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  1. DATE: August 7, 2026 at 07:00AM
    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: Stopping ADHD medication alters sleep rhythms long after discontinuation

    URL: psypost.org/stopping-adhd-medi

    Stopping the common attention-deficit/hyperactivity disorder medication methylphenidate can cause lasting disruptions to sleep and activity rhythms. In a recent animal study, researchers found that both adolescent and adult rats experienced reduced rest quality ten days after they stopped taking the drug. The research was published in the journal Psychopharmacology.

    Children and adults with attention-deficit/hyperactivity disorder, or ADHD, often experience higher rates of sleep disturbances than their peers. These issues range from difficulty falling asleep to experiencing fragmented and shortened periods of rest. Because sleep problems are so common in this population, medical professionals increasingly view ADHD as a condition that affects people throughout the entire day and night.

    The most frequently prescribed treatment for pediatric ADHD is methylphenidate. This psychostimulant helps improve attention and reduce hyperactivity. Patients taking the drug occasionally report side effects like delayed sleep onset and insomnia.

    Treatment discontinuation among people with ADHD is highly prevalent. Medical data suggests that a large portion of patients eventually stop taking their prescribed psychostimulants, with the highest dropout rates occurring among young adults.

    Researchers have debated whether the medication itself worsens existing sleep disturbances or contributes to new sleep disorders later in life. Much of the existing data focuses on the drug’s effects while a patient is actively taking it. Very few clinical or laboratory studies have tracked what happens to sleep patterns once the medication is stopped.

    To answer this question, researchers led by psychologist Leslie R. Amodeo and graduate researcher Carolyn Cueto at California State University, San Bernardino, designed an experiment using an animal model. By observing rats without an underlying disorder, the team aimed to isolate the physiological effects of the drug from the behavioral symptoms of ADHD. They investigated how methylphenidate influenced the natural rest and wake cycles of male and female rats during both adolescence and adulthood.

    The experiment involved one hundred and eight Long-Evans rats divided into groups of 56 adolescents and 52 adults. The animals received either a saline control injection or a specific dose of methylphenidate twice a day for ten days. The researchers administered doses of one or two milligrams per kilogram, which correspond to clinically relevant levels in human patients. To mimic the prolonged exposure typical of medical treatment, the researchers administered the drug in the morning and the evening.

    To measure activity levels, the researchers fitted each rat with a customized spandex jacket equipped with a lightweight commercial activity monitor. These monitors tracked the animals’ physical movements continuously throughout a twenty-four-hour cycle. Rats are nocturnal animals, meaning they are naturally active in the dark and rest when their environment is brightly lit.

    The research team gathered minute-by-minute movement data on three specific days. They analyzed activity on the final day of the medication regimen, on the first day after the drug was stopped, and ten days after the treatment ended.

    On the final day of treatment, the medication increased overall activity levels across both the light and dark phases. Adult rats receiving the higher dose experienced longer and more frequent active periods during their usual waking hours in the dark. The researchers also noticed shifts in the timing of the animals’ daily circadian rhythms, with peak activity occurring later than usual.

    The medication altered the quality of rest during the light phase as well. Female rats in particular showed signs of impaired rest on the last day of the drug regimen. They experienced fewer total rest periods and exhibited more fragmented sleep patterns compared to those receiving the saline control.

    The researchers then stopped the injections and observed the animals during the first twenty-four hours of withdrawal. During this acute discontinuation phase, the rats’ activity patterns began to shift in the opposite direction. The previously sustained periods of wakefulness seen in adult rats shortened and became more erratic.

    During their normal resting phase in the light, the rats undergoing acute withdrawal continued to experience sleep disruptions. Adolescent rats that had received the lower dose of the drug showed shorter rest episodes than their peers in the control group. Both male and female rats experienced an increase in rest fragmentation, meaning their periods of stillness were frequently interrupted by bursts of movement.

    The most pronounced impairments emerged ten days after the animals stopped taking the medication. During this prolonged withdrawal phase, widespread disruptions to rest quality appeared across all age and sex groups. Rats that had been given methylphenidate experienced a drop in both the total number of rest episodes and the average duration of each resting period.

