

Week 1: The “Don’t Touch My Head” Era

You will be allowed to gently wash your hair by now, using a special shampoo.

Week 2: Shedding Starts

Week 3 to 4: Back to Square One

Month 2 to 3: It Can Get Itchy

Month 4 to 6: Hair, Finally!

Month 7 to 12: Full Bloom Season

Recovery time after a hair transplant is not just about healing; it is about growth. Physically, you will be fine after a week or two. But to see visible, satisfying results, expect the full process to stretch over 9 to 12 months.