Day: 02/15/2024

5 Principles for Raising Good Humans

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5 Principles for Raising Good Humans

Dr. Aliza Pressman is a developmental psychologist and an assistant clinical professor in the Division of Behavioral Health Department of Pediatrics at the Icahn School of Medicine at Mount Sinai Hospital. She is cofounding director of The Mount Sinai Parenting Center. Aliza is also the host of the podcast Raising Good Humans.

1. The most powerful environmental influence on children’s growth is their relationship with their parents.

Relationships are so powerful that they actually change the architecture of our children’s brains. Supportive relationships help children thrive. Having a secure attachment with one person, one parent, can buffer the effect that children have from experiencing adversity. This relationship can support their development. It allows them to learn and grow. It soothes their experiences so that they can get through whatever life throws at them.

Every positive relationship with a trusted adult makes a difference. But, of course, the most important relationship is the one they have with you. If kids don’t experience small disappointments throughout their childhood, first of all, that would just not be realistic, but also, they wouldn’t be able to handle the inevitable big disappointments that pop up over the course of a lifetime.

Think about working out. If you stretch and start with modest attainable goals, you’re less likely to injure yourself slowly over time. With small recoverable muscle ruptures and repairs, you can build your endurance and do that triathlon. If you go from a year on the couch to running a 10 K, you are likely to injure yourself to the point where you might have to spend another year on the couch.

Likewise, the psychological concepts of positive, tolerable, and toxic stress refer to the stress response systems’ effects on the body. Positive stress is the normal, healthy part of development. Meeting a new person might cause a brief increase in your child’s heart rate and a wide-eyed look on their face. But that’s a good thing because they’re noticing that something is unfamiliar, and it’s stretching their emotional muscles toward agility.

“Every positive relationship with a trusted adult makes a difference.”

Tolerable stress activates the body’s alert system to an even greater degree. Think about how your child reacts to losing a pet, a scary storm, or falling from a play structure. If the stressful event takes place over a short period of time and there are caring adults with whom your child has existing relationships to support them, tolerable stress has the potential actually to be a building block for resilience.

Toxic stress, on the other hand, is something we would never wish upon any child. Toxic stress is chronic stress that can actually change the structure of the brain. The brain is flooded with hormones. Cortisol in doses that high over a long duration is never going to be a good thing.

But in the presence of a loving caregiver, those things that are categorized as toxic stressors can actually be moved into the category of tolerable, which means that they have the potential to build resilience. That’s how powerful relationships are.

2. All feelings are welcome, but all behaviors are not.

Rules help children feel safe, but they’re often hard for us to sit with because we don’t like witnessing our children in distress or having difficult feelings. It’s hard for us as parents to even stick with rules.

One way to gauge whether you are addressing discipline in a way that keeps your relationship close and honors those rules is to tell yourself all feelings are welcome, but all behaviors are not. So ask yourself, “Did I honor my child’s feelings, and was I clear about my expectations for their behavior?” Rules encompass both boundaries and limits. They go hand in hand with sensitive caregiving regulation and modeling the behaviors we want to see in our children.

3. Mom brain isn’t what you think it is.

In fact, the third largest boost in brain development happens during the transition to parenthood. We get our biggest boost in our first few years of life, then adolescence, and then, surprisingly, right at this transition to parenthood. Yet people historically have thought of it as a time when we don’t remember where our car keys are.

And while it’s true that we might not remember where our car keys are, that’s because we are putting an emphasis on keeping our children alive and helping them thrive, so we don’t have time to worry about where our car keys are. We become parents when our children come into our lives; our needs, our way of being, our families, and our larger communities change along with our kids as they grow. That’s a huge time of motivation for change. That’s why we are more likely to quit drinking or smoking at this time. The transition to parenthood stretches our brains, and not just if we are the biological parent. This is shown to be true in fathers and adoptive parents.

Development doesn’t stop as our children grow. The experience of parenting brings with it countless opportunities to get to know ourselves better. It can encourage us to thrive in ways we may have never dreamed of. To become a better parent is to become a better person. So let’s reframe our conception of Mom brain into something far more positive.

3. Co-regulation is the key to self-regulation.

Babies aren’t born with fully developed capacities for self-regulation. They learn it as their brains develop, and it takes well into adulthood for a brain to fully develop. The part of the brain that houses self-regulation is the prefrontal cortex, which takes between 18 and almost 30 years to develop fully.

A primary way we all learn self-regulation is through a process called co-regulation, which can involve various types of responses, like a warm presence of a person that you love, an acknowledgment of a distress that you’re experiencing, and a calming tone of voice, as well as modeling our own process of calming ourselves down.

“The trick to developing a self-regulation muscle as a person, especially as a parent, is figuring out your personal passcode.”

Whatever it is that you tell yourself, you don’t need to have that alarm system go off. I know that New Yorkers feel safer in New York than anywhere else, and as a New Yorker myself, this makes a lot of sense to me. When I moved to Los Angeles from New York City, I went from living in an apartment building where I had no alarm system. Once I moved to Los Angeles, however, I felt much more nervous and got an alarm system. I wanted to know that if somebody were going to break in, a very loud alarm would send a message to the police. When I walk in the door and hear a slow beeping sound like an alarm, that’s the warning that I hear before a message is sent to security, an ambulance, or a firetruck. That’s what we need to pay attention to in our bodies and in our children’s bodies. That beeping is a stress response that tells us to “fight, flight, or freeze.” That’s our body’s alarm system saying there’s an emergency.

But what if there isn’t an emergency? When we get dysregulated because we have an imagined emergency, that moment of a slow beeping warning is the moment where we can stop, take a breath, drink a glass of water, say a little mantra, and put our hands on our hearts. That stops us from setting off the alarm when there isn’t really a threat. When we do this in front of our kids regularly, they see us take three deep breaths (or whatever our particular passcode to our alarm system is). They are learning co-regulation because they see that we know how to regulate our nervous systems. They can borrow our calm while they’re growing their nervous systems, and that co-regulation is highly linked with self-regulated older kids and adults.

The trick to developing a self-regulation muscle as a person, especially as a parent, is figuring out your personal passcode. Over time, you’ll get better at recognizing the signs that your body is about to start sounding that alarm, and you’ll have more warning time to punch in your personal passcode. That might include things like racing thoughts, difficulty focusing, fast heartbeat, dry mouth butterflies, nausea, cold hands, or quick breathing.

4. Repair is a necessary component of growth.

Like strong trees, humans can sway without snapping, and that’s what we rely on as human parents. Psychologist and professor Ed Tronick’s extensive early research on repair has helped us learn why some children become sad, withdrawn, insecure, or angry while others become happy, curious, affectionate, and self-confident. What he learned was that kids who tend to grow up happy and curious aren’t the ones who never experience negative interactions with their parents. Rather, they’re the ones who have learned to trust their parents or well-meaning humans who are willing to make things right when they go temporarily wrong. It isn’t the conflict or the ruptures that hurt us or our relationships; it’s the lack of repair.

“We repair our relationships by being warm, calm, gentle, respectful, connected, empathetic, loving and accepting, even playful together.”

Tronick’s early studies back in the 1970s may not have been the most ethical, but they looked at the social connection between babies and their caregivers. In the first step of the experiment, the mothers and babies were delightfully connected and involved in complex social interactions. The next step, which was quite heartbreaking, was the disengagement. The first two parts of this experiment dramatically showed the social and emotional connectivity between parents and babies, but it was the third phase, when the caregiver returned, that was even more inspiring. Almost instantly, the babies in the experiment began a reparative process with their mothers and reengaged. That was repair and action.

