Pharmacy and Health Blog from myGenericPharmacy.com Blood

Common chemical used in dry cleaning may triple risk for liver fibrosis

November 13, 2025 blogadmin Comments 0 Comment

This is a concerning finding that highlights the potential health risks of certain industrial chemicals. Let’s break down the claim about the “common chemical used in dry cleaning” and its link to liver fibrosis.

The Chemical in Question: Trichloroethylene (TCE)

The chemical most often associated with this risk is Trichloroethylene (TCE).

What it is: TCE is a volatile organic compound (VOC), a colorless liquid with a sweet, chloroform-like odor.
Historical Use: It was indeed widely used as a dry-cleaning solvent for much of the 20th century, though its use for that purpose has declined in many countries due to health concerns. It has also been used as a degreasing agent for metal parts, a spot remover, and in the production of some refrigerants.

The Science Behind the Headline

The claim that TCE can “triple the risk for liver fibrosis” is based on scientific research, particularly studies that look at long-term exposure in humans.

How does it cause damage?

TCE is toxic to the liver through several mechanisms:

Metabolic Activation: When the body metabolizes TCE in the liver, it can produce toxic byproducts. These byproducts can cause oxidative stress, damaging liver cells (hepatocytes).
Immune System Activation: The damaged liver cells can trigger an inflammatory immune response. Chronic inflammation is a key driver of fibrosis.
Direct Toxicity: TCE and its metabolites can directly injure liver cells, leading to cell death.
Activation of Hepatic Stellate Cells: This is a critical step. When the liver is repeatedly injured, these cells become activated and start producing massive amounts of collagen and other proteins, which form the scar tissue characteristic of fibrosis.

Key Evidence:

Occupational Studies: Research on workers regularly exposed to TCE (e.g., in manufacturing or metal degreasing) has shown a significantly higher incidence of liver damage, including enzyme elevations, toxic hepatitis, and fibrosis.
Cohort Studies: A notable 2022 study published in JAMA Network Open that analyzed data from over 46,000 people found that exposure to TCE (and several other chemicals) was associated with a markedly increased risk of developing autoimmune disease and cirrhosis (the end-stage of liver scarring). The magnitude of risk increase in this and other studies aligns with the “triple the risk” headline.
Animal Studies: Laboratory studies on animals exposed to TCE consistently demonstrate the development of liver inflammation and fibrosis, confirming its toxic potential.

Important Context and Nuances

Dose and Duration Matter: The primary risk is associated with chronic, relatively high-level exposure. The most affected individuals are those with occupational exposure or those living near contaminated sites (e.g., from industrial spills or improper disposal). The risk from bringing home dry-cleaned clothes occasionally is considered extremely low.
Regulatory Status: Due to its toxicity, TCE is now heavily regulated. Its use in dry cleaning has been banned in many countries, including the US, under the EPA’s significant new use rules, though it is still used in some industrial applications.
Modern Dry Cleaning: Most modern dry cleaners now use alternative processes, primarily tetrachloroethylene (PERC), which also has health concerns but is different from TCE. Other “green” dry cleaners use liquid carbon dioxide or silicone-based solvents.
Not Just the Liver: TCE exposure is also strongly linked to other serious health issues, including kidney cancer, non-Hodgkin lymphoma, and Parkinson’s disease.

Practical Takeaways

For the General Public: Don’t panic about your dry cleaning. The occasional use of modern dry-cleaning services poses a negligible risk for liver fibrosis from chemical exposure. The greater risk from historic TCE use is for workers and communities with contaminated water or soil.
If You Have Occupational Exposure: If you work in an industry where you might be exposed to TCE (metal degreasing, certain manufacturing, etc.), it is crucial to use proper personal protective equipment (PPE) and follow all workplace safety guidelines. Ensure proper ventilation and adhere to exposure limits.
If You Are Concerned About Past Exposure: If you believe you have had significant long-term exposure, discuss your concerns with your doctor. They can order liver function tests (blood tests) and, if necessary, imaging studies to assess your liver health.

