Blog

Rethinking Aging

Source https://changingaging.org/culture-change/rethinking-aging/

As an undergraduate student, I was inspired to become a gerontologist after learning about the 1976 research study in which psychologists Ellen Langer and Judith Rodin investigated the effects of choice and enhanced personal responsibility for the aged, which resulted in a groundbreaking study on the impact of loneliness on seniors. They selected two floors of a […]

The post Rethinking Aging appeared first on ChangingAging.

Source https://changingaging.org/culture-change/rethinking-aging/

As an undergraduate student, I was inspired to become a gerontologist after learning about the 1976 research study in which psychologists Ellen Langer and Judith Rodin investigated the effects of choice and enhanced personal responsibility for the aged, which resulted in a groundbreaking study on the impact of loneliness on seniors. They selected two floors of a […]

The post Rethinking Aging appeared first on ChangingAging.

A Faith Community’s Kidney Health Resource

Source: https://www.niddk.nih.gov/health-information/healthy-moments/episodes/faith-communitys-kidney-health-resource

African Americans are at a greater risk for kidney failure than other communities. Make a difference by introducing the Kidney Sundays tool kit in your place of worship.

Source: https://www.niddk.nih.gov/health-information/healthy-moments/episodes/faith-communitys-kidney-health-resource

African Americans are at a greater risk for kidney failure than other communities. Make a difference by introducing the Kidney Sundays tool kit in your place of worship.

For the second week, El Cerebro Que Cura is a bestseller in Catalonia, Spain

Source: https://sharpbrains.com/blog/2019/03/12/for-the-second-week-el-cerebro-que-cura-is-a-bestseller-in-catalonia-spain/

From the official list in el Periódico for the week March 4–10th:

NO FICCIÓN CASTELLANO

1-‘Cómo hacer que te pasen cosas buenas’.  Marian Rojas.  Espasa.  Un libro que quiere ayudar a mejorar nuestras vidas.  200 páginas.  11 semanas.  19,90 euros.

2-‘Come comida real’. Carlos Ríos.  Paidós. Una guía para transformar nuestra salud comiendo saludablemente.  304 páginas.  1 semana.  17 euros.

3-‘Diccionario de las cosas que no supe explicarte’.  Risto Mejide.  Espasa.  Risto Mejide explica sus emociones y experiencias.  206 páginas.  4 semanas.  1…

Source: https://sharpbrains.com/blog/2019/03/12/for-the-second-week-el-cerebro-que-cura-is-a-bestseller-in-catalonia-spain/

From the official list in el Periódico for the week March 4–10th:

NO FICCIÓN CASTELLANO

1-‘Cómo hacer que te pasen cosas buenas’.  Marian Rojas.  Espasa.  Un libro que quiere ayudar a mejorar nuestras vidas.  200 páginas.  11 semanas.  19,90 euros.

2-‘Come comida real’. Carlos Ríos.  Paidós. Una guía para transformar nuestra salud comiendo saludablemente.  304 páginas.  1 semana.  17 euros.

3-‘Diccionario de las cosas que no supe explicarte’.  Risto Mejide.  Espasa.  Risto Mejide explica sus emociones y experiencias.  206 páginas.  4 semanas.  1…

Love Them Today, Before Their Tomorrow’s Taken Away

Source http://feedproxy.google.com/~r/tinybuddha/~3/G2bB9tIH-Vs/

“Before someone’s tomorrow has been taken away, cherish those you love, appreciate them today.” ~Michelle C. Ustaszeski

Last year, my grandfather passed away.

He had gone to the hospital many times before. Sometimes he went for a minor sickness, sometimes for a severe condition. Unfortunately, the last time he went, we found out that he didn’t have much time left. He was diagnosed with last stage bladder cancer.

It was a shock to our family. My grandfather had always been a survivor. He’d survived the war, the darkest moment of the country. We couldn’t imagine he would lose his life to something like this.

I came home as soon as I could after hearing the news. And luckily, when I was home, he was conscious. He was a big man, but I remember seeing him in bed, looking small and fragile like a sick little cat under his too loose clothes. I was thankful for the chance to be with him for the last time, and happy he knew I was there.

After that, I came to visit and check on him every day. On the last day I was home, I hugged him and told him to get well soon, and that I would come back to visit him when he got better.

Before I even said it, I knew it would never happen. I made a promise that I knew I couldn’t keep.

I returned to the city to work and a couple weeks later, I received the news that he had passed away.