The strength we saw in this famous still-face experiment was the repair. What does it look like in everyday life? It might be as simple as apologies, reconnection, or a laugh. We repair our relationships by being warm, calm, gentle, respectful, connected, empathetic, loving and accepting, even playful together. We know when repair has happened. Sometimes, it’s just a shared laugh or a knowing glance. Other times, it’s an explicit conversation. You know it when you feel it, and the more practice you have, the more you grow.

5. Reflection is the key to freedom.

Reflection is a huge part of not only parenting well but “people-ing” well. Reflection might feel like a luxury. Reflection allows you to sit back and think about your experience being parented, why you feel a certain way, and what you might be worried about in the future that’s making you respond in a particular way.

Actually, though, reflection is freedom because when you reflect, you have an understanding of why you are about to be set off or why you can notice that you’re getting frustrated. You can then step back, understand your impulse to react this way, and take a moment to decide exactly how you want to react. That freedom allows you to respond as the parent you most likely want to be. Take the time for reflection and give yourself the freedom to make choices.

Bacteria in your gut can improve your mood − new research in mice tries to zero in on the crucial strains

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Probiotics have been getting a lot of attention recently. These bacteria, which you can consume from fermented foods, yogurt or even pills, are linked to a number of health and wellness benefits, including reducing gastrointestinal distress, urinary tract infections and eczema. But can they improve your mood, too?

Behavior and mental health are complicated. But the short answer, according to my team’s recently published research, is likely yes.

The beneficial bacteria in probiotics become part of a community of other microscopic organisms living in your digestive system called the gut microbiome. Your gut microbiome contains trillions of a diverse range of bacteria, fungi and viruses.

Hundreds of species of bacteria are native to the intestinal tract. Each species can be broken down into hundreds of strains that can also be dramatically different from each other in their metabolism, byproducts and environmental preferences.

This bacterial diversity is why not all probiotics are built the same. Many research groups have shown that specific strains of Lactobacillus have mood-enhancing effects.

But these effects seem to happen only with the right mix of bacteria in the right conditions. For example, a probiotic that can reduce symptoms of stress in someone who is worried about their calculus final may not work in someone with symptoms of post-traumatic stress disorder.

Yogurt parfair on a tablecloth
The probiotics in your yogurt may play a role in boosting mood. 

Studying mood in mice

In my work as a neuroscientist, I study how the gut influences the brain. My team and I recently conducted experiments in mice that support the idea that gut microbiota play a role in regulating stress.

So how do you measure the mood of mice?

First, we needed to understand how stressed mice behave. So we placed them under short periods of stress: They are restrained for two hours each day, given enough room to move around but not enough to groom or stand up. We envision this as the same type of stress people experience when they’re confined to a car or cubical for hours at a time.

Stressed mice soon exhibited depression- and anxiety-like behaviors, which we measured by monitoring how much time they spent hiding when placed in a new environment or how quickly they try to right themselves when flipped upside down.

While it isn’t surprising that stressed mice hide longer and are slower to right themselves, the power of their poop to change their behavior was.

To see if stressed behavior could be transferred through the microbiome, we used another group of mice that were entirely clean. These mice were free from any bacteria, fungi or viruses and lived in a rubber bubble. They essentially had no microbiome at all.

We exposed them to poop from either stressed mice or normal mice by sprinkling soiled bedding in their enclosures. Microbes from the donor mice started to populate the gut microbiomes of the clean mice.

Within a few weeks, the clean mice exposed to poop from stressed mice started to develop stress- and anxiety-like behavior, even though nothing else had changed. Meanwhile, clean mice exposed to poop from normal mice had no differences in their behavior. This finding suggests that the microbes in poop changed the mice’s behavior.

Which bacteria affect mood?

The results of our experiments led us back to our original question: Which bacteria can change your mood?

We started by comparing the microbes in the poop of stressed and normal mice. In our analysis, we found that a group of bacteria called Lactobacillus was greatly reduced in the stressed mice. Research has linked this group of bacteria to stress reduction before. However, Lactobacillus contains over 170 different species and even more strains.

Currently, the probiotic supplements available to patients are unregulated and often untested. In order to reliably get the most effective strains to patients, they need to be properly tested. So we had to come up with a way to test how different strains affect anxious behavior.

Microscopy image of rod-shaped Lactobacillus stained blue
Lactobacillus are a diverse range of bacteria that can provide potential health benefits in people. 

Instead of tackling this colossal task alone, we created a method that other microbiome scientists can also use to look at this group of bacteria as systematically as possible.

To recreate the same experimental conditions for each species of microbe, we created a group of mice with only six species of bacteria in their microbiome, the bare minimum needed for normal and healthy development, which did not include Lactobacillus. This way, we could add individual strains of Lactobacillus back into the mice’s gut microbiome and observe the effects of each strain on their behavior and biology.

We’ve tested two strains so far: Lactobacillus intestinalis ASF360 and Lactobacillus murinus ASF361. Mice with these two strains of Lactobacillus are more resilient to stress and have quieted neural pathways associated with fear.

What’s next?

Our study on how different strains of Lactobacillus affect mood is just the beginning. We hope that our research will open avenues for other scientists to test different probiotics.

While researchers are reaching a consensus that the bacteria in your digestive tract can influence your mood, and vice versa, there is still a lot of testing to be done in both animals and in people.

Our team is starting to develop ways to systematically test which bacteria may provide the best health outcomes in people and which probiotics are the most effective. In the meantime, give the Lactobacillus in your gut some love through a healthy, probiotics-rich diet.

Cannabis products may harbor fungal toxins harmful to human health, but regulations are uneven or nonexistent

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Hemp and cannabis host many fungi inside and outside the plant, most of which are harmless to most people. However, certain types of fungi such as Aspergillus and Fusarium pose potential health concerns, particularly for the immunocompromised, both through direct infection and consumption of the toxins they produce.

There are currently no state or national testing mandates for Fusasrium toxins in cannabis, and regulations vary greatly for Aspergillus toxins. To better understand the effects of these fungi and their toxins on human health and disease, I assembled a research team of plant pathologists and toxicologists to conduct a review of the scientific literature on fungal contaminants in cannabis.

We found that the toxins these fungi produce can make it through the manufacturing process and remain present in many cannabis products.

Fungal toxins in hemp and cannabis

The 2018 U.S. Farm Bill defined hemp as any part of the plant Cannabis sativa with levels of THC at or below 0.3%. THC is the primary component of Cannabis sativa that has psychoactive effects. Parts with higher levels of THC are considered marijuana.

Medical use of cannabis has been approved in most U.S. states and many countries. To provide the maximum potential health benefits associated with cannabis consumption, such as pain relief, plants need to be free of fungal toxins that can cause harm. However, scientists have found fungal toxin levels in hemp flowers and certain cannabis products that exceed acceptable regulatory levels for other food crops.

Microscopy image of the conidial head of Aspergillus, reminiscent of a fleshy daisy
The conidial head, or fungal spore, of Aspergillus. 

