McDonald's Food Mummy Art Show - Update

McDonald's Food Mummy Art Show by Ben Campbell — Kickstarter

 

The project is to fund and enhance an art show featuring a wide variety of work created with and inspired by McDonald's Food. Conceptually, the reason behind the show is to comically highlight the parallels between Ancient Egypt, McDonald's Food, and Modern Society. Some of the more interesting pieces include a hamburger that is over a year old and a life sized mummy made of McDonald's food. Also I would like to incorporate different cultures based off of different fast foods like Taco Bell Aztecs, Pizza Hut Pompeii, and scurvy Pirates made from Long John Silver's.
A short explanation of the reasoning behind the show is as follows.
1. Ancient Egypt was preoccupied with achieving a form of immortality through odd customs such as constructing pyramids and mummification.
2. Modern society is preoccupied with achieving a form of immortality through odd customs such as celebrity status and the construction of corporations.
3. McDonald's is highly representative of American culture, even iconic.

4. McDonald's food doesn't decompose if left to dry out. Seriously, just google it. As such archaeologists from the future will be digging this stuff up thousands of years in the future. Especially if something cataclysmic happens to our society.

5. The questions. What could that something cataclysmic be? How can we prepare for it? Do we still want to invest in distractions and brainwashing instead of real solutions and in each other?
6. And finally, if we don't learn to laugh at ourselves future generations are going to do it for us.
Currently I have two McDonald's food mummies completed and would like to make many more. Other works include preserved hamburgers in commercial plastic cases, McDonald's food skulls, and large scale paintings. The funds generated here will be used to purchase more materials and to pay for gas to haul everything from place to place. Since I am based in Texas, the first shows will be within the state with later shows taking place across the country. If you are interested in booking the show for your gallery or you have any questions, feel free to ask.
Just in case some of you are unsure or on the fence about supporting this project, I'll talk a bit more about myself and what I would hope to accomplish with this and more in the future.
At my core I'm a joker who likes to get people thinking, always have been, always will be. With this Ancient McDonald's Food art show I feel that so far I have done just that and can carry it much further as it and my career develops. I've noticed when people begin to take themselves less seriously and can experience the humorous connections between what were once considered harsh realities, they become open and aware of newer, more vibrant solutions. As such I would like to bring my brand of humor to fields such as pop, geek, and internet culture.
By funding this project you will also be helping me lay the foundation for other really cool endeavors that will more directly impact the world around us in a positive manner as well. Apart from art, sociology, and pop culture I'm really drawn towards engineering, computer science, and architecture. Some of my particular interests include constructing efficient and beautiful geodesic domes for habitation/agriculture, robotics for agriculture, video games that harness our creativity into real world solutions, and all manner of manufacturing.
Lastly I'd like to give away pretty much all of the funds I will have acquired throughout my life and let the people decide how to use them through a social network I'm working on to allow the best, most logical, realistic, and ethical solutions (regardless of who came up with them) to become funded and brought into reality. This idea I feel could truly harness the internet for the betterment of the world at large and addressing potential cataclysms in ways we would be hard pressed to do otherwise.
Any amount helps, even $1 but if you want to really help me out I have some fantastic pieces that would fit well with any serious art collector. So if you're interested check it out, grab a piece of my art, and enjoy the ride.
Also for those unfamiliar with Kickstarter, you will only be charged if the full funding amount is reached. It's all or nothing, so you don't have to worry about your money going towards a project that will fizzle out. And besides that I intend on pursuing and developing this project no matter what happens with this Kickstarter, it would just make things go a bit quicker.
Thanks for your time,
-Ben

Coffee: a caffeinated chronicle

 

A brief history of coffee

Sunshine Green

According to legend, the first cup of coffee came into being in a most magical way. A goat-herd named Kaldi glimpsed the energizing effects of the unique, bright red berries in his flock and took it upon himself to test it out. Such revitalization inspired Kaldi to take the berries to a Muslim holy man. Scared, the holy man tossed them into a fire. Roasted beans were separated from the embers, ground, and dissolved in hot water, creating—you guessed it—the world's first cup of coffee.

Flower Encyclopedia

Coffee beans are derived from several species of the Coffea shrub—most commonly C. canephora and C. arabica. These plants may grow up to 5 feet tall and produce beautiful glossy, dark green leaves. The leaves then ripen to yellow, red, and finally black. Coffea plants are native to Ethiopia, Sudan, and Kenya, and subsaharan Africa. Today, Brazil, Vietnam, Indonesia, and Colombia are the world leaders in coffee production, raising seedlings in nurseries before transferring them outdoors when they are between 6 and 12 months old.

Gimme Coffee

Each berry contains two seeds. It may be surprising to you that these seeds are white. Only when roasted do we see—and smell—the recognizable coffee bean (what I thought were little balls of wood when I was younger). Roasting occurs when the internal temperature of the bean reaches 200º C (392º F), causing caramelization, or starch breakdown, which browns the simple sugars. Acids and oils within the bean weaken, creating its characteristic bitter flavor. Caffeol, one such oil, is generated at 200º C and is largely responsible for coffee's flavor.

The coffee buzz
As you know, the energizing effects of coffee are due to caffeine, this nifty little chemical:

In the plant world, caffeine is a natural pesticide, protecting Coffea, tea plants, and other foods from certain insects. 

In the animal world, caffeine is a drug. A stimulant drug, to be precise.

Inside the body, the chemical adenosine circulates at very high levels. Adenosine is a nucleoside with two main roles:

1. Attached to a ribose sugar, it comprises one of the four constituents of the DNA backbone.

2. Attached to three phosphate groups, it exists as ATP, the energy currency of a living cell.

In addition to these roles, adenosine also acts as an inhibitory neurotransmitter, believed to play a role in suppressing arousal, promoting sleep, and even inducing torpor in hibernating animals. Levels of adenosine increase throughout the day, which may explain why we become increasingly sleepier with each hour after awakening.

Caffeine is unique because it is both water- and lipid-soluble, allowing it to pass the blood-brain barrier and enter the nervous system. In the brain, caffeine works to counteract, or antagonize, the effect of adenosine. Because caffeine and adenosine have similar chemical structures, caffeine (below, red) can bind to adenosine receptors without activating them. In other words, caffeine is a competitive antagonist of adenosine. In this way, the sleep-inducing effect of adenosine (below, white) is blocked, promoting our lovely "coffee buzz."

How Stuff Works

Caffeine has a half-life of ~5 hours, meaning that after 5 hours, half of the caffeine you ingested has been metabolized; after 10 hours, 1/4 of the caffeine is still there—hence potential for a sleepless night if consumed too late in the day.

MUST...HAVE...COFFEE...

The Nutrition Post

Caffeine addiction is not difficult to attain. In response to blocked adenosine receptors, the body will make more. In turn, your body requires more caffeine to block the additional adenosine receptors. A person must drink more coffee, then, to obtain the same degree of wakefulness.

Effects of caffeine include: 

• Increased heart and respiratory rate

• Enhanced fatty acid breakdown and promotes free fatty acids in the bloodstream

• Raised blood pressure

• Increased stomach acid

• Increased urination (a diuretic effect)

• With very high levels can cause a jittery feeling, nervousness, agitation, ringing in the ears, and release of adrenaline

Withdrawal symptoms include headache, irritability, difficulty concentrating, drowsiness, and pain in the stomach and joints. Keep in mind: while these symptoms appear within 12-24 hours of withdrawal, it should all be over after one to five days. Willpower is key!

Coffee may make you lazy?

A study published online Wednesday in Neuropsychopharmacology found that "worker" rats—those who naturally worked harder for reward—were more likely to avoid hard worker when treated with caffeine or amphetamine.

Cocker and colleagues from the University of British Columbia created a rat cognitive effort task (rCET) which allowed rats to choose between an easy or hard task—rats who completed the hard task were doubly rewarded with sugar pellets. 

Those deemed "worker rats," when treated with caffeine or amphetamine, suddenly slacked off; conversely, "slacker rats" worked harder under amphetamine (but not cocaine).

Grad student Jay Hosking interprets these results in terms of human needs. "For some of us, coffee really does the trick for those long hours in the middle of the day, but for other people it makes them too jittery or aroused to concentrate on their work."

 

Cocker PJ, Hosking JG, Benoit J, and Winstanley CA (2012). Sensitivity to Cognitive Effort Mediates Psychostimulant Effects on a Novel Rodent Cost/Benefit Decision-Making Task. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology PMID: 22453140

Related topics: adenosine, caffeine, coffee, sleep, stimulant

Is Exercise Harmful for Some People? | Healthland | TIME.com

 For some healthy people, exercise may actually increase heart risk, according to a paper published this week in the journal PLoS One.


