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You already know how to do it. You just need to be reminded—as I was this week in two different ways. Here it is:

Slow down.

Yep, as we rush through our ever more overscheduled lives, we tend to eat quickly and mindlessly. And as many studies have shown, when you do that, you don’t give your brain time to catch up with your stomach and alert you that you’re full and satisfied. So you eat more than you need or even want, and the pounds pile up.

As a longtime health editor, I know this, of course. But after two recent reminders, I realized I wasn’t practicing it, so I’m going to adopt a slower pace. Here’s why. When I was in Minnesota on a family trip last week, I got to meet my gorgeous new nine-week-old nephew, John Robert IV.

During lunch at a casual restaurant, little John started getting a bit fussy. I told his mom and dad to eat and I’d take him for a while. He loves to be flung over your shoulder and walked around. So I got up after two bites of my gigantic sandwich and made a few circuits of the restaurant with the baby. A few minutes later, I returned and took another bite, then walked again for another 10 minutes or so. When I finally got back to the table and handed off the baby to his mom, I realized I was no longer hungry at all and didn’t even want my fries or the rest of that sandwich. I’m quite sure, however, that I would have snarfed it all down in one sitting if I hadn’t gotten up. We decided that’s how so many new moms lose the baby weight: no time to eat!

My second reminder of this phenomenon was Friday evening at my favorite neighborhood restaurant, Resto, which makes the best hamburgers on the isle of Manhattan. (It’s on 29th between Park and Lex, if you have ever a chance to go.) Now, I don’t eat much red meat, but I do occasionally indulge in Resto’s incredibly juicy and flavorful burger made from short ribs and hanger steak. It’s a modest size, as this is a Belgian-American spot, served with impeccable frites and small salad. I could easily eat it all every time.

But I was with my friend Steve, who had throat surgery that now requires him to eat much more slowly than most people. So I matched his pace, taking tiny bites, really savoring each one, and catching up on his life in between. Sure enough, when I stopped and assessed the situation a little past halfway through, I realized I was full and feeling good. I pushed the plate away and vowed to remember the technique.

“Mindful eating” is the new buzzword for this. And it does work, according to studies that have been done since the 1970s, when we all started getting too busy to sit down and relax with our families at mealtimes. Now, granted, it works best when you really want to eat less. We all have moments of weakness, when only massive doses of chocolate or chips or ice cream will comfort what ails us, and no amount of mindfulness will slow us down. That’s emotional eating, not appetite.

But most of the time, slowing down—and I mean really slowing down so it take 30 minutes or more to finish a meal—can significantly reduce your caloric intake. I could give you dozens of other diet tips, from reducing processed foods and sugars to eating more fiber to getting more sleep and exercise. But taking your time may be the strongest weight-control weapon you have.

University of Michigan pharmacologist Robert U. Simpson, Ph.D., thinks it’s apt to call vitamin D “the heart tranquilizer.”

In studies in rats, Simpson and his team report the first concrete evidence that treatment with activated vitamin D can protect against heart failure. Their results appear in the July issue of the Journal of Cardiovascular Pharmacology.

In the study, treatments with activated vitamin D prevented heart muscle cells from growing bigger – the condition, called hypertrophy, in which the heart becomes enlarged and overworked in people with heart failure. The treatments prevented heart muscle cells from the over-stimulation and increased contractions associated with the progression of heart failure.

About 5.3 million Americans have heart failure, a progressive, disabling condition in which the heart becomes enlarged as it is forced to work harder and harder, making it a challenge even to perform normal daily activities. Many people with heart disease or poorly controlled high blood pressure go on to experience a form of heart failure called congestive heart failure, in which the heart’s inability to pump blood around the body causes weakness and fluid build-up in lungs and limbs. Many people with heart failure, who tend to be older, have been found to be deficient in vitamin D.

“Heart failure will progress despite the best medications,” says Simpson, a professor of pharmacology at the U-M Medical School. “We think vitamin D retards that progression and protects the heart."