Aspergillosis, a lung infection caused by the fungus Aspergillus, is the most potentially harmful fungal infection associated with cannabis consumption. However, our research team determined that Fusarium toxins in cannabis potentially pose a greater risk to human and animal health than Aspergillus. Researchers have isolated 16 species of Fusarium in cannabis flowers. Many produce toxins that negatively affect humans and animals, including by causing nausea, vomiting, diarrhea, cancer, reproductive disruption and kidney impairment.

These toxins can also worsen disease among those with immune disorders. A 2016 survey of 225 organ transplant professionals found that 43% reported cases of fungal infections associated with marijuana use among their patients who may be immunocompromised.

Addressing fungal toxins in cannabis

The extent of fungal toxins in cannabis and hemp products is still unknown because these toxins are rarely regulated.

Testing for Aspergillus in cannabis varies by state, and acceptable toxin levels range from zero tolerance to no action. Many states rely on methods that don’t distinguish between fungi that are or aren’t harmful and do not regulate individual pathogens.

Although Fusarium toxins are not regulated in hemp or cannabis, they are monitored in major food crops such as corn and wheat because of the severe symptoms they can cause in people and animals.

Person in protective wear examining hemp plants.
Fungal toxin regulation in cannabis is inconsistent across states. 

Controlling fungi in crops is essential for both plant and human health. Because hemp cultivation was until recently restricted by law, and no state or federal research funds were available, disease management strategies remain ill-defined.

Although using resistant cultivars for plant production is a safe, economical and environmentally friendly method to control plant diseases, how cannabis develops resistance against pathogens remains poorly understood.

In states where cannabis cultivation is legal, producers must rely on agricultural products approved for hemp. However, few are registered for use on hemp. Although radiation kills fungi and prevents infection in people, this technique is not universally applied and there are currently no methods for removing mycotoxins from cannabis or hemp.

Before producers, consumers and health practitioners can be assured that cannabis products are safe, filling these knowledge gaps is necessary. Additional research on cannabis pathogens and fungal toxins are also needed, as well as better and more consistent methods to regulate medicinal cannabis.

High fat intake sustains sorbitol intolerance after antibiotic-mediated Clostridia depletion from the gut microbiota.

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Highlights

  • •Low fecal SDH is a potential biomarker for sorbitol intolerance
  • •High fat intake after antibiotics impairs microbiota recovery to lower fecal SDH level
  • •Abundant sorbitol-consuming probiotics deplete sorbitol to protect against intolerance
  • •Activating epithelial mitochondria promotes microbiota recovery to rise fecal SDH levels

Summary

Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolved. Here, we show that a history of antibiotic exposure combined with high fat intake triggered long-lasting sorbitol intolerance in mice by reducing Clostridia abundance, which impaired microbial sorbitol catabolism. The restoration of sorbitol catabolism by inoculation with probiotic Escherichia coli protected mice against sorbitol intolerance but did not restore Clostridia abundance. Inoculation with the butyrate producer Anaerostipes caccae restored a normal Clostridia abundance, which protected mice against sorbitol-induced diarrhea even when the probiotic was cleared. Butyrate restored Clostridia abundance by stimulating epithelial peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling to restore epithelial hypoxia in the colon. Collectively, these mechanistic insights identify microbial sorbitol catabolism as a potential target for approaches for the diagnosis, treatment, and prevention of sorbitol intolerance.

Graphical abstract

Introduction

Sorbitol is a naturally occurring polyol that is poorly absorbed by the small intestine, resulting in a low caloric content. Therefore, sorbitol is used as low-calorie sweetener in “sugar-free” foods, such as sugar-free chewing gum, candy, mints, jam, diet drinks, and chocolate.

1

 The estimated daily sorbitol intake in the UK averages 3.5 g,

2

 which comes mostly from its use as sweetener, but sorbitol is also naturally present at low concentrations in some fruits of the Rosaceae family, such as apples, pears, and apricots.

 Excessive consumption of polyols can trap fluid in the colonic lumen to trigger osmotic diarrhea.

 For example, ingestion of 20 g sorbitol can induce symptoms of carbohydrate intolerance in healthy volunteers, including diarrhea, abdominal distention, and flatulence, but most volunteers ingesting 5 g sorbitol do not develop such symptoms.

 Susceptibility to polyol-induced diarrhea varies among individuals, resulting in heightened intolerance in patients with irritable bowel syndrome (IBS)

 or quiescent inflammatory bowel disease (IBD).

 For example, ingesting 5 g of sorbitol can intensify gastrointestinal symptoms in individuals with IBS,

 whereas consuming 3 g of sorbitol can exacerbate gastrointestinal symptoms in IBD patients.

11

Antibiotic treatment can transiently heighten polyol intolerance by disrupting the gut microbiota, which can impair metabolic functions that remove osmotically active solutes.

 In a mouse model of antibiotic-induced sorbitol intolerance, the addition of 5% sorbitol to the drinking water increases fecal water content during treatment with ampicillin or streptomycin (Str), but not in the absence of antibiotic treatment.

 a transient disruption of the microbiota by antibiotics does not explain the prolonged carbohydrate intolerance in patients with IBS or quiescent IBD.

6

,

 Treatment of prolonged polyol intolerance therefore relies on dietary interventions that reduce the intake of polyols and other poorly absorbed mono-, di-, and oligosaccharides.

19

A recent history of antibiotic usage (between 4 and 56 weeks prior to enrollment) in combination with high fat intake is an environmental risk factor in adult patients for developing diarrhea, abdominal distention, and flatulence.

20

 These individuals can be differentiated from IBS patients by their elevated fecal calprotectin levels (between 50 and 200 μg/g feces), which is a marker of intestinal inflammation. However, intestinal inflammation in these individuals does not rise to the level of IBD, which is characterized by fecal calprotectin levels exceeding 250 μg/g feces during active disease.

21

 Patients with low grade mucosal inflammation that is associated with a history of antibiotics and high fat intake thus represents a syndrome located at the intersection of the clinical spectra of IBS and IBD.

22

,

23

,

24

 Elevated fecal calprotectin levels and diarrhea observed in these patients can be recapitulated in mice exposed to high fat intake in combination with a history of Str treatment.

20

 When antibiotics are combined with maintaining mice on a high-fat (HF) diet, microbiota recovery is impaired even 4 weeks after Str treatment, as indicated by increased Enterobacterales (ord. nov.,

25

 phylum Proteobacteria) and reduced Clostridia (phylum Firmicutes) abundance. These changes in the microbiota composition match those in the feces of patients with a history of antibiotics and high fat intake,

20

 and in IBD patients.

26

,

27

,

28

 As mice with a history of antibiotic treatment and high fat intake recapitulate signs of disease seen in patients with diarrhea, abdominal distention, and flatulence, we wanted to investigate whether exposure to these environmental risk factors creates a mouse model for prolonged sorbitol intolerance that can be used to explore approaches for diagnosis, treatment, and prevention.

