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#cardiovascularrisk — Public Fediverse posts

Live and recent posts from across the Fediverse tagged #cardiovascularrisk, aggregated by home.social.

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  1. DATE: September 22, 2026 at 01:38PM
    SOURCE: SOCIALPSYCHOLOGY.ORG

    TITLE: Ozempic Can Change Your Body, But Can It Change Your Well-Being?

    URL: socialpsychology.org/client/re

    Source: Science Daily - Top News

    GLP-1 medications such as Ozempic have reshaped treatment for Type 2 diabetes. These drugs can help patients manage blood sugar, lower cardiovascular risk, and, in many cases, lose a large amount of weight. Yet a new study finds little evidence that they improve mental health, employment, marriage, or overall well-being. Thus, the drugs' broader life effects may be subtler than their dramatic physical health benefits.

    URL: socialpsychology.org/client/re

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Ozempic #GLP1 #Type2Diabetes #WeightLoss #MentalHealth #WellBeing #CardiovascularRisk #DiabetesTreatment #ScienceDaily #WellbeingImpact

  2. DATE: September 22, 2026 at 01:38PM
    SOURCE: SOCIALPSYCHOLOGY.ORG

    TITLE: Ozempic Can Change Your Body, But Can It Change Your Well-Being?

    URL: socialpsychology.org/client/re

    Source: Science Daily - Top News

    GLP-1 medications such as Ozempic have reshaped treatment for Type 2 diabetes. These drugs can help patients manage blood sugar, lower cardiovascular risk, and, in many cases, lose a large amount of weight. Yet a new study finds little evidence that they improve mental health, employment, marriage, or overall well-being. Thus, the drugs' broader life effects may be subtler than their dramatic physical health benefits.

    URL: socialpsychology.org/client/re

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Ozempic #GLP1 #Type2Diabetes #WeightLoss #MentalHealth #WellBeing #CardiovascularRisk #DiabetesTreatment #ScienceDaily #WellbeingImpact

  3. DATE: September 22, 2026 at 01:38PM
    SOURCE: SOCIALPSYCHOLOGY.ORG

    TITLE: Ozempic Can Change Your Body, But Can It Change Your Well-Being?

    URL: socialpsychology.org/client/re

    Source: Science Daily - Top News

    GLP-1 medications such as Ozempic have reshaped treatment for Type 2 diabetes. These drugs can help patients manage blood sugar, lower cardiovascular risk, and, in many cases, lose a large amount of weight. Yet a new study finds little evidence that they improve mental health, employment, marriage, or overall well-being. Thus, the drugs' broader life effects may be subtler than their dramatic physical health benefits.

    URL: socialpsychology.org/client/re

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Ozempic #GLP1 #Type2Diabetes #WeightLoss #MentalHealth #WellBeing #CardiovascularRisk #DiabetesTreatment #ScienceDaily #WellbeingImpact

  4. Trying to Eat Like a Mediterranean Diet Expert? Start With This One Kitchen Staple

    Olive oil usually gets all the attention when people talk about eating Mediterranean. A quieter staple sitting in the same pantry has some of the strongest research behind it of…
    #dining #cooking #diet #food #MediterraneanDiet #cardiovascularrisk #Mediterranean #observationaldata #predimed
    diningandcooking.com/2817097/t

  5. Trying to Eat Like a Mediterranean Diet Expert? Start With This One Kitchen Staple

    Olive oil usually gets all the attention when people talk about eating Mediterranean. A quieter staple sitting in the same pantry has some of the strongest research behind it of…
    #dining #cooking #diet #food #MediterraneanDiet #cardiovascularrisk #Mediterranean #observationaldata #predimed
    diningandcooking.com/2817097/t

  6. Trying to Eat Like a Mediterranean Diet Expert? Start With This One Kitchen Staple

    Olive oil usually gets all the attention when people talk about eating Mediterranean. A quieter staple sitting in the same pantry has some of the strongest research behind it of…
    #dining #cooking #diet #food #MediterraneanDiet #cardiovascularrisk #Mediterranean #observationaldata #predimed
    diningandcooking.com/2817097/t

  7. DATE: September 15, 2026 at 08:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Common antidepressants might help liver cells clear a dangerous type of cholesterol

    URL: psypost.org/common-antidepress

    Common antidepressants might help lower a stubborn, disease-causing type of cholesterol by helping liver cells absorb it from the bloodstream. This unintended side effect could eventually provide a dual-purpose treatment for patients facing both depression and an elevated risk of heart disease. The findings were published in the Journal of Lipid Research.