All my memories of him suddenly came flooding back. He was always there in my childhood. He watched me all day so that my mom could go to work, which meant he was basically a stand in parent.

I remembered the time he gently wrapped a bandage around my head after I ran into a wall and my forehead started bleeding. And how he listened patiently to all my childhood problems, from complaints about a dress that was too old to my side of a fight with my sister. And how he often bought me snacks even though he didn’t have much money to spare.

After I grew up, he was still there while I was studying and busy chasing success and promotions. Yet I only visited him a couple times a year, when I had free time.

I was so used to his presence that I didn’t remember to cherish him while I had the chance.

I remembered one time I came back to visit my old school and realized the tree I used to play under was still there, waiting for me to come back for almost twenty years. I felt like I’d treated my grandfather like that tree. I’d never thought much about how long he’d had to wait for me.

I sobbed, tears running down my cheeks. I couldn’t breathe well. My head was heavy. That tree is now gone. Gone for good. My grandfather is no longer. Now every time I drive by his house, the gate will be locked, the door will be closed, and I’ll no longer see him sitting in his chair, drinking tea, and greeting me with a sparkle in his eyes.

Same street, same house, but it will never be the same.

I didn’t come back home for my grandfather’s funeral because I was pregnant, but many of his other grandchildren showed up. Many of them I hadn’t seen in years, even after hearing about his sickness. In fact, I’d forgotten about their existence. How could I remember? They were never there to talk to him, to be with him when he was conscious. Why did they even show up after he’d passed? What were they doing? Who were they trying to impress?

But then it hit me.

They were just like me. They’d treated him like an old tree whose shadow was always there for them to play under. And they only missed the tree when it was cut down and they were exposed to the sun.

I can’t blame them. It makes sense. Life happens. We get busy. We need to work to pay the bills to buy the house to get the promotion. And we just forget. It’s not until we get burnt that we realize how much we needed that tree, and how much we wish we could feel its shade again.

Maybe it’s time for all of us to slow down, look around, and make sure we spend time with the people who really matter to us.

If you also need to get your priorities in check, like I did…

Make plans to spend time with your loved ones.

I’m sure you’re one of the busiest people in the world. We all are. Or at least that’s what we choose to believe. It’s tempting to spend all our time and energy trying to achieve our goals. When we achieve them, we think, then we’ll allow ourselves to take it easy and be with our loved ones.

But what if when that time comes—if it ever comes at all—our loved ones are no longer there?

Don’t wait till you get the time to prioritize the people you love. Make the time. Make a plan. It’s a choice. One you won’t regret.

Put down your phone and stay present.

How many times have you looked at your phone, read emails or the news, or scanned your notifications while talking to someone?

Yes, you might be able to multitask. But did you really listen to the person in front of you?

Put down your phone and look at your mom’s face when you talk to her. Do you notice the extra wrinkles and gray hair that weren’t there before?

It hurts my heart every time I notice a difference in my mom’s face. It’s like standing still while watching her slowly slip away, knowing there is nothing I can do to stop it. We all have but a short time on this Earth. Don’t trick yourself into believing that there will always be a next time because someday, that conversation will be the last.

After my grandfather died I swore to cherish every moment I have with my loved ones. I make eye contact; I listen to them and hold their hands. I hope all of these moments and memories will sustain me when it’s time for the final goodbye.

Let them know how you feel.

You won’t always feel love for the people you care about. Sometimes they’ll annoy you, or you’ll disagree. And that’s okay. No one, and no relationship, is perfect, and we’re all doing the best we can. The important thing is that you value them, even if your relationship has ups and downs, and let them know you care while you have the chance.

Make sure you tell them how much you appreciate them. Send them random texts to tell them you love them. Bring them flowers and watch their eyes light up. These are the memories we’ll remember when we’re about to leave this world. We won’t think about the job, the house, or the promotions, but the little moments we shared with the people who made us feel loved.

I wish I could still do these things for my grandfather. And I wish I did them more often when I had the chance. But I didn’t. All I can do now is take the lesson with me and show up fully for the people who are still here.

Make the most of your time with your loved ones, because you never know when that time will run out.

About Mai Pham

Mai Pham believes we can create our own happiness. She helps overwhelmed and frustrated people to ditch their stress and enjoy their lives again. Grab her free actionable cheatsheet: 5 Simple Tips to Release Stress and Bring You Calm in Under 5 Minutes and join her free 7 Joyful Days Challenge email course.

