Mary Shomon: Can you give us some background on the hormone leptin as relates to weight loss?
Karilee Shames: Leptin is a hormone from fat cells that, in proper amounts, inhibits food intake and increase caloric burning.
It was not long ago that practitioners in our field were told that leptin would be a major magic bullet to help with weight loss. It was thought that certain kinds of leptin deficiency were responsible for obesity, and thus managing leptin would be a quick and effective solution. Then, researchers found that obese people have, surprisingly, a higher level of leptin. Then the focus shifted to leptin resistance as the culprit, and that hasn't panned out either. Currently, what can be said is that leptin plays the role of "messenger," informing the other organs about the state of fat stores. It's not clear whether it's worth attempting to intervene on and try to directly control.
Mary Shomon: Could you briefly explain the current thinking about leptin?
Richard Shames: To put leptin in perspective, take a quick look at just one array of endocrine signaling in the brain that controls body weight. These are the hormonal signals that mediate meal initiation, types of food intake, blood sugar and insulin levels, satiety (your sense of feeling full), meal termination, and level of fat stores.
"Just thinking about food," as you say in The Thyroid Diet, results in changes in hormone levels that stimulate appetite and salivation.
Here's the science: The stomach releases the peptide ghrelin, which further acts as an appetite stimulator and meal initiation signal. These changes result in increases in peptide Y and agouti-related protein in the arcuate nucleus area, along with the decrease here of alpha-melanocyte stimulating hormone. All this now results in a decrease of melanocortin-4 receptor, accompanied by a decrease in thyrotropin-releasing hormone. These activities also lead to an increase in melanin-concentrating hormone in the lateral hypothalamic area. The result: metabolism slows down and food intake increases. in an attempt to restore the previously burned-off fat.
Mary Shomon: So what does this mean to someone who wants to eat right to reach or maintain a healthy weight?
Karilee Shames: Well, first off, it seems to us that this impressive complexity is better optimized by eating three square meals a day. All these intricate hormone interactions and feedback loops might not be well served cranking up and cranking down six or seven times within fourteen hours.
Instead, the older advice of a smaller number of meals per day may lead to smoother function and fuller recovery time for your hard-working biochemicals. Also, eating at three regular and expected times a day means that when you're not eating, you're not thinking of food or planning when next to eat. And as noted, even thinking about food can trigger some of the chemical reactions.
This seems to be of definite help to large numbers of people because it is at the in-between times that our fabulous complexity can begin to rebalance and adjust itself better. We still have the bodies and chemistry of our ancestors who most likely ate quite intermittently, with long breaks between meals.
Richard Shames, MD graduated Harvard and University of Pennsylvania, did research at the National Institutes of Health with Nobel Prize winner Marshall Nirenberg, and has been in private practice for more than twenty five years. Dr. Shames practices holistic medicine -- with a focus on thyroid and autoimmune conditions -- and has for more than two decades been engaged in the search for answers about thyroid disease. Karilee Halo Shames RN, Ph.D. , Dr. Shames' wife, is herself hypothyroid, and is a Clinical Specialist in Psychiatric Nursing and a Certified Holistic Nurse with a Ph.D.. in Holistic Studies. The Shames are authors of two thyroid-related books, ThyroidPower and Fat Fuzzy and Frazzled?
FOR MORE HELP:
Shomon, Mary J. The Thyroid Diet: Manage Your Metabolism for Lasting Weight Loss, HarperCollins, 2004
Zimmermann-Belsing, T, et. al. "Circulating leptin and thyroid dysfunction," European Journal of Endocrinology, Vol 149, Issue 4, 257-271