Highlights

  • •Low fecal SDH is a potential biomarker for sorbitol intolerance
  • •High fat intake after antibiotics impairs microbiota recovery to lower fecal SDH level
  • •Abundant sorbitol-consuming probiotics deplete sorbitol to protect against intolerance
  • •Activating epithelial mitochondria promotes microbiota recovery to rise fecal SDH levels

Summary

Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolved. Here, we show that a history of antibiotic exposure combined with high fat intake triggered long-lasting sorbitol intolerance in mice by reducing Clostridia abundance, which impaired microbial sorbitol catabolism. The restoration of sorbitol catabolism by inoculation with probiotic Escherichia coli protected mice against sorbitol intolerance but did not restore Clostridia abundance. Inoculation with the butyrate producer Anaerostipes caccae restored a normal Clostridia abundance, which protected mice against sorbitol-induced diarrhea even when the probiotic was cleared. Butyrate restored Clostridia abundance by stimulating epithelial peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling to restore epithelial hypoxia in the colon. Collectively, these mechanistic insights identify microbial sorbitol catabolism as a potential target for approaches for the diagnosis, treatment, and prevention of sorbitol intolerance.

Graphical abstract

Figure thumbnail fx1

Keywords

Sorbitol is a naturally occurring polyol that is poorly absorbed by the small intestine, resulting in a low caloric content. Therefore, sorbitol is used as low-calorie sweetener in “sugar-free” foods, such as sugar-free chewing gum, candy, mints, jam, diet drinks, and chocolate.

1

 The estimated daily sorbitol intake in the UK averages 3.5 g,

2

 which comes mostly from its use as sweetener, but sorbitol is also naturally present at low concentrations in some fruits of the Rosaceae family, such as apples, pears, and apricots.

3

 Excessive consumption of polyols can trap fluid in the colonic lumen to trigger osmotic diarrhea.

4

 For example, ingestion of 20 g sorbitol can induce symptoms of carbohydrate intolerance in healthy volunteers, including diarrhea, abdominal distention, and flatulence, but most volunteers ingesting 5 g sorbitol do not develop such symptoms.

5

 Susceptibility to polyol-induced diarrhea varies among individuals, resulting in heightened intolerance in patients with irritable bowel syndrome (IBS)

6

,

7

 or quiescent inflammatory bowel disease (IBD).

8

,

9

 For example, ingesting 5 g of sorbitol can intensify gastrointestinal symptoms in individuals with IBS,

10

 whereas consuming 3 g of sorbitol can exacerbate gastrointestinal symptoms in IBD patients.

11

Antibiotic treatment can transiently heighten polyol intolerance by disrupting the gut microbiota, which can impair metabolic functions that remove osmotically active solutes.

12

,

13

 In a mouse model of antibiotic-induced sorbitol intolerance, the addition of 5% sorbitol to the drinking water increases fecal water content during treatment with ampicillin or streptomycin (Str), but not in the absence of antibiotic treatment.

14

 However, antibiotic-induced changes in the microbiota composition are short lived, as the gut microbiota regains its normal composition within 5 days after withdrawing Str.

15

,

16

,

17

 Since polyol intolerance resolves as the microbiota recovers after antibiotic treatment,

18

 a transient disruption of the microbiota by antibiotics does not explain the prolonged carbohydrate intolerance in patients with IBS or quiescent IBD.

6

,

7

,

8

,

9

 Treatment of prolonged polyol intolerance therefore relies on dietary interventions that reduce the intake of polyols and other poorly absorbed mono-, di-, and oligosaccharides.

19

A recent history of antibiotic usage (between 4 and 56 weeks prior to enrollment) in combination with high fat intake is an environmental risk factor in adult patients for developing diarrhea, abdominal distention, and flatulence.

20

 These individuals can be differentiated from IBS patients by their elevated fecal calprotectin levels (between 50 and 200 μg/g feces), which is a marker of intestinal inflammation. However, intestinal inflammation in these individuals does not rise to the level of IBD, which is characterized by fecal calprotectin levels exceeding 250 μg/g feces during active disease.

21

 Patients with low grade mucosal inflammation that is associated with a history of antibiotics and high fat intake thus represents a syndrome located at the intersection of the clinical spectra of IBS and IBD.

22

,

23

,

24

 Elevated fecal calprotectin levels and diarrhea observed in these patients can be recapitulated in mice exposed to high fat intake in combination with a history of Str treatment.

20

 When antibiotics are combined with maintaining mice on a high-fat (HF) diet, microbiota recovery is impaired even 4 weeks after Str treatment, as indicated by increased Enterobacterales (ord. nov.,

25

 phylum Proteobacteria) and reduced Clostridia (phylum Firmicutes) abundance. These changes in the microbiota composition match those in the feces of patients with a history of antibiotics and high fat intake,

20

 and in IBD patients.

26

,

27

,

28

 As mice with a history of antibiotic treatment and high fat intake recapitulate signs of disease seen in patients with diarrhea, abdominal distention, and flatulence, we wanted to investigate whether exposure to these environmental risk factors creates a mouse model for prolonged sorbitol intolerance that can be used to explore approaches for diagnosis, treatment, and prevention.

What is the best AFib diet?

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Certain foods, such as caffeine or alcohol, have the potential to trigger AFib. A diet that promotes heart health may help manage and reduce the symptoms of this condition.

Atrial fibrillation (AFib) is a type of arrhythmia that affects the upper chambers of the heart. The electrical impulses that control these chambers fire in a disorganized way, leading to an irregular heartbeat.

AFib itself is not a life threatening condition. However, it can increase the risk of stroke, blood clots, and congestive heart failure. A suitable diet may also decrease the risk of developing other heart conditions alongside AFib.

This article explores foods to eat and avoid with AFib, and other potential tips for managing this condition.

The best AFib diets

A diet rich in vegetables, whole grains, and legumes may help people reduce AFib episodes.

The American Heart Association (AHA)Trusted Source recommends that people with AFib consume foods low in:

A 2023 research article examined medical data from 121,300 people in the United Kingdom. The authors associated diets containing ultra-processed food with an increased risk of AFib.

In contrast, plant-based diets had no association with AFib.

They associated Mediterranean and Dietary Approaches to Stop Hypertension (DASH) diets to lower incidents of AFib. However, the authors noted this association was not significant after considering lifestyle factors.

A 2024 articleTrusted Source suggests plant-based diets and the Mediterranean diet contain components that research links to a lower risk of AFib, including fruits, whole grains, and healthy fats. However, further research is necessary to investigate the benefits.

Mediterranean diet benefits

The Mediterranean diet may also offer the following benefits:

Although diets like the Mediterranean diet may have a positive effect on AFib, people should speak with a healthcare professional, such as a registered dietitian, before changing their diet to manage this condition.

Foods to eat for AFib

The AHATrusted Source lists these foods to eat on the Mediterranean diet:

Meal plans

Mediterranean diet meals should consist of:

  • a good portion of vegetables
  • a source of protein
  • a complex carbohydrate
  • unsaturated fat, such as:
    • olive oil
    • avocado oil
    • flaxseed oil
    • hemp seed oil

If a person needs inspiration for potential meals under the Mediterranean diet, the AHATrusted Source provides a wide range of recipe ideas.

Plant-based diets

If a person is vegetarian or vegan, they can follow a plant-based diet consisting of:

Foods to avoid for AFib

Foods to avoid may include those that directly trigger symptoms and raise the risk of AFib complications. Foods and drinks to avoid may include:

Caffeine and energy drinks

The AHATrusted Source recommends that people avoid excessive amounts of caffeine to lower their risk of AFib. However, a 2019 study found that drinking 1–3 cupsTrusted Source of coffee daily may reduce AFib risk in males.

If a person believes that caffeine could be a personal trigger, they may wish to avoid caffeinated foods and drinks, such as coffee and tea.

People with AFib can also speak with their doctor about the benefits and risks of reducing their caffeine intake.