    Lipoprotein(a) is a complex particle in the blood that carries fats and cholesterol throughout the body. It is structurally similar to low-density lipoprotein, commonly known as bad cholesterol. However, it contains an extra protein called apolipoprotein(a) that makes it particularly prone to causing blockages in arteries. High levels of this molecule are genetic and affect at least a fifth of the population of European descent.

    Traditional cholesterol-lowering medications, such as statins, fail to reduce these specific particles in the blood. The lack of targeted clinical treatments leaves a major gap in preventing cardiovascular disease for many patients. Researchers are actively trying to understand exactly how the human body clears this molecule from circulation.

    Cells absorb molecules from their environment through a process called endocytosis, which involves the cell membrane folding inward to swallow outside material. A specific type of endocytosis called macropinocytosis, or cellular drinking, handles the uptake of this particular cholesterol particle. During cellular drinking, the cell membrane extends outward to gulp large amounts of surrounding fluid and particles.

    Researchers from the University of Otago and the University of New South Wales, led by Nikita Deo, Sally P. A. McCormick, and Gregory M. I. Redpath, wanted to map the mechanics of this cellular drinking. They sought to identify exactly what stimulates liver cells to absorb the particles.

    The research team initially tested a drug called imipramine on human liver cells grown in a laboratory. Imipramine is an older tricyclic antidepressant that previous laboratory studies identified as a blocker of cellular drinking. The researchers treated the liver cells with the drug overnight and then introduced the cholesterol particles into the fluid bathing the cells.

    After a short incubation period, the team measured how much of the substance the cells had absorbed. Instead of blocking the process, the drug caused the cells to absorb nearly three times as much of the cholesterol. The researchers confirmed this was an isolated effect by testing regular bad cholesterol, which the drug did not affect.

    This unexpected outcome prompted the team to test newer, more frequently prescribed antidepressants known as selective serotonin reuptake inhibitors. These drugs treat depression by blocking a specific transport protein from pulling serotonin back into cells. This mechanism leaves more of the mood-regulating chemical active in the space outside the cells.

    The researchers repeated the cell culture experiment using the common drugs citalopram, sertraline, and fluoxetine. Citalopram increased the cholesterol uptake in the liver cells to a degree similar to imipramine. Sertraline and fluoxetine did not alter the uptake levels. A later test with paroxetine showed it also boosted cellular absorption of the particles.

    To figure out how imipramine and citalopram caused this effect, the researchers looked at the outer boundary of the liver cells. The cholesterol molecules must anchor to the cell surface before the cell can swallow them. The team cooled the cells to temporarily halt the swallowing process, added the cholesterol, and used fluorescent tags to measure how much stuck to the outside of the cells.

    Both imipramine and citalopram roughly doubled the amount of cholesterol anchored to the cell surface. The drugs did not change the cells’ ability to bind to standard sugar molecules used as a control. This confirmed that the medications specifically enhanced the cell’s grip on this exact type of cholesterol.

    Because these drugs increase the availability of serotonin outside the cells, the researchers hypothesized that serotonin itself might be driving the surface binding. They added pure serotonin to the liver cell cultures overnight and tracked the cholesterol particles. The serotonin treatment produced the same outcome as the medications.

    The serotonin drastically increased both the amount of cholesterol sticking to the cell surface and the amount the cells eventually absorbed. This suggests the antidepressants enhance cholesterol absorption by increasing local serotonin levels. The serotonin then somehow alters the cell surface to make it more receptive to the passing cholesterol particles.

    The team also explored why sertraline failed to enhance the absorption process despite being in the same class of drugs. Some forms of cellular drinking rely on a specific structural protein called dynamin. Dynamin acts like a lasso, pinching off the newly formed internal pouches so they can detach and drop into the cell interior.

    Previous research shows sertraline can interfere with dynamin, preventing it from pinching off the pouches. The researchers tested this by tracking a different molecule known to require dynamin for absorption. Sertraline blocked this control molecule from entering the cells. Its interference with dynamin likely prevents it from enhancing cholesterol uptake.

    To understand the mechanics of the surface binding, the researchers examined specific anchor proteins on the liver cells. They used fluorescent tags to measure the presence of a receptor known to grab the cholesterol particles. Treating the cells with imipramine or serotonin increased the amount of this receptor on the cell surface.

