best, me: Remembering Tim Bartness

Timothy J. Bartness died on September 24, this year (2015), and the progress of research on obesity will halt in its tracks, or so I feared until I started reading what his students are posting.

Screen Shot 2015-09-26 at 1.10.06 PMIf you didn’t have the good fortune to know him, Tim Bartness was brilliant, hilarious, and intense. He did innovative work on many frontiers. He elucidated how day length controls body fat loss and gain. He showed how chemical messengers in the brain affect hunger. When he studied food intake, he didn’t limit his observations to eating. He also studied food hoarding, or as he called it, “shopping for food.” Tim was on the verge of understanding how adipose tissue talks and listens to the brain.

If you didn’t know that your fat sends and receives neural input and output, then you weren’t up-to-date on the frontiers of obesity research. Tim had recently been appointed to head an obesity institute at Georgia State University. In his short life, he published more than 200 papers that received almost 10,000 citations, and almost 4,000 of these citations occurred since 2010. He had an important impact on his field of research, and had he chosen to study rats or mice instead of hamsters, more of my fellow neuroendocrinologists would recognize and make use of his foundational, inspired research. He would have loved that I said that.

Moreover, Tim Bartness was my science big brother– not the Orwellian big brother-is-watching-you kind, but the “I’ve-always-got-your-back-but-you’ll-never-be-as-great-as-I-am” kind of older sibling. Tim and I shared two of the same academic parents and grandparents (George Wade and Irv Zucker) (Tim’s full academic lineage appears on Neurotree), and so Tim and I learned, lived by, and then handed down the same set of advice, tricks, and scientific standards. Our loyalty to each other was not nepotistic, but based on our shared ideas about what constitutes hard evidence. We were writing a “how-to” manual for survival in our crazy academic science jobs.

I’ve lost a big brother, and the weight of this emptiness has left me weirdly paralyzed with confusion, heart-broken, and deeply sad. It feels almost wrong to think there might be something to be gained.

Of course we have gained from his life, and thanks to the internet, much of what we have gained is all around me and right in my face…in my Facebook to be more exact. On Facebook, I see not only his picture but hear Tim’s voice.

Tim’s voice is clearly living and breathing in the minds of his students and colleagues. What’s more, these voices are versions of George’s and Irv’s teachings, living on, even in these ridiculously young students.

Here are just a small sampling of quotes from Tim’s students and colleagues:Screen Shot 2015-09-26 at 1.10.37 PM

Laura Been: … We are all better scientists (and better people) for having Tim as a mentor and a friend. I can’t write anything without hearing his voice in my head (While vs. Whereas; Since vs. Because; never starting a sentence with an adverb). He will be very missed!!

Nicole Victoria: I refer to a Tim Bartness teaching almost on a daily basis and have passed them on to grad students, post-docs, my post-doc advisor and other colleagues (e.g. Presentations: Question, picture, answer. Only use ‘Since’ when referring to time. Hypotheses are present tense statements that answer your experimental question, whereas predictions are future tense statements using ‘if, then’. Use ‘In addition’ and never ‘Additionally’ to start a sentence…). I started talking about Strong Inference and alternative hypothesis testing at a job interview with the FDA the other day. They loved it; I thought of Tim and sent him a mental thank you. He had a dramatic impact on the GSU biology, psychology and neuroscience groups. Clearly he is going to live on in us all and our interactions with others. So sad to hear that Tim has passed. He was an amazing scientist, mentor and teacher.

Joe Normandin: His door was always open to all of us grad students. I remember stopping by his office many times to run experiments by him (and find out what I was doing wrong).

Pam Patterson: Just heard the incredibly sad news that one of my dissertation committee members, Timothy Bartness, has passed away. I am heartbroken by the news. He has influenced, and will continue to influence, every experiment I design (strong inference!!), every paper/grant I write (the art of if/then statements), and every presentation I give (EVERY line on a graph should have a purpose). I would not be the same scientist I am today without his mentorship, and I know I am not alone. Rest in peace, TJB. I know all of my fellow GSU neuro-peeps would agree: he will be missed.

The high standards to which he held himself had an amazing motivational effect on so many of us. Turned us all into little Bartnessites.

Amy Ross: So very true. I still ask myself quite often, “What would TJB do?”

Kyle Frantz: 1. Funnel from broad to narrow focus in the introduction; from narrow to broad in the discussion. So simple. 2. When colleagues acted up in faculty meetings, he’d comment “no GABA today, eh?”. Just two nuggets from Tim.

Screen Shot 2015-09-26 at 1.11.44 PMAres Patrulis: Tim was truly one-of-a-kind scientist. He prized thinking outside of the box but in a supremely rigorous way. He believed in the question and not scientific fads and went after all of it with passion and verve. Absolutely fearless. He always had, and will continue to have, my full respect. I miss his voice terribly. This is true loss for neuroscience. I could say much more, but this will suffice.

Stephanie Josephine: My heart is heavy over this news. Tim played a huge role in my decision to attend GSU. I owe him a massive amount of gratitude for his willingness to serve on my committees, for giving constant feedback, and his overall incredible scientific inspiration. I have a lot of days where I question some of my career decisions or feel a semblance of bitterness for being overworked and underpaid (“the students don’t care,” I say! Yes, I know, “these kids today….” I say, as more and more of my hairs turn gray). At my dissertation defense, Tim asked me what I wanted to be when I grew up. I answered that I wanted to have a positive influence on undergraduate education, but I didn’t quite know how I was going to do that (I felt, at the time, like that was a terrible answer since I didn’t have a clear trajectory at the time.). I have to say looking at the beautiful memories people are sharing tonight about Tim as an educator and a person reminds me of why we do what we do. Students do care. We’ve all been positively influenced as scientists and people by Tim and it’s quite clear we’re all continuing to share his legacy. RIP TJB.

Dayne Loyd Averett: This is devastating news. I’ve read all of your comments and they are all so touching and funny, and anyone who worked will Tim can relate to each of your wonderful comments. I have never written a grant without hearing Tims voice critiquing the organization and writing. All my grants have the Bartness stamp, bolding, underlining and italicizing, all of it lol. It is obvious he has left a legacy in his alum.

From me (Jill Schneider): This is so bitter sweet to see the hard evidence of your goodness and how you have honored your teachers and blessed your students. They will surely carry on your legacy to places we can’t even imagine. Love you, my brother.

Best, me

(Tim also played the sax, and I think he would have liked you to hear this!)

tim's email 2 Tim's email 1

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Mystery Achievement (So Real)

There’s something strange about the world’s brightest women in science, technology, engineering, and mathematics (STEM) connecting around one common theme: their own personal insecurity. It’s even more remarkable when this unlikely point of connection propels them toward their career goals.

Assoc. V.P. Research and Professor at UCLA

Nancy Wayne, Assoc. V. C. of Research and Professor at UCLA

I experienced this first-hand in a workshop, “Women Advancing Together” sponsored by the Lehigh University’s Department of Biological Sciences and their National Science Foundation Advance Program. It was not unlike hearing women with anorexia nervosa lament their obesity. These women were the cream of their respective crops. They were top-tier university administrators and full professors with long lists of publications and grant proposals rated in the top 9% of those submitted. They were bright, young  assistant professors ranked above hundreds of applicants for the same job, and they were students ranked in the top of their graduating classes. Despite these credentials, they all shared similar stories of serious and even crippling crises of confidence, i.e., self-confidence. More important, I learned that if I stop writing here, or if you stop reading here, we might be part of the evil forces creating the problem. So, please, read on!

Something short of a miracle occurred when the women joined together in this workshop to confront their fears, embrace their true talents, and promote their own future success. This remarkable transformation was accomplished with the encouragement and guidance of the Associate Vice Chancellor for Research and Professor of Neuroscience at the University of California, Nancy Wayne. Thanks, Nancy!

The workshop started with the well-known, dismal statistics, but ended with a transformative twist. First, we were reminded that there is a substantial gender gap in STEM employment, a gap that grows from a crevice to a grand canyon at the ranks of full professor/senior scientist. Only 5% of full professors in engineering are women. Furthermore, there is a persistent wage gap; women who have landed STEM jobs are paid significantly lower salaries than men in the same position. Not encouraging news, but Nancy countered with evidence that low self-esteem is reversible.

