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FDA approves donanemab to treat early Alzheimer’s: What experts think

FDA approves donanemab to treat early Alzheimer’s: What experts think

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The FDA’s approval of donanemab (to be marketed under the brand name Kisunla) is a landmark event in the treatment of Alzheimer’s disease. Here is a comprehensive breakdown of what the experts are saying, reflecting the consensus, the hope, and the caution.

The Headline: A New Era of Treatment

The FDA has approved donanemab, a monoclonal antibody therapy, for the treatment of early symptomatic Alzheimer’s disease. This includes patients with mild cognitive impairment (MCI) or mild dementia stages of the disease, who have a confirmed presence of amyloid plaques in the brain.

Donanemab joins lecanemab (Leqembi) as the second drug in its class to be fully approved in the U.S. that changes the underlying course of the disease by clearing amyloid.

What the Experts Are Saying: A Spectrum of Opinions

The expert reaction is broadly positive but nuanced, characterized by “cautious optimism.” Here’s a breakdown of their key points:

1. The Hopeful and Encouraged View: “A Turning Point”

  • It validates the Amyloid Hypothesis: For decades, the theory that clearing amyloid-beta plaques could slow Alzheimer’s was just that—a theory. The success of donanemab and lecanemab proves that targeting amyloid is a viable therapeutic strategy. Experts see this as a definitive turning point after many past failures.
  • Meaningful Slowing of Decline: In the pivotal clinical trial, donanemab demonstrated a significant slowing of clinical decline by about 35% over 18 months compared to a placebo. For patients and families, this translates to more time to live independently, participate in family events, and manage personal finances.
  • A Dosing Endpoint: A unique and patient-friendly feature of donanemab is that treatment can be stopped once a patient’s amyloid plaques are reduced to a very low level. This “treat-to-clear” protocol means patients aren’t necessarily on the drug for life, potentially reducing long-term costs and side effects.

Expert Quote (Representative): “This is the decade where we go from theory to practice. We now have tools that can meaningfully change the trajectory of this disease. It’s not a cure, but it’s the most important breakthrough we’ve ever had.” – Dr. Ronald Petersen, Director of the Mayo Clinic Alzheimer’s Disease Research Center.

2. The Cautious and Pragmatic View: “A Step, Not a Finish Line”

  • Significant Risks and Side Effects: The most serious side effects are Amyloid-Related Imaging Abnormalities (ARIA). ARIA can manifest as brain swelling (ARIA-E) or micro-bleeds (ARIA-H). While often asymptomatic and detectable only on MRI, it can be serious and, in rare cases, fatal. Expert consensus is that these risks must be carefully managed.
  • Modest Benefit for a High Cost: The 35% slowing is statistically significant, but experts caution that the absolute benefit for an individual patient may feel modest. They weigh this against the very high cost of the drug (Eli Lilly has set a list price of $32,000 per year for donanemab, similar to Leqembi) and the extensive healthcare infrastructure required.
  • The Infrastructure Challenge: Administering these drugs is not simple. It requires:
    • Accurate Early Diagnosis: Confirming early Alzheimer’s with PET scans or cerebrospinal fluid tests.
    • Genetic Testing: For ApoE ε4 status, as carriers have a higher risk of ARIA.
    • Specialized Infusion Centers: For monthly IV treatments.
    • Frequent MRI Monitoring: To check for ARIA.
      Many healthcare systems, especially in rural or underserved areas, are not yet equipped for this.

Expert Quote (Representative): “This is a qualified victory. The benefit is real but incremental, and the risks are substantial. The challenge now is to build a system that can deliver these drugs safely, equitably, and only to those who are likely to benefit.” – Dr. Jason Karlawish, Co-Director of the Penn Memory Center.

3. The Future-Oriented View: “A Foundation to Build Upon”

  • Combination Therapies are the Future: Experts see donanemab not as the end, but as a foundational treatment. The next logical step is to combine amyloid-clearing drugs with therapies that target tau (the other key Alzheimer’s protein) and drugs that protect nerve cells. Donanemab is the “first piece of the puzzle.”
  • Earlier Intervention is Key: The trials show that the earlier you treat, the greater the benefit. This is fueling a massive push for better, cheaper, and more accessible blood tests (e.g., p-tau217) to identify at-risk individuals long before significant symptoms appear.
  • Prevention on the Horizon: The ultimate goal is to use these drugs in the pre-symptomatic stage to prevent the disease altogether. Trials are already underway in this direction.