The review of six previous studies on exercise found that working out worsened at least one measure of heart risk — blood pressure, insulin level or levels of HDL cholesterol or triglycerides — for about 10% of people. About 7% of people declined on at least two measures.

The lead author of the paper, Claude Bouchard, a professor of genetics and nutrition at the Pennington Biomedical Research Center at Louisiana State University, told the New York Times that the finding was “bizarre.”


At the same time, the data, involving 1,687 people, showed that about 10% of people saw outsized gains in at least one measure of heart disease risk — some patients improved 20% to 50%. For other participants, exercise-related rewards ran the gamut, from none to some to significant benefits.


One of the authors of the study was on the committee that provided the scientific evidence underlying the government’s official exercise guidelines for Americans, which recommend at least 150 minutes per week of moderate activity.


The implication here is that the government’s physical activity guidelines are based on rather weak scientific data. The Times’ Gina Kolata writes:

The problem with studies of exercise and health, researchers point out, is that while they often measure things like blood pressure or insulin levels, they do not follow people long enough to see if improvements translate into fewer heart attacks or longer lives. Instead, researchers infer that such changes lead to better outcomes — something that may or may not be true.

Some critics have noted that there is no indication that those who had what Dr. Bouchard is calling an adverse response to exercise actually had more heart attacks or other bad health outcomes. But Dr. Bouchard said if people wanted to use changes in risk factors to infer that those who exercise are healthier, they could not then turn around and say there is no evidence of harm when the risk factor changes go in the wrong direction.

Still, the findings are no excuse not to exercise. For one thing, it’s still not clear why some people had adverse responses to working out. The results couldn’t be explained by how fit participants were (or later became), how strenuously they exercised, whether they were taking medications for blood pressure or cholesterol, or their age, race or gender. “I suspect the most important explanation here will be genomics,” Bouchard told the Boston Globe.

Researchers said it’s important to figure out who will benefit from exercise and who won’t, if we want to able to prescribe exercise individually for better health. “Identifying the predictors of such unwarranted responses and how to prevent them will provide the foundation for personalized exercise prescription,” they wrote.

But for healthy people, experts agree that exercise is a benefit overall. It improves mood, makes you stronger and preserves physical fitness as you age.

So, for now, the authors recommend that people continue exercising as before. If you’ve been sedentary and are starting a new exercise regimen, however, it would be a good idea to check in regularly with your physician to monitor measures of heart health.

Read more: http://healthland.time.com/2012/06/01/is-exercise-harmful-for-some-people/?iid=hl-article-mostpop1#ixzz1whrtI9EV

Is Exercise Harmful for Some People? | Healthland | TIME.com

The New York City Soda Ban, and a Brief History of Bloomberg’s Nudges

The New York City Soda Ban, and a Brief History of Bloomberg’s Nudges


Nothing like a tall, cool drink in the heat of summer, right? Not if it's a sugar-sweetened soda, and not if you're in New York City.


By Alice Park | @aliceparkny | May 31, 2012 | 7




Dorling Kindersley / Getty Images
New York City Mayor Michael Bloomberg is hoping city residents will drink a lot less this summer — less soda, that is.

On Wednesday the famously public health-focused mayor proposed a ban on the sale of large-sized sugar-sweetened beverages — that includes sodas, sweetened teas and coffees, energy drinks and fruit drinks. If approved, the proposal, which is slated to take effect as early as next March, would prohibit restaurants, delis, sports arena vendors, movie theaters and food carts regulated by the city health department from selling sugary beverages in sizes larger than 16 oz. Fines for failing to downsize could be as high as $200.

The ban would apply to food service establishments selling bottled as well as fountain drinks; retailers would have to remove 20-oz. soft drink bottles from their shelves, and delis and restaurants offering self-service fountains wouldn’t be able to give customers cups larger than 16 oz. The ban wouldn’t affect convenience stores or grocery stores and wouldn’t apply to diet drinks, fruit juices, dairy-based drinks like milkshakes or alcoholic beverages.


“Obesity is a nationwide problem, and all over the United States, public health officials are wringing their hands saying, ‘Oh, this is terrible,’” Mr. Bloomberg told the New York Times. “New York City is not about wringing your hands; it’s about doing something.”

During his tenure, Bloomberg has done a lot, initiating several controversial public-health measures, many aimed at reducing obesity by encouraging people to adopt healthier lifestyles. Critics have disparaged him as Nanny Bloomberg for it, but many of the mayor’s sweeping policies have inspired policy makers across the country to do the same. Among his recent actions:

2002: Bloomberg banned public smoking in the city’s bars and restaurants, following the lead of cities like Aspen, Colo., Beverly Hills and San Luis Obispo, Calif., which were the first to bar patrons from lighting up in restaurants and other enclosed public places

2005: At the mayor’s urging, New York became the first city to force restaurants and other food vendors to phase out the use of artificial trans fats, which have been linked to obesity and heart disease. The initiative inspired other cities, including Philadelphia and San Francisco, to pass trans-fat bans of their own. Now entire counties and states are considering regulations that would take the fats out of their food.

2008: New York became the first city to pass a law requiring food service providers to post calorie counts on menus. Seattle and other cities subsequently passed similar laws, and a federal law requiring any restaurant chain with more than 20 locations to publish calorie counts on their menus went into effect this year.
2010: In his first swipe at the soda industry, Bloomberg proposed barring people from using food stamps to purchase sugary sodas. The U.S. Department of Agriculture rejected the proposal saying it would be too difficult to enforce.
2010: Bloomberg urged state legislators to pass a soda tax that would allow the state to collect an additional penny per ounce of sugared soda sold; it failed to pass.
2011: The mayor banned smoking in most outdoor areas in the city, including public parks, plazas and beaches. San Jose, Calif., adopted a similar ban this year, and Boulder, Colo., policy makers are also considering limiting smoking outdoors.
Salt is also on the mayor’s hit list. He wants packaged food makers and restaurants to reduce sodium by 25% in an effort to lower rates of high blood pressure and heart disease.


Improving New Yorkers’ health and eating habits has been one of Bloomberg’s signature missions as mayor. The city subways are plastered with public health messages, such as the graphic anti-obesity advertisements that show a sugary soda turning into fat as it’s poured into a glass. (In March, the Centers for Disease Control and Prevention launched its own series of graphic advertisements: a national anti-smoking campaign.)

Studies are mixed on whether drastic public-health measures like Bloomberg’s can actually change behavior. Some show that people consume less in restaurants where calorie counts are available, for example, than where they aren’t, while others show that people actually tend to consume more when provided with such information. And low-income populations, which tend to have higher rates of obesity and health problems to start with, appear to be the least affected by such changes.

Still, Bloomberg and the city’s health department cite New York’s rising life expectancy as proof that the measures are working.

Beverage makers, not surprisingly, are critical of the new proposal, calling it “zealous” in a statement. “There they go again,” Stefan Friedman, spokesman for the New York City Beverage Association, told the Associated Press.

“The New York City Health Department’s unhealthy obsession with attacking  soft drinks is again pushing them over the top. The city is not going to address the obesity issue by attacking soda because soda is not driving the obesity rates.”

The Coca-Cola Company also defended its products, noting that their beverages contain calorie information. “The people of New York City are much smarter than the New York City Health Department believes,” it said in a statement. “We are transparent with our consumers. They can see exactly how many calories are in every beverage we serve…New Yorkers expect and deserve better than this. They can make their own choices about the beverages they purchase.”

Whether or not it’s responsible for the obesity epidemic, studies show that sugared beverages are a major source of extra calories that can contribute to weight gain.

The ban wouldn’t prevent a customer from ordering several small-sized sugary drinks, of course, or from helping themselves to refills at a fountain, but Bloomberg is hoping that at least at movie theaters and baseball stadiums, the inconvenience of carrying the additional cups will be enough to curb New Yorkers’ sugared drink habit.

The New York City Board of Health needs to approve the measure before it can take effect, which seems likely given the board’s support of the mayor’s previous public health efforts — and because all the members were appointed by Bloomberg. If the mayor has his way, residents and visitors to New York may soon be feeling thirsty for more.

Alice Park is a writer at TIME. Find her on Twitter at @aliceparkny. You can also continue the discussion on TIME’s Facebook page and on Twitter at @TIME.

 

Read more: http://healthland.time.com/2012/05/31/bloombergs-soda-ban-and-other-sweeping-health-measures-in-new-york-city/?iid=hl-article-mostpop1#ixzz1whfMN9JK


Source:
The New York City Soda Ban, and a Brief History of Bloomberg’s Nudges | Healthland | TIME.com

Truth About Salt

Salt, We Misjudged You

        Joon Mo Kang and Susie Choi

By GARY TAUBES

Published: June 2, 2012

Oakland, Calif.