Alcohol

The AHATrusted Source also warns against drinking excessive amounts of alcohol with AFib.

A 2022 meta-analysisTrusted Source suggests alcohol may be a trigger for AFib. The authors suggest that any amount of alcohol may increase the risk of AFib in men, and over 1.4 drinks daily may increase the risk for women.

However, the authors highlight the need for further research into the cause of this gender difference, including whether alcohol type or frequency of consumption has an effect.

Red meat

Red meats such as beef or lamb tend to have higher amounts of saturated fat than white meat. The AHATrusted Source recommends people with AFib consume a diet low in saturated fats.

Processed foods

Processed foods, such as ready meals, carbonated soft drinks, or hot dogs, tend to have large quantities of salt and preservatives. It may be best to limit the intake of these as they can adversely affectTrusted Source the heart.

Sugary foods and drinks

The British Heart Foundation recommends that people choose sugar-free snacks and swap snacks with added sugar with alternatives, such as:

  • fruit
  • Greek yogurt
  • nut butter
  • cashew nuts
  • almonds

Controlling blood sugar levels is particularly important for people with diabetes since diabetes is a risk factorTrusted Source for AFib.

Salt

Someone may have more frequentTrusted Source AFib episodes if they consume food with large quantities of salt. Reducing salt intake may be a useful way to help reduce AFib.

Other tips for managing AFib

There are several other ways a person with AFib can adjust their lifestyle to promote heart health.

Quit smoking

According to a 2018 article, people who smoke may be 2.1 times more likelyTrusted Source to develop AFib. Quitting smoking or not starting smoking at all may significantly improve a person’s risk of getting AFib.

Manage sleep conditions

A 2019 systematic reviewTrusted Source concluded that getting less than six hours of sleep a night or over eight hours a night may increase the risk of AFib.

Sleep deprivation, obstructive sleep apnea, and other sleep disorders that disrupt sleep may also increaseTrusted Source the risk of AFib.

The management of sleep apnea and stress may help a person improve the quality of their sleep.

Improve relaxation

Stress and anxiety have a significant effect on AFib. A 2023 literature reviewTrusted Source suggests that stress or anxiety and AFib may have a bidirectional relationship, in which both can trigger the other.

The authors suggest that stress biomarkers, such as elevated cortisol levels, may play a role in AFib development. However, further research is necessary.

Regular relaxation and stress reduction through activities like yoga may help someone manage these emotions.

Learn about other activities and natural remedies that may help with AFib.

Summary

AFib causes an irregular heartbeat. Several risk factors, such as obesity, high blood pressure, and diabetes, make it more likely that a person will develop AFib.

A healthful, balanced diet can help reduce the risk factors that cause AFib and, in some cases, reduce its symptoms. The Mediterranean diet or a plant-based diet with plenty of fruits, vegetables, and unsaturated fats may be beneficial.

Other changes that may improve AFib include doing moderate exercise several times per week, getting high quality sleep, stopping smoking, and prioritizing time to relax and reduce stress.

6 Ways to Upgrade Your Caesar Salad

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There is no salad more ubiquitous than the caesar, a go-to classic found on menus everywhere from diners to golf clubs to the pricey steakhouse you’ve been dying to try. But if you’re a bit bored with the traditional version, you’re in luck. There are tons of potential ways to tweak or upgrade your greens while still keeping the creamy, tangy taste of your favorite salad. Read ahead for some easy upgrades.

Put It on Pizza

Pizza has long been the final destination for some weird toppings, but trust us, this one is a winner. The garlicky salad dressing replaces tomato sauce on top of dough, and then greens are thrown on after baking for a veggie-heavy take on your typical slice.

Wrap It Up

If you’re looking for something heartier than a salad, putting your caesar into a wrap can make for a more satisfying meal. A wrap is also a great answer to a better brown bag lunch. You’ll be glad that you don’t have to eat yet another boring sandwich during your lunch break. 

Grill Your Produce

If you just want to tweak the classic recipe, you can grill your romaine briefly for a smoky flavor. Adding charred tomatoes into your bowl can also also provide a departure from the norm. 

Swap Out Your Greens

This move may be slightly controversial, but if you have an experimental streak, why not swap out romaine lettuce for something else green? Recipes abound for kale caesar salads, which is a great alternative (so long as you massage your kale to soften it and cut down on the bitterness). You can also reach for brussels sprouts or spinach as a base. 

Rethink Your Croutons

Forget those stale box croutons you bought at the supermarket ages ago. Try your hand at making your own with your preferred spices and herbs and never look back. Searching for other options to add crunch to your meal? You can include nuts or roasted chickpeas instead of croutons.

Add in Some Avocado

For those hunting for a more waistline friendly version of this meal, you can substitute an avocado-based dressing for the original. You won’t lose any of the creaminess with the paleo versions, trust us!

Your caesar salad doesn’t need to be topped with a sad, dry chicken breast. This version features citrusy shrimp and hard boiled eggs for enough protein to keep you full for hours. Get the recipe. 

Plant Protein Kale Caesar Salad Tacos

Tacos and caesar salad? It might sound like an odd food combination, but you’ll change your tune after trying this twist, which also counts quinoa, chickpeas, and avocados as additions, all in a crunchy shell. Get the recipe. 

Brussels Sprouts Caesar Salad

Brussels sprouts make for a unique base for this lemony caesar salad. After shredding them and topping them with dressing, you won’t have to force anyone to finish their vegetables. Get our Brussels Sprouts Caeasar Salad recipe. 

Kale Caesar Salad

Your favorite trendy green and your favorite salad are pretty much a match made in heaven. Throw in some lime instead of lemon for a slightly offbeat flavor addition. Get the recipe.

BLT Caesar Salad

If you’re a bacon fan, you’ve probably already been adding it to your salads for eons. Why not pair it with tomato for a take on the BLT? Bet you won’t even miss the bread. Get the recipe. 

Mustard Greens Salad with Anchovy Dressing

This mustard greens salad is like the older, mature, and better-traveled cousin of the sad diner caesar salad. An anchovy-based dressing calls to mind similar flavors, but crisp pear and gruyere cheese give it a fancier flair. Get our Mustard Greens Salad with Anchovy Dressing recipe. 

Chicken Caesar Pasta Salad

There’s no reason to keep your salad and main course separate when merging the two is this delicious. With easy-to-find, fresh ingredients, this is definitely a crowd-pleaser to bring along to a potluck or dinner party.

Semen Has Its Own Microbiome—And It Might Influence Fertility

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Recent research found a species of bacteria living in semen that’s associated with infertility and has links to the vaginal microbiome

Sperm feritlizing human egg
Human sperm cells fertilizing egg ovum.

Semen was once assumed to be naturally microbe-free; any bacteria found in the fluid was assumed to be a sign of infection. But research over the past decade has shown that semen has its own microbial community, just like microbiomes of the gut and vagina. And now scientists have completed one of the biggest investigations to date on the semen microbiome’s potential link to infertility. Their new findings, published in Scientific Reports, single out a bacterial species that can also be associated with health and fertility issues in the vaginal microbiome.

The semen microbiome can contain a mélange of microbes. Most come from glands in the upper reproductive tract—including the testes, seminal vesicles and prostate—which contribute various components to semen. “Drifter” bacteria from urine and the urethra can also get swept up in the fluid during ejaculation, and microbes from a person’s blood or from their sexual partners might also take up residence in semen.