Confidence in Women EngineersTo support this idea, Nancy showed that women who enter engineering fields have credentials and performance levels equal to those of their male counterparts, but the same women have lower levels of self-esteem and self-confidence correlated with stalled advancement. Another graph showed that, after taking an exam but before receiving their grade, those who underestimate their grade tend to be women, whereas those who overestimate their grade tend to be men. Still another graph showed that women negotiate their salaries far less than do men, and as a result, each individual woman stands to lose more than $500,000.00 in salary by the time they are 60 years of age. Nancy is in a good position to know that the wage gap is reversible because she has successfully corrected her salary and recovered her own lost wages. If this were the end of the workshop, however, the dismal statistics would persist far into the future.

Identity-Safe Environments Work for Women

The important twist in Nancy’s version of the story came when she showed her own published data that she collected while she was training women in medical school. She found that women trainees were less likely than their male counterparts to volunteer for leadership positions. More important, she showed that the trend is reversed by subtle suggestions to the contrary. Nancy documented a fact well-known to psychologists: crises of confidence are either averted by “identity safety” or exaggerated by “stereotype threat” (Davies et al., 2005).

Stereotype threat is the fear that an individual‘s performance will justify a negative stereotype of the group with which the individual identifies. This fear affects performance in a direction that supports the stereotype. A well-known example is that poor math performance occurs when girls are told that “girls are bad at math.” The good news is that the vortex of stereotype threat is not inevitable. The opposite occurs when girls perform math in an identity-safe environment, that is, they are told that girls and boys don’t differ in math ability. Is it a lie to say that girls and boys don’t differ in math? Not if the difference is ameliorated and girls math scores improve by telling that “lie.” The bottom line is, when the stereotype involves women’s identity, stereotype threat can be mitigated by the suggestion that women and men do not differ in their ability.

Women Advancing Together

After the data presentation, Nancy instructed the participants to break into groups of 5-8 for some guided discussion. She first instructed the groups to share a time when they might have experienced self-doubt or a case of “imposter syndrome” (wherein we fail to acknowledge our achievements and therefore fear that we might be exposed as frauds at any given moment). There was no hesitation here, and most women struggled to limit their story to one example. At my table, all of the women spilled out feelings of debilitating anxiety and loneliness as they faced career transitions. The intensity was magnified when women moved up and out, from different countries, cultures, socioeconomic backgrounds, or geographic regions within the same country. During this outpouring of emotion, the discomfort melted away. A reciprocal flow of intimacy, empathy, and support seemed to clear the way for strength and confidence.

After this critical step, the stage was set for the realization that we had all survived and made it through our personal trials. Nancy finessed the group onward to acknowledge and share our talents and skills. We were invited to answer the question “What are your strengths?” There was a moment of silence, and then another outpouring. The skill set at our table was formidable. These women were expert computer programmers, software engineers, chemical engineers, biomedical imaging experts, microscopists, architects, civil and mechanical engineers, teachers, writers, scholars, and facilitators of change. As each woman shared her journey, we all learned different ways of coping with self-doubt.

One fascinating comment came from the women who had grown up in China, where teamwork and humility are valued over individual achievement and self promotion. They said that, after living in the U.S. for a while, they decided to assume the very American idea of the “self made man.” It was funny to realize that this cartoon stereotype actually might be useful. Some prominent American males grow up with this “boot-strap” notion and tend to take it to mythological extremes, but in this case, it works as a tangible point of cross cultural exchange. Picking up on this theme, another woman shared her spin on the boot-strap idea from a classic book entitled “Composing A Life.composing a life Our relaxed, meandering conversation sparked a transformation. Whereas social forces had been conspiring to limit our individuality and advancement, our group forged a bond based on the idea that we can be the authors of our lives, lives that truly exists independent of persistent stereotypes, perceptions, and projections.

If we feel stupid, so what? In STEM, one useful strategy is to face the necessity of feeling stupid while we work at the frontiers of knowledge. By definition, a frontier exists beyond the limits of what is known. Scientists therefore must enjoy and seek out the opportunity to feel stupid because that feeling is the signal that you have found the end of what is known and have courageously leapt off the cliff into the unknown. Authoring new knowledge requires that you first recognize your authentic ignorance about the answer to an important scientific question. Your hypothesis may or may not be true, but there is no guarantee that it will be supported by your data. My own mentor used to say that “Your hypothesis was no less brilliant just because it turned out to be wrong.” There is no point in doing research on a documented fact. Engaging in the scientific process requires the strength to feel stupid until you collect enough data to support (or refute) your hypothesis.

At another table, it was noted that experience in athletics or gaming had provided a foundation for persistence and fortitude. Those of us who played softball know that if you strike out, you don’t quit, you simply step up to the plate in the next inning. There are always new innings, and even if you lose, there are more games, and even if you lose the championships, there will be more seasons. For other women, it helped in times of self doubt to remind themselves of the people who first believed in them, those who opened doors, and provided opportunities. They were buoyed by their fear of disappointing those people and propelled by their desire to prove those people right. Other strategies included sharing fears with supportive friends and reminding each other that stereotype threat can be averted when we establish an identity-safe environment.

A related problem is that traits valued in men are often less valued in women, and these traits are devalued in women by both men and women. In men, leadership qualities are seen as positive, whereas in women they are seen as bossy. Women who are direct, logical, clear, concise, and bold, are labeled “ice queens” or “bitches.” Some women at our table have come to accept that they are not well liked. Women who excel in their field will lose their high status in social circles built on gossip and shared failures, but in the end, this is a good thing. When women seek other women across the disciplines, they find their tribe. We got a taste of this in Nancy’s workshop. We saw that when women persist in their goals while feeling lost or stupid, and when they band together to support each other, the fears and anxiety dissipate, and talent and creativity take over. The best way to combat fears about losing friends and allies is to join forces with women who find themselves in the same dilemma. One of the most gratifying parts of the day came when the participants started trading contact information and making plans for future meetings and collaborations. We learned why Nancy Wayne names her workshops “Women Advancing Together.”

nancy wayne and jms

The best part of it all was knowing that Nancy Wayne and I have been advancing along with another workshop participant and Full Professor and Associate Dean, Jennifer Swann since the 1980’s. Jennifer and I both agree, our friendship with Nancy has been fantastic. Here are the three amigas at happy hour, listening to our science colleague, Assistant Professor Julie Miwa, jamming on the saxaphone and drinking to our mystery achievements.three amigas

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Bad Birds Make Good Birds Feel So Good: It’s In the Genes

Donna Maney's lab found that the more aggressive white-striped morph has a change in the gene for estrogen receptor-alpha that makes expression of this gene more efficient in brain areas important for monogamy, aggression, and parental care.

Donna Maney’s lab found that the more aggressive white-striped morph has a change in the gene for estrogen receptor-alpha that makes expression of this gene more efficient in brain areas important for aggression and parental care.

Donna Maney and colleagues report that

the evolution of complex mating strategies are linked to changes in the gene for the estrogen receptor. Changes in one gene can predispose birds toward a “parental investment strategy” (low levels of competition, high levels of parental care) or a “mating strategy” (high levels of competition, low levels of parental care and exta-pair matings).

That in itself is remarkable, but there is another twist. The birds with the genetic change linked to more aggression and less parental behavior almost invariably mate with birds carrying the other genetic arrangement! We knew that both strategies have their advantages, but now it appears that

the two strategies might be complementary when they occur together in the same couple. One member of the pair is more aggressive and territorial, while the other tends to the nest. In pairs where the male takes on more parental duty, the female is likely to be the one who is more aggressive.

Genes and Behavior

Most people agree that our genes affect some behaviors. Think of Huntington’s disease, in which the devastating loss of motor function, memory, and impulse control are linked to a single gene, HTT. Think about the behavior of different dog breeds. The border collie’s intensity differs from the laid-back demeanor of the Labrador, and both of these tendencies differ from those of the happy yappy terrier. There is no doubt that these behavioral differences came about by selective breeding for specific traits, and that the basis for selective breeding is the heritability of those traits. Heritable traits, those that can be inherited, are affected by genes. No problem, but what about complex social behaviors?

