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Lasix Tablet (Furosemide): Uses, Dosage, Side Effects & FAQs

Lasix Tablet (Furosemide): Uses, Dosage, Side Effects & FAQs

Lasix tablets, also known by their generic name Furosemide, are powerful loop diuretics (water pills). It is commonly prescribed to remove excess fluid from the body and is widely used in conditions related to the heart, kidneys, liver, and blood pressure. You can explore diuretic and heart-related medicines from trusted sources at mygenericpharmacy.com.

What Is Lasix Tablet Used For?

Lasix tablet is mainly used to treat conditions caused by fluid retention (edema), including:

  • Heart failure–related swelling (legs, lungs)
  • Kidney disorders causing fluid buildup
  • Liver disease, such as cirrhosis
  • High blood pressure (hypertension)

How Does Lasix (Furosemide) Work?

Lasix works on the kidneys by increasing urine production. It removes excess water and sodium from the body, which helps reduce swelling, lowers blood pressure, and decreases strain on the heart.

Lasix Tablet Dosage

The dosage of Lasix depends on the patient’s condition and response to treatment:

  • Edema: 20–40 mg once daily (may be adjusted)
  • Heart failure: Dose adjusted gradually by a doctor
  • High blood pressure: Often used along with other BP medicines

Important: Never change the dose without consulting a healthcare professional.

How to Take a Lasix Tablet?

  • Usually taken in the morning
  • Can be taken with or without food
  • Avoid taking it late at night due to frequent urination

Lasix Tablet Side Effects

Like all medicines, Lasix may cause side effects in some people:

  • Frequent urination
  • Dizziness or weakness
  • Low blood pressure
  • Low potassium levels (muscle cramps)
  • Dehydration

Long-term users may require regular blood tests to monitor electrolytes.

Precautions Before Using Lasix

  • Inform your doctor if you have kidney disease or diabetes
  • Use with caution during pregnancy and breastfeeding
  • Avoid excessive alcohol consumption
  • Regular monitoring is essential for long-term use

Frequently Asked Questions (FAQs)

What is the Lasix tablet used for?

Lasix tablet is used to treat fluid retention caused by heart failure, kidney disease, liver disease, and high blood pressure.

Is Lasix used for high blood pressure?

Yes, Lasix can help lower blood pressure by removing excess fluid, although it is usually combined with other antihypertensive medicines.

Can Lasix be taken daily?

Yes, Lasix can be taken daily if prescribed by a doctor. Long-term use requires medical supervision and regular blood tests.

Does Lasix cause potassium loss?

Yes, Lasix can lower potassium levels. Doctors may recommend potassium supplements or potassium-rich foods.

Can Lasix be used for weight loss?

No. Lasix should not be used for weight loss. Any weight reduction is due to water loss, not fat loss, and misuse can be dangerous.

Where can I buy Lasix or similar medicines online?

You can explore a wide range of prescription medicines, including diuretics, from trusted online pharmacies such as mygenericpharmacy.com.

Bottom Line

Lasix (Furosemide) is an effective and widely used diuretic for managing edema, heart failure, and high blood pressure. While it offers significant benefits, it should always be used under medical supervision to avoid dehydration and electrolyte imbalance.

For safe and reliable access to prescription medicines, visit mygenericpharmacy.com.

Rheumatoid Arthritis and Heart Health

Rheumatoid Arthritis and Heart Health

Rheumatoid arthritis can increase the risk of heart disease due to chronic inflammation that damages blood vessels and encourages plaque buildup. Shared risk factors like high blood pressure, obesity, smoking, and a unique effect on blood fats (lipid paradox) further connect RA and heart disease. Individuals with RA can lower their risk of heart disease by managing inflammation with prescribed medications, adopting a heart-healthy lifestyle, and undergoing regular screening for heart disease risk factors.

Rheumatoid arthritis (RA) is an autoimmune form of arthritis that affects more than just your joints. It can also affect other tissues and organs, and it may cause problems in the heart. However, just because you have RA doesn’t mean you’ll have issues with your heart. There are steps you can take to keep your heart healthy and avoid developing heart disease. Read on to find out the connection between rheumatoid arthritis and heart disease and how you can lower your risk factors for developing heart disease if you’re living with RA.

How does RA affect heart health?
Chronic inflammation from RA increases the risk of heart disease. Inflammation damages the blood vessels and can cause plaque to build up in the arteries. Plaque in the arteries can narrow the blood vessels and block blood flow, leading to a heart attack or stroke. Proteins called cytokines are linked to the growth and activity of other immune system cells. These proteins are responsible for both the way RA attacks the joints and the way it damages blood vessels in cardiovascular disease.

Risk factors for both RA and heart disease include:
High blood pressure
If you have RA, your blood pressure is likely to be higher due to:
lack of exercise
certain medications that treat RA, like steroids
less elastic arteries
Inflammation is also linked to higher blood pressure. People with RA may have up to 10 times the amount of inflammation as a person who doesn’t have RA.

Obesity
Having obesity may be linked to the risk of developing RA. According to the Arthritis Foundation, the sore joints associated with RA can make it hard to exercise, and a lack of exercise can cause weight gain.
Additionally, obesity is associated with inflammation and other risk factors for heart disease, including high blood sugar and high blood pressure.
Obesity is also linked to metabolic syndrome. Metabolic syndrome is a group of symptoms that include other risk factors that raise the risk of heart disease, including:
high triglycerides and cholesterol
high blood pressure
high blood sugar
Metabolic syndrome is twice as common in people with RA compared to people who don’t have RA.

Lipid paradox
RA affects the fats in the blood uniquely. Individuals with RA generally have:
Low levels of LDL (bad) cholesterol
High levels of triglycerides
Low levels of HDL (good) cholesterol
While having low levels of LDL is associated with heart health, having too little good cholesterol and high triglycerides can increase the risk of heart disease.

Smoking
People who smoke are more likely to develop RA than people who do not smoke. Further, if you have RA, you’re more likely to have more severe symptoms than someone who does not smoke.
Smoking also makes RA medications less effective. In addition to increasing the risk of and worsening RA, smoking is also a major cause of heart disease. An individual with RA who smokes is 50% more likely to develop heart disease than a person who doesn’t smoke and has RA.

How to reduce the risk
Even though RA increases the risk of heart disease, you can work with your doctor to lower your risk.
One of the easiest ways to protect yourself from heart disease related to RA is by taking the medications your doctor prescribes to control the inflammation from RA.
Disease-modifying antirheumatic drugs (DMARDs) reduce the inflammation associated with RA and may reduce the risk of heart disease. Though people living with RA have an increased risk of heart disease, medical guidelines in the United States don’t have specific recommendations to reduce heart disease if you have RA.