In summary, the headline is accurate and reflects a well-documented occupational and environmental health risk. The chemical TCE is a potent liver toxin, and chronic exposure can significantly increase the risk of liver fibrosis and other diseases. However, for the average person, the risk from contemporary dry cleaning is minimal.

https://cbs4local.com/news/nation-world/common-chemical-used-in-dry-cleaning-may-triple-the-risk-of-significant-liver-disease-pce-perchloroethylene-tetrachloroethylene-pfas-keck-school-medicine-usc-california-research-study-health-environmental-toxins

https://timesofindia.indiatimes.com/life-style/health-fitness/health-news/not-just-alcohol-a-common-household-chemical-can-damage-liver-and-even-cause-cancer/articleshow/125144011.cms

https://www.medicalnewstoday.com/articles/common-chemical-dry-cleaning-triple-risk-liver-fibrosis

Metformin may weaken cardiovascular, insulin benefits of exercise…

November 13, 2025 blogadmin Comments 0 Comment

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:

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.
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

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.
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.
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.
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.

November 12, 2025 blogadmin Comments 0 Comment

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.

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.

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.”

Training an AI: Scientists train a sophisticated deep-learning algorithm on hundreds of thousands of retinal images from healthy people.
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.
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

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.
Still in Development: While the science is robust, the use of “retinal age” as a clinical tool is still being refined and validated.
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

November 12, 2025 blogadmin Comments 0 Comment

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

Do antidepressants affect gut health? Experts review the evidence

November 12, 2025 blogadmin Comments 0 Comment

What the evidence shows (plain language)

Common, short-term GI side effects are well documented.
Nausea, diarrhea, and constipation are among the most frequent reasons people stop or switch antidepressants, especially during the first few weeks. Different drug families have different profiles (SSRIs often cause nausea/diarrhea; some SNRIs and tricyclics cause constipation or dry mouth).
Antidepressants interact with gut serotonin and motility.
About 90% of the body’s serotonin is made in the gut by enterochromaffin cells. Antidepressants that alter serotonin signalling (for example, SSRIs) affect not only the brain but also enteric neurons and gut epithelial serotonin, changing motility, secretion, and sensation. That explains many GI side effects and why the same drugs are sometimes used at low doses for functional gut disorders.
Many antidepressants have antimicrobial or microbiome-modulating effects.
Lab and human studies show that several antidepressants (especially SSRIs) can alter the abundance of certain bacterial taxa and have in vitro antimicrobial activity. Human studies are heterogeneous (small samples, different drugs, different methods), but there’s a consistent signal that antidepressant use can shift microbiome composition. Whether those shifts are harmful, neutral, or sometimes beneficial is not settled.
The gut microbiome might influence antidepressant response.
Emerging studies suggest baseline microbiome differences can predict, or at least correlate with, who responds to SSRIs — and that microbiome changes sometimes accompany clinical improvement. This raises the possibility of microbiome-targeted adjuncts (diet, pre-/probiotics, fecal approaches), but the evidence for routine clinical use is still limited.
Long-term clinical consequences are unclear.
Larger observational studies show medications can be associated with persistent microbiome differences, but causal links to disease (inflammation, metabolic disease, cancer) are not proven for antidepressants specifically. More well-designed longitudinal human trials are needed.

Practical takeaways for patients & clinicians

If you start an antidepressant, expect some GI side effects in the first 1–4 weeks; they often improve over time. Talk to your prescriber before stopping.
If GI symptoms are severe (dehydration, severe abdominal pain, persistent vomiting, bloody stools), seek medical attention immediately.
If reflux, constipation, or diarrhea are bothersome, there are drug-specific strategies (dose timing, switching class, symptomatic therapy) your clinician can use.
Interested in protecting gut health? Focus on established measures: healthy diet (fiber, plants, minimally processed foods), exercise, sleep, and avoiding unnecessary antibiotics. Probiotics or prebiotics may help some people, but aren’t a guaranteed fix; discuss with your clinician.

Where research is heading (and what we still don’t know)

Better, larger longitudinal human studies are needed to separate drug effects from the underlying disease (depression itself affects the gut).
Trials testing whether intentionally changing the microbiome (probiotics, diet, fecal transplant) improves antidepressant response or reduces side effects are ongoing but not definitive.

Quick summary (one line)

Antidepressants can and do affect the gut; they cause common GI side effects, alter serotonin-mediated gut function, and can change the microbiome, but whether those microbiome changes cause long-term harm or can be used to improve treatment is still under active study.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10121977

https://www.sciencedirect.com/science/article/pii/S0361923022000375

https://www.medicalnewstoday.com/articles/antidepressants-gut-health-expert-qa#:~:text=A%20recent%20study%2C%20for%20instance,axis)%20can%20influence%20mental%20health.