But how any of these individual species of bacteria might affect health has largely been a mystery. “I would assume that there are bacteria that are net beneficial, that maybe secrete certain kinds of cytokines or chemicals that improve the fertility milieu for a person—and then there are likely many that have negative effects,” says the new study’s co-author Sriram Eleswarapu, a urologist at the University of California, Los Angeles.

Eleswarapu likens the new research to a “fishing expedition” for bacteria in semen that might be associated with infertility. Around 50 percent of infertility cases are attributed to male individuals and can be identified by doctors, but specific treatment options for sperm are limited and used in select cases. One of the most common procedures is in vitro fertilization, in which a person who can produce sperm only needs to provide a sperm sample, while a person who can become pregnant endures the invasive steps of the process, including hormone drug injections and collecting eggs through an ultrasound probe. Learning how the semen microbiome is involved in infertility—and developing drugs that target specific bacteria—could help even out that burden.

To survey the microbiome, Eleswarapu and his team gathered semen samples from 73 men. About half were fertile and already had children; the other half had originally come to Eleswarapu’s clinic for a fertility consultation. “These are people who have been trying to get pregnant with their partner, and they’ve been unsuccessful,” Eleswarapu says. This latter group’s semen samples had a lower sperm count or motility (the sperm’s ability to swim), both of which can contribute to infertility.

Many bacteria from inside the body don’t grow well in the laboratory, so the researchers turned to genetic sequencing to identify species in the semen microbiome. They found five that were common among all the participants. But high levels of one species, called Lactobacillus iners, corresponded with sperm motility issues in those who were experiencing infertility. L. iners was especially interesting to the researchers because it’s also commonly found in the vaginal microbiome.

Around 90 to 100 percent of a healthy vaginal microbiome is made up of bacteria from the Lactobacillus genus, called lactobacilli, and L. iners is among the four most common species, says Caroline Mitchell, an obstetrician-gynecologist at Massachusetts General Hospital, who wasn’t involved in the new study. To Mitchell, the findings are an indication that the semen and vaginal microbiomes can influence each other.

Still, L. iners isn’t always healthy, or even neutral, in the vaginal microbiome. “Many people have it, and it can be good; it can be bad,” Mitchell says. Some studies show that excessive levels of L. iners in the vaginal microbiome can be associated with bacterial vaginosis, an uncomfortable overgrowth of bacteria. High levels of L. iners in the vaginal microbiome have also been linked to infertility, which lines up with the new findings on the semen microbiome.

Scientists can only speculate about exactly how L. iners could affect sperm motility. It may be related to this species’ production of lactic acid, the same chemical that causes the burning feeling in your muscles during a workout. All lactobacilli produce lactic acid, but L. iners creates a specific variation of the molecule that can induce damaging inflammation—and inflammation has been previously found to impact sperm quality. In the new study, the authors suggest the increased lactic acid from L. iners might prevent sperm from swimming normally.

Other studies have found that several more Lactobacillus species can also harm motility, Mitchell says. Some researchers have hypothesized that the vaginal microbiome’s rich abundance of Lactobacillus slows down unhealthy sperm to increase the chances that a healthy one will fertilize the egg.Having too many lactobacilli in the semen microbiome, however, might hamper even healthy sperm from the start.

Doctors currently treat bacterial vaginosis by combining an antibiotic and a probiotic to help rebalance the vaginal microbiome, and Eleswarapu envisions treating an abnormal semen microbiome in a similar way. The team plans to investigate specific molecules and proteins these bacteria produce and to test whether they slow sperm down in the lab. “If we can identify how they exert that influence,” Eleswarapu says, “then we have some drug targets.”

Novel Drug Combo Offers Hope for Advanced HER2-Negative Breast Cancer

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woman lymph armpit examination. Node-Positive Breast Cancer

Researchers at the Johns Hopkins Kimmel Cancer Center have unveiled a promising new treatment approach for advanced HER2-negative breast cancer, using a three-drug combination that significantly improved responses in patients suffering from the disease.

The study, published in Nature Cancer, involved a combination of a histone deacetylase (HDAC) inhibitor, which halts tumor cell division by inducing chemical changes, along with two types of immunotherapy known as checkpoint inhibitors—working by unleashing the immune system’s power to target and destroy cancer cells.

Led by Evanthia Roussos Torres, PhD, the study enrolled 24 women with HER2-negative metastatic breast cancer, including both hormone receptor-positive and triple-negative cases. The results were striking, with an overall response rate (ORR) of 25 percent across all participants and an even more impressive ORR of 40 percent among those with triple-negative breast cancer.

Breast cancer is the most common cancer among American women, with approximately 300,000 new diagnoses each year in the United States. The majority of these cases are hormone receptor-positive and HER2-negative, underscoring the significance of developing effective treatments for this patient population.

Triple-negative breast cancer, accounting for 10–15 percent of cases, poses particular challenges due to its aggressive nature and limited treatment options.

Importantly, the study demonstrated the safety and tolerability of the combination therapy, with no patients needing to discontinue treatment due to adverse effects. The average progression-free survival (PFS) at six months was 50 percent, indicating that half of the participants experienced no disease progression during this period.

“Our results support the hypothesis that pre-treatment with the HDAC inhibitor entinostat, combined with dual immune checkpoint inhibitors, is a safe and promising strategy for metastatic breast cancer,” Torres said, emphasizing the significance of the findings.

She also underscored the need for further evaluation in larger phase II studies to assess the treatment’s efficacy more comprehensively.

“To our knowledge, this is the first published study that investigates treatment with an HDAC inhibitor in combination with dual immune checkpoint inhibitor therapy in patients with advanced breast cancer,” said Elizabeth Jaffee, PhD, a co-author of the study.

The researchers noted that while immune checkpoint inhibitors have revolutionized the treatment landscape for many solid tumors, their effectiveness in breast cancer has been limited. This novel combination therapy presents a potential solution to this challenge.

“Our study highlights the need for a deeper investigation of the breast cancer tumor microenvironment with a focus on changes in myeloid (immune) cell populations to determine their role in sensitization of the tumor microenvironment to treatment with immune checkpoint inhibitors,” Torres concluded in a press statement.

A Leading Memory Researcher Explains How to Make Precious Moments Last

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Our memories form the bedrock of who we are. Those recollections, in turn, are built on one very simple assumption: This happened. But things are not quite so simple. “We update our memories through the act of remembering,” says Charan Ranganath, a professor of psychology and neuroscience at the University of California, Davis, and the author of the illuminating new book “Why We Remember.” “So it creates all these weird biases and infiltrates our decision making. It affects our sense of who we are.” Rather than being photo-accurate repositories of past experience, Ranganath argues, our memories function more like active interpreters, working to help us navigate the present and future. The implication is that who we are, and the memories we draw on to determine that, are far less fixed than you might think. “Our identities,” Ranganath says, “are built on shifting sand.”about:blank

What is the most common misconception about memory? People believe that memory should be effortless, but their expectations for how much they should remember are totally out of whack with how much they’re capable of remembering.1

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In the 1880s, the pioneering German memory researcher Hermann Ebbinghaus conducted studies suggesting that people lose nearly two-thirds of newly learned information within a day. Another misconception is that memory is supposed to be an archive of the past. We expect that we should be able to replay the past like a movie in our heads. The problem with that assumption is that we don’t replay the past as it happened; we do it through a lens of interpretation and imagination. about:blank