However, the European League Against Rheumatism (EULAR) recommends that you be screened every 5 years for risk factors of heart disease. You can also make some lifestyle changes to help lower your risk of heart disease.

The American Heart Association suggests the following tips to reduce the risk of heart disease:
eating a balanced diet of vegetables, fruits, and whole grains
Getting at least 150 minutes of aerobic exercise per week
maintaining a healthy weight
avoiding smoking or quitting
managing any health conditions like RA that raise your risk of heart disease
Taking any medication prescribed by a doctor to prevent heart disease, like statins

RA increases the risk of developing heart disease due to inflammation and shared risk factors. Though there’s an increased risk, you can take steps to lower the chances of developing heart disease even if you’re living with RA. Some things you can do to lower your risk include taking your medications as prescribed, eating a balanced diet, getting regular exercise, avoiding or quitting smoking, and maintaining a healthy weight.

Reference:
https://www.healthline.com/health/rheumatoid-arthritis/rheumatoid-arthritis-and-heart-health#takeaway

Medications that have been suggested by doctors worldwide are available on the link below
https://mygenericpharmacy.com/category/arthritis

Polyphenol-rich cocoa, coffee, and berries may help support heart health

Polyphenol-rich cocoa, coffee, and berries may help support heart health

Polyphenol-rich foods, such as cocoa, coffee, and berries, are consistently linked to cardiovascular benefits. Their power comes from a complex interplay of bioactive compounds that work through multiple pathways in the body. Here’s a breakdown of how each supports heart health and the key mechanisms at play.

1. How They Work: Key Mechanisms

Polyphenols are plant compounds with potent antioxidant and anti-inflammatory effects. For heart health specifically, they contribute by:

  • Improving Endothelial Function: They boost the production of nitric oxide, a molecule that relaxes and dilates blood vessels, improving blood flow and lowering blood pressure.
  • Reducing Oxidation of LDL Cholesterol: Oxidized LDL is a key driver of plaque formation in arteries (atherosclerosis). Polyphenols act as antioxidants, protecting LDL particles from this damaging oxidation.
  • Lowering Inflammation: Chronic inflammation is a root cause of many cardiovascular diseases. Polyphenols inhibit inflammatory pathways.
  • Improving Insulin Sensitivity: They can help regulate blood sugar, which is crucial because insulin resistance is a major risk factor for heart disease.
  • Modulating Gut Microbiota: As discussed earlier, some polyphenols are metabolized by gut bacteria into beneficial compounds that reduce systemic inflammation and improve metabolic health.

2. A Closer Look at Each Food

Cocoa (Dark Chocolate):

  • Key Polyphenols: Flavanols, especially epicatechin.
  • Evidence-Based Benefits: Numerous studies and meta-analyses show that cocoa flavanols can lower blood pressure, improve blood vessel flexibility, reduce LDL oxidation, and improve platelet function (making blood less “sticky”). The effect is significant enough that the European Food Safety Authority (EFSA) has approved a health claim stating that cocoa flavanols help maintain normal blood vessel elasticity.
  • Important: Benefits are linked to high-flavanol cocoa or dark chocolate with >70% cocoa content. Milk chocolate and highly processed cocoa have much lower polyphenol levels.

Coffee:

  • Key Polyphenols: Hydroxycinnamic acids, most notably chlorogenic acid.
  • Evidence-Based Benefits: Large observational studies consistently show a link between moderate coffee consumption (3-4 cups per day) and a reduced risk of heart failure, stroke, and coronary heart disease. Chlorogenic acid is associated with improved blood vessel function and may help lower blood pressure. Coffee also contains other bioactive compounds and minerals like magnesium.
  • Note: The benefits are seen with filtered coffee. Unfiltered coffee (like French press or Turkish) contains diterpenes that can raise LDL cholesterol in some individuals.

Berries (Blueberries, Strawberries, Raspberries, etc.):

  • Key Polyphenols: Anthocyanins (which give them their vibrant color), flavonols, and ellagitannins.
  • Evidence-Based Benefits: Berry consumption is strongly linked to improved cardiovascular risk profiles. Regular intake is associated with reduced blood pressure, improved HDL cholesterol, lower oxidized LDL, and better arterial stiffness. The famous “Nurses’ Health Study” found that women with the highest intake of anthocyanins (mainly from berries) had a significantly lower risk of heart attack.

3. Synergistic Effect & Practical Advice

The greatest benefit comes from a dietary pattern rich in a variety of these polyphenol sources, along with other heart-healthy foods (vegetables, nuts, whole grains, oily fish).

How to incorporate them:

  • Cocoa: Use natural, non-alkalized cocoa powder in smoothies or oatmeal. Enjoy a small square of high-quality dark chocolate (70-85% cocoa) as a treat.
  • Coffee: Enjoy 1-4 cups of freshly brewed, filtered coffee per day, ideally without large amounts of added sugar and cream.
  • Berries: Aim for at least 1-2 servings daily—fresh or frozen (freezing preserves polyphenols well). Add to yogurt, cereal, salads, or eat as a snack.

Important Consideration: While these foods are powerful components of a preventative diet, they are not a replacement for medical treatment in individuals with existing heart conditions. Always discuss significant dietary changes with a healthcare provider.

Conclusion: Your statement is well-supported by science. Regularly consuming polyphenol-rich cocoa, coffee, and berries as part of a balanced diet is a delicious and effective strategy for supporting long-term heart health.

Reference:
https://www.medicalnewstoday.com/articles/polyphenol-rich-foods-cocoa-coffee-berries-olive-oil-support-heart-health

Medications that have been suggested by doctors worldwide are available on the link below
https://mygenericpharmacy.com/category/disease/heart-disease

A ‘spoonful’ of black cumin seed powder a day may help lower cholesterol

A ‘spoonful’ of black cumin seed powder a day may help lower cholesterol

You’ve touched on another promising area of research for a functional food. Let’s break down the evidence for black cumin seed (Nigella sativa) and its potential cholesterol-lowering effects.

The Core Evidence

A growing body of clinical research suggests that daily supplementation with black cumin seed oil or powder can indeed improve cholesterol and other cardiovascular risk factors.

  • Meta-Analyses (The Gold Standard of Evidence): Multiple meta-analyses (which pool data from many randomized controlled trials) have concluded that Nigella sativa supplementation significantly reduces:
    • Total Cholesterol
    • LDL (“bad”) Cholesterol
    • Triglycerides
    • Fasting Blood Sugar
    • It also tends to increase HDL (“good”) Cholesterol, though this effect is sometimes less pronounced.
  • Typical Dose & Form: Benefits are seen with doses of 1-3 grams per day of powder or oil, typically taken for 8-12 weeks. A “spoonful” in common parlance often means ~1 teaspoon (roughly 2-3 grams).

