Study: Subway Sandwiches Are Worse Than We Think

We still underestimate how many calories we're getting at most fast food restaurants. The effect is most drastic at Subway, where a marketing "health halo" seems responsible.

James Hamblin, MD, is The Atlantic's Health editor.



PROBLEM: Under Obamacare, major fast food chains will be required to print calorie counts on menus. The idea presumes that we still don't really know what we're getting into with fast food. Don't we?


METHODOLOGY: Researchers led by Dr. Jason Block at Harvard surveyed people at fast food restaurants across New England. They talked with 1877 adults, 1178 adolescents, and 330 children at places like McDonald's, Dunkin Donuts, KFC, and Subway, among others.

They asked customers to save their receipts, then estimate how many calories were in their meals. Most of the customers ended up being non-white, 65 percent of the adults and 57 percent of the school-age children were obese, and 40 percent reported eating at that same restaurant chain at least once per week.

RESULTS: The average meal was 836 calories for adults, 756 for adolescents, and 733 for kids. Two-thirds of people underestimated that. One quarter underestimated it by at least 500 calories.

The underestimation in adults averaged 175 calories and got larger as the number of calories in the meal increased. Subway was the most insidious, with adolescent estimates averaging around 500 calories on the low side. Adults and adolescents eating at Subway estimated 20 and 25 percent lower than those at McDonald's, respectively. Here's how the underestimation looked between restaurants:

Calories estimated minus actual calories [BMJ]

IMPLICATIONS: Most people eating at these restaurants were obese, and most underestimated how many calories they were actually taking in. So, maybe calorie-counts on menus are a good thing. The researchers also discuss Subway's branding as a sort of "health halo" of which to be wary.

Of course, calorie count isn't the only measure of foods' healthfulness -- a 230-calorie veggie sub is better than 230 calories worth of jelly donut -- it's just the only measure in this study.

A footnote: 41 people were excluded from the study as outliers because their meals exceeded 4000 calories.

The full study, "Consumers' Estimation of Calorie Content at Fast Food Restaurants" is published in the journal BMJ.

Smoking a cigarette while riding the Tour de France. 1920s

Alcohol Addiction Relapse

Alcohol Addiction Relapse Might Be Thwarted By Turning Off Brain Trigger

By Jennifer O'Brien on June 23, 2013

 
Researchers at the Ernest Gallo Clinic and Research Center at UC San Francisco have been able to identify and deactivate a brain pathway linked to memories that cause alcohol cravings in rats, a finding that may one day lead to a treatment option for people who suffer from alcohol abuse disorders and other addictions.

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In the study, researchers were able to prevent the addicted animals from seeking alcohol and drinking it, the equivalent of relapse.

“One of the main causes of relapse is craving, triggered by the memory by certain cues – like going into a bar, or the smell or taste of alcohol,” said lead author Segev Barak, PhD, at the time a postdoctoral fellow in the lab of co-senior author Dorit Ron, PhD, a Gallo Center investigator and UCSF professor of neurology.
 
“We learned that when rats were exposed to the smell or taste of alcohol, there was a small window of opportunity to target the area of the brain that reconsolidates the memory of the craving for alcohol and to weaken or even erase the memory, and thus the craving”he said.
The study, also supervised by co-senior author PatriciH. Janak, PhD, a Gallo Center investigator and UCSF professor of neurology, was published online on June 23 in Nature Neuroscience.

Neural Mechanism That Triggers Alcohol Memorya 

In the first phase of the study, rats had the choice to freely drink water or alcohol over the course of seven weeks, and during this time developed a high preference for alcohol.
In the next phase, they had the opportunity to access alcohol for one hour a day, which they learned to do by pressing a lever. They were then put through a 10-day period of abstinence from alcohol.

Following this period, the animals were exposed for five minutes to just the smell and taste of alcohol, which cued them to remember how much they liked drinking it. The researchers then scanned the animals’ brains, and identified the neural mechanism responsible for the reactivation of the memory of the alcohol – a molecular pathway mediated by an enzyme known as mammalian target of rapamycin complex 1 (mTORC1).
They found that just a small drop of alcohol presented to the rats turned on the mTORC1 pathway specifically in a select region of the amygdala, a structure linked to emotional reactions and withdrawal from alcohol, and cortical regions involved in memory processing.

They further showed that once mTORC1 was activated, the alcohol-memory stabilized (reconsolidated) and the rats relapsed on the following days, meaning in this case, that they started again to push the lever to dispense more alcohol.