Expert Quote (Representative): “Donanemab is a critical proof-of-concept. It tells us we’re on the right path. Now, we need to build on this success by targeting other aspects of the disease and moving treatment earlier, ultimately aiming for prevention.” – Dr. Reisa Sperling, Director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital.

Connecting Back to the Predictive Tool

This approval makes the predictive tool for Alzheimer’s risk mentioned in the previous article even more relevant.

  • Early Identification is Everything: With an effective treatment now available, identifying people at high risk for memory decline before it becomes significant is crucial. The predictive tool (using APOE, MMSE, and subjective complaints) could be a first-line, low-cost method to flag individuals who should then undergo more definitive testing (amyloid PET or blood tests) to see if they are candidates for donanemab.
  • A Pathway to Treatment: The workflow becomes: Risk Calculator -> Confirmatory Amyloid Test -> Donanemab Treatment. This creates a proactive pathway from risk assessment to intervention.

Conclusion: A Watershed Moment with Work Ahead

The consensus among experts is clear: The FDA’s approval of donanemab is a watershed moment for the Alzheimer’s field. It provides a new, effective treatment option that meaningfully slows the disease.

However, it comes with significant challenges regarding safety, cost, and healthcare delivery. The excitement is tempered by a sober understanding of the work required to integrate this therapy into real-world practice. For patients and families, it represents a new, tangible hope—a chance to buy more quality time in the early stages of a devastating disease.

Reference:
https://www.fda.gov/drugs/news-events-human-drugs/fda-approves-treatment-adults-alzheimers-disease
https://www.medicalnewstoday.com/articles/fda-approves-alzheimers-drug-donanemab
https://www.alz.org/alzheimers-dementia/treatments/donanemab
https://www.neurologylive.com/view/eli-lilly-anti-amyloid-therapy-donanemab-gains-eu-approval-alzheimer-disease

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

New tool predicts future Alzheimer’s-related memory risk based on 3 factors

New tool predicts future Alzheimer’s-related memory risk based on 3 factors

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The Headline: A New, Accessible Risk Calculator

Researchers have developed a new, relatively simple tool that can estimate an individual’s risk of developing memory and thinking problems related to Alzheimer’s disease in the future. Unlike expensive or invasive tests like PET scans or spinal taps, this tool uses easily obtainable information, making it a potential game-changer for primary care and public health.

The tool is often referred to as a risk stratification model or cognitive impairment risk calculator.

The 3 Key Factors

The predictive power of the tool comes from a combination of three primary factors. While the exact weighting in the algorithm is complex, these are the core elements:

  1. A Specific Genetic Marker: APOE-e4 Allele
    • What it is: The APOE gene comes in several forms, and the APOE-e4 variant is the strongest known genetic risk factor for late-onset Alzheimer’s disease.
    • How it’s measured: Through a simple blood or saliva test (like a direct-to-consumer DNA kit). Inheriting one copy of e4 from a parent increases risk; having two copies increases it significantly.
    • Why it matters: This factor provides a baseline biological risk that the other factors can amplify or moderate.
  2. A Memory Test Score: The Mini-Mental State Examination (MMSE)
    • What it is: A brief, 30-point questionnaire used extensively in clinical and research settings to screen for cognitive impairment. It tests orientation, memory, attention, and language.
    • How it’s measured: Administered by a healthcare professional in about 10 minutes.
    • Why it matters: It provides a snapshot of current cognitive function. A lower score, even within the “normal” range, can indicate the very earliest, subtle signs of decline.
  3. Subjective Memory Complaints
    • What it is: The individual’s own perception that their memory or thinking skills have declined. This isn’t about occasionally misplacing keys, but a persistent, noticeable change confirmed by the person or a close family member.
    • How it’s measured: Through a standardized interview or questionnaire.
    • Why it matters: A person’s subjective experience of their own cognitive decline is a powerful predictor. It often precedes measurable deficits on objective tests and can indicate early brain changes.