The Active Compound & How It May Work

The primary bioactive component is thymoquinone (TQ), which is responsible for most of its therapeutic effects. The proposed mechanisms for lowering cholesterol include:

  1. Reducing Cholesterol Synthesis: TQ may inhibit key enzymes (like HMG-CoA reductase) in the liver that are involved in the body’s internal production of cholesterol. (This is a similar, though likely weaker, mechanism to that of statin drugs).
  2. Enhancing Cholesterol Excretion: It may promote the excretion of bile acids (which are made from cholesterol), forcing the liver to pull more cholesterol from the blood to make new bile.
  3. Potent Antioxidant & Anti-inflammatory Effects: Chronic inflammation and oxidative stress are deeply linked to atherosclerosis (plaque buildup). By reducing these, black cumin seed may improve overall vascular health and LDL particle quality.
  4. Improving Insulin Sensitivity: Since high blood sugar and cholesterol often go hand-in-hand (metabolic syndrome), improving insulin resistance has a beneficial downstream effect on lipid profiles.

Important Caveats and Context

  1. Adjunct, Not Replacement: The effect is moderate. For individuals with severely high cholesterol, black cumin seed is not a replacement for prescribed statins or other cholesterol-lowering medications. It is best viewed as a dietary adjunct or a preventive measure for those with mildly elevated levels.
  2. Whole Food vs. Supplement: The studies often use standardized oil extracts or powdered seeds. The concentration of thymoquinone can vary in store-bought seeds.
  3. Safety & Side Effects: Generally recognized as safe (GRAS) for culinary use. In supplemental doses, it is well-tolerated but can cause mild digestive upset for some. Important interactions:
    • It may slow blood clotting and should be used cautiously by those on anticoagulant drugs (like warfarin, aspirin, clopidogrel).
    • It may lower blood pressure and blood sugar, so monitoring is advised for those on related medications.
    • Pregnant women are typically advised to avoid therapeutic doses due to potential uterine stimulant effects.
  4. The “Spoonful” Advice: While a teaspoon a day is a common traditional and researched dose, it’s not a one-size-fits-all prescription. Starting with a smaller amount (e.g., 1/2 teaspoon) to assess tolerance is prudent.

Practical Conclusion

The statement that “a spoonful of black cumin seed powder a day may help lower cholesterol” is supported by scientific evidence. It fits into the category of a functional food with proven medicinal properties.

For someone looking to improve their cardiovascular health naturally, adding black cumin seed to their diet (e.g., sprinkled on salads, yogurt, or in smoothies) is a reasonable and likely beneficial strategy, provided they have no contraindications.

However, for diagnosed hyperlipidemia, this should be done in consultation with a doctor, as part of a broader plan that includes diet, exercise, and possibly medication. It’s a powerful seed, but not a magic bullet.

Reference:
https://www.medicalnewstoday.com/articles/spoonful-black-cumin-seed-powder-daily-may-help-lower-cholesterol
https://www.sciencealert.com/a-daily-sprinkle-of-cumin-seeds-can-help-lower-cholestrol-study-finds
https://www.news-medical.net/news/20251118/Daily-black-cumin-intake-improves-blood-lipids-and-reduces-obesity-risk.aspx

Medications that have been suggested by doctors worldwide are available on the link below
https://mygenericpharmacy.com/category/products/disease/heart-disease

3 New Findings on AFib and What They Mean

3 New Findings on AFib and What They Mean

If you’re among the 1 in 5 U.S. adults who have an abnormal heart rhythm problem called atrial fibrillation, there’s been a flurry of new research about the condition that offers some guidance on your everyday choices and how those impact your risk of recurrence.

“The major risk is stroke, and preventing stroke is the name of the game with AFib.
Three new studies shed light on some common questions: whether your morning coffee matters, whether a diabetes drug might help lower recurrence risk, and what new data reveals about AFib’s link to dementia.


Here’s what the latest research suggests:
Coffee doesn’t increase the risk of recurrent atrial fibrillation. A small but well-designed new study showed that people who drank a cup of coffee daily were not more likely than non-coffee drinkers to have a repeat atrial fibrillation episode after successful treatment with electrical cardioversion – a quick procedure where a doctor delivers a brief, controlled shock to the heart to put it back into a normal rhythm. People in the study agreed ahead of time to be randomly assigned to one of two groups: those who continued drinking coffee as they did before the study, and those who abstained for six months.

Why it matters: Many people and even some doctors still assume coffee triggers AFib, a long-held bit of “common wisdom” that isn’t backed by strong evidence, Prystowsky said. It’s a top concern for newly diagnosed patients, but experts say coffee is rarely a problem except in people with palpitations. The design of this latest study, randomizing people before asking them to keep drinking or abstain, makes the results particularly trustworthy, he said.

What you can do: If you’re going to change one beverage you consume to manage atrial fibrillation risk, go ahead and keep drinking coffee and instead focus on reducing or cutting out alcohol.


Metformin helped reduce AFib recurrence in a small study of people with overweight and obesity. In a study of 99 people with overweight or obesity who had an ablation procedure, where doctors burn or freeze tiny areas of heart tissue to stop the abnormal signals that cause AFib, those who took the type 2 diabetes drug metformin after ablation were less likely to have recurrent AFib. None of the people in the study had diabetes, although 40% of them met prediabetic blood sugar criteria. The study was presented at an American Heart Association conference this month and hasn’t been published in a peer-reviewed journal.

Why it matters: Doctors are talking about this study because it’s another step toward understanding the connection between weight and AFib risk. An important previous study showed that people who lost 10% of their body weight were six times more likely to survive four years without recurrence. “It wasn’t just weight loss, though,” Prystowsky said, noting that those who lost weight had improved glucose and blood pressure levels.
Interestingly, in this latest metformin study, people saw AFib benefits without significant weight loss. That suggests the drug may be affecting the body in other ways, possibly through metabolism, inflammation, or fat around the heart, though researchers don’t yet know the exact mechanism, Prystowsky said.

What you can do: “The most important takeaway from this small study is reinforcing the idea that the management of obesity makes a huge difference in outcomes for atrial fibrillation,” Philbin said. He and Prystowsky agreed the study was too small for a doctor to recommend that a patient take metformin to reduce AFib risk, though. The study was “hypothesis-forming rather than game-changing, but it reinforces some ideas we know about atrial fibrillation that we know will work: you should exercise. You should lose weight. You should not drink alcohol,” Philbin said. He and his colleagues plan to explore whether AFib patients benefit from six weeks of supervised exercise and dietitian guidance the way heart attack survivors do.