THE first time I questioned the conventional wisdom on the nature of a healthy diet, I was in my salad days, almost 40 years ago, and the subject was salt. Researchers were claiming that salt supplementation was unnecessary after strenuous exercise, and this advice was being passed on by health reporters. All I knew was that I had played high school football in suburban Maryland, sweating profusely through double sessions in the swamplike 90-degree days of August. Without salt pills, I couldn’t make it through a two-hour practice; I couldn’t walk across the parking lot afterward without cramping.


While sports nutritionists have since come around to recommend that we should indeed replenish salt when we sweat it out in physical activity, the message that we should avoid salt at all other times remains strong. Salt consumption is said to raise blood pressure, cause hypertension and increase the risk of premature death. This is why the Department of Agriculture’s dietary guidelines still consider salt Public Enemy No. 1, coming before fats, sugars and alcohol. It’s why the director of the Centers for Disease Control and Prevention has suggested that reducing salt consumption is as critical to long-term health as quitting cigarettes.


And yet, this eat-less-salt argument has been surprisingly controversial — and difficult to defend. Not because the food industry opposes it, but because the actual evidence to support it has always been so weak.


When I spent the better part of a year researching the state of the salt science back in 1998 — already a quarter century into the eat-less-salt recommendations — journal editors and public health administrators were still remarkably candid in their assessment of how flimsy the evidence was implicating salt as the cause of hypertension.


“You can say without any shadow of a doubt,” as I was told then by Drummond Rennie, an editor for The Journal of the American Medical Association, that the authorities pushing the eat-less-salt message had “made a commitment to salt education that goes way beyond the scientific facts.”


While, back then, the evidence merely failed to demonstrate that salt was harmful, the evidence from studies published over the past two years actually suggests that restricting how much salt we eat can increase our likelihood of dying prematurely. Put simply, the possibility has been raised that if we were to eat as little salt as the U.S.D.A. and the C.D.C. recommend, we’d be harming rather than helping ourselves.


WHY have we been told that salt is so deadly? Well, the advice has always sounded reasonable. It has what nutritionists like to call “biological plausibility.” Eat more salt and your body retains water to maintain a stable concentration of sodium in your blood. This is why eating salty food tends to make us thirsty: we drink more; we retain water. The result can be a temporary increase in blood pressure, which will persist until our kidneys eliminate both salt and water.


The scientific question is whether this temporary phenomenon translates to chronic problems: if we eat too much salt for years, does it raise our blood pressure, cause hypertension, then strokes, and then kill us prematurely? It makes sense, but it’s only a hypothesis. The reason scientists do experiments is to find out if hypotheses are true.


In 1972, when the National Institutes of Health introduced the National High Blood Pressure Education Program to help prevent hypertension, no meaningful experiments had yet been done. The best evidence on the connection between salt and hypertension came from two pieces of research. One was the observation that populations that ate little salt had virtually no hypertension. But those populations didn’t eat a lot of things — sugar, for instance — and any one of those could have been the causal factor. The second was a strain of “salt-sensitive” rats that reliably developed hypertension on a high-salt diet. The catch was that “high salt” to these rats was 60 times more than what the average American consumes.


Still, the program was founded to help prevent hypertension, and prevention programs require preventive measures to recommend. Eating less salt seemed to be the only available option at the time, short of losing weight. Although researchers quietly acknowledged that the data were “inconclusive and contradictory” or “inconsistent and contradictory” — two quotes from the cardiologist Jeremiah Stamler, a leading proponent of the eat-less-salt campaign, in 1967 and 1981 — publicly, the link between salt and blood pressure was upgraded from hypothesis to fact.


In the years since, the N.I.H. has spent enormous sums of money on studies to test the hypothesis, and those studies have singularly failed to make the evidence any more conclusive. Instead, the organizations advocating salt restriction today — the U.S.D.A., the Institute of Medicine, the C.D.C. and the N.I.H. — all essentially rely on the results from a 30-day trial of salt, the 2001 DASH-Sodium study. It suggested that eating significantly less salt would modestly lower blood pressure; it said nothing about whether this would reduce hypertension, prevent heart disease or lengthen life.


While influential, that trial was just one of many. When researchers have looked at all the relevant trials and tried to make sense of them, they’ve continued to support Dr. Stamler’s “inconsistent and contradictory” assessment. Last year, two such “meta-analyses” were published by the Cochrane Collaboration, an international nonprofit organization founded to conduct unbiased reviews of medical evidence. The first of the two reviews concluded that cutting back “the amount of salt eaten reduces blood pressure, but there is insufficient evidence to confirm the predicted reductions in people dying prematurely or suffering cardiovascular disease.” The second concluded that “we do not know if low salt diets improve or worsen health outcomes.”


The idea that eating less salt can worsen health outcomes may sound bizarre, but it also has biological plausibility and is celebrating its 40th anniversary this year, too. A 1972 paper in The New England Journal of Medicine reported that the less salt people ate, the higher their levels of a substance secreted by the

kidneys, called renin, which set off a physiological cascade of events that seemed to end with an increased risk of heart disease. In this scenario: eat less salt, secrete more renin, get heart disease, die prematurely.


With nearly everyone focused on the supposed benefits of salt restriction, little research was done to look at the potential dangers. But four years ago, Italian researchers began publishing the results from a series of clinical trials, all of which reported that, among patients with heart failure, reducing salt consumption increased the risk of death.


Those trials have been followed by a slew of studies suggesting that reducing sodium to anything like what government policy refers to as a “safe upper limit” is likely to do more harm than good. These covered some 100,000 people in more than 30 countries and showed that salt consumption is remarkably stable among populations over time. In the United States, for instance, it has remained constant for the last 50 years, despite 40 years of the eat-less-salt message. The average salt intake in these populations — what could be called the normal salt intake — was one and a half teaspoons a day, almost 50 percent above what federal agencies consider a safe upper limit for healthy Americans under 50, and more than double what the policy advises for those who aren’t so young or healthy. This consistency, between populations and over time, suggests that how much salt we eat is determined by physiological demands, not diet choices.


One could still argue that all these people should reduce their salt intake to prevent hypertension, except for the fact that four of these studies — involving Type 1 diabetics, Type 2 diabetics, healthy Europeans and patients with chronic heart failure — reported that the people eating salt at the lower limit of normal were more likely to have heart disease than those eating smack in the middle of the normal range. Effectively what the 1972 paper would have predicted.


Proponents of the eat-less-salt campaign tend to deal with this contradictory evidence by implying that anyone raising it is a shill for the food industry and doesn’t care about saving lives. An N.I.H. administrator told me back in 1998 that to publicly question the science on salt was to play into the hands of the industry. “As long as there are things in the media that say the salt controversy continues,” he said, “they win.”


When several agencies, including the Department of Agriculture and the Food and Drug Administration, held a hearing last November to discuss how to go about getting Americans to eat less salt (as opposed to whether or not we should eat less salt), these proponents argued that the latest reports suggesting damage from lower-salt diets should simply be ignored. Lawrence Appel, an epidemiologist and a co-author of the DASH-Sodium trial, said “there is nothing really new.” According to the cardiologist Graham MacGregor, who has been promoting low-salt diets since the 1980s, the studies were no more than “a minor irritation that causes us a bit of aggravation.”


This attitude that studies that go against prevailing beliefs should be ignored on the basis that, well, they go against prevailing beliefs, has been the norm for the anti-salt campaign for decades. Maybe now the prevailing beliefs should be changed. The British scientist and educator Thomas Huxley, known as Darwin’s bulldog for his advocacy of evolution, may have put it best back in 1860. “My business,” he wrote, “is to teach my aspirations to conform themselves to fact, not to try and make facts harmonize with my aspirations.”







A Robert Wood Johnson Foundation Independent Investigator in Health Policy Research and the author of “Why We Get Fat.”

A version of this op-ed appeared in print on June 3, 2012, on page SR8 of the New York edition with the headline: Salt, We Misjudged You.









 

David Katz, M.D.: Soda, Supply, and Demand: Can We Share a Taste for Change?