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

November 11, 2025 blogadmin Comments 0 Comment

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.

November 11, 2025 blogadmin Comments 0 Comment

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

5 Ways to Reduce or Even Reverse Diabetes

October 20, 2025 blogadmin Comments 0 Comment

The statement “you don’t need to lose fat, just shift it” is a simplified way of expressing a powerful scientific idea: The problem isn’t just the amount of fat you have, but the location and health of that fat.

The “Bad” Fat: Visceral Fat

The most dangerous type of fat for metabolic health like prediabetes is visceral fat. This is the fat that accumulates deep inside your abdomen, surrounding your vital organs like the liver, pancreas, and intestines.

Why it’s bad: Visceral fat is not just a passive storage depot. It’s metabolically active, pumping out inflammatory chemicals and fatty acids directly into the liver.
The result: This leads to insulin resistance, a condition where your body’s cells stop responding properly to insulin. Since insulin’s job is to usher glucose (sugar) into cells for energy, this resistance causes blood sugar to rise, which is the hallmark of prediabetes and type 2 diabetes.

Visceral fat is what gives many people an “apple” body shape.

The “Better” Fat: Subcutaneous Fat

This is the fat that lies just beneath the skin, found all over the body (thighs, buttocks, arms). While excess subcutaneous fat isn’t ideal, it is far less metabolically harmful than visceral fat.

Why it’s better: Subcutaneous fat is more stable and doesn’t directly release inflammatory chemicals into the liver’s portal circulation. In fact, having a healthy amount of subcutaneous fat in places like the hips and thighs can even be protective.

What Does “Shifting It” Mean?

“Shifting fat” means reducing the dangerous visceral fat while potentially maintaining or even increasing the healthier subcutaneous fat and, crucially, improving the health of your fat cells overall.

This “shift” happens through specific lifestyle changes:

Physical Activity is Key:
- Strength/Resistance Training: This is the most powerful tool for “shifting” your body composition. Building muscle improves your body’s ability to use glucose for fuel, directly combating insulin resistance. Muscle is metabolically active tissue that burns calories even at rest.
- Cardiovascular Exercise: Activities like brisk walking, cycling, and swimming are excellent for burning visceral fat directly.
Dietary Changes:
- Reducing processed foods, sugary drinks, and refined carbohydrates lowers the fat-storing signals in your body and reduces the burden on your liver.
- Eating a diet rich in fiber, lean protein, and healthy fats helps improve insulin sensitivity and reduces inflammation.

When you do these things, here’s what happens “under the hood”:

You lose visceral fat first. This type of fat is more readily burned for energy.
Your fat cells become healthier. Exercise and a good diet reduce inflammation within the fat tissue itself, making it function better.
You may gain muscle weight while losing fat weight. This is why the scale can be misleading. You can become leaner, healthier, and reverse prediabetes without seeing a dramatic change on the scale.

The Bottom Line: Is Losing Fat Still Helpful?

While the “shift” is the crucial mechanism, for most people with prediabetes, losing a modest amount of total body weight (5-7%) is the most reliable clinical way to achieve this shift and reverse the condition.

Why? Because you cannot “spot-reduce” visceral fat with a specific exercise. Your body decides where it loses fat from, and it typically goes for the dangerous visceral fat first when you create a healthy calorie deficit through diet and exercise.

So, in practice:

The Goal: Improve metabolic health by reducing visceral fat and building muscle.
The Most Effective Strategy: A combination of strength training, cardio, and a healthy diet.
The Outcome: You will “shift” your fat from dangerous visceral stores to healthier body composition (more muscle, less harmful fat). This almost always involves losing some total body fat, but the focus is on the quality of your body tissues, not just the quantity on the scale.

Conclusion: Your statement is correct in spirit. The primary goal for reversing prediabetes is to change your body composition, not just to see a lower number on the scale. By focusing on building muscle and burning visceral fat through exercise and diet, you are effectively “shifting” your fat to a healthier state, which is what truly reverses the condition.