    The activity monitors revealed that the animals’ sleep-like states remained highly fragmented long after the stimulant had left their biological systems. Sleep fragmentation involves frequent physical arousals that interrupt continuous rest. In human populations, this type of fragmented rest is linked to memory impairment, increased physical stress, and metabolic dysfunction.

    While the findings demonstrate a link between methylphenidate withdrawal and altered rest patterns in an animal model, rats process medications differently than humans. The rats used in this study also did not have a neurological equivalent of ADHD. People taking the medication for a diagnosed condition might experience different physiological responses than a non-diseased animal subject.

    The researchers measured sleep-like behavior using activity monitors that track physical movement rather than brain waves. True sleep architecture requires monitoring electrical activity in the brain to identify specific sleep stages. Relying on physical stillness provides a useful approximation for rest, but it does not capture the deeper neurological shifts associated with entering deep sleep.

    Future research will need to explore exactly how early exposure to stimulants alters the brain’s long-term sleep and arousal circuitry. Previous rodent studies have suggested that withdrawing from stimulants can alter glucose metabolism in the hypothalamus, a brain region critical to regulating wakefulness. Researchers hope to determine if these prolonged sleep disturbances contribute to changes in cognitive function or reward processing later in life. Understanding these extended withdrawal effects could help doctors better manage the treatment plans of patients who eventually stop taking their medication.

    The study, “Methylphenidate leads to disruptions in rest/wake patterns after discontinuation,” was authored by Carolyn Cueto, Magdalena R. Gonzales, Alexandra N. Tejada, Kimberly Guerrero Leon, Alexandra Mora, Andrew Cabrera, and Leslie R. Amodeo.

    URL: psypost.org/stopping-adhd-medi

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #ADHD #MethylphenidateWithdrawal #SleepDisruption #CircadianRhythms #RestQuality #MedicationDiscontinuation #ADHDResearch #SleepHealth #Psychopharmacology #AnimalStudy

  2. DATE: August 7, 2026 at 07:00AM
    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: Stopping ADHD medication alters sleep rhythms long after discontinuation

    URL: psypost.org/stopping-adhd-medi

    Stopping the common attention-deficit/hyperactivity disorder medication methylphenidate can cause lasting disruptions to sleep and activity rhythms. In a recent animal study, researchers found that both adolescent and adult rats experienced reduced rest quality ten days after they stopped taking the drug. The research was published in the journal Psychopharmacology.

    Children and adults with attention-deficit/hyperactivity disorder, or ADHD, often experience higher rates of sleep disturbances than their peers. These issues range from difficulty falling asleep to experiencing fragmented and shortened periods of rest. Because sleep problems are so common in this population, medical professionals increasingly view ADHD as a condition that affects people throughout the entire day and night.

    The most frequently prescribed treatment for pediatric ADHD is methylphenidate. This psychostimulant helps improve attention and reduce hyperactivity. Patients taking the drug occasionally report side effects like delayed sleep onset and insomnia.

    Treatment discontinuation among people with ADHD is highly prevalent. Medical data suggests that a large portion of patients eventually stop taking their prescribed psychostimulants, with the highest dropout rates occurring among young adults.

    Researchers have debated whether the medication itself worsens existing sleep disturbances or contributes to new sleep disorders later in life. Much of the existing data focuses on the drug’s effects while a patient is actively taking it. Very few clinical or laboratory studies have tracked what happens to sleep patterns once the medication is stopped.

    To answer this question, researchers led by psychologist Leslie R. Amodeo and graduate researcher Carolyn Cueto at California State University, San Bernardino, designed an experiment using an animal model. By observing rats without an underlying disorder, the team aimed to isolate the physiological effects of the drug from the behavioral symptoms of ADHD. They investigated how methylphenidate influenced the natural rest and wake cycles of male and female rats during both adolescence and adulthood.

    The experiment involved one hundred and eight Long-Evans rats divided into groups of 56 adolescents and 52 adults. The animals received either a saline control injection or a specific dose of methylphenidate twice a day for ten days. The researchers administered doses of one or two milligrams per kilogram, which correspond to clinically relevant levels in human patients. To mimic the prolonged exposure typical of medical treatment, the researchers administered the drug in the morning and the evening.

    To measure activity levels, the researchers fitted each rat with a customized spandex jacket equipped with a lightweight commercial activity monitor. These monitors tracked the animals’ physical movements continuously throughout a twenty-four-hour cycle. Rats are nocturnal animals, meaning they are naturally active in the dark and rest when their environment is brightly lit.

