Randi Hutter Epstein M.D. M.P.H.

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Transforming Our Thinking About Bad, and Even Good, Stress

Many who knew Bruce S. McEwen, Ph.D., either at The Rockefeller University where he ran a laboratory or as a guest at one of his homes in New Jersey or Maine, said the same thing:  For a high-powered New York City-based scientist, McEwen was unusually serene.

But McEwen was deep in stress for more than 50 years.

He conducted pioneering work on stress in the brain in the 1960s and trained a generation of the leaders in the field. I had the privilege of speaking with him a few months ago while exploring the truth behind the old adage about stress hindering fertility.

We had a few fruitful conversations–not  limited to fertility. We chatted stress and its broader impact on health. We talked even talked about the good stress.

Last week, I was devastated to hear that he died after complications from a stroke. McEwen was 81. One of his articles was published on the day he died: January 2, 2020.

In the New York Times obituary that I wrote and that came out today, I touched on his discoveries. His initial study showed that corticosterone, a stress hormone, latched onto the hippocampus, the brain center for learning and memory. This research paved the way for others to show that unrelenting stress causes a spike in stress hormones (cortisol along with other chemical mediators) that shrinks parts of the hippocampus (and swells the amygdala, known for vigilance against a threat).

What drew me to McEwen was, of course, his fascinating research but also that he practiced what he preached. If you were lucky enough to catch a few minutes with him, somehow his approach to life wafted through the room or phone lines, as the case may be. You felt a little more, well, calmer. Perhaps it was his Midwestern mild manner (he grew up in Michigan) compared to my New Yorker neuroses.

Since immersing myself in his research over the past weeks, going over our conversations and listening to his many talks on YouTube, I’ve been reciting a few of his lessons, like mantras. They remind me that a few minutes a day to unwind, to take deep breaths, or to meditate has both immediate and long-term health implications.

  • Reducing stress is good for your brain, right down to the genetic switches.
  • Fleeting stress is a good thing: the kind that energizes you for, say, a talk or test.
  • Stress is not something that happens to you, but the way you respond.

That last one is a tricky one because, in the thick of freaking out about some frustrating incident or a screw-up at work, it’s easy to believe that our racing heart, our shallow breath, our nail-biting infuriation is the right way, or the only way,  to behave. It’s not me. It’s everything done to me. But it’s at those moments, when you realize that the day may be going off course (it may be something you did wrong that needs to be fixed; or something someone did wrong to you), but you can still control your physical responses. You cannot deep breathe away a mishap but you can control the way you allow your thoughts to dwell.

McEwen leaves a massive legacy in neuroscience: he ushered in a new way of thinking about stress. And yet, according to his wide network of friends, students, and colleagues, he also leaves behind another important lesson:

McEwen was kind, supportive, and engaged in life inside and outside his lab. He played tennis, drew, painted, and enjoyed a good glass of red wine with family and friends. He was a dog-person (which ranks high in my books). Students remember his Schnauzer wandering the Rockefeller and sometimes in the faculty club.

Does niceness and companionship help people cope with stress? I would say so. And, in turn, it just may foster better focus and learning. To be sure, avoiding bad stress and engaging in good stress is not a guarantee against every chronic ailment, but it will certainly make the journey more pleasant.McEwen, Bruce S. and Huda Akil, “Revisiting the Stress Concept: Implications for Stress Disorders,” The Journal of Neuroscience, January 2, 2020 40:1 12-21

Here’s a link to his thoughts about good, tolerable and toxic stress.

 

REFERENCE: McEwen, Bruce S. and Huda Akil, “Revisiting the Stress Concept: Implications for Stress Disorders,” The Journal of Neuroscience, January 2, 2020 40:1 12-21

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The Secret Behind the World’s First IVF Baby

Behind Every Successful Man is Strong woman. Or is it “wise woman”? Or maybe it’s this: “Behind every successful man is a woman who provides a strong foundation.” I read that somewhere.