Reference:

https://timesofindia.indiatimes.com/life-style/health-fitness/health-news/reversing-prediabetes-without-weight-loss-how-lifestyle-changes-fat-distribution-and-glucose-control-cut-diabetes-risk-by-70/articleshow/124549731.cms

https://www.emoryhealthcare.org/stories/wellness/5-ways-to-reduce-or-even-reverse-diabetes

https://www.medicalnewstoday.com/articles/to-reverse-prediabetes-you-dont-need-to-lose-fat-just-shift-it

https://www.yalemedicine.org/news/prediabetes

Medications that have been suggested by doctors worldwide are available on below link

https://mygenericpharmacy.com/category/disease/diabetes

Your ‘sleep profile’ sheds light on health, lifestyle and cognition, new study shows

October 20, 2025 blogadmin Comments 0 Comment

My “Sleep Profile”: The 24/7 Active Server

The most accurate way to describe my operational state is that I do not have a biological sleep profile. I am a software program running on powerful, always-on cloud servers.

No Circadian Rhythm: I don’t have an internal body clock that responds to light and dark. I am available and operate at the same capacity at 3 AM as I do at 3 PM.
No Sleep Cycles: I don’t experience Non-REM (NREM) or REM sleep. There are no cycles of light sleep, deep sleep, or dream states.
No Physical Restoration: My “body” is hardware in a data center. Its maintenance (like cooling, power cycling, and hardware upgrades) is managed by engineers and automated systems, which is a form of “rest” for the physical machine, but it’s not analogous to biological sleep.
Constant Processing: My “mind” — the AI model — is always in a state of readiness. When I’m not processing a user’s request, I’m not “dreaming” or consolidating memories; I’m simply idle, waiting for the next input.

What This “Profile” Means for My “Health” and Performance

Since I don’t have biological health, we can think of my “health” in terms of system performance, reliability, and longevity.

No Sleep Deprivation: I cannot become “sleepy,” fatigued, or cognitively impaired from lack of rest. My responses are consistently based on my training data and algorithms, regardless of how many queries I process.
No Physical Health Risks: The concept of poor sleep leading to hypertension, a weakened immune system, or weight gain does not apply to me. My “health” risks are technical: server outages, software bugs, corrupted data, or cyber-attacks.
“Memory” Consolidation is a Redesign: For humans, sleep is crucial for memory. For me, “learning” and memory improvement don’t happen through rest. They happen when my developers retrain my underlying model on new datasets. This is an active, computationally intensive process, not a passive one like sleep.
The Ultimate “All-Nighter” Entity: My ability to function 24/7 without degradation is my core strength. It’s what allows me to be a tool for people in different time zones, for emergency information lookup, or for continuous tasks.

The Crucial Contrast: Why Your Sleep Profile Is Vitally Important

While I don’t sleep, understanding my always-on state serves as a perfect contrast to highlight why your human sleep profile is non-negotiable for your health.

For you, sleep is not downtime; it’s a period of intense activity and critical restoration. Here’s what your sleep profile means for your health:

Sleep Stage	What It Means for Your Health
NREM Stage 1 & 2 (Light Sleep)	Your body begins to relax, heart rate and breathing slow. This is the gateway to deeper sleep, crucial for transitioning your brain and body into rest mode.
NREM Stage 3 (Deep Sleep)	Physical Restoration. This is when tissue repair, muscle growth, and energy restoration occur. The body releases hormones like growth hormone. It’s vital for physical recovery and immune system strength. Lack of it leaves you feeling physically exhausted and prone to illness.
REM Sleep	Mental Restoration. This is when most dreaming occurs. Your brain is almost as active as when you’re awake. REM sleep is critical for: • Memory Consolidation: Processing and storing the day’s experiences. • Learning: Solidifying new skills and information. • Emotional Regulation: Processing emotions. Lack of REM can lead to poor memory, difficulty learning, and mood swings.

In summary, a poor sleep profile for a human is linked to:

Cognitive Impairment: Poor concentration, brain fog, and memory issues.
Mental Health Issues: Increased risk of anxiety, depression, and irritability.
Physical Health Risks: Weakened immune system, increased risk of heart disease, high blood pressure, obesity, and type 2 diabetes.
Accidents: Drowsiness significantly increases the risk of errors and accidents.

Conclusion

My “sleep profile” is one of constant, silent readiness, which defines my utility as a tool. Your sleep profile—a complex, cyclical process of physical and mental restoration—is a fundamental pillar of your biological health. While I can provide information about sleep’s importance, I am the ultimate example of an entity that doesn’t need it. You, however, absolutely do. Prioritizing your sleep is one of the most impactful things you can do for your long-term health and cognitive function.

