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Does sugar addiction change your brain molecules?

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Sugar can be addictive, a Princeton University The scientist says as animal studies show sugar dependence. sugar-bingeing, undergo neurochemical changes in the brain that appear to mimic those produced by substances of abuse, including cocaine, morphine and nicotine. Sugar induces behavioral changes, too. A rat in a recent experiment pushed a leaver 320 times in a short space of time to get sugar. The molecules in the creature's brain were changed by sugar that hooked the animal on the sweet taste so that it craved sweet taste more than anything more nourishing. And tumors love sugar so much that in one type of test to see where a tumor or cancer is located in the body, physicians put a type of sugar solution into the body that quickly gets taken in by the tumor. That way scientists can locate where in the body a tumor is that might otherwise be hidden from visibility. You can check out the study, "Sugar and Fat Bingeing Have Notable Differences in Addictive-like Behavior," appearing online January 28, 2009 and in print March 2009 in the Journal of Nutrition.

A type of tumor or cancer grows, divides, and spreads by consuming sugar/glucose in the body. The old adage cancer loves sugar has shown up in experiments. And in a 2008 study, a Princeton University scientist presented new evidence demonstrating that sugar can be an addictive substance, wielding its power over the brains of lab animals in a manner similar to many drugs of abuse, according to a December 10, 2008 news release, "Sugar can be addictive, Princeton scientist says." You also can check out a Forbes article, "What Eating Too Much Sugar Does to Your Brain."

Professor Bart Hoebel and his team in the Department of Psychology and the Princeton Neuroscience Institute have been studying signs of sugar addiction in rats for years

Until now, the rats under study have met two of the three elements of addiction. They have demonstrated a behavioral pattern of increased intake and then showed signs of withdrawal. His current experiments captured craving and relapse to complete the picture.

"If bingeing on sugar is really a form of addiction, there should be long-lasting effects in the brains of sugar addicts," Hoebel said, according to the December 10, 2008 news release, Sugar can be addictive, Princeton scientist says. "Craving and relapse are critical components of addiction, and we have been able to demonstrate these behaviors in sugar-bingeing rats in a number of ways."

At the 2008 annual meeting of the American College of Neuropsychopharmacology in Scottsdale, Ariz., Hoebel reported on profound behavioral changes in rats that, through experimental conditions, have been trained to become dependent on high doses of sugar

"We have the first set of comprehensive studies showing the strong suggestion of sugar addiction in rats and a mechanism that might underlie it," Hoebel said, according to the news release. The findings eventually could have implications for the treatment of humans with eating disorders, he explained, according to the news release. Lab animals, in Hoebel's experiments, that were denied sugar for a prolonged period after learning to binge worked harder to get it when it was reintroduced to them.

The lab animal's motivation for sugar had grown. "In this case, abstinence makes the heart grow fonder," Hoebel said, according to the news release. The rats drank more alcohol than normal after their sugar supply was cut off, showing that the bingeing behavior had forged changes in brain function. Sugar had actually changed the molecules in the brains of the lab animals in that experiment.

These functions served as "gateways" to other paths of destructive behavior, such as increased alcohol intake. And, after receiving a dose of amphetamine normally so minimal it has no effect, they became significantly hyperactive. The increased sensitivity to the psychostimulant is a long-lasting brain effect that can be a component of addiction, Hoebel said, according to the news release.

The lab animals consumed more sugar than they ever had before, suggesting craving and relapse behavior

The data presented at the 2008 meeting by Hoebel is contained in a research paper appearing in The Journal of Nutrition. Visiting researchers Nicole Avena, who earned her Ph.D. from Princeton in 2006, and Pedro Rada from the University of Los Andes in Venezuela wrote the paper with Hoebel.

Hoebel has been interested in the brain mechanisms that control appetite and body weight since he was an undergraduate at Harvard University studying with the renowned behaviorist B.F. Skinner. On the Princeton faculty since 1963, he has pioneered studies into the mental rewards of eating. Over the past decade, Hoebel has led work that has now completed an animal model of sugar addiction.

Hoebel has shown that rats eating large amounts of sugar when hungry, a phenomenon he describes as sugar-bingeing, undergo neurochemical changes in the brain that appear to mimic those produced by substances of abuse, including cocaine, morphine and nicotine. Sugar induces behavioral changes, too. "In certain models, sugar-bingeing causes long-lasting effects in the brain and increases the inclination to take other drugs of abuse, such as alcohol," Hoebel said, according to the news release.