Get in the conversation! Click here to leave a comment on the site.

The post Love Them Today, Before Their Tomorrow’s Taken Away appeared first on Tiny Buddha.

Source http://feedproxy.google.com/~r/tinybuddha/~3/G2bB9tIH-Vs/

“Before someone’s tomorrow has been taken away, cherish those you love, appreciate them today.” ~Michelle C. Ustaszeski

Last year, my grandfather passed away.

He had gone to the hospital many times before. Sometimes he went for a minor sickness, sometimes for a severe condition. Unfortunately, the last time he went, we found out that he didn’t have much time left. He was diagnosed with last stage bladder cancer.

It was a shock to our family. My grandfather had always been a survivor. He’d survived the war, the darkest moment of the country. We couldn’t imagine he would lose his life to something like this.

I came home as soon as I could after hearing the news. And luckily, when I was home, he was conscious. He was a big man, but I remember seeing him in bed, looking small and fragile like a sick little cat under his too loose clothes. I was thankful for the chance to be with him for the last time, and happy he knew I was there.

After that, I came to visit and check on him every day. On the last day I was home, I hugged him and told him to get well soon, and that I would come back to visit him when he got better.

Before I even said it, I knew it would never happen. I made a promise that I knew I couldn’t keep.

I returned to the city to work and a couple weeks later, I received the news that he had passed away.

All my memories of him suddenly came flooding back. He was always there in my childhood. He watched me all day so that my mom could go to work, which meant he was basically a stand in parent.

I remembered the time he gently wrapped a bandage around my head after I ran into a wall and my forehead started bleeding. And how he listened patiently to all my childhood problems, from complaints about a dress that was too old to my side of a fight with my sister. And how he often bought me snacks even though he didn’t have much money to spare.

After I grew up, he was still there while I was studying and busy chasing success and promotions. Yet I only visited him a couple times a year, when I had free time.

I was so used to his presence that I didn’t remember to cherish him while I had the chance.

I remembered one time I came back to visit my old school and realized the tree I used to play under was still there, waiting for me to come back for almost twenty years. I felt like I’d treated my grandfather like that tree. I’d never thought much about how long he’d had to wait for me.

I sobbed, tears running down my cheeks. I couldn’t breathe well. My head was heavy. That tree is now gone. Gone for good. My grandfather is no longer. Now every time I drive by his house, the gate will be locked, the door will be closed, and I’ll no longer see him sitting in his chair, drinking tea, and greeting me with a sparkle in his eyes.

Same street, same house, but it will never be the same.

I didn’t come back home for my grandfather’s funeral because I was pregnant, but many of his other grandchildren showed up. Many of them I hadn’t seen in years, even after hearing about his sickness. In fact, I’d forgotten about their existence. How could I remember? They were never there to talk to him, to be with him when he was conscious. Why did they even show up after he’d passed? What were they doing? Who were they trying to impress?

But then it hit me.

They were just like me. They’d treated him like an old tree whose shadow was always there for them to play under. And they only missed the tree when it was cut down and they were exposed to the sun.

I can’t blame them. It makes sense. Life happens. We get busy. We need to work to pay the bills to buy the house to get the promotion. And we just forget. It’s not until we get burnt that we realize how much we needed that tree, and how much we wish we could feel its shade again.

Maybe it’s time for all of us to slow down, look around, and make sure we spend time with the people who really matter to us.

If you also need to get your priorities in check, like I did…

Make plans to spend time with your loved ones.

I’m sure you’re one of the busiest people in the world. We all are. Or at least that’s what we choose to believe. It’s tempting to spend all our time and energy trying to achieve our goals. When we achieve them, we think, then we’ll allow ourselves to take it easy and be with our loved ones.

But what if when that time comes—if it ever comes at all—our loved ones are no longer there?

Don’t wait till you get the time to prioritize the people you love. Make the time. Make a plan. It’s a choice. One you won’t regret.

Put down your phone and stay present.

How many times have you looked at your phone, read emails or the news, or scanned your notifications while talking to someone?

Yes, you might be able to multitask. But did you really listen to the person in front of you?

Put down your phone and look at your mom’s face when you talk to her. Do you notice the extra wrinkles and gray hair that weren’t there before?

It hurts my heart every time I notice a difference in my mom’s face. It’s like standing still while watching her slowly slip away, knowing there is nothing I can do to stop it. We all have but a short time on this Earth. Don’t trick yourself into believing that there will always be a next time because someday, that conversation will be the last.