    Citalopram did not increase this specific receptor. However, it did boost the presence of an accessory protein that helps orchestrate the swallowing process. The precise mechanism linking citalopram, serotonin, and this accessory protein requires further mapping.

    Finally, the team tracked where the cholesterol went after the cells swallowed it. They used chemical markers to see if the cells sent the particles to internal compartments meant for degradation or compartments meant for recycling material back outside the cell. The cells treated with imipramine and citalopram routed the extra cholesterol into the recycling compartments.

    The researchers suspect this recycling process strips the harmful lipid component from the particle before sending the harmless protein portion back into the bloodstream. If true, the overall impact would still be a reduction in cardiovascular risk.

    This study relied exclusively on isolated cells in a laboratory. The behavior of these drugs and the cholesterol particles might differ inside a living human body. The liver interacts with many different tissues and chemical signals that a petri dish cannot replicate.

    Additionally, the concentration of citalopram used in the main experiments was roughly twice the maximum dose prescribed to human patients. The serotonin levels tested were also much higher than typical biological conditions. While the paroxetine tests matched clinical doses, animal studies or human trials are needed to verify if these medications can safely lower this dangerous cholesterol in patients.

    People suffering from depression often exhibit higher levels of this specific cholesterol, elevating their risk of heart attacks and strokes. Identifying an existing, affordable medication that manages both mood and cardiovascular risk could simplify treatment regimens for vulnerable patients.

    The study, “Antidepressants stimulate lipoprotein(a) macropinocytosis via serotonin-enhanced cell surface binding,” was authored by Nikita Deo, Halima Siddiqui, Katie Peppercorn, Golnoush Madani, Alexandria Rutherford-Blyth, Malcolm Rutledge, Michael J. A. Williams, Sally P. A. McCormick, and Gregory M. I. Redpath.

    URL: psypost.org/common-antidepress

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Lipoprotein(a) #antidepressants #serotonin #macropinocytosis #liverhealth #cardiovascularrisk #cholesterollowering #statinsfail #dualtherapy #lipidresearch

  8. DATE: September 15, 2026 at 08:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Common antidepressants might help liver cells clear a dangerous type of cholesterol

    URL: psypost.org/common-antidepress

    Common antidepressants might help lower a stubborn, disease-causing type of cholesterol by helping liver cells absorb it from the bloodstream. This unintended side effect could eventually provide a dual-purpose treatment for patients facing both depression and an elevated risk of heart disease. The findings were published in the Journal of Lipid Research.

    Lipoprotein(a) is a complex particle in the blood that carries fats and cholesterol throughout the body. It is structurally similar to low-density lipoprotein, commonly known as bad cholesterol. However, it contains an extra protein called apolipoprotein(a) that makes it particularly prone to causing blockages in arteries. High levels of this molecule are genetic and affect at least a fifth of the population of European descent.

    Traditional cholesterol-lowering medications, such as statins, fail to reduce these specific particles in the blood. The lack of targeted clinical treatments leaves a major gap in preventing cardiovascular disease for many patients. Researchers are actively trying to understand exactly how the human body clears this molecule from circulation.

    Cells absorb molecules from their environment through a process called endocytosis, which involves the cell membrane folding inward to swallow outside material. A specific type of endocytosis called macropinocytosis, or cellular drinking, handles the uptake of this particular cholesterol particle. During cellular drinking, the cell membrane extends outward to gulp large amounts of surrounding fluid and particles.

    Researchers from the University of Otago and the University of New South Wales, led by Nikita Deo, Sally P. A. McCormick, and Gregory M. I. Redpath, wanted to map the mechanics of this cellular drinking. They sought to identify exactly what stimulates liver cells to absorb the particles.

    The research team initially tested a drug called imipramine on human liver cells grown in a laboratory. Imipramine is an older tricyclic antidepressant that previous laboratory studies identified as a blocker of cellular drinking. The researchers treated the liver cells with the drug overnight and then introduced the cholesterol particles into the fluid bathing the cells.

    After a short incubation period, the team measured how much of the substance the cells had absorbed. Instead of blocking the process, the drug caused the cells to absorb nearly three times as much of the cholesterol. The researchers confirmed this was an isolated effect by testing regular bad cholesterol, which the drug did not affect.