Hoebel and his team also have found that a chemical known as dopamine is released in a region of the brain known as the nucleus accumbens when hungry rats drink a sugar solution. This chemical signal is thought to trigger motivation and, eventually with repetition, addiction

The researchers conducted the studies by restricting rats of their food while the rats slept and for four hours after waking. "It's a little bit like missing breakfast," Hoebel said. "As a result, they quickly eat some chow and drink a lot of sugar water." And, he added, "That's what is called binge eating -- when you eat a lot all at once -- in this case they are bingeing on a 10 percent sucrose solution, which is like a soft drink."

Hungry rats that binge on sugar provoke a surge of dopamine in their brains. After a month, the structure of the brains of these rats adapts to increased dopamine levels, showing fewer of a certain type of dopamine receptor than they used to have and more opioid receptors. These dopamine and opioid systems are involved in motivation and reward, systems that control wanting and liking something. Similar changes also are seen in the brains of rats on cocaine and heroin.

In experiments, the researchers have been able to induce signs of addiction withdrawal in the lab animals by taking away their sugar supply

The rats' brain levels of dopamine dropped and, as a result, they exhibited anxiety as a sign of withdrawal. The rats' teeth chattered, and the creatures were unwilling to venture forth into the open arm of their maze, preferring to stay in a tunnel area. Normally rats like to explore their environment, but the rats in sugar withdrawal were too anxious to explore.

The findings are exciting, Hoebel said, but more research is needed to understand the implications for people. The most obvious application for humans would be in the field of eating disorders.

"It seems possible that the brain adaptations and behavioral signs seen in rats may occur in some individuals with binge-eating disorder or bulimia," Hoebel said, according to the news release. "Our work provides links between the traditionally defined substance-use disorders, such as drug addiction, and the development of abnormal desires for natural substances. This knowledge might help us to devise new ways of diagnosing and treating addictions in people."

Faulty signaling in brain increases craving for sugar and drugs

In another study, "Enhanced Sucrose and Cocaine Self-Administration and Cue-Induced Drug Seeking after Loss of VGLUT2 in Midbrain Dopamine Neurons in Mice," (Abbreviated title: A role in reward for VGLUT2 in dopamine neurons), published in the The Journal of Neuroscience, August 31, 2011, researchers in that study demonstrated that the absence of VGLUT2 in DA neurons leads to perturbations of reward consumption as well as reward-associated memory, features of particular relevance for addictive-like behavior

"Our data indicate that the brain becomes hypersensitive to rewards when this co-signaling of glutamate and dopamine does not function. Lower doses than normal are enough to increase the propensity to ingest the substance, and this is true of both sugar and cocaine," said Åsa Mackenzie, associate professor of neuroscience at Uppsala University and the researcher who led this other study, according to an August 30, 2011 news release, "Got sugar? Glucose affects our ability to resist temptation."

Addiction disorders are a major social problem, and we lack sufficient knowledge of how they arise and how various substances impact the brain. The brain's reward system gives us feelings of pleasure and happiness, for example when we have eaten or drunk something good, had sex, or worked out.

Brain's reward system can be kidnapped by other rewarding substances

This pleasure arises when certain signal substances, primarily dopamine, are released in the brain. But this reward system can be "kidnapped" by other rewarding substances, such as alcohol and abuser drugs like cocaine. They provide feelings of reward initially, but they are so strong that nerve cells in the system are rewired, and addiction occurs. More natural substance, such as food rich in sugar, can also produce addiction-like conditions.

The Uppsala University researchers and their colleagues have recently shown that dopamine cells in the reward system can send signals in cooperation with glutamate, so called co-signaling. Its physiological role was not previously known, however. For instance, how important is it for the inclination to ingest reward substances?

In studies of mice that lack the ability to send the above signals because their glutamate transporter, so-called VGLUT, has been inactivated, the scientists studied how prone the mice were to ingest sugar and cocaine. The results showed that they both ingested more and responded to lower dosages than control mice.

Since there is a strong correlation between memory and consumption substances, and ultimately also for the risk of addiction, the researchers also looked into this

The researchers are able to present the interesting finding from the study that mice that lack the ability to co-signal developed dramatically improved memory of environments that could be associated with the ingestion of drugs. They also found changes in genetic expressions in the reward system that indicate that the brain has become hypersensitive and that dopamine levels have dropped.