 

There are good reasons -- both upstream and down -- why Mayor Bloomberg should want to ban the sale of enormous sodas in New York City.
The distal, downstream reasons are dire health outcomes aided and abetted by soda consumption: obesity, diabetes, and even heart disease, cancer, and stroke in children as well as adults. This toxic tide is well documented, as is the important contribution the empty calories and copious sugar of soft drinks (and related sugar-sweetened beverages that often do a better job of hiding their nature under an evocative name like "sports" drink) make to it.
The proximal, upstream reasons are that people buy enormous sodas in enormous quantities because one, they tend to think more for less is a bargain; and two, they like it!
Mayor Bloomberg presumably has concluded that these are not likely to change, and the only way to get past them and deal with those downstream consequences and their costs is to take the decision out of your hands and into his own, at least partially.
Perhaps he's right, and that's why debate is spirited on both sides of the "Should we ban big sodas?" divide. (My closest colleagues are divided on the issue.)
But I am more sanguine on removing these upstream impediments to healthful change. I think a prod to common sense, and a well-tended meme could do the job. The first of these upstream barriers is obsolete nonsense that doesn't withstand the meanest application of common sense; and the second can be fixed by nurturing our nature.

1) The notion that more -- measured in calories -- is better used to make sense. It made sense throughout the long sweep of human history during which calories were a rate-limiting commodity in the struggle to survive. It made sense even more recently when calories were still relatively scarce and hard to get, and physical activity unavoidable. It made so much sense, in fact, that we equated food/calories with security and success, and spoke of bringing home the bacon, being the breadwinner, and making dough.

It made sense THEN. But now, it makes as much sense as bringing coals to Newcastle!

Getting more of what you don't have enough of is a good thing. Getting more of what you already have too much of is anything but!

More calories and more sugar at no or little extra charge means getting fat and probably sick for free -- and winning the opportunity to spend a fortune trying to fix that! Come on folks, wake up and smell the SlimFast -- this is NOT a bargain anymore! In the modern era, nutrients per dollar -- vitality per dollar -- are far better measures of food value than volume or calories. More nutritious foods do not need to cost more, particularly when the right metrics are used -- but they are certainly WORTH more. It's past time for our culture to start acting accordingly.


2) Regarding the second, the fact that people like soda -- I'll start with the personal. I used to drink soda as a kid, being raised on a typical American diet until I was old enough to see the light and take matters into my own hands.

Since I first gave up soda (I have not had one in literally decades at this point), I have had several occasions to taste it -- whether on purpose or accidentally -- and had this basic reaction: yuck. When one doesn't drink soft drinks for some time and then goes back, they taste far more like what they are -- extremely sweet, highly processed and rather dubious concoctions -- than the treat we pretend them to be.

I don't dislike soda because soda isn't good for me. I dislike soda because I dislike soda! Once I gave my taste buds a soda-free holiday, they did the rest. They went through rehab, rediscovered their native predilection for native foods, and made it easy for me to avoid soda for the rest of my life. I don't like it. It's too sweet, too overtly "factory food."

But getting taste buds not to like something isn't enough. The rest of the job is getting them to like foods -- love foods -- that love you back. This, too, is within reach.
A large volume of research I have reviewed for several of the books I've written, 20 years of clinical practice, and personal experience convince me that taste buds are malleable little fellas: When they can't be with a food they love, they pretty readily learn to love the food they're with. And once they do, familiarity becomes a powerful reinforcing agent. We like what we know.

This can work for good, or ill. Bathe your taste buds all day long -- knowingly, or unknowingly -- in copious additions of sugar and salt, and you will come to prefer more and more of these. Dial down your exposures, and you can reverse-engineer this process, rehabilitate your taste buds, and come to love food far more likely to love you back.

Most of the evidence I've encountered -- both published and personal -- suggests that habituation to new and improved versions of foods and recipes happens in as little as two weeks, or even less. A good example is a transition from whole milk to skim milk.

If you like whole milk and try skim, it tastes a bit like dishwater at first. If you stick with skim milk for a few days, it becomes hard to remember what the problem was. Hang in there for a week or two, and you will register the taste and texture of skim milk as just... milk. Retry whole milk at this point, and it will make you think of wallpaper paste.

The same basic principle applies to all foods. And there is enormous opportunity to trade up choices within food categories, and derive stunning health benefits -- acclimation, but no real heavy lifting, required.

So here's the thing: If it takes only about two weeks to adjust to new and better foods, then what stands between us and the dietary promised land where we can all as a matter of routine love foods that love us back, is a hill only two weeks high. For far too long, we have been making a mountain out of this molehill!

But to climb it requires the coordinated efforts of the supply side, and the demand side.

For their part, food suppliers like to contend they are only feeding us what we want, just trying to keep the customer satisfied. But the reality is that they helped create the prevailing palate, and are now profiting mightily from feeding it. They share in the responsibility of rehabilitating it by providing reformulated products that are genuinely better for our health -- not products that merely pretend to be.

But the industry is right to note they can't sell what we won't buy! And the precautionary tales they cite -- the fate of McLean Deluxe or Alphabits cereal (nutritionally improved, only to fail commercially) -- are valid. If we want truly better food choices, we have to choose them when they become available!

So to change demand, we have to change supply; and to change supply, we have to change demand. This has "impasse" written all over it, and it's why we have been stuck on this side of the molehill for so long.

But I believe we can get over it. Imagine a program in which the "taste for change" is shared by both demand and supply. We might, for instance, develop a public service campaign to raise awareness in the population about the adaptability of taste buds, about that two-week-high hill of taste habituation, and about the need to give new and better-for-you products a trial period of a couple of weeks before reaching a verdict.

This campaign could, in theory, be timed to anticipate a whole new crop of better-for-you products released by major food companies -- just like movie trailers are released to build the buzz for a new movie. If you've seen a trailer and think you are going to love a movie, you don't walk out if the first few minutes happen to be slow going. You have expectations, and you give them a chance. By the end, you may well wind up loving the film. Could we perhaps cultivate the same "give it a reasonable chance" attitude about new and better-for-us foods?

Ideally, these products would be subjected to an objective measure of nutritional quality in the R&D phase so we could all be confident they are TRULY better for us, and not merely depend on the company saying so.

If we prime the public reception for such products, perhaps we would see robust sales when they are introduced. If people know to hang in there for a couple of weeks, they could adjust to the new formulations and actually learn to prefer them.

And if better-for-you products come to be preferred, it would encourage food companies to produce more of them -- and less of the alternative. Of course we are naturally, genetically adapted to like sweet -- along with salt, fat, calories, and variety. Predilections for all of these favored survival during the long sweep of human history before the advent of agriculture, and for some time afterward.

Human babies are born with a preference for sweet, and it's a good thing. They might otherwise turn up their tiny noses at the first, critical, life-sustaining substance: mother's milk, sweetened with lactose.

And that preference for sweet is preserved into adulthood -- because it leads away from poisons, which tend to be bitter, and toward the quickly available energy in honey and wild fruits. Our Stone Age ancestors who didn't like sweet might forego such sustenance, making them less likely to survive and reproduce. And let's face it: People who don't survive to reproduce make very poor ancestors!

But this is just our nature -- it ignores the power of nurture! Richard Dawkins, arguably the most influential evolutionary biologist since Darwin, argues brilliantly at the close of his seminal book The Selfish Gene that unthinking genes got us here -- but they do not control our destiny! Units of cultural transmission -- units of choice -- called memes can carry the day.

We can make health a prevailing cultural meme by replacing our unconscious adaptations with conscious choices. It's true, we are adapted to like sweet. But we are also adapted to be terrestrial -- yet can learn to swim, and to hold our breath under water. We are adapted to ambulate -- but can learn to ride a bike. Both require skills we can, by choice, obtain.

We can choose what we chew -- and swallow -- as well! We can replace the thoughtlessness of genes with the thoughtfulness of memes. We can make health a meme. But only by choice!

The current impasse -- junky foods feeding junk-loving palates -- was engineered, and can be reverse-engineered. The hill is not all that high, and the prize on the other side is truly great.

We can get there from here, but only if we acknowledge the interdependence of supply and demand, and share a taste for change.



-fin




Dr. David L. Katz; www.davidkatzmd.com
www.turnthetidefoundation.org

Find Dr. David Katz on Facebook.
Follow Dr. David Katz on Twitter.
For more on David Katz, M.D., click here.
For more on diet and nutrition, click here.

 


 Source:
David Katz, M.D.: Soda, Supply, and Demand: Can We Share a Taste for Change?

Mark Hyman, MD: The Last Diet You Will Ever Need

Why is it that we believe we can feed our bodies industrial, nutrient-depleted food-like substances empty of life and be healthy? How did we come to believe that food industry chemicals and processing could replace nature-made foods?

A hundred years ago all food was organic, local, seasonal, fresh or naturally-preserved by ancient methods. All food was food. Now less than 3 percent of our agricultural land is used to grow fruits and vegetables, which should make up 80 percent of our diet. Today there are not even enough fruits and vegetables in this country to allow all Americans to follow the government guidelines to eat five to nine servings a day.