Another study just linked AFib with dementia risk. Published this month in JACC: Advances, the analysis looked at 670,745 Medicare patients 65 and older and found that those who developed AFib after non-cardiac surgery were more likely to later be diagnosed with dementia. In cardiac surgery patients, dementia rates were similar regardless of AFib (about 4%). But after non-cardiac surgery, dementia was diagnosed in nearly 13% of people with AFib, versus 9% without – a 20% increased risk. Non-cardiac procedures ranged widely, with orthopedic (including joint replacements), gastrointestinal, and circulatory surgeries most common.

Why it matters: The study authors wrote it was “notable” that cardiac surgery patients who developed AFib weren’t more likely to get dementia, suggesting their AFib may have been triggered by the surgery itself. They couldn’t explain why non-cardiac surgery patients had a higher dementia risk and found no clear contributing factors like high blood pressure, diabetes, or prior stroke or heart failure. They hypothesized that undetected mild strokes or heart attacks, which can damage the brain and blood vessels, might play a role. The link between AFib and dementia is established, and while silent strokes and heart attacks are suspected contributors, the data shows a link rather than a cause. Prystowsky tells patients who get AFib after non-cardiac surgery that they have a higher risk of recurrence and need to be aware of it.

What you can do: If you’re heading into surgery, worrying about AFib shouldn’t be at the top of your list, Prystowsky said. But if you like to be prepared, both Philbin and Prystowsky advised that wearing a device like a smartwatch that can check your pulse and rhythm can help you spot any issues early. And if you’ve already had AFib after a non-cardiac surgery, regular monitoring is especially important – and you should call your doctor if your device flags an abnormal pulse or rhythm.


Reference:
https://www.webmd.com/heart-disease/atrial-fibrillation/news/20251118/3-new-findings-on-afib-and-what-they-mean
https://my.clevelandclinic.org/health/diseases/16765-atrial-fibrillation-afib
https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20350624

Medications that have been suggested by doctors worldwide are available on the link below:
https://mygenericpharmacy.com/category/products/disease/heart-disease

Metformin may weaken cardiovascular, insulin benefits of exercise…

Metformin may weaken cardiovascular, insulin benefits of exercise…

This is a fascinating and nuanced topic that sits at the intersection of two foundational treatments for type 2 diabetes. The headline is based on real research, but it requires important context to be fully understood. Here’s a breakdown of what the science says, what it means, and who should be concerned.

The Core Finding: The “Metformin-Exercise Interaction”

The claim originates primarily from a series of studies, most notably a 2013 randomized controlled trial published in The Journal of Clinical Endocrinology & Metabolism and other follow-up research.

The studies found that in older, overweight, or pre-diabetic adults, taking metformin seemed to blunt some of the key physiological benefits of exercise compared to a placebo group that did the same exercise regimen.

The blunted benefits were specifically in two areas:

  1. Insulin Sensitivity: Exercise is one of the most powerful ways to improve insulin sensitivity. The studies found that the group taking metformin saw a significantly smaller improvement in insulin sensitivity from their exercise training than the placebo group.
  2. Mitochondrial Function: Exercise trains your muscles’ mitochondria (the cellular power plants) to become more efficient and numerous. The metformin group showed a reduced improvement in markers of mitochondrial health.

The proposed mechanism is that metformin and exercise act on the same pathway, but in somewhat opposing ways.

  • Exercise signals through AMPK (AMP-activated protein kinase), a cellular energy sensor. When you exercise, you deplete energy, activating AMPK. This tells the cell to ramp up energy production (improve mitochondria) and increase glucose uptake (improve insulin sensitivity).
  • Metformin also works primarily by activating AMPK.

The theory is that by chronically activating AMPK pharmacologically, metformin might “pre-empt” or dull the cell’s robust response to the natural AMPK signal from exercise. It’s as if the cell is already being “shouted at” by the drug, so it doesn’t “hear” the shout from exercise as clearly.

Crucial Context and Limitations

This is where the “may” in the headline becomes critically important. This interaction is not a universal rule and has several important caveats:

  • Population Specific: The effect has been most consistently observed in at-risk, non-diabetic individuals (e.g., those with pre-diabetes or insulin resistance) and older, overweight populations. The evidence is much less clear for people with established type 2 diabetes.
  • Benefit Blunting vs. Benefit Elimination: The studies show a reduction in the improvement, not a complete elimination. The metformin+exercise group still saw benefits—just not as much as the exercise-only group.
  • Cardiovascular Benefits Are Broader: The term “cardiovascular benefits” can be misleading. While mitochondrial and insulin-sensitivity improvements are crucial for metabolic cardiovascular health, exercise provides a host of other cardiovascular benefits that are likely NOT blunted by metformin, such as:
    • Lowering blood pressure
    • Improving cholesterol levels
    • Strengthening the heart muscle
    • Improving endothelial function (blood vessel health)
    • aiding in weight management

What This Means For You: Practical Takeaways

  1. For People with Type 2 Diabetes: Do NOT stop taking metformin. For you, the proven, powerful benefits of metformin in controlling blood glucose and reducing the risk of diabetes complications far outweigh the potential slight blunting of exercise’s effect on insulin sensitivity. The combination of metformin and exercise is still a cornerstone of effective diabetes management.
  2. For People with Pre-Diabetes: This is the group where the conversation is most relevant. If you are using exercise as your primary tool to prevent the onset of type 2 diabetes, it’s worth having a discussion with your doctor. They might consider whether lifestyle intervention alone is sufficient before adding metformin. However, for many, the combination is still recommended as the most effective strategy.
  3. For Healthy Individuals or Athletes: This research is likely not relevant to you. Metformin is not prescribed for this population, and the studies did not involve them.
  4. The Overarching Principle: Exercise is Non-Negotiable. Regardless of whether you take metformin, exercise remains one of the most powerful health interventions available. Its benefits extend far beyond the specific metrics that might be slightly blunted. The worst decision you could make based on this research is to stop exercising.

Conclusion

The statement “Metformin may weaken cardiovascular, insulin benefits of exercise” is scientifically accurate but easily misinterpreted.

  • The Science: It appears that metformin can attenuate some of the specific cellular and metabolic adaptations to exercise, particularly improvements in insulin sensitivity and mitochondrial biogenesis, likely through competing actions on the AMPK pathway.
  • The Reality: For the vast majority of people taking metformin (especially those with type 2 diabetes), this potential interaction is a minor consideration. The powerful, combined benefits of both the medication and physical activity make them a winning combination for long-term health.