Genes, Hormones, Monogamy, and Parental Care

We know that species differ in their mating strategies. Some species tend toward monogamy in that they show a strong preference for mating with a familiar partner, the parent of their own offspring. In these species, fathers tend to share the parental care of their own offspring, and these behaviors are often incompatible with high levels of aggressive competition. Other species tend toward promiscuity (multiple mating partners and no pair-bonds) and in these species, females tend to bear the burden of offspring care. We know quite a bit about hormonal control of these behaviors in certain species. Hormones are secreted from endocrine glands, and they act by binding to receptors. Hormone-receptor binding stimulates or inhibits the neural circuits that control behavior. In male prairie voles and marmoset monkeys, monogamy is linked to a number of hormones, two of which are oxytocin and vasopressin. Promiscuous species differ from monogamous species in the distribution of these receptors in the brain. One specific gene encodes the vasopressin V1A receptor, and monogamy in male voles is linked to the distribution of brain V1A receptors, which in turn is a consequence of the gene for this receptor. One form of the gene (a polymorphism) is linked with monogamy. How strong is the link between hormone receptor distribution and monogamy? In terms of their vasopressin and oxytocin receptors, monogamous marmoset monkeys look more like monogamous prairie voles than they look like promiscuous species of monkeys! Hormonal influences on monogamy and parental behaviors in birds and mammals are well accepted, and this line of research has provided insights into child neglect and abuse, postpartum depression, and autism.


Donna Maney and her students study song birds that are monogamous, but can be divided into two types, “dads or cads.” They study hormonally-mediated aggressive song and parental behavior in wild birds that form pair bonds with different levels of exclusivity. In biology, we say these species are “monogamous,” but this does not mean they don’t have sex with more than one partner.  In these song birds, they all form pair bonds, but high levels of aggression and territoriality and low levels of offspring care are correlated with more “philandering,” that is, mating with multiple partners. In male birds, sex and aggressive behaviors are linked to hormones like testosterone from the testes and estradiol made from testosterone in the brain. As you will see, this model system affords unique advantages.

Two Morphs of White-throated Sparrow (Dads or Cads)

To link the evolution of behavior to specific genes, we need a snapshot of evolution in action, that is, we need two groups emerging within one population. Maney chose to study two different wild morphs within one population of white-throated sparrows (Zonotrichia albicollis). The morphs differ in their degree of aggressive song and parental care, as well as their propensity for multiple mating partners. As pictured at the top of this post, the tan-striped morph shows more parental behavior, more exclusive pair bonds, and less aggressive song, whereas the white-striped morph forms pair bonds, but also copulates freely with other birds. The white-striped males are less parental. Aggression can be easily measured by recording the species-typical song in response to that of an intruding male. Videos of the aggressive songs and display can be seen in the video here.

The two morphs also differ at chromosome 2, or ZAL2. Sparrows of the white-striped, aggressive morph all have at least one copy of a rearranged chromosome 2, ZAL2m, whereas the tan-striped sparrows never have this inverted chromosome. Donna Maney set out to study gene differences on this inverted chromosome that might explain differences in complex social behavior.

What’s Estrogen Got To Do With It?

In both morphs, the onset of aggressive, territorial song is correlated with increases in testosterone secreted from the testes during the breeding season (spring). Thus, you might suspect that the white-striped morph is more aggressive due to higher levels of testosterone. You would be wrong. When testosterone levels are equalized, the behavioral differences persist. There is something else going on. In the brains of sparrows and many song bird species, testosterone is converted to estradiol. Aggressive song is blocked by treatments that prevent conversion of testosterone to estradiol or by treatments that block estradiol binding to the estrogen receptor-alpha (ER-alpha) (reviewed by Kiran Soma). Receptors for estradiol, in particular ER-alpha, are located in brain areas involved in aggression, including the medial amygdala. Parental behavior is related to ER-alpha in other brain areas, including the medial preoptic area. The differences between the morphs might be related to differences in ER-alpha in the amygdala and preoptic area.

Just to remind you, Maney and colleagues knew that wild males of the more aggressive, white-striped morphs all have at least one copy of a rearranged copy of chromosome 2 (the rearranged chromosome is called ZAL2m). It turns out, the gene for ER-alpha, called ESR1, is located on this chromosome. Yes. Maney and her colleagues hypothesized that the rearrangement in the chromosome led to a change in ESR1 that led to elevated sensitivity to estradiol, and hence, higher levels of aggression and less parental behavior.

Indeed, Horton et al. found that the white-striped sparrows’ aggression was associated with a more efficient transcription of the gene, ESR1. That is, when the DNA is transcribed to messenger RNA, it occurred at a greater rate in the more aggressive, less parental, white-striped birds. More transcription might led to more translation, and hence more ER-alpha.  This would be expected to render the white-striped birds more sensitive to estradiol’s effects on behavior.

Furthermore, Horton et al., found that in the white-throated morphs, territorial singing and ESR1 expression were higher in a region of the medial amygdala associated with aggression.  Similarly, levels of nest provisioning were predicted by the level of ESR1 expression in the medial preoptic area. Thus, Maney’s group 1) linked a genetic change to a change in behavior, 2) linked a genetic change to a change in efficiency of gene transcription, 3) linked a change in gene expression in a particular brain area to a change in a particular behavior.

Together, these results are consistent with the idea that a genetic change in the gene for the estrogen receptor-alpha has led to the evolution of two different morphs of sparrow that differ in complex social behaviors. These experiments were done using wild birds from natural environments, not just laboratory animals. This and other work on this species was blogged by the awesome, Grrlscientist, at the Guardian. To the best of my knowledge, the Horton et al. article is the first such report in any vertebrate species.

It Takes All Kinds of Birds

Depending on your personal bias, you probably jump to the conclusion that one morph is better than the other, and one morph will win out. Exclusive pair bonds and low levels of aggression might result in more offspring if the offspring receive more parental care. The investment in parental care leads to a pay off in terms of number of reproductively successful offspring.  On the other hand, aggressive, less parental birds can win larger territories and a greater abundance of resources (food and shelter). As this blog documents, the more energy, the greater the reproductive success. Read our latest review for more info on energy and reproduction. I wonder whether the frequency of the different morphs would change depending on the availability of energy in the environment. In any case, this means that in the white-stripe, “Don Draper-like” morph, greater investment in competition for resources might lead to more matings, greater fertility, and higher levels of long-term reproductive success. Maney tells us that these two morphs are not in competition, and probably not about to evolve into two separate species.

In reality, almost all white-throated sparrow breeding pairs consist of one individual with and one without the inverted ZAL2m chromosome. The females also differ in their level of parental investment. In other words, the tan-striped morph invariably mates with the white-striped morph, and the tan-striped male or tan-striped female takes up the slack at the nest. This increases the frequency of heterozygous individuals, and maintains the inverted chromosome ZAL2m in the population. Presumably, there is an evolutionary advantage to both the original version of chromosome 2 and the inverted chromosome ZAL2m, perhaps related to differential parental investment. It’s fascinating that the tan-striped males tend to mate with the more aggressive and territorial females and pick up the slack in the parenting department.

Maney and colleagues and their elegant experiments have shown that in white-throated sparrows, rearrangement of a specific gene, ESR1, is one of the genetic changes that underlies the emergence of two different, complementary life-history strategies.

Human Beings

In birds, voles, and monkeys, the behaviors are measured with precision, and these animals can’t deny, lie about, or exaggerate their sex behaviors. A number of studies have associated human monogamous/promiscuous and parental/nonparental tendencies with genetic polymorphisms, but it’s reasonable to wonder whether monogamy can be studied with any precision in people with such complicated sexuality. When it comes to sex, people are inhibited, shy, disingenuous, priggish, or boastful, rather than factual. Questions about human sexuality might have to wait until sex researchers get a hold of the data compiled by the NSA (that is, data compiled when the agents aren’t spying on their own love interests). Ah, yes. Therein lies a clue.