What most of us are left with is industrial food. And who knows what lurks in the average boxed, packaged, or canned factory-made science project.

When a French fry has more than 20 ingredients and almost all of them are not potato, or when a fast food hamburger contains very little meat, or when the average teenager consumes 34 teaspoons of sugar a day, we are living in a food nightmare, a sci-fi horror show.

The very fact that we are having a national conversation about what we should eat, that we are struggling with the question about what the best diet is, is symptomatic of how far we have strayed from the natural conditions that gave rise to our species, from the simple act of eating real, whole, fresh food. When it becomes a revolutionary act to eat real food, we are in trouble.

The food industry, which is the second biggest employer in America after the federal government, heavily influences the media and government agencies that regulate it (U.S. Department of Agriculture, Food and Drug Administration and Congress) and intentionally confuses and confounds us.

Low-fat is good -- so anything with a "low-fat" on the label must be healthy. But Coke is 100 percent fat-free and that doesn't make it a health food. Now we are told to eat more whole grains, so a few flecks of whole grains are sprinkled on sugary cereals. That doesn't make them a health food either.

The best advice is to avoid foods with health claims on the label, or better yet avoid foods with labels in the first place.

In the 21st century our tastes buds, our brain chemistry, our biochemistry, our hormones and our kitchens have been hijacked by the food industry. The food-like substances proffered by the industrial food system food trick our taste buds into momentary pleasure, but not our biology, which reacts, rejects and reviles the junk plied on our genes and our hormonal and biochemical pathways. We need to unjunk our biology.

Industrial processing has given rise to an array of addictive, fattening, metabolism-jamming chemicals and compounds including aspartame, MSG (monosodium glutamate), high-fructose corn syrup and trans fats, to name the biggest offenders.

MSG is used to create fat mice so researchers can study obesity. MSG is an excito-toxin that stimulates your brain to eat uncontrollably. When fed to mice, they pig out and get fat. It is in 80 percent of processed foods and mostly disguised as "natural flavorings."

And trans fat, for example, is derived from a real food -- vegetable oil -- chemically altered to resist degradation by bacteria, which is why modern cookies last on the shelf for years.

But the ancient energy system of your cells is descended from bacteria and those energy factories, or mitochondria, cannot process these trans fats either. Your metabolism is blocked and weight gain and Type 2 diabetes ensue.

Your tongue can be fooled and your brain can become addicted to the slick combinations of fat, sugar, and salt pumped into factory-made foods, but your biochemistry cannot, and the result is the disaster of obesity and chronic disease we have in America today.

No wonder 68 percent of Americans are overweight. No wonder that from 1960 to today obesity rates have risen from 13 percent to 36 percent and soon will reach 42 percent. Over the last decade the rate of pre-diabetes or diabetes in teenagers has risen from 9 percent to 23 percent.

Really? Almost one in four of our kids now has pre-diabetes or Type 2 diabetes? And 37 percent of normal weight kids have one or more cardiovascular risk factors, such as high blood pressure, high cholesterol or high blood sugar, because even though factory food doesn't make them fat, it makes them sick!

It is time to take our kitchens and our homes back. Transforming the food industry seems monumental, a gigantic undertaking. But it is not. It is a small problem. In the small places in our lives, our shopping carts, the fridge, the cupboard, the kitchen and on our dining room table is where all the power is.

It is the hundreds of little choices, the small actions you make every day, that will topple the monolithic food industry. This century is littered with the bodies and institutions of fallen despots and despotic regimes -- from the fall of the Berlin wall to the Arab spring. There is no force more powerful than a small group of individuals with a desire to end injustice and abuse.

A very simple idea can break through the confusion and plant the seeds of a revolution. Our bodies were designed to run on real food. Our natural default state is health. We need to simplify our way of eating.

Unjunk our diet, detoxify our bodies and our minds and we heal. Simply choose foods such as vegetables, fruits, nuts, seeds, healthy oils (olive oil, fish oil, avocado and coconut oil), small amounts of whole grains and beans and lean animal protein including small wild fish, grass fed meat, and farm eggs.

There are no diets, no calorie counting, and no measuring fats, carbs or protein grams. None of that matters if you choose real, whole, fresh, live foods. If you choose quality, the rest takes care of itself.

When you eat empty industrial food with addictive chemicals and sugar, your body craves more, looking for nutrients in a dead food where none are to be found. Yet after eating nutrient dense fresh food for a few days the biological addiction to industrial food is broken, and in a few more days your cells begin to rejuvenate and you heal from the inside out.

And the side effects are all good ones: effortless weight loss, reversal of high blood pressure, diabetes, high cholesterol, clearing of brain fog, lifting of depression and fatigue and even better skin, hair and nails.

What is more important than what you take out of your diet is what you put in. Add in the good stuff and there won't be room for the bad. Mother Nature is the best pharmacist and food is the most powerful drug on the planet. It works faster, better and cheaper than any other pharmaceutical.

Whole, real food spiced up with a few super foods such as chia, hemp, parsley, cilantro, coconut and green juicing can beneficially affect thousands of genes, regulate dozens of hormones, and enhance the function of tens of thousands of protein networks.

Dinner is a date with the doctor. What you put at the end of your fork is more powerful than anything you will ever find at the bottom of a prescription bottle. The roadmap to health is simple: eat real food, practice self-love rather than self-loathing, imagine yourself well, get sufficient sleep, and incorporate movement into your life. The solution to our health crisis and obesity epidemic is not complicated.

Health and happiness are often just a few days away. Each of us has the capacity to make the small changes in our lives that will create big changes in our food landscape, our agriculture and even our government policies.

I hope you will use the power of your fork to be part of the start of a true food revolution.

Now I'd like to hear from you...

Have you changed your eating habits to include more real food?

What have you done to create a healthier diet for your family?

Have you eliminated MSG from your diet?





Mark Hyman, M.D.



Mark Hyman, M.D. is a practicing physician, founder of The UltraWellness Center, a four-time New York Times bestselling author, and an international leader in the field of Functional Medicine. You can follow him on Twitter, connect with him on LinkedIn, watch his videos on YouTube, become a fan on Facebook, and subscribe to his newsletter.
For more by Mark Hyman, M.D., click here.


 Source:
 Mark Hyman, MD: The Last Diet You Will Ever Need

China researchers link obesity to bacteria

 

December 19th, 2012 in Overweight and Obesity

Chinese researchers have identified a bacteria which may cause obesity, according to a new paper suggesting diets that alter the presence of microbes in humans could combat the condition.

Researchers in Shanghai found that mice bred to be resistant to obesity even when fed high-fat foods became excessively overweight when injected with a kind of human bacteria and subjected to a rich diet.

The bacterium—known as enterobacter—had been linked with obesity after being found in high quantities in the gut of a morbidly obese human volunteer, said the report, written by researchers at Shanghai's Jiaotong University.

The mice were injected with the bacterium for up to 10 weeks as part of the experiment.

The experiments show that the bacterium "may causatively contribute to the development of obesity" in humans, according to the paper published in the peer-reviewed journal of the International Society for Microbial Ecology (ISMEJ).

A human patient lost over 30 kilograms in nine weeks after being placed on a diet of "whole grains, traditional Chinese medicinal foods and prebiotics", which reduced the bacterium's presence in the patient's gut to "undetectable" levels, the paper said.


One of the report's authors, Zhao Liping, lost 20 kilograms in two years after adopting a diet of fermented probiotic foods such as bitter melon to adjust the balance of bacteria in his gut, the American magazine Science said in an article this year on his previous research.

Zhao's work on the role of bacteria in obesity is inspired by traditional Chinese beliefs that the gut is the "foundation for human health", Science reported.

The scientists wrote in their latest paper that they "hope to identify more such obesity-inducing bacteria from various human populations" in future research.

Obesity worldwide has more than doubled since 1980,
 according to the World Health Organisation, with 
more than 500 million adults worldwide suffering from the condition according to 2008 statistics.



(c) 2012 AFP
"China researchers link obesity to bacteria." December 19th, 2012.


Source:
http://medicalxpress.com/news/2012-12-china-link-obesity-bacteria.html

China researchers link obesity to bacteria

....................................................................

*Remember ulcers were discovered to be caused by bacteria after years of other things, like stress, were blamed for causing the condition.

Grapefruit and Drugs Often Don't Mix - NYTimes.com

This is somewhat shocking information but you may see one of your medications on the list.  It is very informative to go to the list and compare the drugs you take currently with the list to protect yourself from harm.

List:  http://www.cmaj.ca/content/suppl/2012/11/26/cmaj.120951.DC1/grape-bailey-1-at.pdf

 

John Cohoe

The Consumer

Advice on money and health.