    The research team gathered minute-by-minute movement data on three specific days. They analyzed activity on the final day of the medication regimen, on the first day after the drug was stopped, and ten days after the treatment ended.

    On the final day of treatment, the medication increased overall activity levels across both the light and dark phases. Adult rats receiving the higher dose experienced longer and more frequent active periods during their usual waking hours in the dark. The researchers also noticed shifts in the timing of the animals’ daily circadian rhythms, with peak activity occurring later than usual.

    The medication altered the quality of rest during the light phase as well. Female rats in particular showed signs of impaired rest on the last day of the drug regimen. They experienced fewer total rest periods and exhibited more fragmented sleep patterns compared to those receiving the saline control.

    The researchers then stopped the injections and observed the animals during the first twenty-four hours of withdrawal. During this acute discontinuation phase, the rats’ activity patterns began to shift in the opposite direction. The previously sustained periods of wakefulness seen in adult rats shortened and became more erratic.

    During their normal resting phase in the light, the rats undergoing acute withdrawal continued to experience sleep disruptions. Adolescent rats that had received the lower dose of the drug showed shorter rest episodes than their peers in the control group. Both male and female rats experienced an increase in rest fragmentation, meaning their periods of stillness were frequently interrupted by bursts of movement.

    The most pronounced impairments emerged ten days after the animals stopped taking the medication. During this prolonged withdrawal phase, widespread disruptions to rest quality appeared across all age and sex groups. Rats that had been given methylphenidate experienced a drop in both the total number of rest episodes and the average duration of each resting period.

    The activity monitors revealed that the animals’ sleep-like states remained highly fragmented long after the stimulant had left their biological systems. Sleep fragmentation involves frequent physical arousals that interrupt continuous rest. In human populations, this type of fragmented rest is linked to memory impairment, increased physical stress, and metabolic dysfunction.

    While the findings demonstrate a link between methylphenidate withdrawal and altered rest patterns in an animal model, rats process medications differently than humans. The rats used in this study also did not have a neurological equivalent of ADHD. People taking the medication for a diagnosed condition might experience different physiological responses than a non-diseased animal subject.

    The researchers measured sleep-like behavior using activity monitors that track physical movement rather than brain waves. True sleep architecture requires monitoring electrical activity in the brain to identify specific sleep stages. Relying on physical stillness provides a useful approximation for rest, but it does not capture the deeper neurological shifts associated with entering deep sleep.

    Future research will need to explore exactly how early exposure to stimulants alters the brain’s long-term sleep and arousal circuitry. Previous rodent studies have suggested that withdrawing from stimulants can alter glucose metabolism in the hypothalamus, a brain region critical to regulating wakefulness. Researchers hope to determine if these prolonged sleep disturbances contribute to changes in cognitive function or reward processing later in life. Understanding these extended withdrawal effects could help doctors better manage the treatment plans of patients who eventually stop taking their medication.

    The study, “Methylphenidate leads to disruptions in rest/wake patterns after discontinuation,” was authored by Carolyn Cueto, Magdalena R. Gonzales, Alexandra N. Tejada, Kimberly Guerrero Leon, Alexandra Mora, Andrew Cabrera, and Leslie R. Amodeo.

    URL: psypost.org/stopping-adhd-medi

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

    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 #ADHD #MethylphenidateWithdrawal #SleepDisruption #CircadianRhythms #RestQuality #MedicationDiscontinuation #ADHDResearch #SleepHealth #Psychopharmacology #AnimalStudy

  3. DATE: August 5, 2026 at 06:00PM
    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: Animal studies suggest that reproductive behavior fully recovers after puberty-blocking treatment ends

    URL: psypost.org/animal-studies-sug

    Recent research provides evidence that temporarily pausing puberty with the drug leuprolide delays reproductive development in adolescent rats but allows for full physical and behavioral maturation after the treatment stops. The findings suggest that the brain and body adjust to the medication through specific genetic changes, enabling normal reproductive function to eventually emerge. These two related studies were published in the journals Biology of Sex Differences and Hormones and Behavior.