Well, if humans share anything in common with white-throated sparrows, it would surely be reflected in our musical archives…


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When I’m Sixty Five

Special dedication to

Jacques Balthazart!

quail mating

birthday greetings

bottle of winejuliper

Pictured, a Valentine, a birthday greeting, a bottle of wine, and a Jupiler



Jacques Balthazart is a true leader in behavioral neuroendocrinology, the study of how hormones affect the brain and behavior. His retirement demanded a fitting tribute, but there was a problem. When it comes to international conference organizers, nobody does it better than Jacquesyoung jacques Balthazart. So, who would throw this party? No worries. The Belgian government’s policy requiring mandatory retirement at age 65 turned out to be the catalyst for a nonpareil scientific meeting (throughout this blog, all words underlined are links). It also turned out to be an outrageous birthday party and a creative plan to continue research on his own terms. Last week, the combination of foundational research, cutting-edge science, Belgian beer, and collegiality led to the conference’s new nom de plume: The International Conference Honoring Brilliant Balthazart (ICHBB).

Jacques is shown above and to the right just moments before the party, and below, just a few days into the party.


Photo by GianCarlo Panzica of Jacques Balthazart, 65,  in a gift hat symbolizing his dual loyalty to Belgium and the U.S.
dave me scottish guy beerjon
ICHBB Conference photos by GianCarlos Panzika

After all, when you are the premier conference organizer, entertainer, and hub of your scientific community, it makes sense that you should plan, host, and orchestrate your own birthday retirement party!

team jacques

“Team Jacques” adapted from a funny photo by Julie Bakker

The first ICHBB was named the International Conference on Hormones Brain and Behavior and held in Bielfeld, Germany in 1982. It was conceived and developed from Jacques’ isolation as one of the few behavioral endocrinologists in Belgium. His uncontrollable desire for scientific interaction led him to invite about 40 premier behavioral endocrinologists from around the world to Bielfeld. To his surprise, they all showed up; it was an unqualified success; and everyone wanted to do it again and again. And again. In subsequent years, Jacques personally nursed the ICHBB in his home town of Liege (in 1984, 1989, and 2014) and affectionately nurtured the conference when it was hosted by others in France, Italy, and Spain.

liege buttfly bushes  2 I learned some things about Jacques’ life that I hope will be shared, remembered, and handed down to our academic offspring! First, necessity is the mother of invention in that some of Jacques’ biggest contributions to science come from his ability to embrace his authentic small-town lifestyle while uniting the world of behavioral neuroendocrinology. He was born, raised, educated, bred, and “retired” in Liege, Belgium, far less a tourist destination than a very pleasant place to grow up, and Jacques truly loves Liege. Many Americans have never even heard of Belgium, let alone, Liege, but one thing is very clear. Liege is “on the map” in the minds of behavioral endocrinologists. This just shows that there is no point in whining about where you work. I know behavioral endocrinologists at big U.S. medical schools, at Yale, or in big universities like UC-Berkeley who feel more isolated than Jacques.

liege night

liege dogs in bar

liege dob in bar 2

Scenes from Liege














This idea was confirmed by plenary speaker, Kathy Olsen, former deputy director of the National Science Foundation, chief scientist for NASA, and associate director and deputy director of science in the executive offices of the President of the United States of America. According to Kathy, there is no one else to blame for putting Liege on the map other than Jacques Balthazart.


Kathy Olsen (right) shown with Vicki Luine and Yasuo Sakuma (left)

In terms of hormones and behavior, Jacques brought the world to Liege. I was surprised to learn that the man we know as the hub of our global science community is very much a local family man. Jacques’ father was a local architect, and his mother worked as a full-time homemaker and mother of two children. Jacques was educated from primary school on up through college in his home town of Liege. It was at the University of Liege that he fell in love with one of his biology professors, the beautiful and enviably fit, Claire (apparently she still runs 10K a day!). In addition to having a successful career in biology, Claire is a super friendly, social, community-oriented woman-about-town. Jacques, on the other hand, is not nearly as involved with his local friends and relatives. Though Claire chides Jacques for not remembering neighbors who have known Jacques his whole life, Jacques, ironically, is the social glue holding together a giant global network of scholars and friends, many of whom traveled far and wide to celebrate Jacques’ birthday. In one of Jacques’ presentations this week, he showed a world map dotted in every continent with markers showing where he has friends who will meet him at the airport.

nicole stripeyriters
Lauren Riters and family (left) and Nicole Cameron with a lot of French stripes (right)


Nicole, Lauren, Lauren’s son, Nancy Forger and Geert DeVries (left) and cannibals on the menu (below)

A Bad Bromance

Everyone in behavioral endocrinology knows that Jacques Balthazart has co-authored numerous landmark articles with Greg Ball, begging the question “How did this fertile collaboration begin?” During the various tributes at the conference, we learned that in 1983, Greg Ball was a graduate student at the Institute for Animal Behavior at Rutgers-Newark, where Jacques Balthazart was a distinguished visitor. Jacques, however, was not impressed with that Greg Ball character!

Jacques recalls Greg as a “lazy, long-haired hippie hanging around drinking coffee and pontificating in the break room all day long in a booming voice that could be heard all over the department.” As they say, first impressions are the best. Well, except the lazy part, because Greg’s and Jacques’ publications together number at least 400, and somewhere between 110-115 of those articles are co-authored by Ball and Balthazart or Balthazart and Ball.

The Ball and Balthazart Bromance was finally consummated (scientifically) a few years later in Germany. Greg Ball, then a postdoc with John Wingfield, was invited to speak at the conference. Greg was put up in a small dormatory-like room with a single bathroom shared by the adjacent room. Greg was brushing his teeth when his new next door neighbor, Jacques Balthazart, burst into the bathroom. “Well, well, well, we meet again!” Only this time, the Greg-Jacques Belgian beer bromance began in earnest (Wait? Who’s Ernest?) From the time of that meeting, Jacques Balthazart and Greg Ball became fast friends and insanely productive collaborators.

Incidentally, you can trace the academic family trees of these characters and that of your own mentor at Greg Ball’s tree is probably the most interesting, reaching straight back to Niko Tinbergen and Konrad Lorenz.

Peg McCarthy, Greg Ball’s beloved spousal unit, in her plenary lecture, explained that Jacques was a daunting obstacle blocking Greg’s affections for Peg in the initial stages of their courtship. At first, it was clear to Peg that Jacques would always be Greg’s “first wife.” It seemed she could never compete with Jacques. Luckily, Jacques came to adore Peg, and now warmly accepts Peg as a sisterwife. Suffice to say, that if all sisterwives were like Jacques and Peg, we would all be Mormons.

peg and greg

me peg colin
Greg Ball and Peg McCarthy (left) and a nicer pic of Peg with me and Colin Saldanha

world cup

   Celebrating Belgium Moving Up In the World Cup 2014

To Sir Jacques With Love

The entire meeting was infused with enormous gratitude and affection from Jacques’ present and former students, postdocs, collaborators, family, and friends. Greg Ball gave a “What I learned from Jacques” speech that I wish all graduate students could hear. The highlights included

1) PUBLISH all of your data immediately. You never know when or how your results will be useful to other scientists, and none of it will matter if it is not published.

2) Time is precious, so, collect data, and write without fail, regardless of how late you stayed up the night before. No excuses. As Jacques would say, you have one 33 cl (Jupiler) at lunch and then bike back to work!

3) Be brave about methods. If it’s been done, you can do it.

4) Good ideas come from many sources, so, go to meetings and host your own.

5) Good colleagues can be good friends.

jacques at poster jacquest and jeff poster

Jacques and Jeff Blaustein are not at all faking interest in my poster presentation. Photo taken by Vicki Luine.

In any case, there were so many excellent talks and posters at the meeting, demonstrating that Jacques will live on through his scholarship and mentoring as long as human civilization survives. Happily we learned that Jacques will continue working at the University of Liege, without the unpleasant duties of his old position, but instead intensifying focus on the research that he loves. This is one of the benefits of launching the careers of young, outstanding scientists and scholars. Shown below are ICHBB attendees who came to honor Jacques: Dave Grattan, Colin Saldanha, Kiran Soma, Jim Pfaus (with son, Josh), Thierry Charlier, Chuck Roselli and many others in the group photos.

jacques with dave gratten jacques w:colin and kiren

jaques anne etgen

jacques chuck vicki jim









jim thierrymug


Enjoy the next phase, Jacques! Your work is alive and well in all of our research programs. See you soon.

jacques juliper

The above photo of Jacques and the preceding six were taken by GianCarlo Panzica.

There will be more pictures available through the website for the ICHBB. Meanwhile, you will find some links to seminal Balthazart discoveries here and here.