How the Tool Was Developed and Works

  • The Data Source: Researchers built this model by analyzing data from large, long-term studies of older adults (e.g., the Alzheimer’s Disease Neuroimaging Initiative – ADNI). They tracked thousands of people with normal cognition, noting who developed Mild Cognitive Impairment (MCI) or Alzheimer’s dementia over time.
  • The Algorithm: Using machine learning, they identified which combination of factors at the study’s start most accurately predicted who would later develop cognitive problems. The interplay of the genetic risk (APOE-e4), a slightly lower current test score (MMSE), and the presence of subjective complaints proved to be a highly predictive triad.
  • The Output: The tool generates a percentage or a risk category (e.g., low, medium, high) for the likelihood of developing memory issues within a specific timeframe, such as the next 2-5 years.

Significance and Potential Benefits

  1. Early Identification: It can flag at-risk individuals long before significant symptoms appear, moving towards a model of prevention rather than reaction.
  2. Accessibility and Cost-Effectiveness: It uses simple, low-cost measures, making it feasible for use in a primary care doctor’s office.
  3. Enrolling the Right People in Clinical Trials: This is a major hurdle. By identifying high-risk individuals, researchers can enroll them in prevention trials for new drugs and therapies, increasing the chances of finding effective treatments.
  4. Empowering Lifestyle Changes: A person deemed “high-risk” would have a powerful motivation to adopt brain-healthy behaviors, such as:
    • Managing blood pressure and cholesterol
    • Engaging in regular physical exercise
    • Maintaining a healthy diet (e.g., Mediterranean diet)
    • Staying socially and cognitively active

Important Limitations and Considerations

  • It’s a Prediction, Not a Diagnosis: This tool estimates risk, not certainty. A high score does not mean a person will develop Alzheimer’s, and a low score does not guarantee they won’t.
  • Focus on a Specific Group: Many of these models were developed and validated in populations of a certain age (often 65+) and specific ethnicities. Their accuracy may vary for younger or more diverse groups.
  • Ethical and Psychological Implications: Knowing one’s high genetic and cognitive risk can cause significant anxiety. Any use of this tool must be accompanied by proper counseling to explain the results and their implications.
  • It’s a Starting Point: A high-risk score would likely lead to more comprehensive testing with a neurologist to rule out other causes and confirm the findings.

Conclusion

This new predictive tool represents a significant step forward in the fight against Alzheimer’s. By demystifying risk through three key factors—genetics, current cognitive performance, and personal experience—it provides a practical and powerful way to identify vulnerable individuals earlier than ever before. This opens the door to more targeted prevention strategies and more efficient research, ultimately bringing us closer to a future where Alzheimer s-related memory loss can be prevented or significantly delayed.

Reference:
https://www.medicalnewstoday.com/articles/new-tool-predicts-future-alzheimers-memory-risk-age-genetics
https://pmc.ncbi.nlm.nih.gov/articles/PMC11071573/
https://www.sciencedirect.com/science/article/pii/S2274580725002675
https://newsnetwork.mayoclinic.org/discussion/mayo-clinic-scientists-create-tool-to-predict-alzheimers-risk-years-before-symptoms-begin/#

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

Exercise may help counter depressive, anxiety-like symptoms from Western diet

Exercise may help counter depressive, anxiety-like symptoms from Western diet

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The Core Finding: “Rewiring” the Brain

The headline captures the essence of a significant shift in how scientists understand psychedelic therapy. The “rewiring” metaphor refers to the concept of neuroplasticity—the brain’s ability to form new neural connections and reorganize itself.

Traditional antidepressants (like SSRIs) work by gradually altering brain chemistry, primarily by increasing the levels of neurotransmitters like serotonin. Their effect is often described as “dampening” negative emotional responses.

Psychedelics like psilocybin (the active compound in “magic mushrooms”) appear to work differently and more rapidly. They don’t just modulate chemistry; they seem to induce a temporary state of heightened neuroplasticity. This means the brain becomes more flexible and open to change, potentially allowing it to break out of rigid, negative thought patterns associated with depression.