Always consult your doctor before making any changes to your medication or exercise regimen. They can provide personalized advice based on your specific health status and goals.

https://www.pharmacytimes.com/view/metformin-may-diminish-the-cardiometabolic-benefits-of-exercise

https://www.medicalnewstoday.com/articles/metformin-diabetes-lower-exercise-benefits

https://scitechdaily.com/popular-diabetes-drug-metformin-may-cancel-out-exercise-benefits-study-warns

https://mygenericpharmacy.com/category/disease/heart-disease

Blood vessels in eyes may help predict heart disease and biological aging risk.

Blood vessels in eyes may help predict heart disease and biological aging risk.

That’s a fascinating and accurate insight. This field of research is growing rapidly and holds significant promise for non-invasive health diagnostics.
Here’s a detailed breakdown of how the blood vessels in your eyes (the retina) can serve as a window to your heart health and biological age.

Why the Retina is a Unique “Window”
The retina is the only place in the body where you can directly and non-invasively view microvascular blood vessels (arterioles and venules). These tiny vessels are sensitive to the same pressures and damage that affect the entire circulatory system, including the heart and brain. Changes in their structure and function often mirror what’s happening in vessels you can’t see.

  1. Predicting Heart Disease Risk
    The condition of the retinal vessels, known as Retinal Vascular Caliber, is a key indicator.

What Doctors Look For:
Narrowing of Arterioles: This is a classic sign of hypertension (high blood pressure). The constant high pressure causes the vessel walls to thicken, making the central light reflex (the visible column of blood) appear narrower.

Arteriovenous (AV) Nicking: This occurs when a hardened retinal artery compresses a vein where they cross, causing the vein to appear “nicked” or pinched. It’s a sign of chronic hypertension and advanced vascular damage.

Microaneurysms, Hemorrhages, and Cotton-Wool Spots: These are signs of more severe damage, often seen in diabetic retinopathy and hypertensive retinopathy. Since diabetes is a major risk factor for heart disease, these findings are a red flag for systemic cardiovascular issues.

The Link to Heart Disease:
The same processes that damage retinal vessels—inflammation, oxidative stress, and endothelial dysfunction also damage the coronary arteries supplying the heart.

Studies have shown that people with narrower retinal arterioles and wider venules have a higher risk of developing hypertension, coronary heart disease, heart failure, and stroke, even after accounting for traditional risk factors like smoking and cholesterol.

  1. Predicting Biological Aging Risk
    This is an even more cutting-edge application. The concept is that the “age” of your retinal vessels may be a better indicator of your overall health and mortality risk than your chronological age.

Retinal Age Gap: Researchers are using advanced AI to analyze retinal images and predict a person’s “biological age” based on the health of their retinal vasculature. How it works: A deep learning model is trained on thousands of retinal images from healthy people to learn what a “normal” retina looks like at different chronological ages.

The Key Finding: People whose retinas look “older” than their actual age (a positive “retinal age gap”) have a significantly higher risk of death from all causes, and specifically from cardiovascular disease. A large study found that every 1-year increase in the retinal age gap was associated with a 2-3% increase in all-cause and cause-specific mortality risk.

Why it Reflects Biological Aging:
The retina is part of the central nervous system (it’s an extension of the brain). Its health is closely linked to brain health. The microvasculature in the retina is sensitive to cumulative lifelong damage from factors like high blood pressure, high blood sugar, and oxidative stress—all key drivers of biological aging.

Therefore, an “aged” retina suggests accelerated aging and cumulative damage throughout the entire body’s vascular and neurological systems. The Future: AI and Routine Screening
The traditional method of a doctor manually examining the retina is being supercharged by Artificial Intelligence.

Automated Analysis: AI algorithms can now quickly and accurately measure retinal vessel caliber, detect lesions, and even calculate a “retinal age” from a simple, non-invasive photograph.

Potential for Widespread Use: Because retinal imaging is quick, cheap, and non-invasive, it has the potential to become a powerful tool for mass screening. A routine eye exam could one day provide a risk assessment for heart disease, stroke, and overall health, prompting earlier intervention.

The blood vessels in your eyes are far more than just tools for vision. They are a unique and accessible mirror of your body’s circulatory and neurological health. By examining them, doctors and AI can get an early, direct look at the silent damage caused by conditions like hypertension and diabetes, potentially predicting your risk for major heart events and even your rate of biological aging.

Disclaimer: This information is for educational purposes only. While retinal health is an exciting area of predictive medicine, it is not a standalone diagnostic tool. Always consult with your primary care physician and a cardiologist for a comprehensive assessment of your heart disease risk.

This is a fascinating and rapidly advancing area of research. The claim that blood vessels in the eyes can help predict heart disease and biological aging risk is strongly supported by scientific evidence.

Here’s a detailed breakdown of how it works, the science behind it, and what it means for the future.

The Window to Your Health: The Retina

The back of your eye, called the retina, is the only place in the body where doctors can directly and non-invasively view a network of tiny blood vessels (microvasculature) and nerves.

The health of these small vessels is a mirror of the health of similar-sized vessels throughout your body, including in your brain, heart, and kidneys. Damage to these microvessels is often a very early sign of systemic (whole-body) diseases.


1. Predicting Heart Disease (Cardiovascular Risk)

The link between the retina and heart disease primarily revolves around a condition known as Retinopathy.

How it Works:

  • Shared Physiology: The small vessels in your retina are similar in size, structure, and function to the small vessels that supply the heart muscle itself. Factors that damage one are likely to damage the other.
  • The Damage Process: Conditions like high blood pressure (hypertension) and atherosclerosis (clogging of the arteries) don’t just affect large arteries. They also cause:
    • Narrowing (Arteriolosclerosis): The retinal arteries become thicker and narrower.
    • AV Nicking: Where arteries cross over veins, they can compress them, a sign of chronic high blood pressure.
    • Hemorrhages & Microaneurysms: Weakened vessel walls can leak blood or form tiny bulges.
  • What Doctors Look For: An eye doctor (ophthalmologist) or even an AI algorithm analyzing a retinal image can identify these changes. Their presence is classified as Hypertensive Retinopathy or, if related to diabetes, Diabetic Retinopathy.

The Evidence:
Multiple large-scale studies have shown that people with these retinal changes have a significantly higher risk of:

  • Coronary heart disease
  • Heart failure
  • Stroke
  • Death from cardiovascular causes

Essentially, the retina acts as an “early warning system,” showing damage from high blood pressure and vascular disease long before a major cardiac event like a heart attack occurs.