Whatever. This week was the 40th birthday of Louise Brown, the world’s first test tube baby. (July 25th to be precise). We celebrate Louise but we really celebrate Dr. Robert Edwards, the Cambridge University doctor who made it all happen.

But guess what? There was a woman behind his greatness. Back in the late 1970s, Dr. Georgeanna Jones, director of reproductive endocrinology at Johns Hopkins hospital, told Edwards to tweak with the chemicals in the culture media into one that she knew would allow the sperm/egg union to flourish.

When Edwards won the Nobel Prize in 2010, Hopkins had their own tiny ceremony in the department of obstetrics and gynecology. I was there when about a dozen of us watched the unveiling of a small plaque commemorating Dr. Georgeanna Jones and Dr. Howard W. Jones, Jr. (her husband) for providing the advice that led to Edward’s Nobel Prize.

Dr. Howard was there that day ,too. .He told me the advice was all Georgeanna, not him. I never met Dr. Georgeanna. She died in 2005. (Howard Jones died at the age of 104, in 2015, mentally sharp until his very last breath.)

The Joneses went on to create America’s first test tube baby in 1981.

But on this week, when we celebrate Brown’s 40th birthday (she was born, July 25th, 1978), we should also raise a toast to the woman who made it all possible. Dr. Georgeanna Seegar Jones.
You can read more about her accomplishments in my book, AROUSED: The History of Hormones and How They Control Just About Everything. And if you happen to have been born because of the Joneses—and knew either of them—I’d love to hear your story.

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Pregnancy Hormones but No Panda Pregnancy

The National Zoo in Washington D.C. announced today that Mei Xiang, a 19-year-old panda isn’t pregnant after all. It was just a “pseudo pregnancy,” or fake pregnancy. Seems she had all the signs (nesting, eating less) and even hormonal changes. But the one thing she didn’t have was a fetus in her womb.

So, what was going on with her hormones? In short, some animals after sex or artificial insemination, have a rise in certain pregnancy hormones can rise for a few weeks.   Then without a fetus gestating, the levels eventually go back to the non-pregnant state. That seems to have been Mei Xiang’s  story. She had a progesterone surge but an ultrasound didn’t find a fetus

In an article aptly called, “Pseudopregnancy in the Bitch,” and published in the Journal of Small Animal Practice in 1986, the authors explain that the condition has to do with the way post-coital hormones are released from the pituitary gland, a gland that dangles off the brain.  It’s not uncommon in mammals that go through estrus, which is different from humans that menstruate. (Estrus means that the lining of the womb is absorbed back into the body after the egg is released but there is no conception. For many species, the females are only sexually active during estrus. Humans menstruate—that means they bleed and sometimes have sex  when they aren’t fertile.) In humans (but not pandas) “pseudopregnancy” also called pseudocyesis and is listed in the DSM-5, the psychiatrists bible of mental disorders.

At 20, the Mei Xiang is considered on the older end for giving birth, but the National Zoo veterinarians aren’t giving up hope yet.

For further reading on pregnancy hormones and a pioneering researcher, check out Chapter Six in my latest book: Aroused: The History of Hormones and How They Control Just About Everything 

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Hungry: Could it Be Your Hormones

For many of us, the fourth of July means fireworks and food. But here’s the thing: unlike colder weather festivals, such as Thanksgiving, it’s harder to cover up our bulging bellies. Can’t we just have a little self-control?

Well, maybe not. Emerging evidence reveals that our drive to eat may be controlled by our hormones.

People with glitches in the hormone, leptin, for instance—or in the way the body responds to it, are voraciously hungry all the time. Left to their own desires, they become morbidly obese and suffer from all of the consequences that go along with that. Scientists have developed leptin shots that help many people with this rare disorder, allowing them to enjoy hunger and fullness for the first time in their lives. But some folks with a leptin defect have enough of the hormone, but their bodies do not respond to the “I-feel-full” signals. That means that all the leptin in the world won’t stop their cravings. Scientists are beginning to understand their chemical dysfunction. There are a few drugs in the pipeline but no cure yet.