Breaking Down the Science: What the Studies Show

Several key studies have contributed to this “rewiring” theory:

  1. The “Reset” Hypothesis: Research using fMRI scans has shown that depression can cause the brain to fall into rigid, repetitive patterns of activity, particularly in a network called the Default Mode Network (DMN). The DMN is associated with self-referential thought, the “inner critic,” and mind-wandering. In depression, it’s often overactive.
    • What Psychedelics Do: Under the influence of psilocybin, the DMN temporarily breaks down or becomes less organized. This is thought to correlate with the subjective experience of “ego dissolution” or a loss of the rigid sense of self. When the DMN re-establishes itself, it may do so in a more flexible, less dominant way, effectively “resetting” this circuit.
  2. Growth of Neuronal Connections: Preclinical studies on animals have shown that psychedelics like psilocybin promote:
    • Dendritogenesis: The growth of new dendrites, the branch-like parts of neurons that receive signals.
    • Spinogenesis: The formation of new dendritic spines, the tiny protrusions where synapses (connections between neurons) are formed.
    • Increased Synaptogenesis: The creation of entirely new synapses.
      This literal physical “rewiring” increases the brain’s connectivity and computational capacity, potentially providing the hardware needed for new, healthier thought patterns to take root.
  3. The Role of Therapy (The Crucial Ingredient): The “rewiring” isn’t automatic. The psychedelic experience is often intense and can be challenging. The therapeutic context is critical. The drug-induced state of plasticity is paired with supported psychotherapy.
    • The therapist helps guide the patient through their experience.
    • In the following days and weeks, during the “plastic window,” the therapist helps the patient integrate their insights, process old traumas, and solidify new, healthier perspectives.

In essence, the psychedelic doesn’t cure depression on its own. It opens a critical window of opportunity where the brain is more receptive to change, and psychotherapy helps guide that change in a positive direction.

Key Takeaways and Implications

  • Rapid and Sustained Effect: Clinical trials have demonstrated that a single dose (or two) of psilocybin, when combined with therapy, can result in fast and significant reductions in depressive symptoms, with effects lasting for several months. This is a stark contrast to the weeks it can take for SSRIs to begin working.
  • Treatment-Resistant Depression: This approach shows immense promise for individuals who have not responded to conventional antidepressants, offering a new hope where other options have failed.
  • A Paradigm Shift in Psychiatry: This moves beyond the simple “chemical imbalance” model of depression towards a “circuit and plasticity” model. It focuses on the brain’s dynamic structure and its ability to heal itself.
  • Not a DIY Treatment: It is crucial to emphasize that this research is conducted in a strictly controlled medical setting. Self-medicating with psychedelics carries significant risks, including psychological distress and the potential to trigger latent mental health conditions.

The Road Ahead

While the results are promising, this is still an emerging field.

  • Larger-Scale Trials: More extensive Phase 3 clinical trials are underway to firmly establish efficacy and safety for regulatory approval.
  • Decriminalization vs. Medicalization: There’s an ongoing discussion about the legal and regulatory pathways, distinguishing between medical use and broader decriminalization.
  • Accessibility: If approved, a major challenge will be scaling this intensive, therapist-guided model to make it accessible and affordable.

In conclusion, the idea that psychedelics “rewire” the brain is a powerful and scientifically-grounded metaphor for a potentially revolutionary new approach to treating mental health disorders by harnessing the brain’s innate capacity for healing and change.

Exercise may help counter depressive, anxiety-like symptoms from the Western diet. Of course. This is another excellent example of how lifestyle interventions can powerfully impact mental health, creating a compelling parallel to the psychedelics research.

Here’s a detailed breakdown of the connection between exercise and counteracting the mental health effects of a Western diet.

The Core Finding: Exercise as a Protective Buffer

The headline points to a key concept: the negative mental health impacts of a Western diet are not fixed. Exercise can act as a powerful, non-pharmacological buffer, mitigating the inflammatory and metabolic damage that can lead to depressive and anxiety-like symptoms.

Breaking Down the Science: The Diet-Brain-Exercise Connection

1. The Problem: How a Western Diet Harms the Brain

A Western Diet (high in saturated fats, refined sugars, and processed foods) doesn’t just affect the body; it directly impacts the brain through several pathways:

  • Chronic Systemic Inflammation: Poor diet triggers the immune system, leading to widespread, low-grade inflammation. Inflammatory markers (cytokines) can cross the blood-brain barrier, disrupting the function of neurotransmitters like serotonin and dopamine, which are crucial for mood regulation.
  • Oxidative Stress: Diets high in processed foods generate free radicals, causing cellular damage in the brain.
  • Hippocampal Damage: The hippocampus, a brain region critical for memory and mood regulation, is particularly vulnerable. A Western diet can reduce the production of Brain-Derived Neurotrophic Factor (BDNF), a key protein for neuron health and survival, leading to impaired neurogenesis (the creation of new neurons) in this area. This shrinkage is a well-documented feature of depression.
  • Gut-Brain Axis Disruption: The diet alters the gut microbiome, promoting the growth of harmful bacteria that can produce inflammatory compounds and disrupt the communication network between the gut and the brain.