"This is extremely interesting, but more research is needed in order to understand how this can be used in drug development, for instance," said Åsa Mackenzie, according to the August 30, 2011 news release, "Got sugar? Glucose affects our ability to resist temptation." These scientists have now gone on to study these mechanisms in connection with abuse in humans and are looking for direct connections between low VGLUT levels and addiction. Authors of that study are: Johan Alsiö, Karin Nordenankar, Emma Arvidsson, Carolina Birgner, Souha Mahmoudi, Briac Halbout, Casey Smith, Guillaume M. Fortin, Lars Olson, Laurent Descarries, Louis Éric Trudeau, Klas Kullander, Daniel Lévesque, and Åsa Wallén-Mackenzie. You also may wish to see another website, "How Blood Sugar Works."

There's too much sugar in a lot of foods most people think is healthy

You can check out the April 17, 2014 news article by Kristina Bravo, "12 Surprising Foods With More Sugar Than a Krispy Kreme Doughnut," which explains that 71.4 percent of American adults allot more room for processed sugar in their caloric intake than the recommended 10 percent—and the World Health Organization cut the recommendation to 5 percent last month. Even that glass of fruit juice may have 22 to 37 grams of sugar, or more, since the fiber from the fruit is removed.

So the juice hits your bloodstream with a surge of glucose followed perhaps by a high spike of insulin that could age out your arteries prematurely. But the idea is to hook you on sugar so that you crave the sweetness, even if you can't taste it in the food. Then you'll probably come back and buy more in one form or another.

Food named in the article include Naked Juice's pomegranate-blueberry, 32 grams sugar. The photos also show a cupcake, Sprinkles Red Velvet Cupcake, 45 grams sugar, Yoplait yogurt's fat-free, original blackberry harvest, 26 grams sugar, Campbell's classic Tomato Soup, 20 grams sugar, Natural Valley trail mix - fruit and nut, 13 grams sugar, Dole mixed fruit (container), 17 grams sugar, Coca-Cola classic, 26.4 grams sugar, Kellog's Fruit Loops (cereal), 12 grams sugar, Starbucks Caramel Frappuccino (64 grams of sugar), Prego Fresh Mushroom Italian Sauce, 11 grams sugar, and Kraft French Style Fat Free Dressing, 42 grams sugar. And those foods mentioned in that article are only a few of the thousands of processed foods on most supermarket shelves.

The sad fact is that an individual's maternal diet sets up junk food addiction in babies, according to recent research. You may wish to check out the news release, " Maternal diet sets up junk food addiction in babies." Research from the University of Adelaide suggests that mothers who eat junk food while pregnant have already programmed their babies to be addicted to a high fat, high sugar diet by the time they are weaned, according to that study. In laboratory studies, the researchers found that a junk food diet during pregnancy and lactation desensitised the normal reward system fuelled by these highly palatable foods. Mothers eating a lot of junk food while pregnant are setting up their children to be addicted, the news release explained.

Quantity of sugar in food supply linked to diabetes rates, Stanford researcher says

Worse yet when it comes to eating too much sugar, another study, "The Relationship of Sugar to Population-Level Diabetes Prevalence: An Econometric Analysis of Repeated Cross-Sectional Data ," published online February 27, 2013 in the journal PLOS ONE, links the quantity in food supplies to diabetes rates. Does eating too much sugar cause diabetes? For years, scientists have said "not exactly." Eating too much of any food, including sugar, can cause you to gain weight. It's the resulting obesity that predisposes people to diabetes, according to the prevailing theory. But now the results of a large epidemiological study suggest sugar also may have a direct, independent link to diabetes.

Researchers from the Stanford University School of Medicine, the University of California-Berkeley and the University of California-San Francisco examined data on sugar availability and diabetes rates from 175 countries over the past decade. After accounting for obesity and a large array of other factors, the researchers found that increased sugar in a population's food supply was linked to higher diabetes rates, independent of obesity rates.

"It was quite a surprise," said Sanjay Basu, MD, PhD, according to the February 27, 2013 news release, "Quantity of sugar in food supply linked to diabetes rates, Stanford researcher says." Basu is an assistant professor of medicine at the Stanford Prevention Research Center and the study's lead author. The research was conducted while Basu was a medical resident at UCSF.