After my grandfather died I swore to cherish every moment I have with my loved ones. I make eye contact; I listen to them and hold their hands. I hope all of these moments and memories will sustain me when it’s time for the final goodbye.

Let them know how you feel.

You won’t always feel love for the people you care about. Sometimes they’ll annoy you, or you’ll disagree. And that’s okay. No one, and no relationship, is perfect, and we’re all doing the best we can. The important thing is that you value them, even if your relationship has ups and downs, and let them know you care while you have the chance.

Make sure you tell them how much you appreciate them. Send them random texts to tell them you love them. Bring them flowers and watch their eyes light up. These are the memories we’ll remember when we’re about to leave this world. We won’t think about the job, the house, or the promotions, but the little moments we shared with the people who made us feel loved.

I wish I could still do these things for my grandfather. And I wish I did them more often when I had the chance. But I didn’t. All I can do now is take the lesson with me and show up fully for the people who are still here.

Make the most of your time with your loved ones, because you never know when that time will run out.

About Mai Pham

Mai Pham believes we can create our own happiness. She helps overwhelmed and frustrated people to ditch their stress and enjoy their lives again. Grab her free actionable cheatsheet: 5 Simple Tips to Release Stress and Bring You Calm in Under 5 Minutes and join her free 7 Joyful Days Challenge email course.

Get in the conversation! Click here to leave a comment on the site.

The post Love Them Today, Before Their Tomorrow’s Taken Away appeared first on Tiny Buddha.

A new culprit in cognitive decline in Alzheimer’s disease

Source: https://womensbrainhealth.org/think-outside-the-box/a-new-culprit-in-cognitive-decline-in-alzheimers-disease

by Science Daily: It has long been known that patients with Alzheimer’s disease have abnormalities in the vast network of blood vessels in the brain. Some of these alterations may also contribute to age-related cognitive decline in people without dementia…….

Source: https://womensbrainhealth.org/think-outside-the-box/a-new-culprit-in-cognitive-decline-in-alzheimers-disease

by Science Daily: It has long been known that patients with Alzheimer’s disease have abnormalities in the vast network of blood vessels in the brain. Some of these alterations may also contribute to age-related cognitive decline in people without dementia…….

Have Specific Genetic Examples of Antagonistic Pleiotropy Been Identified in Humans?

Source https://www.fightaging.org/archives/2019/03/have-specific-genetic-examples-of-antagonistic-pleiotropy-been-identified-in-humans/

Pleiotropy occurs when a single gene affects more than one distinct and seemingly unrelated trait. Antagonistic pleiotropy occurs when one of those traits is harmful. It is widely considered to be an important foundation for the evolution of aging, in that natural selection operates strongly during early life, a period characterized by tooth and claw battles for survival and reproductive success. Evolution will select for genes, mechanisms, and biological systems that operate well early and run down later, or otherwise cause harm in later life. The adaptive immune system is an example of the type, a system that works very well right out of the gate in youth, but cannot possibly function indefinitely. It devotes resources to all pathogens encountered, and eventually simply runs out of capacity. The decline of the immune system is much more complex than that simple sketch, of course, and has numerous distinct causes, but the example serves.

In the broader sense, why doesn’t the body repair itself indefinitely? The antagonistic pleiotropy hypothesis suggests that the fierce selection pressure in early life will strip away anything that isn’t absolutely vital to immediate survival and reproductive success. Long-term investment in repair and maintenance simply cannot survive this evolutionary arms race, in which even a tiny loss of advantage may well lead to extinction of the lineage. This might lead us to wonder how the lowly hydra manages to be functionally immortal, actually ageless – but it is only one among countless species that all undergo degenerative aging. Perhaps we are seeing the hydra shortly before its inevitable extinction at the hands of a slightly more efficient rival.

The two commentaries here follow on from a recent paper that discussed antagonistic pleiotropy and the evidence for it. Everyone involved in the exchange appears to support the antagonistic pleiotropy hypothesis; the debate is over whether or not specific named genes in humans are clearly pleiotropic in this way, and whether the evidence in support of that position is robust. As the authors of the original paper note, the challenge inherent in human data is that it produces correlations rather than the definitive causation that can be obtained from a well-designed animal study.