2. Predicting Biological Aging Risk

This is an even more cutting-edge application. The concept is that the condition of your retinal vessels can reveal your “biological age” as opposed to your “chronological age.”

How it Works: Researchers use a metric called the “Retinal Age Gap.”

  1. Training an AI: Scientists train a sophisticated deep-learning algorithm on hundreds of thousands of retinal images from healthy people.
  2. Learning the Pattern: The AI learns what a “healthy” retina looks like at different chronological ages (e.g., age 40, 50, 60). It becomes an expert at predicting someone’s age just from their retinal scan.
  3. Calculating the Gap: The AI then analyzes a new person’s retina and gives a “retinal age” prediction. The difference between this predicted biological age and the person’s actual chronological age is the “Retinal Age Gap.”
    • Example: If the AI says your retina looks like that of a 50-year-old, but you are only 45, you have a +5-year Retinal Age Gap.

What the Research Shows:
A large study published in the British Journal of Ophthalmology found that:

  • A large Retinal Age Gap (e.g., your retina is “older” than you are) is significantly associated with a higher risk of death, particularly from cardiovascular disease.
  • This link remained strong even after accounting for traditional risk factors like age, smoking, and BMI.

Why is this a powerful indicator?
The retina is part of the central nervous system (it’s an extension of the brain). Its health is intimately tied to the overall health of your circulatory system and cellular aging processes. An “older” retina suggests accelerated aging and cumulative damage throughout the body’s vascular and neurological systems.


The Future: AI and Retinal Scans

This research is moving quickly from the lab to the clinic, powered by Artificial Intelligence (AI).

  • Automated Screening: AI can analyze a routine retinal photo in seconds, providing a quantitative and objective assessment of cardiovascular risk and biological age.
  • Accessibility: A quick, non-invasive retinal scan could become a standard part of a general health check-up, not just an eye exam, making advanced risk prediction more accessible.
  • Personalized Medicine: It could help doctors identify high-risk individuals earlier, allowing for more aggressive and personalized preventative strategies (like lifestyle changes and medications).

Limitations and Important Caveats

  1. It’s a Predictor, Not a Crystal Ball: A retinal scan is a powerful risk indicator, but it’s not a definitive diagnosis. It adds to the overall picture alongside blood tests, blood pressure readings, and family history.
  2. Still in Development: While the science is robust, the use of “retinal age” as a clinical tool is still being refined and validated.
  3. Cannot Replace Specific Tests: It won’t tell you your exact cholesterol levels or if a specific artery is blocked. It assesses the health of your microvasculature, which is a proxy for systemic health.

Conclusion

The idea that the blood vessels in your eyes can predict heart disease and biological aging is not science fiction; it’s solid science. Your retina provides a unique, real-time window into the health of your entire circulatory system and the pace of your body’s aging. With the help of AI, this “window” is poised to become a revolutionary tool in preventative medicine, helping people take control of their health long before serious problems arise.

https://www.medicalnewstoday.com/articles/blood-vessels-eyes-predict-heart-disease-biological-aging-risk

https://health.medicaldialogues.in/health-topics/eye-health/eye-scans-may-predict-heart-disease-and-biological-ageing-say-researchers-157448

https://healthsci.mcmaster.ca/aging-in-plain-sight-what-new-research-says-the-eyes-reveal-about-aging-and-cardiovascular-risk

D3 supplements could halve the risk of a second heart attack

D3 supplements could halve the risk of a second heart attack

That’s a very interesting and significant claim, and it’s based on emerging research. Let’s break down what the science currently says about this. The statement that “Vitamin D3 supplements could halve the risk of a second heart attack” is a simplified summary of the findings from a specific, and quite important, clinical trial.

The Key Study: The VITAL Rhythm Trial
The most direct evidence for this claim comes from a sub-study of the large-scale VITAL trial, published in 2020. What was the main VITAL trial? A major study investigating whether vitamin D3 (2000 IU/day) or omega-3 fatty acids could prevent heart attacks, strokes, and cancer in generally healthy adults. The main results were modest.

What did the VITAL Rhythm sub-study find? This part of the trial specifically looked at people who had a previous heart attack. They found that among these participants, those who took vitamin D3 had a significantly lower risk of having a subsequent major cardiovascular event, including a fatal heart attack. The risk reduction was indeed reported to be around 50%.

How Might Vitamin D Help the Heart?
The proposed mechanisms are biologically plausible:

Reducing Inflammation: Chronic inflammation is a key driver of atherosclerosis (hardening of the arteries). Vitamin D has anti-inflammatory properties.

Improving Vascular Function: Vitamin D may help the lining of blood vessels (the endothelium) function better, keeping them flexible and healthy.

Regulating Blood Pressure: It plays a role in the renin-angiotensin system, which helps control blood pressure.

Modulating Immune Response: It may help stabilize arterial plaques, making them less likely to rupture and cause a blockage.

Important Nuances and Caveats
While the findings are promising, it’s crucial to understand the context and limitations:

Not for Primary Prevention: The dramatic benefit was seen only in people who had already experienced a heart attack (this is called “secondary prevention”). For the general population without a history of heart attack, vitamin D supplementation has not shown a clear benefit in preventing a first heart attack.

Correlation is Not Causation (Yet): While this was a randomized controlled trial (the gold standard), more research is needed to confirm these results and firmly establish vitamin D as a standard secondary prevention therapy.

The “Baseline Level” Hypothesis: A leading theory is that the benefit is most pronounced in people who are deficient in vitamin D to begin with. Correcting a deficiency may be what’s driving the benefit, rather than supplementing in people who already have sufficient levels.

Dosage Matters: The study used a high dose (2000 IU/day). This should not be taken without considering one’s baseline levels and consulting a doctor.

Not a Magic Bullet: Vitamin D supplementation is not a substitute for proven heart attack prevention strategies, such as:
Statin medications
Blood pressure control
Aspirin or other antiplatelet drugs (as prescribed)
Smoking cessation
A healthy diet and regular exercise

What Should You Do?
Get Tested: If you have a history of heart disease or have had a heart attack, ask your doctor to check your 25-hydroxyvitamin D blood level. This is the only way to know your status.
Discuss with Your Doctor: Based on your test results and overall health, your doctor can determine if supplementation is right for you and what the appropriate dose would be.

Focus on a Comprehensive Plan: View vitamin D as a potential part of a comprehensive cardiac rehabilitation and prevention plan, not a standalone solution.