And finally, here’s a funky version of what I’m sure Jacques’ mentees are thinking…


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He’s A Rebel! Paul Heideman visits Lehigh

     This week the Schneider lab had the pleasure of hosting one of our scienImagece heroes, Paul Heideman from The College of William and Mary. He doesn’t wear a leather jacket or anything, and in fact, he looks like a typical white-guy professor. We’re still wondering exactly how he left us so inspired and energized, like we just discovered the thrill of science all over again.

He’s a loner, Dottie, a rebel

     Like most of us, Paul came up the ranks when everyone was advised to learn super cool state-of-the-art molecular techniques, to work on conditional knock-out/knock-in-optogenetic-whatever-the-hell mice, and to focus on cellular mechanism. Did he do this? No. Is he tenured? Yes. Is he funded? Yes, well funded. Is he happy? He seems pretty darn ecstatic.

     Second, he studies the one thing that most biologists avoid like the plague: Individual differences. Most scientists seek to minimize them. They like groups that show little natural variance, and they omit outliers.

      Hating individual differences makes sense in a way. When a drug works to reduce pain or fight infection, you want it to do so reliably in just about everyone. Will a new drug X decrease depression? We want a clean result. We want to see clear differences in depression between the drug-treated and placebo-treated groups. We want as little variation as possible within the groups. Face it. Too much variation within the treated group, and the drug is not going to market.

Vive la diffe’rence!

Image      Paul solved the problem of individual differences by embracing them. He started his career in the field, trying to figure out why some equatorial animals are seasonal breeders and some aren’t.  Fruit bats (a.k.a., flying foxes) that inhabit particular islands in the Philippines breed only in certain seasons, whereas  those on other islands begin their breeding season months later. Presumably, this ensures that offspring are born at the time when they are most likely to survive. But what is the source of the difference?

      To be a seasonal breeder, you need an internal clock, a reliable cue in the environment to set your clock (like the availability of food or the day length), and a sensory system to detect the environmental cue. Also, you need your clock and your senses to be connected to your reproductive system, and ultimately, to your gonads (ovaries or testes). What’s up with a nonseasonal breeder? Is the clock broken or are they deaf to the alarm? Is there a disconnect between the clock and the gonad?

Now What?

Image     Paul was stuck. He just couldn’t figure this out in the field. In order to uncover the internal brain mechanisms, he needed to have animals in the lab. Commercially available lab animals, however, will not do. They gots no variance in the thing he wanted to study. Most lab animals are uniformly year-round breeders. He would have to create a lab population that had the same variation that exists in nature.

     Being a rebel, he did what all of his colleagues were not doing. He trapped wild mice (Peromyscus leucopus) from the wild, brought them to his laboratory, and began crossbreeding. He kept the population large enough to avoid inbreeding (breeding close relatives tends to decrease heritable variation). Now he had a lab population that contained most of the variation that existed in the wild. How would he make use of this to answer his questions about individual differences in seasonality?

     The next thing he did was brilliant. This base population served as the starting point for a selective breeding program. He started breeding lines of mice that differed in their seasonality. By breeding seasonal males to seasonal females, and unseasonal males to unseasonal females for many generations, he ended up with two groups of animals that differed from each other. They didn’t just differ by accidental inbreeding, or for other unknown reasons. They differed because they were selectively bred for those traits he wanted to study.

     Paul has created and maintained a scientific gold mine. He can expose the two groups to winter conditions, measure their hormones and neuropeptide levels, and figure out what accounts for their differential response to the changing season. He can even sequence their genome and look for differences. He can get answers to questions like “How does evolution change the reproductive system?” “Can natural selection change hormone levels or does it change hormone receptors?” “In nonseasonal animals, is their internal clock broken or are they simply blind to the seasons?”

      To find out the answers, you can check out Paul’s work here and here. Paul writes, “I have worked on multiple populations, but my current mice all come from one population. That’s important to me because I can say that all this variation is just from one little population — and that suggests that other mammals, including humans, might also contain large amounts of variation.”

    I agree and I think it’s especially cool that selection has created wildly different strategies for survival and reproduction within the same species. In this case, you’ve got cautious mice that take the hint that winter is on the way by shutting down the reproductive system in order to conserve energy for survival in the cold. In the same population, you’ve also got flexible mice that will breed willy nilly as long as they can. If the winter is mild, the sexy mice beat the conservatives by producing litters and getting more genes into the next generation. If winter is harsh, the conservatives will win the gamble because they will be the only ones to survive to breed in spring. It takes all kinds. Vive la diffe’rence!

Paul gives a great talk. He gives all of his attention to the students, and he has tons of helpful advice about teaching behavioral endocrinology and science writing. Plus. . .

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Happy Fat Tuesday from Schneider Lab

As Fat Tuesday approaches, my mind turns to cycles of indulgence and moderation. This is not news to women. They are quite familiar with regular, repeated bouts of uncontrollable appetite. Women are more prone to obesity and binge eating, and their binges are more likely to occur at a certain phase of the menstrual cycle. These differences are related, at least in part, to changes in hormones secreted from the ovaries. The ovaries secrete steroid hormones, such as estradiol and progesterone. Changes in estradiol and progesterone secretion alter the steroid environment in the brain and body, so that when hunger strikes, we might feel “just peckish” at one stage of the menstrual cycle or ravenously hungry at another phase.

How does this work? I received a four-year research grant from the National Science Foundation in 2013 to study ovarian hormone effects on appetite.

One clue to understanding estradiol is that it affects sexual desire and hunger for food in the opposite direction. In the middle of the menstrual cycle, when estradiol levels are highest, the appetite for food falls to its lowest level. This is the time when females are most fertile and sexual desire peaks (although sexual activity can occur any time during the menstrual cycle). As women approach menstruation, progesterone levels and the appetite for food rise while sexual desire tends to fall. Similarly, after menopause, as the ovarian hormones wane so does sexual urgency (to different degrees, depending on the individual).

So, changes in hunger for food are correlated with changes ovarian steroid hormones, but correlations cannot tell you what causes what. My work started by looking for brain hormones secreted by cells with steroid receptors, brain hormones that increase the appetite for food and decrease the desire for sex. The problem is, we can’t really muck around in our own brains to study these hormones (neuropeptides). It’s difficult to study human food intake and sexual behavior because people lie about how much and what they eat. Don’t even get me started on measuring their sexual desire. No thanks. I like to study Syrian hamsters because I can precisely control what they eat, and they ovulate like clockwork every 4 days, unlike women who ovulate every 24-32 days. Plus, hamsters have a great way to demonstrate their hunger. After a period of dieting (say, we feed them only 75% of their normal daily food intake for a week), when we give them back their food, they increase their food hoarding. The hungrier they are the more food they carry in their cheek pouches from a distant source to their home cage. We can measure hamster sexual desire and hunger for food quite easily and accurately.

1 SFRR CHAPTER 3 fig hamsters hoarding over cycle

Hamster food hoarding (mean and s.e.m.) over the four days of the ovulatory cycle in food-restricted (open triangles, dotted lines) and food-unlimited (solid circles and lines) females housed with the choice between staying home, visiting a male, or hoarding food. The predominant sex behavior of the food-restricted female is shown in a cartoon above the hoarding data. On day 4 of the cycle, the periovulatory day, the females show mating behavior. On day 3, they show vaginal scent marking but do not mate. On days 1 and 2 they spend more time hoarding food than visiting the male. (Adapted from Klingerman et al., 2010 by Jay Alexander)

            Candice Klingerman (a former grad student in my lab at Lehigh University and now a real professor at Bloomsburg University), found that hamsters on calorie-restricting diets show little interest in males and spend most of their time busily hoarding food, except on the day of ovulation. As ovulation approaches, however, they spend more and more time near the males. What you might find surprising is unrestricted females are obsessed with males throughout the ovulatory cycle! Whether they are ovulating or not, they ignore the food and spend more than 75% of their time leaving vaginal scent marks near the males. Like most rodents, they mate only on the day of ovulation, but the chubbier, calorie-unrestricted females prefer males over food every day of their four-day cycle. The differences between the calorie-restricted and unrestricted females are illustrated in the graph to the right, where you can see that calorie-restricted females do lots of food hoarding on most days of the cycle, with a conspicuous dip at the time of ovulation. The unrestricted females’ hoarding levels are low and flat throughout the cycle because they spend most of their time with the male (Klingerman et al., 2010).

