Skip Breakfast, Get Fat
Skip Breakfast, Get Fat
But more meals, if smaller, could make you thinner, study finds
FRIDAY, July 11 (HealthDayNews) — It’s a prime piece of conventional wisdom: Eat right before you go to bed and you’ll get fat.
But new research suggests that late eaters are no more likely to be overweight than anyone else. It’s what you consume the rest of the day — especially in the morning — that counts.
Americans who regularly skip breakfast are 4.5 times more likely to be fat, researchers found. But, in good news for the nibblers among us, those who eat four or more meals a day are actually on the thinner side.
“”We tend to eat because of external cues instead of internal cues — we eat until the plate’s clean. If the plate has a lot less food on it, perhaps you’ll be eating less,”" says Ruth Kava, director of nutrition with the American Council on Science and Health.
Researchers launched their study because experts don’t fully understand how eating habits — such as the timing and frequency of meals — are tied to obesity, says study co-author Yunsheng Ma, an assistant professor of epidemiology at the University of Massachusetts Medical School.
The researchers examined a national cholesterol study that took place from 1994 to 1998. A total of 499 people reported five times a year on what they ate over 24 hours.
The findings of the study appear in the current issue of the American Journal of Epidemiology.
Ma and his colleagues found people who ate more than three times a day were about half as likely to be fat as those who ate three or fewer times a day. Ma suspects the difference may have something to do with fewer spikes in blood sugar levels among the frequent eaters.
Insulin levels go up when blood sugar rises, contributing to hunger and the buildup of fat, Ma says. Similar factors may be at work among those who frequently eat breakfast or dinner away from home, he says. The study found they were 4.5 times more likely to be fat.
Someone who eats breakfast at home might settle for a small, convenient meal, Kava says. “”But if you go out, there’s all kinds of tempting things like bacon and eggs and hash browns. Maybe you tend to indulge a little bit more. You don’t have to do the work or clean up.”"
And what about the link between skipping breakfast and tipping the scales?
“”You have not broken the fast soon enough to only need a moderate amount of calories,”" says Gail Frank, a professor of nutrition at California State University at Long Beach and a spokeswoman for the American Dietetic Association. “”You are starving. How does the normal person respond? They eat, and they keep eating to compensate.”"
As for the study’s rebuttal of the time-honored belief in the fattening properties of late-night meals, Ma says more research is needed to confirm that finding.
But it makes sense, Frank says, and counteracts the “”myth”" about the hazards of midnight munching.
The body continues digesting through the night, she says, even when people are asleep and not active. “”The body doesn’t know when the lights go off,”" she says.
SOURCES: Yunsheng Ma, Ph.D., assistant professor, epidemiology, University of Massachusetts Medical School, Worcester; Ruth Kava, Ph.D, R.D. director, nutrition, American Council on Science and Health, New York City; Gail Frank, DrPH, R.D., professor, nutrition, California State University at Long Beach, and spokeswoman, American Dietetic Association; July 1, 2003, American Journal of Epidemiology
Acetyl L-Carntine vs. L-Carnitine
The Essential Difference Between the Carnitines
Do you lack energy, or feel tired and physically or mentally unprepared to take on the tasks of the day? This is not unusual, especially as we age, and today’s topic may help explain some of the reasons for this energy deficit.
Two natural compounds produced by our tissues, L-carnitine and acetyl-L-carnitine (ALC), are similar in that both have identical chemical core structures. However, one (ALC) contains an extra component, an acetic acid bound to the core molecule (in what is known as an ester linkage). It turns out that this extra chemical piece makes a significant difference in how this molecule behaves in our body relative to its non-acetylated cousin, L-carnitine. These differences are described below, but first a brief summary of how these molecules normally function in our body.
L-carnitine functions as a vehicle to ferry fat constituents (fatty acids) across a membrane barrier into the cell’s energy-producing machine, the mitochondria, where the fat is converted to energy. Equally important, L-carnitine works in the reverse direction, too. It ferries toxic products produced during fat metabolism out of the mitochondria. This latter step helps maintain the mitochondria as clean-burning, energy-efficient machines.
We are all aware of the fact that as we age, our energy level diminishes. This decrease in energy parallels a decrease in the plasma level of L-carnitine. L-carnitine also decreases under conditions of stress, both psychological and physical. Consequently, it is described as a conditionally essential nutrient. This simply means that when our bodies cannot produce enough of it to meet demand, we need to increase the intake of this nutrient.