    This unexpected outcome prompted the team to test newer, more frequently prescribed antidepressants known as selective serotonin reuptake inhibitors. These drugs treat depression by blocking a specific transport protein from pulling serotonin back into cells. This mechanism leaves more of the mood-regulating chemical active in the space outside the cells.

    The researchers repeated the cell culture experiment using the common drugs citalopram, sertraline, and fluoxetine. Citalopram increased the cholesterol uptake in the liver cells to a degree similar to imipramine. Sertraline and fluoxetine did not alter the uptake levels. A later test with paroxetine showed it also boosted cellular absorption of the particles.

    To figure out how imipramine and citalopram caused this effect, the researchers looked at the outer boundary of the liver cells. The cholesterol molecules must anchor to the cell surface before the cell can swallow them. The team cooled the cells to temporarily halt the swallowing process, added the cholesterol, and used fluorescent tags to measure how much stuck to the outside of the cells.

    Both imipramine and citalopram roughly doubled the amount of cholesterol anchored to the cell surface. The drugs did not change the cells’ ability to bind to standard sugar molecules used as a control. This confirmed that the medications specifically enhanced the cell’s grip on this exact type of cholesterol.

    Because these drugs increase the availability of serotonin outside the cells, the researchers hypothesized that serotonin itself might be driving the surface binding. They added pure serotonin to the liver cell cultures overnight and tracked the cholesterol particles. The serotonin treatment produced the same outcome as the medications.

    The serotonin drastically increased both the amount of cholesterol sticking to the cell surface and the amount the cells eventually absorbed. This suggests the antidepressants enhance cholesterol absorption by increasing local serotonin levels. The serotonin then somehow alters the cell surface to make it more receptive to the passing cholesterol particles.

    The team also explored why sertraline failed to enhance the absorption process despite being in the same class of drugs. Some forms of cellular drinking rely on a specific structural protein called dynamin. Dynamin acts like a lasso, pinching off the newly formed internal pouches so they can detach and drop into the cell interior.

    Previous research shows sertraline can interfere with dynamin, preventing it from pinching off the pouches. The researchers tested this by tracking a different molecule known to require dynamin for absorption. Sertraline blocked this control molecule from entering the cells. Its interference with dynamin likely prevents it from enhancing cholesterol uptake.

    To understand the mechanics of the surface binding, the researchers examined specific anchor proteins on the liver cells. They used fluorescent tags to measure the presence of a receptor known to grab the cholesterol particles. Treating the cells with imipramine or serotonin increased the amount of this receptor on the cell surface.

    Citalopram did not increase this specific receptor. However, it did boost the presence of an accessory protein that helps orchestrate the swallowing process. The precise mechanism linking citalopram, serotonin, and this accessory protein requires further mapping.

    Finally, the team tracked where the cholesterol went after the cells swallowed it. They used chemical markers to see if the cells sent the particles to internal compartments meant for degradation or compartments meant for recycling material back outside the cell. The cells treated with imipramine and citalopram routed the extra cholesterol into the recycling compartments.

    The researchers suspect this recycling process strips the harmful lipid component from the particle before sending the harmless protein portion back into the bloodstream. If true, the overall impact would still be a reduction in cardiovascular risk.

    This study relied exclusively on isolated cells in a laboratory. The behavior of these drugs and the cholesterol particles might differ inside a living human body. The liver interacts with many different tissues and chemical signals that a petri dish cannot replicate.

    Additionally, the concentration of citalopram used in the main experiments was roughly twice the maximum dose prescribed to human patients. The serotonin levels tested were also much higher than typical biological conditions. While the paroxetine tests matched clinical doses, animal studies or human trials are needed to verify if these medications can safely lower this dangerous cholesterol in patients.

    People suffering from depression often exhibit higher levels of this specific cholesterol, elevating their risk of heart attacks and strokes. Identifying an existing, affordable medication that manages both mood and cardiovascular risk could simplify treatment regimens for vulnerable patients.

    The study, “Antidepressants stimulate lipoprotein(a) macropinocytosis via serotonin-enhanced cell surface binding,” was authored by Nikita Deo, Halima Siddiqui, Katie Peppercorn, Golnoush Madani, Alexandria Rutherford-Blyth, Malcolm Rutledge, Michael J. A. Williams, Sally P. A. McCormick, and Gregory M. I. Redpath.