In summary, the claim is based on solid, recent research and is up-and-coming for a specific high-risk group, heart attack survivors. However, it is not a recommendation for the general public to start high-dose vitamin D supplementation for heart health, and it should always be implemented under the guidance of a medical professional.

A new randomized trial called TARGET-D (reported at the AHA Scientific Sessions 2025 and in Intermountain Health press materials) found that tailored vitamin D₃ supplementation, adjusting doses to reach and maintain target blood levels (≈40–80 ng/mL), was associated with about a 50% lower risk of a second heart attack in people who recently had a myocardial infarction. The result is promising but preliminary (abstract / press release), and it did not reduce the trial’s composite major-adverse-cardiac-event (MACE) endpoint. More peer-reviewed data are needed before changing practice.

Vitamin D has known effects on inflammation, vascular function, and the renin–angiotensin system; observational studies have linked low vitamin D to worse cardiovascular outcomes. Tailoring doses to achieve a biological target (instead of giving everyone the same pill) is a different strategy from many prior trials.

Past large randomized trials and meta-analyses generally did not find that unselected vitamin D supplementation prevents heart attacks or other major cardiovascular events. The new TARGET-D result is from an abstract/conference presentation and institutional press releases, promising but preliminary until a full peer-reviewed paper appears and the finding is replicated in other trials.

If you’ve had a heart attack, don’t change or start high-dose vitamin D on your own based on news alone. Discuss vitamin D testing and any supplementation with your cardiologist or primary care clinician. If you’ve had a heart attack, don’t change or start high-dose vitamin D on your own based on news alone. Discuss vitamin D testing and any supplementation with your cardiologist or primary care clinician.

The study used monitoring + individualized dosing (some people needed much higher daily intakes than typical OTC doses), so safety monitoring (blood 25-OH-D, calcium) matters if doses are high. Vitamin D toxicity is uncommon but can occur with very large, unmonitored doses.

This is an interesting and potentially important finding: targeted vitamin D₃ supplementation reduced recurrent MI risk in this single trial, but it is not yet definitive. Expect investigators to publish the full results, and for guideline-level changes to require replication and peer review. Until then, vitamin D testing and discussion with your clinician is the prudent route.

https://newsroom.heart.org/news/heart-attack-risk-halved-in-adults-with-heart-disease-taking-tailored-vitamin-d-doses?utm_source=chatgpt.com

https://news.intermountainhealth.org/targeted-vitamin-d3-supplementation-cuts-risk-of-heart-attack-patients-having-a-second-heart-attack-in-half-intermountain-study-shows/?utm_source=chatgpt.com

Long-term melatonin use linked to 90% greater heart failure risk.

Long-term melatonin use linked to 90% greater heart failure risk.

Approximately 16% of people worldwide suffer from insomnia. A person can enhance the quality of their sleep in a variety of ways, including by taking melatonin supplements. Previous research indicates that using melatonin supplements may pose certain risks. According to a recent study, taking melatonin supplements over an extended period of time may increase the risk of heart failure. According to research, 16% of people worldwide suffer from insomnia, which is the inability to fall or stay asleep. A person can enhance the quality of their sleep in a variety of ways. Among them are behavioral adjustments like maintaining proper sleep hygiene, exercising during the day, and avoiding certain foods right before bed. Other individuals who have trouble falling asleep may choose to use medical interventions, such as prescription drugs or over-the-counter remedies like melatonin supplements, a hormone that the body produces naturally and is crucial.

12-month or longer melatonin use linked to 90% greater heart failure risk
Researchers examined medical records from TriNetX for nearly 131,000 adults who had been diagnosed with insomnia, with an average age of roughly 56. Approximately 65,000 study participants reported taking melatonin for at least a year after receiving a prescription for it at least once. According to the study’s findings, individuals who took melatonin for longer than a year had a 90% higher risk of heart failure over five years than those who did not. Additionally, participants had an 82% higher risk of heart failure if they had filled at least two melatonin prescriptions at least ninety days apart. Furthermore, during the five-year follow-up period, researchers found that melatonin users were roughly 3.5 times more likely to be hospitalized for heart failure and twice as likely to die from any cause.

Melatonin supplements are widely thought of as a safe and ‘natural’ option to support better sleep, so it was striking to see such consistent and significant increases in serious health outcomes, even after balancing for many other risk factors, Ekenedilichukwu Nnadi, and lead author of the study, said in a press release. Worse insomnia, depression/anxiety or the use of other sleep-enhancing medicines might be linked to both melatonin use and heart risk. Also, while the association we found raises safety concerns about the widely used supplement, our study cannot prove a direct cause-and-effect relationship. This means more research is needed to test melatonin’s safety for the heart, Nnadi explained

Unexpected findings on melatonin and heart health are noteworthy
Melatonin is widely regarded by both the public and many in the medical community as a safe, ‘natural’ sleep aid, so it was striking to see a potential link to serious health issues like heart failure, Mody explained. While this study shows an association and not a direct cause-and-effect relationship, the consistency and significance of the increased risks are noteworthy. It’s particularly unexpected given that some previous research has suggested potential cardiovascular benefits of melatonin, such as its antioxidant properties.

This new study challenges the conventional wisdom regarding long-term melatonin use for chronic insomnia, for which it is not an indicated treatment in the United States, she continued. According to Mody, these findings suggest a re-evaluation of how we counsel patients about sleep aids and underscore the importance of discussing long-term supplement use. My concern is that insomnia may actually be masking signs and symptoms of early heart failure in some of these cases, so this research also highlights the importance of ruling out different causes of insomnia, particularly since the treatment market for insomnia aids is not strongly regulated.

Further research is needed to confirm the findings
According to Mody, the research’s next steps should concentrate on a number of crucial areas to elucidate the results and their consequences for patient care, such as causality and confirmation. She explained, “First and foremost, more research is needed to confirm these findings and to determine if there is a direct cause-and-effect relationship between long-term melatonin use and heart failure. The best way to determine whether melatonin is safe for the heart would be to conduct randomized controlled trials. Research will need to investigate the biological mechanism by which long-term melatonin use might increase the risk of heart failure if a causal link is established, Mody continued. Given that melatonin has been shown to have protective effects on the cardiovascular system, this would be a major change

How can I improve my sleep without taking melatonin?
Melatonin is available in a variety of formulations, including high and low doses, as well as slow and immediate release, none of which are FDA regulated, according to Ni’s initial response to the study. Therefore, there are worries that the levels of melatonin drugs and supplements may differ significantly. It is difficult to determine whether a particular amount or kind of melatonin is linked to an increase in heart failure.