    Adolescents who experience distress because their gender identity does not match their sex assigned at birth are sometimes prescribed puberty-blocking medications. These drugs, known as gonadotropin-releasing hormone agonists, temporarily pause physical changes like breast development or facial hair growth. Leuprolide is one commonly used medication in this category. Delaying these physical changes gives young people time to explore their gender identity without the stress of developing unwanted physical traits.

    A research team led by Fay Guarraci at Southwestern University initiated a series of experiments to understand how protracted puberty suppression affects brain and reproductive development. The researchers wanted to track both the behavioral and biological changes that occur during and after leuprolide administration. Because long-term physiological studies on human adolescents are limited, animal models help scientists observe how the brain and reproductive systems respond to these hormone-altering drugs over time.

    In the first study, published in 2023, Guarraci and her colleagues tested how leuprolide affected the physical and behavioral development of 40 adolescent Long-Evans rats. The sample included 24 female rats and 16 male rats. Starting on postnatal day 25, which corresponds to early adolescence in rats, the scientists administered daily injections of either 50 micrograms per kilogram of leuprolide or a neutral saltwater solution for 25 days. The researchers monitored the rats daily for physical signs of puberty, such as vaginal opening in females and penile development in males.

    Following the treatment period, the authors placed the rats in specialized chambers to observe their sexual motivation and mating behaviors. They recorded how much time the subjects chose to spend with male or female stimulus rats and tracked specific reproductive actions. The female subjects were tested during their first reproductive cycle after the drug was stopped. The male subjects underwent weekly behavioral tests for a month to track their development over a longer timeframe.

    The researchers observed that leuprolide delayed the physical onset of puberty. Female rats receiving the drug reached puberty at an average of 45.9 days of age, compared to 38.1 days for those receiving the saltwater solution. Male rats receiving the drug reached puberty at an average of 45.0 days, compared to 39.0 days for the control group. During the treatment window, the female rats did not experience normal reproductive cycles.

    Once the leuprolide injections ended, the female rats rapidly resumed normal reproductive function. Within a week, they displayed typical mating behaviors and became pregnant at absolute rates comparable to the control group. The male rats took longer to recover from the puberty-blocking effects. During the initial post-treatment tests, the leuprolide-treated males showed reduced sexual motivation toward females and engaged in fewer mating behaviors. By the fourth week after treatment ended, the treated males exhibited sexual behavior that matched the control group.

    To understand the biological mechanisms driving these behavioral changes, the researchers conducted a second study, published in 2025. This experiment involved 16 female and 17 male adolescent rats, using the exact same 25-day leuprolide treatment protocol. Instead of observing behavior after the drug was stopped, the scientists analyzed the rats’ brains and blood hormone levels on the final day of treatment. They specifically measured the activity of genes related to reproduction in the pituitary gland and the hypothalamus, two brain regions that control hormone production.

    Leuprolide once again delayed physical puberty, pushing the onset back by about five days in females (from 37.25 to 42.25 days) and ten days in males (from 39.50 to 49.67 days). Blood tests indicated that the circulating levels of sex hormones like testosterone and estrogen were not statistically significantly different between the treated and untreated rats at the end of the 25-day window. However, the genetic analysis showed distinct changes in how the brain was preparing for reproduction.

    In the pituitary gland, both male and female rats treated with leuprolide showed increased activity in genes responsible for producing estrogen receptors and gonadotropin-releasing hormone receptors. In the hypothalamus, the effects differed by sex. Male rats receiving the drug had lower activity of the Kiss1 gene in the preoptic area, a brain region involved in sexual behavior. This gene produces kisspeptin, a protein that helps trigger puberty.

    In a different section of the hypothalamus called the mediobasal region, the Kiss1 gene was highly active in both treated males and females. The scientists note that this heightened gene activity likely represents the brain attempting to compensate for the drug’s suppressive effects. The brain continues to mature and build the necessary reproductive architecture even while the physical manifestation of puberty is stalled.

    Applying findings from animal models to human biology requires noting that rats and humans mature on vastly different timelines. The precise brain mechanisms governing puberty also feature species-specific variations, meaning a one-week recovery period in rats does not correspond to a specific timeframe in human adolescents.

    Animal studies remain highly useful, however, because they allow scientists to directly examine brain tissue and track genetic changes across a full developmental lifespan. Observing these molecular adaptations in a controlled environment provides evidence about how the mammalian brain responds to protracted puberty suppression that would be impossible to gather from human patients.