The patient didn’t overdose on medication.  She overdosed on grapefruit juice.

The 42-year-old was barely responding when her husband brought her to the emergency room. Her heart rate was slowing, and her blood pressure was falling.

Doctors had to insert a breathing tube, and then a pacemaker, to revive her.

They were mystified: The patient’s husband said she suffered from migraines and was taking a blood pressure drug called verapamil to help prevent the headaches. But blood tests showed she had an alarming amount of the drug in her system, five times the safe level.

Did she overdose? Was she trying to commit suicide? It was only after she recovered that doctors were able to piece the story together.

“The culprit was grapefruit juice,” said Dr. Unni Pillai, a nephrologist in St. Louis, Mo., who treated the woman several years ago and later published a case report.

“She loved grapefruit juice, and she had such a bad migraine, with nausea and vomiting, that she could not tolerate anything else.”

The previous week, she had been subsisting mainly on grapefruit juice. Then she took verapamil, one of dozens of drugs whose potency is dramatically increased if taken with grapefruit. In her case, the interaction was life-threatening.

Last month, Dr. David Bailey, a Canadian researcher who first described this interaction more than two decades ago, released an updated list of medications affected by grapefruit. There are now 85 such drugs on the market, he noted, including common cholesterol-lowering drugs, new anticancer agents, and some synthetic opiates and psychiatric drugs, as well as certain immunosuppressant medications taken by organ transplant patients, some AIDS medications, and some birth control pills and estrogen treatments. (The full list is online; your browser must be configured to handle PDF files.)

“What drove us to write this paper was the number of new drugs that have come out in the last four years,” said Dr. Bailey, a clinical pharmacologist at the Lawson Health Research Institute, who first discovered the interaction by accident in the 1990s.

How often such reactions occur, however, and how often they are triggered in people consuming regular amounts of juice is debated by scientists. Dr. Bailey believes many cases are missed because doctors don’t think to ask if patients are consuming grapefruit or grapefruit juice.

Even if such incidents are rare, Dr. Bailey argued, they are predictable and entirely avoidable. Many hospitals no longer serve juice, and some prescriptions carry stickers warning patients to avoid grapefruit.

“The bottom line is that even if the frequency is low, the consequences can be dire,” he said. “Why do we have to have a body count before we make changes?”

For 43 of the 85 drugs now on the list, consumption with grapefruit can be life-threatening, Dr. Bailey said. Many are linked to an increase in heart rhythm, known as torsade de pointes, that can lead to death. It can occur even without underlying heart disease and has been seen in patients taking certain anticancer agents, erythromycin and other anti-infective drugs, some cardiovascular drugs like quinidine, the antipsychotics lurasidone and ziprasidone, gastrointestinal agents cisapride and domperidone, and solifenacin, used to treat overactive bladders.

Taken with grapefruit, other drugs like fentanyl, oxycodone and methadone can cause fatal respiratory depression. The interaction also can be caused by other citrus fruits, including Seville oranges, limes and pomelos; one published case report has suggested that pomegranate may increase the potency of certain drugs.

Older people may be more vulnerable, because they are more likely to be both taking medications and drinking more grapefruit juice. The body’s ability to cope with drugs also weakens with age, experts say.

Under normal circumstances, the drugs are metabolized in the gastrointestinal tract, and relatively little is absorbed, because an enzyme in the gut called CYP3A4 deactivates them. But grapefruit contains natural chemicals called furanocoumarins, that inhibit the enzyme, and without it the gut absorbs much more of a drug and blood levels rise dramatically.

For example, someone taking simvastatin (brand name Zocor) who also drinks a small 200-milliliter, or 6.7 ounces, glass of grapefruit juice once a day for three days could see blood levels of the drug triple, increasing the risk for rhabdomyolysis, a breakdown of muscle that can cause kidney damage.

Estradiol and ethinyl estradiol, forms of estrogen used in oral contraceptives and hormone replacement, also interact with grapefruit juice. In one case in the journal Lancet, a 42-year-old woman taking the birth control pill Yaz developed a very serious clot that threatened her leg several days after she started eating just one grapefruit a day, said Dr. Lucinda Grande, a physician in Lacey, Wash., and an author of the case report.

But Dr. Grande also noted that the patient had other risk factors and the circumstances were unusual. “The reason we published it as a case report was because it was so uncommon,” she said. “We need to be careful not to exaggerate this.”

Some drugs that have a narrow “therapeutic range” — where having a bit too much or too little can have serious consequences — require vigilance with regard to grapefruit, said Patrick McDonnell, clinical professor of pharmacy practice at Temple University. These include immunosuppressant agents like cyclosporine that are taken by transplant patients to prevent rejection of a donor organ, he said.

Still, Dr. McDonnell added, most patients suffering adverse reactions are consuming large amounts of grapefruit. “There’s a difference between an occasional section of grapefruit and someone drinking 16 ounces of grapefruit juice a day,” he said.

And, he cautioned, “Not all drugs in the same class respond the same way.” While some statins are affected by grapefruit, for instance, others are not.

Here is some advice from experts for grapefruit lovers:

¶ If you take oral medication of any kind, check the list to see if it interacts with grapefruit. Make sure you understand the potential side effects of an interaction; if they are life-threatening or could cause permanent injury, avoid grapefruit altogether. Some drugs, such as clopidogrel, may be less effective when taken with grapefruit.

¶ If you take one of the listed drugs a regular basis, keep in mind that you may want to avoid grapefruit, as well as pomelo, lime and marmalade. Be on the lookout for symptoms that could be side effects of the drug. If you are on statins, this could be unusual muscle soreness.

¶It is not enough to avoid taking your medicine at the same time as grapefruit. You must avoid consuming grapefruit the whole period that you are on the medication.

¶In general, it is a good idea to avoid sudden dramatic changes in diet and extreme diets that rely on a narrow group of foods. If you can’t live without grapefruit, ask your doctor if there’s an alternative drug for you.

 

Readers may submit comments or questions for The Consumer by e-mail to consumer@nytimes.com.

A version of this article appeared in print on 12/18/2012, on page D6 of the NewYork edition with the headline: Grapefruit Is a Culprit In More Drug Reactions.

Grapefruit and Drugs Often Don't Mix - NYTimes.com

http://well.blogs.nytimes.com/2012/12/17/grapefruit-is-a-culprit-in-more-drug-reactions/

Synthetic Pot Sends Thousands to Hospital | Sci-Tech Today

Not only is getting sick from the stuff a problem...


Synthetic Pot Sends Thousands to Hospital
By Donna Leinwand Leger

December 8, 2012 8:52AM





The Drug Abuse Warning Network says drugs like Spice and K2, marketed as legal, fake pot and labeled as herbal incense, are sending teenagers and young adults to emergency rooms around the country. In 59% of the cases, doctors found no other substance, differing from most emergency department visits involving illicit drugs.



K2, Spice and other synthetic drugs that mimic a marijuana high sent 11,406 people -- mostly teenagers and young adults -- to the emergency room in 2010, according to the first report on the substances from the federal government's Drug Abuse Warning Network.

The report, the first to analyze the impact of the popular herbal incense, found that children ages 12 to 17 accounted for a third of the emergency room visits. Young adults ages 18 to 24 accounted for an additional 35%.

In 59% of the cases involving patients ages 12 to 29, doctors found no other substance, differing from most emergency department visits involving illicit drugs and painkiller abuse.

Marijuana, the most popular illicit drug with 18 million regular users, sent 461,028 people to the emergency room in 2010.

"This report confirms that synthetic drugs cause substantial damage to public health and safety," Office of National Drug Control Policy Director Gil Kerlikowske said.

Spice and K2, marketed as legal, fake pot and labeled as herbal incense, emerged in 2009 as popular drugs among teens and college students, who could buy the substances online and in convenience stores.

Problems quickly emerged. Doctors reported teenagers arriving in the emergency room with high fevers and strange behavior.

Police in Nebraska in 2010 arrested a teenage boy who had smoked Wicked X, herbal incense coated with synthetic cannabinoids. The teen careened his truck into the side of a house and then continued driving.

At least 18 states outlawed the substances and the Drug Enforcement Administration instituted an emergency ban. In July, Congress banned sales of K2, Spice and other synthetic drugs under the Food and Drug Administration Safety and Innovation Act.





© 2012 USA TODAY under contract with YellowBrix. All rights reserved.