“The smell and taste of alcohol were such strong cues that we could target the memory specifically without impacting other memories, such as a craving for sugar,” said Barak, who added that the 

Ron research group has been doing brain studies for many years and has never seen such a robust and specific activation in the brain.

Drug that Erases the Memory of Alcohol

In the next part of the study, the researchers set out to see if they could prevent the reconsolidation of the memory of alcohol by inhibiting mTORC1, thus preventing relapse. 

When mTORC1 was inactivated using a drug called rapamycin, administered immediately after the exposure to the cue (smell, taste), there was no relapse to alcohol-seeking the next day.
Strikingly, drinking remained suppressed for up to 14 days, the end point of the study. 

These results suggest that rapamycin erased the memory of alcohol for a long period, said Ron.

The authors said the study is an important first step, but that more research is needed to determine how mTORC1 contributes to alcohol memory reconsolidation and whether turning off mTORC1 with rapamycin would prevent relapse for more than two weeks.

The authors also said it would be interesting to test if rapamycin, an FDA-approved drug currently used to prevent organ rejection after transplantation, or other mTORC1 inhibitors that are currently being developed in pharmaceutical companies, would prevent relapse in human alcoholics.

“One of the main problems in alcohol abuse disorders is relapse, and current treatment options are very limited.” Barak said. 

“Even after detoxification and a period of rehabilitation, 70 to 80 percent of patients will relapse in the first several years. It is really thrilling that we were able to completely erase the memory of alcohol and prevent relapse in these animals. This could be a revolution in treatment approaches for addiction, in terms of erasing unwanted memories and thereby manipulating the brain triggers that are so problematic for people with addictions.”

The other co-authors of the paper are Feng Liu, PhD, Sami Ben Hamida, PhD, Quinn V. Yowell, BS, Jeremie Neasta, PhD, and Viktor Kharazia, PhD, all of the Gallo Center and UCSF Department of Neurology.

The study was supported by funds from the National Institute on Alcohol Abuse and Alcoholism and funds from the State of California for Medical Research on Alcohol and Substance Abuse administered through UCSF.


The UCSF-affiliated Ernest Gallo Clinic and Research Center is one of the world’s preeminent academic centers for the study of the biological basis of alcohol and substance use disorders. Gallo Center discoveries of potential molecular targets for the development of therapeutic medications are extended through preclinical and proof-of-concept clinical studies.
 

Source: http://www.ucsf.edu/news/2013/06/107001/addiction-relapse-might-be-thwarted-turning-brain-trigger
  

Brain Freeze

Why do we get Brain Freeze? [Sphenopalatine Ganglioneuralgia]

Posted on May 29, 2012 by Wiley Life Sciences Blog

Have you ever wondered why you get “brain freeze” when you eat something cold such as ice cream or a milkshake? That sudden pain in your forehead is known in medicine as sphenopalatine ganglioneuralgia.

It is caused by having something cold touch the roof of the mouth (palate), or the total immersion in water that is generally below 15°C (or 10°C or even 5°C for some acclimated open water swimmers). It is believed to result from a nerve response causing rapid constriction and swelling of blood vessels or a “referring” of pain from the roof of the mouth to the head.

An ice cream headache is the direct result of the rapid cooling and rewarming of the capillaries in the sinuses. A similar but painless blood vessel response causes the face to appear “flushed” after being outside on a cold day. In both instances, the cold temperature causes the capillaries in the sinuses to constrict and then experience extreme rebound dilation as they warm up again.
In the palate, this dilation is sensed by nearby pain receptors, which then send signals back to the brain via the trigeminal nerve, one of the major nerves of the facial area. This nerve also senses facial pain, so as the neural signals are conducted the brain interprets the pain as coming from the forehead—the same “referred pain” phenomenon seen in heart attacks. 

Brain-freeze pain may last from a few seconds to a few minutes. Research suggests that the same vascular mechanism and nerve implicated in “brain freeze” cause the aura (sensory disturbance) and pulsatile (throbbing pain) phases of migraines.

How do we stop brain freeze? WikiHow explains.

Find more interesting stories on the official Neuroscience Facebook page

 

How do we stop brain freeze? WikiHow explains.

Find more interesting stories on the official Neuroscience Facebook page


Source:  http://wisciblog.com/2012/05/29/why-do-we-get-brain-freeze-sphenopalatine-ganglioneuralgia/

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Levity never hurts a person thus, this funny article is included here for your enjoyment.

Always laugh when you can. It is cheap medicine. 

— Lord Byron