How much are we capable of remembering, from both an episodic2

2
Episodic memory is the term for the memory of life experiences. and a semantic3

3
Semantic memory is the term for the memory of facts and knowledge about the world. standpoint? It’s exceptionally hard to answer the question of how much we can remember. What I’ll say is that we can remember an extraordinary amount of detail that would make you feel at times as if you have a photographic memory. We’re capable of these extraordinary feats. I would argue that we’re all everyday-memory experts, because we have this exceptional semantic memory, which is the scaffold for episodic memory. I know it sounds squirmy to say, “Well, I can’t answer the question of how much we remember,” but I don’t want readers to walk away thinking memory is all made up. about:blank

But if memories are malleable, what are the implications for how we understand our “true” selves? At the risk of being pretentious, I’ll get philosophical for a second.about:blank

You’re not being pretentious. OK, good, because I always have this critical peer reviewer in the back of my head saying, “Don’t say that!” But your question gets to a major purpose of memory, which is to give us an illusion of stability in a world that is always changing. Because if we look for memories, we’ll reshape them into our beliefs of what’s happening right now. We’ll be biased in terms of how we sample the past. We have these illusions of stability, but we are always changing. And depending on what memories we draw upon, those life narratives can change.about:blank

Tell me more about what you mean when you say “illusion.” I probably overstated it with the word “illusion,” but there is an illusionary component. I think we have this illusion that much of the world is cause and effect. But the reason, in my opinion, that we have that illusion is that our brain is constantly trying to find the patterns. One thing that makes the human brain so sophisticated is that we have a longer timeline in which we can integrate information than many other species. That gives us the ability to say: “Hey, I’m walking up and giving money to the cashier at the cafe. The barista is going to hand me a cup of coffee in about a minute or two.” This is everyday fortunetelling that we do. There’s nothing that says that the barista won’t throw this coffee at me. There is this illusion that we know exactly what’s going to happen, but the fact is we don’t. Memory can overdo it: Somebody lied to us once, so they are a liar; somebody shoplifted once, they are a thief. If people have a vivid memory of something that sticks out, that will overshadow all their knowledge about the way things work. So there’s kind of an illusion there.about:blank

If what we’re remembering, or the emotional tenor of what we’re remembering, is dictated by how we’re thinking in a present moment, what can we really say about the truth of a memory? I think of memory more like a painting than a photograph. There’s often photorealistic aspects of a painting, but there’s also interpretation. As a painter evolves, they could revisit the same subject over and over and paint differently based on who they are now. We’re capable of remembering things in extraordinary detail, but we infuse meaning into what we remember. We’re designed to extract meaning from the past, and that meaning should have truth in it. But it also has knowledge and imagination and, sometimes, wisdom.about:blank

I think everyone has seemingly inexplicable memories that stick with us. One for me is, a lifetime ago, sitting in an internship and locking eyes with a person across the room — whom I never spoke to. This two-second interaction is still kicking around in my head 20 years later. What could explain that? Neuroscience is terrible for picking out any one thing and saying why it happened. But if you think about it from an evolutionary perspective, memory, often, is educated guesses by the brain about what’s important. So what’s important? Things that are scary, things that get your desire going, things that are surprising. Maybe you were attracted to this person, and your eyes dilated, your pulse went up. Maybe you were working on something in this high state of excitement, and your dopamine was up. Maybe she had a T-shirt on, and it was like, “Oh, I know about that.” It could be any of those things, but they’re all important in some way, because if you’re a brain, you want to take what’s surprising, you want to take what’s motivationally important for survival, what’s new.about:blank

On the more intentional side, are there things that we might be able to do in the moment to make events last in our memories? In some sense, it’s about being mindful. If we want to form a new memory, focus on aspects of the experience you want to take with you. If you’re with your kid, you’re at a park, focus on the parts of it that are great, not the parts that are kind of annoying. Then you want to focus on the sights, the sounds, the smells, because those will give you rich detail later on when you remember it. Another part of it, too, is that we kill ourselves by inducing distractions in our world. We have alerts on our phones. We check email habitually. So you don’t remember being there, because to some extent you were never really there in the first place. If you set time with your child, don’t check email, and turn off your alerts. That’s the idea. Technology can be helpful for memory, but usually not in the way we use it. You’re not really there if you’re mindlessly taking pictures, because it takes over the experience. When we go on trips, I take candid shots. These are the things that bring you back to moments. If you capture the feelings and the sights and the sounds that bring you to the moment, as opposed to the facts of what happened, that is a huge part of getting the best of memory.about:blank

I’m thinking of concerts where you see people watch the whole show through their phones. You’re saying that the emotional connection to the event later onwill be dimmer for them than if they’d mostly kept their phone in their pocket, even at the expense of a more complete record? There’s conflicting data on taking pictures: Most of the data suggests that it’s bad for memory, but there’s one study that found that it could be good for memory if you’re focused on the details that would put you back into that moment. For instance, I saw the Descendents. They came out for the encore, and Bill Stevenson4

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The drummer for the Descendents, a long-running California punk band. comes out in front of the stage. He’s like: I want to take a look at this audience. I’ve been playing for 40 years, and I’m finally at a point where I get to appreciate the audience. I took a picture of that, and that was one of the highlights of the show for me — seeing these guys who were a soundtrack for my adolescence be human beings in that moment. about:blank

I oftenfind myself going back to music that I associate with melancholy memories. Yeah, I mean, you’ve got a legion of Smiths fans all over the world who do that.about:blank

But what is the neuroscientific or psychologists’ explanation for why we would be drawn to re-experiencing melancholy memories? That’s a great question. The science part of it is that we know for a fact that people tend to reminisce more about certain periods in their life. They call it the reminiscence bump.5

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As Ranganath writes in “Why We Remember,” the “reminiscence bump” — the centrality of memories from the ages of about 10 to 30 — shows up when people list their favorite movies, books or music, which tend to come from that period in peoples’ lives. These are the most formative years for our sense of self in some ways. We’re becoming independent from our parents, and we’re developing our careers and building relationships and so forth. When you reminisce about those periods, you go back to the highs and lows, the beginnings and ends. Typically, those are the things that you remember the most in life. It depends on what you need in the moment. Sometimes we get solace from going back to these melancholy times and saying, “Hey, I feel better now” or “I’ve grown from the experience.” We still need to process that stuff, and we go back. Music has this weird ability to trigger emotional response. about:blank

Can you still picture the first concert you went to?6

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In “Why We Remember,” Ranganath writes that the first rock concert he ever went to was one given by the British rock band Def Leppard. I think I can. I remember that Joe Elliott’s voice was just nowhere near as good as it was on “Pyromania.” Rick Savage was still pretty handsome in person. You can’t help but notice that. Steve Clark was supercool, with his scarf and everything. He looked rock ’n’ roll. That’s what I can remember. about:blank

In the book, you say this concert is a central memory. It was.about:blank

When do you think it happened? It must have been 1985.about:blank

Def Leppard was not on tour in 1985.7

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Def Leppard’s drummer, Rick Allen, lost his arm in a car accident on Dec. 31, 1984. The band did not play live again until August 1986. Oh! Brutal! about:blank

Does that matter for the memory? That was a silly example, but this goes back to the question of whether the factual truth of a memory matters to how we interpret it. I think it matters to have some truth, but then again, many of the truths we cling to depend on our own perspective. There’s a great experiment on this. These researchers had people read this story about a house.8