The U-M researchers wanted to show whether a form of vitamin D could have beneficial effects on hearts that have developed or are at risk of developing heart failure. They used a breed of laboratory rats predisposed to develop human-like heart failure.

The researchers measured the effects of activated Vitamin D (1,25 dihydroxyvitamin D3, a form called calcitriol) in rats given a normal diet or a high-salt diet, compared to control group rats given either of the same two diets, but no vitamin D treatment. The rats on the high-salt diet were likely to develop heart failure within months.

The rats on the high-salt diet, comparable to the fast food that many humans feast on, quickly revealed the difference vitamin D could make.

“From these animals, we have obtained exciting and very important results,” Simpson says.

After 13 weeks, the researchers found that the heart failure-prone rats on the high-salt diet that were given the calcitriol treatment had significantly lower levels of several key indicators of heart failure than the untreated high-salt diet rats in the study. The treated rats had lower heart weight. Also, the left ventricles of the treated rats’ hearts were smaller and their hearts worked less for each beat while blood pressure was maintained, indicating that their heart function did not deteriorate as it did in the untreated rats. Decreased heart weight, meaning that enlargement was not occurring, also showed up in the treated rats fed a normal diet, compared to their untreated counterparts.

Simpson and his colleagues have explored vitamin D’s effects on heart muscle and the cardiovascular system for more than 20 years. In 1987, when Simpson showed the link between vitamin D and heart health, the idea seemed far-fetched and research funding was scarce. Now, a number of studies worldwide attest to the vitamin D-heart health link (see citations below).

The new heart insights add to the growing awareness that widespread vitamin D deficiency—thought to affect one-third to one-half of U.S. adults middle-aged and older—may be putting people at greater risk of many common diseases. Pharmaceutical companies are developing anti-cancer drugs using vitamin D analogs, which are synthetic compounds that produce vitamin D’s effects. There’s also increasing interest in using vitamin D or its analogs to treat autoimmune disorders.

In more than a dozen types of tissues and cells in the body, activated vitamin D acts as a powerful hormone, regulating expression of essential genes and rapidly activating already expressed enzymes and proteins. In the heart, Simpson’s team has revealed precisely how activated vitamin D connects with specific vitamin D receptors and produces its calming, protective effects. Those results appeared in the February issue of Endocrinology.

Sunlight causes the skin to make activated vitamin D. People also get vitamin D from certain foods and vitamin D supplements. Taking vitamin D supplements and for many people, getting sun exposure in safe ways, are certainly good options for people who want to keep their hearts healthy. But people with heart failure or at risk of heart failure will likely need a drug made of a compound or analog of vitamin D that will more powerfully produce vitamin D’s effects in the heart if they are to see improvement in their symptoms, Simpson says.

Vitamin D analogs already are on the market for some conditions. One present drawback of these compounds is that they tend to increase blood calcium to undesirable levels. Simpson’s lab is conducting studies of a specific analog which may be less toxic, so efforts to develop a vitamin D-based drug to treat heart failure are moving a step closer to initial trials in people.

In addition to Simpson, other U-M authors include Peter Mancuso, Ph.D., of the U-M Department of Environmental Health Sciences; Ayesha Rahman, Ph.D., Stephen D. Hershey, M.D., Loredana Dandu and Karl A. Nibbelink, M.D. of the Department of Pharmacology in the U-M Medical School.

Funding for the study came from the National Institutes of Health.

Patents related to this research have been applied for by the U-M Office of Technology Transfer.

The new study, from Germany, adds to the scientific evidence linking deficiency of this sex hormone with increased death from all causes over time–so-called "all-cause mortality."

The results should serve as a warning for men with low testosterone to have a healthier lifestyle, including weight control, regular exercise and a healthy diet, said lead author Robin Haring, a PhD student from Ernst-Moritz-Arndt University of Greifswald, Institute for Community Medicine.

"It is very possible that lifestyle determines levels of testosterone," he said.