However, considering that melatonin is not subject to FDA regulation, the study is undoubtedly concerning, he said. Ni strongly suggests that people who may be taking melatonin think about other ways to enhance the quality of their sleep. He clarified, for instance, that a lot of people have sleep apnea but are unaware of it and mistakenly believe that they just need to take a sleep aid to help them sleep. Given that sleep apnea is linked to an increased risk of heart disease, melatonin users in the study may have sleep issues.

I should also mention that melatonin and high dosages seem to have a paradoxical effect on sleep; that is, taking too much melatonin may actually make it difficult for you to fall asleep. I typically advise my patients to take no more than 1 to 3 mg of melatonin per night. Additionally, I tell my patients that because the melatonin hormone’s effect on sleepiness is gradual, it usually needs to be taken at least an hour or two before attempting to fall asleep.

https://www.medicalnewstoday.com/articles/long-term-melatonin-use-linked-to-90-greater-heart-failure-risk

https://mygenericpharmacy.com/category/disease/sleep-disorder

High levels of heart damage biomarker may signal increased dementia risk.

High levels of heart damage biomarker may signal increased dementia risk.

Recent research suggests that higher levels of certain heart-damage biomarkers may signal an increased risk of developing dementia later in life. I’ll walk you through what has been found, what it might mean, and what we don’t yet know. A large long-term study found that people aged approximately 45-69 who had higher mid-life levels of the cardiac biomarker High‑sensitivity cardiac troponin I (hs-troponin I), which signals subtle heart muscle injury, had a significantly higher risk of being diagnosed with dementia decades later.

Specifically, those with the highest troponin levels had about a 38% higher risk of dementia compared with the lowest troponin group. The elevated troponin levels showed up 7 to 25 years before the dementia diagnosis. In a subset of participants with brain MRI, higher troponin levels were associated with smaller hippocampal volume and less grey matter brain changes consistent with aging/degeneration.

More broadly, a review article notes that several cardiac biomarkers, including troponins, N‑terminal pro­ B‑type natriuretic peptide (NT-proBNP, a marker of cardiac/ventricular stress), and Growth‑differentiation factor 15 (GDF15, a marker of vascular stress), are associated with cognitive impairment or brain changes even in people without overt heart disease. A meta-analysis of coronary heart disease (CHD) found that people with CHD have a higher odds (~1.45 times) of developing cognitive impairment or dementia compared to those without CHD.

What it might mean — possible mechanisms
Here are some ways in which subtle heart damage / cardiovascular dysfunction might contribute to brain aging and dementia risk:
Reduced cerebral perfusion / heart-brain blood flow link: If the heart muscle is damaged (even subtly), cardiac output or the efficiency of circulation might decline, which could impair blood flow to the brain over the years. The brain is highly sensitive to its blood supply.

Vascular damage and micro-injuries: Biomarkers of cardiac injury or stress also correlate with vascular stress. This may manifest in the brain as white matter changes, microinfarcts, or reduced brain tissue volume (as found in the MRI subset).

Shared risk factors: Many heart injury markers are elevated in the presence of high blood pressure, diabetes, high cholesterol, obesity, smoking, etc. These risk factors also contribute to dementia. So part of the association may be explained by overlapping risk pathways.

Early warning / silent damage: The troponin elevations in the study were associated with “subclinical” heart damage (i.e., no overt symptomatic heart disease at baseline). That suggests damage begins much earlier than clinical diagnoses and may set the stage for brain aging for decades.

What we don’t yet caution:
These findings are observational in nature. That means we can’t yet say the elevated troponin caused the dementia, only that there’s an association. Indeed, the Mendelian-randomisation study found little evidence for a causal effect of genetically elevated cardiac biomarkers on dementia risk.

Exactly what threshold of troponin (or other biomarkers) is meaningful, and at what ages, is not yet firmly established. While plausible pathways exist (blood flow, microvascular injury, overlap of cardiovascular & cerebrovascular disease), the precise chain of events linking heart damage → brain injury → dementia remains under investigation.

Many of the studies focus on specific cohorts (e.g., the Whitehall II Study in the UK) and mostly middle-aged adults initially without heart disease. Whether the same associations hold in other populations, ethnicities, or older age groups is still being defined. If elevated cardiac biomarker levels identify a higher risk of dementia, we don’t yet have solid evidence that intervening specifically based on these biomarker levels (e.g., in addition to standard cardiovascular care) will reduce dementia risk.

Implications for health & prevention:
Mid-life heart health appears increasingly important for brain health in later life. What happens to the heart, vessels, and circulation may matter for the brain decades later. Monitoring cardiovascular risk factors (blood pressure, lipids, diabetes, smoking, obesity, physical activity) remains very important because these are modifiable and already known to influence dementia risk.

The idea of using cardiac biomarkers (like troponin) as part of a dementia risk assessment is emerging but not yet ready for routine clinical use solely for that purpose. For individuals, focusing on good cardiovascular health is also brain-health care. Eat healthy, exercise, manage weight/diabetes/hypertension, avoid smoking, and keep cholesterol/lipids in check. For clinicians/researchers: These findings may guide future work on early identification of who is at risk, and possibly on targeting brain-protective interventions earlier in those with evidence of silent cardiovascular damage.

Elevated levels of cardiac injury biomarkers (especially high-sensitivity troponin) measured in mid-life are associated with an increased risk of dementia many years later, potentially reflecting that silent heart damage is setting the stage for brain aging/neurovascular injury. While this doesn’t prove causation, it strengthens the notion that the heart-brain connection is significant and that protecting cardiovascular health may help reduce dementia risk. If you like, I can pull up the full study details (sample size, follow-up years, exact biomarker levels, cognitive outcomes) and we can discuss how strong the evidence is and what it might mean for clinical practice. Would you like that?

Additionally, scientists discovered that study participants with high levels of troponin between the ages of 45 and 69 experienced a quicker decline in their memory, thinking, and problem-solving abilities. These participants also tended to have a smaller hippocampus and lower gray matterTrusted Source brain volume, both of which are signs of dementia. Poor heart health in middle age puts people at increased risk of dementia in later life,

Damage to the brain seen in people with dementia accumulates slowly over the decades before symptoms develop. Control of risk factors common to both heart disease, stroke, and dementia in middle age, such as high blood pressure, may slow or even stop the development of dementia as well as cardiovascular disease. We now need to carry out studies to investigate how well troponin levels in the blood can predict future dementia risk. Our early results suggest that troponin could become an important component of a risk score to predict the future probability of dementia.

https://www.medicalnewstoday.com/articles/high-levels-troponin-heart-damage-biomarker-middle-age-increased-dementia-risk