2. The Solution: How Exercise Counteracts These Effects

Exercise acts as a direct antidote to nearly every negative effect of the Western diet on the brain:

  • Exercise is Anti-Inflammatory: Physical activity directly reduces the levels of pro-inflammatory cytokines and stimulates the production of natural anti-inflammatory molecules. It effectively “fights fire with fire” at a biological level.
  • Boosts BDNF and Neuroplasticity: This is the “rewiring” parallel. Exercise is one of the most potent natural boosters of BDNF. By increasing BDNF, it promotes neurogenesis in the hippocampus, strengthens existing neurons, and enhances synaptic plasticity—effectively repairing and protecting the brain from dietary damage.
  • Reduces Oxidative Stress: Regular exercise enhances the body’s own antioxidant defense systems, helping to neutralize the damaging free radicals produced by a poor diet.
  • Regulates the Gut-Brain Axis: Studies suggest that exercise can positively alter the composition of the gut microbiome, increasing the abundance of beneficial, anti-inflammatory bacteria and improving gut barrier function, which prevents “leaky gut” and subsequent inflammation.
  • Neurotransmitter Regulation: Like antidepressants, exercise increases the availability of key neurotransmitters like serotonin, norepinephrine, and endorphins, which can immediately improve mood and reduce anxiety.

Key Takeaways and Implications

  • A Powerful Two-Way Street: This research highlights that both diet and exercise are active regulators of brain biology. You can’t out-exercise a consistently terrible diet, but you can significantly mitigate its mental health consequences with consistent physical activity.
  • Preventative and Therapeutic: Exercise isn’t just for treating existing symptoms; it’s a potent preventative strategy for those who may find it difficult to completely avoid a Western-style diet.
  • Accessibility and Empowerment: Unlike specialized psychedelic therapy, exercise is a highly accessible, low-cost intervention that empowers individuals to take an active role in their mental wellness.

The Road Ahead

  • Dosage: Future research will continue to refine the “dose” of exercise—what type (aerobic vs. resistance), intensity, and frequency—that is most effective for mental health protection.
  • Personalization: As with all treatments, exercise will not be a one-size-fits-all solution, but it remains a foundational tool for brain health.
  • Public Health Policy: This science strengthens the argument for promoting physical activity and improving nutritional standards as core components of public mental health initiatives.

In conclusion, the finding that “exercise may help counter depressive, anxiety-like symptoms from Western diet” underscores that physical activity is not just for physical fitness. It is a fundamental pillar of mental health resilience, directly protecting the brain from the modern world’s dietary challenges.

Reference:

https://www.medicalnewstoday.com/articles/exercise-help-counter-depressive-anxiety-symptoms-western-diet-fat-sugar
https://pmc.ncbi.nlm.nih.gov/articles/PMC12537415/
https://www.mayoclinic.org/diseases-conditions/depression/in-depth/depression-and-exercise/art-20046495

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

Psychedelics may ‘rewire’ brain to improve depression treatment: study

Psychedelics may ‘rewire’ brain to improve depression treatment: study

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The Core Finding: “Rewiring” the Brain

The headline captures the essence of a significant shift in how scientists understand psychedelic therapy. The “rewiring” metaphor refers to the concept of neuroplasticity—the brain’s ability to form new neural connections and reorganize itself.

Traditional antidepressants (like SSRIs) work by gradually altering brain chemistry, primarily by increasing the levels of neurotransmitters like serotonin. Their effect is often described as “dampening” negative emotional responses.

Psychedelics like psilocybin (the active compound in “magic mushrooms”) appear to work differently and more rapidly. They don’t just modulate chemistry; they seem to induce a temporary state of heightened neuroplasticity. This means the brain becomes more flexible and open to change, potentially allowing it to break out of rigid, negative thought patterns associated with depression.