You can see from the figure above that living in an “all-you-can-eat” buffet masks the effects of the ovarian cycle on the appetites for food and sex. Females on the “all-you-can-eat” diet consistently prefer to court males rather than stock their larder with food. Those females that are calorie-limited save all their sexual ardor for the small window of fertility on the day of ovulation. They spend the rest of the ovulatory cycle busily hoarding food. In the wild, this would ensure that there will be plenty of energy available for their offspring if their mating results in a pregnancy. This result makes me wonder whether our understanding of sex hormones has been clouded by studying animals housed in small cages with unlimited food. It makes me wonder how much our own species has diverged from our ancestors, now that we have adopted a sedentary lifestyle with food available in office vending machines, coffee break rooms, fast food restaurants, and well-stocked homes. No wonder we sit around watching Game of Thrones.

What are the brain differences between the hamsters on a limited-calorie diet and the hamsters at the “all-you-can-eat” buffet? I suspected that I would be able to find a brain hormone (neuropeptide) secreted by cells that have steroid receptors. I further suspected that the secretion of this neuropeptide is increased by food restriction. A review of the literature revealed many such chemicals. I have posted a handy table in a previous blog post here.

At the moment, we are interested in gonadotropin inhibiting hormone, GnIH. The figure below shows a hamster brain cell (neuron) that produces GnIH (a neuropeptide), which is stained red. Those GnIH cells that were activated by food restriction are shown in red with a green/yellow dot in the middle. These are cells labeled for GnIH and Fos, a marker for cellular activation. I got interested in GnIH when my colleague, Lance Kriegsfeld at the University of California at Berkeley, showed that GnIH inhibits reproduction in Syrian hamsters.


Brain cells stained for GnIH (red) and Fos (green). The red stain represents GnIH which occurs in the cytoplasm and thus colors a wide area of the cell body. The greed stain represents the proto-oncogene product Fos, a protein that is synthesized upon cellular activation. Fos resides within the cell nucleus. Cells that are red with a green/yellow stained nucleus are double-labeled with GnIH and Fos. These represent GnIH-containing cells that have been activated by food restriction. (Photograph and immunohistochemistry by Noah Benton)

Some of my other great colleagues in Australia (e.g., Iain Clarke) were showing that GnIH increases food intake in sheep, monkeys, and rats. GnIH sounded promising. Thus, I approached Lance about studying the effects of GnIH on the appetites for food and sex in Syrian hamsters. My student Candice Klingerman partnered with a grad student from the Kriegsfeld lab, Wilbur P. Williams. Together, Klingerman and Williams found that the level of calorie restriction was a good predictor of the level of GnIH cell activation (Klingerman, Williams, et al., 2011).

           This suggested that GnIH might be part of the system that orchestrates the appetities for food and sex. This was confirmed by Noah Benton (Lehigh) and David Piekarski (UC-Berkeley). They administered GnIH to the brains of well fed females, and found that the GnIH-treated hamsters acted like they were starving. Their sexual appetites were lowered and their hunger for food was increased by GnIH treatment in the brain.

            Another prediction you can make based on the hoarding data shown above is that GnIH will have different effects depending on the day of the ovualtory cycle (and the levels of estradiol and progesterone secreted from the ovary). Consistent with this idea, my student Noah Benton is finding that in food-restricted females, the activity of GnIH is elevated only during the nonfertile periods of the female cycle. In the figure above, GnIH cells are shown in red, and the activation of those cells is indicated by the central dot stained green for Fos, a protein that shows up in cells that have been activated. Noah double-labeled cells for both Fos and GnIH in food-restricted and food-unlimited females on every day of the ovulatory cycle. On nonfertile days of the cycle, there are significantly more GnIH cells activated in food-restricted compared to food-unlimited females. As you would predict from their sexy behavior, however, on the day of ovulation, GnIH is not elevated by food restriction. Go, Noah!

GnIH activity is usually elevated in food-restricted females, except at ovulation. We think the effects of GnIH are dampened by one of the hormones that is high around the time of ovulation. Noah Benton’s dissertation work will determine which ovarian steroid hormones and receptor are important for these effects. Will it be estradiol, progesterone, or testosterone? Place your bets.

Many obesity researchers think that appetite suppressing hormones are suppose to function to preserve our youthful figures and keep our body weights in fashionable and healthy limits. The work of my students shows that an important function of these hormones is to orchestrate the appetites for food and sex, perhaps to maximize reproductive success in environments where energy availability fluctuates. These effects are short-lived and change rapidly in the small time window of fertility (basically 1 day of the 4-day ovulatory cycle). It is probably unrealistic to expect any one of these neuropeptides to be a long-term or permanent cure obesity. Maybe we should think more broadly about how all this obesity has come about, and put some energy into understanding the link between energy balance (food intake, body fat storage, and energy expenditure) and reproduction.

Meanwhile, happy Mardi Gras! 



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March 1, 2014 · 4:40 pm

Sex and Food and. . . on the Table


oldie but goodie

“Sex and food and. . .” What pops into your mind to finish this sentence? For me it’s “rock and roll” (I substitute food for drugs because I don’t need drugs). If you are more punk than new wave it’s “Food, Sex, and Ewe,” and for the hip hopsters it’s “Sex, Food, and Sports.” The latter is also true for Seinfeld fans. Don’t Google “food and sex” though, you might get distracted.

“Sex-and-food” is the key to life. This grammatical impossibility stems from the fact that in the brain, the desires for sex and food seem to be one and the same, sometimes two sides of the same coin. In my upcoming book “Sex and food and. .” (Oxford University Press), I begin by noting that in every-day language food is sexy and sex is foodie;

“In both word and deed, we express our entangled appetites for food and sex, almost as if we confuse the two. In everyday language, food is sexy and sex is foodie. Chocolate is orgasmic and our lovers are delicious. In The Bible we are told to be fruitful and multiply. In Shakespeare’s Sonnet 118 he uses food metaphors for budding romance, for the “sweetness” of true love, and for the “bitter sauces” of infidelity.”

Just a smidgen of the evidence for the food-sex connection is presented in the table below. These 40-or-so chemical messengers have documented effects on ingestive behavior. They either increase or decrease the amount of food eaten per unit time. The same chemical messengers have clear, repeatable effects on reproductive processes, often including sexual desire and performance. In fact, compounds pushed as anti-obesity drugs by some researchers are being pushed as libido-enhancer by others. Our table reveals information useful for a wide range of scientists, not just those narcissists who feel that all research must have medical application. For more on this topic check out our new preprint now available online (it will be published open access).

TABLE 1. A list of hormones and neuropeptides that influence both food intake and reproduction. From Schneider et al., 2013, When do we eat? Ingestive behavior, survival, and reproductive success, Hormones and Behavior, published online ahead of print.