What about the rest of us? Do these exciting clues mean that we can tweak our appetite hormones so we can feel fuller sooner and shed those extra pounds? Can we pop a pill before the weekend barbeque and control the urge to go for seconds?

To be sure, there are self-help books and supplements galore with all sorts of dubious claims to boost your leptin hormone. But here’s the thing: Leptin has been in the spotlight ever since it was discovered in 1994, yet there are so many other chemical signals that control how much we eat, how we burn calories, and what we choose to pile on our plates.

We are a complicated stew of chemicals. When it comes to hunger and satiety, there’s neuropeptide Y, agouti-related peptide, melanocyte-stimulating hormone, ghrelin, insulin-like peptide and the list goes on and on.

So sure, blame your hormones for driving you to the dessert table. But don’t try to “cure” your urges with some dubious supplement.

And sometimes, well, we eat even when we don’t feel those hormonally driven hunger pangs. Sometimes we eat when we’re not hungry because we are, after all, human.

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Predicting Criminal Behavior

In 1924, two rich teenagers from the suburbs of Chicago murdered a kid in their neighborhood. They were caught right away and the trial became known as the crime of the century. The gruesome story of Richard Loeb and Nathan Leopold became fodder for national newspapers and would inspire four films, several books and one play.

During the trial, the killers’ parents hired doctors who tried to convince the judge that the boys weren’t responsible for their own actions. Their faulty hormones made them do it. One doctor, using state-of-the-art tools of the time said he spotted a defective pineal (a gland in the brain) that triggered a lack of inhibition. Today we know the pineal gland emits bursts of melatonin that control our circadian rhythm, our internal clock. In other words, it has nothing to do with compelling someone to kill. In Leopold and Loeb’s time, it was connected ever-so-tentatively to sex and intellect. The doctor explained that because of Leopold’s hard pineal, he had too much libido, even for a 19-year-old boy, and not enough inhibition.

The judge said he was intrigued by this new field of endocrinology (the study of hormones), but these insights were not going to keep two murderers out of jail. The boys were each sentenced to life in prison.

For nearly a century, we have tried to use all kinds of tests to predict human behavior. Around the same time as the trial, Dr. Louis Berman, a New York City doctor, claimed he could look at people and figure out which of their many hormone-spewing glands controlled them. He labeled people “thyroid types” or “adrenal types” based on some dubious assessment. He also said he could forecast their future—whether, based on their hormones, they’d become leaders or movie stars, or criminals. Berman’s ambitions were lofty: he wanted to use his “skills” to evaluate school children and predict their futures. If a kid were destined for a wayward life, he’d prescribe preventive hormone therapy. He wrote books that the public adored and his colleagues loathed. Still, like many ideas based on conjure rather than data, his theory faded away.

We’ve tried for nearly a century to figure out ways to predict who is likely to be a killer, and then take extra cautions with those people. Last week, during a news conference about the flu epidemic, Alex M. Azar, the U.S. Department of Health and Human Services Secretary began by addressing the recent Florida massacre saying the administration needs to be “laser-focused on getting Americans with mental illness the help they need.”

That’s a nice idea. Those with mental health issues should get the therapy they deserve. We don’t need to stigmatize mental illness even further by assuming that anyone suffering from mental illness is a potential murderer. In a scientific article in 2105 published in the American Journal of Public Health, the authors write that the mentally ill are “far more likely to be assaulted by others or shot by the police than to commit violent crimes themselves.”

I’ve spent the past seven years exploring the history of hormones and the science of hormones and behavior. We’ve made great strides. We have more insight into the ways that hormones can make us moody or hungry or tired. We have hormone medicines that can help people with dysfunctional glands. But our notions of predicting a “killer instinct” are, at best, wishy-washy.

We are kidding ourselves if we think we can predict the next killer with tests based on hormones or surveys or any kind of chemical assessments. Politicians and others may look to these studies because they provide a good sound bite, but we need to reread the history of medicine and the recent history of killing sprees to appreciate that it’s highly unlikely we are going to find the sure-fire predictive test and then provide all of the best preventive care necessary to prevent the next massacre.