    Drug doses used in experimental models do not always translate exactly to the proportional doses prescribed in clinical settings. Future research could isolate smaller, more specific clusters of cells within the hypothalamus to see exactly where these genetic changes originate. Tracking hormone and gene expression over a longer timeline after the medication is stopped would also help clarify how the brain readjusts. Testing different doses of the medication could provide additional context regarding how the body manages chemical puberty suppression.

    The study, “Chronic periadolescent leuprolide exposure affects the development of reproductive physiology and behavior of female and male rats differently, but both mature after treatment termination,” was authored by Fay A. Guarraci, Layla Avendano, Megan Kelly, Cleriza Estoesta, Bernard Sencherey, Hannah S. Valdivia, Amanda Gale, Lily Yepez, Jasmine B. Belfield, Kristen M. Carter, Natalie Williams, and Andrea C. Gore.

    The study, “Chronic periadolescent leuprolide exposure affects the expression of multiple genes in the hypothalamus and pituitary gland with a different pattern of expression in female and male Long-Evans rats,” was authored by Fay A. Guarraci, Ian M. Klepcyk, Lindsay M. Thompson, Madeline Streifer, Emily N. Hilz, Grace Hudson, Sarah H. Meerts, and Andrea C. Gore.

    URL: psypost.org/animal-studies-sug

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

    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 #PubertyBlockers #Leuprolide #ReproductiveDevelopment #AdolescentResearch #AnimalStudy #HormonesAndBehavior #BiologyOfSexDifferences #Kiss1 #Hypothalamus #PituitaryGland

  4. DATE: August 5, 2026 at 06:00PM
    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: Animal studies suggest that reproductive behavior fully recovers after puberty-blocking treatment ends

    URL: psypost.org/animal-studies-sug

    Recent research provides evidence that temporarily pausing puberty with the drug leuprolide delays reproductive development in adolescent rats but allows for full physical and behavioral maturation after the treatment stops. The findings suggest that the brain and body adjust to the medication through specific genetic changes, enabling normal reproductive function to eventually emerge. These two related studies were published in the journals Biology of Sex Differences and Hormones and Behavior.

    Adolescents who experience distress because their gender identity does not match their sex assigned at birth are sometimes prescribed puberty-blocking medications. These drugs, known as gonadotropin-releasing hormone agonists, temporarily pause physical changes like breast development or facial hair growth. Leuprolide is one commonly used medication in this category. Delaying these physical changes gives young people time to explore their gender identity without the stress of developing unwanted physical traits.

    A research team led by Fay Guarraci at Southwestern University initiated a series of experiments to understand how protracted puberty suppression affects brain and reproductive development. The researchers wanted to track both the behavioral and biological changes that occur during and after leuprolide administration. Because long-term physiological studies on human adolescents are limited, animal models help scientists observe how the brain and reproductive systems respond to these hormone-altering drugs over time.

    In the first study, published in 2023, Guarraci and her colleagues tested how leuprolide affected the physical and behavioral development of 40 adolescent Long-Evans rats. The sample included 24 female rats and 16 male rats. Starting on postnatal day 25, which corresponds to early adolescence in rats, the scientists administered daily injections of either 50 micrograms per kilogram of leuprolide or a neutral saltwater solution for 25 days. The researchers monitored the rats daily for physical signs of puberty, such as vaginal opening in females and penile development in males.

    Following the treatment period, the authors placed the rats in specialized chambers to observe their sexual motivation and mating behaviors. They recorded how much time the subjects chose to spend with male or female stimulus rats and tracked specific reproductive actions. The female subjects were tested during their first reproductive cycle after the drug was stopped. The male subjects underwent weekly behavioral tests for a month to track their development over a longer timeframe.

    The researchers observed that leuprolide delayed the physical onset of puberty. Female rats receiving the drug reached puberty at an average of 45.9 days of age, compared to 38.1 days for those receiving the saltwater solution. Male rats receiving the drug reached puberty at an average of 45.0 days, compared to 39.0 days for the control group. During the treatment window, the female rats did not experience normal reproductive cycles.