    URL: psypost.org/common-antidepress

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Lipoprotein(a) #antidepressants #serotonin #macropinocytosis #liverhealth #cardiovascularrisk #cholesterollowering #statinsfail #dualtherapy #lipidresearch

  9. DATE: September 15, 2026 at 08:00AM
    SOURCE: PSYPOST.ORG

    ** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
    -------------------------------------------------

    TITLE: Common antidepressants might help liver cells clear a dangerous type of cholesterol

    URL: psypost.org/common-antidepress

    Common antidepressants might help lower a stubborn, disease-causing type of cholesterol by helping liver cells absorb it from the bloodstream. This unintended side effect could eventually provide a dual-purpose treatment for patients facing both depression and an elevated risk of heart disease. The findings were published in the Journal of Lipid Research.

    Lipoprotein(a) is a complex particle in the blood that carries fats and cholesterol throughout the body. It is structurally similar to low-density lipoprotein, commonly known as bad cholesterol. However, it contains an extra protein called apolipoprotein(a) that makes it particularly prone to causing blockages in arteries. High levels of this molecule are genetic and affect at least a fifth of the population of European descent.

    Traditional cholesterol-lowering medications, such as statins, fail to reduce these specific particles in the blood. The lack of targeted clinical treatments leaves a major gap in preventing cardiovascular disease for many patients. Researchers are actively trying to understand exactly how the human body clears this molecule from circulation.

    Cells absorb molecules from their environment through a process called endocytosis, which involves the cell membrane folding inward to swallow outside material. A specific type of endocytosis called macropinocytosis, or cellular drinking, handles the uptake of this particular cholesterol particle. During cellular drinking, the cell membrane extends outward to gulp large amounts of surrounding fluid and particles.

    Researchers from the University of Otago and the University of New South Wales, led by Nikita Deo, Sally P. A. McCormick, and Gregory M. I. Redpath, wanted to map the mechanics of this cellular drinking. They sought to identify exactly what stimulates liver cells to absorb the particles.

    The research team initially tested a drug called imipramine on human liver cells grown in a laboratory. Imipramine is an older tricyclic antidepressant that previous laboratory studies identified as a blocker of cellular drinking. The researchers treated the liver cells with the drug overnight and then introduced the cholesterol particles into the fluid bathing the cells.

    After a short incubation period, the team measured how much of the substance the cells had absorbed. Instead of blocking the process, the drug caused the cells to absorb nearly three times as much of the cholesterol. The researchers confirmed this was an isolated effect by testing regular bad cholesterol, which the drug did not affect.

    This unexpected outcome prompted the team to test newer, more frequently prescribed antidepressants known as selective serotonin reuptake inhibitors. These drugs treat depression by blocking a specific transport protein from pulling serotonin back into cells. This mechanism leaves more of the mood-regulating chemical active in the space outside the cells.

    The researchers repeated the cell culture experiment using the common drugs citalopram, sertraline, and fluoxetine. Citalopram increased the cholesterol uptake in the liver cells to a degree similar to imipramine. Sertraline and fluoxetine did not alter the uptake levels. A later test with paroxetine showed it also boosted cellular absorption of the particles.

    To figure out how imipramine and citalopram caused this effect, the researchers looked at the outer boundary of the liver cells. The cholesterol molecules must anchor to the cell surface before the cell can swallow them. The team cooled the cells to temporarily halt the swallowing process, added the cholesterol, and used fluorescent tags to measure how much stuck to the outside of the cells.

    Both imipramine and citalopram roughly doubled the amount of cholesterol anchored to the cell surface. The drugs did not change the cells’ ability to bind to standard sugar molecules used as a control. This confirmed that the medications specifically enhanced the cell’s grip on this exact type of cholesterol.

    Because these drugs increase the availability of serotonin outside the cells, the researchers hypothesized that serotonin itself might be driving the surface binding. They added pure serotonin to the liver cell cultures overnight and tracked the cholesterol particles. The serotonin treatment produced the same outcome as the medications.

    The serotonin drastically increased both the amount of cholesterol sticking to the cell surface and the amount the cells eventually absorbed. This suggests the antidepressants enhance cholesterol absorption by increasing local serotonin levels. The serotonin then somehow alters the cell surface to make it more receptive to the passing cholesterol particles.

    The team also explored why sertraline failed to enhance the absorption process despite being in the same class of drugs. Some forms of cellular drinking rely on a specific structural protein called dynamin. Dynamin acts like a lasso, pinching off the newly formed internal pouches so they can detach and drop into the cell interior.