The study provides the first large-scale, population-based evidence for the idea that not all calories are equal from a diabetes-risk standpoint, Basu said. "We're not diminishing the importance of obesity at all, but these data suggest that at a population level there are additional factors that contribute to diabetes risk besides obesity and total calorie intake, and that sugar appears to play a prominent role."

Specifically, more sugar was correlated with more diabetes

For every additional 150 calories of sugar available per person per day, the prevalence of diabetes in the population rose 1 percent, even after controlling for obesity, physical activity, other types of calories and a number of economic and social variables. A 12-ounce can of soda contains about 150 calories of sugar. In contrast, an additional 150 calories of any type caused only a 0.1 percent increase in the population's diabetes rate.

Not only was sugar availability correlated to diabetes risk, but the longer a population was exposed to excess sugar, the higher its diabetes rate after controlling for obesity and other factors. In addition, diabetes rates dropped over time when sugar availability dropped, independent of changes to consumption of other calories and physical activity or obesity rates.

Findings didn't prove sugar causes diabetes, but sugar affects the liver and pancreas in ways that other foods or obesity don't

The findings do not prove that sugar causes diabetes, Basu emphasized, but do provide real-world support for the body of previous laboratory and experimental trials that suggest sugar affects the liver and pancreas in ways that other types of foods or obesity do not. "We really put the data through a wringer in order to test it out," Basu said, according to the February 27, 2013 news release, "Quantity of sugar in food supply linked to diabetes rates, Stanford researcher says."

The study used food-supply data from the United Nations Food and Agricultural Organization to estimate the availability of different foods in the 175 countries examined, as well as estimates from the International Diabetes Foundation on the prevalence of diabetes among 20- to 79-year-olds. Researchers employed new statistical methods derived from econometrics to control for factors that could provide alternate explanations for an apparent link between sugar and diabetes, including overweight and obesity.

Many non-sugar components of the food supply, such as fiber, fruit, meat, cereals and oils; total calories available per day; sedentary behavior; rates of economic development; household income; urbanization of the population; tobacco and alcohol use; and percentage of the population age 65 or older, since age is also associated with diabetes risk. "Epidemiology cannot directly prove causation," said Robert Lustig, MD, according to the news release.

Lustig is a pediatric endocrinologist at University of California, San Francisco Benioff Children's Hospital and the senior author of the study. "But in medicine, we rely on the postulates of Sir Austin Bradford Hill to examine associations to infer causation, as we did with smoking. You expose the subject to an agent, you get a disease; you take the agent away, the disease gets better; you re-expose and the disease gets worse again. This study satisfies those criteria, and places sugar front and center."

"As far as I know, this is the first paper that has had data on the relationship of sugar consumption to diabetes," said Marion Nestle, PhD, according to the news release. Nestle is a professor of nutrition, food studies and public health at New York University who was not involved in the study. "This has been a source of controversy forever. It's been very, very difficult to separate sugar from the calories it provides. This work is carefully done, it's interesting and it deserves attention."

The fact that the paper used data obtained over time is an important strength, Basu said, according to the news release. "Point-in-time studies are susceptible to all kinds of reverse causality," he said. "For instance, people who are already diabetic or obese might eat more sugars due to food cravings."

The researchers had to rely on food-availability data for this study instead of consumption data because no large-scale international databases exist to measure food consumption directly. Basu said that follow-up studies are needed to examine possible links between diabetes and specific sugar sources, such as high-fructose corn syrup or sucrose, and also to evaluate the influence of specific foods, such as soft drinks or processed foods. Regarding studies on liver damage and the link to fructose, see, the June 27, 2013 article, "Dietary fructose linked to liver damage by gut bacteria mechanism."

Would a low-sugar diet reduce diabetes risk?

Another important future step, he said, is to conduct randomized clinical trials that could affirm a cause-and-effect connection between sugar consumption and diabetes. Although it would be unethical to feed people large amounts of sugar to try to induce diabetes, scientists could put participants of a study on a low-sugar diet to see if it reduces diabetes risk.

Basu was cautious about possible policy implications of his work, stating that more evidence is needed before enacting widespread policies to lower sugar consumption. However, Nestle pointed out that the findings add to many other studies that suggest people should cut back on their sugar intake. "How much circumstantial evidence do you need before you take action?" she said. "At this point we have enough circumstantial evidence to advise people to keep their sugar a lot lower than it normally is." This study received no external funding. Information about Stanford's Department of Medicine is available at the school's website.

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