    Once the leuprolide injections ended, the female rats rapidly resumed normal reproductive function. Within a week, they displayed typical mating behaviors and became pregnant at absolute rates comparable to the control group. The male rats took longer to recover from the puberty-blocking effects. During the initial post-treatment tests, the leuprolide-treated males showed reduced sexual motivation toward females and engaged in fewer mating behaviors. By the fourth week after treatment ended, the treated males exhibited sexual behavior that matched the control group.

    To understand the biological mechanisms driving these behavioral changes, the researchers conducted a second study, published in 2025. This experiment involved 16 female and 17 male adolescent rats, using the exact same 25-day leuprolide treatment protocol. Instead of observing behavior after the drug was stopped, the scientists analyzed the rats’ brains and blood hormone levels on the final day of treatment. They specifically measured the activity of genes related to reproduction in the pituitary gland and the hypothalamus, two brain regions that control hormone production.

    Leuprolide once again delayed physical puberty, pushing the onset back by about five days in females (from 37.25 to 42.25 days) and ten days in males (from 39.50 to 49.67 days). Blood tests indicated that the circulating levels of sex hormones like testosterone and estrogen were not statistically significantly different between the treated and untreated rats at the end of the 25-day window. However, the genetic analysis showed distinct changes in how the brain was preparing for reproduction.

    In the pituitary gland, both male and female rats treated with leuprolide showed increased activity in genes responsible for producing estrogen receptors and gonadotropin-releasing hormone receptors. In the hypothalamus, the effects differed by sex. Male rats receiving the drug had lower activity of the Kiss1 gene in the preoptic area, a brain region involved in sexual behavior. This gene produces kisspeptin, a protein that helps trigger puberty.

    In a different section of the hypothalamus called the mediobasal region, the Kiss1 gene was highly active in both treated males and females. The scientists note that this heightened gene activity likely represents the brain attempting to compensate for the drug’s suppressive effects. The brain continues to mature and build the necessary reproductive architecture even while the physical manifestation of puberty is stalled.

    Applying findings from animal models to human biology requires noting that rats and humans mature on vastly different timelines. The precise brain mechanisms governing puberty also feature species-specific variations, meaning a one-week recovery period in rats does not correspond to a specific timeframe in human adolescents.

    Animal studies remain highly useful, however, because they allow scientists to directly examine brain tissue and track genetic changes across a full developmental lifespan. Observing these molecular adaptations in a controlled environment provides evidence about how the mammalian brain responds to protracted puberty suppression that would be impossible to gather from human patients.

    Drug doses used in experimental models do not always translate exactly to the proportional doses prescribed in clinical settings. Future research could isolate smaller, more specific clusters of cells within the hypothalamus to see exactly where these genetic changes originate. Tracking hormone and gene expression over a longer timeline after the medication is stopped would also help clarify how the brain readjusts. Testing different doses of the medication could provide additional context regarding how the body manages chemical puberty suppression.

    The study, “Chronic periadolescent leuprolide exposure affects the development of reproductive physiology and behavior of female and male rats differently, but both mature after treatment termination,” was authored by Fay A. Guarraci, Layla Avendano, Megan Kelly, Cleriza Estoesta, Bernard Sencherey, Hannah S. Valdivia, Amanda Gale, Lily Yepez, Jasmine B. Belfield, Kristen M. Carter, Natalie Williams, and Andrea C. Gore.

    The study, “Chronic periadolescent leuprolide exposure affects the expression of multiple genes in the hypothalamus and pituitary gland with a different pattern of expression in female and male Long-Evans rats,” was authored by Fay A. Guarraci, Ian M. Klepcyk, Lindsay M. Thompson, Madeline Streifer, Emily N. Hilz, Grace Hudson, Sarah H. Meerts, and Andrea C. Gore.

    URL: psypost.org/animal-studies-sug

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

    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 #PubertyBlockers #Leuprolide #ReproductiveDevelopment #AdolescentResearch #AnimalStudy #HormonesAndBehavior #BiologyOfSexDifferences #Kiss1 #Hypothalamus #PituitaryGland

  5. Monkey study casts doubt on need for an omicron-specific booster - Enlarge / A vial of the current Moderna COVID-19 vaccine. (credit: Gett... - arstechnica.com/?p=1832385 #infectiousdisease #vaccineefficacy #publichealth #animalstudy #coronavirus #sars-cov-2 #covid-19 #variants #science #booster #moderna #monkeys #omicron