    Previous research shows sertraline can interfere with dynamin, preventing it from pinching off the pouches. The researchers tested this by tracking a different molecule known to require dynamin for absorption. Sertraline blocked this control molecule from entering the cells. Its interference with dynamin likely prevents it from enhancing cholesterol uptake.

    To understand the mechanics of the surface binding, the researchers examined specific anchor proteins on the liver cells. They used fluorescent tags to measure the presence of a receptor known to grab the cholesterol particles. Treating the cells with imipramine or serotonin increased the amount of this receptor on the cell surface.

    Citalopram did not increase this specific receptor. However, it did boost the presence of an accessory protein that helps orchestrate the swallowing process. The precise mechanism linking citalopram, serotonin, and this accessory protein requires further mapping.

    Finally, the team tracked where the cholesterol went after the cells swallowed it. They used chemical markers to see if the cells sent the particles to internal compartments meant for degradation or compartments meant for recycling material back outside the cell. The cells treated with imipramine and citalopram routed the extra cholesterol into the recycling compartments.

    The researchers suspect this recycling process strips the harmful lipid component from the particle before sending the harmless protein portion back into the bloodstream. If true, the overall impact would still be a reduction in cardiovascular risk.

    This study relied exclusively on isolated cells in a laboratory. The behavior of these drugs and the cholesterol particles might differ inside a living human body. The liver interacts with many different tissues and chemical signals that a petri dish cannot replicate.

    Additionally, the concentration of citalopram used in the main experiments was roughly twice the maximum dose prescribed to human patients. The serotonin levels tested were also much higher than typical biological conditions. While the paroxetine tests matched clinical doses, animal studies or human trials are needed to verify if these medications can safely lower this dangerous cholesterol in patients.

    People suffering from depression often exhibit higher levels of this specific cholesterol, elevating their risk of heart attacks and strokes. Identifying an existing, affordable medication that manages both mood and cardiovascular risk could simplify treatment regimens for vulnerable patients.

    The study, “Antidepressants stimulate lipoprotein(a) macropinocytosis via serotonin-enhanced cell surface binding,” was authored by Nikita Deo, Halima Siddiqui, Katie Peppercorn, Golnoush Madani, Alexandria Rutherford-Blyth, Malcolm Rutledge, Michael J. A. Williams, Sally P. A. McCormick, and Gregory M. I. Redpath.

    URL: psypost.org/common-antidepress

    -------------------------------------------------

    Private, vetted email list for mental health professionals: clinicians-exchange.org

    Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

    -------------------------------------------------

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Lipoprotein(a) #antidepressants #serotonin #macropinocytosis #liverhealth #cardiovascularrisk #cholesterollowering #statinsfail #dualtherapy #lipidresearch

  10. The 5 Best Cereals to Reduce Stroke Risk, According to Cardiologists and Dietitians

    Reviewed by Dietitian Maria Laura Haddad-Garcia Credit: Getty Images. EatingWell design. Key Points High-fiber, low-added-sugar breakfast cereals can…
    #NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #addedsugars #bloodpressure #bloodsugar #breakfastcereals #cardiovascularrisk #EatingWell #morningcereal #ShreddedWheat
    newsbeep.com/us/716225/

  11. Why Mediterranean Women Rarely Snack the Way Americans Do

    Italian researchers in 2024 reported that shared, unhurried meals were associated with better mental health, reduced cortisol, decreased depression, and lower cardiovascular risk, underscoring the s…
    #dining #cooking #diet #food #MediterraneanDiet #cardiovascularrisk #Italianresearchers #mainmeals #mealpatterns #Mediterranean #Mentalhealth
    diningandcooking.com/2666172/w

  12. Why Mediterranean Women Rarely Snack the Way Americans Do

    Italian researchers in 2024 reported that shared, unhurried meals were associated with better mental health, reduced cortisol, decreased depression, and lower cardiovascular risk, underscoring the s…
    #dining #cooking #diet #food #MediterraneanDiet #cardiovascularrisk #Italianresearchers #mainmeals #mealpatterns #Mediterranean #Mentalhealth
    diningandcooking.com/2666172/w