Synthetic Pot Sends Thousands to Hospital | Sci-Tech Today

LINK: 

ALCOHOL'S DAMAGING EFFECTS ON THE BRAIN

Number 63                          October 2004

ALCOHOL’S DAMAGING EFFECTS ON THE BRAIN

Difficulty walking, blurred vision, slurred speech, slowed reaction times, impaired memory: Clearly, alcohol affects the brain. Some of these impairments are detectable after only one or two drinks and quickly resolve when drinking stops. On the other hand, a person who drinks heavily over a long period of time may have brain deficits that persist well after he or she achieves sobriety. Exactly how alcohol affects the brain and the likelihood of reversing the impact of heavy drinking on the brain remain hot topics in alcohol research today.
We do know that heavy drinking may have extensive and far–reaching effects on the brain, ranging from simple “slips” in memory to permanent and debilitating conditions that require lifetime custodial care. And even moderate drinking leads to short–term impairment, as shown by extensive research on the impact of drinking on driving.
A number of factors influence how and to what extent alcohol affects the brain (1), including

• how much and how often a person drinks;
• the age at which he or she first began drinking, and how long he or she has been drinking;
• the person’s age, level of education, gender, genetic background, and family history
• of alcoholism;
• whether he or she is at risk as a result of prenatal alcohol exposure; and
• his or her general health status.

This Alcohol Alert reviews some common disorders associated with alcohol–related brain damage and the people at greatest risk for impairment. It looks at traditional as well as emerging therapies for the treatment and prevention of alcohol–related disorders and includes a brief look at the high–tech tools that are helping scientists to better understand the effects of alcohol on the brain.

BLACKOUTS AND MEMORY LAPSES

Alcohol can produce detectable impairments in memory after only a few drinks and, as the amount of alcohol increases, so does the degree of impairment. Large quantities of alcohol, especially when consumed quickly and on an empty stomach, can produce a blackout, or an interval of time for which the intoxicated person cannot recall key details of events, or even entire events.
Blackouts are much more common among social drinkers than previously assumed and should be viewed as a potential consequence of acute intoxication regardless of age or whether the drinker is clinically dependent on alcohol (2). White and colleagues (3) surveyed 772 college undergraduates about their experiences with blackouts and asked, “Have you ever awoken after a night of drinking not able to remember things that you did or places that you went?” Of the students who had ever consumed alcohol, 51 percent reported blacking out at some point in their lives, and 40 percent reported experiencing a blackout in the year before the survey. Of those who reported drinking in the 2 weeks before the survey, 9.4 percent said they blacked out during that time. The students reported learning later that they had participated in a wide range of potentially dangerous events they could not remember, including vandalism, unprotected sex, and driving.

Binge Drinking and Blackouts

• Drinkers who experience blackouts typically drink too much and too quickly, which causes their blood alcohol levels to rise very rapidly. College students may be at particular risk for experiencing a blackout, as an alarming number of college students engage in binge drinking. Binge drinking, for a typical adult, is defined as consuming five or more drinks in about 2 hours for men, or four or more drinks for women.

Equal numbers of men and women reported experiencing blackouts, despite the fact that the men drank significantly more often and more heavily than the women. This outcome suggests that regardless of the amount of alcohol consumption, females—a group infrequently studied in the literature on blackouts—are at greater risk than males for experiencing blackouts. A woman’s tendency to black out more easily probably results from differences in how men and women metabolize alcohol. Females also may be more susceptible than males to milder forms of alcohol–induced memory impairments, even when men and women consume comparable amounts of alcohol (4).

ARE WOMEN MORE VULNERABLE

TO ALCOHOL’S EFFECTS ON THE BRAIN?

Women are more vulnerable than men to many of the medical consequences of alcohol use. For example, alcoholic women develop cirrhosis (5), alcohol–induced damage of the heart muscle (i.e., cardiomyopathy) (6), and nerve damage (i.e., peripheral neuropathy) (7) after fewer years of heavy drinking than do alcoholic men. Studies comparing men and women’s sensitivity to alcohol–induced brain damage, however, have not been as conclusive.
Using imaging with computerized tomography, two studies (8,9) compared brain shrinkage, a common indicator of brain damage, in alcoholic men and women and reported that male and female alcoholics both showed significantly greater brain shrinkage than control subjects. Studies also showed that both men and women have similar learning and memory problems as a result of heavy drinking (10). The difference is that alcoholic women reported that they had been drinking excessively for only about half as long as the alcoholic men in these studies. This indicates that women’s brains, like their other organs, are more vulnerable to alcohol–induced damage than men’s (11).
Yet other studies have not shown such definitive findings. In fact, two reports appearing side by side in the American Journal of Psychiatry contradicted each other on the question of gender–related vulnerability to brain shrinkage in alcoholism (12,13). Clearly, more research is needed on this topic, especially because alcoholic women have received less research attention than alcoholic men despite good evidence that women may be particularly vulnerable to alcohol’s effects on many key organ systems.

BRAIN DAMAGE FROM OTHER CAUSES

People who have been drinking large amounts of alcohol for long periods of time run the risk of developing serious and persistent changes in the brain. Damage may be a result of the direct effects of alcohol on the brain or may result indirectly, from a poor general health status or from severe liver disease.
For example, thiamine deficiency is a common occurrence in people with alcoholism and results from poor overall nutrition. Thiamine, also known as vitamin B1, is an essential nutrient required by all tissues, including the brain. Thiamine is found in foods such as meat and poultry; whole grain cereals; nuts; and dried beans, peas, and soybeans. Many foods in the United States commonly are fortified with thiamine, including breads and cereals. As a result, most people consume sufficient amounts of thiamine in their diets. The typical intake for most Americans is 2 mg/day; the Recommended Daily Allowance is 1.2 mg/day for men and 1.1 mg/day for women (14).

Wernicke–Korsakoff Syndrome

Up to 80 percent of alcoholics, however, have a deficiency in thiamine (15), and some of these people will go on to develop serious brain disorders such as Wernicke–Korsakoff syndrome (WKS) (16). WKS is a disease that consists of two separate syndromes, a short–lived and severe condition called Wernicke’s encephalopathy and a long–lasting and debilitating condition known as Korsakoff’s psychosis.
The symptoms of Wernicke’s encephalopathy include mental confusion, paralysis of the nerves that move the eyes (i.e., oculomotor disturbances), and difficulty with muscle coordination. For example, patients with Wernicke’s encephalopathy may be too confused to find their way out of a room or may not even be able to walk. Many Wernicke’s encephalopathy patients, however, do not exhibit all three of these signs and symptoms, and clinicians working with alcoholics must be aware that this disorder may be present even if the patient shows only one or two of them. In fact, studies performed after death indicate that many cases of thiamine deficiency–related encephalopathy may not be diagnosed in life because not all the “classic” signs and symptoms were present or recognized.

Human Brain

Schematic drawing of the human brain, showing regions vulnerable to alcoholism-related abnormalities.

Approximately 80 to 90 percent of alcoholics with Wernicke’s encephalopathy also develop Korsakoff’s psychosis, a chronic and debilitating syndrome characterized by persistent learning and memory problems. Patients with Korsakoff’s psychosis are forgetful and quickly frustrated and have difficulty with walking and coordination (17). Although these patients have problems remembering old information (i.e., retrograde amnesia), it is their difficulty in “laying down” new information (i.e., anterograde amnesia) that is the most striking. For example, these patients can discuss in detail an event in their lives, but an hour later might not remember ever having the conversation.
Treatment

The cerebellum, an area of the brain responsible for coordinating movement and perhaps even some forms of learning, appears to be particularly sensitive to the effects of thiamine deficiency and is the region most frequently damaged in association with chronic alcohol consumption. Administering thiamine helps to improve brain function, especially in patients in the early stages of WKS. When damage to the brain is more severe, the course of care shifts from treatment to providing support to the patient and his or her family (18). Custodial care may be necessary for the 25 percent of patients who have permanent brain damage and significant loss of cognitive skills (19).
Scientists believe that a genetic variation could be one explanation for why only some alcoholics with thiamine deficiency go on to develop severe conditions such as WKS, but additional studies are necessary to clarify how genetic variants might cause some people to be more vulnerable to WKS than others.

LIVER DISEASE

Most people realize that heavy, long–term drinking can damage the liver, the organ chiefly responsible for breaking down alcohol into harmless byproducts and clearing it from the body. But people may not be aware that prolonged liver dysfunction, such as liver cirrhosis resulting from excessive alcohol consumption, can harm the brain, leading to a serious and potentially fatal brain disorder known as hepatic encephalopathy (20).
Hepatic encephalopathy can cause changes in sleep patterns, mood, and personality; psychiatric conditions such as anxiety and depression; severe cognitive effects such as shortened attention span; and problems with coordination such as a flapping or shaking of the hands (called asterixis). In the most serious cases, patients may slip into a coma (i.e., hepatic coma), which can be fatal.
New imaging techniques have enabled researchers to study specific brain regions in patients with alcoholic liver disease, giving them a better understanding of how hepatic encephalopathy develops. These studies have confirmed that at least two toxic substances, ammonia and manganese, have a role in the development of hepatic encephalopathy. Alcohol–damaged liver cells allow excess amounts of these harmful byproducts to enter the brain, thus harming brain cells.
Treatment

Physicians typically use the following strategies to prevent or treat the development of hepatic encephalopathy.