Byars and Voskarides: Genes that improved fitness also cost modern humans, evidence for genes with antagonistic effects on longevity and disease

Austad and Hoffmann reviewed the current state-of-the-art on what support there is for the theory of antagonistic pleiotropy and what implications this has for modern medicine regarding improving human health and longevity. Although the authors focus on examples in both wild populations and laboratory conditions, the review states that there are no compelling examples in humans where the underlying genes or alleles that carry this tradeoff have been identified. This fails to acknowledge recent studies, mostly published the last two years, where excellent progress has been made in identifying such genes and below, we describe several examples.

Two studies in 2017 uncovered evidence for antagonistic pleiotropy in genes related to coronary heart disease (CAD) and fitness, and diseases related to ageing. The first found that CAD genes in humans are significantly enriched for fitness (increased lifetime reproductive success) relative to the rest of the genome, with evidence that the direction of their effects on CAD and fitness are antagonistic. This study provides a possible reason why genes carrying health risks have persisted in human populations. The second found evidence for multiple variants in genes related to ageing that exhibited antagonistic pleiotropic effects. They found higher risk allele frequencies with large effect sizes for late-onset diseases (relative to early-onset diseases) and an excess of variants with antagonistic effects expressed through early and late life diseases.

There also exists other recent tangible evidence of antagonistic pleiotropy in specific human genes. The SPATA31 gene has been found under strong positive genomic selection. Long-lived individuals carry fewer SPATA31 copy numbers. On the other hand, its overexpression in fibroblast cells leads to premature senescence, this being the case in people having multiple copies of the gene. During human evolution, more copies of this gene have likely been favored since this protein is important in sensing and repairing UV-induced DNA damage. Unfortunately, the cost is cell senescence and premature aging.

Austad and Hoffmann: Response to genes that improved fitness also cost modern humans: evidence for genes with antagonistic effects on longevity and disease

Byars and Voskarides, responding to our review of empirical support for the antagonistic pleiotropy theory of the evolution of aging, feel that we have ‘failed to acknowledge’ recent human studies supporting the theory. Indeed, we mentioned no human studies because we had intended our review to present only the strongest evidence supporting the theory which has been done almost entirely in laboratory model organisms. For this reason, while we mentioned a few studies from natural populations, we emphasized how such nonexperimental studies could be consistent with the antagonistic pleiotropy mechanisms, but could not be cleanly attributed to it. Experimental studies establish cause-and-effect in a way that correlational studies cannot.

It is an unfortunate truth about research on humans that because experimental studies are often impossible, results are almost inevitably correlational, which in our view makes virtually any single study highly suggestive at best, but never compelling. To illustrate why, we consider one of the studies adduced by Byars and Voskarides, although we could have chosen any of the others. That study identifies numerous human alleles pre-disposing individuals to coronary artery disease (CAD) but also conferring reproductive advantages early in life. This is a very nice study given the limitations of human research. The best that could be done with available data was done. Note, however, that one of the first lessons of statistical reasoning is that correlation does not equal causation and, yes, genomic associations are correlations.

Our point in noting these things is certainly not to denigrate the study by Byars et al. or the other studies cited. These are some very fine studies using state-of-the-art genomic analyses. We simply wanted to explain why we consider such studies less compelling as support for the antagonistic pleiotropy theory than experimental studies done in model laboratory organisms with specific and purposeful manipulation of specific individual genes.

Source https://www.fightaging.org/archives/2019/03/have-specific-genetic-examples-of-antagonistic-pleiotropy-been-identified-in-humans/

Pleiotropy occurs when a single gene affects more than one distinct and seemingly unrelated trait. Antagonistic pleiotropy occurs when one of those traits is harmful. It is widely considered to be an important foundation for the evolution of aging, in that natural selection operates strongly during early life, a period characterized by tooth and claw battles for survival and reproductive success. Evolution will select for genes, mechanisms, and biological systems that operate well early and run down later, or otherwise cause harm in later life. The adaptive immune system is an example of the type, a system that works very well right out of the gate in youth, but cannot possibly function indefinitely. It devotes resources to all pathogens encountered, and eventually simply runs out of capacity. The decline of the immune system is much more complex than that simple sketch, of course, and has numerous distinct causes, but the example serves.