Central “Orexigenic” Peptides Ingestive Effects Reproductive Effects
agouti-related protein (AgRP), HS04, SHU9119 (MCR antagonists) increases food intake in fish (Schjolden et al., 2009), birds (Strader et al., 2003), and mammals (Rossi et al., 1998; Stark, 1998), and food hoarding in hamsters (Day and Bartness, 2004) inhibits gonadotropin secretion in fish (Zhang et al., 2012), inhibits LH in the presence of estradiol in female rats (Schioth et al., 2001; Watanobe et al., 1999), stimulates LH in male mammals (Stanley et al., 1999), ablation of AgRP gene restores fertility in ob/ob mice (Wu et al., 2012)
alarin Increases food intake in male rats (Van Der Kolk et al., 2010) stimulates LH secretion in castrated male rats (Van Der Kolk et al., 2010)
β-endorphin increases food intake in fish (de Pedro et al., 1995b) (reviewed in (Lin et al., 2000)), birds (Deviche and Schepers, 1984; Maney and Wingfield, 1998; Yanagita et al., 2008), and rats (Grandison and Guidotti, 1977; McKay et al., 1981) mediates stress-induced suppression of LH in fish (Ganesh and Chabbi, 2013), birds (Sakurai et al., 1986), inhibits LH secretion and sexual performance (Hughes et al., 1987, 1990; Sirinathsinghji et al., 1983), but might also increase sexual motivation in rats (Mitchell and Stewart, 1990; Torii et al., 1999),
galanin increases food intake in fish (De Pedro et al., 1995a; Lin et al., 2000; Nelson and Sheridan, 2006; Volkoff et al., 2005) and rats (Kyrkouli et al., 1990) stimulates LH secretion in birds (Hall and Cheung, 1991),  steroid-primed rats (Sahu et al., 1987)
galanin-like peptide (GALP) increases food intake in rats (Matsumoto et al., 2002), also decreases food intake in mice (Krasnow et al., 2003) stimulates LH secretion in male mice and rats and in estradiol-treated female rats (Krasnow et al., 2003; Matsumoto et al., 2001; Uenoyama et al., 2008)
gamma aminobutyric acid (GABA) might not mediate hyperphagic effects of orexin in fish (Facciolo et al., 2011); increases food intake in rats (Basso and Kelley, 1999) increases gonadotropin release in fish (Kah et al., 1992); GABA-BR decreases excitability of mouse GnRH-I neurons (Zhang et al., 2009); GABA-AR excitatory for mouse GnRH-I neurons (DeFazio et al., 2002; Moenter and DeFazio, 2005)
melanin-concentrating hormone (MCH) increases food intake in rats (Presse et al., 1996), but decreases food intake in fish (Shimakura et al., 2008) inhibits LH secretion in rats (Tsukamura et al., 2000a)
neuropeptide Y (NPY) increases food intake in fish (de Pedro et al., 2000; Lopez-Patino et al., 1999), frogs (Crespi et al., 2004), snakes (Morris and Crews, 1990), birds (Strader and Buntin, 2001), rats (Stanley and Leibowitz, 1984) and food hoarding in hamsters (Dailey and Bartness, 2009) increases gonadotropin release in fish (Peng et al., 1993), inhibits steroid biosynthesis in frogs (Beaujean et al., 2002), inhibits sex behavior in snakes (Morris and Crews, 1990), inhibits LH in the absence of estradiol, stimulates LH in the presence of estradiol in rats (Crowley et al., 1985; Sahu et al., 1987) (Sahu et al., 1987), inhibits sex behavior in rats (Ammar et al., 2000)
orexin/hypocretin increases food intake in fish (Lin et al., 2000; Volkoff et al., 1999; Volkoff et al., 2005), and rats  (Sakurai et al., 1998), but not in birds (da Silva et al., 2008) inhibits spawning in fish (Hoskins et al., 2008), inhibits LH in rats with little or no estradiol (Furuta et al., 2002), stimulates LH in rats with high  levels of estradiol  (Pu et al., 1998)
gonadotropin inhibiting hormone (GnIH) increases food intake in birds (Tachibana et al., 2005), mice, sheep, and monkeys (Clarke et al., 2012; Johnson et al., 2007; Tachibana et al., 2005) inhibits GnRH and LH secretion and sex behavior in fish (Moussavi et al., 2012), birds (Bentley et al., 2006; Satake et al., 2001) and blocks the LH surge in sheep and inhibits LH secretion in rats and female hamsters (Bentley et al., 2006; Johnson et al., 2007; Kriegsfeld et al., 2006; Smith et al., 2008)
Peripheral “Orexigenic” Hormones Ingestive Effects Reproductive Effects
corticosteroids chronically elevated levels increase food intake in fish (Bernier et al., 2004),  amphibians (Crespi et al., 2004), birds (Astheimer et al., 1992), and rats (Hamelink et al., 1994; McLaughlin et al., 1987; Stevenson and Franklin, 1970) inhibits a wide array of reproductive parameters in fish including parental behavior (Carragher et al., 1989; O’Connor et al., 2009) reviewed by (Milla et al., 2009), inhibits steroid synthesis and spermatogenesis in amphibians (Moore and Zoeller, 1985; Moore and Jessop, 2003), inhibits sex behavior in snakes (Lutterschmidt et al., 2004; Moore and Jessop, 2003), stimulates gonadotropin secretion at low doses in birds (Etches and Cunningham, 1976), inhibits HPG function at chronically high doses in birds (Etches et al., 1984), and mammals (Vreeburg et al., 1988)
ghrelin (gut) increases food intake in fish (goldfish and tilapia), but decreases food intake in rainbow trout (Jonsson, 2013; Jonsson et al., 2010), decreases food intake in birds (Kaiya et al., 2009), increases food intake in rats and mice (Tschop et al., 2000; Wren et al., 2000) and food hoarding in Siberian hamsters (Keen-Rhinehart and Bartness, 2005) stimulates LH release from fish (Grey et al., 2010), inhibits GnRH, LH secretion and sex behavior in rats and mice (Fernandez-Fernandez et al., 2004; Furuta et al., 2001; Shah and Nyby, 2010)
insulin (pancreas) chronically elevated levels increase body weight, adiposity, and food intake in birds (Nir and Levy, 1973), rats (Booth and Brookover, 1968; Friedman, 1977; Friedman et al., 1982; Houpt, 1974) systemic treatment inhibits LH secretion at doses that increase food intake in hamsters not allowed to overeat (Wade et al., 1991), inhibits LH secretion in sheep treated peripherally with saline but not with glucose (Clarke et al., 1990)
motilin (gut) increases food intake in fasted rats (Garthwaite, 1985) inhibits LH secretion in rats (Tsukamura et al., 2000b)
progesterone (gonads, adrenals) reverses the weight reducing effects of estradiol on body weight and food intake in rodents (Hervey and Hervey, 1966, 1969; Zucker et al., 1972) synergizes with estradiol to stimulate female sexual performance in rats (Dempsey et al., 1936), enhances estradiol feedback on LH in female rats (Chappell and Levine, 2000), mimics testosterone in male rats (Witt et al., 1995)
testosterone (gonads, adrenals) increases food intake and growth in rats (Siegel et al., 1981) stimulates sexual motivation in females (de Jonge et al., 1986; Everitt and Herbert, 1970) and sexual performance in male rats (Davidson, 1966; Davidson and Bloch, 1969)
Central “Anorectic” Peptides Ingestive Effects Reproductive Effects
α-melanocyte stimulating hormone (α-MSH), melanotan- II (MT-II), PT-141 decreases food intake in fish (Kang et al., 2011; Schjolden et al., 2009), amphibians (Carpenter and Carr, 1996), birds (Kawakami et al., 2000; Tachibana et al., 2007),  and rats (Vergoni et al., 1986), and food hoarding in Siberian  hamsters (Keen-Rhinehart and Bartness, 2007a; Shimizu et al., 1989) enhances electric organ discharge in  electric fish (Markham et al., 2009), Stimulates LH secretion and sex behavior in rats (Alde and Celis, 1980; Thody et al., 1981)
Cocaine and amphetamine-regulated transcript (CART) decreases food intake in fish (Volkoff et al., 2005), birds (Tachibana et al., 2003), rats (Kristensen et al., 1998) stimulates GnRH secretion in rats (Lebrethon et al., 2000; Parent et al., 2000)
Cholecystokinin (CCK) decreases food intake in fish (Himick and Peter, 1994; Volkoff et al., 2005), birds (Tachibana et al., 2012), rats (Gibbs et al., 1973) and food hoarding in Siberian hamsters (Bailey and Dela-Fera, 1995; Figlewicz et al., 1989; Teubner and Bartness, 2010) stimulates GnRH and LH secretion in rats (Ichimaru et al., 2003; Kimura et al., 1983)CCK in the medial preoptic areas is required for estradiol-induced lordosis in rats (Dornan et al., 1989; Holland et al., 1997)