Acetyl-L-carnitine is just as active as L-carnitine in transporting fatty acids into the mitochondria. However, as described below, that extra acetyl group confers additional properties to this form of L-carnitine, which make it superior to its non-acetylated cousin. Both compounds increase energy Acetyl L-Carnitine or ALC Physical Energy Fat Metabolism Brain Protection Neurotransmission
Experiments with rats show a dramatic decrease (between 50-70%) in the activity level of old rats as compared to the young animal. Old rats, too, get tired with age! This decrease, as mentioned above, parallels a decrease in the amount of L-carnitine present in the animal’s tissues and blood.
This observation led researchers to investigate whether the old energy-deficient animals could be transformed into more energetic, youthful animals by feeding them a diet enriched with L-carnitine. Supplying L-carnitine to the diet increased the ambulatory activity of the old rats almost two-fold. The experiment was repeated with ALC, and it too increased the animals’ activity level to about an equal degree. So both compounds worked equally well in improving the old rats’ energy levels. ALC protects the brain
One of the two cousins, ALC, stands out with respect to its effects on the brain and nervous system. First, ALC is more effectively transported into the central nervous system. It more readily traverses the blood-brain barrier
Brain Cell Growth Boosted By DHEA Supplements
‘Anti-aging’ hormone DHEA Found to Boost Brain Cell Growth August 24, 2004
Human neural stem cells, exposed in a lab dish to the steroid DHEA, exhibit a remarkable uptick in growth rates, suggesting that the hormone may play a role in helping the brain produce new cells, according to a new study published this week in the online edition of the Proceedings of the National Academy of Sciences (PNAS).
The new work, conducted by a team of scientists at the University of Wisconsin-Madison, provides some of the first direct evidence of the biological effects of DHEA on the human nervous system, according to Clive Svendsen, the study’s senior author and an authority on brain stem cells at UW-Madison’s Waisman Center.
“What we saw was that DHEA significantly increased the division of the cells,” said Svendsen, a UW-Madison professor of anatomy and neurology. “It also increased the number of neurons produced by the stem cells, prompting increased neurogenesis of cells in culture.”
DHEA or dehydroepiandrosterone is among the most abundant naturally occurring steroids in the blood of young humans, but levels decline with age and its physiological effects are poorly understood.
A synthetic form of the hormone is sold over-the-counter as a dietary supplement in the US, thought to have anti-aging properties and to offer prevention against cancer and heart disease, Alzheimer’s and other diseases. But scientists know relatively little about the drug and its basic biological effects on humans.
“We don’t know much about DHEA, but this new work adds a piece to the puzzle,” said Svendsen, who conducted the study with colleagues Masatoshi Suzuki, Lynda S. Wright, Padma Marwah and Henry A. Lardy, all of UW-Madison. “This is the first real evidence of DHEA’s effects on human neural cells.”
Svendsen and Suzuki carried out the experiments by growing human fetal neural stem cells in culture. The cells form aggregates known as ‘neurospheres,’ which were exposed to a cocktail of DHEA and growth and inhibitory factors, and observed a 29 per cent increase in new brain cells compared to cells grown in a medium with the same factors, but without DHEA.
“We saw such a pure effect of DHEA,” Svendsen said.
“It’s the only steroid we tested that had such a direct effect on stem cell growth and new neuron formation,” according to Suzuki.
The new work is important because it provides a direct window to the controversial hormone’s effects on critical human cells. Similar studies have been conducted in mice and rats, but those models have shortcomings that are difficult to address, Svendsen notes.
“There are previous studies in rats that suggest DHEA is neuroprotective, but the problem with DHEA in rats is that it is not a major metabolite in that animal so its effects may not be the same as those seen in humans,” he said. According to Lardy, metabolic products of DHEA hormone have also been shown to aid memory retention in old mice.
Despite hints from the studies in rodents that DHEA may play a role in enhancing the brain and memory, the new findings reported in the PNAS article were a surprise, he said.
“We assumed the compounds we were testing would be more active than DHEA in brain stem cells,” Lardy explains. In previous studies, Lardy, with Wisconsin biochemistry colleagues James Ntambi and Brian Fox, showed that DHEA blocked a step in fat synthesis.
“The effects of DHEA on brain stem cells is a completely new finding,” said Lardy. “The problem of whether DHEA itself is having this effect, or if there’s another metabolite of the hormone involved, still exists.”
One of the intriguing aspects of the new work, according to Svendsen, is the possibility that DHEA could have some positive effects on the adult human brain.
It is known that DHEA amounts fall progressively during aging, and reduced levels of DHEA have been reported in both adolescents and adults with major depressive disorders. And given the fact that adult humans have neural stem cells that continue to make new neurons in some parts of the brain, there is a possibility that DHEA could play a role in moderating the genesis of new brain cells.