All About Smoking, Eating And Thinking: New Research On The Brain, Hormones And Behavior
PITTSBURGH, June 19, 2006 — Certain hormones may make it more difficult for some to quit smoking, according to results of a study being presented at the 6th International Congress of Neuroendocrinology (ICN 2006) in Pittsburgh June 19 – 22 at the David L. Lawrence Convention Center. Other research focusing on the interaction between hormones and the brain and its influence on behavior include a laboratory study suggesting the immune system could help curb one’s appetite and animal research indicating what may be responsible for that yen for sweets.
Following are summaries of these studies’ findings as well as one giving perspective on the use of estrogen therapy for improving memory and brain power in women during menopause.
Hormones make it even harder for some to kick the habit
If quitting smoking weren’t already hard enough, researchers are now saying that for some, kicking the habit may be even more difficult due to changes in levels of certain stress hormones.
Prior studies led researchers to believe that cortisol, a stress hormone that can contribute to depression, may make quitting more of a challenge. However, a Yale University School of Medicine study has found that cortisol levels alone may not be as useful for predicting the ability to quit as the ratio of DHEA (another stress hormone) to cortisol. Indeed, research has shown that DHEA may protect the brain against some potential deleterious effects of cortisol. Participants who relapsed eight days after abstinence from cigarettes were more likely to have a drop in the ratio between DHEA and cortisol as measured in their plasma than smokers able to maintain abstinence. According to lead researcher Ann Rasmusson, M.D., director of the neuroendocrine laboratory in Yale’s department of psychiatry, this finding indicates that the DHEA/cortisol ratio may prove to be a useful diagnostic tool for determining who is likely to have a more difficult time kicking the habit and also may serve as a potential target for smoking cessation treatment interventions.
One lump or two? Oxytocin influences a sweet tooth
We all have weaknesses for certain kinds of food. Some of us can’t refuse a second helping of cake, while others can’t stay away from the chips and dip. It’s not merely a lack of willpower that leads us to indulge in our “trigger” foods, either.
Research by Janet Amico, M.D., professor of medicine and pharmaceutical sciences, University of Pittsburgh schools of Medicine and Pharmacy, Regis Vollmer, Ph.D., professor of pharmaceutical sciences, School of Pharmacy, and colleagues, identified an oxytocin deficiency as a contributing factor in developing a sweet tooth. In more recent studies, Dr. Amico and her team sought to determine if the same hormone that fosters a hankering for sweets leads to a love affair with fatty snacks, as well. Results suggest that oxytocin may be to blame for sugar cravings, but that influence does not appear to extend to the desire of fatty foods.
In the study, Dr. Amico’s team compared two groups of mice – normal animals and those without the ability to produce oxytocin – to see if they had particular preference for drinking solutions with either added sugar or fat. While the oxytocin-deficient mice showed markedly greater intake of the sugar solution than their wild-type counterparts, both groups seemed to like the fat-enhanced drink just the same. Oxytocin is a hormone that plays a role in physical and emotional responses, induces labor, encourages maternal behavior and promotes positive relationship interactions. This work establishes a new role for oxytocin in influencing food tastes and limiting intake of sweets. Whether oxytocin also plays this same role in humans is not yet known, but the investigators hope to extend these studies to people. Perhaps abnormalities in the production of oxytocin may lead to excessive ingestion of sweet-tasting substances in humans.
Confused at midlife: Clear thinking about estrogen therapy and the menopausal brain
While normal aging itself can result in a decline of certain cognitive abilities, many women at midlife complain specifically of difficulties in maintaining focus and concentration – of feeling wooly-headed. But even those with younger and sharper minds are finding the information about estrogen therapy confusing.
Some studies on hormone therapy indicate that estrogen supplementation can help boost brain power during the menopausal transition, when some aspects of cognition, particularly verbal memory, may begin to deteriorate. Other studies, particularly the Women’s Health Initiative Memory Study (WHIMS) published in 2004, find no benefit – and even some risk – associated with hormone replacement therapy. A large randomized controlled trial of more than 7,000 women, WHIMS found that estrogen fails to protect against cognitive aging in women who begin treatment after age 65. While these sets of findings appear to be at odds with one another, taken together, they indicate that estrogen supplementation can have the greatest benefit if begun during a woman’s transition into menopause – generally between the ages of 45 and 55 – rather than years after menstruation ceases. According to Barbara B. Sherwin, Ph.D., James McGill Professor of Psychology at McGill University in Montreal, this so-called “critical period hypothesis” is taking hold and is supported by a body of research that includes basic science, small animal, primate as well as human studies.
The next fad in weight loss: The cytokine diet?
Might we be able to turn our immune system against another kind of foe besides infections and viruses? How about fat? Researchers from the Centre National de la Recherche Scientifique (CNRS) at the Pasteur Institute and the University of Lille, France, have evidence suggesting the possibility. According to their studies, cytokine interleukin-7 (IL-7), an element of the immune system that is critical for maintaining the proper store of immune cells, also prevents obesity-prone mice from getting fat.
The researchers used a common mouse model for obesity that involves inducing lesions in the hypothalamus—a part of the brain that regulates appetite—using a common food additive, monosodium glutamate (MSG). As expected, these mice packed on extra ounces—up to 28 percent of their normal body weight. Another set of mice was injected with a single infusion of IL-7 after being given MSG. Interestingly, these mice neither developed lesions nor did they gain weight.
According to doctoral student Laurence Macia and co-authors, the results indicate for the first time that IL-7 interacts with the hypothalamus, and moreover, this interaction is related to the brain’s regulation of appetite. Perhaps the immune and neuroendocrine systems are more closely linked than previously thought, they conclude.
Held in a different part of the world every four years under the auspices of the International Neuroendocrine Federation, this year’s congress – Bridging Neuroscience and Endocrinology – is being sponsored by the American Neuroendocrine Society and the University of Pittsburgh School of Medicine. The first full day of the program, June 20, is being held in conjunction with the 10th Annual Meeting of the Society for Behavioral Neuroendocrinology.
Formerly the International Society of Neuroendocrinology, the International Neuroendocrine Federation consists of six member societies and seven regional groups, representing all parts of the world. The federation’s president is John A. Russell, MBChB, Ph.D., chair of neuroendocrinology, University of Edinburgh. The chair of the ICN 2006 scientific program is Iain J. Clarke, Ph.D., professorial fellow in the department of physiology at Monash University in Australia. Tony Plant, Ph.D., professor of cell biology and physiology and director of the Center for Research in Reproductive Physiology, University of Pittsburgh School of Medicine, is chair of the local organizing committee.