In the broader sense, why doesn’t the body repair itself indefinitely? The antagonistic pleiotropy hypothesis suggests that the fierce selection pressure in early life will strip away anything that isn’t absolutely vital to immediate survival and reproductive success. Long-term investment in repair and maintenance simply cannot survive this evolutionary arms race, in which even a tiny loss of advantage may well lead to extinction of the lineage. This might lead us to wonder how the lowly hydra manages to be functionally immortal, actually ageless – but it is only one among countless species that all undergo degenerative aging. Perhaps we are seeing the hydra shortly before its inevitable extinction at the hands of a slightly more efficient rival.

The two commentaries here follow on from a recent paper that discussed antagonistic pleiotropy and the evidence for it. Everyone involved in the exchange appears to support the antagonistic pleiotropy hypothesis; the debate is over whether or not specific named genes in humans are clearly pleiotropic in this way, and whether the evidence in support of that position is robust. As the authors of the original paper note, the challenge inherent in human data is that it produces correlations rather than the definitive causation that can be obtained from a well-designed animal study.

Byars and Voskarides: Genes that improved fitness also cost modern humans, evidence for genes with antagonistic effects on longevity and disease

Austad and Hoffmann reviewed the current state-of-the-art on what support there is for the theory of antagonistic pleiotropy and what implications this has for modern medicine regarding improving human health and longevity. Although the authors focus on examples in both wild populations and laboratory conditions, the review states that there are no compelling examples in humans where the underlying genes or alleles that carry this tradeoff have been identified. This fails to acknowledge recent studies, mostly published the last two years, where excellent progress has been made in identifying such genes and below, we describe several examples.

Two studies in 2017 uncovered evidence for antagonistic pleiotropy in genes related to coronary heart disease (CAD) and fitness, and diseases related to ageing. The first found that CAD genes in humans are significantly enriched for fitness (increased lifetime reproductive success) relative to the rest of the genome, with evidence that the direction of their effects on CAD and fitness are antagonistic. This study provides a possible reason why genes carrying health risks have persisted in human populations. The second found evidence for multiple variants in genes related to ageing that exhibited antagonistic pleiotropic effects. They found higher risk allele frequencies with large effect sizes for late-onset diseases (relative to early-onset diseases) and an excess of variants with antagonistic effects expressed through early and late life diseases.

There also exists other recent tangible evidence of antagonistic pleiotropy in specific human genes. The SPATA31 gene has been found under strong positive genomic selection. Long-lived individuals carry fewer SPATA31 copy numbers. On the other hand, its overexpression in fibroblast cells leads to premature senescence, this being the case in people having multiple copies of the gene. During human evolution, more copies of this gene have likely been favored since this protein is important in sensing and repairing UV-induced DNA damage. Unfortunately, the cost is cell senescence and premature aging.

Austad and Hoffmann: Response to genes that improved fitness also cost modern humans: evidence for genes with antagonistic effects on longevity and disease

Byars and Voskarides, responding to our review of empirical support for the antagonistic pleiotropy theory of the evolution of aging, feel that we have ‘failed to acknowledge’ recent human studies supporting the theory. Indeed, we mentioned no human studies because we had intended our review to present only the strongest evidence supporting the theory which has been done almost entirely in laboratory model organisms. For this reason, while we mentioned a few studies from natural populations, we emphasized how such nonexperimental studies could be consistent with the antagonistic pleiotropy mechanisms, but could not be cleanly attributed to it. Experimental studies establish cause-and-effect in a way that correlational studies cannot.

It is an unfortunate truth about research on humans that because experimental studies are often impossible, results are almost inevitably correlational, which in our view makes virtually any single study highly suggestive at best, but never compelling. To illustrate why, we consider one of the studies adduced by Byars and Voskarides, although we could have chosen any of the others. That study identifies numerous human alleles pre-disposing individuals to coronary artery disease (CAD) but also conferring reproductive advantages early in life. This is a very nice study given the limitations of human research. The best that could be done with available data was done. Note, however, that one of the first lessons of statistical reasoning is that correlation does not equal causation and, yes, genomic associations are correlations.

Our point in noting these things is certainly not to denigrate the study by Byars et al. or the other studies cited. These are some very fine studies using state-of-the-art genomic analyses. We simply wanted to explain why we consider such studies less compelling as support for the antagonistic pleiotropy theory than experimental studies done in model laboratory organisms with specific and purposeful manipulation of specific individual genes.