  13. Why Mediterranean Women Rarely Snack the Way Americans Do

    Italian researchers in 2024 reported that shared, unhurried meals were associated with better mental health, reduced cortisol, decreased depression, and lower cardiovascular risk, underscoring the s…
    #dining #cooking #diet #food #MediterraneanDiet #cardiovascularrisk #Italianresearchers #mainmeals #mealpatterns #Mediterranean #Mentalhealth
    diningandcooking.com/2666172/w

  14. Study Finds Certain Food Preservatives May Increase Cardiovascular Risks

    📰 Original title: High blood pressure, heart attacks linked to common preservatives in food

    🤖 IA: It's clickbait ⚠️
    👥 Users: It's clickbait ⚠️

    View full AI summary: en.killbait.com/study-finds-ce

    #health #preservatives #hearthealth #cardiovascularrisk

  15. Study Finds Certain Food Preservatives May Increase Cardiovascular Risks

    📰 Original title: High blood pressure, heart attacks linked to common preservatives in food

    🤖 IA: It's clickbait ⚠️
    👥 Users: It's clickbait ⚠️

    View full AI summary: en.killbait.com/study-finds-ce

    #health #preservatives #hearthealth #cardiovascularrisk

  16. Study Finds Certain Food Preservatives May Increase Cardiovascular Risks

    📰 Original title: High blood pressure, heart attacks linked to common preservatives in food

    🤖 IA: It's clickbait ⚠️
    👥 Users: It's clickbait ⚠️

    View full AI summary: en.killbait.com/study-finds-ce

    #health #preservatives #hearthealth #cardiovascularrisk

  17. LLY’s Oral GLP-1 Pill Foundayo Shows Heart Benefits in Diabetes Study

    Eli Lilly and Company LLY announced that a phase III study, ACHIEVE-4, evaluating its newly approved oral GLP-1…
    #NewsBeep #News #Medication #AU #Australia #cardiovascularrisk #EliLillyandCompany #FDA #Health #insulinglargine #Obesity #typeIIdiabetes
    newsbeep.com/au/617392/

  18. Nguy cơ biến chứng tim mạch ở người hút thuốc lá lâu năm rất cao, kể cả ở người trẻ dưới 40 tuổi. Theo bác sĩ, hút thuốc là một trong những yếu tố chính gây nhồi máu cơ tim, đột quỵ ngoài bệnh nền và yếu tố bẩm sinh. Bảo vệ sức khỏe tim mạch bằng cách từ bỏ thuốc lá là cần thiết và cấp bách.

    #TimMach #HutThuocLa #NhomiMacCoTim #DotQuy #Suckhoe #HeartHealth #Smoking #CardiovascularRisk #VietnameseHealth

    vietnamnet.vn/nguy-co-bien-chu

  19. Nutritionist shares gut-friendly diet for a healthy heart, recommends eating 30 plant based foods every week

    What we eat not just feeds our taste buds and stomach, but also shapes our gut microbiota –…
    #NewsBeep #News #Nutrition #cardiovascularrisk #gutfriendlyfoods #guthealth #gutmicrobiota #Health #heartfriendlyfood #hearthealth #UK #UnitedKingdom
    newsbeep.com/uk/157504/

  20. American Heart Association launches PREVENT equations: Revolutionary tool for personalized cardiovascular risk assessment, offering precise health insights for adults with high blood pressure. #Healthcare #CardiovascularRisk

  21. American Heart Association launches PREVENT equations: Revolutionary tool for personalized cardiovascular risk assessment, offering precise health insights for adults with high blood pressure. #Healthcare #CardiovascularRisk

  22. 📄 'Treatment of Plaque Psoriasis with Guselkumab Reduces Systemic Inflammatory Burden as Measured by Neutrophil/Lymphocyte Ratio, Platelet/Lymphocyte Ratio, and Monocyte/Lymphocyte Ratio: A post hoc Analysis of Three Randomised Clinical Trials' - an article in the #KargerPublishers research collection on #ScienceOpen:

    🔎🔗 scienceopen.com/document?vid=a

    #PlaquePsoriasis #Guselkumab #SystemicInflammation #CardioDerm #IL23Inhibitor #CardiovascularRisk

  23. CW: Covid-19, cardiovascular risk

    Given everything we now know about how covid-19 infection increases cardiovascular risk in the months following infection, is there any research on how to mitigate that risk?

    For example, it seems logical that taking aspirin for a few months after the infection might reduce the risk, but is anyone looking into whether it actually does?

    #Covid19 #LongCovid #CardiovascularRisk #HeartAttack #Stroke