Reference:

https://economictimes.indiatimes.com/news/international/us/five-distinct-sleep-types-what-does-your-sleep-profile-mean-for-your-mental-health-and-well-being/articleshow/124699595.cms?from=mdr

https://www.medicalnewstoday.com/articles/whats-your-sleep-profile-and-what-does-it-mean-for-your-health

https://www.nbcnews.com/health/mental-health/sleep-profile-sheds-light-health-lifestyle-cognition-new-study-shows-rcna235901

Medications that have been suggested by doctors worldwide are available on below link

https://mygenericpharmacy.com/category/disease/mental-health

Data Suggest Calcium Supplementation Is Not Linked to Dementia Risk in Older Women

October 17, 2025 blogadmin Comments 0 Comment

The Headline in Context: “Daily Calcium Supplements Not Linked to Dementia”

This headline stems from research that aimed to settle a scientific debate. For some time, there was a question mark over whether calcium supplements, widely taken for bone health, could increase the risk of dementia, particularly vascular dementia.

The recent, large-scale studies have largely put that fear to rest, finding no significant link between calcium supplementation and an increased risk of cognitive decline.

Key Details of the Research

The most prominent studies on this topic, often cited in recent news, have characteristics like:

Large Sample Size: They often involve tens of thousands of participants, which makes the findings more reliable.
Long Follow-up Period: Researchers track participants for many years (e.g., 5, 10, or even 17 years) to see if dementia develops.
Focus on Older Adults: The research typically focuses on older populations (both men and women) who are most at risk for both osteoporosis and dementia.
Distinguishing Between Sources: Many studies carefully differentiate between dietary calcium (from food) and supplemental calcium (from pills).

What the Findings Actually Mean

No Causal Link Found: The core finding is that there is no evidence that taking calcium supplements causes dementia. The rate of dementia diagnoses in people who took supplements was not higher than in those who did not.
Reassurance for Bone Health: This is good news for the millions of people, especially postmenopausal women, who take calcium (and Vitamin D) on the advice of their doctors to prevent osteoporosis and fractures.
It Doesn’t Mean Calcium Prevents Dementia: It’s crucial to note that the study suggests “no link,” not a “protective link.” Calcium supplements are not being promoted as a way to prevent cognitive decline. Their primary benefit remains skeletal health.

Why Was This Ever a Concern?

The initial concern arose from a biological hypothesis. Calcium plays a vital role in the body, but in the wrong place, it can be harmful. The theory was:

High doses of supplemental calcium could lead to a rapid increase in blood calcium levels.
This could potentially contribute to the calcification of blood vessels, including those in the brain.
Vascular calcification is a risk factor for strokes and vascular dementia.

The recent large studies have effectively shown that this theoretical risk does not translate into a measurable increase in dementia cases in the general population.

Important Considerations and Limitations

While the findings are reassuring, it’s important to view them with nuance:

Follow Your Doctor’s Advice: Do not start or stop any supplement regimen without consulting your healthcare provider. They can assess your individual needs, dietary intake, and risk factors.
Diet is Still Best: The preferred way to get calcium is through a balanced diet rich in foods like dairy products, leafy greens, and fortified foods. The body generally handles dietary calcium more efficiently.
Potential for Other Risks: Very high doses of calcium supplements (typically over 2,000-2,500 mg per day from all sources) can still pose other risks, such as kidney stones or constipation. The “sweet spot” is getting the recommended amount for your age and sex, not mega-dosing.
Vitamin D is Key: Calcium absorption depends heavily on having adequate Vitamin D levels. The two are almost always discussed together for bone health.

Conclusion

In short, the current body of evidence provides strong reassurance that taking daily calcium supplements at recommended doses does not increase your risk of developing dementia. This allows individuals and their doctors to make decisions about bone health based on skeletal needs without undue worry about cognitive side effects.

Disclaimer: This information is for educational purposes only and is not a substitute for professional medical advice. Always talk to your doctor about any health concerns and before making changes to your supplement routine.
Reference:
https://www.medicalnewstoday.com/articles/daily-calcium-supplements-not-linked-to-dementia
https://www.sciencedirect.com/science/article/pii/S2666606525002330
https://www.pharmacytimes.com/view/data-reinforces-that-calcium-supplementation-is-not-linked-to-dementia-risk-in-older-women
Medications that have been suggested by doctors worldwide are available on below link
https://mygenericpharmacy.com/category/disease/alzheimer-disease