Breaking Down the Science: What the Studies Show

Several key studies have contributed to this “rewiring” theory:

  1. The “Reset” Hypothesis: Research using fMRI scans has shown that depression can cause the brain to fall into rigid, repetitive patterns of activity, particularly in a network called the Default Mode Network (DMN). The DMN is associated with self-referential thought, the “inner critic,” and mind-wandering. In depression, it’s often overactive.
    • What Psychedelics Do: Under the influence of psilocybin, the DMN temporarily breaks down or becomes less organized. This is thought to correlate with the subjective experience of “ego dissolution” or a loss of the rigid sense of self. When the DMN re-establishes itself, it may do so in a more flexible, less dominant way, effectively “resetting” this circuit.
  2. Growth of Neuronal Connections: Preclinical studies on animals have shown that psychedelics like psilocybin promote:
    • Dendritogenesis: The growth of new dendrites, the branch-like parts of neurons that receive signals.
    • Spinogenesis: The formation of new dendritic spines, the tiny protrusions where synapses (connections between neurons) are formed.
    • Increased Synaptogenesis: The creation of entirely new synapses.
      This literal physical “rewiring” increases the brain’s connectivity and computational capacity, potentially providing the hardware needed for new, healthier thought patterns to take root.
  3. The Role of Therapy (The Crucial Ingredient): The “rewiring” isn’t automatic. The psychedelic experience is often intense and can be challenging. The therapeutic context is critical. The drug-induced state of plasticity is paired with supported psychotherapy.
    • The therapist helps guide the patient through their experience.
    • In the following days and weeks, during the “plastic window,” the therapist helps the patient integrate their insights, process old traumas, and solidify new, healthier perspectives.

In essence, the psychedelic doesn’t cure depression on its own. It opens a critical window of opportunity where the brain is more receptive to change, and psychotherapy helps guide that change in a positive direction.

Key Takeaways and Implications

  • Rapid and Sustained Effect: Clinical trials have demonstrated that a single dose (or two) of psilocybin, when combined with therapy, can result in fast and significant reductions in depressive symptoms, with effects lasting for several months. This is a stark contrast to the weeks it can take for SSRIs to begin working.
  • Treatment-Resistant Depression: This approach shows immense promise for individuals who have not responded to conventional antidepressants, offering a new hope where other options have failed.
  • A Paradigm Shift in Psychiatry: This moves beyond the simple “chemical imbalance” model of depression towards a “circuit and plasticity” model. It focuses on the brain’s dynamic structure and its ability to heal itself.
  • Not a DIY Treatment: It is crucial to emphasize that this research is conducted in a strictly controlled medical setting. Self-medicating with psychedelics carries significant risks, including psychological distress and the potential to trigger latent mental health conditions.

The Road Ahead

While the results are promising, this is still an emerging field.

  • Larger-Scale Trials: More extensive Phase 3 clinical trials are underway to firmly establish efficacy and safety for regulatory approval.
  • Decriminalization vs. Medicalization: There’s an ongoing discussion about the legal and regulatory pathways, distinguishing between medical use and broader decriminalization.
  • Accessibility: If approved, a major challenge will be scaling this intensive, therapist-guided model to make it accessible and affordable.

In conclusion, the idea that psychedelics “rewire” the brain is a powerful and scientifically-grounded metaphor for a potentially revolutionary new approach to treating mental health disorders by harnessing the brain’s innate capacity for healing and change.

Reference:

https://www.medicalnewstoday.com/articles/psychedelics-may-rewire-memory-circuits-key-to-mental-health
https://www.ucsf.edu/news/2022/04/422606/psilocybin-rewires-brain-people-depression
https://pmc.ncbi.nlm.nih.gov/articles/PMC8209538

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

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

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

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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:

  1. 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).
  2. Immune System Activation: The damaged liver cells can trigger an inflammatory immune response. Chronic inflammation is a key driver of fibrosis.
  3. Direct Toxicity: TCE and its metabolites can directly injure liver cells, leading to cell death.
  4. 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

  1. 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.
  2. 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.
  3. 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.
  4. 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…

Metformin may weaken cardiovascular, insulin benefits of exercise…

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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.

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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

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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

Do antidepressants affect gut health? Experts review the evidence

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What the evidence shows (plain language)

  1. 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).
  2. 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.
  3. 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.
  4. 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.
  5. 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.

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

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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