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The study was “Recall of Previously Unrecallable Information Following a Shift in Perspective,” by Richard C. Anderson and James W. Pichert. One group of subjects is told, I want you to read this story from the perspective of a prospective home buyer. When they remember it, they remember all the features of the house that are described in the thing. Another group is told, I want you to remember this from the perspective of a burglar. Those people tend to remember the valuables in the house and things that you would want to take. But what was interesting was then they switched the groups around. All of a sudden, peoplecould pull up a number of details that they didn’t pull up before. It was always there, but they just didn’t approach it from that mind-set. Sowe do have a lot of information that we can get if we change our perspective, and this ability to change our perspective is exceptionally important for being accurate. It’s exceptionally important for being able to grow and modify our beliefs. But it’s exceptionally hard. about:blank

People get stuck in memories, whether they’re traumatic or more benignly negative. What are ways people can get unstuck? It’s very hard. You know, the training environment I was in was very down on psychoanalysis, but it always comes back to memory. A lot of that benefit is from the sharing of memories. Maybe it’s a sad memory, but I’m telling you with the goal of helping me get over it. That in and of itself changes my perspective. We know that people tailor their message for the listener. Then you reflect it back to me and reorganize it as an outsider. Once we go back and forth, we’re updating the memory to something that’s no longer my own. It’s now shared. When you tell someone, “You shouldn’t be ashamed,” it changes that whole relationship with the past. The first patient I ever did therapy with, he had a driving phobia. He worked through the behavior-therapy part, which is just drive, drive, drive until you habituate that biological fear response. But he didn’t feel better. Eventually he told me that he had a memory. How much of this was true, how much of it wasn’t, I didn’t know, but it didn’t matter. He was gay, and he came out of the closet with his dad and got into an argument with him and then was in the car afterward and got into a car accident.about:blank

Pretty clear! Yeah, exactly. It was about processing that memory and what it meant to him. He hadn’t told this to anyone; I don’t know that he had even thought about it that much. That was deep for me.about:blank

Do you think there is some core unchanging self? Something that makes us us? Or is it all just this flowing assemblage of interpretations of memories that make the present make sense? Is that sense of self static? I would say that some parts of it are. Memory gives us the power to shift our sense of who we are. If you believe you’re a failure, a lot of the power of thinking positive is remembering those times when you weren’t and being able to supplement those beliefs. There’s a dynamic sense of the self. I grew up in an immigrant family under challenging circumstances, and that part of myself is locked away from most anyone I interact with. We have these little compartments that are rooted somewhat in memory that we can access at different moments.about:blank

You say in the book that you dealt with racism growing up.9

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Ranganath, who is 52, grew up in San Jose, Calif. Is that what you’re talking about? Yeah. It was a different time, and there were very few people who weren’t white in my neighborhood. At the same time, my parents were also concerned about fitting in. There was a sense of, “At home, we have this Indian identity, but when you go out to other people’s houses, you can eat meat and do what you need to do to fit in.” On both sides, I’m being told, You’re different. I haven’t talked about this. When I was a kid, my teachers said I had attention-deficit disorder. I was impulsive. All my teachers hated me. They said I should have skipped a grade, but socially I wasn’t there. So I was different in that way too. All this stuff gave me this weird sense of self. I didn’t understand normal behavior well enough to be normal, but I desperately wanted to fit in. That’s where psychology really got to me, especially once I started to see that nobody really gets the truth. Everybody has weird flaws in their judgment. about:blank

But what do you do with those negative formative memories? I put things in little compartments. Inside, I’m this nerd who’s picked last. When I’m feeling bad, those memories are there, and that’s who I feel like. It’s a constant putting on the right hat at the right moment. Sometimes it feels like masking. But who I am now is the only reality. All that past stuff is grist for the mill, but it’s not reality. That is the part that I struggle with. That’s the part that, when I was doing therapy, I tried to remind other people of. A lot of it is just reminding yourself, This is who I am now. Because it’s not like my being a nerd and being hated back then is more real than getting to do an interview now with somebody who interviewed Iggy Pop.10

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“Iggy Pop Isn’t About to Whitewash His Past,” published Jan. 1, 2023. This is reality, and nothing else matters.

A Man Fell Victim to ‘Alaskapox’, a Mysterious Virus From the Wilderness.

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strange light in a dark forest at night silhouette of person standing in the dark forest with light dark night in forest at fog time surreal night forest scene horror halloween concept fairytale

  • An Alaska man recently died following complications from the ‘Alaskapox’ virus.
  • Only discovered in 2015, this is the first reported case of the virus ending in death.
  • The Alaskapox virus is believed to spread from small mammals to humans, but scientists aren’t sure exactly how.

Before 2015, we didn’t even know about a new ‘Alaskapox’ virus. Now, that rare virus has claimed the life of an elderly Alaskan man, and the location of Alaskapox (AKPV) seems to have spread across the state.

In a bulletin released by the Alaska Section of Epidemiology, details about the rare virus—the first-ever case was spotted in a female in 2015, and a total of seven AKPV cases have been reported to epidemiologists in total—reveal both its history just how bad its affects can be.

In September of 2023, an elderly man from the Kenai Peninsula (in a highly immunocompromised state) was treated off and on for six weeks for a tender area under his right shoulder. The condition only worsened, and the infection did not respond to antibiotics. He was eventually hospitalized, as the infection impacted his ability to move his right arm. The infection grew while the man stayed in an Anchorage hospital, and multiple tests eventually submitted to the Centers for Disease Control and Prevention were consistent with AKPV. The patient was never able to fully recover and died in January.

“This is the first case of severe Alaskapox infection resulting in hospitalization and death,” the bulletin states. “The patient’s immunocompromised status likely contributed to illness severity.”

But this also represented the first case of AKPV outside of the interior region near Fairbanks, where all previous cases of AKPV were reported. This indicates, unfortunately, that “AKPV appears to be more geographically widespread in Alaska’s small mammals than previously known and warrants increased statewide awareness among clinicians.”

In this most recent case, experts believe that the man contracted the virus through a stray cat he was caring for. They can’t be certain, though.

AKPV is believed to live within small mammals—most commonly red-backed voles and shrews. The mechanism by which the virus spreads from the mammals to humans isn’t yet known. Belonging to the same Orthopoxvirus genus as smallpox, there’s no current evidence that the AKPV can spread between humans, but other viruses in the same family can spread via direct contact with skin lesions

Before the Kenai Peninsula case, all previous cases were found in people living near Fairbanks, and all caused skin lesions. Some people also had swollen lymph nodes and joint or muscle pain. None were hospitalized for the virus, and the lesions healed after a few weeks.

The most recent case may have included a stray cat that regularly hunted small mammals scratching the man near the area in which the skin irritation started. Serum and mucosal swabs collected from the cat were submitted to the CDC for antibody and orthopoxviral testing, but all were negative.

“The route of exposure in this case remains unclear,” the state wrote, but leaves open the thought that the scratches from the cat still represent a “possible source of inoculation through fomite transmission.” This is further bolstered by the fact that the man lived alone in a forested area with no recent travel, no contact with someone who had recently traveled, and no contact with anyone displaying lesions.

While still quite rare, the latest AKPV case deepens the mystery surrounding the relatively young virus.