In the study, Haring and co-workers looked at death from any cause in nearly 2,000 men aged 20 to 79 years who were living in northeast Germany and who participated in the Study of Health in Pomerania (SHIP). Follow-up averaged 7 years. At the beginning of the study, 5 percent of these men had low blood testosterone levels, defined as the lower end of the normal range for young adult men. The men with low testosterone were older, more obese, and had a greater prevalence of diabetes and high blood pressure, compared with men who had higher testosterone levels, Haring said.

Men with low testosterone levels had more than 2.5 times greater risk of dying during the next 10 years compared to men with higher testosterone, the study found. This difference was not explained by age, smoking, alcohol intake, level of physical activity, or increased waist circumference (a risk factor for diabetes and heart disease), Haring said.

In cause-specific death analyses, low testosterone predicted increased risk of death due to cardiovascular disease and cancer but not death of any other single cause.

DPC Biermann, Bad Nauheim, Germany, provided the testosterone reagent, and Novo Nordisc provided partial funding for this analysis.

Detailed results will be presented at The Endocrine Society's 90th Annual Meeting in San Francisco.

"We want to understand the mechanisms behind the current epidemic of childhood obesity," said Dr. Kjersti M. Aagaard-Tillery, assistant professor of obstetrics and gynecology at BCM. "What efforts can we take in pregnancy to affect this problem? Is it that the mom is obese or is exposure to a high fat diet the problem?"

A consortium of researchers from BCM, the University of Utah Health Sciences in Salt Lake and the Oregon National Primate Research Center teamed up to study what happens to the offspring of non-human primate mothers fed a diet consisting of 35 percent fat. When compared to those who ate a 13 percent fat diet, the offspring of these animals had non-alcoholic fatty liver disease (comparable to that found in obese human youngsters). In fact, their triglycerides (one form of fat measured in blood) were three times higher than those of the normal offspring.

In some cases, the mothers on the high fat diet did not become obese themselves but their offspring suffered the same ill effects as those of moms who did become obese.

At a molecular level, Aagaard and her collaborators found modifications in the DNA backbone – the histones – of the offspring of the mothers who ate a high fat diet. This is called an epigenetic change, which means that while it does not affect the DNA code per se, it still affects the way that the genes are regulated and the degree to which they are expressed (the so-called "histone code").

"We found that there were genes that were differentially regulated in the livers of the offspring whose mothers had a high fat diet, and that these changes were associated with histone alterations," she said. "The genes affected were not always those associated with obesity."

She is now trying to find out why these gene changes exist and how they might affect the animals later in life. She is interested in looking at whether they are the direct result of permanent modifications in the histones in both the liver and brain, and whether they further relate to specific changes in the chemical modifications (or methylation) of the regulatory regions of genes.

Others who took part in this work include Kevin Grove and Jacalyn Bishop of the Oregon Health Science University, Oregon National Primate Research Center and Xingrao Ke, Qi Fu, Robert McKnight, and Robert H. Lane of the University of Utah Health Sciences in Salt Lake.

Funding for this work came from the 2007 National Institutes of Health Director's New Innovators Award to Aagaard, the National Institute of Digestive and Diabetes and Kidney Diseases and the National Institute of Child Health and Human Development.

Presented at this week's Endocrine Society annual meeting, in San Francisco, the new research found that sedentary, obese women lost almost five times as much weight on the "big breakfast" diet as did women following a traditional, restrictive low-carbohydrate diet.

"We treat obese people by telling them to eat less and exercise more, but that does not take into account feelings of carb cravings and hunger. We have to change our approach and find a diet that can control cravings and hunger," said the study's lead author, Dr. Daniela Jakubowicz, a clinical professor at Virginia Commonwealth University and an endocrinologist at the Hospital de Clinicas Caracas in Venezuela.

Jakubowicz explained that when you wake in the morning, your body is primed to look for food. Your metabolism is revved up, and levels of cortisol and adrenaline are at their highest. Your brain needs energy right away, and if you don't eat or you eat too little, the brain needs to find another fuel source. To do this, it activates an emergency system that pulls energy from muscle, destroying muscle tissue in the process. Then when you eat later, the body and brain are still in high-alert mode, so the body saves energy from the food as fat, she said.