Corticotropin releasing hormone (CRH) decreases food intake in fish (De Pedro et al., 1993; Matsuda et al., 2008), amphibians (Crespi et al., 2004), birds (Denbow et al., 1999; Furuse et al., 1997), rats (Heinrichs and Richard, 1999; Levine et al., 1983; Morley and Levine, 1982; Negri et al., 1985) and food hoarding in rats (Cabanac and Richard, 1995) reviewed by (Carr, 2002) inhibits spawning in fish (Mousa and Mousa, 2006), inhibits LH secretion and lordosis in rats (Olster and Ferin, 1987) and sex behavior in Syrian hamsters (Jones et al., 2002)
Dopamine (DA) decreases food intake in fish (Leal et al., 2013), rats (Heffner et al., 1977), increases food hoarding in rats (Borker and Mascarenhas, 1991; Kelley and Stinus, 1985), and reward (Wise, 2004) inhibits gonadotropin secretion in fish (Omeljaniuk et al., 1989), stimulates sexual arousal, motivation and reward in birds (Cornil et al., 2005), rats and hamsters (Agmo and Picker, 1990; Meisel and Mullins, 2006)
Glucagon-like peptide (GLP-I) decreases food intake in fish (Silverstein et al., 2001), birds (Tachibana et al., 2006), rats (Turton et al., 1996) stimulates LH secretion (Beak et al., 1998)
Gonadotropin releasing hormone (GnRH I or II) decreases food intake in fish (Hoskins et al., 2008; Nishiguchi et al., 2012), and female musk shrews (Kauffman and Rissman, 2004b) stimulates LH secretion in fish (Moussavi et al., 2012), birds (Chowdhury and Yoshimura, 2004), stimulates LH secretion and sex behavior in amphibians and reptiles (Alderete et al., 1980; Licht et al., 1984), rats and sheep and sex behavior in shrews and mice (Kauffman and Rissman, 2004a; Kauffman et al., 2005) (Temple et al., 2003) (Moss and McCann, 1975) (Clarke and Cummins, 1982)
Insulin-like Growth Factor -1 (IGF-I in CNS) ICV treatment decreases food intake in diabetic, but not normal rats (Lu et al., 2001), required for post-fast hyperphagia in rats (Todd et al., 2007) restores LH surge amplitude in middle-aged rats (Todd et al., 2010), required for the LH surge, estrous behavior, estrous cycles in rats (Etgen and Acosta-Martinez, 2003; Quesada and Etgen, 2002; Todd et al., 2007), and for sex behavior in rats (Etgen and Acosta-Martinez, 2003)
Kisspeptin decreases food intake in mice (Stengel et al., 2011) stimulates GnRH and LH secretion in fish (Moussavi et al., 2012; Tena-Sempere et al., 2012), stimulates testicular expression of ER-a in frogs (Chianese et al., 2013), rats (Gottsch et al., 2004; Irwig et al., 2004)
Norepinephrine decreases food intake in birds (Denbow, 1983) and stimulates food intake in rats (Ritter and Epstein, 1975) inhibits LH secretion in rats (Iwata et al., 2011), stimulates sex behavior in birds (Cornil et al., 2005) and rats (Nock and Feder, 1979)
Oxytocin decreases food intake in birds (Jonaidi et al., 2003), rats (Olson et al., 1991) stimulates GnRH and LH secretion sex behavior in rats (Rettori et al., 1997; Whitman and Albers, 1995)
Secretin decreases food intake in  rats (Cheng et al., 2011a) stimulates LH secretion in rats (Babu and Vijayan, 1983)
Serotonin (5HT) decreases food intake in birds (Denbow et al., 1982), rats (Blundell, 1977) stimulates LH in the presence of estradiol in rats (Coen and MacKinnon, 1979) Inhibits LH secretion in the absence of estradiol in rats (Coen et al., 1980) (Koh et al., 1984)
Thyrotropin releasing hormone decreases food intake in rats (Vijayan and McCann, 1977) and Siberian hamsters (Steward et al., 2003) stimulates LH secretion in pituitary in vitro not in vivo in rats (Fujihara and Shiino, 1983), and indirectly by effects on thyroid hormones in rats (Barrett et al., 2007)
Urocortin decreases food intake in fish, amphibians, birds, and rats (Spina et al., 1996) stimulates LH secretion in ewes (Holmberg et al., 2001), inhibits LH secretion in rats (Li et al., 2005; Nemoto et al., 2010), directly inhibits Leydig cell function in rats (Rivier, 2008)
Peripheral “Anorectic” Hormones Ingestive Effects Reproductive Effects
Adiponectin (adipocytes) decreases food intake in rats (Bassi et al., 2012), increases food intake in mice (Kubota et al., 2007), decreases body weight and increases energy expenditure, insulin sensitivity, and ffa oxidation without effect on food intake in rats (Fruebis et al., 2001; Qi et al., 2004) implicated in embryo implantation and fetal development in pigs and women (Palin et al., 2012), inhibits ovarian steroidogenesis in cows (Lagaly et al., 2008), inhibits GnRH and LH in rats and in GnRH cell cultures (Cheng et al., 2011b; Lu et al., 2008)
Adrenocorticotropic hormone (ACTH) decreases food intake in rats (Vergoni et al., 1986) stimulated LH secretion in female rats inhibits LH secretion in male rats (indirect via adrenals) (Mann et al., 1985; Putnam et al., 1991)
Bombesin (gut) decreases food intake in fish (Volkoff et al., 2005), birds (Savory and Hodgkiss, 1984; Tachibana et al., 2010), and rats (Gibbs et al., 1979) stimulates LH secretion in rats (Babu and Vijayan, 1983)
Cholecystokinin (gut) decreases food intake in fish (Volkoff et al., 2005), birds (Savory and Hodgkiss, 1984), and hoarding in Siberian hamsters (Gibbs et al., 1973; Qian et al., 1999; Teubner and Bartness, 2010) simulates LH secretion in rats (Perera et al., 1993); Inhibits lordosis duration in rats (Mendelson and Gorzalka, 1984), but see central effects in Table 1.1
Estradiol (gonads, adrenals, adipocytes, brain) decreases body weight and food intake in fish (Leal et al., 2009), lizards (Shanbhag and Prasad, 1992), obese but not lean hens (Jaccoby et al., 1995; Jaccoby et al., 1996), rats (Nunez et al., 1980; Roepke et al., 2010; Roy and Wade, 1977; Zucker, 1969) and food hoarding in Syrian hamsters (Klingerman et al., 2010) stimulates sexual receptivity and vitellogenesis and has negative feedback on LH in fish, frogs, lizards and birds (Chakraborty and Burmeister, 2009; Cheng, 1973; Crews, 1975; Gavaud, 1986; Gibbins and Robinson, 1982a, b; Licht et al., 1985; Liley, 1972; Mason and Adkins, 1976; McCreery and Licht, 1984; Redshaw et al., 1969; Shanbhag and Prasad, 1992; Yu et al., 1981), and stimulates LH surges in female rats (Chazal et al., 1974) and female sex behavior in rats (Dempsey et al., 1936; Powers, 1970), increases courtship and sexual behaviors in hamsters (Ciaccio and Lisk, 1973; Ciaccio et al., 1979; Takahashi et al., 1985)
Insulin (ICV treatment) decreases food intake in rats and baboons (Chavez et al., 1995; Woods et al., 1979) stimulates LH pulses in rats, pigs, and diabetic sheep and non diabetic ovariectomized sheep (Bucholtz et al., 2000; Cox et al., 1987; Daniel et al., 2000; Kovacs et al., 2003; Miller et al., 1995), inhibits LH in ad libitum-fed ovariectomized lambs (Hileman et al., 1993)
Insulin-like growth factor increases body weight gain at superphysiological concentrations (Gruaz et al., 1997) does not accelerate reproductive development in female rats (Gruaz et al., 1997)
Leptin (adipocytes, liver) decreases body weight, adiposity, and food intake in fish (Crespi and Denver, 2006; Murashita et al., 2008), and mice (Campfield et al., 1995; Halaas et al., 1995; Pelleymounter et al., 1995) and food hoarding in Syrian hamsters (Buckley and Schneider, 2003) while increasing energy expenditure mammalian leptin increases gonadotropin secretion in fish (Peyon et al., 2003; Peyon et al., 2001), delays the summertime regression of the testes in lizards (Putti et al., 2009), delays fasting-induced cessation of egg laying, follicular regression, and follicle wall apoptosis in chickens (Paczoska-Eliasiewicz et al., 2003), reverses the effects of metabolic challenges on gonadotropin secretion in mice (Ahima et al., 1996; Barash et al., 1996), estrous cycles, and steroid-induced sex behavior (the latter only in ad libitum fed female hamsters) (Schneider et al., 2007; Schneider et al., 1997; Wade et al., 1997)
Resistin transient decreases in food intake in rats (Tovar et al., 2005) promotes ovarian steroid secretion in rats (Maillard et al., 2011)

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