• Treatment that lowers blood ammonia concentrations, such as administering L–ornithine L–aspartate.
• Techniques such as liver–assist devices, or “artificial livers,” that clear the patients’ blood of harmful toxins. In initial studies, patients using these devices showed lower amounts of ammonia circulating in their blood, and their encephalopathy became less severe (21).
• Liver transplantation, an approach that is widely used in alcoholic cirrhotic patients with severe (i.e., end–stage) chronic liver failure. In general, implantation of a new liver results in significant improvements in cognitive function in these patients (22) and lowers their levels of ammonia and manganese (23).

ALCOHOL AND THE DEVELOPING BRAIN

Drinking during pregnancy can lead to a range of physical, learning, and behavioral effects in the developing brain, the most serious of which is a collection of symptoms known as fetal alcohol syndrome (FAS). Children with FAS may have distinct facial features (see illustration). FAS infants also are markedly smaller than average. Their brains may have less volume (i.e., microencephaly). And they may have fewer numbers of brain cells (i.e., neurons) or fewer neurons that are able to function correctly, leading to long–term problems in learning and behavior.

Fetal Alcohol Syndrome

Children with fetal alcohol syndrome (FAS) may have distinct facial features.

Treatment

Scientists are investigating the use of complex motor training and medications to prevent or reverse the alcohol–related brain damage found in people prenatally exposed to alcohol (24). In a study using rats, Klintsova and colleagues (25) used an obstacle course to teach complex motor skills, and this skills training led to a re–organization in the adult rats’ brains (i.e., cerebellum), enabling them to overcome the effects of the prenatal alcohol exposure. These findings have important therapeutic implications, suggesting that complex rehabilitative motor training can improve motor performance of children, or even adults, with FAS.
Scientists also are looking at the possibility of developing medications that can help alleviate or prevent brain damage, such as that associated with FAS. Studies using animals have yielded encouraging results for treatments using antioxidant therapy and vitamin E. Other preventive therapies showing promise in animal studies include 1–octanol, which ironically is an alcohol itself. Treatment with l–octanol significantly reduced the severity of alcohol’s effects on developing mouse embryos (26). Two molecules associated with normal development (i.e., NAP and SAL) have been found to protect nerve cells against a variety of toxins in much the same way that octanol does (27). And a compound (MK–801) that blocks a key brain chemical associated with alcohol withdrawal (i.e., glutamate) also is being studied. MK–801 reversed a specific learning impairment that resulted from early postnatal alcohol exposure (28).

Though these compounds were effective in animals, the positive results cited here may or may not translate to humans. Not drinking during pregnancy is the best form of prevention; FAS remains the leading preventable birth defect in the United States today.

GROWING NEW BRAIN CELLS

For decades scientists believed that the number of nerve cells in the adult brain was fixed early in life. If brain damage occurred, then, the best way to treat it was by strengthening the existing neurons, as new ones could not be added. In the 1960s, however, researchers found that new neurons are indeed generated in adulthood—a process called neurogenesis (29). These new cells originate from stem cells, which are cells that can divide indefinitely, renew themselves, and give rise to a variety of cell types. The discovery of brain stem cells and adult neurogenesis provides a new way of approaching the problem of alcohol–related changes in the brain and may lead to a clearer understanding of how best to treat and cure alcoholism (30).
For example, studies with animals show that high doses of alcohol lead to a disruption in the growth of new brain cells; scientists believe it may be this lack of new growth that results in the long–term deficits found in key areas of the brain (such as hippocampal structure and function) (31,32). Understanding how alcohol interacts with brain stem cells and what happens to these cells in alcoholics is the first step in establishing whether the use of stem cell therapies is an option for treatment (33).

SUMMARY

Alcoholics are not all alike. They experience different degrees of impairment, and the disease has different origins for different people. Consequently, researchers have not found conclusive evidence that any one variable is solely responsible for the brain deficits found in alcoholics. Characterizing what makes some alcoholics vulnerable to brain damage whereas others are not remains the subject of active research (34).
The good news is that most alcoholics with cognitive impairment show at least some improvement in brain structure and functioning within a year of abstinence, though some people take much longer (35–37). Clinicians must consider a variety of treatment methods to help people stop drinking and to recover from alcohol–related brain impairments, and tailor these treatments to the individual patient.
Advanced technology will have an important role in developing these therapies. Clinicians can use brain–imaging techniques to monitor the course and success of treatment, because imaging can reveal structural, functional, and biochemical changes in living patients over time. Promising new medications also are in the early stages of development, as researchers strive to design therapies that can help prevent alcohol’s harmful effects and promote the growth of new brain cells to take the place of those that have been damaged by alcohol.

SIDEBAR Using High–Tech Tools to Assess Alcoholic Brain Damage Researchers studying the effects of alcohol use on the brain are aided by advanced technology such as magnetic resonance imaging (MRI), diffusion tensor imaging (DTI), positron emission tomography (PET), and electrophysiological brain mapping. These tools are providing valuable insight into how alcohol affects the brain’s structure and function. Long–term heavy drinking may lead to shrinking of the brain and deficiencies in the fibers (white matter) that carry information between brain cells (gray matter). MRI and DTI are being used together to assess the brains of patients when they first stop chronic heavy drinking and again after long periods of sobriety, to monitor for possible relapse to drinking (38). Memory formation and retrieval are highly influenced by factors such as attention and motivation (39). Studies using MRI are helping scientists to determine how memory and attention improve with long-time abstinence from alcohol, as well as what changes take place when a patient begins drinking again. The goal of these studies is to determine which alcohol–induced effects on the brain are permanent and which ones can be reversed with abstinence. PET imaging is allowing researchers to visualize, in the living brain, the damage that results from heavy alcohol consumption (40). This “snapshot” of the brain’s function enables scientists to analyze alcohol’s effects on various nerve cell communication systems (i.e., neurotransmitter systems) as well as on brain cell metabolism and blood flow within the brain. These studies have detected deficits in alcoholics, particularly in the frontal lobes, which are responsible for numerous functions associated with learning and memory, as well as in the cerebellum, which controls movement and coordination. PET also is a promising tool for monitoring the effects of alcoholism treatment and abstinence on damaged portions of the brain and may help in developing new medications to correct the chemical deficits found in the brains of people with alcohol dependence. Another high–tech tool, electroencephalography (EEG), records the brain’s electrical signals (41). Small electrodes are placed on the scalp to detect this electrical activity, which then is magnified and graphed as brain waves (i.e., neural oscillations). These brain waves show real–time activity as it happens in the brain. Many male alcoholics have a distinctive electrophysiological profile—that is, a low amplitude of their P3 components (see figure). P3 amplitudes in women alcoholics also are reduced, although to a lesser extent than in men. For many years it was assumed that the P3 deficit observed in alcoholics was the result of alcohol’s damage to the brain. Then it was determined that while many of the clinical symptoms and electrophysiological measures associated with alcoholism return to normal after abstinence, the P3 amplitude abnormality persists (42). The P3 component is reduced in alcoholics compared with control subjects. This continued deficit in long–term abstinent alcoholics suggests that P3 deficits may be a marker of risk for alcohol dependence, rather than a result of alcohol use. In fact, a number of studies have since reported low P3 amplitudes in young people who have not started drinking alcohol but who are at high risk for developing alcoholism, such as young sons of alcoholic fathers (43,44). Markers such as the P3 can help identify people who may be at greatest risk for developing problems with alcohol. END OF SIDEBAR

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Resources

Source material for this Alcohol Alert originally appeared in the journal Alcohol Research & Health, “Alcoholic Brain Damage” (Vol. 27, No. 2, 2003). Alcohol Research and Health is the quarterly, peer–reviewed journal published by the National Institute on Alcohol Abuse and Alcoholism. Each issue of AR&H provides in–depth focus on a single topic in the field of alcohol research. Back issues of Alcohol Research & Health and additional resources can be downloaded from NIAAA’s Web site, www.niaaa.nih.gov. Subscriptions are available from the Superintendent of Documents for $25. Write to New Orders, Superintendent of Documents, P.O. Box 371954, Pittsburgh, PA 15250–7954; or fax 202/512–2250.

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Prepared: October 2004

Source:
ALCOHOL'S DAMAGING EFFECTS ON THE BRAIN

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