Compounding the problem, your levels of the brain chemical serotonin are highest in the morning, which means your craving levels are at the lowest when you first wake up, and you may not feel much like eating, Jakubowicz said. But, as the day wears on, serotonin levels dip, and you get cravings for chocolate or cookies, and the like. If you eat these foods, your serotonin levels rise, and your body begins to associate good feelings with them, creating an addictive cycle, she said.

To combat both the addiction cycle and the hunger that inevitably seems to come with calorie reduction, Jakubowicz and her colleagues designed the "big breakfast" diet. In this eating plan, your breakfast accounts for roughly half of your daily calories, and breakfast includes milk, 3 ounces of lean meat, two slices of cheese, two whole grain servings, one fat serving and one ounce of milk chocolate or candy.

The high protein, carbohydrate mix gives the body the initial energy boost it needs in the morning. Throughout the rest of the day, the meals are made up of protein and complex carbohydrates, like vegetables. Because protein is digested slowly, Jakubowicz said, you won't feel hungry.

And, she said, by having a small piece of chocolate or candy when serotonin levels are high, it won't taste as good, and the brain won't feel the same serotonin boost, which will eventually help cut down on cravings.

In the study of 94 obese, sedentary women with metabolic syndrome, half were told to eat the big breakfast diet containing about 1,240 calories, while the other half ate a 1,085 calorie high-protein, low carbohydrate diet for eight months.

At the end of the eight months, those on the more restrictive low-carb diet lost an average of almost 9 pounds. But those on the big breakfast diet lost nearly40pounds. That translated to an average body mass loss of 4.5 percent for those on the low-carb diet and a 21.3 percent average loss for those on the big breakfast plan.

Additionally, those on the big breakfast plan reported feeling less hungry and had fewer carbohydrate cravings.

Nutritionist Geri Brewster, a wellness consultant at Northern Westchester Hospital Center in Mount Kisco, N.Y., said she already recommends a large, well-balanced breakfast to all of her clients, because it helps to keep blood sugar levels stable.

She said if you eat a traditional breakfast, something like cereal or a doughnut, your blood sugar and insulin levels spike. Once that blood sugar is used up, you'll still have excess insulin circulating, which makes you hungry and makes you crave carbohydrates.

A second study presented at the meeting reinforced the idea that biological changes occur when you carry excess weight, Brewster said. This study found that women who are overweight don't experience a drop in leptin levels after exercise like lean women do.

Leptin is a hormone that plays a role in appetite regulation and metabolism. Brewster said she wasn't surprised by these findings, because once the body is overweight, it tries to maintain that size. "Fat cells become mini-endocrine systems themselves to maintain obesity," she said, and keeping leptin levels elevated is likely one way the body does that.

A new study, by Michael Rosenbaum and colleagues, at Columbia University Medical Center, New York, has provided new insight into the critical interaction between the hormone leptin and the brain's response to weight loss.

Leptin levels fall as obese individuals lose weight. So, the authors set out to see whether changes in leptin levels altered activity in the regions of the brain known to have a role in regulating food intake.

They observed that activity in these regions of the brain in response to visual food-related cues changed after an obese individual successfully lost weight. However, these changes in brain activity were not observed if the obese individual who had successfully lost weight was treated with leptin. These data are consistent with the idea that the decrease in leptin levels that occurs when an individual loses weight serves to protect the body against the loss of body fat.

Further, both the authors and, in an accompanying commentary, Rexford Ahima, at the University of Pennsylvania School of Medicine, Philadelphia, suggest that leptin therapy after weight loss might improve weight maintenance by overriding this fat-loss defense.

Sean William Maynard was 10 pounds and 14 ounces, but when Abigail Rose Maynard was born, she outweighed her brother with 12 pounds, 3 ounces. Together, the twins tipped the scales at 23 pounds, 1 ounce.  The heaviest twins on record in the country were born in Arkansas in 1927. They weighed a total of 27 pounds, 12 ounces.