Depression Can Increase Stroke Risk

Source: https://womensbrainhealth.org/think-it-over/depression-can-increase-stroke-risk

by Judy George for MedPage Today: Depressive symptoms were tied to an increased risk of ischemic stroke, a prospective cohort study of largely Hispanic older adults found. Over 14 years of follow-up, older adults who had elevated depressive symptoms were……

Source: https://womensbrainhealth.org/think-it-over/depression-can-increase-stroke-risk

by Judy George for MedPage Today: Depressive symptoms were tied to an increased risk of ischemic stroke, a prospective cohort study of largely Hispanic older adults found. Over 14 years of follow-up, older adults who had elevated depressive symptoms were……

Daxko Acquires GroupEx PRO to Bring Streamlined, Integrated Group Fitness Program Management to a Growing Number of Health and Wellness Centers

Source https://www.clubindustry.com/news-central/daxko-acquires-groupex-pro-bring-streamlined-integrated-group-fitness-program

Club Industry was not involved in the creation of this content.

BIRMINGHAM, Ala., March 8, 2019 /PRNewswire/ — Daxko announced today that it acquired GroupEx PRO, a privately held best of breed, web-based group exercise management portal utili

Source https://www.clubindustry.com/news-central/daxko-acquires-groupex-pro-bring-streamlined-integrated-group-fitness-program

Club Industry was not involved in the creation of this content.

BIRMINGHAM, Ala., March 8, 2019 /PRNewswire/ — Daxko announced today that it acquired GroupEx PRO, a privately held best of breed, web-based group exercise management portal utili

Sleep apnea may be tied to increased Alzheimer’s biomarker in brain

Source: https://womensbrainhealth.org/think-it-over/sleep-apnea-may-be-tied-to-increased-alzheimers-biomarker-in-brain

by Mayo Clinic: People who stop breathing during sleep may have higher accumulations of the toxic protein tau, a biological hallmark of Alzheimer’s disease, in part of the brain that manages memory, navigation and perception of time. Recent evidence has supported……

Source: https://womensbrainhealth.org/think-it-over/sleep-apnea-may-be-tied-to-increased-alzheimers-biomarker-in-brain

by Mayo Clinic: People who stop breathing during sleep may have higher accumulations of the toxic protein tau, a biological hallmark of Alzheimer’s disease, in part of the brain that manages memory, navigation and perception of time. Recent evidence has supported……

Seafood fraud again and again

Source https://www.foodpolitics.com/2019/03/seafood-fraud-again-and-again/

Seafood fraud, long a problem (I wrote about it in What to Eat), is still a problem.  The latest evidence comes from a report from the New York State Attorney General.

Investigators tested fish and found widespread mislabeling of just about every type of fish except striped bass.

I wish the figure displayed percentages instead of absolute numbers, but you get the idea.  Examples:

  • Lemon sole       87.5%
  • Red snapper     67.0%
  • “Wild” salmon  27.6% (in quotes because some was farmed)

Overall, the investigation found 27% of seafood purchases to be mislabeled.  Some conclusions:

  • Mislabeling was worse at some supermarkets more than others; for example, five chains had mislabeling rates of 50% or higher.
  • Some fish are mislabeled more than others, especially lemon sole, red snapper, and grouper.
  • Substitutes were cheaper, less desirable fish, sometimes with higher levels of mercury.
  • Mislabeling was common throughout the state, but the mislabeling rate for New York City was nearly 43%.

If ever there was a call for caveat emptor, this is it.

What to do?  Ask.  Complain. Demand regulation.

Source https://www.foodpolitics.com/2019/03/seafood-fraud-again-and-again/

Seafood fraud, long a problem (I wrote about it in What to Eat), is still a problem.  The latest evidence comes from a report from the New York State Attorney General.

Investigators tested fish and found widespread mislabeling of just about every type of fish except striped bass.

I wish the figure displayed percentages instead of absolute numbers, but you get the idea.  Examples:

  • Lemon sole       87.5%
  • Red snapper     67.0%
  • “Wild” salmon  27.6% (in quotes because some was farmed)

Overall, the investigation found 27% of seafood purchases to be mislabeled.  Some conclusions:

  • Mislabeling was worse at some supermarkets more than others; for example, five chains had mislabeling rates of 50% or higher.
  • Some fish are mislabeled more than others, especially lemon sole, red snapper, and grouper.
  • Substitutes were cheaper, less desirable fish, sometimes with higher levels of mercury.
  • Mislabeling was common throughout the state, but the mislabeling rate for New York City was nearly 43%.

If ever there was a call for caveat emptor, this is it.

What to do?  Ask.  Complain. Demand regulation.

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